[Federal Register Volume 79, Number 242 (Wednesday, December 17, 2014)]
[Proposed Rules]
[Pages 75233-75411]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2014-28674]



[[Page 75233]]

Vol. 79

Wednesday,

No. 242

December 17, 2014

Part II





Environmental Protection Agency





-----------------------------------------------------------------------





40 CFR Parts 50, 51, 52, et al.





-----------------------------------------------------------------------





National Ambient Air Quality Standards for Ozone; Proposed Rule

Federal Register / Vol. 79 , No. 242 / Wednesday, December 17, 2014 / 
Proposed Rules

[[Page 75234]]


-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 52, 53, and 58

[EPA-HQ-OAR-2008-0699; FRL-9918-43-OAR]
RIN 2060-AP38


National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency.

ACTION: Proposed rule.

-----------------------------------------------------------------------

SUMMARY: Based on its review of the air quality criteria for ozone 
(O3) and related photochemical oxidants and national ambient 
air quality standards (NAAQS) for O3, the Environmental 
Protection Agency (EPA) proposes to make revisions to the primary and 
secondary NAAQS for O3 to provide requisite protection of 
public health and welfare, respectively. The EPA is proposing to revise 
the primary standard to a level within the range of 0.065 to 0.070 
parts per million (ppm), and to revise the secondary standard to within 
the range of 0.065 to 0.070 ppm, which air quality analyses indicate 
would provide air quality, in terms of 3-year average W126 index 
values, at or below a range of 13-17 ppm-hours. The EPA proposes to 
make corresponding revisions in data handling conventions for 
O3 and conforming changes to the Air Quality Index (AQI); to 
revise regulations for the prevention of significant deterioration 
(PSD) program to add a transition provision for certain applications; 
and to propose schedules and convey information related to implementing 
any revised standards. The EPA is proposing changes to the 
O3 monitoring seasons, the Federal Reference Method (FRM) 
for monitoring O3 in the ambient air, Federal Equivalent 
Method (FEM) procedures for testing, and the Photochemical Assessment 
Monitoring Stations (PAMS) network.
    Along with proposing exceptional event schedules related to 
implementing any revised O3 standards, the EPA is proposing 
to apply this same schedule approach to other future revised NAAQS and 
to remove obsolete regulatory language for expired exceptional event 
deadlines. The EPA is proposing to make minor changes to the procedures 
and time periods for evaluating potential FRMs and equivalent methods 
(including making the requirements for nitrogen dioxide consistent with 
the requirements for O3) and to remove an obsolete 
requirement for the annual submission of documentation by manufacturers 
of certain particulate matter monitors. For additional information, see 
the Executive Summary, section I.A.

DATES: Written comments on this proposed rule must be received by March 
17, 2015.
    Public Hearings: The EPA intends to hold three public hearings on 
this proposed rule in January 2015. These will be announced in a 
separate Federal Register notice that provides details, including 
specific dates, times, addresses, and contact information for these 
hearings.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2008-0699, to the EPA by one of the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the online instructions for submitting comments.
     Email: A-and-R-Docket@epa.gov. Include docket ID No. EPA-
HQ-OAR-2008-0699 in the subject line of the message.
     Fax: (202) 566-9744.
     Mail: Environmental Protection Agency, EPA Docket Center 
(EPA/DC), Mailcode 28221T, Attention Docket ID No. OAR-2008-0699, 1200 
Pennsylvania Ave. NW., Washington, DC 20460. Please include a total of 
two copies.
     Hand/Courier Delivery: EPA Docket Center, Room 3334, EPA 
WJC West Building, 1301 Constitution Ave. NW., Washington, DC. Such 
deliveries are only accepted during the Docket's normal hours of 
operation, and special arrangements should be made for deliveries of 
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2008-0699. The EPA's policy is that all comments received will be 
included in the public docket without change and may be made available 
online at www.regulations.gov, including any personal information 
provided, unless the comment includes information claimed to be 
Confidential Business Information (CBI) or other information whose 
disclosure is restricted by statute. Do not submit information that you 
consider to be CBI or otherwise protected through www.regulations.gov 
or email. The www.regulations.gov Web site is an ``anonymous access'' 
system, which means the EPA will not know your identity or contact 
information unless you provide it in the body of your comment. If you 
send an email comment directly to the EPA without going through 
www.regulations.gov your email address will be automatically captured 
and included as part of the comment that is placed in the public docket 
and made available on the Internet. If you submit an electronic 
comment, the EPA recommends that you include your name and other 
contact information in the body of your comment and with any disk or 
CD-ROM you submit. If the EPA cannot read your comment due to technical 
difficulties and cannot contact you for clarification, the EPA may not 
be able to consider your comment. Electronic files should avoid the use 
of special characters, any form of encryption, and be free of any 
defects or viruses. For additional information about EPA's public 
docket visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
    Docket: The EPA has established dockets for these actions as 
discussed above. All documents in these dockets are listed on the 
www.regulations.gov Web site. This includes documents in the rulemaking 
docket (Docket ID No. EPA-HQ-OAR-2008-0699) and a separate docket, 
established for the Integrated Science Assessment (ISA) (Docket No. 
EPA-HQ-ORD-2011-0050) that has have been incorporated by reference into 
the rulemaking docket. Although listed in the index, some information 
is not publicly available, e.g., CBI or other information whose 
disclosure is restricted by statute. Certain other material, such as 
copyrighted material, is not placed on the Internet and may be viewed, 
with prior arrangement, at the EPA Docket Center. Publicly available 
docket materials are available either electronically in 
www.regulations.gov or in hard copy at the Air and Radiation Docket and 
Information Center, EPA/DC, EPA WJC West Building, Room 3334, 1301 
Constitution Ave. NW., Washington, DC. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744 and the telephone number for the Air and Radiation Docket and 
Information Center is (202) 566-1742. For additional information about 
EPA's public docket visit the EPA Docket Center homepage at: http://www.epa.gov/epahome/dockets.htm.

FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards, U.S. Environmental Protection Agency, Mail code C504-06, 
Research Triangle Park, NC 27711; telephone: (919) 541-1146; fax: (919) 
541-0237; email: stone.susan@epa.gov.

SUPPLEMENTARY INFORMATION:

[[Page 75235]]

General Information

What should I consider as I prepare my comments for EPA?

    1. Submitting CBI. Do not submit this information to the EPA 
through www.regulations.gov or email. Clearly mark the part or all of 
the information that you claim to be CBI. For CBI information in a disk 
or CD ROM that you mail to EPA, mark the outside of the disk or CD ROM 
as CBI and then identify electronically within the disk or CD ROM the 
specific information that is claimed as CBI. In addition to one 
complete version of the comment that includes information claimed as 
CBI, a copy of the comment that does not contain the information 
claimed as CBI must be submitted for inclusion in the public docket. 
Information so marked will not be disclosed except in accordance with 
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments, 
remember to:
     Identify the rulemaking by docket number and other 
identifying information (subject heading, Federal Register date and 
page number).
     Follow directions--The agency may ask you to respond to 
specific questions or organize comments by referencing a Code of 
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives, 
and substitute language for your requested changes.
     Describe any assumptions and provide any technical 
information and/or data that you used.
     Provide specific examples to illustrate your concerns, and 
suggest alternatives.
     Explain your views as clearly as possible, avoiding the 
use of profanity or personal threats.
     Make sure to submit your comments by the comment period 
deadline identified.

Availability of Related Information

    A number of documents relevant to this rulemaking are available on 
EPA Web sites. The ISA for Ozone and Related Photochemical Oxidants is 
available on the EPA's National Center for Environmental Assessment 
(NCEA) Web site. To obtain this document, go to http://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open a 
page with a link to the February 2013 ISA. The 2014 Policy Assessment 
(PA), Health and Welfare Risk and Exposure Assessments (HREA and WREA, 
respectively), and other related technical documents are available on 
EPA's Office of Air Quality Planning and Standards (OAQPS) Technology 
Transfer Network (TTN) Web site. The final 2014 PA is available at: 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pa.html, and the 
final 2014 Health and Welfare Risk and Exposure Assessments and other 
related technical documents are available at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_rea.html. These and other related 
documents are also available for inspection and copying in the EPA 
docket identified above.

Environmental Justice

    Analyses evaluating the potential implications of a revised 
O3 NAAQS for environmental justice populations are discussed 
in appendix 9A of the Regulatory Impact Analysis (RIA) that accompanies 
this notice of proposed rulemaking. The RIA is available on the Web, 
through the EPA's Technology Transfer Network Web site at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html.

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Executive Summary
    B. Legislative Requirements
    C. Related Control Programs To Implement O3 Standards
    D. Review of Air Quality Criteria and Standards for 
O3
    E. Ozone Air Quality
II. Rationale for Proposed Decision on the Primary Standard
    A. Approach
    B. Health Effects Information
    1. Overview of Mechanisms
    2. Nature of Effects
    3. Adversity of O3 Effects
    4. Ozone-Related Impacts on Public Health
    C. Human Exposure and Health Risk Assessments
    1. Air Quality Adjustment
    2. Exposure Assessment
    3. Quantitative Health Risk Assessments
    D. Conclusions on the Adequacy of the Current Primary Standard
    1. Summary of Evidence-Based Considerations in the PA
    2. Summary of Exposure- and Risk-Based Considerations in the PA
    3. Policy Assessment Conclusions on the Current Standard
    4. CASAC Advice
    5. Administrator's Proposed Conclusions Concerning the Adequacy 
of the Current Standard
    E. Conclusions on the Elements of the Primary Standard
    1. Indicator
    2. Averaging Time
    3. Form
    4. Level
    F. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
    A. Approach
    B. Welfare Effects Information
    1. Nature of Effects and Biologically Relevant Exposure Metric
    2. Potential Impacts on Public Welfare
    C. Exposure and Risk Assessment Information
    1. Air Quality Analyses
    2. Tree Seedling Growth, Productivity, Carbon Storage and 
Associated Ecosystem Services
    3. Crop Yield
    4. Visible Foliar Injury
    D. Conclusions on Adequacy of the Current Secondary Standard
    1. Evidence- and Exposure/Risk-Based Considerations in the 
Policy Assessment
    2. CASAC Advice
    3. Administrator's Proposed Conclusions on Adequacy of the 
Current Standard
    E. Consideration of Alternative Secondary Standards
    1. Indicator
    2. Consideration of a Cumulative, Seasonal Exposure-based 
Standard in the Policy Assessment
    3. CASAC Advice
    4. Air Quality Analyses
    5. Administrator's Proposed Conclusions
    F. Proposed Decision on the Secondary Standard
V. Appendix U: Interpretation of the Primary and Secondary NAAQS for 
O3
    A. Background
    B. Data Selection Requirements
    C. Data Reporting and Data Handling Requirements
    D. Considerations for the Possibility of a Distinct Secondary 
Standard
    E. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to Proposed O3 Standards
    A. Background
    B. Revisions to the Length of the Required O3 
Monitoring Seasons
    C. Revisions to the Photochemical Assessment Monitoring Stations 
(PAMS)
    1. Network Design
    2. Speciated VOC Measurements
    3. Carbonyl Sampling
    4. Nitrogen Oxides Sampling
    5. Meteorology Measurements
    6. PAMS Season
    7. Timing and Other Implementation Issues
    D. Addition of a New Federal Reference Method (FRM) for 
O3
    E. Revisions to the Procedures for Testing Performance 
Characteristics and Determining Comparability Between Candidate 
Methods and Reference Methods
VII. Implementation of Proposed O3 Standards
    A. NAAQS Implementation Plans
    1. Background
    2. Timing of Rules and Guidance
    3. Section 110 State Implementation Plans
    4. Nonattainment Area Requirements
    B. Implementing a Distinct Secondary O3 NAAQS, if One 
is Established
    C. Designation of Areas

[[Page 75236]]

    D. Prevention of Significant Deterioration and Nonattainment New 
Source Review Programs for the Proposed Revised Primary and 
Secondary O3 NAAQS
    1. Prevention of Significant Deterioration (PSD)
    2. Nonattainment New Source Review
    E. Transportation and General Conformity Programs
    1. What are transportation and general conformity?
    2. Why is the EPA discussing transportation and general 
conformity in this proposed rulemaking?
    3. When would transportation and general conformity apply to 
areas designated nonattainment for a revised O3 NAAQS, if 
one is established?
    4. Will transportation and general conformity apply to a 
distinct secondary O3 NAAQS, if one is established?
    5. What impact would the implementation of a revised 
O3 NAAQS have on a State's transportation and/or general 
conformity SIP?
    F. How Background O3 Is Addressed in CAA 
Implementation Provisions
    1. Introduction
    2. Exceptional Events Exclusions
    3. Rural Transport Areas
    4. International Transport
VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review and 
Executive Order 13563: Improving Regulation and Regulatory Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With 
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From 
Environmental Health & Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect 
Energy Supply, Distribution, or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions To Address 
Environmental Justice in Minority Populations and Low-Income 
Populations
References

I. Background

A. Executive Summary

    This section summarizes information about the purpose of this 
regulatory action (I.A.1), the major provisions of this proposal 
(I.A.2), and provisions related to implementation (I.A.3).
1. Purpose of This Regulatory Action
    Sections 108 and 109 of the Clean Air Act (CAA) govern the 
establishment, review, and revision, as appropriate, of the NAAQS to 
protect public health and welfare. The CAA requires the EPA to 
periodically review the air quality criteria--the science upon which 
the standards are based--and the standards themselves. This rulemaking 
is being conducted pursuant to these statutory requirements. The 
schedule for completing this review is established by a federal court 
order, which requires that the EPA sign a proposal by December 1, 2014, 
and make a final determination by October 1, 2015.
    The EPA completed its most recent review of the O3 NAAQS 
in 2008. As a result of that review, EPA took four principal actions: 
(1) Revised the level of the 8-hour primary O3 standard to 
0.075 parts per million (ppm); (2) expressed the standard to three 
decimal places; (3) revised the 8-hour secondary O3 standard 
by making it identical to the revised primary standard; and (4) made 
conforming changes to the AQI for O3.
    In subsequent litigation, the U.S. Court of Appeals for the 
District of Columbia Circuit upheld the EPA's 2008 primary 
O3 standard, but remanded the 2008 secondary standard. State 
of Mississippi v. EPA, 744 F. 3d 1334 (D.C. Cir. 2013). With respect to 
the primary standard, the court held that the EPA reasonably determined 
that the existing primary standard, set in 1997, did not protect public 
health with an adequate margin of safety and required revision. In 
upholding the EPA's revised primary standard, the court dismissed 
arguments that the EPA should have adopted a more stringent standard. 
The court remanded the secondary standard to the EPA after rejecting 
the EPA's explanation for setting the secondary standard identical to 
the revised 8-hour primary standard. The court held that because the 
EPA had failed to identify a level of air quality requisite to protect 
public welfare, the EPA's comparison between the primary and secondary 
standards for determining if requisite protection for public welfare 
was afforded by the primary standard failed to comply with the CAA.
    This proposal reflects the Administrator's proposed conclusions 
based on a review of the O3 NAAQS that began in September 
2008. In conducting this review, the EPA has carefully evaluated the 
currently available scientific literature on the health and welfare 
effects of ozone, focusing particularly on the new literature available 
since the conclusion of the previous review in 2008. In addition, the 
EPA has also addressed the remand of the Agency's 2008 decision on the 
secondary standard. Between 2008 and 2014, the EPA prepared draft and 
final versions of the Integrated Science Assessment, the Health and 
Welfare Risk and Exposure Assessments, and the Policy Assessment. 
Multiple drafts of these documents were available for public review and 
comment, and as required by the CAA, were peer-reviewed by the Clean 
Air Scientific Advisory Committee (CASAC), an independent scientific 
advisory committee established by the CAA and charged with providing 
advice to the Administrator. The final documents reflect the EPA 
staff's consideration of the comments and recommendations made by CASAC 
and the public on draft versions of these documents.
2. Summary of Major Provisions
    The EPA is proposing that the current primary O3 
standard set at a level of 0.075 ppm is not requisite to protect public 
health with an adequate margin of safety, and that it should be revised 
to provide increased public health protection. Specifically, the EPA is 
proposing to retain the indicator (ozone), averaging time (8-hour) and 
form (annual fourth-highest daily maximum, averaged over 3 years) of 
the existing primary O3 standard and is proposing to revise 
the level of that standard to within the range of 0.065 ppm to 0.070 
ppm. The EPA is proposing this revision to increase public health 
protection, including for ``at-risk'' populations such as children, 
older adults, and people with asthma or other lung diseases, against an 
array of O3-related adverse health effects. For short-term 
O3 exposures, these effects include decreased lung function, 
increased respiratory symptoms and pulmonary inflammation, effects that 
result in serious indicators of respiratory morbidity such as emergency 
department visits and hospital admissions, and all-cause (total 
nonaccidental) mortality. For long-term O3 exposures, these 
health effects include a variety of respiratory morbidity effects and 
respiratory mortality. Recognizing that the CASAC recommended a range 
of levels from 0.060 ppm to 0.070 ppm, and that levels as low as 0.060 
ppm could potentially be supported, the Administrator solicits comment 
on alternative standard levels below 0.065 ppm, and as low as 0.060 
ppm. However, the Administrator notes that setting a standard below 
0.065 ppm, down to 0.060 ppm, would inappropriately place very little 
weight on the uncertainties in the health effects evidence and 
exposure/risk information. Given alternative views of the currently 
available evidence and information expressed by some commenters, the 
EPA is taking comment on both the Administrator's proposed decision to 
revise the current primary O3 standard and the option of 
retaining that standard.
    In addition to proposing changes to the level of the standard, the 
EPA is

[[Page 75237]]

proposing conforming changes to the Air Quality Index (AQI) by 
proposing to set an AQI value of 100 equal to the level of the 8-hour 
primary O3 standard, and proposing adjustments to the AQI 
values of 50, 150, 200 and 300.
    The EPA also proposes to revise the secondary standard to provide 
increased protection against vegetation-related effects on public 
welfare. As an initial matter, the Administrator proposes to conclude 
that air quality in terms of a three-year average seasonal W126 index 
value, based on the three consecutive month period within the 
O3 season with the maximum index value, with daily exposures 
cumulated for the 12-hour period from 8:00 a.m. to 8:00 p.m., within 
the range from 13 ppm-hrs to 17 ppm-hrs would provide the requisite 
protection against known or anticipated adverse effects to the public 
welfare. The EPA solicits comment on this proposed conclusion. In 
considering how to achieve that level of air quality, the Administrator 
recognizes that air quality data analyses suggest that air quality in 
terms of three-year average W126 index values of a range at or below 13 
to 17 ppm-hrs would be provided by a secondary standard level within 
the range of 0.065 to 0.070 ppm, and that to the extent areas need to 
take action to attain a standard in the range of 0.065 to 0.070 ppm, 
those actions would also improve air quality as measured by the W126 
metric. Thus, the Administrator proposes to revise the level of the 
current secondary standard to within the range of 0.065 to 0.070 ppm. 
The EPA solicits comments on this proposed revision of the secondary 
standard.
    The EPA also solicits comments on the alternative approach of 
revising the secondary standard to a W126-based form, averaged over 
three years, with a level within the range of 13 ppm-hrs to 17 ppm-hrs. 
The EPA additionally solicits comments on such a distinct secondary 
standard with a level within the range extending below 13 ppm-hrs down 
to 7 ppm-hrs. Further, the EPA solicits comments on retaining the 
current secondary standard without revision, along with the alternative 
views of the evidence that would support retaining the current 
standard.
3. Provisions Related to Implementation
    As directed by the CAA, reducing pollution to meet national air 
quality standards always has been a shared task, one involving the 
federal government, states, tribes and local air agencies. This 
partnership has proved effective since the EPA first issued 
O3 standards more than three decades ago, and is evidenced 
by significantly lower O3 levels throughout the country. To 
provide a foundation that helps air agencies build successful 
strategies for attaining new O3 standards, the EPA will 
continue to move forward with federal regulatory programs, such as the 
proposed Clean Power Plan and the final Tier 3 motor vehicle emissions 
standards. To facilitate the development of CAA-compliant 
implementation plans and strategies to attain new standards, the EPA 
intends to issue timely and appropriate implementation guidance and, 
where appropriate and consistent with the law, new rulemakings to 
streamline regulatory burdens and provide flexibility in 
implementation. In addition, given the regional nature of O3 
air pollution, the EPA will continue to work with states to address 
interstate transport of O3 and O3 precursors.
    This notice contains several proposed provisions related to 
implementation of the proposed standards. In addition to revisions to 
the primary and secondary NAAQS, the EPA is proposing to make 
corresponding revisions in data handling conventions for O3; 
to revise regulations for the Prevention of Significant Deterioration 
(PSD) permitting program to add a provision grandfathering certain 
pending permits from certain requirements with respect to the proposed 
revisions to the O3 NAAQS; and to convey schedules and 
information related to implementing any revised standards.
    In conjunction with proposing exceptional event schedules related 
to implementing any revised O3 standards, the EPA is also 
proposing to extend the new schedule approach to other future revised 
NAAQS and to remove obsolete regulatory language associated with 
expired exceptional event deadlines for historical standards for both 
O3 and other NAAQS pollutants. The EPA is also proposing to 
make minor changes to the procedures and time periods for evaluating 
potential FRMs and equivalent methods, including making the 
requirements for nitrogen dioxide consistent with the requirements for 
O3, and removing an obsolete requirement for the annual 
submission of documentation by manufacturers of certain particulate 
matter monitors.

B. Legislative Requirements

    Two sections of the CAA govern the establishment and revision of 
the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to 
identify and list certain air pollutants and then to issue air quality 
criteria for those pollutants. The Administrator is to list those air 
pollutants that in her ``judgment, cause or contribute to air pollution 
which may reasonably be anticipated to endanger public health or 
welfare;'' ``the presence of which in the ambient air results from 
numerous or diverse mobile or stationary sources;'' and ``for which . . 
. [the Administrator] plans to issue air quality criteria . . . .'' Air 
quality criteria are intended to ``accurately reflect the latest 
scientific knowledge useful in indicating the kind and extent of all 
identifiable effects on public health or welfare which may be expected 
from the presence of [a] pollutant in the ambient air . . . .'' 42 
U.S.C. 7408(b). Section 109 (42 U.S.C. 7409) directs the Administrator 
to propose and promulgate ``primary'' and ``secondary'' NAAQS for 
pollutants for which air quality criteria are issued. Section 109(b)(1) 
defines a primary standard as one ``the attainment and maintenance of 
which in the judgment of the Administrator, based on such criteria and 
allowing an adequate margin of safety, are requisite to protect the 
public health.'' \1\ A secondary standard, as defined in section 
109(b)(2), must ``specify a level of air quality the attainment and 
maintenance of which, in the judgment of the Administrator, based on 
such criteria, is requisite to protect the public welfare from any 
known or anticipated adverse effects associated with the presence of 
[the] pollutant in the ambient air.'' \2\
---------------------------------------------------------------------------

    \1\ The legislative history of section 109 indicates that a 
primary standard is to be set at ``the maximum permissible ambient 
air level . . . which will protect the health of any [sensitive] 
group of the population,'' and that, for this purpose, ``reference 
should be made to a representative sample of persons comprising the 
sensitive group rather than to a single person in such a group.'' S. 
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).
    \2\ Welfare effects as defined in section 302(h) (42 U.S.C. 
7602(h)) include, but are not limited to, ``effects on soils, water, 
crops, vegetation, man-made materials, animals, wildlife, weather, 
visibility and climate, damage to and deterioration of property, and 
hazards to transportation, as well as effects on economic values and 
on personal comfort and well-being.''
---------------------------------------------------------------------------

    The requirement that primary standards provide an adequate margin 
of safety was intended to address uncertainties associated with 
inconclusive scientific and technical information available at the time 
of standard setting. It was also intended to provide a reasonable 
degree of protection against hazards that research has not yet 
identified. See State of Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. 
Cir. 2013) (``By requiring an `adequate margin of safety', Congress was 
directing EPA to build a buffer to protect against uncertain and 
unknown dangers to human health''); see also Lead Industries 
Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980); American 
Petroleum Institute v. Costle,

[[Page 75238]]

665 F.2d 1176, 1186 (D.C. Cir. 1981); American Farm Bureau Federation 
v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 2009); Association of Battery 
Recyclers v. EPA, 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both kinds of 
uncertainties are components of the risk associated with pollution at 
levels below those at which human health effects can be said to occur 
with reasonable scientific certainty. Thus, in selecting primary 
standards that provide an adequate margin of safety, the Administrator 
is seeking not only to prevent pollution levels that have been 
demonstrated to be harmful but also to prevent lower pollutant levels 
that may pose an unacceptable risk of harm, even if the risk is not 
precisely identified as to nature or degree. The CAA does not require 
the Administrator to establish a primary NAAQS at a zero-risk level or 
at background concentrations, see Lead Industries v. EPA, 647 F.2d at 
1156 n.51; State of Mississippi v. EPA, 744 F. 3d at 1351, but rather 
at a level that reduces risk sufficiently so as to protect public 
health with an adequate margin of safety.
    In addressing the requirement for an adequate margin of safety, the 
EPA considers such factors as the nature and severity of the health 
effects, the size of sensitive population(s) \3\ at risk, and the kind 
and degree of the uncertainties that must be addressed. The selection 
of any particular approach for providing an adequate margin of safety 
is a policy choice left specifically to the Administrator's judgment. 
See Lead Industries Association v. EPA, 647 F.2d at 1161-62; State of 
Mississippi, 744 F. 3d at 1353.
---------------------------------------------------------------------------

    \3\ As used here and similarly throughout this document, the 
term ``population'' refers to people having a quality or 
characteristic in common, including a specific pre-existing illness 
or a specific age or life stage.
---------------------------------------------------------------------------

    In setting primary and secondary standards that are ``requisite'' 
to protect public health and welfare, respectively, as provided in 
section 109(b), the EPA's task is to establish standards that are 
neither more nor less stringent than necessary for these purposes. In 
so doing, the EPA may not consider the costs of implementing the 
standards. See generally, Whitman v. American Trucking Associations, 
531 U.S. 457, 465-472, 475-76 (2001). Likewise, ``[a]ttainability and 
technological feasibility are not relevant considerations in the 
promulgation of national ambient air quality standards.'' American 
Petroleum Institute v. Costle, 665 F. 2d at 1185.
    Section 109(d)(1) requires that ``not later than December 31, 1980, 
and at 5-year intervals thereafter, the Administrator shall complete a 
thorough review of the criteria published under section 108 and the 
national ambient air quality standards . . . and shall make such 
revisions in such criteria and standards and promulgate such new 
standards as may be appropriate . . . .'' Section 109(d)(2) requires 
that an independent scientific review committee ``shall complete a 
review of the criteria . . . and the national primary and secondary 
ambient air quality standards . . . and shall recommend to the 
Administrator any new . . . standards and revisions of existing 
criteria and standards as may be appropriate . . . .'' Since the early 
1980's, the Clean Air Scientific Advisory Committee (CASAC) has 
performed this independent review function.\4\
---------------------------------------------------------------------------

    \4\ Lists of CASAC members and of members of the CASAC Ozone 
Review Panel are available at: http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommitteesSubCommittees/Ozone%20Review%20Panel.
---------------------------------------------------------------------------

C. Related Control Programs To Implement O3 Standards

    States are primarily responsible for ensuring attainment and 
maintenance of ambient air quality standards once the EPA has 
established them. Under section 110 of the CAA, and related provisions, 
states are to submit, for the EPA's approval, state implementation 
plans (SIPs) that provide for the attainment and maintenance of such 
standards through control programs directed to sources of the 
pollutants involved. The states, in conjunction with the EPA, also 
administer the PSD program (CAA sections 160 to 169). In addition, 
federal programs provide for nationwide reductions in emissions of 
O3 precursors and other air pollutants through the federal 
motor vehicle and motor vehicle fuel control program under title II of 
the CAA (sections 202 to 250) which involves controls for emissions 
from mobile sources and controls for the fuels used by these sources, 
and new source performance standards for stationary sources under 
section 111 of the CAA. For some stationary sources, the national 
emissions standards for hazardous air pollutants under section 112 of 
the CAA may provide ancillary reductions in O3 precursors.
    After the EPA establishes a new or revised NAAQS, the CAA directs 
the EPA and the states to take steps to ensure that the new or revised 
NAAQS is met. One of the first steps, known as the initial area 
designations, involves identifying areas of the country that either are 
attaining or not attaining the new or revised NAAQS along with the 
nearby areas that contribute to the violations. Upon designation of 
nonattainment areas, certain states would then be required to develop 
SIPs to attain the standards. In developing their attainment plans, 
states would first take into account projected emission reductions from 
federal and state rules that have been already adopted at the time of 
plan submittal. A number of significant emission reduction programs 
that will lead to reductions of O3 precursors are in place 
today or are expected to be in place by the time any new SIPs will be 
due. Examples of such rules include the Nitrogen Oxides 
(NOX) SIP Call, Clean Air Interstate Rule (CAIR), and Cross-
State Air Pollution Rule (CSAPR),\5\ regulations controlling onroad and 
nonroad engines and fuels, the utility and industrial boilers hazardous 
air pollutant rules, and various other programs already adopted by 
states to reduce emissions from key emissions sources. States would 
then evaluate the level of additional emission reductions needed for 
each nonattainment area to attain the O3 standards ``as 
expeditiously as practicable,'' and adopt new state regulations as 
appropriate. Section VII of this preamble includes additional 
discussion of designation and implementation issues associated with any 
revised O3 NAAQS.
---------------------------------------------------------------------------

    \5\ The Cross-State Air Pollution Rule was recently upheld by 
the Supreme Court in Environmental Protection Agency v. EME Homer 
City Generation, U.S. (2014). The DC Circuit has since lifted the 
stay of the rule. Order, Document #1518738, EME Homer City 
Generation, L.P. v. EPA, Case #11-1302 (D.C. Cir. Oct. 23, 2014).
---------------------------------------------------------------------------

D. Review of Air Quality Criteria and Standards for O3
    The EPA first established primary and secondary NAAQS for 
photochemical oxidants in 1971 (36 FR 8186, April 30, 1971). The EPA 
set both primary and secondary standards at a level of 0.08 parts per 
million (ppm), 1-hr average, total photochemical oxidants, not to be 
exceeded more than one hour per year. The EPA based the standards on 
scientific information contained in the 1970 Air Quality Criteria for 
Photochemical Oxidants (U.S. DHEW, 1970). The EPA initiated the first 
periodic review of the NAAQS for photochemical oxidants in 1977. Based 
on the 1978 Air Quality Criteria for Ozone and Other Photochemical 
Oxidants (U.S. EPA, 1978), the EPA published proposed revisions to the 
original NAAQS in 1978 (43 FR 16962) and final revisions in 1979 (44 FR 
8202). At that time, the EPA revised the level of the primary and 
secondary standards from 0.08 to 0.12 ppm and changed the

[[Page 75239]]

indicator from photochemical oxidants to O3, and the form of 
the standards from a deterministic (i.e., not to be exceeded more than 
one hour per year) to a statistical form. This statistical form defined 
attainment of the standards as occurring when the expected number of 
days per calendar year with maximum hourly average concentration 
greater than 0.12 ppm equaled one or less.
    Following the final decision in the 1979 review, the City of 
Houston challenged the Administrator's decision arguing that the 
standard was arbitrary and capricious because natural O3 
concentrations and other physical phenomena in the Houston area made 
the standard unattainable in that area. The U.S. Court of Appeals for 
the District of Columbia Circuit (D.C. Circuit) rejected this argument, 
holding (as noted above) that attainability and technological 
feasibility are not relevant considerations in the promulgation of the 
NAAQS. The court also noted that the EPA need not tailor the NAAQS to 
fit each region or locale, pointing out that Congress was aware of the 
difficulty in meeting standards in some locations and had addressed 
this difficulty through various compliance related provisions in the 
CAA. See API v. Costle, 665 F.2d 1176, 1184-6 (D.C. Cir. 1981).
    In 1982, the EPA announced plans to revise the 1978 Air Quality 
Criteria document (47 FR 11561), and in 1983, the EPA initiated the 
second periodic review of the O3 NAAQS (48 FR 38009). The 
EPA subsequently published the 1986 Air Quality Criteria for Ozone and 
Other Photochemical Oxidants (U.S. EPA, 1986) and the 1989 Staff Paper 
(U.S. EPA, 1989). Following publication of the 1986 Air Quality 
Criteria Document (AQCD), a number of scientific abstracts and articles 
were published that appeared to be of sufficient importance concerning 
potential health and welfare effects of O3 to warrant 
preparation of a Supplement (U.S. EPA, 1992). On August 10, 1992, under 
the terms of a court order, the EPA published a proposed decision to 
retain the existing primary and secondary standards (57 FR 35542). The 
notice explained that the proposed decision would complete the EPA's 
review of information on health and welfare effects of O3 
assembled over a 7-year period and contained in the 1986 AQCD and its 
1992 Supplement. The proposal also announced the EPA's intention to 
proceed as rapidly as possible with the next review of the air quality 
criteria and standards for O3 in light of emerging evidence 
of health effects related to 6- to 8-hour O3 exposures. On 
March 9, 1993, the EPA concluded the review by affirming its proposed 
decision to retain the existing primary and secondary standards (58 FR 
13008).
    In August 1992, the EPA announced plans to initiate the third 
periodic review of the air quality criteria and O3 NAAQS (57 
FR 35542). In December 1996, the EPA proposed to replace the then-
existing 1-hour primary and secondary standards with 8-hour average 
O3 standards set at a level of 0.08 ppm (equivalent to 0.084 
ppm using standard rounding conventions) (61 FR 65716). The EPA also 
proposed to establish a new distinct secondary standard using a 
biologically based cumulative, seasonal form. The EPA completed this 
review on July 18, 1997 (62 FR 38856) by setting the primary standard 
at a level of 0.08 ppm, based on the annual fourth-highest daily 
maximum 8-hr average concentration, averaged over three years, and 
setting the secondary standard identical to the revised primary 
standard. In reaching this decision, the EPA identified several reasons 
supporting its decision to reject a potential alternate standard set at 
0.07 ppm. Most importantly, the EPA pointed out the scientific 
uncertainty at lower concentrations and placed significant weight on 
the fact that no CASAC panel member supported a standard level set 
lower than 0.08 ppm (62 FR 38868). In addition to noting the 
uncertainties in the health evidence for exposure concentrations below 
0.08 ppm and the advice of CASAC, the EPA noted that a standard set at 
a level of 0.07 ppm would be closer to peak background concentrations 
that infrequently occur in some areas due to nonanthropogenic sources 
of O3 precursors (62 FR 38856, 38868; July 18, 1997).
    On May 14, 1999, in response to challenges by industry and others 
to the EPA's 1997 decision, the D.C. Circuit remanded the O3 
NAAQS to the EPA, finding that section 109 of the CAA, as interpreted 
by the EPA, effected an unconstitutional delegation of legislative 
authority. American Trucking Assoc. v. EPA, 175 F.3d 1027, 1034-1040 
(D.C. Cir. 1999) (``ATA I''). In addition, the court directed that, in 
responding to the remand, the EPA should consider the potential 
beneficial health effects of O3 pollution in shielding the 
public from the effects of solar ultraviolet (UV) radiation, as well as 
adverse health effects. Id. at 1051-53. In 1999, the EPA petitioned for 
rehearing en banc on several issues related to that decision. The court 
granted the request for rehearing in part and denied it in part, but 
declined to review its ruling with regard to the potential beneficial 
effects of O3 pollution. 195 F.3d 4, 10 (D.C. Cir., 1999) 
(``ATA II''). On January 27, 2000, the EPA petitioned the U.S. Supreme 
Court for certiorari on the constitutional issue (and two other 
issues), but did not request review of the ruling regarding the 
potential beneficial health effects of O3. On February 27, 
2001, the U.S. Supreme Court unanimously reversed the judgment of the 
D.C. Circuit on the constitutional issue. Whitman v. American Trucking 
Assoc., 531 U.S. 457, 472-74 (2001) (holding that section 109 of the 
CAA does not delegate legislative power to the EPA in contravention of 
the Constitution). The Court remanded the case to the D.C. Circuit to 
consider challenges to the O3 NAAQS that had not been 
addressed by that court's earlier decisions. On March 26, 2002, the 
D.C. Circuit issued its final decision on remand, finding the 1997 
O3 NAAQS to be ``neither arbitrary nor capricious,'' and so 
denying the remaining petitions for review. American Trucking 
Associations, Inc. v. EPA, 283 F.3d 355, 379 (D.C. Cir., 2002) (``ATA 
III'').
    Specifically, in ATA III, the D.C. Circuit upheld the EPA's 
decision on the 1997 O3 standard as the product of reasoned 
decision-making. With regard to the primary standard, the court made 
clear that the most important support for EPA's decision to revise the 
standard was the health evidence of insufficient protection afforded by 
the then-existing standard (``the record is replete with references to 
studies demonstrating the inadequacies of the old one-hour standard''), 
as well as extensive information supporting the change to an 8-hour 
averaging time. 283 F.3d at 378. The court further upheld the EPA's 
decision not to select a more stringent level for the primary standard 
noting ``the absence of any human clinical studies at ozone 
concentrations below 0.08 [ppm]'' which supported EPA's conclusion that 
``the most serious health effects of ozone are `less certain' at low 
concentrations, providing an eminently rational reason to set the 
primary standard at a somewhat higher level, at least until additional 
studies become available.'' Id. (internal citations omitted). The Court 
also pointed to the significant weight that the EPA properly placed on 
the advice it received from CASAC. Id. at 379. In addition, the court 
noted that ``although relative proximity to peak background 
O3 concentrations did not, in itself, necessitate a level of 
0.08 [ppm], EPA could consider that factor when choosing among the 
three alternative levels.'' Id.
    Independently of the litigation, the EPA responded to the court's 
remand to

[[Page 75240]]

consider the potential beneficial health effects of O3 
pollution in shielding the public from effects of UV radiation. The EPA 
provisionally determined that the information linking changes in 
patterns of ground-level O3 concentrations to changes in 
relevant patterns of exposures to UV radiation of concern to public 
health was too uncertain, at that time, to warrant any relaxation in 
1997 O3 NAAQS. The EPA also expressed the view that any 
plausible changes in UV-B radiation exposures from changes in patterns 
of ground-level O3 concentrations would likely be very small 
from a public health perspective. In view of these findings, the EPA 
proposed to leave the 1997 8-hour NAAQS unchanged (66 FR 57268, Nov. 
14, 2001). After considering public comment on the proposed decision, 
the EPA published its final response to this remand on January 6, 2003, 
re-affirming the 8-hour O3 NAAQS set in 1997 (68 FR 614).
    The EPA initiated the fourth periodic review of the air quality 
criteria and O3 standards in September 2000 with a call for 
information (65 FR 57810). The schedule for completion of that review 
was ultimately governed by a consent decree resolving a lawsuit filed 
in March 2003 by plaintiffs representing national environmental and 
public health organizations, who maintained that the EPA was in breach 
of a mandatory legal duty to complete review of the O3 NAAQS 
within a statutorily mandated deadline. On July 11, 2007, the EPA 
proposed to revise the level of the primary standard within a range of 
0.075 to 0.070 ppm (72 FR 37818). Documents supporting this proposed 
decision included the Air Quality Criteria for Ozone and Other 
Photochemical Oxidants (U.S. EPA, 2006a) and the Staff Paper (U.S. EPA, 
2007) and related technical support documents. The EPA also proposed 
two options for revising the secondary standard: (1) Replace the 
current standard with a cumulative, seasonal standard, expressed as an 
index of the annual sum of weighted hourly concentrations cumulated 
over 12 daylight hours during the consecutive 3-month period within the 
O3 season with the maximum index value, set at a level 
within the range of 7 to 21 ppm-hrs, or (2) set the secondary standard 
identical to the proposed primary standard. The EPA completed the 
review with publication of a final decision on March 27, 2008 (73 FR 
16436). In that final rule, the EPA revised the NAAQS by lowering the 
level of the 8-hour primary O3 standard from 0.08 ppm to 
0.075 ppm, not otherwise revising the primary standard, and adopting a 
secondary standard identical to the revised primary standard. In May 
2008, state, public health, environmental, and industry petitioners 
filed suit challenging the EPA's final decision on the 2008 
O3 standards. On September 16, 2009, the EPA announced its 
intention to reconsider the 2008 O3 standards, and initiated 
a rulemaking to do so. At the EPA's request, the Court held the 
consolidated cases in abeyance pending the EPA's reconsideration of the 
2008 decision.
    On January 19, 2010 (75 FR 2938), the EPA issued a notice of 
proposed rulemaking to reconsider the 2008 final decision. In that 
notice, the EPA proposed that further revisions of the primary and 
secondary standards were necessary to provide a requisite level of 
protection to public health and welfare. The EPA proposed to decrease 
the level of the 2008 8-hour primary standard from 0.075 ppm to a level 
within the range of 0.060 to 0.070 ppm, and to change the secondary 
standard to a new cumulative, seasonal standard expressed as an annual 
index of the sum of weighted hourly concentrations, cumulated over 12 
hours per day (8 a.m. to 8 p.m.), during the consecutive 3-month period 
within the O3 season with a maximum index value, set at a 
level within the range of 7 to 15 ppm-hours. The Agency also solicited 
CASAC review of the proposed rule on January 25, 2010 and solicited 
additional CASAC advice on January 26, 2011. After considering comments 
from CASAC and the public, the EPA prepared a draft final rule, which 
was submitted for interagency review pursuant to Executive Order 12866. 
On September 2, 2011, consistent with the direction of the President, 
the Administrator of the Office of Information and Regulatory Affairs 
(OIRA), Office of Management and Budget (OMB), returned the draft final 
rule to the EPA for further consideration. In view of this return and 
the fact that the Agency's next periodic review of the O3 
NAAQS required under CAA section 109 had already begun (as announced on 
September 29, 2008), the EPA deferred the decisions involved in the 
reconsideration until it completed its statutorily required periodic 
review.
    In light of EPA's decision to consolidate the reconsideration with 
the current review, the D.C. Circuit proceeded with the litigation on 
the 2008 final decision. On July 23, 2013, the Court upheld the EPA's 
2008 primary O3 standard, but remanded the 2008 secondary 
standard to the EPA. State of Mississippi v. EPA, 744 F.3d 1334. With 
respect to the primary standard, the court first held that the EPA 
reasonably determined that the existing standard was not requisite to 
protect public health with an adequate margin of safety, and 
consequently required revision. Specifically, the court noted that 
there were ``numerous epidemiologic studies linking health effects to 
exposure to ozone levels below 0.08 ppm and clinical human exposure 
studies finding a causal relationship between health effects and 
exposure to ozone levels at and below 0.08 ppm.'' 744 F.3d at 1345. The 
court also specifically endorsed the weight of evidence approach 
utilized by the EPA in its deliberations. Id. at 1344.
    The court went on to reject arguments that the EPA should have 
adopted a more stringent primary standard. Dismissing arguments that a 
clinical study (as properly interpreted by the EPA) showing effects at 
0.06 ppm necessitated a standard level lower than that selected, the 
court noted that this was a single, limited study. Id. at 1350. With 
respect to the epidemiologic evidence, the court accepted the EPA's 
argument that there could be legitimate uncertainty that a causal 
relationship between O3 and 8-hour exposures less than 0.075 
ppm exists, so that associations at lower levels reported in 
epidemiologic studies did not necessitate a more stringent standard. 
Id. at 1351-52.\6\
---------------------------------------------------------------------------

    \6\ The court cautioned, however, that ``perhaps more [clinical] 
studies like the Adams studies will yet reveal that the 0.060 ppm 
level produces significant adverse decrements that simply cannot be 
attributed to normal variation in lung function,'' and further 
cautioned that ``agencies may not merely recite the terms 
`substantial uncertainty' as a justification for their actions.'' 
Id. at 1350, 1357 (internal citations omitted).
---------------------------------------------------------------------------

    The court also rejected arguments that an 8-hour primary standard 
of 0.075 ppm failed to provide an adequate margin of safety, noting 
that margin of safety considerations involved policy judgments by the 
agency, and that by setting a standard ``appreciably below'' the level 
of the current standard (0.08 ppm), the agency had made a reasonable 
policy choice. Id. Finally, the court rejected arguments that the EPA's 
decision was inconsistent with CASAC's scientific recommendations 
because CASAC had been insufficiently clear in its recommendations 
whether it was providing scientific or policy recommendations, and the 
EPA had reasonably addressed CASAC's policy recommendations. Id. at 
1357-58.
    With respect to the secondary standard, the court held that because 
the EPA had failed to identify a level of air quality requisite to 
protect public welfare, the EPA's comparison between

[[Page 75241]]

the primary and secondary standards for determining if requisite 
protection for public welfare was afforded by the primary standard did 
not comply with the CAA. The court thus rejected the EPA's explanation 
for setting the secondary standard identical to the revised 8-hour 
primary standard, and remanded the secondary standard to the EPA. Id. 
at 1360-62.
    At the time of the court's decision, the EPA had already completed 
significant portions of its next statutorily required periodic review 
of the O3 NAAQS. On September 29, 2008, the EPA announced 
the initiation of a new periodic review of the air quality criteria for 
O3 and related photochemical oxidants and issued a call for 
information in the Federal Register (73 FR 56581, Sept. 29, 2008). A 
wide range of external experts, as well as the EPA staff, representing 
a variety of areas of expertise (e.g., epidemiology, human and animal 
toxicology, statistics, risk/exposure analysis, atmospheric science, 
ecology, biology, plant science, ecosystem services) participated in a 
workshop. This workshop was held on October 28-29, 2008 in Research 
Triangle Park, NC. The workshop provided an opportunity for a public 
discussion of the key policy-relevant issues around which the EPA would 
structure this O3 NAAQS review and the most meaningful new 
science that would be available to inform our understanding of these 
issues.
    Based in part on the workshop discussions, the EPA developed a 
draft Integrated Review Plan (IRP) outlining the schedule, process, and 
key policy-relevant questions that would guide the evaluation of the 
air quality criteria for O3 and the review of the primary 
and secondary O3 NAAQS. A draft of the IRP was released for 
public review and comment in September 2009. This IRP was the subject 
of a consultation with the CASAC on November 13, 2009 (74 FR 54562; 
October 22, 2009).\7\ The EPA considered comments received from that 
consultation and from the public in finalizing the plan and in 
beginning the review of the air quality criteria. The EPA's overall 
plan and schedule for this review is presented in the Integrated Review 
Plan for the Ozone National Ambient Air Quality Standards.\8\
---------------------------------------------------------------------------

    \7\ See http://yosemite.epa.gov/sab/sabproduct.nsf/WebProjectsbyTopicCASAC!OpenView for more information on CASAC 
activities related to the current O3 NAAQS review.
    \8\ EPA 452/R-11-006; April 2011; Available: http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_OzoneIRP.pdf.
---------------------------------------------------------------------------

    As part of the process of preparing the O3 ISA, the 
EPA's NCEA hosted a workshop to review and discuss preliminary drafts 
of key sections of the ISA on August 6, 2010 (75 FR 42085, July 20, 
2010). The CASAC and the public reviewed the first external review 
draft ISA (U.S. EPA, 2011a; 76 FR 10893, February 28, 2011) at a 
meeting held in May 19-20, 2011 (76 FR 23809; April 28, 2011). Based on 
CASAC and public comments, NCEA prepared a second draft ISA (U.S. EPA, 
2011b; 76 FR 60820, September 30, 2011). CASAC and the public reviewed 
this draft at a January 9-10, 2012 (76 FR 236, December 8, 2011) 
meeting. Based on CASAC and public comments, NCEA prepared a third 
draft ISA (U.S. EPA 2012a; 77 FR 36534; June 19, 2012), which was 
reviewed at a CASAC meeting in September 2012. The EPA released the 
final ISA (EPA/600/R-10/076F) in February 2013.
    The EPA presented its plans for conducting the Risk and Exposure 
Assessments (REAs) that build on the scientific evidence presented in 
the ISA, in two planning documents titled Ozone National Ambient Air 
Quality Standards: Scope and Methods Plan for Health Risk and Exposure 
Assessment and Ozone National Ambient Air Quality Standards: Scope and 
Methods Plan for Welfare Risk and Exposure Assessment (henceforth, 
Scope and Methods Plans).\9\ These planning documents outlined the 
scope and approaches that staff planned to use in conducting 
quantitative assessments, as well as key issues that would be addressed 
as part of the assessments. The EPA released these documents for public 
comment in April 2011, and consulted with CASAC on May 19-20, 2011 (76 
FR 23809; April 28, 2011). In designing and conducting the initial 
health risk and welfare risk assessments, the EPA considered CASAC 
comments (Samet, 2011) on the Scope and Methods Plans and also 
considered public comments. In May 2012, the EPA issued a memo titled 
Updates to Information Presented in the Scope and Methods Plans for the 
Ozone NAAQS Health and Welfare Risk and Exposure Assessments that 
described changes to elements of the scope and methods plans and 
provided a brief explanation of each change and the reason for it.
---------------------------------------------------------------------------

    \9\ EPA-452/P-11-001 and -002; April 2011; Available: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pd.html.
---------------------------------------------------------------------------

    In July 2012, the EPA made the first drafts of the Health and 
Welfare REAs available for CASAC review and public comment (77 FR 
42495, July 19, 2012). The first draft PA \10\ was made available for 
CASAC review and public comment in August 2012. These documents were 
reviewed by the CASAC O3 Panel at a public meeting in 
September 2012. The second draft REAs and PA, made available by the EPA 
in January 2014 (79 FR 4694, January 29, 2014), were prepared with 
consideration of advice from CASAC (Frey and Samet, 2012a, 2012b) and 
comments from the public. These drafts were reviewed by the CASAC 
O3 Panel at a public meeting on March 25-27, 2014. The CASAC 
issued final reports on the second drafts of the HREA on July 1, 2014 
(Frey, 2014a), and the WREA on June 18, 2014 (Frey, 2014b), 
respectively. The CASAC issued a final report on the second draft PA on 
June 26, 2014 (Frey, 2014c). The final versions of the HREA (U.S. EPA 
2014a), WREA (U.S. EPA, 2014b), and PA (U.S. EPA, 2014c) were made 
available by the EPA in August, 2014. These documents reflect staff's 
consideration of the comments and recommendations made by CASAC, as 
well as comments made by members of the public, in their review of the 
draft versions of these documents.
---------------------------------------------------------------------------

    \10\ The PA is prepared by the staff in the EPA's Office of Air 
Quality Planning and Standards (OAQPS). It presents a staff 
evaluation of the policy implications of the key scientific and 
technical information in the ISA and REAs for the EPA's 
consideration. The PA provides a transparent evaluation, and staff 
conclusions, regarding policy considerations related to reaching 
judgments about the adequacy of the current standards, and if 
revision is considered, what revisions may be appropriate to 
consider. The PA is intended to help ``bridge the gap'' between the 
agency's scientific assessments presented in the ISA and REAs, and 
the judgments required of the EPA Administrator in determining 
whether it is appropriate to retain or revise the NAAQS.
---------------------------------------------------------------------------

E. Ozone Air Quality

    Ozone is formed near the Earth's surface due to chemical 
interactions involving solar radiation and precursor pollutants 
including volatile organic compounds (VOCs), nitrogen oxides 
(NOX), methane (CH4) and carbon monoxide (CO). 
The precursor emissions leading to O3 formation can result 
from both man-made sources (e.g., motor vehicles and electric power 
generation) and natural sources (e.g., vegetation and wildfires). 
Occasionally, O3 that is created naturally in the 
stratosphere can also contribute to O3 levels near the 
surface. Once formed, O3 can be transported by winds before 
eventually being removed from the atmosphere via chemical reactions or 
deposition to surfaces. In sum, O3 concentrations are 
influenced by complex interactions between precursor emissions, 
meteorological conditions, and surface characteristics.
    In order to continuously assess O3 air pollution levels, 
state and local environmental agencies operate O3 monitors 
at various locations and

[[Page 75242]]

subsequently submit the data to the EPA. At present, there are 
approximately 1,400 monitors across the U.S. reporting hourly 
O3 averages during the times of the year when local 
O3 pollution can be important. Much of this monitoring is 
focused on O3 measurements in urban areas where precursor 
emissions tend to be largest, as well as locations directly downwind of 
these areas, but there are also over 100 sites in rural areas where 
high levels of O3 can periodically exist due to transport 
from upwind sources. Based on data from this national network, the EPA 
estimates that approximately 133 million Americans live in counties 
where O3 concentrations were above the level of the existing 
health-based NAAQS of 0.075 ppm at least 4 days in 2012. High 
O3 values can occur almost anywhere within the contiguous 48 
states, although locations in California, Texas, and the Northeast 
Corridor are especially subject to poor O3 air quality. From 
a temporal perspective, the highest daily peak O3 
concentrations generally tend to occur during the afternoon within the 
warmer months due to higher solar radiation and other conducive 
meteorological conditions during these times. The exceptions to this 
general rule include: (1) Some rural sites where transport of 
O3 from upwind areas of regional production can occasionally 
result in high nighttime levels of O3, (2) high-elevation 
sites periodically influenced by stratospheric intrusions, and (3) 
certain locations in the western U.S. where large quantities of 
O3 precursors emissions associated with oil and gas 
development can be trapped by strong inversions associated with snow 
cover during the colder months and efficiently converted to 
O3.
    One of the challenging aspects of developing plans to reduce 
emissions leading to high O3 concentrations is that the 
response of O3 to precursor reductions is nonlinear. In 
particular, NOX causes both the formation and destruction of 
O3. The net impact of NOX emissions on 
O3 concentrations depends on the local quantities of 
NOX, VOC, and sunlight which interact in a set of complex 
chemical reactions. In some areas, such as urban centers where 
NOX emissions typically are high, NOX leads to 
the net destruction of O3, making O3 levels lower 
in the immediate vicinity. This phenomenon is particularly pronounced 
under conditions that lead to low O3 concentrations (i.e. 
during cool, cloudy weather and at night when photochemical activity is 
limited or nonexistent). However, while NOX can initially 
destroy O3 near the emission sources, these same 
NOX emissions eventually do react to form more O3 
downwind. Photochemical model simulations suggest that the additional 
expected reductions in NOX emissions will slightly increase 
O3 concentrations on days with lower O3 
concentrations in areas in close proximity to NOX sources, 
while at the same time decreasing the highest O3 
concentrations in outlying areas. See generally, U.S. EPA, 2014a 
(section 2.2.1).
    At present, both the primary and secondary NAAQS use the annual 
fourth-highest daily maximum 8-hour concentration, averaged over 3 
years, as the form of the standard. An additional air quality metric, 
referred to as W126, is often used to assess cumulative impact of 
O3 exposure on ecosystems and vegetation. W126 is a seasonal 
aggregate of weighted hourly O3 values observed between 8 
a.m. and 8 p.m. As O3 precursor emissions have decreased 
across the U.S., O3 design values \11\ have concurrently 
shown a modest downward trend. Ozone design values decreased by 
approximately 9% on average between 2000 and 2012. Air quality model 
simulations estimate that peak O3 levels will continue to 
improve over the next decade as additional reductions in O3 
precursors from power plants, motor vehicles, and other sources are 
realized.
---------------------------------------------------------------------------

    \11\ A design value is a statistic that describes the air 
quality status of a given location relative to the level of the 
NAAQS.
---------------------------------------------------------------------------

    In addition to being affected by changing emissions, future 
O3 concentrations will also be affected by climate change. 
Modeling studies in EPA's Interim Assessment (U.S. EPA, 2009b) and 
cited in support of the 2009 Endangerment Finding (74 FR 66,496; Dec. 
15, 2009) show that, while the impact is not uniform, climate change 
has the potential to cause increases in summertime O3 
concentrations over substantial regions of the country, with increases 
tending to occur during higher peak pollution episodes in the summer, 
if offsetting emissions reductions are not made. Increases in 
temperature are expected to be the principal factor in driving any 
ozone increases, although increases in stagnation frequency may also 
contribute (Jacob and Winner, 2009). These increases in O3 
pollution over broad areas of the U.S., including in the largest 
metropolitan areas with the worst O3 problems, increase the 
risk of morbidity and mortality. Children, people with asthma or other 
lung diseases, older adults, and people who are active outdoors, 
including outdoor workers, are among the most vulnerable to these 
O3-related health effects. If unchecked, climate change has 
the potential to offset some of the improvements in O3 air 
quality, and therefore some of the improvements in public health, that 
are expected from reductions in emissions of O3 precursors.
    Another challenging aspect of the O3 issue is the 
involvement of sources of O3 and O3 precursors 
beyond those from domestic, anthropogenic sources. Modeling analyses 
have suggested that nationally the majority of O3 
exceedances are predominantly caused by anthropogenic emissions from 
within the U.S. However, observational and modeling analyses have 
concluded that O3 concentrations in some locations in the 
U.S. can be substantially influenced by sources that may not be suited 
to domestic control measures. In particular, certain high-elevation 
sites in the western U.S. are impacted by a combination of non-local 
sources like international transport, stratospheric O3, and 
O3 originating from wildfire emissions. Ambient 
O3 from these non-local sources is collectively referred to 
as background O3. See generally section 2.4 of the Policy 
Assessment (U.S. EPA, 2014c). The analyses suggest that, at these 
locations, there can be episodic events with substantial background 
contributions where O3 concentrations approach or exceed the 
level of the current NAAQS (i.e., 75 ppb). These events are relatively 
infrequent and the EPA has policies that allow for the exclusion of air 
quality monitoring data from design value calculations when they are 
substantially affected by certain background influences. Wildfires pose 
a direct threat to air quality and public safety--threats that can be 
mitigated through management of wildland vegetation. The use of 
wildland prescribed fire can influence the occurrence of catastrophic 
wildfires which may help manage the contribution of wildfires to 
background O3 levels and periodic peak O3 events. 
Prescribed fire mimics a natural process necessary to manage and 
maintain fire-adapted ecosystems and climate change adaptation, while 
reducing risk of uncontrolled emissions from catastrophic wildfires. 
Wildfire emissions may make it more challenging to meet the NAAQS. 
However, the CAA requires the EPA to set the NAAQS at levels requisite 
to protect public health and welfare without regard to the source of 
the pollutant. API, 665 F. 2d at 1185-86. The EPA may consider 
proximity to background levels as a factor in the decision whether and 
how to revise the NAAQS when considering levels within the range of 
reasonable values

[[Page 75243]]

supported by the air quality criteria and judgments of the 
Administrator. ATA III, 283 F. 3d at 379. It is in the implementation 
process that states and the EPA can address how to develop effective 
public policy in locations in which background sources contribute 
substantially to high O3. Section VII.F provides more detail 
about how background O3 can be addressed via CAA 
implementation provisions.

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the Administrator's rationale for her 
proposed decision to revise the existing primary O3 standard 
by lowering the level of the standard to within the range of 0.065 to 
0.070 ppm. As discussed more fully below, this rationale draws from the 
thorough review in the ISA of the available scientific evidence, 
published through July 2011, on human health effects associated with 
the presence of O3 in the ambient air. This rationale also 
takes into account: (1) Analyses of O3 air quality, human 
exposures to O3, and O3-associated health risks, 
as presented and assessed in the HREA; (2) the EPA staff assessment of 
the most policy-relevant scientific evidence and exposure/risk 
information in the PA; (3) CASAC advice and recommendations, as 
reflected in discussions of drafts of the ISA, REA, and PA at public 
meetings, in separate written comments, and in CASAC's letters to the 
Administrator; and (4) public input received during the development of 
these documents, either in connection with CASAC meetings or 
separately.
    Section II.A below provides an overview of the approaches used to 
consider the scientific evidence and exposure/risk information as it 
relates to the primary O3 standard. This includes summaries 
of the approach adopted by the Administrator in the 2008 review of the 
O3 NAAQS and of the approach adopted in the PA in the 
current review. Section II.B summarizes the body of evidence for health 
effects attributable to short- or long-term O3 exposures, 
with a focus on effects for which the ISA judges that there is a 
``causal'' or a ``likely to be causal'' relationship with O3 
exposures. Section II.C summarizes the HREA's quantitative estimates of 
O3 exposures and health risks, including key results and 
uncertainties. Sections II.D and II.E present the Administrator's 
proposed conclusions on the adequacy of the current primary 
O3 standard and alternative primary standards, respectively.

A. Approach

    In the 2008 review of the O3 NAAQS, Administrator 
Stephen L. Johnson revised the level of the 8-hour primary 
O3 standard from 0.08 ppm \12\ to 0.075 ppm (75 parts per 
billion (ppb) \13\). This decision was based on his consideration of 
the available scientific evidence and exposure/risk information, the 
advice and recommendations of CASAC, and comments from the public. The 
Administrator placed primary emphasis on the body of available 
scientific evidence, while viewing the results of exposure and risk 
assessments as providing supporting information. Specifically, he 
judged that a standard set at 75 ppb would be appreciably below the 
concentration at which adverse effects had been demonstrated in the 
controlled human exposure studies available at that time (i.e., 80 
ppb), and would provide a significant increase in protection compared 
to the then-current standard. The Administrator further concluded that 
the body of evidence did not support setting a lower standard level, 
given the increasing uncertainty in the evidence at lower O3 
concentrations (U.S. EPA, 2014c, Chapter 1).
---------------------------------------------------------------------------

    \12\ Due to rounding convention, the 1997 standard level of 0.08 
ppm corresponded to 0.084 ppm (84 ppb).
    \13\ The level of the O3 standard is specified as 
0.075 ppm rather than 75 ppb. However, in the PA we refer to ppb, 
which is most often used in the scientific literature and in the 
ISA, in order to avoid the confusion that could result from 
switching units when discussing the evidence in relation to the 
standard level. Similarly, in the preamble to this notice we refer 
to ppb.
---------------------------------------------------------------------------

    In the current review, the EPA's approach to informing decisions on 
the primary O3 standard builds upon the general approach 
used in the last review and reflects the broader body of scientific 
evidence, updated exposure/risk information, and advances in 
O3 air quality modeling now available. This approach, 
described in detail in the PA (U.S. EPA, 2014c, section 1.3.1), is 
based most fundamentally on using the EPA's assessment of the available 
scientific evidence and associated quantitative analyses to inform the 
Administrator's judgments regarding a primary standard for 
O3 that is ``requisite'' (i.e., neither more nor less 
stringent than necessary) to protect public health with an adequate 
margin of safety. Specifically, it is based on consideration of the 
available body of scientific evidence assessed in the ISA (U.S. EPA, 
2013a), exposure and risk analyses presented in the HREA (U.S. EPA, 
2014a), advice and recommendations from CASAC (Frey, 2014a, c), and 
public comments. Based on the application of this approach, the PA 
assesses and integrates the evidence and information, and reaches 
conclusions for the Administrator's consideration about the range of 
policy options that could be supported. The remainder of this section 
describes the PA's approach to reviewing the primary O3 
standard, and to informing the Administrator's proposed decisions on 
the current and alternative standards.
    As an initial matter, the PA recognizes that the final decision to 
retain or revise the current primary O3 standard is a public 
health policy judgment to be made by the Administrator and will draw 
upon the available scientific evidence for O3-attributable 
health effects and on analyses of population exposures and health 
risks, including judgments about the appropriate weight to assign the 
range of uncertainties inherent in the evidence and analyses. The PA's 
general approach to informing these public health policy judgments 
recognizes that the available health effects evidence reflects a 
continuum from relatively higher O3 concentrations, at which 
scientists generally agree that health effects are likely to occur, 
through lower concentrations, at which the likelihood and magnitude of 
a response become increasingly uncertain. Therefore, the conclusions in 
the PA reflect an interpretation of the available scientific evidence 
and exposure/risk information that, in the views of the EPA staff, 
neither overstates nor understates the strengths and limitations of 
that evidence and information.\14\ This approach is consistent with the 
requirements of sections 108 and 109 of the CAA, as well as with how 
the EPA and the courts have historically interpreted the CAA.
---------------------------------------------------------------------------

    \14\ Draft versions of the PA were subject to review by CASAC 
and the final PA reflects consideration of the advice received from 
CASAC during the review process. CASAC concluded that ``Overall, we 
find the Second Draft PA to be adequate for its intended purpose of 
providing a strong scientific basis for findings regarding the 
inadequacy of current primary and secondary ozone air quality 
standards'' (Frey, 2014c, p. v).
---------------------------------------------------------------------------

    The PA draws upon an integrative synthesis of the entire body of 
available scientific evidence for O3-related health effects, 
including the evidence newly available in the current review and the 
evidence from previous reviews, as presented in the ISA (U.S. EPA, 
2013a). Consideration of the scientific evidence is based fundamentally 
on information from controlled human exposure and epidemiologic 
studies, supplemented by information from animal toxicology studies. In 
the PA, such evidence informs the consideration of the health

[[Page 75244]]

endpoints and at-risk populations \15\ on which to focus the current 
review, and the consideration of the O3 concentrations at 
which various health effects can occur.
---------------------------------------------------------------------------

    \15\ In this review, the term ``at-risk population'' is used to 
encompass populations or lifestages that have a greater likelihood 
of experiencing health effects related to exposure to an air 
pollutant due to a variety of factors; other terms used in the 
literature include susceptible, vulnerable, and sensitive. These 
factors may be intrinsic, such as genetic factors, lifestage, or the 
presence of preexisting diseases, or they may be extrinsic, such as 
socioeconomic status (SES), activity pattern and exercise level, or 
increased pollutant exposures (U.S. EPA 2013, p. lxx, 8-1, 8-2). The 
courts and the CAA's legislative history refer to these at-risk 
subpopulations as ``susceptible'' or ``sensitive'' populations. See, 
e.g., American Lung Ass'n v. EPA, 134 F. 3d 388, 389 (D.C. Cir. 
1998) (``NAAQS must protect not only average health individuals, but 
also `sensitive citizens'--children, for example, or people with 
asthma, emphysema, or other conditions rendering them particularly 
vulnerable to air pollution'' (quoting S. Rep. No. 91-1196 at 10).
---------------------------------------------------------------------------

    Since the 2008 review of the O3 NAAQS, the EPA has 
developed formal frameworks for characterizing the strength of the 
scientific evidence with regard to health effects associated with 
exposures to O3 in ambient air and factors that may increase 
risk in some populations or lifestages. These frameworks provide the 
basis for robust, consistent, and transparent processes for evaluating 
the scientific evidence, including uncertainties in the evidence, and 
for drawing weight-of-evidence conclusions on air pollution-related 
health effects and at-risk populations. These frameworks for 
characterizing the strength of the scientific evidence are discussed in 
detail in the ISA (U.S. EPA, 2013a, Preamble; Chapter 8).
    With regard to characterization of health effects, the ISA uses a 
five-level hierarchy to classify the overall weight of evidence into 
one of the following categories: causal relationship, likely to be a 
causal relationship, suggestive of a causal relationship, inadequate to 
infer a causal relationship, and not likely to be a causal relationship 
(U.S. EPA, 2013a, Preamble Table II). In using the weight-of-evidence 
approach to inform judgments about the degree of confidence that 
various health effects are likely to be caused by exposure to 
O3, confidence increases as the number of studies 
consistently reporting a particular health endpoint grows and as other 
factors, such as biological plausibility and the strength, consistency, 
and coherence of evidence, increase. Conclusions about biological 
plausibility and about the consistency and coherence of O3-
related health effects are drawn from the integration of epidemiologic 
studies with mechanistic information from controlled human exposure and 
animal toxicological studies, as discussed in the ISA (U.S. EPA, 2013a, 
EPA Framework for Causal Determination, p. 1viii). The PA places the 
greatest weight on the health effects for which the evidence has been 
judged in the ISA to support a ``causal'' or a ``likely to be causal'' 
relationship with O3 exposures.
    The PA further considers the evidence base assessed in the ISA with 
regard to the types and levels of exposure at which health effects are 
indicated. This consideration of the evidence, which directly informs 
conclusions regarding the adequacy of current or alternative standards, 
differs from consideration of the evidence in the ISA with regard to 
overarching determinations of causality. Therefore, studies that inform 
determinations of causality may or may not be concluded to be 
informative with regard to the adequacy of the current or alternative 
standards.\16\
---------------------------------------------------------------------------

    \16\ For example, the PA judges that health studies evaluating 
exposure concentrations near or below the level of the current 
standard and epidemiologic studies conducted in locations meeting 
the current standard are particularly informative when considering 
the adequacy of the public health protection provided by the current 
standard (U.S. EPA, 2014c, Chapters 3 and 4).
---------------------------------------------------------------------------

    As with health endpoints, the ISA's characterization of the weight 
of evidence for potential at-risk populations is based on the 
evaluation and synthesis of evidence from across scientific 
disciplines. The ISA uses the collective evidence to examine the 
coherence of effects across disciplines and to determine the biological 
plausibility of reported effects. Based on this approach, the ISA 
characterizes the evidence for a number of ``factors'' that have the 
potential to place populations at increased risk for O3-
related effects. The categories considered in evaluating the evidence 
for these potential at-risk factors are ``adequate evidence,'' 
``suggestive evidence,'' ``inadequate evidence,'' and ``evidence of no 
effect.'' For the ``adequate evidence'' category, the ISA concludes 
that this category is appropriate when multiple high-quality studies 
show ``there is substantial, consistent evidence within a discipline to 
conclude that a factor results in a population or lifestage being at 
increased risk of air pollutant-related health effect(s) relative to 
some reference population or lifestage'' (U.S. EPA, 2013a, p. 8-2). In 
addition, where applicable, the ``adequate evidence'' category reflects 
a conclusion that there is coherence in the evidence across 
disciplines. The other categories reflect greater uncertainty in the 
evidence. In this review, the PA focuses on those factors for which the 
ISA judges there is adequate evidence of increased risk (U.S. EPA, 
2013a, Table 8-5). At-risk populations are discussed in more detail in 
section 3.1.5 of the PA (U.S. EPA, 2014c) and these categories are 
discussed in more detail in the ISA (U.S. EPA, 2013a, chapter 8, Table 
8-1).
    Using the available scientific evidence to inform conclusions on 
the current and alternative standards is complicated by the recognition 
that a population-level threshold has not been identified below which 
it can be concluded with confidence that O3-attributable 
effects do not occur (U.S. EPA, 2013a, section 2.5.4.4). In the absence 
of a discernible threshold, the PA's general approach to considering 
the available O3 health evidence involves characterizing 
confidence in the extent to which O3-attributable effects 
occur, and the extent to which such effects are adverse, over the 
ranges of O3 exposure concentrations evaluated in controlled 
human exposure studies and over the distributions of ambient 
O3 concentrations in locations where epidemiologic studies 
have been conducted. As noted above, the PA recognizes that the 
available health effects evidence reflects a continuum from relatively 
high O3 concentrations, at which scientists generally agree 
that adverse health effects are likely to occur, through lower 
concentrations, at which the likelihood and magnitude of a response 
become increasingly uncertain. Aspects of the approach used in this 
review to evaluate evidence from controlled human exposure and 
epidemiologic studies, respectively, are discussed below.
    Controlled human exposure studies provide direct evidence of 
relationships between pollutant exposures and human health effects 
(U.S. EPA, 2013a, p.lx). Controlled human exposure studies provide data 
with the highest level of confidence since they provide human effects 
data under closely monitored conditions and can provide exposure 
response relationships. Such studies are particularly useful in 
defining the specific conditions under which pollutant exposures can 
result in health impacts, including the exposure concentrations, 
durations, and ventilation rates under which effects can occur. As 
discussed in the ISA, controlled human exposure studies provide clear 
and compelling evidence for an array of human health effects that are 
directly attributable to acute exposures to O3 per se (i.e., 
as opposed to O3 and other photochemical oxidants, for which 
O3 is an indicator, or other co-occurring pollutants) (U.S. 
EPA, 2013a, Chapter 6). Together with animal toxicological studies, 
which can provide

[[Page 75245]]

information about more serious health outcomes as well as the effects 
of long-term exposures and mode of action, controlled human exposure 
studies also help to provide biological plausibility for health effects 
observed in epidemiologic studies.
    The PA considers the evidence from controlled human exposure 
studies in two ways. First, the PA considers the extent to which 
controlled human exposure studies provide evidence for health effects 
following exposures to different O3 concentrations, down to 
the lowest-observed-effects levels in those studies. Second, the PA 
uses these studies to help evaluate the extent to which there is 
confidence in health effect associations reported in epidemiologic 
studies down through lower ambient O3 concentrations, where 
the likelihood and magnitude of O3-attributable effects 
become increasingly uncertain.
    The PA considers the range of O3 exposure concentrations 
evaluated in controlled human exposure studies, including 
concentrations near or below the level of the current standard. The PA 
considers both group mean responses, which provide insight into the 
extent to which observed changes are due to O3 exposures 
rather than to chance alone, and interindividual variability in 
responses, which provides insight into the fraction of the population 
that might be affected by such O3 exposures (U.S. EPA, 
2013a, section 6.2.1.1). When considering the relative weight to place 
on various controlled human exposure studies, the discussion in the PA 
focuses on the exposure conditions evaluated (e.g., exercising versus 
resting, exposure duration); the nature, magnitude, and likely 
adversity of effects over the range of reported O3 exposure 
concentrations; the statistical precision of reported effects; and the 
consistency of results across studies for a given health endpoint and 
exposure concentration. In addition, because controlled human exposure 
studies typically involve healthy individuals and do not evaluate the 
most sensitive individuals in the population (U.S. EPA, 2013a, Preamble 
p. lx), when considering the implications of these studies for 
evaluation of the current and alternative standards, the PA also 
considers the extent to which reported effects are likely to reflect 
the magnitude and/or severity of effects in at-risk groups.
    The PA also considers epidemiologic studies of short- and long-term 
O3 concentrations in ambient air. Epidemiologic studies 
provide information on associations between variability in ambient 
O3 concentrations and variability in various health 
outcomes, including lung function decrements, respiratory symptoms, 
school absences, hospital admissions, emergency department visits, and 
premature mortality (U.S. EPA, 2013a, Chapters 6 and 7). Epidemiologic 
studies can inform understanding of the effects in the study population 
(which may include at-risk groups) of real-world exposures to the range 
of O3 concentrations in ambient air, as well as provide 
evidence of associations between ambient O3 levels and more 
serious acute and chronic health effects that cannot be assessed in 
controlled human exposure studies. For these studies, the degree of 
uncertainty introduced by confounding variables (e.g., other 
pollutants, temperature) and other factors (e.g., effects modifiers 
such as averting behavior) affects the level of confidence that the 
health effects being investigated are attributable to O3 
exposures, alone and in combination with copollutants.
    Available epidemiologic studies have generally not indicated a 
discernible population threshold below which O3 is no longer 
associated with health effects (U.S. EPA, 2013a, section 2.5.4.4). 
However, the currently available epidemiologic evidence indicates 
decreased confidence in reported concentration-response relationships 
for O3 concentrations at the lower ends of ambient 
distributions due to the low density of data in this range (U.S. EPA, 
2013a, section 2.5.4.4). As discussed more fully in Chapter 1 of the PA 
(U.S. EPA, 2014c), the general approach to considering the results of 
epidemiologic studies within the context of the current and alternative 
standards focuses on characterizing the range of ambient O3 
concentrations over which studies indicate the most confidence in 
O3-associated health effects, and the concentrations below 
which confidence in such health effect associations becomes appreciably 
lower.
    In placing emphasis on specific epidemiologic studies, as in past 
reviews, the discussion in the PA focuses on the epidemiologic studies 
conducted in the U.S. and Canada. Such studies reflect air quality and 
exposure patterns that are likely more typical of the U.S. population, 
since studies conducted outside the U.S. and Canada may well reflect 
different demographic and air pollution characteristics.\17\ The PA 
also focuses on studies reporting associations with effects judged in 
the ISA (U.S. EPA, 2013a) to be robust to confounding by other factors, 
including co-occurring air pollutants.
---------------------------------------------------------------------------

    \17\ Though the PA recognizes that a broader body of studies, 
including international studies, informs the causal determinations 
in the ISA.
---------------------------------------------------------------------------

    To put staff conclusions about O3-related health effects 
into a broader public health context, the PA also considers exposure 
and risk estimates from the HREA, which develops and applies models to 
estimate human exposures to O3 and O3-related 
health risks in urban study areas across the United States (U.S. EPA, 
2014a). The HREA estimates exposures of concern, based on interpreting 
quantitative exposure estimates within the context of controlled human 
exposure study results; lung function risks, based on applying 
exposure-response relationships from controlled human exposure studies 
to quantitative estimates of exposures; and epidemiologic-based risk 
estimates, based on applying concentration-response relationships drawn 
from epidemiologic studies to adjusted air quality. Each of these types 
of assessments is discussed briefly below.
    As in the 2008 review, the HREA estimates exposures at or above 
benchmark concentrations of 60, 70, and 80 ppb, reflecting exposure 
concentrations of concern based on the available health evidence.\18\ 
Estimates of exposures of concern, defined as personal exposures while 
at moderate or greater exertion to 8-hour average ambient O3 
levels, at or above these discrete benchmark concentrations provide 
perspective on the public health risks of O3-related health 
effects that have been demonstrated in controlled human exposure and 
toxicological studies. However, because of a lack of exposure-response 
information across a range of exposure concentrations in these studies, 
these risks cannot be assessed using a quantitative risk assessment. 
Though this analysis is conducted using discrete benchmark 
concentrations, information from the broad body of evidence indicates 
that health-relevant exposures are more appropriately viewed as a 
continuum with greater confidence and certainty about the existence of 
health effects at higher O3 exposure concentrations and less 
confidence and certainty at lower exposure concentrations. This 
approach recognizes that there is no sharp breakpoint within the 
exposure-response relationship for exposure concentrations at and above 
80 ppb down to 60 ppb.
---------------------------------------------------------------------------

    \18\ For example, see 75 FR 2945-2946 (January 19, 2010) and 73 
FR 16441-16442 (March 27, 2008) discussing ``exposures of concern.''
---------------------------------------------------------------------------

    Within the context of this continuum, estimates of exposures of 
concern at these discrete benchmark

[[Page 75246]]

concentrations provide some perspective on the public health impacts of 
O3-related health effects, such as pulmonary inflammation, 
that are plausibly linked to the more serious effects seen in 
epidemiologic studies but cannot be evaluated in quantitative risk 
assessments. They also help elucidate the extent to which such impacts 
may be reduced by meeting the current and alternative standards. 
Estimates of the number of people likely to experience exposures of 
concern cannot be directly translated into quantitative estimates of 
the number of people likely to experience specific health effects due 
to individual variability in responsiveness. Only a subset of 
individuals can be expected to experience such adverse health effects, 
and at-risk populations or lifestages, such as people with asthma or 
children, are expected to be affected more by such exposures than 
healthy adults.
    The HREA also generates quantitative estimates of O3 
health risks for air quality adjusted to just meet the current \19\ and 
alternative standards. One approach to estimating O3 health 
risks is to combine modeled exposure estimates with exposure-response 
relationships derived from controlled human exposure studies of 
O3-induced health effects. The HREA uses this approach to 
estimate the occurrence of O3-induced lung function 
decrements in at-risk populations, including school-age children, 
school-age children with asthma, adults with asthma, and older adults. 
The available exposure-response information does not support this 
approach for other endpoints evaluated in controlled human exposure 
studies (U.S. EPA, 2014a, section 2.3).
---------------------------------------------------------------------------

    \19\ For purposes of the exposure and risk estimates with 
adjusted air quality, the REA considered any value <76 ppb to be 
``just meeting'' the current 75 ppb standard (U.S. EPA, 2014a).
---------------------------------------------------------------------------

    The other approach used in this review to estimate O3-
associated health risks is to apply concentration-response 
relationships derived from short- and/or long-term epidemiologic 
studies to air quality adjusted to just meet current and alternative 
standards. The concentration-response relationships drawn from 
epidemiologic studies are based on population exposure surrogates, such 
as 8-hour concentrations averaged across monitors and over more than 
one day (U.S. EPA, 2013a, Chapter 6). The HREA presents epidemiologic-
based risk estimates for O3-associated mortality, hospital 
admissions, emergency department visits, and respiratory symptoms (U.S. 
EPA, 2014a, section 2.3). These estimates are derived from the full 
distributions of ambient O3 concentrations estimated for the 
study locations.\20\ In addition, the HREA estimates mortality risks 
associated with various portions of distributions of short-term 
O3 concentrations (U.S. EPA, 2014a). The PA considers risk 
estimates based on the full distributions of ambient O3 
concentrations and, when available, estimates of the risk associated 
with various portions of those ambient distributions.\21\ In doing so, 
the PA takes note of the ISA conclusions regarding confidence in linear 
concentration-response relationships over distributions of ambient 
concentrations (see above), and of the extent to which health effect 
associations at various ambient O3 concentrations are 
supported by the evidence from experimental studies for effects 
following specific O3 exposures.
---------------------------------------------------------------------------

    \20\ In previous reviews, including the 2008 review and 
reconsideration, such risks were separately estimated for 
O3 concentrations characterized as above policy-relevant 
background concentrations. Policy-relevant background concentrations 
were defined as the distribution of O3 concentrations 
attributable to sources other than anthropogenic emissions of 
O3 precursor emissions (e.g., VOC, CO, NOX) in 
the U.S., Canada, and Mexico. The decision in this review to 
estimate total risk across the full range of O3 
concentrations reflects consideration of advice from CASAC (Frey and 
Samet, 2012b).
    \21\ In a series of sensitivity analyses, the HREA also 
evaluates a series of threshold models for respiratory mortality 
associated with long-term O3 concentrations. The PA 
considers these risk estimates based on threshold models, in 
addition to HREA core estimates based on the linear model (U.S. EPA, 
2014a, sections 3.2.3.2, 4.4.2.3).
---------------------------------------------------------------------------

B. Health Effects Information

    This section outlines key information contained in the ISA (U.S. 
EPA, 2013a, Chapters 4 to 8) and in the PA (U.S. EPA, 2014c, Chapters 3 
and 4) on the known or potential effects on public health which may be 
expected from the presence of O3 in the ambient air. The 
information highlighted here summarizes: (1) New information available 
on potential mechanisms for health effects associated with exposure to 
O3 (II.B.1); (2) the nature of effects that have been 
associated directly with both short- and long-term exposure to 
O3 and indirectly with the presence of O3 in 
ambient air (II.B.2); (3) considerations related to the adversity of 
O3-attributable health effects (II.B.3); and (4) 
considerations in characterizing the public health impact of 
O3, including the identification of ``at risk'' populations 
(II.B.4).
    The decision in the 2008 rulemaking emphasized the large number of 
epidemiologic studies published since the 1997 review that continued to 
report associations with respiratory hospital admissions and emergency 
department visits, as well as additional health endpoints, including 
the effects of acute (short-term and prolonged) and chronic exposures 
to O3 on lung function decrements and enhanced respiratory 
symptoms in asthmatic individuals, school absences, and premature 
mortality. It also emphasized controlled human exposure studies showing 
respiratory effects with prolonged O3 exposures at levels 
below 80 ppb, changes in lung host defenses, and increased airway 
responsiveness, and animal toxicology studies that provided information 
about mechanisms of action.
    The ISA (U.S. EPA, 2013a) prepared for this review emphasizes a 
large number of new epidemiologic studies published since the last 
review on effects associated with both short- and long-term exposures, 
including new epidemiologic studies about risk factors. It also 
emphasizes important new information from controlled human exposure, 
dosimetry and toxicology studies. Highlights of the new evidence 
included:

    (1) Two controlled human exposure studies new since the 2008 
review are now available that examine respiratory effects associated 
with prolonged, 6.6-hour, O3 exposures to levels of 72 
ppb \22\ and 60 ppb. These studies observed effects in healthy 
adults, including lung function decrements combined with respiratory 
symptoms at 72 ppb, and lung function decrements and pulmonary 
inflammation at 60 ppb. These studies expand on evidence of lung 
function decrements with O3 exposure at 60 ppb available 
in the last review, and provide new evidence of airway inflammation, 
a mechanism by which O3 may cause other more serious 
respiratory effects (e.g., asthma exacerbations).
---------------------------------------------------------------------------

    \22\ As noted below, for the 70 ppb exposure concentration, 
Schelegle et al. (2009) reported that the actual mean exposure 
concentration was 72 ppb.
---------------------------------------------------------------------------

    (2) Recent multicity and single city epidemiologic studies 
continue to report associations between short-term O3 
exposures and respiratory hospital admissions and respiratory 
emergency department visits. Recent multicity studies and a multi-
continent study have reported consistent positive associations 
between short-term O3 exposure and total (nonaccidental) 
mortality, expanding upon evidence available in the last review. 
They also observed associations between O3 exposure and 
cardiovascular and respiratory mortality.\23\
---------------------------------------------------------------------------

    \23\ The consideration of ambient O3 concentrations 
in the locations of these epidemiologic studies are discussed in 
sections II.D.1.b and II.E.4.a below, for the current standard and 
alternative standards, respectively.
---------------------------------------------------------------------------

    (3) Recent controlled human exposure studies reporting systemic 
inflammation and cardiac changes provide support for the expanded 
body of epidemiologic evidence for

[[Page 75247]]

cardiovascular mortality, although lack of coherence with 
epidemiologic studies of cardiovascular morbidity remains an 
important uncertainty.
    (4) New epidemiologic studies provide expanded evidence for 
respiratory effects associated with long-term or repeated 
O3 concentrations (e.g., seasonal average of 1- or 8-hour 
daily max concentrations). Recent studies report interactions 
between exercise or different genetic variants and both new-onset 
asthma in children and increased respiratory symptom effects in 
individuals with asthma; additional studies of respiratory morbidity 
and mortality support the association between long-term exposure to 
O3 and a range of respiratory health effects.
    (5) New evidence of risk factors (i.e., people with certain 
genetic variants related to antioxidant status or inflammation, and 
people with reduced intake of antioxidant nutrients) strengthens our 
understanding of the potential modes of action from O3-
induced effects.
1. Overview of Mechanisms
    The purpose of this section is to describe the ISA's 
characterization of the key events and pathways that contribute to 
health effects resulting from both short-term and long-term exposures 
to O3. The information in this section draws from section 
5.3 of the ISA (U.S. EPA, 2013a). Mode of action refers to a sequence 
of key events and processes that result in a given toxic effect. 
Elucidation of mechanisms provides a more detailed understanding of 
these key events and processes. Experimental evidence elucidating modes 
of action and/or mechanisms contributes to our understanding of the 
biological plausibility of adverse O3-related health 
effects, including respiratory effects and effects outside the 
respiratory system (U.S. EPA, 2013a, Chapters 6 and 7).
    Figure 3.1 in the PA (U.S. EPA, 2014c) shows the current 
understanding of key events in the toxicity pathway of O3, 
based on the available evidence. These key events are described briefly 
here and in more detail in section 3.1.1 of the PA. The initial key 
event is the formation of secondary oxidation products in the 
respiratory tract (U.S. EPA, 2013a, section 5.3). This mainly involves 
direct reactions with components of the extracellular lining fluid 
(ELF). Although the ELF has inherent capacity to quench (based on 
individual antioxidant capacity), this capacity can be overwhelmed, 
especially with exposure to elevated concentrations of O3. 
The resulting secondary oxidation products transmit signals to the 
epithelium, pain receptive nerve fibers and, if present, immune cells 
(i.e., eosinophils, dendritic cells and mast cells) involved in 
allergic responses. Thus, the available evidence indicates that the 
effects of O3 are mediated by components of ELF and by the 
multiple cell types found in the respiratory tract. Further, oxidative 
stress is an implicit part of this initial key event.
    It is well understood that secondary oxidation products initiate 
numerous responses at the cellular, tissue, and whole organ level of 
the respiratory system. These responses include the activation of 
neural reflexes leading to lung function decrements, airway 
obstruction, and extrapulmonary effects such as slow resting heart 
rate; initiation of inflammation; alteration of barrier epithelial 
function; sensitization of bronchial smooth muscle; modification of 
lung host defenses; and airways remodeling (U.S. EPA, 2013a, section 
5.3.10, Figure 5-8). Each of these effects is discussed in more detail 
in section 3.1.1 of the PA (U.S. EPA, 2014c).
    Persistent inflammation and injury, which are observed in animal 
models of chronic and intermittent exposure to O3, are 
associated with airways remodeling (see Section 7.2.3 of the ISA, U.S. 
EPA 2013). Chronic intermittent exposure to O3 has also been 
shown to result in effects on the developing lung and immune system. 
Systemic inflammation and vascular oxidative/nitrosative stress are 
also key events in the toxicity pathway of O3. 
Extrapulmonary effects of O3 occur in numerous organ 
systems, including the cardiovascular, central nervous, reproductive, 
and hepatic systems (U.S. EPA, 2013a, sections 6.3 to 6.5 and sections 
7.3 to 7.5).
    Responses to O3 exposure are variable within the 
population. Studies have shown a large range of pulmonary function 
(i.e., spirometric) responses to O3 among healthy young 
adults, while responses within an individual are relatively consistent 
over time. Other responses to O3 have also been 
characterized by a large degree of interindividual variability. For 
example, a 3- to 20-fold difference among subjects in their studies in 
airways inflammation (i.e., neutrophilia influx) following 
O3 exposure has been reported (Schelegle et al., 1991 and 
Devlin et al., 1991, respectively). Reproducibility of an individual's 
inflammatory response to O3 exposure in humans, measured as 
sputum neutrophilia, was demonstrated by Holz et al (1999). Since 
individual inflammatory responses were relatively consistent across 
time, it was thought that inflammatory responsiveness reflected an 
intrinsic characteristic of the subject (Mudway and Kelly, 2000). While 
the basis for the observed interindividual variability in 
responsiveness to O3 is not clear, section 5.4.2 of the ISA 
discusses mechanisms that may underlie the variability in responses 
seen among individuals. Certain functional genetic polymorphisms, pre-
existing conditions or diseases, nutritional status, lifestages, and 
co-exposures contribute to altered risk of O3-induced 
effects. Experimental evidence for such O3-induced changes 
contributes to our understanding of the biological plausibility of 
adverse O3-related health effects, including a range of 
respiratory effects as well as effects outside the respiratory system 
(e.g., cardiovascular effects) (U.S. EPA, 2013a, Chapters 6 and 7).
2. Nature of Effects
    The health effects of O3 are described in detail and 
assessed in the ISA (U.S. EPA, 2013a). Based on this assessment, the 
ISA determined that a ``causal'' relationship exists between short-term 
exposure to O3 in ambient air \24\ and effects on the 
respiratory system and that a ``likely to be causal'' relationship \25\ 
exists between long-term exposure to O3 in ambient air and 
respiratory effects (U.S. EPA 2013a, pp. 1-6 to 1-7). As stated in the 
ISA, ``[c]ollectively, a very large amount of evidence spanning several 
decades supports a relationship between exposure to O3 and a 
broad range of respiratory effects'' (US. EPA, 2013a, p. 1-6). The ISA 
summarizes the longstanding body of evidence for O3 
respiratory effects as follows (U.S. EPA, 2013a, p. 1-5):
---------------------------------------------------------------------------

    \24\ In determining that a causal relationship exists for 
O3 with specific health effects, the EPA has concluded 
that ``[e]vidence is sufficient to conclude that there is a causal 
relationship with relevant pollutant exposures'' (U.S. EPA, 2013a, 
p. lxiv).
    \25\ In determining a ``likely to be a causal'' relationship 
exists for O3 with specific health effects, the EPA has 
concluded that ``[e]vidence is sufficient to conclude that a causal 
relationship is likely to exist with relevant pollutant exposures, 
but important uncertainties remain'' (U.S. EPA, 2013a, p. lxiv).

    The clearest evidence for health effects associated with 
exposure to O3 is provided by studies of respiratory 
effects. Collectively, a very large amount of evidence spanning 
several decades supports a relationship between exposure to 
O3 and a broad range of respiratory effects (see Section 
6.2.9 and Section 7.2.8). The majority of this evidence is derived 
from studies investigating short-term exposures (i.e., hours to 
weeks) to O3, although animal toxicological studies and 
recent epidemiologic evidence demonstrate that long-term exposure 
---------------------------------------------------------------------------
(i.e., months to years) may also harm the respiratory system.

Additionally, the ISA determined that the relationships between short-
term exposures to O3 in ambient air and both total mortality 
and cardiovascular effects are likely to be causal, based on expanded 
evidence bases in the current review (U.S. EPA, 2013a, pp. 1-7 to 1-

[[Page 75248]]

8). In the ISA, the EPA additionally determined that the currently 
available evidence for additional endpoints is ``suggestive'' of causal 
relationships between short-term (central nervous system effects) and 
long-term exposure (cardiovascular effects, reproductive and 
developmental effects, central nervous system effects and total 
mortality) to ambient O3.
    Consistent with emphasis in past reviews on O3 health 
effects for which the evidence is strongest, in this review the EPA 
places the greatest emphasis on studies of health effects that have 
been judged in the ISA to be caused by, or likely to be caused by, 
O3 exposures (U.S. EPA, 2013a, section 2.5.2). This section 
discusses the evidence for health effects attributable to O3 
exposures, with a focus on respiratory morbidity and mortality effects 
attributable to short- and long-term exposures, and cardiovascular 
system effects (including mortality) and total mortality attributable 
to short-term exposures. This section focuses particularly on 
considering the extent to which the scientific evidence available in 
the current review has been strengthened since the last review, and the 
extent to which important uncertainties and limitations in the evidence 
from the last review have been addressed.
    a. Respiratory Effects--Short-Term
    The 2006 O3 AQCD concluded that there was clear, 
consistent evidence of a causal relationship between short-term 
O3 exposure and respiratory effects (U.S. EPA, 2006a). This 
conclusion was substantiated by evidence from controlled human exposure 
and toxicological studies indicating a range of respiratory effects in 
response to short-term O3 exposures, including pulmonary 
function decrements and increases in respiratory symptoms, lung 
inflammation, lung permeability, and airway hyperresponsiveness. 
Toxicological studies provided additional evidence for O3-
induced impairment of host defenses. Combined, these findings from 
experimental studies provided support for epidemiologic evidence, in 
which short-term increases in ambient O3 concentration were 
consistently associated with decreases in lung function in populations 
with increased outdoor exposures, especially children with asthma and 
healthy children; increases in respiratory symptoms and asthma 
medication use in children with asthma; and increases in respiratory-
related hospital admissions and asthma-related emergency department 
visits (U.S. EPA, 2013a, pp. 6-1 to 6-2).
    As discussed in detail in the ISA (U.S. EPA, 2013a, section 6.2.9), 
studies evaluated since the completion of the 2006 O3 AQCD 
support and expand upon the strong body of evidence that, in the last 
review, indicated a causal relationship between short-term 
O3 exposures and respiratory health effects. Recent 
controlled human exposure studies conducted in young, healthy adults 
with moderate exertion have reported forced expiratory volume in 1 
second (FEV1) decrements and pulmonary inflammation 
following prolonged exposures to O3 concentrations as low as 
60 ppb, and respiratory symptoms following exposures to concentrations 
as low as 72 ppb (based on group mean responses).\26\ Epidemiologic 
studies provide evidence that increases in ambient O3 
exposures are associated with lung function decrements, increases in 
respiratory symptoms, and pulmonary inflammation in children with 
asthma; increases in respiratory-related hospital admissions and 
emergency department visits; and increases in respiratory mortality. 
Some of these studies report such associations even for O3 
concentrations at the low end of the distribution of daily 
concentrations. Recent epidemiologic studies report that associations 
with respiratory morbidity and mortality are stronger during the warm/
summer months and remain robust after adjustment for copollutants. 
Recent toxicological studies reporting O3-induced 
inflammation, airway hyperresponsiveness, and impaired lung host 
defense continue to support the biological plausibility and modes of 
action for the O3-induced respiratory effects observed in 
the controlled human exposure and epidemiologic studies. Further 
support is provided by recent studies that found O3-
associated increases in indicators of airway inflammation and oxidative 
stress in children with asthma (U.S. EPA, 2013a, section 6.2.9). 
Together, epidemiologic and experimental studies support a continuum of 
respiratory effects associated with O3 exposure that can 
result in respiratory-related emergency department visits, hospital 
admissions, and/or mortality (U.S. EPA, 2013a, section 6.2.9).
---------------------------------------------------------------------------

    \26\ Schelegle et al. (2009) reported a statistically 
significant increase in respiratory symptoms in healthy adults at a 
target O3 exposure concentration of 70 ppb, averaged over 
the study period. For this 70 ppb target exposure concentration, 
Schelegle et al. (2009) reported that the actual mean exposure 
concentration was 72 ppb.
---------------------------------------------------------------------------

    Across respiratory endpoints, evidence indicates antioxidant 
capacity may modify the risk of respiratory morbidity associated with 
O3 exposure (U.S. EPA, 2013a, section 6.2.9, p. 6-161). The 
potentially elevated risk of populations with diminished antioxidant 
capacity and the reduced risk of populations with sufficient 
antioxidant capacity is supported by epidemiologic studies and from 
controlled human exposure studies. Additional evidence characterizes 
O3-induced decreases in antioxidant levels as a key event in 
the mode of action for downstream effects.
    Key aspects of this evidence are discussed below with regard to 
lung function decrements; pulmonary inflammation, injury, and oxidative 
stress; airway hyperresponsiveness; respiratory symptoms and medication 
use; lung host defense; allergic and asthma-related responses; hospital 
admissions and emergency department visits; and respiratory 
mortality.\27\
---------------------------------------------------------------------------

    \27\ CASAC concurred that these were ``the kinds of identifiable 
effects on public health that are expected from the presence of 
ozone in the ambient air'' (Frey 2014c, p. 3).
---------------------------------------------------------------------------

i. Lung Function Decrements
    In the 2008 review, a large number of controlled human exposure 
studies\28\ reported O3-induced lung function decrements in 
young, healthy adults engaged in intermittent, moderate exertion 
following 6.6 hour exposures to O3 concentrations at or 
above 80 ppb. Although two studies also reported effects following 
exposures to lower concentrations, an important uncertainty in the last 
review was the extent to which exposures to O3 
concentrations below 80 ppb result in lung function decrements. In 
addition, in the last review epidemiologic panel studies had reported 
O3-associated lung function decrements in a variety of 
different populations (e.g., children, outdoor workers) likely to 
experience increased exposures. In the current review, additional 
controlled human exposure studies are available that have evaluated 
exposures to O3 concentrations of 60 or 72 ppb. The 
available evidence from controlled human exposure and panel studies is

[[Page 75249]]

assessed in detail in the ISA (U.S. EPA, section 6.2.1) and is 
summarized below.
---------------------------------------------------------------------------

    \28\ The controlled human exposure studies emphasized in the PA 
utilize only healthy adult subjects. In the near absence of 
controlled human exposure data for children, HREA estimates of lung 
function decrements are based on the assumption that children 
exhibit the same lung function responses following O3 
exposures as healthy 18 year olds (U.S. EPA, 2014a, section 6.2.4 
and 6.5). This assumption is justified in part by the findings of 
McDonnell et al. (1985), who reported that children (8-11 years old) 
experienced FEV1 responses similar to those observed in 
adults (18-35 years old). Thus, the conclusions about the occurrence 
of lung function decrements that follow generally apply to children 
as well as to adults.
---------------------------------------------------------------------------

    Controlled exposures to O3 concentrations that can be 
found in the ambient air can result in a number of lung function 
effects, including decreased inspiratory capacity, mild 
bronchoconstriction, and rapid, shallow breathing patterns during 
exercise. Reflex inhibition of inspiration results in a decrease in 
forced vital capacity (FVC) and total lung capacity (TLC) and, in 
combination with mild bronchoconstriction, contributes to a decrease in 
FEV1 (U.S. EPA, 2013a, section 6.2.1.1). Accumulating 
evidence indicates that such effects are mediated by activation of 
sensory nerves, resulting in the involuntary truncation of inspiration 
and a mild increase in airway obstruction due to bronchoconstriction 
(U.S. EPA, 2013a, section 5.3.10).
    Data from controlled human exposure studies show that increasing 
the duration of O3 exposures and increasing ventilation 
rates decreases the O3 exposure concentrations required to 
impair lung function. Ozone exposure concentrations well above those 
typically found in ambient air are required to impair lung function in 
healthy resting adults, while exposure to O3 concentrations 
at or below those in the ambient air have been reported to impair lung 
function in healthy adults exposed for longer durations while 
undergoing intermittent, moderate exertion (U.S. EPA, 2013a, section 
6.2.1.1). With repeated O3 exposures over several days, 
FEV1 responses become attenuated in both healthy adults and 
adults with mild asthma, though this attenuation of response is lost 
after about a week without exposure (U.S. EPA, 2013a, section 6.2.1.1; 
p. 6-27).
    When considering controlled human exposure studies of 
O3-induced lung function decrements, the ISA and PA evaluate 
both group mean changes in lung function and the interindividual 
variability in the magnitude of responses. An advantage of 
O3 controlled human exposure studies (i.e., compared to the 
epidemiologic panel studies discussed below) is that reported effects 
necessarily result from exposures to O3 itself.\29\ To the 
extent studies report statistically significant decrements in mean lung 
function following O3 exposures after controlling for other 
factors, these studies provide greater confidence that measured 
decrements are due to the O3 exposure itself, rather than to 
chance alone. As discussed below, group mean changes in lung function 
are often small, especially following exposures to relatively low 
O3 concentrations (e.g., 60 ppb). However, even when group 
mean decrements in lung function are small, some individuals could 
experience decrements that are ``clinically meaningful'' (Pellegrino et 
al., 2005; ATS, 1991) with respect to criteria for spirometric testing, 
and/or that could be considered adverse with respect to public health 
policy decisions (see section II.B.3, below).
---------------------------------------------------------------------------

    \29\ The ISA notes that the use of filtered air responses as a 
control for the assessment of responses following O3 
exposure in controlled human exposure studies serves to eliminate 
alternative explanations other than O3 itself in causing 
the measured responses (U.S. EPA, 2013a, section 6.2.1.1).
---------------------------------------------------------------------------

    At the time of the last review, a number of controlled human 
exposure studies had reported lung function decrements in young, 
healthy adults following prolonged (6.6-hour) exposures while at 
moderate exertion to O3 concentrations at and above 80 ppb. 
In addition, there were two controlled human exposure studies by Adams 
(2002, 2006) that examined lung function effects following exposures to 
60 ppb O3. The EPA's analysis of the data from the Adams 
(2006) study reported a small but statistically significant 
O3-induced decrement in group mean FEV1 following 
exposures of young, healthy adults to 60 ppb O3 while at 
moderate exertion, when compared with filtered air controls (Brown et 
al., 2008).\30\ Further examination of the post-exposure 
FEV1 data, and mean data for other time points and other 
concentrations, indicated that the temporal pattern of the response to 
60 ppb O3 was generally consistent with the temporal 
patterns of responses to higher O3 concentrations in this 
and other studies (75 FR 2950, January 19, 2010). This suggested a 
pattern of response following exposures to 60 ppb O3 that 
was consistent with a dose-response relationship, rather than random 
variability. See also State of Mississippi v. EPA, F. 3d at 1347 
(upholding EPA's interpretation of the Adams studies).
---------------------------------------------------------------------------

    \30\ Adams (2006) did not find effects on FEV1 at 60 
ppb to be statistically significant. In an analysis of the Adams 
(2006) data, Brown et al. (2008) showed that even after removal of 
potential outliers, the average effect on FEV1 at 60 ppb 
was small, but highly statistically significant (p <0.002) using 
several common statistical tests.
---------------------------------------------------------------------------

    Figure 6-1 in the ISA summarizes the currently available evidence 
from multiple controlled human exposure studies evaluating group mean 
changes in FEV1 following prolonged O3 exposures 
(i.e., 6.6 hours) in young, healthy adults engaged in moderate levels 
of physical activity (U.S. EPA, 2013a, section 6.2.1.1). With regard to 
the group mean changes reported in these studies, the ISA specifically 
notes the following (U.S. EPA, 2013a, section 6.2.1.1, Figure 6-1):
    1. Prolonged exposure to 40 ppb O3 results in a small 
decrease in group mean FEV1 that is not statistically 
different from responses following exposure to filtered air (Adams, 
2002; Adams, 2006).
    2. Prolonged exposure to an average O3 concentration of 
60 ppb results in group mean FEV1 decrements ranging from 
1.8% to 3.6% (Adams 2002; Adams, 2006; \31\ Schelegle et al., 2009; 
\32\ Kim et al., 2011). Based on data from multiple studies, the 
weighted average group mean decrement was 2.7%. In some analyses, these 
group mean decrements in lung function were statistically significant 
(Brown et al., 2008; Kim et al., 2011), while in other analyses they 
were not (Adams, 2006; Schelegle et al., 2009).\33\
---------------------------------------------------------------------------

    \31\ Adams (2006); (2002) both provide data for an additional 
group of 30 healthy subjects that were exposed via facemask to 60 
ppb (square-wave) O3 for 6.6 hours with moderate exercise 
(VE = 23 L/min per m\2\ BSA). These subjects are 
described on page 133 of Adams (2006) and pages 747 and 761 of Adams 
(2002). The FEV1 decrement may be somewhat increased due 
to a target VE of 23 L/min per m\2\ BSA relative to other 
studies having the target VE of 20 L/min per m\2\ BSA. 
The facemask exposure is not expected to affect the FEV1 
responses relative to a chamber exposure.
    \32\ For the 60 ppb target exposure concentration, Schelegle et 
al. (2009) reported that the actual mean exposure concentration was 
63 ppb.
    \33\ Adams (2006) did not find effects on FEV1 at 60 
ppb to be statistically significant. In an analysis of the Adams 
(2006) data, Brown et al. (2008) addressed the more fundamental 
question of whether there were statistically significant differences 
in responses before and after the 6.6 hour exposure period and found 
the average effect on FEV1 at 60 ppb to be small, but 
highly statistically significant using several common statistical 
tests, even after removal of potential outliers. Schelegle et al. 
(2009) reported that, compared to filtered air, the largest change 
in FEV1 for the 60 ppb protocol occurred after the sixth 
(and final) exercise period.
---------------------------------------------------------------------------

    3. Prolonged exposure to an average O3 concentration of 
72 ppb results in a statistically significant group mean decrement in 
FEV1 of about 6% (Schelegle et al., 2009).\34\
---------------------------------------------------------------------------

    \34\ As noted above, for the 70 ppb exposure group, Schelegle et 
al. (2009) reported that the actual mean exposure concentration was 
72 ppb.
---------------------------------------------------------------------------

    4. Prolonged square-wave exposure to average O3 
concentrations of 80 ppb, 100 ppb, or 120 ppb O3 results in 
statistically significant group mean decrements in FEV1 
ranging from 6 to 8%, 8 to 14%, and 13 to 16%, respectively (Folinsbee 
et al., 1988; Horstman et al., 1990; McDonnell et al., 1991; Adams, 
2002; Adams, 2003; Adams, 2006).
    As illustrated in Figure 6-1 of the ISA, there is a smooth dose-
response

[[Page 75250]]

curve without evidence of a threshold for exposures between 40 and 120 
ppb O3 (U.S. EPA, 2013a, Figure 6-1). When these data are 
taken together, the ISA concludes that ``mean FEV1 is 
clearly decreased by 6.6-hour exposures to 60 ppb O3 and 
higher concentrations in [healthy, young adult] subjects performing 
moderate exercise'' (U.S. EPA, 2013a, p. 6-9).
    With respect to interindividual variability in lung function, in an 
individual with relatively ``normal'' lung function, with recognition 
of the technical and biological variability in measurements, within-day 
changes in FEV1 of >=5% are clinically meaningful 
(Pellegrino et al., 2005; ATS, 1991). The ISA (U.S. EPA, 2013a, section 
6.1.) focuses on individuals with >10% decrements in FEV1 
for two reasons. A 10% FEV1 decrement is accepted by the 
American Thoracic Society (ATS) as an abnormal response and a 
reasonable criterion for assessing exercise-induced bronchoconstriction 
(Dryden et al., 2010; ATS, 2000). (U.S. EPA, 2013a, section 6.2.1.1). 
Also, some individuals in the Schelegle et al. (2009) study experienced 
5-10% FEV1 decrements following exposure to filtered air.
    In previous NAAQS reviews, the EPA has made judgments regarding the 
potential implications for individuals experiencing FEV1 
decrements of varying degrees of severity.\35\ For people with lung 
disease, the EPA judged that moderate functional decrements (e.g., 
FEV1 decrements >10% but <20%, lasting up to 24 hours) would 
likely interfere with normal activity for many individuals, and would 
likely result in more frequent use of medication (75 FR 2973, January 
19, 2010). In previous reviews CASAC has endorsed these conclusions. In 
the context of standard setting, in the last review of the 
O3 NAAQS CASAC indicated that it is appropriate to focus on 
the lower end of the range of moderate functional responses (e.g., 
FEV1 decrements >=10%) when estimating potentially adverse 
lung function decrements in people with lung disease, especially 
children with asthma (Henderson, 2006c; transcript of CASAC meeting, 
day 8/24/06, page 149). More specifically, CASAC stated that ``[a] 10% 
decrement in FEV1 can lead to respiratory symptoms, 
especially in individuals with pre-existing pulmonary or cardiac 
disease. For example, people with chronic obstructive pulmonary disease 
have decreased ventilatory reserve (i.e., decreased baseline 
FEV1) such that a >=10% decrement could lead to moderate to 
severe respiratory symptoms'' (Samet, 2011). In this review, CASAC 
reiterated its support for this conclusion, stating that ``[a]n FEV1 
decrement of >=10% is a scientifically relevant surrogate for adverse 
health outcomes for people with asthma and lung disease'' (Frey, 2014c 
p. 3). Therefore, in considering interindividual variability in 
O3-induced lung function decrements in the current review, 
the EPA also focuses on the extent to which individuals were reported 
to experience FEV1 decrements of 10% or greater.\36\
---------------------------------------------------------------------------

    \35\ Such judgments have been made for decrements in 
FEV1 as well as for increased airway responsiveness and 
symptomatic responses (e.g., cough, chest pain, wheeze). Ranges of 
pulmonary responses and their associated potential impacts are 
presented in Tables 3-2 and 3-3 of the 2007 Staff Paper (U.S. EPA, 
2007).
    \36\ The approach to using results from controlled human 
exposure studies conducted in healthy adults to provide perspective 
on the potential public health impacts of O3-related 
respiratory health effects is discussed in section II.A above, and 
in sections II.C.2 and II.C.3 below.
---------------------------------------------------------------------------

    New studies (Schelegle et al., 2009; Kim et al., 2011) add to the 
previously available evidence for interindividual variability in the 
responses of healthy adults following exposures to O3. 
Following prolonged exposures to 80 ppb O3 while at moderate 
exertion, the proportion of healthy adults experiencing FEV1 
decrements greater than 10% was 17% by Adams (2006), 26% by McDonnell 
(1996), and 29% by Schelegle et al. (2009). Following exposures to 60 
ppb O3, that proportion was 20% by Adams (2002), 3% by Adams 
(2006), 16% by Schelegle et al. (2009), and 5% by Kim et al. (2011). 
Across these studies, the weighted average proportion (i.e., based on 
numbers of subjects in each study) of young, healthy adults with >10% 
FEV1 decrements is 25% following exposure to 80 ppb 
O3 and 10% following exposure to 60 ppb O3, for 
6.6 hours at moderate exertion (U.S. EPA, 2013a, page 6-18 and 6-
19).\37\ \38\ The ISA notes that responses within an individual tend to 
be reproducible over a period of several months, indicating that 
interindividual differences reflect differences in intrinsic 
responsiveness. Given this, the ISA concludes that ``[t]hough group 
mean decrements are biologically small and generally do not attain 
statistical significance, a considerable fraction of exposed 
individuals experience clinically meaningful decrements in lung 
function'' when exposed for 6.6 hours to 60 ppb O3 during 
quasi continuous, moderate exertion (U.S. EPA, 2013a, section 6.2.1.1, 
p. 6-20).
---------------------------------------------------------------------------

    \37\ The ISA notes that by considering responses uncorrected for 
filtered air exposures, during which lung function typically 
improves (which would increase the size of the change, pre-and post-
exposure), 10% is an underestimate of the proportion of healthy 
individuals that are likely to experience clinically meaningful 
changes in lung function following exposure for 6.6 hours to 60 ppb 
O3 during intermittent moderate exertion (U.S. EPA, 2012, 
section 6.2.1.1).
    \38\ Based on the data available at 60 ppb, 1% of subjects 
experienced decrements >20% (also uncorrected for filtered air 
exposures).
---------------------------------------------------------------------------

    This review has marked an advance in the ability to make reliable 
quantitative predictions of the potential lung function response to 
ozone exposure, and thus to reasonably predict the degree of 
interindividual response of lung function to that exposure. McDonnell 
et al. (2012) and Schelegle et al. (2012) developed models using data 
on O3 exposure concentrations, ventilation rates, duration 
of exposures, and lung function responses from a number of controlled 
human exposure studies. See section 6.2.1.1 of the ISA (U.S. EPA 2013a, 
p. 6-15). The McDonnell et al. (2012) and Schelegle et al. (2012) 
studies analyzed large datasets to fit compartmental models that 
included the concept of a dose of onset in lung function response or a 
response threshold based upon the inhaled O3 dose. The 
McDonnell et al. (2012) model was fit to a dataset consisting of the 
FEV1 responses of 741 young, healthy adults (18-35 years of 
age) from 23 individual controlled exposure studies. Concentrations 
across individual studies ranged from 40 ppb to 400 ppb,\39\ activity 
level ranged from rest to heavy exercise, duration of exposure was from 
2 to 7.6 hours. The extension of the McDonnell et al. (2012) model to 
children and older adults is discussed in section 6.2.4 of the HREA 
(U.S. EPA, 2014a). Schelegle et al. (2012) also analyzed a large 
dataset with substantial overlap to that used by McDonnell et al. 
(2012). The Schelegle et al. (2012) model was fit to the 
FEV1 responses of 220 young healthy adults (taken from a 
dataset of 704 individuals) from 21 individual controlled exposure 
studies. The resulting empirical models can estimate the frequency 
distribution of individual responses for any exposure scenario as well 
as summary measures of the distribution such as the mean or median 
response and the proportions of individuals with FEV1 
decrements >10%, 15%, and 20%.
---------------------------------------------------------------------------

    \39\ Responses to O3 in these studies were adjusted 
for responses observed following exposure to filtered air.
---------------------------------------------------------------------------

    The predictions of the McDonnell and Schelegle models are 
consistent with the observed results from the individual studies of 
O3-induced FEV1 decrements. Specifically, 
McDonnell et al. (2012) estimated that 9% of healthy exercising adults 
would experience FEV1 decrements greater than 10% following

[[Page 75251]]

6.6 hour exposure to 60 ppb O3, and that 22% would 
experience such decrements following exposure to 80 ppb O3 
(U.S. EPA, 2013a, p. 6-18 and Figure 6-3).\40\ Schelegle et al. (2012) 
estimated that, for a prolonged (6.6 hours) O3 exposure with 
moderate, quasi-continuous exercise, the average dose of onset for 
FEV1 decrement would be reached following 4 to 5 hours of 
exposure to 60 ppb, and following 3 to 4 hours of exposure to 80 ppb. 
However, 14% of the individuals were estimated to have a dose of onset 
that was less than 40% of the average. Those individuals were estimated 
to reach their dose of onset following 1 to 2 hours of exposure to 50 
to 80 ppb O3 (U.S. EPA, 2013a, p. 6-16), which is consistent 
with the threshold FEV1 responses reported by McDonnell et 
al. (2012).
---------------------------------------------------------------------------

    \40\ Also consistent with the data from published studies (see 
above), this model predicts that 1% of people would experience 
FEV1 decrements >20% following 6.6 hour exposure to 60 
ppb O3.
---------------------------------------------------------------------------

    CASAC agreed that these models mark a significant technical advance 
over the exposure-response modeling approach used in the last review 
(Frey, 2014a), stating that ``the comparison of the MSS [McDonnell-
Stewart-Smith] model results to those obtained with the exposure-
response (E-R) model is of tremendous importance. Typically, the MSS 
model gives results about a factor of three higher than the E-R model 
for school-aged children, which is expected because the MSS model 
includes responses for a wider range of exposure protocols (under 
different levels of exertion, lengths of exposure, and patterns of 
exposure concentrations) than the E-R model'' (Frey, 2014a, p. 7). 
CASAC explicitly found ``the updated and expanded lung finds the MSS 
model to be scientifically and biologically defensible.'' (Frey, 2014a, 
pp. 2, 8).
    As discussed above and in the ISA (U.S EPA, 2013a, Section 5.3.2), 
secondary oxidation products formed following O3 exposures 
can activate neural reflexes leading to decreased lung function. The 
McDonnell and Schelegle models included mathematical approaches to 
simulate the potential protective effect of antioxidants in the ELF at 
lower ambient O3 concentrations, and include a dose 
threshold below which changes in lung function do not occur.
    Epidemiologic studies \41\ have consistently linked short-term 
increases in ambient O3 concentrations with lung function 
decrements in diverse populations and lifestages, including children 
attending summer camps, adults exercising or working outdoors, and 
groups with pre-existing respiratory diseases such as asthmatic 
children (U.S. EPA, 2013a, section 6.2.1.2). Some of these studies 
reported O3-associated lung function decrements accompanied 
by respiratory symptoms \42\ in asthmatic children (Just et al., 2002; 
Mortimer et al., 2002; Ross et al., 2002; Gielen et al., 1997; Romieu 
et al., 1997; Thurston et al., 1997; Romieu et al., 1996). In contrast, 
studies of children in the general population have reported similar 
O3-associated lung function decrements but without 
accompanying respiratory symptoms (Ward et al., 2002; Gold et al., 
1999; Linn et al., 1996) (U.S. EPA, 2013a, section 6.2.1.2).
---------------------------------------------------------------------------

    \41\ Unless otherwise specified, the epidemiologic studies 
discussed in the PA evaluate only adults.
    \42\ Reversible loss of lung function in combination with the 
presence of symptoms meets the ATS definition of adversity (ATS, 
2000).
---------------------------------------------------------------------------

    Several epidemiologic panel studies \43\ reported statistically 
significant associations with lung function decrements at relatively 
low ambient O3 concentrations. For outdoor recreation or 
exercise, associations were reported in analyses restricted to 1-hour 
average O3 concentrations less than 80 ppb (Spektor et al., 
1988a; Spektor et al., 1988b), 60 ppb (Brunekreef et al., 1994; Spektor 
et al., 1988a), and 50 ppb (Brunekreef et al., 1994). Among outdoor 
workers, Brauer et al. (1996) found a robust association with daily 1-
hour max O3 concentrations less than 40 ppb. Ulmer et al. 
(1997) found a robust association in schoolchildren with 30-minute 
maximum O3 concentrations less than 60 ppb. For 8-hour 
average O3 concentrations, associations with lung function 
decrements in children with asthma were found to persist at 
concentrations less than 80 ppb in a U.S. multicity study (Mortimer et 
al., 2002) and less than 51 ppb in a study conducted in the Netherlands 
(Gielen et al., 1997).
---------------------------------------------------------------------------

    \43\ Panel studies include repeated measurements of health 
outcomes, such as respiratory symptoms, at the individual level 
(U.S. EPA, 2013a, p. 1x).
---------------------------------------------------------------------------

    Epidemiologic panel studies investigating the effects of short-term 
exposure to O3 provided information on potential confounding 
by copollutants such as particulate matter with a median aerodynamic 
diameter less than or equal to 2.5 microns (PM2.5), 
particulate matter with a median aerodynamic diameter less than or 
equal to 10 microns (PM10), nitrogen dioxide 
(NO2), or sulfur dioxide (SO2). These studies 
varied in how they evaluated confounding. Some studies of subjects 
exercising outdoors indicated that ambient concentrations of 
copollutants such as NO2, SO2, or acid aerosol 
were low, and thus not likely to confound associations observed for 
O3 (Hoppe et al., 2003; Brunekreef et al., 1994; Hoek et 
al., 1993). In other studies of children with increased outdoor 
exposures, O3 was consistently associated with decreases in 
lung function, whereas other pollutants such as PM2.5, 
sulfate, and acid aerosol individually showed variable associations 
across studies (Thurston et al., 1997; Castillejos et al., 1995; Berry 
et al., 1991; Avol et al., 1990; Spektor et al., 1988a). Studies that 
conducted copollutant modeling generally found O3-associated 
lung function decrements to be robust (i.e., most copollutant-adjusted 
effect estimates fell within the 95% confidence interval (CI) of the 
single-pollutant effect estimates) (U.S. EPA, 2013a, Figure 6-10 and 
Table 6-14). Most O3 effect estimates for lung function were 
robust to adjustment for temperature, humidity, and copollutants such 
as PM2.5, PM10, NO2, or 
SO2. Although examined in only a few epidemiologic studies, 
O3 also remained associated with decreases in lung function 
with adjustment for pollen or acid aerosols (U.S. EPA, 2013a, section 
6.2.1.2).
    Several epidemiologic studies demonstrated the protective effects 
of vitamin E and vitamin C supplementation, and increased dietary 
antioxidant intake, on O3-induced lung function decrements 
(Romieu et al., 2002) (U.S. EPA, 2013a, Figure 6-7 and Table 6-8).\44\ 
These results provide support for the new, quantitative models 
(McDonnell et al., 2012; Schelegle et al., 2012), discussed above, 
which make use of the concept of oxidant stress to estimate the 
occurrence of lung function decrements following exposures to 
relatively low O3 concentrations.
---------------------------------------------------------------------------

    \44\ Evidence from controlled human exposure studies is mixed, 
suggesting that supplementation may be ineffective in the absence of 
antioxidant deficiency (U.S. EPA, 2013a, p. 5-63).
---------------------------------------------------------------------------

    In conclusion, new information from controlled human exposure 
studies considerably strengthens the evidence and reduces the 
uncertainties, relative to the evidence that was available at the time 
of the 2008 review, regarding the presence and magnitude of lung 
function decrements in healthy adults following prolonged exposures to 
O3 concentrations below 80 ppb. As discussed in Section 
6.2.1.1 in the ISA (U.S. EPA, 2013, p. 6-12), there is information 
available from four separate studies that evaluated exposures to 60 ppb 
O3 (Kim et al., 2011; Schelegle et al., 2009; Adams 2002; 
2006). Although not consistently statistically significant, group mean 
FEV1 decrements following exposures to 60 ppb O3 
are consistent

[[Page 75252]]

among these studies. Moreover, as is illustrated in Figure 6-1 of the 
ISA (U.S. EPA, 2013a), the group mean FEV1 responses at 60 
ppb fall on a smooth intake dose-response curve for exposures between 
40 and 120 ppb O3. Based on the data in these studies, 10% 
of young, healthy adults experience clinically meaningful decrements in 
lung function when exposed for 6.6 hours to 60 ppb O3 during 
intermittent, moderate exertion. One recent study has also reported 
statistically significant decrements following exposures to 72 ppb 
O3 (Schelegle et al., 2009). Predictions from newly 
developed quantitative models are consistent with these experimental 
results. Additionally, as discussed in more detail in section II.B.4 
below, epidemiologic studies continue to provide evidence of lung 
function decrements in people who are active outdoors, including people 
engaged in outdoor recreation or exercise, children, and outdoor 
workers, at low ambient O3 concentrations. While few new 
epidemiologic studies of O3-associated lung function 
decrements are available in this review, previously available studies 
have reported associations with decrements, including at relatively low 
ambient O3 concentrations.
ii. Pulmonary Inflammation, Injury, and Oxidative Stress
    Ozone exposures result in increased respiratory tract inflammation 
and epithelial permeability. Inflammation is a host response to injury, 
and the induction of inflammation is evidence that injury has occurred. 
Oxidative stress has been shown to play a key role in initiating and 
sustaining O3-induced inflammation. Secondary oxidation 
products formed as a result of reactions between O3 and 
components of the ELF can increase the expression of molecules (i.e., 
cytokines, chemokines, and adhesion molecules) that can enhance airway 
epithelium permeability (U.S. EPA, 2013a, sections 5.3.3 and 5.3.4). As 
discussed in detail in the ISA (U.S. EPA, 2013a, section 6.2.3), 
O3 exposures can initiate an acute inflammatory response 
throughout the respiratory tract that has been reported to persist for 
at least 18-24 hours after exposure.
    Inflammation induced by exposure of humans to O3 can 
have several potential outcomes: (1) Inflammation induced by a single 
exposure (or several exposures over the course of a summer) can resolve 
entirely; (2) continued acute inflammation can evolve into a chronic 
inflammatory state; (3) continued inflammation can alter the structure 
and function of other pulmonary tissue, leading to diseases such as 
asthma; (4) inflammation can alter the body's host defense response to 
inhaled microorganisms, particularly in potentially at-risk populations 
or lifestages such as the very young and old; and (5) inflammation can 
alter the lung's response to other agents such as allergens or toxins 
(U.S. EPA, 2013a, section 6.2.3). Thus, lung injury and the resulting 
inflammation provide a mechanism by which O3 may cause other 
more serious morbidity effects (e.g., asthma exacerbations).\45\
---------------------------------------------------------------------------

    \45\ CASAC also addressed this issue: ``The CASAC believes that 
these modest changes in FEV1 are usually associated with 
inflammatory changes, such as more neutrophils in the 
bronchoalveolar lavage fluid. Such changes may be linked to the 
pathogenesis of chronic lung disease'' (Frey, 2014a p. 2).
---------------------------------------------------------------------------

    In the last review, controlled human exposure studies reported 
O3-induced airway inflammation following exposures at or 
above 80 ppb and animal toxicological studies provided evidence for 
increases in inflammation and permeability in rabbits at levels as low 
as 100 ppb O3. In the current review, the link between 
O3 exposures and airway inflammation and injury has been 
evaluated in additional controlled human exposure studies, as well as 
in recent epidemiologic studies. Controlled human exposure studies have 
generally been conducted in young, healthy adults or in adults with 
asthma using lavage (proximal airway and bronchoalveolar), bronchial 
biopsy, and more recently, induced sputum. These studies have evaluated 
one or more indicators of inflammation, including neutrophil \46\ (PMN) 
influx, markers of eosinophilic inflammation, increased permeability of 
the respiratory epithelium, and/or prevalence of proinflammatory 
molecules (U.S. EPA, 2013a, section 6.2.3.1). Epidemiologic studies 
have generally evaluated associations between ambient O3 and 
markers of inflammation and/or oxidative stress, which plays a key role 
in initiating and sustaining inflammation (U.S. EPA, 2013a, section 
6.2.3.2).
---------------------------------------------------------------------------

    \46\ Referred to as either neutrophils or polymorphonuclear 
neutrophils (or PMNs), these are the most abundant type of white 
blood cells in mammals. PMNs are recruited to the site of injury 
following trauma and are the hallmark of acute inflammation. The 
presence of PMNs in the lung has long been accepted as a hallmark of 
inflammation and is an important indicator that O3 causes 
inflammation in the lungs. Neutrophilic inflammation of tissues 
indicates activation of the innate immune system and requires a 
complex series of events, that then are normally followed by 
processes that clear the evidence of acute inflammation.
---------------------------------------------------------------------------

    There is an extensive body of evidence from controlled human 
exposure studies indicating that short-term exposures to O3 
can cause pulmonary inflammation. A single acute exposure (1-4 hours) 
of humans to moderate concentrations of O3 (200-600 ppb) 
while exercising at moderate to heavy intensities resulted in a number 
of cellular and biochemical changes in the lung, including inflammation 
characterized by increased numbers of PMNs, increased permeability of 
the epithelial lining of the respiratory tract, cell damage, and 
production of proinflammatory molecules (i.e., cytokines and 
prostaglandins, U.S. EPA, 2006a). A meta-analysis of 21 controlled 
human exposure studies (Mudway and Kelly, 2004) using varied 
experimental protocols (80-600 ppb O3 exposures; 1-6.6 hours 
exposure duration; light to heavy exercise; bronchoscopy at 0-24 hours 
post-O3 exposure) reported that PMN influx in healthy 
subjects is linearly associated with total O3 dose.
    Several studies, including one published since the last review 
(Alexis et al., 2010), have reported O3-induced increases in 
PMN influx and permeability following exposures at or above 80 ppb 
(Alexis et al., 2010; Peden et al., 1997; Devlin et al., 1991), and 
eosinophilic inflammation following exposures at or above 160 ppb 
(Scannell et al., 1996; Peden et al., 1997; Hiltermann et al., 1999; 
Vagaggini et al., 2002). In addition, one recent controlled human 
exposure study has reported O3-induced PMN influx following 
exposures of healthy adults to 60 ppb O3 (Kim et al., 2011), 
the lowest concentration at which inflammatory responses have been 
evaluated in human studies.
    As with FEV1 responses to O3, inflammatory 
responses to O3 are generally reproducible within 
individuals, with some individuals experiencing more severe 
O3-induced airway inflammation than indicated by group 
averages (Holz et al., 2005; Holz et al., 1999). Unlike O3-
induced decrements in lung function, which are attenuated following 
repeated exposures over several days (U.S. EPA, 2013a, section 
6.2.1.1), some markers of O3-induced inflammation and tissue 
damage remain elevated during repeated exposures, indicating ongoing 
damage to the respiratory system (U.S. EPA, 2013a, section 6.2.3.1).
    Most controlled human exposure studies have reported that 
asthmatics experience larger O3-induced inflammatory 
responses than non-asthmatics.\47\ Specifically, asthmatics

[[Page 75253]]

exposed to 200 ppb O3 for 4-6 hours with exercise show 
significantly more neutrophils in bronchoalveolar lavage fluid (BALF) 
than similarly exposed healthy individuals (Scannell et al., 1996; 
Basha et al., 1994). Bosson et al. (2003) reported significantly 
greater expression of a variety of pro-inflammatory cytokines in 
asthmatics, compared to healthy subjects, following exposure to 200 ppb 
O3 for 2 hours. In addition, research available in the last 
review, combined with a recent study newly available in this review, 
indicates that pretreatment of asthmatics with corticosteroids can 
prevent the O3-induced inflammatory response in induced 
sputum, though pretreatment did not prevent FEV1 decrements 
(Vagaggini et al., 2001; 2007). In contrast, Stenfors et al. (2002) did 
not detect a difference in the O3-induced increases in 
neutrophil numbers between 15 subjects with mild asthma and 15 healthy 
subjects by bronchial wash at the 6 hours postexposure time point, 
although the neutrophil increase in the asthmatic group was on top of 
an elevated baseline.
---------------------------------------------------------------------------

    \47\ When evaluated, these studies have also reported 
O3-induced respiratory symptoms in asthmatics. 
Specifically, Scannell et al. (1996), Basha et al. (1994), and 
Vagaggini et al. (2001, 2007) reported increased symptoms in 
addition to inflammation.
---------------------------------------------------------------------------

    In people with allergic airway disease, including people with 
rhinitis and asthma, evidence available in the last review indicated 
that proinflammatory mediators also cause accumulation of eosinophils 
in the airways (Jorres et al., 1996; Peden et al., 1995 and 1997; 
Frampton et al., 1997; Hiltermann et al., 1999; Holz et al., 2002; 
Vagaggini et al., 2002). The eosinophil, which increases inflammation 
and allergic responses, is the cell most frequently associated with 
exacerbations of asthma (72 FR 37846, July 11, 2007).
    Studies reporting inflammatory responses and markers of lung injury 
have clearly demonstrated that there is important variation in the 
responses of exposed subjects (72 FR 37831, July 11, 2007). Some 
individuals also appear to be intrinsically more susceptible to 
increased inflammatory responses from O3 exposure (Holz et 
al., 2005). In healthy adults exposed to each 80 and 100 ppb 
O3, Devlin et al. (1991) observed group average increases in 
neutrophilic inflammation of 2.1- and 3.8-fold, respectively. However, 
there was a 20-fold range in inflammatory responses between individuals 
at both concentrations. Relative to an earlier, similar study conducted 
at 400 ppb (Koren et al., 1989), Devlin et al. (1991) noted that 
although some of the study population showed little or no increase in 
inflammatory and cellular injury indicators analyzed after exposures to 
lower levels of O3 (i.e., 80 and 100 ppb), others had 
changes that were as large as those seen when subjects were exposed to 
400 ppb O3. The study authors concluded that, ``while the 
population as a whole may have a small inflammatory response to near-
ambient levels of ozone, there may be a significant subpopulation that 
is very sensitive to these low levels'' (Devlin et al., 1991).
    A number of studies report that O3 exposures increase 
epithelial permeability. Increased BALF protein, suggesting 
O3-induced changes in epithelial permeability, has been 
reported at 1 hour and 18 hours postexposure (Devlin et al., 1997; 
Balmes et al., 1996). A meta-analysis of results from 21 publications 
(Mudway and Kelly, 2004) for varied experimental protocols (80-600 ppb 
O3; 1-6.6 hours duration; light to heavy exercise; 
bronchoscopy at 0-24 hours post-O3 exposure; healthy 
subjects), showed that increased BALF protein is associated with total 
inhaled O3 dose. As noted in the 2009 PM ISA (U.S. EPA, 
2009a), it has been postulated that changes in permeability associated 
with acute inflammation may provide increased access of inhaled 
antigens, particles, and other inhaled substances deposited on lung 
surfaces to the smooth muscle, interstitial cells, immune cells 
underlying the epithelium, and the blood (U.S. EPA, 2013a, sections 
5.3.4, 5.3.5). As has been observed with FEV1 responses, 
within individual changes in permeability are correlated with changes 
following sequential O3 exposures (Que et al., 2011). 
Changes in permeability and AHR apear to be mediated by different 
pathways. Animal toxicology studies have provided some support for this 
hypothesis (Adamson and Prieditis, 1995; Chen et al., 2006), though 
these studies did not specifically evaluate O3 exposures 
(U.S. EPA, 2009a).
    The limited epidemiologic evidence reviewed in the 2006 
O3 AQCD (U.S. EPA, 2006a) reported associations between 
short-term increases in ambient O3 concentrations and 
airways inflammation in children (1-hour max O3 of 
approximately 100 ppb). In the 2006 O3 AQCD (U.S. EPA, 
2006a), there was limited evidence for increases in nasal lavage levels 
of inflammatory cell counts and molecules released by inflammatory 
cells (i.e., eosinophilic cationic protein, and myeloperoxidases). 
Since 2006, as a result of the development of less invasive methods, 
there has been a large increase in the number of studies assessing 
ambient O3-associated changes in airway inflammation and 
oxidative stress, the types of biological samples collected, and the 
types of indicators. Most of these recent studies have evaluated 
biomarkers of inflammation or oxidative stress in exhaled breath, nasal 
lavage fluid, or induced sputum (U.S. EPA, 2013a, section 6.2.3.2). 
These recent studies form a larger database to establish coherence with 
findings from controlled human exposure and animal studies that have 
measured the same or related biological markers. Additionally, results 
from these studies provide further biological plausibility for the 
associations observed between ambient O3 concentrations and 
respiratory symptoms and asthma exacerbations.
    A number of epidemiologic studies provide evidence that short-term 
increases in ambient O3 exposure increase pulmonary 
inflammation and oxidative stress in children, including those with 
asthma (Sienra-Monge et al., 2004; Barraza-Villarreal et al., 2008; 
Romieu et al., 2008; Berhane et al., 2011). Multiple studies examined 
and found increases in exhaled nitric oxide (eNO)\48\ (Berhane et al., 
2011; Khatri et al., 2009; Barraza-Villarreal et al., 2008). In some 
studies of subjects with asthma, increases in ambient O3 
concentration at the same lag were associated with both increases in 
pulmonary inflammation and respiratory symptoms (Khatri et al., 2009; 
Barraza-Villarreal et al., 2008). Although more limited in number, 
epidemiologic studies also found associations with cytokines such as 
IL-6 or IL-8 (Barraza-Villarreal et al., 2008; Sienra-Monge et al., 
2004), eosinophils (Khatri et al., 2009), antioxidants (Sienra-Monge et 
al., 2004), and indicators of oxidative stress (Romieu et al., 2008) 
(U.S. EPA, 2013a, section 6.2.3.2). Because associations with 
inflammation were attenuated with higher antioxidant intake in the 
study by Sienra-Monge et al. (2004), this study provides additional 
evidence that inhaled O3 is likely to be an important source 
of reactive oxygen species in airways and/or may increase pulmonary 
inflammation via oxidative stress-mediated mechanisms among all age 
groups. Limitations in some recent studies have contributed to 
inconsistent results in adults (U.S. EPA, 2013a, section 6.2.3.2).
---------------------------------------------------------------------------

    \48\ Exhaled NO has been shown to be a useful biomarker for 
airway inflammation in large population-based studies (Linn et al., 
2009) (U.S. EPA, 2013a, section 7.2.4).
---------------------------------------------------------------------------

    Exposure to ambient O3 on multiple days can result in 
larger increases in pulmonary inflammation and oxidative stress, as 
discussed in section 6.2.3.2 of the ISA (U.S. EPA, 2013a). In studies 
that examined multiple O3 lags,

[[Page 75254]]

multiday averages of 8-hour maximum or 8-hour average concentrations 
were associated with larger increases in pulmonary inflammation and 
oxidative stress (Berhane et al., 2011; Delfino et al., 2010; Sienra-
Monge et al., 2004), consistent with controlled human exposure (U.S. 
EPA, 2013a, section 6.2.3.1) and animal studies (U.S. EPA, 2013a, 
section 6.2.3.3) reporting that some markers of pulmonary inflammation 
remain elevated with O3 exposures repeated over multiple 
days. Evidence from animal toxicological studies also clearly indicates 
that O3 exposures result in damage and inflammation in the 
lung (U.S. EPA, 2013a, section 5.3). In the few studies that evaluated 
the potential for confounding, O3 effect estimates were not 
confounded by temperature or humidity, and were robust to adjustment 
for PM2.5 or PM10 (Barraza-Villarreal et al., 
2008; Romieu et al., 2008; Sienra-Monge et al., 2004).
    In conclusion, a relatively small number of controlled human 
exposure studies evaluating O3-induced airway inflammation 
have become available since the last review. For purposes of reviewing 
the current O3 NAAQS, the most important of these recent 
studies reported a statistically significant increase in airway 
inflammation in healthy adults at moderate exertion following exposures 
to 60 ppb O3, the lowest concentration that has been 
evaluated for inflammation. In addition, a number of recent 
epidemiologic studies report O3-associated increases in 
markers of pulmonary inflammation, particularly in children. Thus, 
recent studies continue to support the evidence for airway inflammation 
and injury that was available in previous reviews, with new evidence 
for such effects following exposures to lower concentrations than had 
been evaluated previously.
iii. Airway Hyperresponsiveness
    Airway hyperresponsiveness (AHR) refers to a condition in which the 
conducting airways undergo enhanced bronchoconstriction in response to 
a variety of stimuli. Airway hyperresponsiveness is an important 
consequence of exposure to ambient O3 because its presence 
reflects a change in airway smooth muscle reactivity, and indicates 
that the airways are predisposed to narrowing upon inhalation of a 
variety of ambient stimuli including specific triggers (i.e., 
allergens) and nonspecific triggers (e.g., SO2, and cold 
air). People with asthma are generally more sensitive to 
bronchoconstricting agents than those without asthma, and the use of an 
airway challenge to inhaled bronchoconstricting agents is a diagnostic 
test in asthma (U.S. EPA, 2013, section 6.2.2). Standards for airway 
responsiveness testing have been developed for the clinical laboratory 
(ATS, 2000), although variation in the methodology for administering 
the bronchoconstricting agent may affect the results (Cockcroft et al., 
2005). There is a wide range of airway responsiveness in people without 
asthma, and responsiveness is influenced by a number of factors, 
including cigarette smoke, pollutant exposures, respiratory infections, 
occupational exposures, and respiratory irritants. Dietary antioxidants 
have been reported to attenuate O3-induced bronchial 
hyperresponsiveness in people with asthma (Trenga et al., 2001).
    Evidence for airway hyperresponsiveness (AHR) following 
O3 exposures is derived primarily from controlled human 
exposure and toxicological studies (U.S. EPA, 2013a, section 6.2.2). 
Airway responsiveness is often quantified by measuring changes in 
pulmonary function following the inhalation of an aerosolized allergen 
or a nonspecific bronchoconstricting agent (e.g., methacholine), or 
following exposure to a bronchoconstricting stimulus such as cold air. 
In the last review, controlled human exposure studies of mostly adults 
(>=18 years of age) had shown that exposures to O3 
concentrations at or above 80 ppb increase airway responsiveness, as 
indicated by a reduction in the concentration of specific (e.g., 
ragweed) and non-specific (e.g., methacholine) agents required to 
produce a given reduction in lung function (e.g., as measured by 
FEV1 or specific airway resistance) (U.S. EPA, 2013a, 
section 6.2.2.1). This O3-induced AHR has been reported to 
be dose-dependent (Horstman et al., 1990). Animal toxicology studies 
have reported O3-induced AHR in a number of species, with 
some rat strains exhibiting hyperresponsiveness following 4-hour 
exposures to O3 concentrations as low as 50 ppb (Depuydt et 
al., 1999). Since the last review, there have been relatively few new 
controlled human exposure and animal toxicology studies of 
O3 and AHR, and no new studies have evaluated exposures to 
O3 concentrations at or below 80 ppb (U.S. EPA, 2013a, 
section 6.2.2.1).
    Airway hyperresponsiveness is linked with the accumulation and/or 
activation of eosinophils in the airways of asthmatics, which is 
followed by production of mucus and a late-phase asthmatic response 
(section II.B.4.a.ii). In a study of 16 intermittent asthmatics, 
Hiltermann et al. (1999) found that there was a significant inverse 
correlation between the O3-induced change in the percentage 
of eosinophils in induced sputum and the concentration of methacholine 
causing a 20% decrease in FEV1. Hiltermann et al. (1999) 
concluded that the results point to the role of eosinophils in 
O3-induced AHR. Increases in O3-induced 
nonspecific airway responsiveness incidence and duration could have 
important clinical implications for children and adults with asthma, 
such as exacerbations of their disease.
    Airway hyperresponsiveness after O3 exposure appears to 
resolve more slowly than changes in FEV1 or respiratory 
symptoms (Folinsbee and Hazucha, 2000). Studies suggest that 
O3-induced AHR usually resolves 18 to 24 hours after 
exposure, but may persist in some individuals for longer periods 
(Folinsbee and Hazucha, 1989). Furthermore, in studies of repeated 
exposure to O3, changes in AHR tend to be somewhat less 
susceptible to attenuation with consecutive exposures than changes in 
FEV1 (Gong et al., 1997; Folinsbee et al., 1994; Kulle et 
al., 1982; Dimeo et al., 1981) (U.S. EPA, 2013a, section 6.2.2). In 
animal studies a 3-day continuous exposure resulted in attenuation of 
O3-induced AHR (Johnston et al., 2005) while repeated 
exposures for 2 hours per day over 10 days did not (Chhabra et al., 
2010), suggesting that attenuation could be lost when repeated 
exposures are interspersed with periods of rest (U.S. EPA, 2013a, 
section 6.2.2.2).
    As mentioned above, in addition to human subjects a number of 
species, including nonhuman primates, dogs, cats, rabbits, and rodents, 
have been used to examine the effect of O3 exposure on AHR, 
(U.S. EPA, 1996, Table 6-14; and U.S. EPA, 2006a, Annex Table AX5-12, 
p. AX5-36). A body of animal toxicology studies, including some recent 
studies conducted since the last review, provides support for the 
O3-induced AHR reported in humans (U.S. EPA, 2013a, section 
6.2.2.2). Although most of these studies evaluated O3 
concentrations above those typically found in ambient air in cities in 
the United States (i.e., most studies evaluated O3 
concentrations of 100 ppb or greater), one study reported that a very 
low exposure concentration (50 ppb for 4 hours) induced AHR in some rat 
strains (Depuydt et al., 1999). Additional recent rodent studies 
reported O3-induced AHR following exposures to O3 
concentrations from 100 to 500 ppb (Johnston et al., 2005; Chhabra et 
al., 2010; Larsen et al., 2010).

[[Page 75255]]

In characterizing the relevance of these exposure concentrations, the 
ISA noted that a study using radiolabeled O3 suggests that 
even very high O3 exposure concentrations in rodents could 
be equivalent to much lower exposure concentrations in humans. 
Specifically, a 2000 ppb (2 ppm) O3 exposure concentration 
in resting rats was reported to be roughly equivalent to a 400 ppb 
exposure concentration in exercising humans (Hatch et al., 1994). Given 
this relationship, the ISA noted that animal data obtained in resting 
conditions could underestimate the risk of effects for humans (U.S. 
EPA, 2013a, section 2.4, p. 2-14).
    The 2006 AQCD (U.S. EPA, 2006a, p. 6-34) concluded that spirometric 
responses to O3 are independent of inflammatory responses 
and markers of epithelial injury (Balmes et al., 1996; Blomberg et al., 
1999; Torres et al., 1997). Significant inflammatory responses to 
O3 exposures that did not elicit significant spirometric 
responses have been reported (Holz et al., 2005). A recent study (Que 
et al., 2011) indicates that AHR also appears to be mediated by a 
differing physiologic pathway. These results from controlled human 
exposure studies indicate that O3-induced lung function 
decrements, inflammatory responses and pulmonary injury (leading to 
increased epithelial permeability), and AHR, are mediated by apparently 
different physiologic pathways. Except for lung function decrements, we 
do not have concentration or exposure response information about the 
other, potentially more sensitive,\49\ clinical endpoints (i.e., 
inflammation, increased epithelial permeability, AHR) that would allow 
us to quantitatively estimate the size of the population affected and 
the magnitude of their responses.
---------------------------------------------------------------------------

    \49\ CASAC noted that ``while measures of FEV1 are quantitative 
and readily obtainable in humans, they are not the only measures--
and perhaps not the most sensitive measures--of the adverse health 
effects induced by ozone exposure.'' (Henderson, 2006).
---------------------------------------------------------------------------

    In summary, a strong body of controlled human exposure and animal 
toxicological studies, most of which were available in the last review 
of the O3 NAAQS, report O3-induced AHR after 
either acute or repeated exposures (U.S. EPA, 2013a, section 6.2.2.2). 
People with asthma often exhibit increased airway responsiveness at 
baseline relative to healthy controls, and they can experience further 
increases in responsiveness following exposures to O3. 
Studies reporting increased airway responsiveness after O3 
exposure contribute to a plausible link between ambient O3 
exposures and increased respiratory symptoms in asthmatics, and 
increased hospital admissions and emergency department visits for 
asthma (U.S. EPA, 2013a, section 6.2.2.2).
iv. Respiratory Symptoms and Medication Use
    Respiratory symptoms are associated with adverse outcomes such as 
limitations in activity, and are the primary reason for people with 
asthma to use quick relief medication and seek medical care. Studies 
evaluating the link between O3 exposures and such symptoms 
allow a direct characterization of the clinical and public health 
significance of ambient O3 exposure. Controlled human 
exposure and toxicological studies have described modes of action 
through which short-term O3 exposures may increase 
respiratory symptoms by demonstrating O3-induced AHR (U.S. 
EPA, 2013a, section 6.2.2) and pulmonary inflammation (U.S. EPA, 2013a, 
section 6.2.3).
    The link between subjective respiratory symptoms and O3 
exposures has been evaluated in both controlled human exposure and 
epidemiologic studies, and the link with medication use has been 
evaluated in epidemiologic studies. In the last review, several 
controlled human exposure studies reported respiratory symptoms 
following exposures to O3 concentrations at or above 80 ppb. 
In addition, one study reported such symptoms following exposures to 60 
ppb O3, though the increase was not statistically different 
from filtered air controls. Epidemiologic studies reported associations 
between ambient O3 and respiratory symptoms and medication 
use in a variety of locations and populations, including asthmatic 
children living in U.S. cities. In the current review, additional 
controlled human exposure studies have evaluated respiratory symptoms 
following exposures to O3 concentrations below 80 ppb and 
recent epidemiologic studies have evaluated associations with 
respiratory symptoms and medication use (U.S. EPA, 2013a, sections 
6.2.1, 6.2.4).
    In controlled human exposure studies available in the last review 
as well as newly available studies, statistically significant increases 
in respiratory symptoms have been reported in healthy adult volunteers 
engaged in intermittent, moderate exertion following 6.6 hour exposures 
to average O3 concentrations of 80 ppb (Adams, 2003; Adams, 
2006; Schelegle et al., 2009) and 72 ppb (Schelegle et al., 2009). Such 
symptoms have been reported to increase with increasing O3 
exposure concentrations, duration of exposure, and activity level 
(McDonnell et al., 1999).
    Results have been less consistent for lower exposure 
concentrations. A recent study by Schelegle et al. (2009) reported a 
statistically significant increase in respiratory symptoms in healthy 
adults following 6.6 hour exposures to an average O3 
concentration of 72 ppb, but not 60 ppb. Kim et al. (2011) also did not 
find statistically significant increases in respiratory symptoms 
following exposures of healthy adults to 60 ppb O3. Adams 
(2006) reported an increase in respiratory symptoms in healthy adults 
during a 6.6 hour exposure protocol with an average O3 
exposure concentration of 60 ppb. This increase was significantly 
different from initial respiratory symptoms, but not from filtered air 
controls. The findings for O3-induced respiratory symptoms 
in controlled human exposure studies, and the evidence integrated 
across disciplines describing underlying modes of action, provide 
biological plausibility for epidemiologic associations observed between 
short-term increases in ambient O3 concentration and 
increases in respiratory symptoms (U.S. EPA, 2013a, section 6.2.4).
    In epidemiologic panel studies of respiratory symptoms, data 
typically are collected by having subjects (or their parents) record 
symptoms and medication use in a diary without direct supervision by 
study staff. Several limitations of symptom reports are well 
recognized, as described in the ISA (U.S. EPA, 2013a, section 6.2.4). 
Nonetheless, symptom diaries remain a convenient tool to collect 
individual-level data from a large number of subjects and allow 
modeling of associations between daily changes in O3 
concentration and daily changes in respiratory morbidity over multiple 
weeks or months. Importantly, many of the limitations in these studies 
are sources of random measurement error that can bias effect estimates 
to the null or increase the uncertainty around effect estimates (U.S. 
EPA, 2013a, section 6.2.4). Because respiratory symptoms are associated 
with limitations in activity and daily function and are the primary 
reason for using medication and seeking medical care, the evidence is 
directly coherent with the associations consistently observed between 
increases in ambient O3 concentration and increases in 
asthma emergency department visits, discussed below (U.S. EPA, 2013a, 
section 6.2.4).
    Most epidemiologic studies of O3 and respiratory 
symptoms and medication use have been conducted in children

[[Page 75256]]

and/or adults with asthma, with fewer studies, and less consistent 
results, in non-asthmatic populations (U.S. EPA, 2013a, section 6.2.4). 
The 2006 AQCD (U.S. EPA, 2006a, U.S. EPA, 2013a, section 6.2.4) 
concluded that the collective body of epidemiologic evidence indicated 
that short-term increases in ambient O3 concentrations are 
associated with increases in respiratory symptoms in children with 
asthma. A large body of single-city and single-region studies of 
asthmatic children provides consistent evidence for associations 
between short-term increases in ambient O3 concentrations 
and increased respiratory symptoms and asthma medication use in 
children with asthma (U.S. EPA, 2013a, Figure 6-12, Table 6-20, p. 79).
    Methodological differences among studies make comparisons across 
recent multicity studies of respiratory symptoms difficult. Because of 
fewer person-days of data (Schildcrout et al., 2006) or examination of 
19-day averages of ambient O3 concentrations (O'Connor et 
al., 2008), the ISA did not give greater weight to results from recent 
multicity studies than results from single-city studies (U.S. EPA, 
2013a, section 6.2.4.5).\50\ While evidence from the few available U.S. 
multicity studies is less consistent (O'Connor et al., 2008; 
Schildcrout et al., 2006; Mortimer et al., 2002), the overall body of 
epidemiologic evidence with respect to the association betweeen 
exposure to O3 and respiratory symptoms in asthmatic 
children remains compelling (U.S. EPA, 2013a, section 6.2.4.1). 
Findings from a small body of studies indicate that O3 is 
also associated with increased respiratory symptoms in adults with 
asthma (Khatri et al., 2009; Feo Brito et al., 2007; Ross et al., 2002) 
(U.S. EPA, 2013a, section 6.2.4.2).
---------------------------------------------------------------------------

    \50\ Though, as discussed below, for other endpoints (e.g., 
hospital admissions, emergency department visits) the ISA focused 
primarily on multicity studies.
---------------------------------------------------------------------------

    Available evidence indicates that O3-associated 
increases in respiratory symptoms are not confounded by temperature, 
pollen, or copollutants (primarily PM) (U.S. EPA, 2013a, section 
6.2.4.5; Table 6-25; Romieu et al., 1996; Romieu et al., 1997; Thurston 
et al., 1997; Gent et al., 2003). However, identifying the independent 
effects of O3 in some studies was complicated due to the 
high correlations observed between O3 and PM or different 
lags and averaging times examined for copollutants. Nonetheless, the 
ISA noted that the robustness of associations in some studies of 
individuals with asthma, combined with findings from controlled human 
exposure studies for the direct effects of O3 exposure, 
provide substantial evidence supporting the independent effects of 
short-term ambient O3 exposure on respiratory symptoms (U.S. 
EPA, 2013a, section 6.2.4.5).
    Epidemiologic studies of medication use have reported associations 
with 1-hour maximum O3 concentrations and with multiday 
average O3 concentrations (Romieu et al., 2006; Just et al., 
2002). Some studies reported O3 associations for both 
respiratory symptoms and asthma medication use (Escamilla-Nu[ntilde]ez 
et al., 2008; Romieu et al., 2006; Schildcrout et al., 2006; Jalaludin 
et al., 2004; Romieu et al., 1997; Thurston et al., 1997) while others 
reported associations for either respiratory symptoms or medication use 
(Romieu et al., 1996; Rabinovitch et al., 2004; Just et al., 2002; 
Ostro et al., 2001).
    In summary, both controlled human exposure and epidemiologic 
studies have reported respiratory symptoms attributable to short-term 
O3 exposures. In the last review, the majority of the 
evidence from controlled human exposure studies in young, healthy 
adults was for symptoms following exposures to O3 
concentrations at or above 80 ppb. Although studies that have become 
available since the last review have not reported increased respiratory 
symptoms in young, healthy adults following exposures with moderate 
exertion to 60 ppb, one recent study did report increased symptoms 
following exposure to 72 ppb O3. As was concluded in the 
2006 O3 AQCD (U.S. EPA, 2006a; U.S. EPA, 1996), the 
collective body of epidemiologic evidence indicates that short-term 
increases in ambient O3 concentration are associated with 
increases in respiratory symptoms in children with asthma (U.S. EPA, 
2013a, section 6.2.4). Recent studies of respiratory symptoms and 
medication use, primarily in asthmatic children, add to this evidence. 
In a smaller body of studies, increases in ambient O3 
concentration were associated with increases in respiratory symptoms in 
adults with asthma.
v. Lung Host Defense
    The mammalian respiratory tract has a number of closely integrated 
defense mechanisms that, when functioning normally, provide protection 
from the potential health effects of exposures to a wide variety of 
inhaled particles and microbes. These defense mechanisms include 
mucociliary clearance, alveolobronchiolar transport mechanism, alveolar 
macrophages,\51\ and adaptive immunity \52\ (U.S. EPA, 2013a, section 
6.2.5). The previous O3 AQCD (U.S. EPA, 2006a) concluded 
that animal toxicological studies provided evidence that acute exposure 
to O3 concentrations as low as 100 to 500 ppb can increase 
susceptibility to infectious diseases due to modulation of these lung 
host defenses. This conclusion was based, in large part, on animal 
studies of alveolar macrophage function and mucociliary clearance (U.S. 
EPA, 2013a, section 6.2.5).
---------------------------------------------------------------------------

    \51\ Phagocytic white blood cells within the alveoli of the 
lungs that ingest inhaled particles.
    \52\ The adaptive immune system, is also known as the acquired 
immune system. Acquired immunity creates immunological memory after 
an initial response to a specific pathogen, leading to an enhanced 
response to subsequent encounters with that same pathogen.
---------------------------------------------------------------------------

    Integrating animal study results with human exposure evidence, the 
2006 Criteria Document concluded that available evidence indicates that 
short-term O3 exposures have the potential to impair host 
defenses in humans, primarily by interfering with alveolar macrophage 
function. Any impairment in alveolar macrophage function may lead to 
decreased clearance of microorganisms or nonviable particles. 
Compromised alveolar macrophage functions in asthmatics may increase 
their susceptibility to other O3 effects, the effects of 
particles, and respiratory infections (U.S. EPA, 2006a, p. 8-26). These 
conclusions were based largely on studies conducted in animals exposed 
for several hours up to several weeks to O3 concentrations 
from 100 to 250 ppb (Hurst et al., 1970; Driscoll et al., 1987; Cohen 
et al., 2002). Consistent with the animal evidence, a controlled human 
exposure study available in the last review had reported decrements in 
the ability of alveolar macrophages to phagocytize yeast following 
exposures of healthy volunteers to O3 concentrations of 80 
and 100 ppb for 6.6 hours during moderate exercise (Devlin et al., 
1991).
    Alveolobronchiolar transport mechanisms refers to the transport of 
particles deposited in the deep lung (alveoli) which may be removed 
either up through the respiratory tract (bronchi) by alveolobronchiolar 
transport or through the lymphatic system. The pivotal mechanism of 
alveolobronchiolar transport involves the movement of alveolar 
macrophages with ingested particles to the bottom of the conducting 
airways. These airways are lined with ciliated epithelial cells and 
cells that produce mucous, which surrounds the macrophages. The 
ciliated epithelial cells move the

[[Page 75257]]

mucous packets up the resiratory tract, hence the term ``mucociliary 
escalator.'' Although some studies show reduced tracheobronchial 
clearance after O3 exposure (U.S. EPA, 2013a, section 
6.2.5.1), alveolar clearance of deposited material is accelerated, 
presumably due to macrophage influx, which in itself can be damaging.
    With regard to adaptive immunity, a limited number of epidemiologic 
studies have examined associations between O3 exposure and 
hospital admissions or emergency department visits for respiratory 
infection, pneumonia, or influenza. Results have been mixed, and in 
some cases conflicting (U.S. EPA, 2013a, sections 6.2.7.2 and 6.2.7.3). 
With the exception of influenza, it is difficult to ascertain whether 
cases of respiratory infection or pneumonia are of viral or bacterial 
etiology. A recent study that examined the association between 
O3 exposure and respiratory hospital admissions in response 
to an increase in influenza intensity observed an increase in 
respiratory hospital admissions (Wong et al., 2009), but information 
from toxicological studies of O3 and viral infections is 
ambiguous.
    In summary, relatively few studies conducted since the last review 
have evaluated the effects of O3 exposures on lung host 
defense. When the available evidence is taken as a whole, the ISA 
concludes that acute O3 exposures impair the host defense 
capability of animals, primarily by depressing alveolar macrophage 
function and perhaps also by decreasing mucociliary clearance of 
inhaled particles and microorganisms. Coupled with limited evidence 
from controlled human exposure studies, this suggests that humans 
exposed to O3 could be predisposed to bacterial infections 
in the lower respiratory tract (U.S. EPA, 2013a, section 6.2.5.5).
vi. Allergic and Asthma-Related Responses
    Effects resulting from combined exposures to O3 and 
allergens have been studied in a variety of animal species, generally 
as models of experimental asthma. Pulmonary function and AHR in animal 
models of asthma are discussed in detail in Section 6.2.1.3 and Section 
6.2.2.2, respectively, in the ISA (U.S. EPA, 2013a). Studies of 
allergic and asthma-related responses are discussed in detail in 
sections 5.3.6 and 6.2.6 of the ISA (U.S. EPA, 2013a).
    Evidence available in the last review indicates that O3 
exposure skews immune responses toward an allergic phenotype and could 
also make airborne allergens more allergenic. In humans, allergic 
rhinoconjunctivitis symptoms are associated with increases in ambient 
O3 concentrations (Riediker et al., 2001). Controlled human 
exposure studies have observed O3-induced changes indicating 
allergic skewing. Airway eosinophils, which are white blood cells that 
participate in allergic disease and inflammation, were observed to 
increase in volunteers with atopy \53\ and mild asthma (Peden et al., 
1997). In a more recent study, expression of IL-5, a cytokine involved 
in eosinophil recruitment and activation, was increased in subjects 
with atopy but not in healthy subjects (Hernandez et al., 2010). 
Epidemiologic studies describe associations between eosinophils in both 
short- (U.S. EPA, 2013a, section 6.2.3.2) and long-term (U.S. EPA, 
2013a, section 7.2.5) O3 exposure, as do chronic exposure 
studies in non-human primates. Collectively, findings from these 
studies suggest that O3 can induce or enhance certain 
components of allergic inflammation in individuals with allergy or 
allergic asthma.
---------------------------------------------------------------------------

    \53\ Atopy is a predisposition toward developing certain 
allergic hypersensitivity reactions. A person with atopy typically 
presents with one or more of the following: eczema (atopic 
dermatitis), allergic rhinitis (hay fever), allergic conjunctivitis, 
or allergic asthma.
---------------------------------------------------------------------------

    Evidence available in the last review indicates that O3 
may also increase AHR to specific allergen triggers (75 FR 2970, 
January 19, 2010). Two studies (J[ouml]rres et al., 1996; Holz et al., 
2002) observed increased airway responsiveness to O3 
exposure with bronchial allergen challenge in subjects with preexisting 
allergic airway disease. Ozone-induced exacerbation of airway 
responsiveness persists longer and attenuates more slowly than 
O3-induced lung function decrements and respiratory symptom 
responses and can have important clinical implications for asthmatics. 
Animal toxicology studies indicate that O3 enhances 
inflammatory and allergic responses to allergen challenge in sensitized 
animals. In addition to exacerbating existing allergic responses, 
toxicology studies indicate that O3 can also act as an 
adjuvant to produce sensitization in the respiratory tract. Along with 
its pro-allergic effects (inducing or enhancing certain components of 
allergic inflammation in individuals with allergy or allergic asthma), 
O3 could also make airborne allergens more allergenic. When 
combined with NO2, O3 has been shown to enhance 
nitration of common protein allergens, which may increase their 
allergenicity (Franze et al., 2005).
vii. Hospital Admissions and Emergency Department Visits
    The 2006 O3 AQCD evaluated numerous studies of 
respiratory-related emergency department visits and hospital 
admissions. These were primarily time-series studies conducted in the 
U.S., Canada, Europe, South America, Australia, and Asia. Based on such 
studies, the 2006 O3 AQCD concluded that ``the overall 
evidence supports a causal relationship between acute ambient 
O3 exposures and increased respiratory morbidity resulting 
in increased emergency department visits and [hospital admissions] 
during the warm season'' \54\ (U.S. EPA, 2006a). This conclusion was 
``strongly supported by the human clinical, animal toxicologic[al], and 
epidemiologic evidence for [O3-induced] lung function 
decrements, increased respiratory symptoms, airway inflammation, and 
airway hyperreactivity'' (U.S. EPA, 2006a).
---------------------------------------------------------------------------

    \54\ Epidemiologic associations for O3 are more 
robust during the warm season than during cooler months (e.g., 
smaller measurement error, less potential confounding by 
copollutants). Rationale for focusing on warm season epidemiologic 
studies for O3 can be found at 72 FR 37838-37840.
---------------------------------------------------------------------------

    The results of recent studies largely support the conclusions of 
the 2006 O3 AQCD (U.S. EPA, 2013a, section 6.2.7). Since the 
completion of the 2006 O3 AQCD, relatively fewer studies 
conducted in the U.S., Canada, and Europe have evaluated associations 
between short-term O3 concentrations and respiratory 
hospital admissions and emergency department visits, with a growing 
number of studies conducted in Asia. This epidemiologic evidence is 
discussed in detail in the ISA (U.S. EPA, 2013a, section 6.2.7).\55\
---------------------------------------------------------------------------

    \55\ The consideration of ambient O3 concentrations 
in the locations of these epidemiologic studies are discussed in 
sections II.D.1.b and II.E.4.a below, for the current standard and 
alternative standards, respectively.
---------------------------------------------------------------------------

    In considering this body of evidence, the ISA focused primarily on 
multicity studies because they examine associations with respiratory-
related hospital admissions and emergency department visits over large 
geographic areas using consistent statistical methodologies (U.S. EPA, 
2013a, section 6.2.7.1). The ISA also focused on single-city studies 
that encompassed a large number of daily hospital admissions or 
emergency department visits, included long study-durations, were 
conducted in locations not represented by the larger studies, or 
examined population-specific characteristics that may impact the risk 
of O3-related health effects but were not evaluated in the 
larger studies (U.S. EPA, 2013a, section 6.2.7.1). When

[[Page 75258]]

examining the association between short-term O3 exposure and 
respiratory health effects that require medical attention, the ISA 
distinguishes between hospital admissions and emergency department 
visits because it is likely that a small percentage of respiratory 
emergency department visits will be admitted to the hospital; 
therefore, respiratory emergency department visits may represent 
potentially less serious, but more common outcomes (U.S. EPA, 2013a, 
section 6.2.7.1).
    Several recent multicity studies (e.g., Cakmak et al., 2006; Dales 
et al., 2006) and a multi-continent study (Katsouyanni et al., 2009) 
report associations between short-term O3 concentrations and 
increased respiratory-related hospital admissions and emergency 
department visits. These multicity studies are supported by results 
from single-city studies also reporting consistent positive 
associations using different exposure assignment approaches (i.e., 
average of multiple monitors, single monitor, population-weighted 
average) and averaging times (i.e., 1-hour max and 8-hour max) (U.S. 
EPA, 2013a, sections 6.2.7.1 to 6.2.7.5). When examining cause-specific 
respiratory outcomes, recent studies report positive associations with 
hospital admissions and emergency department visits for asthma 
(Strickland et al., 2010; Stieb et al., 2009) and chronic obstructive 
pulmonary disease (COPD) (Stieb et al., 2009; Medina-Ramon et al., 
2006), with more limited evidence for pneumonia (Medina-Ramon et al., 
2006; Zanobetti and Schwartz, 2006). In seasonal analyses (U.S. EPA, 
2013a, Figure 6-19, Table 6-28), stronger associations were reported in 
the warm season or summer months, when O3 concentrations are 
higher, compared to the cold season, particularly for asthma 
(Strickland et al., 2010; Ito et al., 2007) and COPD (Medina-Ramon et 
al., 2006). The available evidence indicates that children are at 
greatest risk for effects leading to O3-associated hospital 
admissions and emergency department visits (Silverman and Ito, 2010; 
Mar and Koenig, 2009; Villeneuve et al., 2007).
    Although the collective evidence across studies indicates a mostly 
consistent positive association between O3 exposure and 
respiratory-related hospital admissions and emergency department 
visits, the magnitude of these associations may be underestimated to 
the extent members of study populations modify their behavior in 
response to air quality forecasts, and to the extent such behavior 
modification increases exposure misclassification (U.S. EPA, 2013, 
Section 4.6.6). Studies examining the potential confounding effects of 
copollutants have reported that O3 effect estimates remained 
relatively robust upon the inclusion of PM and gaseous pollutants in 
two-pollutant models (U.S. EPA, 2013a, Figure 6-20, Table 6-29). 
Additional studies that conducted copollutant analyses, but did not 
present quantitative results, also support these conclusions 
(Strickland et al., 2010; Tolbert et al., 2007; Medina-Ramon et al., 
2006) (U.S. EPA, 2013a, section 6.2.7.5).
    In the last review, studies had not evaluated the concentration-
response relationship between short-term O3 exposure and 
respiratory-related hospital admissions and emergency department 
visits. A preliminary examination of this relationship in studies that 
have become available since the last review found no evidence of a 
deviation from linearity when examining the association between short-
term O3 exposure and asthma hospital admissions (U.S. EPA, 
2013a, page 6-157; Silverman and Ito, 2010). In addition, an 
examination of the concentration-response relationship for 
O3 exposure and pediatric asthma emergency department visits 
found no evidence of a threshold at O3 concentrations as low 
as 30 ppb (for daily maximum 8-hour concentrations) (Strickland et al., 
2010). However, in both studies there is uncertainty in the shape of 
the concentration-response curve at the lower end of the distribution 
of O3 concentrations due to the low density of data in this 
range (U.S. EPA, 2013a, page 6-157).
viii. Respiratory Mortality
    The controlled human exposure, epidemiologic, and toxicological 
studies discussed in section 6.2 of the ISA (U.S. EPA, 2013a) provide 
evidence for respiratory morbidity effects, including emergency 
department visits and hospital admissions, in response to short-term 
O3 exposures. Moreover, evidence from experimental studies 
indicates multiple potential pathways of respiratory effects from 
short-term O3 exposures, which support the continuum of 
respiratory effects that could potentially result in respiratory-
related mortality in adults (U.S. EPA, 2013a, section 6.2.8). The 2006 
O3 AQCD found inconsistent evidence for associations between 
short-term O3 concentrations and respiratory mortality (U.S. 
EPA, 2006a). Although some studies reported a strong positive 
association between O3 and respiratory mortality, additional 
studies reported small associations or no associations. New 
epidemiologic evidence for respiratory mortality is discussed in detail 
in section 6.2.8 of the ISA (U.S. EPA, 2013a). The majority of recent 
multicity studies have reported positive associations between short-
term O3 exposures and respiratory mortality, particularly 
during the summer months (U.S. EPA, 2013a, Figure 6-36).
    Specifically, recent multicity studies from the U.S. (Zanobetti and 
Schwartz, 2008b), Europe (Samoli et al., 2009), Italy (Stafoggia et 
al., 2010), and Asia (Wong et al., 2010), as well as a multi-continent 
study (Katsouyanni et al., 2009), reported associations between short-
term O3 concentrations and respiratory mortality (U.S. EPA, 
2013a, Figure 6-37, page 6-259). With respect to respiratory mortality, 
summer-only analyses were consistently positive and most were 
statistically significant. All-year analyses had more mixed results, 
but most were positive.
    Of the studies evaluated, only the studies by Katsouyanni et al. 
(2009) and by Stafoggia et al. (2010) analyzed the potential for 
copollutant confounding of the O3-respiratory mortality 
relationship. Based on the results of these analyses, the ISA concluded 
that O3 respiratory mortality risk estimates appear to be 
moderately to substantially sensitive (e.g., increased or attenuated) 
to inclusion of PM10. However, in the APHENA study 
(Katsouyanni et al., 2009), the mostly every-6th-day sampling schedule 
for PM10 in the Canadian and U.S. datasets greatly reduced 
their sample size and limits the interpretation of these results (U.S. 
EPA, 2013a, section 6.2.8).
    In summary, recent epidemiologic studies support and reinforce the 
epidemiologic evidence for O3-associated respiratory 
hospital admissions and emergency department visits from the last 
review. In addition, the evidence for associations with respiratory 
mortality has been strengthened since the last review, with the 
addition of several large multicity studies. The biological 
plausibility of the associations reported in these studies is supported 
by the experimental evidence for respiratory effects.
b. Respiratory Effects--Long-Term
    Since the last review, the body of evidence indicating the 
occurrence of respiratory effects due to long-term O3 
exposure has been strengthened. This evidence is discussed in detail in 
the ISA (U.S. EPA, 2013a, Chapter 7) and summarized below for new-onset 
asthma and asthma prevalence, asthma hospital admissions, pulmonary 
structure and function, and respiratory mortality.

[[Page 75259]]

i. New-Onset Asthma and Asthma Prevalence
    Asthma is a heterogeneous disease with a high degree of temporal 
variability. The on-set, progression, and symptoms can vary within an 
individual's lifetime, and the course of asthma may vary markedly in 
young children, older children, adolescents, and adults. In the 
previous review, longitudinal cohort studies that examined associations 
between long-term O3 exposures and the onset of asthma in 
adults and children indicated a direct effect of long-term 
O3 exposures on asthma risk in adults (McDonnell et al., 
1999, 15-year follow-up; Greer et al., 1993, 10-year follow-up) and 
effect modification by O3 in children (McConnell et al., 
2002). Since that review, additional studies have evaluated 
associations with new onset asthma, further informing our understanding 
of the potential gene-environment interactions, mechanisms, and 
biological pathways associated with incident asthma.
    In children, the relationship between long-term O3 
exposure and new-onset asthma has been extensively studied in the 
Children's Health Study (CHS), a long-term study that was initiated in 
the early 1990's which has evaluated effects in several cohorts of 
children. The CHS was initially designed to examine whether long-term 
exposure to ambient pollution was related to chronic respiratory 
outcomes in children in 12 communities in southern California. In the 
CHS, new-onset asthma was classified as having no prior history of 
asthma at study entry with subsequent report of physician-diagnosed 
asthma at follow-up, with the date of onset assigned to be the midpoint 
of the interval between the interview date when asthma diagnosis was 
first reported and the previous interview date. The results of one 
study (McConnell et al., 2002) available in the previous review 
indicated that within high O3 communities, asthma risk was 
3.3 times greater for children who played three or more outdoor sports 
as compared with children who played no sports.
    For this review, as discussed in section 7.2.1.1 of the ISA (U.S. 
EPA, 2013a), recent studies from the CHS provide evidence for gene-
environment interactions in effects on new-onset asthma by indicating 
that the lower risks associated with specific genetic variants are 
found in children who live in lower O3 communities. These 
studies indicate that the risk for new-onset asthma is related in part 
to genetic susceptibility, as well as behavioral factors and 
environmental exposure. The onset of a chronic disease, such as asthma, 
is partially the result of a sequence of biochemical reactions 
involving exposures to various environmental agents metabolized by 
enzymes related to a number of different genes. Oxidative stress has 
been proposed to underlie the mechanistic hypotheses related to 
O3 exposure. Genetic variants may impact disease risk 
directly, or modify disease risk by affecting internal dose of 
pollutants and other environmental agents and/or their reaction 
products, or by altering cellular and molecular modes of action. 
Understanding the relation between genetic polymorphisms and 
environmental exposure can help identify high-risk subgroups in the 
population and provide better insight into pathway mechanisms for these 
complex diseases.
    The CHS analyses (Islam et al., 2008; Islam et al., 2009; Salam et 
al., 2009) have found that asthma risk is related to interactions 
between O3 and variants in genes for enzymes such as heme-
oxygenase (HO-1), arginases (ARG1 and 2), and glutathione S transferase 
P1 (GSTP1). Biological plausibility for these findings is provided by 
evidence that these enzymes have antioxidant and/or anti-inflammatory 
activity and participate in well-recognized modes of action in asthma 
pathogenesis. As O3 is a source of oxidants in the airways, 
oxidative stress serves as the link among O3 exposure, 
enzyme activity, and asthma. Further, several lines of evidence 
demonstrate that secondary oxidation products of O3 initiate 
the key modes of action that mediate downstream health effects (U.S. 
EPA, 2013a, section 5.3). For example, HO-1 responds rapidly to 
oxidants, has anti-inflammatory and antioxidant effects, relaxes airway 
smooth muscle, and is induced in the airways during asthma. Cross-
sectional studies by Akinbami et al. (2010) and Hwang et al. (2005) 
provide further evidence relating O3 exposures with asthma 
prevalence. Gene-environment interactions are discussed in detail in 
Section 5.4.2.1 in the ISA (U.S. EPA, 2013a).
ii. Asthma Hospital Admissions
    In the 2006 AQCD, studies on O3-related hospital 
discharges and emergency department visits for asthma and respiratory 
disease mainly looked at short-term (daily) metrics. The short-term 
O3 studies presented in section 6.2.7.5 of the ISA (U.S. 
EPA, 2013a) and discussed above in section 3.1.2.1 continue to indicate 
that there is evidence for increases in both hospital admissions and 
emergency department visits in children and adults related to all 
respiratory outcomes, including asthma, with stronger associations in 
the warm months. New studies, discussed in section 7.2.2 of the ISA 
(U.S. EPA, 2013a) also evaluated long-term O3 exposure 
metrics, providing a new line of evidence that suggests a positive 
exposure-response relationship between the first hospital admission for 
asthma and long-term O3 exposure, although the ISA cautions 
in attributing the associations in that study to long-term exposures 
since there is potential for short-term exposures to contribute to the 
observed associations.
    Evidence associating long-term O3 exposure to first 
asthma hospital admission in a positive concentration-response 
relationship is provided in a retrospective cohort study (Lin et al., 
2008b). This study investigated the association between chronic 
exposure to O3 and childhood asthma admissions by following 
a birth cohort of more than 1.2 million babies born in New York State 
(1995-1999) to first asthma admission or until December 31, 2000. Three 
annual indicators (all 8-hour maximum from 10:00 a.m. to 6:00 p.m.) 
were used to define chronic O3 exposure: (1) Mean 
concentration during the follow-up period (41.06 ppb); (2) mean 
concentration during the O3 season (50.62 ppb); and (3) 
proportion of follow-up days with O3 levels >70 ppb. The 
effects of copollutants were controlled, and interaction terms were 
used to assess potential effect modifications. A positive association 
between chronic exposure to O3 and childhood asthma hospital 
admissions was observed, indicating that children exposed to high 
O3 levels over time are more likely to develop asthma severe 
enough to be admitted to the hospital. The various factors were 
examined and differences were found for younger children (1-2 years), 
poor neighborhoods, Medicaid/self-paid births, geographic region and 
others. As shown in the ISA, Figure 7-3 (U.S. EPA, 2013a, p. 7-16), 
positive concentration-response relationships were observed. Asthma 
admissions were significantly associated with increased O3 
levels for all chronic exposure indicators.
    In considering the relationship between long-term pollutant 
exposures and chronic disease health endpoints, where chronic 
pathologies are found with acute expression of chronic disease, 
K[uuml]nzli (2012) hypothesizes that if the associations of pollution 
with events are much larger in the long-term studies, it provides some 
indirect evidence that air pollution increases the pool of subjects 
with chronic disease, and that more acute events are to be

[[Page 75260]]

expected to be seen for higher exposures. The results of Lin et al 
(2008a) for first asthma hospital admission, presented in Figure 7-3 
(U.S. EPA, 2013a, p. 7-16), show effects estimates that are larger than 
those reported in a study of childhood asthma hospital admission in New 
York State (Silverman and Ito, 2010), discussed above. The ISA (U.S. 
EPA, 2013a, p. 7-16) notes that this provides some support for the 
hypothesis that O3 exposure may not only have triggered the 
events but also increased the pool of asthmatic children, but cautions 
in attributing the associations in the Lin et al. (2008) study to long-
term exposures since there is potential for short-term exposures to 
contribute to the observed associations.
iii. Pulmonary Structure and Function
    In the 2006 O3 AQCD, few epidemiologic studies had 
investigated the effect of chronic O3 exposure on pulmonary 
function. The definitive 8-year follow-up analysis of the first cohort 
of the CHS (U.S. EPA, 2013a, section 7.2.3.1) provided little evidence 
that long-term exposure to ambient O3 was associated with 
significant deficits in the growth rate of lung function in children. 
The strongest evidence was for medium-term effects of extended 
O3 exposures over several summer months on lung function 
(FEV1) in children, i.e., reduced lung function growth being 
associated with higher ambient O3 levels. Short-term 
O3 exposure studies presented in the ISA (U.S. EPA, 2013a, 
section 6.2.1.2) provide a cumulative body of epidemiologic evidence 
that strongly supports associations between ambient O3 
exposure and decrements in lung function among children. A later CHS 
study (Islam et al., 2007) included in this review (U.S. EPA, 2013a, 
section 7.2.3.1) also reported no substantial differences in the effect 
of O3 on lung function. However, in a more recent CHS study, 
Breton et al. (2011) hypothesized that genetic variation in genes on 
the glutathione metabolic pathway may influence the association between 
ambient air pollutant exposures and lung function growth in children, 
and found that variation in the GSS locus was associated with 
differences in risk of children for lung function growth deficits 
associated ambient air pollutants, including O3. A recent 
study (Rojas-Martinez et al., 2007) of long-term exposure to 
O3, described in section 7.2.3.1 of the ISA (U.S. EPA, 
2013a, p. 7-19), observed a relationship with pulmonary function 
declines in school-aged children where O3 and other 
pollutant levels were higher (90 ppb at high end of the range) than 
those in the CHS. Two studies of adult cohorts provide mixed results 
where long-term exposures were at the high end of the range.
    Long-term studies in animals allow for greater insight into the 
potential effects of prolonged exposure to O3 that may not 
be easily measured in humans, such as structural changes in the 
respiratory tract. Despite uncertainties, epidemiologic studies 
observing associations of O3 exposure with functional 
changes in humans can attain biological plausibility in conjunction 
with long-term toxicological studies, particularly O3-
inhalation studies performed in non-human primates whose respiratory 
systems most closely resemble that of the human. An important series of 
studies, discussed in section 7.2.3.2 of the ISA (U.S. EPA, 2013a), 
have used nonhuman primates to examine the effect of O3 
alone, or in combination with an inhaled allergen, house dust mite 
antigen (HDMA), on morphology and lung function. Animals exhibit the 
hallmarks of allergic asthma defined for humans (NHLBI, 2007). These 
studies and others have demonstrated changes in pulmonary function and 
airway morphology in adult and infant nonhuman primates repeatedly 
exposed to environmentally relevant concentrations of O3 
(U.S. EPA, 2013a, section 7.2.3.2).
    The initial observations in adult nonhuman primates have been 
expanded in a series of experiments using infant rhesus monkeys 
repeatedly exposed to 0.5 ppm O3 starting at 1 month of age 
(Plopper et al., 2007; Schelegle et al. 2003). The purpose of these 
studies was to determine if a cyclic regimen of O3 
inhalation would amplify the allergic responses and structural 
remodeling associated with allergic sensitization and inhalation in the 
infant rhesus monkey; they provide evidence of an O3-induced 
change in airway resistance and responsiveness provides biological 
plausibility of long-term exposure, or repeated short-term exposures, 
to O3 contributing to the effects of asthma in children.
    In addition, significant structural changes in the respiratory 
tract development, during which conducting airways increase in diameter 
and length, have been observed in infant rhesus monkeys after cyclic 
exposure to O3 (Fanucchi et al., 2006). These effects are 
noteworthy because of their potential contribution to airway 
obstruction and AHR which are central features of asthma. A number of 
studies in both non-human primates and rodents demonstrate that 
O3 exposure can increase collagen synthesis and deposition, 
including fibrotic-like changes in the lung (U.S. EPA, 2013a, section 
7.2.3.2).
    Collectively, evidence from animal studies strongly suggests that 
chronic O3 exposure is capable of damaging the distal 
airways and proximal alveoli, resulting in lung tissue remodeling and 
leading to apparent irreversible changes. Potentially, persistent 
inflammation and interstitial remodeling play an important role in the 
progression and development of chronic lung disease. Further discussion 
of the modes of action that lead to O3-induced morphological 
changes can be found in section 5.3.7 of the ISA (U.S. EPA, 2013a). 
Discussion of mechanisms involved in lifestage susceptibility and 
developmental effects can be found in section 5.4.2.4 of the ISA (U.S. 
EPA, 2013a). The findings reported in chronic animal studies offer 
insight into potential biological mechanisms for the suggested 
association between seasonal O3 exposure and reduced lung 
function development in children as observed in epidemiologic studies 
(U.S. EPA, 2013a, section 7.2.3.1).
iv. Respiratory Mortality
    A limited number of epidemiologic studies have assessed the 
relationship between long-term exposure to O3 and mortality 
in adults. The 2006 O3 AQCD concluded that an insufficient 
amount of evidence existed ``to suggest a causal relationship between 
chronic O3 exposure and increased risk for mortality in 
humans'' (U.S. EPA, 2006a). Though total and cardio-pulmonary mortality 
were considered in these studies, respiratory mortality was not 
specifically considered.
    In the most recent follow-up analysis of the American Cancer 
Society (ACS) cohort (Jerrett et al., 2009), cardiopulmonary deaths 
were separately subdivided into respiratory and cardiovascular deaths, 
rather than combined as in the Pope et al. (2002) work. Increased 
O3 exposure was associated with the risk of death from 
respiratory causes, and this effect was robust to the inclusion of 
PM2.5. The association between increased O3 
concentrations and increased risk of death from respiratory causes was 
insensitive to the use of different models and to adjustment for 
several ecologic variables considered individually. The authors 
reported that when seasonal averages of 1-hour daily maximum 
O3 concentrations ranged from 33 to 104 ppb, there was no 
statistical deviation from a linear concentration-response relationship 
between O3 and respiratory mortality across 96 U.S. cities 
(U.S. EPA, 2013a, section 7.7). However, the authors also

[[Page 75261]]

evaluated the degree to which models incorporating thresholds provided 
a better fit to the data. Based on these analyses, Jerrett et al. 
(2009) reported ``limited evidence'' for an effect threshold at an 
O3 concentration of 56 ppb (p=0.06).
    Additionally, a recent multicity time series study (Zanobetti and 
Schwartz, 2011), which followed (from 1985 to 2006) four cohorts of 
Medicare enrollees with chronic conditions that might predispose to 
O3-related effects, observed an association between long-
term (warm season) exposure to O3 and elevated risk of 
mortality in the cohort that had previously experienced an emergency 
hospital admission due to COPD. A key limitation of this study is the 
inability to control for PM2.5, because data were not 
available in these cities until 1999.
c. Cardiovascular Effects
    A relatively small number of studies have examined the potential 
effect of short-term O3 exposure on the cardiovascular 
system. The 2006 O3 AQCD (U.S. EPA, 2006a, p. 8-77) 
concluded that ``O3 directly and/or indirectly contributes 
to cardiovascular-related morbidity,'' but added that the body of 
evidence was limited. This conclusion was based on a controlled human 
exposure study that included hypertensive adult males; a few 
epidemiologic studies of physiologic effects, heart rate variability, 
arrhythmias, myocardial infarctions, and hospital admissions; and 
toxicological studies of heart rate, heart rhythm, and blood pressure.
    More recently, the body of scientific evidence available that has 
examined the effect of O3 on the cardiovascular system has 
expanded. There is an emerging body of animal toxicological evidence 
demonstrating that short-term exposure to O3 can lead to 
autonomic nervous system alterations (in heart rate and/or heart rate 
variability) and suggesting that proinflammatory signals may mediate 
cardiovascular effects. Interactions of O3 with respiratory 
tract components result in secondary oxidation product formation and 
subsequent production of inflammatory mediators, which have the 
potential to penetrate the epithelial barrier and to initiate toxic 
effects systemically. In addition, animal toxicological studies of 
long-term exposure to O3 provide evidence of enhanced 
atherosclerosis and ischemia/reperfusion (I/R) injury, corresponding 
with development of a systemic oxidative, proinflammatory environment. 
Recent experimental and epidemiologic studies have investigated 
O3-related cardiovascular events and are summarized in 
section 6.3 of the ISA (U.S. EPA, 2013a). Overall, the ISA summarized 
the evidence in this review as follows (U.S. EPA, 2013a, p. 6-211).

    In conclusion, animal toxicological studies demonstrate 
O3-induced cardiovascular effects, and support the strong 
body of epidemiologic evidence indicating O3-induced 
cardiovascular mortality. Animal toxicological and controlled human 
exposure studies provide evidence for biologically plausible 
mechanisms underlying these O3-induced cardiovascular 
effects. However, a lack of coherence with epidemiologic studies of 
cardiovascular morbidity remains an important uncertainty.

    Controlled human exposure studies discussed in previous AQCDs have 
not demonstrated any consistent extrapulmonary effects. In this review, 
evidence from controlled human exposure studies suggests cardiovascular 
effects in response to short-term O3 exposure (U.S. EPA, 
2013a, section 6.3.1) and provides some coherence with evidence from 
animal toxicology studies. Controlled human exposure studies also 
support the animal toxicological studies by demonstrating 
O3-induced effects on blood biomarkers of systemic 
inflammation and oxidative stress, as well as changes in biomarkers 
that can indicate the potential for increased clotting following 
O3 exposures. Increases and decreases in high frequency 
heart rate variability (HRV) have been reported following relatively 
low (120 ppb during rest) and high (300 ppb with exercise) 
O3 exposures, respectively. These changes in cardiac 
function observed in animal and human studies provide preliminary 
evidence for O3-induced modulation of the autonomic nervous 
system through the activation of neural reflexes in the lung (U.S. EPA 
2013a, section 5.3.2).
    Overall, the ISA concludes that the available body of epidemiologic 
evidence examining the relationship between short-term exposures to 
O3 concentrations and cardiovascular morbidity is 
inconsistent (U.S. EPA, 2013a, section 6.3.2.9). Across studies, 
different definitions (i.e., ICD-9 diagnostic codes) were used for both 
all-cause and cause-specific cardiovascular morbidity (U.S. EPA, 2013a, 
Tables 6-35 to 6-39), which may contribute to inconsistency in results. 
However, within diagnostic categories, no consistent pattern of 
association was found with O3. Generally, the epidemiologic 
studies used nearest air monitors to assess O3 
concentrations, with a few exceptions that used modeling or personal 
exposure monitors. The inconsistencies in the associations observed 
between short-term O3 and cardiovascular disease (CVD) 
morbidities are unlikely to be explained by the different exposure 
assignment methods used (U.S. EPA, 2013a, section 4.6). The wide 
variety of biomarkers considered and the lack of consistency among 
definitions used for specific cardiovascular disease endpoints (e.g., 
arrhythmias, HRV) make comparisons across studies difficult.
    Despite the inconsistent evidence for an association between 
O3 concentration and CVD morbidity, mortality studies 
indicate a consistent positive association between short-term 
O3 exposure and cardiovascular mortality in multicity 
studies and in a multi-continent study. When examining mortality due to 
CVD, epidemiologic studies consistently observe positive associations 
with short-term exposure to O3. Additionally, there is some 
evidence for an association between long-term exposure to O3 
and mortality, although the association between long-term ambient 
O3 concentrations and cardiovascular mortality can be 
confounded by other pollutants (U.S. EPA, 2013a). The ISA (U.S. EPA 
2013a, section 6.3.4) states that taken together, the overall body of 
evidence across the animal and human studies is sufficient to conclude 
that there is likely to be a causal relationship between relevant 
short-term exposures to O3 and cardiovascular system 
effects.
d. Total Mortality
    The 2006 O3 AQCD concluded that the overall body of 
evidence was highly suggestive that short-term exposure to 
O3 directly or indirectly contributes to nonaccidental and 
cardiopulmonary-related mortality in adults, but additional research 
was needed to more fully establish underlying mechanisms by which such 
effects occur (U.S. EPA, 2013a, p. 2-18). In building on the 2006 
evidence for mortality, the ISA states the following (U.S. EPA, 2013a, 
p. 6-261).

    The evaluation of new multicity studies that examined the 
association between short-term O3 exposures and mortality 
found evidence that supports the conclusions of the 2006 AQCD. These 
new studies reported consistent positive associations between short-
term O3 exposure and all-cause (nonaccidental) mortality, 
with associations persisting or increasing in magnitude during the 
warm season, and provide additional support for associations between 
O3 exposure and cardiovascular and respiratory mortality.

    The 2006 O3 AQCD reviewed a large number of time-series 
studies of associations between short-term O3 exposures and 
total mortality including single- and multicity studies, and meta-
analyses. In the large U.S. multicity

[[Page 75262]]

studies that examined all-year data, effect estimates corresponding to 
single-day lags ranged from a 0.5-1% increase in all-cause 
(nonaccidental) total mortality per a 20 ppb (24-hour), 30 ppb (8-hour 
maximum), or 40 ppb (1-hour maximum) increase in ambient O3 
(U.S. EPA, 2013a, section 6.6.2). Available studies reported some 
evidence for heterogeneity in O3 mortality risk estimates 
across cities and across studies. Studies that conducted seasonal 
analyses reported larger O3 mortality risk estimates during 
the warm or summer season. Overall, the 2006 O3 AQCD 
identified robust associations between various measures of daily 
ambient O3 concentrations and all-cause mortality, which 
could not be readily explained by confounding due to time, weather, or 
copollutants. With regard to cause-specific mortality, consistent 
positive associations were reported between short-term O3 
exposure and cardiovascular mortality, with less consistent evidence 
for associations with respiratory mortality. The majority of the 
evidence for associations between O3 and cause-specific 
mortality were from single-city studies, which had small daily 
mortality counts and subsequently limited statistical power to detect 
associations. The 2006 O3 AQCD concluded that ``the overall 
body of evidence is highly suggestive that O3 directly or 
indirectly contributes to nonaccidental and cardiopulmonary-related 
mortality'' (U.S. EPA, 2013a, section 6.6.1).
    Recent studies have strengthened the body of evidence that supports 
the association between short-term O3 concentrations and 
mortality in adults. This evidence includes a number of studies 
reporting associations with nonaccidental as well as cause-specific 
mortality. Multi-continent and multicity studies have consistently 
reported positive and statistically significant associations between 
short-term O3 concentrations and all-cause mortality, with 
evidence for larger mortality risk estimates during the warm or summer 
months (U.S. EPA, 2013a, Figure 6-27; Table 6-42). Similarly, 
evaluations of cause-specific mortality have reported consistently 
positive associations with O3, particularly in analyses 
restricted to the warm season (U.S. EPA, 2013a, Figure 6-37; Table 6-
53).\56\
---------------------------------------------------------------------------

    \56\ Respiratory mortality is discussed in more detail above.
---------------------------------------------------------------------------

    In assessing the evidence for O3-related mortality, the 
2006 AQCD also noted that multiple uncertainties remained regarding the 
relationship between short-term O3 concentrations and 
mortality, including the extent of residual confounding by 
copollutants; characterization of the factors that modify the 
O3-mortality association; the appropriate lag structure for 
identifying O3-mortality effects; and the shape of the 
O3-mortality concentration-response function and whether a 
threshold exists. Many of the studies, published since the last review, 
have attempted to address one or more of these uncertainties. The ISA 
(U.S. EPA, 2013a, section 6.6.2) discusses the extent to which recent 
studies have evaluated these uncertainties in the relationship between 
O3 and mortality.
    In particular, recent studies have evaluated different statistical 
approaches to examine the shape of the O3-mortality 
concentration-response relationship and to evaluate whether a threshold 
exists for O3-related mortality. In an analysis of the 
National Morbidity and Mortality Air Pollution Study (NMMAPS) data, 
Bell et al. (2006) evaluated the potential for a threshold in the 
O3-mortality relationship. The authors reported positive and 
statistically significant associations with mortality in a variety of 
restricted analyses, including analyses restricted to days with 24-hour 
area-wide average O3 concentrations below 60, 55, 50, 45, 
40, 35, and 30 ppb. In these restricted analyses O3 effect 
estimates were of similar magnitude, were statistically significant, 
and had similar statistical precision. In analyses restricted to days 
with 24-hour average O3 concentrations below 25 ppb, the 
O3 effect estimate was similar in magnitude to the effect 
estimates resulting from analyses with the higher cutoffs, but had 
somewhat lower statistical precision, with the estimate approaching 
statistical significance (i.e., based on observation of Figure 2 in 
Bell et al., 2006). In analyses restricted to days with lower 24-hour 
average O3 concentrations (i.e., below 20 and 15 ppb), 
effect estimates were similar in magnitude to analyses with higher 
cutoffs, but with notably less statistical precision, and were not 
statistically significant (i.e., confidence intervals included the 
null, indicating no O3-associated mortality, based on 
observation of Figure 2 in Bell et al., 2006). Ozone was no longer 
positively associated with mortality when the analysis was restricted 
to days with 24-hour O3 concentrations below 10 ppb. Given 
the relatively small number of days included in these restricted 
analyses, especially for cut points of 20 ppb and below,\57\ 
statistical uncertainty is increased.
---------------------------------------------------------------------------

    \57\ For example, Bell et al. (2006) reported that for analyses 
restricted to 24-hour O3 concentrations at or below 20 
ppb, 73% of days were excluded on average across the 98 communities.
---------------------------------------------------------------------------

    Bell et al. (2006) also evaluated the shape of the concentration-
response relationship between O3 and mortality. Although the 
results of this analysis suggested the lack of threshold in the 
O3-mortality relationship, the ISA noted that it is 
difficult to interpret such a curve because: (1) There is uncertainty 
around the shape of the concentration-response curve at 24-hour average 
O3 concentrations generally below 20 ppb; and (2) the 
concentration-response curve does not take into consideration the 
heterogeneity in O3-mortality risk estimates across cities 
(U.S. EPA, 2013a, section 6.6.2.3).
    Several additional studies have used the NMMAPS dataset to evaluate 
the concentration-response relationship between short-term 
O3 concentrations and mortality. For example, using the same 
data as Bell et al. (2006), Smith et al. (2009) conducted a subset 
analysis, but instead of restricting the analysis to days with 
O3 concentrations below a cutoff, the authors only included 
days above a defined cutoff (cutoffs from 15 and 60 ppb). The results 
of this analysis were consistent with those reported by Bell et al. 
(2006). Specifically, the authors reported consistent positive 
associations for all cutoff concentrations up to concentrations where 
the total number of days available were so limited that the variability 
around the central estimate was increased (i.e., cutoff values at or 
above about 50 ppb) (U.S. EPA, 2013a, section 6.6.2.3). In addition, 
using NMMAPS data for 1987-1994 for Chicago, Pittsburgh, and El Paso, 
Xia and Tong (2006) reported evidence for a threshold around a 24-hour 
average O3 concentration of 25 ppb, though the threshold 
values estimated in the analysis were sometimes in the range of where 
data density was low (U.S. EPA, 2013a, section 6.6.2.3). Stylianou and 
Nicolich (2009) examined the existence of thresholds following an 
approach similar to Xia and Tong (2006) using data from NMMAPS for nine 
major U.S. cities (i.e., Baltimore, Chicago, Dallas/Fort Worth, Los 
Angeles, Miami, New York, Philadelphia, Pittsburgh, and Seattle) for 
the years 1987-2000. The authors reported that the estimated 
O3-mortality risks varied across the nine cities, with the 
models exhibiting apparent thresholds in the 10-45 ppb range for 
O3 (24-hour average). However, given the city-to-city 
variation in risk estimates, combining the city-specific estimates into 
an overall estimate complicates the interpretation of the results. 
Additional studies in

[[Page 75263]]

Europe, Canada, and Asia did not report the existence of a threshold 
(Katsouyanni et al., 2009), with inconsistent and/or inconclusive 
results across cities, or a non-linear relationship in the 
O3-mortality concentration-response curve (Wong et al., 
2010).
3. Adversity of O3 Effects
    In making judgments as to when various O3-related 
effects become regarded as adverse to the health of individuals, in 
previous NAAQS reviews, the EPA has relied upon the guidelines 
published by the American Thoracic Society (ATS) and the advice of 
CASAC. In 2000, the ATS published an official statement on ``What 
Constitutes an Adverse Health Effect of Air Pollution?'' (ATS, 2000), 
which updated and built upon its earlier guidance (ATS, 1985). The 
earlier guidance defined adverse respiratory health effects as 
``medically significant physiologic changes generally evidenced by one 
or more of the following: (1) Interference with the normal activity of 
the affected person or persons, (2) episodic respiratory illness, (3) 
incapacitating illness, (4) permanent respiratory injury, and/or (5) 
progressive respiratory dysfunction,'' while recognizing that 
perceptions of ``medical significance'' and ``normal activity'' may 
differ among physicians, lung physiologists and experimental subjects 
(ATS, 1985). The 2000 ATS guidance builds upon and expands the 1985 
definition of adversity in several ways. The guidance concludes that 
transient, reversible loss of lung function in combination with 
respiratory symptoms should be considered adverse. There is also a more 
specific consideration of population risk (ATS, 2000). Exposure to air 
pollution that increases the risk of an adverse effect to the entire 
population is adverse, even though it may not increase the risk of any 
individual to an unacceptable level. For example, a population of 
asthmatics could have a distribution of lung function such that no 
individual has a level associated with clinically important impairment. 
Exposure to air pollution could shift the distribution to lower levels 
that still do not bring any individual to a level that is associated 
with clinically relevant effects. However, this would be considered to 
be adverse because individuals within the population would have 
diminished reserve function, and therefore would be at increased risk 
to further environmental insult (U.S. EPA, 2013a, p. lxxi; and 75 FR at 
35526/2, June 22, 2010).
    The ATS also concluded that elevations of biomarkers such as cell 
types, cytokines and reactive oxygen species may signal risk for 
ongoing injury and more serious effects or may simply represent 
transient responses, illustrating the lack of clear boundaries that 
separate adverse from nonadverse events. More subtle health outcomes 
also may be connected mechanistically to health effects that are 
clearly adverse, so that small changes in physiological measures may 
not appear clearly adverse when considered alone, but may be part of a 
coherent and biologically plausible chain of related health outcomes 
that include responses that are clearly adverse, such as mortality 
(U.S. EPA, 2014c, section 3.1.2.1).
    In this review, the new evidence provides further support for 
relationships between O3 exposures and a spectrum of health 
effects, including effects that meet the ATS criteria for being adverse 
(ATS, 1985 and 2000). The ISA determination that there is a causal 
relationship between short-term O3 exposure and a full range 
of respiratory effects, including respiratory morbidity (e.g., lung 
function decrements, respiratory symptoms, inflammation, hospital 
admissions, and emergency department visits) and mortality, provides 
support for concluding that short-term O3 exposure is 
associated with adverse effects (U.S. EPA, 2013a, section 2.5.2). 
Overall, including new evidence of cardiovascular system effects, the 
evidence supporting an association between short-term O3 
exposures and total (nonaccidental, cardiopulmonary) respiratory 
mortality is stronger in this review (U.S. EPA, 2013a, section 2.5.2). 
And the judgment of likely causal associations between long-term 
measures of O3 exposure and respiratory effects such as new-
onset asthma, prevalence of asthma, asthma symptoms and control, and 
asthma hospital admissions provides support for concluding that long-
term O3 exposure is associated with adverse effects ranging 
from episodic respiratory illness to permanent respiratory injury or 
progressive respiratory decline (U.S. EPA, 2013a, section 7.2.8).
    Application of the ATS guidelines to the least serious category of 
effects related to ambient O3 exposures, which are also the 
most numerous and, therefore, are also potentially important from a 
public health perspective, involves judgments about which medical 
experts on CASAC panels and public commenters have in the past 
expressed diverse views. To help frame such judgments, in past reviews, 
the EPA has defined gradations of individual functional responses 
(e.g., decrements in FEV1 and airway responsiveness) and 
symptomatic responses (e.g., cough, chest pain, wheeze), together with 
judgments as to the potential impact on individuals experiencing 
varying degrees of severity of these responses. These gradations were 
used in the 1997 O3 NAAQS review and slightly revised in the 
2008 review (U.S. EPA, 1996, p. 59; 2007, p. 3-72; 72 FR 37849, July 
11, 2007). These gradations and impacts are summarized in Tables 3-2 
and 3-3 in the 2007 O3 Staff Paper (U.S. EPA, 2007, pp. 3-74 
to 3-75).
    For active healthy people, including children, moderate levels of 
functional responses (e.g., FEV1 decrements of >=10% but 
<20%, lasting 4 to 24 hours) and/or moderate symptomatic responses 
(e.g., frequent spontaneous cough, marked discomfort on exercise or 
deep breath, lasting 4 to 24 hours) would likely interfere with normal 
activity for relatively few sensitive individuals (U.S. EPA, 2007, p. 
3-72; 72 FR 37849, July 11, 2007); whereas large functional responses 
(e.g., FEV1 decrements >=20%, lasting longer than 24 hours) 
and/or severe symptomatic responses (e.g., persistent uncontrollable 
cough, severe discomfort on exercise or deep breath, lasting longer 
than 24 hours) would likely interfere with normal activities for many 
sensitive individuals (U.S. EPA, 2007, p. 3-72; 72 FR 37849, July 11, 
2007) and, therefore, would be considered adverse under ATS guidelines. 
For the purpose of estimating potentially adverse lung function 
decrements in active healthy people in the 2008 O3 NAAQS 
review, the CASAC panel for that review indicated that a focus on the 
mid to upper end of the range of moderate levels of functional 
responses is most appropriate (e.g., FEV1 decrements >=15% 
but <20%) (Henderson, 2006; U.S. EPA, 2007, p. 3-76). In this review, 
CASAC concurred that the ``[e]stimation of FEV1 decrements 
of >=15% is appropriate as a scientifically relevant surrogate for 
adverse health outcomes in active healthy adults'' (Frey, 2014c, p. 3). 
However, for children and adults with lung disease, even moderate 
functional (e.g., FEV1 decrements >=10% but <20%, lasting up 
to 24 hours) or symptomatic responses (e.g., frequent spontaneous 
cough, marked discomfort on exercise or with deep breath, wheeze 
accompanied by shortness of breath, lasting up to 24 hours) would 
likely interfere with normal activity for many individuals, and would 
likely result in additional and more frequent use of

[[Page 75264]]

medication (U.S. EPA, 2007, p. 3-72; 72 FR 37849, July 11, 2007). For 
people with lung disease, large functional responses (e.g., 
FEV1 decrements >=20%, lasting longer than 24 hours) and/or 
severe symptomatic responses (e.g., persistent uncontrollable cough, 
severe discomfort on exercise or deep breath, persistent wheeze 
accompanied by shortness of breath, lasting longer than 24 hours) would 
likely interfere with normal activity for most individuals and would 
increase the likelihood that these individuals would seek medical 
treatment (U.S. EPA, 2007, p. 3-72; 72 FR 37849, July 11, 2007). In the 
last O3 NAAQS review, for the purpose of estimating 
potentially adverse lung function decrements in people with lung 
disease the CASAC panel indicated that a focus on the lower end of the 
range of moderate levels of functional responses is most appropriate 
(e.g., FEV1 decrements >=10%) (Henderson, 2006; U.S. EPA, 
2007, p. 3-76). In addition, in their letter advising the Administrator 
on the reconsideration of the 2008 final decision, CASAC stated that 
``[a] 10% decrement in FEV1 can lead to respiratory symptoms, 
especially in individuals with pre-existing pulmonary or cardiac 
disease. For example, people with chronic obstructive pulmonary disease 
have decreased ventilatory reserve (i.e., decreased baseline 
FEV1) such that a >=10% decrement could lead to moderate to 
severe respiratory symptoms'' (Samet, 2011). In this review, CASAC 
concurred that ``[a]n FEV1 decrement of >=10% is a scientifically 
relevant surrogate for adverse health outcomes for people with asthma 
and lung disease'' (Frey, 2014c, p. 3).
    In judging the extent to which these impacts represent effects that 
should be regarded as adverse to the health status of individuals, in 
previous NAAQS reviews, the EPA has also considered whether effects 
were experienced repeatedly during the course of a year or only on a 
single occasion (U.S. EPA, 2007). Although some experts would judge 
single occurrences of moderate responses to be a nuisance, especially 
for healthy individuals, a more general consensus view of the adversity 
of such moderate responses emerges as the frequency of occurrence 
increases. Thus it has been judged that repeated occurrences of 
moderate responses, even in otherwise healthy individuals, may be 
considered to be adverse since they could well set the stage for more 
serious illness (61 FR 65723). The CASAC panel in the 1997 NAAQS review 
expressed a consensus view that these ``criteria for the determination 
of an adverse physiological response were reasonable'' (Wolff, 1995). 
In the review completed in 2008, estimates of repeated occurrences 
continued to be an important public health policy factor in judging the 
adversity of moderate lung function decrements in healthy and asthmatic 
people (72 FR 37850, July 11, 2007).
    Evidence new to this review indicates that 6.6-hour exposures to 60 
ppb O3 during moderate exertion can result in pulmonary 
inflammation in healthy adults (based on study mean). As discussed in 
the ISA, the initiation of inflammation can be considered as evidence 
that injury has occurred. Inflammation induced by a single 
O3 exposure can resolve entirely but, as noted in the ISA 
(U.S. EPA, 2013a, p. 6-76), ``continued acute inflammation can evolve 
into a chronic inflammatory state,'' which would be adverse.
    Responses measured in controlled human exposure studies indicate 
that the range of effects elicited in humans exposed to ambient 
O3 concentrations include: Decreased inspiratory capacity; 
mild bronchoconstriction; rapid, shallow breathing pattern during 
exercise; and symptoms of cough and pain on deep inspiration (U.S. EPA, 
2013a, section 6.2.1.1). Young, healthy adults exposed for 6.6 hours to 
O3 concentrations >=60 ppb, while engaged in intermittent 
moderate exertion, develop reversible, transient decrements in lung 
function. In addition, depending on the exposure concentration and the 
duration of exposure, young healthy adults have been shown to 
experience symptoms of breathing discomfort and inflammation if minute 
ventilation or duration of exposure is increased sufficiently (U.S. 
EPA, 2013a, section 6.2.1.1). Among healthy subjects there is 
considerable interindividual variability in the magnitude of the 
FEV1 responses, but when data were combined across studies 
at 60 ppb (U.S. EPA, 2013a, pp. 6-17 to 6-18), 10% of healthy subjects 
had >10% FEV1 decrements. Moreover, consistent with the 
findings of the ISA (U.S. EPA, 2013a, section 6.2.1.1), CASAC concluded 
that ``[a]sthmatic subjects appear to be at least as sensitive, if not 
more sensitive, than non-asthmatic subjects in manifesting ozone-
induced pulmonary function decrements'' (Frey, 2014c, p. 4). The 
combination of lung function decrements and respiratory symptoms, which 
has been considered adverse in previous reviews, has been demonstrated 
in healthy adults following prolonged (6.6 hour) exposures, while at 
intermittent moderate exertion, to 72 ppb. For these types of effects, 
information from controlled human exposure studies, which provides an 
indication of the magnitude and thus adversity of effects at different 
O3 concentrations, combined with estimates of occurrences in 
the population from the HREA, provide information about their 
importance from a policy perspective.
4. Ozone-Related Impacts on Public Health
    Setting standards to provide appropriate public health protection 
requires consideration of the factors that put populations at greater 
risk from O3 exposure. In order to estimate the potential 
for public health impacts, it is important to consider not only the 
adversity of the health effects, but also the populations at greater 
risk and potential behaviors that may reduce exposures.
a. Identification of At-Risk Populations and Lifestages
    The currently available evidence expands the understanding of 
populations that were identified to be at greater risk of 
O3-related health effects at the time of the last review 
(i.e., people who are active outdoors, people with lung disease, 
children and older adults and people with increased responsiveness to 
O3) and supports the identification of additional factors 
that may lead to increased risk (U.S. EPA, 2006, section 3.6.2; U.S. 
EPA, 2013a, Chapter 8). Populations and lifestages may be at greater 
risk for O3-related health effects due to factors that 
contribute to their susceptibility and/or vulnerability to 
O3. The definitions of susceptibility and vulnerability have 
been found to vary across studies, but in most instances 
``susceptibility'' refers to biological or intrinsic factors (e.g., 
lifestage, sex, preexisting disease/conditions) while ``vulnerability'' 
refers to non-biological or extrinsic factors (e.g., socioeconomic 
status [SES]) (U.S. EPA, 2013a, p. 8-1; U.S. EPA, 2010c, 2009d). In 
some cases, the terms ``at-risk'' and ``sensitive'' have been used to 
encompass these concepts more generally. In the ISA and PA, ``at-risk'' 
is the all-encompassing term used to define groups with specific 
factors that increase their risk of O3-related health 
effects.
    There are multiple avenues by which groups may experience increased 
risk for O3-induced health effects. A population or 
lifestage \58\ may exhibit greater effects than other populations or 
lifestages exposed to the same

[[Page 75265]]

concentration or dose, or they may be at greater risk due to increased 
exposure to an air pollutant (e.g., time spent outdoors). A group with 
intrinsically increased risk would have some factor(s) that increases 
risk through a biological mechanism and, in general, would have a 
steeper concentration-risk relationship, compared to those not in the 
group. Factors that are often considered intrinsic include pre-existing 
asthma, genetic background, and lifestage. A group of people could also 
have extrinsically increased risk, which would be through an external, 
non-biological factor, such as socioeconomic status (SES) and diet. 
Some groups are at risk of increased internal dose at a given exposure 
concentration, for example, because of breathing patterns. This 
category would include people who work or exercise outdoors. Finally, 
there are those who might be placed at increased risk for experiencing 
greater exposures by being exposed to higher O3 
concentrations. This would include, for example, groups of people with 
greater exposure to ambient O3 due to less availability or 
use of home air conditioners such that they are more likely to be in 
locations with open windows on high O3 days. Some groups may 
be at increased risk of O3-related health effects through a 
combination of factors. For example, children tend to spend more time 
outdoors when O3 levels are high, and at higher levels of 
activity than adults, which leads to increased exposure and dose, and 
they also have biological, or intrinsic, risk factors (e.g., their 
lungs are still developing) (U.S. EPA, 2013a, Chapter 8). An at-risk 
population or lifestage is more likely to experience adverse health 
effects related to O3 exposures and/or, develop more severe 
effects from exposure than the general population.
---------------------------------------------------------------------------

    \58\ Lifestages, which in this case includes childhood and older 
adulthood, are experienced by most people over the course of a 
lifetime, unlike other factors associated with at-risk populations.
---------------------------------------------------------------------------

i. People With Specific Genetic Variants
    There is adequate evidence for populations with certain genotypes 
being more at-risk than others to the effects of O3 exposure 
on health (U.S. EPA, 2013a, section 8.1). Controlled human exposure and 
epidemiologic studies have reported evidence of O3-related 
increases in respiratory symptoms or decreases in lung function with 
variants including GSTM1, GSTP1, HMOX1, and NQO1. NQO1 deficient mice 
were found to be resistant to O3-induced AHR and 
inflammation, providing biological plausibility for results of studies 
in humans. Additionally, studies of rodents have identified a number of 
other genes that may affect O3-related health outcomes, 
including genes related to innate immune signaling and pro- and anti-
inflammatory genes, which have not been investigated in human studies.
ii. People With Asthma
    Previous O3 AQCDs identified individuals with asthma as 
a population at increased risk of O3-related health effects. 
Multiple new epidemiologic studies included in the ISA have evaluated 
the potential for increased risk of O3-related health 
effects in people with asthma, including: Lung function; symptoms; 
medication use; AHR; and airway inflammation (also measured as exhaled 
nitric oxide fraction, or FeNO). A study of lifeguards in Texas 
reported decreased lung function with short-term O3 exposure 
among both individuals with and without asthma; however, the decrease 
was greater among those with asthma (Thaller et al., 2008). A Mexican 
study of children ages 6-14 detected an association between short-term 
O3 exposure and wheeze, cough, and bronchodilator use among 
asthmatics but not non-asthmatics, although this may have been the 
result of a small non-asthmatic population (Escamilla-Nu[ntilde]ez et 
al., 2008). A study of modification by AHR (an obligate condition among 
asthmatics) reported greater short-term O3-associated 
decreases in lung function in elderly individuals with AHR, especially 
among those who were obese (Alexeeff et al., 2007). With respect to 
airway inflammation, in one study, a positive association was reported 
for airway inflammation among asthmatic children following short-term 
O3 exposure, but the observed association was similar in 
magnitude to that of non-asthmatics (Barraza-Villarreal et al., 2008). 
Similarly, another study of children in California reported an 
association between O3 concentration and FeNO that persisted 
both among children with and without asthma as well as those with and 
without respiratory allergy (Berhane et al., 2011). Finally, Khatri et 
al. (2009) found no association between short-term O3 
exposure and altered lung function for either asthmatic or non-
asthmatic adults, but did note a decrease in lung function among 
individuals with allergies.
    New evidence for difference in effects among asthmatics has been 
observed in studies that examined the association between O3 
exposure and altered lung function by asthma medication use. A study of 
children with asthma living in Detroit reported a greater association 
between short-term O3 and lung function (i.e., 
FEV1) for corticosteroid users compared with 
noncorticosteroid users (Lewis et al., 2005). Conversely, another study 
found decreased lung function among noncorticosteroid users compared to 
users, although in this study, a large proportion of non-users were 
considered to be persistent asthmatics (Hern[aacute]ndez-Cadena et al., 
2009). Lung function was not related to short-term O3 
exposure among corticosteroid users and non-users in a study taking 
place during the winter months in Canada (Liu et al., 2009). 
Additionally, a study of airway inflammation reported a 
counterintuitive inverse association with O3 of similar 
magnitude for all groups of corticosteroid users and non-users (Qian et 
al., 2009).
    Controlled human exposure studies that have examined the effects of 
O3 on adults with asthma and healthy controls are limited. 
Based on studies reviewed in the 1996 and 2006 O3 AQCDs, 
subjects with asthma appeared to be more sensitive to acute effects of 
O3 in terms of FEV1 and inflammatory responses 
than healthy non-asthmatic subjects. For instance, Horstman et al. 
(1995) observed that mild-to-moderate asthmatics, on average, 
experienced double the O3-induced FEV1 decrement 
of healthy subjects (19% versus 10%, respectively, p=0.04). Moreover, a 
statistically significant positive correlation between FEV1 
responses to O3 exposure and baseline lung function was 
observed in individuals with asthma, i.e., responses increased with 
severity of disease. Minimal evidence exists suggesting that 
individuals with asthma have smaller O3-induced 
FEV1 decrements than healthy subjects (3% versus 8%, 
respectively) (Mudway et al., 2001). However, the asthmatics in that 
study also tended to be older than the healthy subjects, which could 
partially explain their lesser response since FEV1 responses 
to O3 exposure diminish with age. Individuals with asthma 
also had significantly more neutrophils in the BALF (18 hours 
postexposure) than similarly exposed healthy individuals (Peden et al., 
1997; Scannell et al., 1996; Basha et al., 1994). Furthermore, a study 
examining the effects of O3 on individuals with atopic 
asthma and healthy controls reported that greater numbers of 
neutrophils, higher levels of cytokines and hyaluronan, and greater 
expression of macrophage cell-surface markers were observed in induced 
sputum of atopic asthmatics compared with healthy controls (Hernandez 
et al., 2010). Differences in O3-induced epithelial cytokine 
expression were noted in bronchial biopsy samples from asthmatics and 
healthy controls (Bosson et al., 2003). Cell-surface marker and 
cytokine expression results, and the

[[Page 75266]]

presence of hyaluronan, are consistent with O3 having 
greater effects on innate and adaptive immunity in these asthmatic 
individuals. In addition, studies have demonstrated that O3 
exposure leads to increased bronchial reactivity to inhaled allergens 
in mild allergic asthmatics (Kehrl et al., 1999; Jorres et al., 1996) 
and to the influx of eosinophils in individuals with pre-existing 
allergic disease (Vagaggini et al., 2002; Peden et al., 1995). Taken 
together, these results point to several mechanistic pathways which 
could account for the enhanced sensitivity to O3 in subjects 
with asthma (U.S. EPA, 2013a, section 5.4.2.2).
    As noted in the previous review (72 FR 37846, July 11, 2007) 
asthmatics present a differential response profile for cellular, 
molecular, and biochemical parameters (U.S. EPA, 2006a, Figure 8-1) 
that are altered in response to acute O3 exposure. Ozone-
induced increases in neutrophils, IL-8 and protein were found to be 
significantly higher in the BAL fluid from asthmatics compared to 
healthy subjects, suggesting mechanisms for the increased sensitivity 
of asthmatics (Basha et al., 1994; McBride et al., 1994; Scannell et 
al., 1996; Hiltermann et al., 1999; Holz et al., 1999; Bosson et al., 
2003). Neutrophils, or PMNs, are the white blood cell most associated 
with inflammation. IL-8 is an inflammatory cytokine with a number of 
biological effects, primarily on neutrophils. The major role of this 
cytokine is to attract and activate neutrophils. Protein in the airways 
is leaked from the circulatory system, and is a marker for increased 
cellular permeability.
    Bronchial constriction following provocation with O3 
and/or allergens presents a two-phase response. The early response is 
mediated by release of histamine and leukotrienes that leads to 
contraction of smooth muscle cells in the bronchi, narrowing the lumen 
and decreasing the airflow. In people with allergic airway disease, 
including people with rhinitis and asthma, these mediators also cause 
accumulation of eosinophils in the airways (Bascom et al., 1990; Jorres 
et al., 1996; Peden et al., 1995 and 1997; Frampton et al., 1997a; 
Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002; 
Vagaggini et al., 2002). In asthma, the eosinophil, which increases 
inflammation and allergic responses, is the cell most frequently 
associated with exacerbations of the disease. A study by Bosson et al. 
(2003) evaluated the difference in O3-induced bronchial 
epithelial cytokine expression between healthy and asthmatic subjects. 
After O3 exposure the epithelial expression of IL-5 and GM-
CSF increased significantly in asthmatics, compared to healthy 
subjects. Asthma is associated with Th2-related airway response 
(allergic response), and IL-5 is an important Th2-related cytokine. The 
O3-induced increase in IL-5, and also in GM-CSF, which 
affects the growth, activation and survival of eosinophils, may 
indicate an effect on the Th2-related airway response and on airway 
eosinophils. The authors reported that the O3-induced Th2-
related cytokine responses that were found within the asthmatic group 
may indicate a worsening of their asthmatic airway inflammation and 
thus suggest a plausible link to epidemiological data indicating 
O3-associated increases in bronchial reactivity and hospital 
admissions.
    The accumulation of eosinophils in the airways of asthmatics is 
followed by production of mucus and a late-phase bronchial constriction 
and reduced airflow. In a study of 16 intermittent asthmatics, 
Hiltermann et al. (1999) found that there was a significant inverse 
correlation between the O3-induced change in the percentage 
of eosinophils in induced sputum and the change in PC20, the 
concentration of methacholine causing a 20% decrease in 
FEV1. Characteristic O3-induced inflammatory 
airway neutrophilia at one time was considered a leading mechanism of 
airway hyperresponsiveness. However, Hiltermann et al. (1999) 
determined that the O3-induced change in percentage 
neutrophils in sputum was not significantly related to the change in 
PC20. These results are consistent with the results of Zhang et al. 
(1995), which found neutrophilia in a murine model to be only 
coincidentally associated with airway hyperresponsiveness, i.e., there 
was no cause and effect relationship (U.S. EPA, 2006a, AX 6-26). 
Hiltermann et al. (1999) concluded that the results point to the role 
of eosinophils in O3-induced airway hyperresponsiveness. 
Increases in O3-induced nonspecific airway responsiveness 
incidence and duration could have important clinical implications for 
asthmatics.
    Toxicological studies provide additional evidence of the biological 
basis for the greater effects of O3 among those with asthma 
or AHR (U.S. EPA, 2013a, section 8.2.2). In animal toxicological 
studies, an asthmatic phenotype is modeled by allergic sensitization of 
the respiratory tract. Many of the studies that provide evidence that 
O3 exposure is an inducer of AHR and remodeling utilize 
these types of animal models. For example, a series of experiments in 
infant rhesus monkeys have shown these effects, but only in monkeys 
sensitized to house dust mite allergen. Similarly, adverse changes in 
pulmonary function were demonstrated in mice exposed to O3; 
enhanced inflammatory responses were in rats exposed to O3, 
but only in animals sensitized to allergen. In general, it is the 
combined effects of O3 and allergic sensitization which 
result in measurable effects on pulmonary function. In a pulmonary 
fibrosis model, exposure to O3 for 5 days increased 
pulmonary inflammation and fibrosis, along with the frequency of 
bronchopneumonia in rats. Thus, short-term exposure to O3 
may enhance damage in a previously injured lung (U.S. EPA, 2013a, 
section 8.2.2).
    In the 2006 O3 AQCD, the potential for individuals with 
asthma to have greater risk of O3-related health effects was 
supported by a number of controlled human exposure studies, evidence 
from toxicological studies, and a limited number of epidemiologic 
studies. In section 8.2.2, the ISA reports that in the recent 
epidemiologic literature some, but not all, studies report greater risk 
of health effects among individuals with asthma. Studies examining 
effect measure modification of the relationship between short-term 
O3 exposure and altered lung function by corticosteroid use 
provided limited evidence of O3-related health effects. 
However, recent studies of behavioral responses have found that studies 
do not take into account individual behavioral adaptations to 
forecasted air pollution levels (such as avoidance and reduced time 
outdoors), which may underestimate the observed associations in studies 
that examined the effect of O3 exposure on respiratory 
health (Neidell and Kinney, 2010). This could explain some 
inconsistency observed among recent epidemiologic studies. The evidence 
from controlled human exposure studies provides support for increased 
detriments in FEV1 and greater inflammatory responses to 
O3 in individuals with asthma than in healthy individuals 
without a history of asthma. The collective evidence for increased risk 
of O3-related health effects among individuals with asthma 
from controlled human exposure studies is supported by recent 
toxicological studies which provide biological plausibility for 
heightened risk of asthmatics to respiratory effects due to 
O3 exposure. Overall, the ISA finds there is adequate 
evidence for asthmatics to be an at-risk population.
iii. Children
    Children are considered to be at greater risk from O3 
exposure because their respiratory systems undergo lung

[[Page 75267]]

growth until about 18-20 years of age and are therefore thought to be 
intrinsically more at risk for O3-induced damage (U.S. EPA, 
2006a). It is generally recognized that children spend more time 
outdoors than adults, and, therefore, would be expected to have higher 
exposure to O3 than adults. Children aged 11 years and older 
and adults have higher absolute ventilation rates than younger children 
aged 1-11 years. However, younger children have higher ventilation 
rates relative to their lung volumes, which tends to increase dose 
normalized to lung surface area. In all ages, exercise intensity has a 
substantial effect on ventilation rate, high intensity activity results 
in nearly double the ventilation rate for moderate activity. For more 
information on time spent outdoors and ventilation rate differences by 
age group, see section 4.4.1 in the ISA (U.S. EPA, 2013a).
    The 1996 O3 AQCD reported clinical evidence that 
children, adolescents, and young adults (<18 years of age) appear, on 
average, to have nearly equivalent spirometric responses to 
O3 exposure, but have greater responses than middle-aged and 
older adults (U.S. EPA, 1996). Symptomatic responses (e.g., cough, 
shortness of breath, pain on deep inspiration) to O3 
exposure, however, appear to increase with age until early adulthood 
and then gradually decrease with increasing age (U.S. EPA, 1996). 
Complete lung growth and development is not achieved until 18-20 years 
of age in women and the early 20s for men; pulmonary function is at its 
maximum during this time as well.
    Recent epidemiologic studies have examined different age groups and 
their risk to O3-related respiratory hospital admissions and 
emergency department visits. Evidence for greater risk in children was 
reported in several studies. A study in Cyprus of short-term 
O3 concentrations and respiratory hospital admissions 
detected possible effect measure modification by age with a larger 
association among individuals <15 years of age compared with those >15 
years of age; the effect was apparent only with a 2-day lag (Middleton 
et al., 2008). Similarly, a Canadian study of asthma-related emergency 
department visits reported the strongest O3-related 
associations among 5- to 14-year olds compared to the other age groups 
(ages examined 0-75+) (Villeneuve et al., 2007). Greater O3-
associated risk in asthma-related emergency department visits were also 
reported among children (<15 years) as compared to adults (15 to 64 
years) in a study from Finland (Halonen et al., 2009). A study of New 
York City hospital admissions demonstrated an increase in the 
association between O3 exposure and asthma-related hospital 
admissions for 6- to 18-year olds compared to those <6 years old and 
those >18 years old (Silverman and Ito, 2010). When examining long-term 
O3 exposure and asthma-related hospital admissions among 
children, associations were determined to be larger among children 1 to 
2 years old compared to children 2 to 6 years old (Lin et al., 2008). A 
few studies reported positive associations among both children and 
adults and no modification of the effect by age.
    The evidence reported in epidemiologic studies is supported by 
recent toxicological studies which observed O3-induced 
health effects in immature animals. Early life exposures of multiple 
species of laboratory animals, including infant monkeys, resulted in 
changes in conducting airways at the cellular, functional, ultra-
structural, and morphological levels. The studies conducted on infant 
monkeys are most relevant for assessing effects in children. Carey et 
al. (2007) conducted a study of O3 exposure in infant rhesus 
macaques, whose respiratory tract closely resemble that of humans. 
Monkeys were exposed either acutely or in episodes designed to mimic 
human exposure. All monkeys acutely exposed to O3 had 
moderate to marked necrotizing rhinitis, with focal regions of 
epithelial exfoliation, numerous infiltrating neutrophils, and some 
eosinophils. The distribution, character, and severity of lesions in 
episodically exposed infant monkeys were similar to that of acutely 
exposed animals. Neither exposure protocol for the infant monkeys 
produced mucous cell metaplasia proximal to the lesions, an adaptation 
observed in adult monkeys exposed in another study (Harkema et al., 
1987). Functional and cellular changes in conducting airways were 
common manifestations of exposure to O3 among both the adult 
and infant monkeys (Plopper et al., 2007). In addition, the lung growth 
of the distal conducting airways in the infant monkeys was 
significantly stunted by O3 and this aberrant development 
was persistent 6 months postexposure (Fanucchi et al., 2006).
    Age may also affect the inflammatory response to O3 
exposure. Toxicological studies reported that the difference in effects 
among younger lifestage test animals may be due to age-related changes 
in antioxidants levels and sensitivity to oxidative stress. Further 
discussion of these studies may be found in section 8.3.1.1 of the ISA 
(U.S. EPA, 2013a, p. 8-18).
    The previous and recent human clinical and toxicological studies 
reported evidence of increased risk from O3 exposure for 
younger ages, which provides coherence and biological plausibility for 
the findings from epidemiologic studies. Although there was some 
inconsistency, generally, the epidemiologic studies reported positive 
associations among both children and adults or just among children. The 
interpretation of these studies is limited by the lack of consistency 
in comparison age groups and outcomes examined. However, overall, the 
epidemiologic, controlled human exposure, and toxicological studies 
provide adequate evidence that children are potentially at increased 
risk of O3-related health effects.
iv. Older adults
    The ISA notes that older adults are at greater risk of health 
effects associated with O3 exposure through a variety of 
intrinsic pathways (U.S. EPA, 2013a, section 8.3.1.2). In addition, 
older adults may differ in their exposure and internal dose. Older 
adults were outdoors for a slightly longer proportion of the day than 
adults aged 18-64 years. For more information on time spent outdoors by 
age group, see Section 4.4 in the ISA (U.S. EPA, 2013a). The gradual 
decline in physiological processes that occurs with aging may lead to 
increased risk of O3-related health effects (U.S. EPA, 
2006a). Respiratory symptom responses to O3 exposure appears 
to increase with age until early adulthood and then gradually decrease 
with increasing age (U.S. EPA, 1996); lung function responses to 
O3 exposure also decline from early adulthood (U.S. EPA, 
1996). The reductions of these responses with age may put older adults 
at increased risk for continued O3 exposure. In addition, 
older adults, in general, have a higher prevalence of preexisting 
diseases compared to younger age groups and this may also lead to 
increased risk of O3-related health effects (U.S. EPA, 
2013a, section 8.3.1.2). With the number of older Americans increasing 
in upcoming years (estimated to increase from 12.4% of the U.S. 
population to 19.7% between 2000 to 2030, which is approximately 35 
million and 71.5 million individuals, respectively) this group 
represents a large population potentially at risk of O3-
related health effects (SSDAN CensusScope, 2010a; U.S. Census Bureau, 
2010).
    The majority of recent studies reported greater effects of short-
term O3 exposure and mortality among older adults, which is 
consistent with the findings of the 2006 O3 AQCD. A study 
(Medina-Ram[oacute]n and Schwartz, 2008)

[[Page 75268]]

conducted in 48 cities across the U.S. reported larger effects among 
adults >=65 years old compared to those <65 years. Further 
investigation of this study population revealed a trend of 
O3-related mortality risk that gets larger with increasing 
age starting at age 51 (Zanobetti and Schwartz, 2008a). Another study 
conducted in 7 urban centers in Chile reported similar results, with 
greater effects in adults >=65 years old (Cakmak et al., 2007). More 
recently, a study conducted in the same area reported similar 
associations between O3 exposure and mortality in adults 
aged <64 years old and 65 to 74 years old, but the risk was increased 
among the older age group (Cakmak et al., 2011). A study performed in 
China reported greater effects in populations >=45 years old (compared 
to 5 to 44 year olds), with statistically significant effects present 
only among those >=65 years old (Kan et al., 2008). An Italian study 
reported higher risk of all-cause mortality associated with increased 
O3 concentrations among individuals >=85 year old as 
compared to those 35 to 84 years old (Stafoggia et al., 2010). The Air 
Pollution and Health: A European and North American Approach (APHENA) 
project examined the association between O3 exposure and 
mortality for those <75 and >=75 years of age. In Canada, the 
associations for all-cause and cardiovascular mortality were greater 
among those >=75 years old. In the U.S., the association for all-cause 
mortality was slightly greater for those <75 years of age compared to 
those >=75 years old in summer-only analyses. No consistent pattern was 
observed for CVD mortality. In Europe, slightly larger associations for 
all-cause mortality were observed in those <75 years old in all-year 
and summer-only analyses. Larger associations were reported among those 
<75years for CVD mortality in all-year analyses, but the reverse was 
true for summer-only analyses (Katsouyanni et al., 2009).
    With respect to epidemiologic studies of O3 exposure and 
hospital admissions, a positive association was reported between short-
term O3 exposure and respiratory hospital admissions for 
adults >=65 years old but not for those adults aged 15 to 64 years 
(Halonen et al., 2009). In the same study, no association was observed 
between O3 concentration and respiratory mortality among 
those >=65 years old or those 15 to 64 years old. No modification by 
age (40 to 64 year olds versus >64 year olds) was observed in a study 
from Brazil examining O3 levels and COPD-related emergency 
department visits.
    Although some outcomes reported mixed findings regarding an 
increase in risk for older adults, recent epidemiologic studies report 
consistent positive associations between short-term O3 
exposure and mortality in older adults. The evidence from mortality 
studies is consistent with the results reported in the 2006 
O3 AQCD and is supported by toxicological studies providing 
biological plausibility for increased risk of effects in older adults. 
Also, older adults may be experiencing increased exposure compared to 
younger adults. Overall, the ISA (U.S. EPA, 2013a) concludes adequate 
evidence is available indicating that older adults are at increased 
risk of O3-related health effects.
v. People With Diets Lower in Vitamins C and E
    Diet was not examined as a factor potentially affecting risk in 
previous O3 AQCDs, but recent studies have examined 
modification of the association between O3 and health 
effects by dietary factors. Because O3 mediates some of its 
toxic effects through oxidative stress, the antioxidant status of an 
individual is an important factor that may contribute to increased risk 
of O3-related health effects. Supplementation with vitamins 
C and E has been investigated in a number of studies as a means of 
inhibiting O3-mediated damage.
    Two epidemiologic studies have examined effect modification by diet 
and found evidence that certain dietary components are related to the 
effect O3 has on respiratory outcomes. In one recent study, 
the effects of fruit/vegetable intake and Mediterranean diet were 
examined. Increases in these food patterns, which have been noted for 
their high vitamins C and E and omega-3 fatty acid content, were 
positively related to lung function in asthmatic children living in 
Mexico City, and modified by O3 exposure (Romieu et al., 
2009). Another study examined supplementation of the diets of asthmatic 
children in Mexico with vitamins C and E (Sienra-Monge et al., 2004). 
Associations were detected between short-term O3 exposure 
and nasal airway inflammation among children in the placebo group but 
not in those receiving the supplementation.
    The epidemiologic evidence is supported by controlled human 
exposure studies, discussed in section 8.4.1 of the ISA (U.S. EPA, 
2013a), that have shown that the first line of defense against 
oxidative stress is antioxidants-rich extracellular lining fluid (ELF) 
which scavenges free radicals and limit lipid peroxidation. Exposure to 
O3 depletes antioxidant levels in nasal ELF probably due to 
scrubbing of O3; however, the concentration and the activity 
of antioxidant enzymes either in ELF or plasma do not appear to be 
related to O3 responsiveness. Controlled studies of dietary 
antioxidant supplementation have demonstrated some protective effects 
of [alpha]-tocopherol (a form of vitamin E) and ascorbate (vitamin C) 
on spirometric measures of lung function after O3 exposure 
but not on the intensity of subjective symptoms and inflammatory 
responses. Dietary antioxidants have also afforded partial protection 
to asthmatics by attenuating postexposure bronchial 
hyperresponsiveness. Toxicological studies discussed in section 8.4.1 
of the ISA (U.S. EPA, 2013a) provide evidence of biological 
plausibility to the epidemiologic and controlled human exposure 
studies.
    Overall, the ISA (U.S. EPA, 2013a) concludes adequate evidence is 
available indicating that individuals with diets lower in vitamins C 
and E are at risk for O3-related health effects. The 
evidence from epidemiologic studies is supported by controlled human 
exposure and toxicological studies.
vi. Outdoor Workers
    Studies included in the 2006 O3 AQCD reported that 
individuals who participate in outdoor activities or work outside to be 
a population at increased risk based on consistently reported 
associations between O3 exposure and respiratory health 
outcomes in these groups (U.S. EPA, 2006a). Outdoor workers are exposed 
to ambient O3 concentrations for a greater period of time 
than individuals who spend their days indoors. As discussed in section 
4.7 of the ISA (U.S. EPA, 2013a) outdoor workers sampled during the 
work shift had a higher ratio of personal exposure to fixed-site 
monitor concentrations than health clinic workers who spent most of 
their time indoors. Additionally, an increase in dose to the lower 
airways is possible during outdoor exercise due to both increases in 
the amount of air breathed (i.e., minute ventilation) and a shift from 
nasal to oronasal breathing. The association between FEV1 
responses to O3 exposure and minute ventilation is discussed 
more fully in section 6.2.3.1 of the 2006 O3 AQCD (U.S. EPA, 
2006a).
    Previous studies have shown that increased exposure to 
O3 due to outdoor work leads to increased risk of 
O3-related health effects, specifically decrements in lung 
function (U.S. EPA, 2006a). The strong evidence from the 2006 
O3 AQCD, which demonstrated increased exposure, dose, and 
ultimately risk of O3-related health effects in this 
population, supports the

[[Page 75269]]

conclusion that there is adequate evidence to indicate that increased 
exposure to O3 through outdoor work increases the risk of 
O3-related health effects.
    In some cases, it is difficult to determine a factor that results 
in increased risk of effects. For example, previous assessments have 
included controlled human exposure studies in which some healthy 
individuals demonstrate greater O3-related health effects 
compared to other healthy individuals. Interindividual variability has 
been observed for lung function decrements, symptomatic responses, 
pulmonary inflammation, AHR, and altered epithelial permeability in 
healthy adults exposed to O3, and these results tend to be 
reproducible within a given individual over a period of several months 
indicating differences in the intrinsic responsiveness. In many cases 
the reasons for the variability is not clear. This may be because one 
or some of the factors described above have not been evaluated in 
studies, or it may be that additional, unidentified factors influence 
individual responses to O3 (U.S. EPA, 2013a, section 8.5).
    As discussed in chapter 8 of the ISA (U.S. EPA, 2013a), there is a 
lack of information regarding the extent to which some factors may 
increase risk from O3 exposures. Due to this lack of 
information, the ISA concluded that for some factors, such as sex, SES, 
and obesity, there is only ``suggestive'' evidence of increased risk, 
or that for a number of factors the evidence is inadequate to draw 
conclusions about potential increase in risk of effects. Overall, the 
factors for which the ISA concludes there is adequate evidence of 
increased risk for experiencing O3-related effects were 
related to asthma, lifestage (children and older adults), genetic 
variability, dietary factors, and working outdoors.
b. Size of At-Risk Populations
    One consideration in the assessment of potential public health 
impacts is the size of various population groups for which there is 
adequate evidence of increased risk for health effects associated with 
O3-related air pollution exposure (U.S. EPA, 2014c, section 
3.1.5.2). The factors for which the ISA judged the evidence to be 
``adequate'' with respect to contributing to increased risk of 
O3-related effects among various populations and lifestages 
included: asthma; childhood and older adulthood; diets lower in 
vitamins C and E; certain genetic variants; and working outdoors (U.S. 
EPA, 2013a, section 8.5). No statistics are available to estimate the 
size of an at-risk population based on nutritional status or genetic 
variability.
    With regard to asthma, Table 3-7 in the PA (U.S. EPA, 2014c, 
section 3.1.5.2) summarizes information on the prevalence of current 
asthma by age in the U.S. adult population in 2010 (Schiller et al. 
2012; children--Bloom et al., 2011). Individuals with current asthma 
constitute a fairly large proportion of the population, including more 
than 25 million people. Asthma prevalence tends to be higher in 
children than adults. Within the U.S., approximately 8.2% of adults 
have reported currently having asthma (Schiller et al., 2012) and 9.5% 
of children have reported currently having asthma (Bloom et al., 
2011).\59\
---------------------------------------------------------------------------

    \59\ As noted below (II.C.3.a.ii), asthmatics can experience 
larger O3-induced respiratory effects than non-asthmatic, 
healthy adults. The responsiveness of asthmatics to O3 
exposures could depend on factors that have not been well-evaluated 
such as asthma severity, the effectiveness of asthma control, or the 
prevalence of medication use.
---------------------------------------------------------------------------

    With regard to lifestages, based on U.S. census data from 2010 
(Howden and Meyer, 2011), about 74 million people, or 24% of the U.S. 
population, are under 18 years of age and more than 40 million people, 
or about 13% of the U.S. population, are 65 years of age or older. 
Hence, a large proportion of the U.S. population (i.e., more than a 
third) is included in age groups that are considered likely to be at 
increased risk for health effects from ambient O3 exposure.
    With regard to outdoor workers, in 2010, approximately 11.7% of the 
total number of people (143 million people) employed, or about 16.8 
million people, worked outdoors one or more days per week (based on 
worker surveys).\60\ Of these, approximately 7.4% of the workforce, or 
about 7.8 million people, worked outdoors three or more days per week.
---------------------------------------------------------------------------

    \60\ The O*NET program is the nation's primary source of 
occupational information. Central to the project is the O*NET 
database, containing information on hundreds of standardized and 
occupation-specific descriptors. The database, which is available to 
the public at no cost, is continually updated by surveying a broad 
range of workers from each occupation. http://www.onetcenter.org/overview.html. http://www.onetonline.org/find/descriptor/browse/Work_Context/4.C.2/.
---------------------------------------------------------------------------

    The health statistics data illustrate what is known as the 
``pyramid'' of effects. At the top of the pyramid, there are 
approximately 2.5 million deaths from all causes per year in the U.S. 
population, with about 250 thousand respiratory-related deaths (CDC-
WONDER, 2008). For respiratory health diseases, there are nearly 3.3 
million hospital discharges per year (HCUP, 2007), 8.7 million 
respiratory emergency department visits (HCUP, 2007), 112 million 
ambulatory care visits (Woodwell and Cherry, 2004), and an estimated 
700 million restricted activity days per year due to respiratory 
conditions (Adams et al., 1999). Combining small risk estimates with 
relatively large baseline levels of health outcomes can result in quite 
large public health impacts. Thus, even a small percentage reduction in 
O3 health impacts on cardiopulmonary diseases would reflect 
a large number of avoided cases.
c. Impacts of Averting Behavior
    The activity pattern of individuals is an important determinant of 
their exposure (U.S. EPA, 2013a, section 4.4.1). Variation in 
O3 concentrations among various microenvironments means that 
the amount of time spent in each location, as well as the level of 
activity, will influence an individual's exposure to ambient 
O3. Activity patterns vary both among and within 
individuals, resulting in corresponding variations in exposure across a 
population and over time. Individuals can reduce their exposure to 
O3 by altering their behaviors, such as by staying indoors, 
being active outdoors when air quality is better, and by reducing their 
activity levels or reducing the time being active outdoors on high-
O3 days (U.S. EPA, 2013a, section 4.4.2).
    The widely reported Air Quality Index (AQI) conveys advice to the 
public, and particularly at-risk populations, on reducing short- or 
prolonged-exposures on days when ambient levels of common, criteria air 
pollutants (except lead), are elevated (www.airnow.gov). Information 
communicated by the AQI is based on the evidence and exposure/risk 
information assessed in the review of the NAAQS; it is updated and 
revised as necessary during the review of each standard. Proposed 
changes to the AQI sub-index for O3, based on evidence and 
exposure/risk information assessed in this review, are discussed in 
section III below.
    The AQI describes the potential for health effects from 
O3 (and other individual pollutants) in six color-coded 
categories of air-quality, ranging from Good (green), Moderate 
(yellow), Unhealthy for Sensitive Groups (orange), Unhealthy (red), and 
Very Unhealthy (purple), and Hazardous (maroon). Levels in the 
unhealthy ranges (i.e., Unhealthy for Sensitive Groups and above) come 
with recommendations about reducing exposure. Forecasted and actual AQI 
values for O3 are reported to the public

[[Page 75270]]

during the O3 season. The AQI advisories explicitly state 
that children, older adults, people with lung disease, and people who 
are active outdoors, may be at greater risk from exposure to 
O3. People are advised to reduce exposure depending on the 
predicted O3 levels and the likelihood of risk. This advice 
includes being active outdoors when air quality is better, and reducing 
activity levels or reducing the time being active outdoors on high-
O3 days. Staying indoors to reduce exposure is not 
recommended until air quality reaches the Very Unhealthy or Hazardous 
categories.
    Evidence of individual averting behaviors in response to AQI 
advisories has been found in several studies, including activity 
pattern and epidemiologic studies, especially for the at-risk 
populations, such as children, older adults, and people with asthma, 
who are targeted by the advisories. Such effects are less pronounced in 
the general population, possibly due to the opportunity cost of 
behavior modification. Epidemiologic evidence from a study (Neidell and 
Kinney, 2010) conducted in the 1990's in Los Angeles, CA reports 
increased asthma hospital admissions among children and older adults 
when O3 alert days (1-hour max O3 concentration 
>200 ppb) were excluded from the analysis of daily hospital admissions 
and O3 concentrations (presumably thereby eliminating 
averting behavior based on high O3 forecasts). If averting 
behavior reduces exposure to ambient O3, then epidemiologic 
studies that do not account for averting behavior may produce effect 
estimates that are biased toward the null due to exposure 
misclassification (U.S. EPA, 2013, section 4.6.6).

C. Human Exposure and Health Risk Assessments

    To put judgments about health effects that are adverse for 
individuals into a broader public health context, the EPA has developed 
and applied models to estimate human exposures to O3 and 
O3-associated health risks. Exposure and risk estimates 
based on such models are presented and assessed in the HREA (U.S. EPA, 
2014a). In reviewing the draft HREA, CASAC expressed the view that the 
document is ``well-written, founded based upon comprehensive analyses 
and adequate for its intended purpose'' (Frey, 2014a, p. 1). Analyses 
in the HREA inform consideration of the O3 exposures and 
health risks that could be allowed by the current standard and 
alternative standards, and consideration of the kind and degree of 
uncertainties inherent in estimates of O3 exposures and 
health risks.
    The following sections discuss the air quality adjustment approach 
used in the HREA for exposure and health risk estimates (II.C.1); the 
approach taken to estimate exposures, key exposure results, and 
important uncertainties (II.C.2); and the approaches taken to estimate 
O3 health risks, key risk results, and important 
uncertainties (II.C.3).
1. Air Quality Adjustment
    As discussed above (section I.E), O3 is formed near the 
Earth's surface due to chemical interactions involving solar radiation 
and precursor pollutants including VOCs, NOX, CH4 
and CO. The response of O3 to changes in precursor 
concentrations is nonlinear. In particular, NOX causes both 
the formation and destruction of O3. The net impact of 
NOX emissions on O3 concentrations depends on the 
local quantities of NOX, VOC, and sunlight, which interact 
in a set of complex chemical reactions. In some areas, such as urban 
centers where NOX emissions typically are high, 
NOX leads to the net destruction of O3, 
decreasing O3 concentrations in the immediate vicinity. This 
phenomenon is particularly pronounced under conditions that lead to low 
ambient O3 concentrations (i.e. during cool, cloudy weather 
and at night when photochemical activity is limited or nonexistent). 
However, while NOX can initially destroy O3 near 
emission sources, these same NOX emissions eventually react 
to form O3 downwind of those sources. Photochemical model 
simulations suggest that reductions in NOX emissions will 
slightly increase O3 concentrations near NOX 
sources on days with lower O3 concentrations, while at the 
same time decreasing the highest O3 concentrations in 
outlying areas. The atmospheric chemistry that influences ambient 
O3 concentrations is discussed in more detail in the ISA 
(U.S. EPA, 2013a, Chapter 3) and the PA (U.S. EPA, 2014c, Chapter 2) 
(see also Frey, 2014a, pp. 10 and 11).
    The HREA uses a photochemical model to estimate sensitivities of 
O3 to changes in precursor emissions in order to estimate 
ambient O3 concentrations that would just meet the current 
and alternative standards (U.S. EPA, 2014a, Chapter 4).\61\ For the 15 
urban study areas evaluated in the HREA,\62\ this model-based 
adjustment approach estimates hourly O3 concentrations at 
each monitor location when modeled U.S. anthropogenic precursor 
emissions (i.e., NOX, VOC) \63\ are reduced. The HREA 
estimates air quality that just meets the current and alternative 
standards for the 2006-2008 and 2008-2010 periods.\64\
---------------------------------------------------------------------------

    \61\ The HREA uses the Community Multi-scale Air Quality (CMAQ) 
photochemical model instrumented with the higher order direct 
decoupled method (HDDM) to estimate O3 concentrations 
that would occur with the achievement of the current and alternative 
O3 standards (U.S. EPA, 2014a, Chapter 4).
    \62\ The urban study areas assessed are Atlanta, Baltimore, 
Boston, Chicago, Cleveland, Dallas, Denver, Detroit, Houston, Los 
Angeles, New York, Philadelphia, Sacramento, St. Louis, and 
Washington, DC.
    \63\ Exposure and risk analyses for most urban study areas focus 
on reducing U.S. anthropogenic NOX emissions alone. The 
exceptions are Chicago and Denver. Exposure and risk analyses for 
Chicago and Denver are based on reductions in emissions of both 
NOX and VOC (U.S. EPA, 2014a, section 4.3.3.1; Appendix 
4D).
    \64\ These simulations are illustrative and do not reflect any 
consideration of specific control programs designed to achieve the 
reductions in emissions required to meet the specified standards. 
Further, these simulations do not represent predictions of when, 
whether, or how areas might meet the specified standards.
---------------------------------------------------------------------------

    As discussed in Chapter 4 of the HREA (U.S. EPA, 2014a), this 
approach to adjusting air quality models the physical and chemical 
atmospheric processes that influence ambient O3 
concentrations. Compared to the quadratic rollback approach used in 
previous reviews, it provides more realistic estimates of the spatial 
and temporal responses of O3 to reductions in precursor 
emissions. Because ambient NOX can contribute both to the 
formation and destruction of O3 (U.S. EPA, 2014a, Chapter 
4), as discussed above, the response of ambient O3 
concentrations to reductions in NOX emissions is more 
variable than indicated by the quadratic rollback approach. This 
improved approach to adjusting O3 air quality is consistent 
with recommendations from the National Research Council of the National 
Academies (NRC, 2008). In addition, CASAC strongly supported the 
improved approach, stating that ``the quadratic rollback approach has 
been replaced by a scientifically more valid Higher-order Decoupled 
Direct Method (HDDM)'' and that ``[t]he replacement of the quadratic 
rollback procedure by the HDDM procedure is important and supported by 
the CASAC'' (Frey, 2014a, pp.1 and 3).
    Consistent with the O3 chemistry summarized above, in 
locations and time periods when NOX is predominantly 
contributing to O3 formation (e.g., downwind of important 
NOX sources, where the highest O3 concentrations 
often occur), model-based adjustment to the current and alternative 
standards decreases

[[Page 75271]]

estimated ambient O3 concentrations compared to recent 
monitored concentrations (U.S. EPA, 2014a, section 4.3.3.2). In 
contrast, in locations and time periods when NOX is 
predominantly contributing to O3 titration (e.g., in urban 
centers with high concentrations of NOX emissions, where 
ambient O3 concentrations are often suppressed and thus 
relatively low \65\), model-based adjustment increases ambient 
O3 concentrations compared to recent monitored 
concentrations (U.S. EPA, 2014a, section 4.3.3.2; Frey, 2014a, p. 10).
---------------------------------------------------------------------------

    \65\ Titration is also prominent during time periods when 
photochemistry is limited, and ambient O3 concentrations 
are relatively low, such as at night and on cool, cloudy days (U.S. 
EPA, 2014a, Chapter 4).
---------------------------------------------------------------------------

    Within urban study areas, the overall impacts of model-based air 
quality adjustment are to reduce the O3 concentrations at 
the upper ends of ambient distributions and to increase the 
O3 concentrations at the lower ends of those distributions 
(U.S. EPA, 2014a, section 4.3.3.2, Figures 4-9 and 4-10).\66\ Seasonal 
means of daily O3 concentrations generally exhibit only 
modest changes upon model adjustment, reflecting the seasonal balance 
between daily decreases in relatively higher concentrations and 
increases in relatively lower concentrations (U.S. EPA, 2014a, Figures 
4-9 and 4-10). The resulting compression in the seasonal distributions 
of ambient O3 concentrations is evident in all of the urban 
study areas evaluated, though the degree of compression varies 
considerably across areas (U.S. EPA, 2014a, Figures 4-9 and 4-10).
---------------------------------------------------------------------------

    \66\ It is important to note that sensitivity analyses in the 
HREA indicate that the increases in low O3 concentrations 
are smaller when NOX and VOC emissions are reduced than 
when only NOX emissions are reduced (U.S. EPA, 2014a, 
Appendix 4-D, section 4.7).
---------------------------------------------------------------------------

    This compression in the distributions of ambient O3 
concentrations has important implications for exposure and risk 
estimates in urban study areas. Estimates influenced largely by the 
upper ends of the distribution of ambient concentrations (i.e., 
exposures of concern and lung function risk estimates, as discussed in 
sections 3.2.2 and 3.2.3.1 of the PA (U.S. EPA, 2014c)) decrease with 
adjustment of air quality to the current and alternative standards. In 
contrast, seasonal risk estimates influenced by the full distribution 
of ambient O3 concentrations (i.e., epidemiology-based risk 
estimates, as discussed in section 3.2.3.2 of the PA) either decrease 
or increase in response to air quality adjustment, depending on the 
balance between the daily decreases in high O3 
concentrations and increases in low O3 concentrations.\67\
---------------------------------------------------------------------------

    \67\ In addition, because epidemiology-based risk estimates use 
``area-wide'' average O3 concentrations, calculated by 
averaging concentrations across multiple monitors in urban study 
areas (U.S. EPA, 2014c, section 3.2.3.2), risk estimates on a given 
day depend on the daily balance between increasing and decreasing 
O3 concentrations at the individual monitors that are 
averaged together to calculate the ``area-wide'' concentration.
---------------------------------------------------------------------------

    In their review of the second draft HREA, CASAC considered this 
issue, in particular noting that ``reductions in nitrogen oxides 
emissions can lead to less scavenging of ozone and free radicals, 
resulting in locally higher levels of ozone'' (Frey, 2014a, p. 10). 
CASAC recommended that ``the EPA should identify and discuss whether 
and to what extent health risks in the urban core may be affected by 
NOX reductions or other possible strategies'' and, in 
particular, concluded that it would ``be of interest to learn if there 
would be any children or outdoor workers in the more urban areas who 
would experience significantly higher exposures to ozone as a result of 
possible changes in the ozone NAAQS'' (Frey, 2014a, p. 10). Consistent 
with this advice, the exposure and risk implications of the spatial and 
temporal patterns of ambient O3 following air quality 
adjustment in urban study areas are discussed in the final HREA (U.S. 
EPA, 2014a, Chapter 9) and the final PA (U.S. EPA, 2014c, sections 
3.2.2, 3.2.3), and are summarized below within the context of the PA's 
consideration of exposure estimates (II.D.2.a) and risk estimates 
(II.D.2.b and II.D.2.c).
2. Exposure Assessment
    This section discusses the HREA assessment of human exposures to 
O3. Section II.C.2.a provides an overview of the approach 
used in the HREA to assessing exposures and the approach in the PA to 
considering exposure estimates, and summarizes key results. Section 
II.C.2.b summarizes the important uncertainties in exposure estimates.
a. Overview and Summary of Key Results
    The exposure assessment presented in the HREA (U.S. EPA, 2014a, 
Chapter 5) provides estimates of the number and percent of people 
exposed to various concentrations of ambient O3, while at 
specified exertion levels. The HREA estimates exposures in the 15 urban 
study areas for four study groups, all school-age children (ages 5 to 
18), asthmatic school-age children, asthmatic adults (ages 19 to 95), 
and all older adults (ages 65 to 95), reflecting the evidence 
indicating that these populations are at increased risk for 
O3-attributable effects (U.S. EPA, 2013a, Chapter 8). An 
important purpose of these exposure estimates is to provide perspective 
on the extent to which air quality adjusted to just meet the current 
O3 NAAQS could be associated with exposures to O3 
concentrations reported to result in respiratory effects.\68\ Estimates 
of such ``exposures of concern'' provide perspective on the potential 
public health impacts of O3-related effects, including 
effects that cannot currently be evaluated in a quantitative risk 
assessment.\69\
---------------------------------------------------------------------------

    \68\ In addition, the range of modeled personal exposures to 
ambient O3 provide an essential input to the portion of 
the health risk assessment based on exposure-response functions (for 
lung function decrements) from controlled human exposure studies. 
The health risk assessment based on exposure-response information is 
discussed below (II.C.3).
    \69\ In this review, the term ``exposure of concern'' is defined 
as a personal exposure, while at moderate or greater exertion, to 8-
hour average ambient O3 concentrations at and above 
specific benchmarks. As discussed below, benchmarks represent 
exposure concentrations at which O3-induced health 
effects are known to occur, or can reasonably be anticipated to 
occur, in some individuals.
---------------------------------------------------------------------------

    In the absence of large scale exposure studies that encompass the 
general population, as well as at-risk populations, modeling is the 
preferred approach to estimating exposures to O3 (U.S. EPA, 
2014a, Chapter 5). The use of exposure modeling also facilitates the 
estimation of exposures resulting from ambient O3 
concentrations differing from those present during exposure studies. In 
the HREA, population exposures to ambient O3 concentrations 
are estimated using the current version of the Air Pollutants Exposure 
(APEX) model. The APEX model simulates the movement of individuals 
through time and space and estimates their exposures to a given 
pollutant in indoor, outdoor, and in-vehicle microenvironments (U.S. 
EPA, 2014a, section 5.1.3). APEX takes into account important factors 
that contribute to total human exposure to ambient O3, 
including the temporal and spatial distributions of people and 
O3 concentrations throughout an urban area, the variation of 
O3 concentrations within various microenvironments, and the 
effects of exertion on breathing rate in exposed individuals (U.S. EPA, 
2014a, section 5.1.3). To the extent spatial and/or temporal patterns 
of ambient O3 concentrations are altered upon model 
adjustment, as discussed above, exposure estimates reflect population 
exposures to those altered patterns.
    The HREA estimates 8-hour exposures at or above benchmark 
concentrations of

[[Page 75272]]

60, 70, and 80 ppb for individuals engaged in moderate or greater 
exertion (i.e., to approximate conditions in the controlled human 
exposure studies on which benchmarks are based). Benchmarks reflect 
exposure concentrations at which O3-induced respiratory 
effects are known to occur in some healthy adults engaged in moderate, 
intermittent exertion, based on evidence from controlled human exposure 
studies (U.S. EPA, 2013a, section 6.2; U.S. EPA, 2014c, section 
3.1.2.1). The amount of weight to place on the estimates of exposures 
at or above specific benchmark concentrations depends in part on the 
weight of the scientific evidence concerning health effects associated 
with O3 exposures at those benchmark concentrations. It also 
depends on judgments about the importance, from a public health 
perspective, of the health effects that are known or can reasonably be 
inferred to occur as a result of exposures at benchmark concentrations 
(U.S. EPA, 2014c, sections 3.1.3, 3.1.5).
    As discussed in more detail above (II.B.2), the health evidence 
that supports evaluating exposures of concern at or above benchmark 
concentrations of 60, 70, and 80 ppb comes from a large body of 
controlled human exposure studies reporting a variety of respiratory 
effects in healthy adults. The lowest O3 exposure 
concentration for which controlled human exposure studies have reported 
respiratory effects in healthy adults is 60 ppb (based on changes in 
group mean responses), with more evidence supporting this benchmark 
concentration in the current review than in the last review. In healthy 
adults, 6.6 hour exposures to 60 ppb O3 have been reported 
to decrease lung function and to increase airway inflammation. 
Exposures of healthy adults to 72 ppb O3 for 6.6 hours have 
been reported to result in larger average lung function decrements, 
compared to 60 ppb, as well as in increased respiratory symptoms. 
Exposures of healthy adults to 80 ppb O3 for 6.6 hours have 
been reported to result in larger average lung function decrements than 
following exposures to 60 or 72 ppb and, depending on the study, to 
increase airway inflammation, increase respiratory symptoms, increase 
airways responsiveness, and decrease lung host defense (based on 
changes in group means) (U.S. EPA, 2014c, section 3.1.2.1). In 
commenting on the evidence for benchmark concentrations, CASAC stated 
the following (Frey, 2014c, p. 6):

The 80 ppb-8hr benchmark level represents an exposure level for 
which there is substantial clinical evidence demonstrating a range 
of ozone-related effects including lung inflammation and airway 
responsiveness in healthy individuals. The 70 ppb-8hr benchmark 
level reflects the fact that in healthy subjects, decreases in lung 
function and respiratory symptoms occur at concentrations as low as 
72 ppb and that these effects almost certainly occur in some people, 
including asthmatics and others with low lung function who are less 
tolerant of such effects, at levels of 70 ppb and below. The 60 ppb-
8hr benchmark level represents the lowest exposure level at which 
ozone-related effects have been observed in clinical studies of 
healthy individuals. Based on its scientific judgment, the CASAC 
finds that the 60 ppb-8hr exposure benchmark is relevant for 
consideration with respect to adverse effects on asthmatics.

    In considering estimates of O3 exposures of concern at 
or above benchmarks of 60, 70, and 80 ppb, the PA focuses on modeled 
exposures for school-age children (ages 5-18), including asthmatic 
school-age children, which are key at-risk populations identified in 
the ISA (U.S. EPA, 2014c, section 3.1.5). The percentages of children 
estimated to experience exposures of concern are considerably larger 
than the percentages estimated for adult populations (i.e., 
approximately 3-fold larger across urban study areas) (U.S. EPA, 2014a, 
section 5.3.2 and Figures 5-5 to 5-8). The larger exposure estimates 
for children are due primarily to the larger percentage of children 
estimated to spend an extended period of time being physically active 
outdoors when O3 concentrations are elevated (U.S. EPA, 
2014a, sections 5.3.2 and 5.4.1).
    Although exposure estimates differ between children and adults, the 
patterns of results across the urban study areas and years are similar 
among all of the populations evaluated (U.S. EPA, 2014a, Figures 5-5 to 
5-8). Therefore, while the PA highlights estimates in children, 
including asthmatic school-age children, it also notes that the 
patterns of exposures estimated for children represent the patterns 
estimated for adult asthmatics and older adults.
    Table 1 below summarizes key results from the exposure assessment. 
Table 1 presents estimates of the percentages and numbers of all 
school-aged children estimated to experience exposures of concern when 
air quality was adjusted to just meet the current and alternative 8-
hour O3 standards. The percentage of all school-age children 
in the 15 urban study areas estimated to experience exposures of 
concern declines when comparing just meeting the current standard to 
just meeting alternative 8-hour O3 standards. Substantial 
variability is evident across years and urban study areas, as indicated 
by the ranges of averaged estimates and estimates for worst-case years 
and study areas. As discussed below, the interindividual variability in 
responsiveness following exposures of concern means that only a subset 
of individuals who are exposed at and above a given benchmark 
concentration would actually be expected to experience respiratory 
effects.

Table 1--Summary of Estimated Exposures of Concern in All School-age Children for the Current and Alternative O3
                                         Standards in Urban Study Areas
----------------------------------------------------------------------------------------------------------------
                                                                                                   % Children--
                                   Standard level     Average %     Average number of children    worst year and
     Benchmark  concentration           (ppb)         children      exposed  [average number of     worst area
                                                    exposed \70\     asthmatic children] \71\
----------------------------------------------------------------------------------------------------------------
                                   One or more exposures of concern per season
----------------------------------------------------------------------------------------------------------------
>=80 ppb.........................              75           0-0.3  27,000 [3,000]..............              1.1
                                               70           0-0.1  3,700 [300].................              0.2
                                               65               0  300 [0].....................                0
                                               60               0  100 \72\ [0]................                0
>=70 ppb.........................              75         0.6-3.3  362,000 [40,000]............              8.1
                                               70         0.1-1.2  94,000 [10,000].............              3.2
                                               65           0-0.2  14,000 [2,000]..............              0.5
                                               60               0  1,400 [200].................              0.1
>=60 ppb.........................              75          9.5-17  2,316,000 [246,000].........             25.8
                                               70        3.3-10.2  1,176,000 [126,000].........             18.9
                                               65           0-4.2  392,000 [42,000]............              9.5

[[Page 75273]]

 
                                               60           0-1.2  70,000 [8,000]..............              2.2
----------------------------------------------------------------------------------------------------------------
                                   Two or more exposures of concern per season
----------------------------------------------------------------------------------------------------------------
>=80 ppb.........................              75               0  600 [100]...................              0.1
                                               70               0  0 [0].......................                0
                                               65               0  0 [0].......................                0
                                               60               0  0 [0].......................                0
>=70 ppb.........................              75         0.1-0.6  46,000 [5,000]..............              2.2
                                               70           0-0.1  5,400 [600].................              0.4
                                               65               0  300 [100]...................                0
                                               60               0  0 [0].......................                0
>=60 ppb.........................              75         3.1-7.6  865,000 [93,000]............             14.4
                                               70         0.5-3.5  320,000 [35,000]............              9.2
                                               65           0-0.8  67,000 [7,500]..............              2.8
                                               60           0-0.2  5,100 [700].................              0.3
----------------------------------------------------------------------------------------------------------------

b. Key Uncertainties
---------------------------------------------------------------------------

    \70\ Estimates for each urban case study area were averaged for 
the years evaluated in the HREA (2006 to 2010). Ranges reflect the 
ranges across urban study areas. Estimates smaller than 0.05% were 
rounded downward to zero (from U.S. EPA, 2014a, Tables 5-11 and 5-
12).
    \71\ Numbers of children exposed in each urban case study area 
were averaged over the years 2006 to 2010. These averages were then 
summed across urban study areas. Numbers were rounded to nearest 
thousand unless otherwise indicated. Estimates smaller than 50 were 
rounded downward to zero (from U.S. EPA, 2014a, Appendix 5F Table 
5F-5). See below for discussion of uncertainties in exposure 
estimates.
    \72\ As discussed in section 4.3.3 of the HREA, the model-based 
air quality adjustment approach used to estimate risks associated 
with the current and alternative standards was unable to estimate 
the distribution of ambient O3 concentrations in New York 
City upon just meeting an alternative standard with a level of 60 
ppb. Therefore, for the 60 ppb standard level the numbers of 
children and asthmatic children reflect all of the urban study areas 
except New York.
---------------------------------------------------------------------------

    In considering exposure estimates within the context of the current 
and alternative O3 standards, the PA also notes important 
uncertainties in these estimates. For example, due to variability in 
responsiveness, only a subset of individuals who experience exposures 
at or above a benchmark concentration can be expected to experience 
health effects.\73\ Given the lack of sufficient exposure-response 
information for most of the health effects that informed benchmark 
concentrations, estimates of the number of people likely to experience 
exposures at or above benchmark concentrations generally cannot be 
translated into quantitative estimates of the number of people likely 
to experience specific health effects.\74\ The PA views health-relevant 
exposures as a continuum with greater confidence and less uncertainty 
about the existence of adverse health effects at higher O3 
exposure concentrations, and less confidence and greater uncertainty as 
one considers lower exposure concentrations. This view draws from the 
overall body of available health evidence, which indicates that as 
exposure concentrations increase, the incidence, magnitude, and 
severity of effects increases.
---------------------------------------------------------------------------

    \73\ As noted below (II.C.3.a.ii), in the case of asthmatics, 
responsiveness to O3 could depend on factors that have 
not been well-evaluated, such as asthma severity, the effectiveness 
of asthma control, or the prevalence of medication use.
    \74\ The exception to this is lung function decrements, as 
discussed below (and in U.S. EPA, 2014c, section 3.2.3.1).
---------------------------------------------------------------------------

    Though the PA indicates less confidence in the likelihood of 
adverse health effects as O3 exposure concentrations 
decrease, it also notes that the controlled human exposure studies that 
provided the basis for health benchmark concentrations have not 
evaluated at-risk populations. Compared to the healthy individuals 
included in controlled human exposure studies, members of at-risk 
populations (e.g., asthmatics, children) could be more likely to 
experience adverse effects, could experience larger and/or more serious 
effects, and/or could experience effects following exposures to lower 
O3 concentrations. The CASAC expressed similar views in 
their advice to the Administrator (Frey, 2014a, pp. 7 and 14). In 
considering estimated exposures of concern (U.S. EPA, 2014c, section 
3.4), the PA notes that concerns about the potential for adverse health 
effects, including effects in at-risk populations must be balanced 
against the increasing uncertainty regarding the likelihood of such 
effects following exposures to lower O3 concentrations.
    Uncertainties associated with the APEX exposure modeling also have 
the potential to be important (U.S. EPA, 2014a, section 5.5.2, Table 5-
6). For example, the HREA concludes that exposures of concern could be 
underestimated for some individuals who are frequently and routinely 
active outdoors during the warm season (U.S. EPA, 2014a, section 
5.5.2). This could include outdoor workers and children who are 
frequently active outdoors. The HREA specifically notes that long-term 
diary profiles (i.e., monthly, annual) do not exist for such 
populations, limiting the extent to which APEX outputs reflect people 
who follow similar daily routines resulting in high exposures, over 
extended periods of time.
    In order to evaluate one dimension of the potential implications of 
this uncertainty for exposure estimates, the HREA reports the results 
of limited exposure model sensitivity analyses using subsets of 
activity diaries specifically selected to reflect groups spending a 
larger proportion of time being active outdoors during the 
O3 season. When diaries were selected to mimic activity 
patterns performed by outdoor workers, the percent of modeled 
individuals estimated to experience exposures of concern was higher 
than the other adult populations evaluated. The percentages of outdoor 
workers estimated to experience exposures of concern were generally 
similar to the percentages estimated for children (i.e., using the full 
database of diary profiles) in the worst-case urban study area and year 
(i.e., urban study area and year with the largest percent of children 
estimated to experience exposures of concern) (U.S. EPA, 2014a, section 
5.4.3.2, Figure 5-14). In

[[Page 75274]]

addition, when diaries were restricted to children who did not report 
any time spent inside a school or performing paid work (i.e., to mimic 
children spending large portions of their time outdoors during the 
summer), the number experiencing exposures of concern increased by 
approximately 30% (U.S. EPA, 2014a, section 5.4.3.1). Though these 
sensitivity analyses are limited to single urban study areas, and 
though there is uncertainty associated with diary selection approaches 
to mimic highly exposed populations, they suggest the possibility that 
some at-risk groups could experience more frequent exposures of concern 
than indicated by estimates made using the full database of activity 
diary profiles.
    In further considering activity diaries, the HREA also notes that 
growing evidence indicates that people can change their behavior in 
response to high O3 concentrations, reducing the time spent 
being active outdoors (U.S. EPA, 2014a, section 5.4.3.3). Commonly 
termed ``averting behaviors,'' these altered activity patterns could 
reduce personal exposure concentrations. Therefore, the HREA also 
performed limited sensitivity analyses to evaluate the potential 
implications of averting behavior for estimated exposures of concern. 
These analyses suggest that averting behavior could reduce the 
percentages of children estimated to experience exposures of concern at 
or above the 60 or 70 ppb benchmark concentrations by approximately 10 
to 30%, with larger reductions possible for the 80 ppb benchmark (U.S. 
EPA, 2014a, Figure 5-15). As discussed above for other sensitivity 
analyses, these analyses are limited to a single urban case study area 
and are subject to uncertainties associated with assumptions about the 
prevalence and duration of averting behaviors. However, the results 
suggest that exposures of concern could be overestimated, particularly 
in children (Neidell, 2009; U.S. EPA, 2013, Figures 4-7 and 4-8), if 
the possibility for averting behavior is not incorporated into 
estimates.
3. Quantitative Health Risk Assessments
    For some health endpoints, there is sufficient scientific evidence 
and information available to support the development of quantitative 
estimates of O3-related health risks. In the last review of 
the O3 NAAQS, the quantitative health risk assessment 
estimated O3-related lung function decrements, respiratory 
symptoms, respiratory-related hospital admissions, and nonaccidental 
and cardiorespiratory-related mortality (U.S. EPA, 2007). In those 
analyses, both controlled human exposure and epidemiologic studies were 
used for the quantitative assessment of O3-related human 
health risks.
    In the current review, for short-term O3 concentrations, 
the HREA estimates lung function decrements; respiratory symptoms in 
asthmatics; hospital admissions and emergency department visits for 
respiratory causes; and all-cause mortality (U.S. EPA, 2014a). For 
long-term O3 concentrations, the HREA estimates respiratory 
mortality (U.S. EPA, 2014a).\75\ Estimates of O3-induced 
lung function decrements are based on exposure modeling, combined with 
exposure-response relationships from controlled human exposure studies 
(U.S. EPA, 2014a, Chapter 6). Estimates of O3-associated 
respiratory symptoms, hospital admissions and emergency department 
visits, and mortality are based on concentration-response relationships 
from epidemiologic studies (U.S. EPA, 2014a, Chapter 7). As with the 
exposure assessment discussed above, O3-associated health 
risks are estimated for recent air quality and for ambient 
concentrations adjusted to just meet the current and alternative 
O3 standards, based on 2006-2010 air quality and adjusted 
precursor emissions. The following sections discuss the lung function 
risk assessment (II.C.3.a) and the epidemiology-based morbidity and 
mortality risk assessments (II.C.3.b) from the HREA, including 
important sources of uncertainty in these estimates.
---------------------------------------------------------------------------

    \75\ Estimates of O3-associated respiratory mortality 
are based on the study by Jerrett et al. (2009). This study used 
seasonal averages of 1-hour daily maximum O3 
concentrations to estimate long-term concentrations.
---------------------------------------------------------------------------

a. Lung Function Risk Assessment
    Section II.C.3.a.i provides an overview of the approach used in the 
HREA to assessing lung function risks, an overview of the approach in 
the PA to considering lung function risk estimates, and a summary of 
key results. Section II.C.3.a.ii presents a summary of key 
uncertainties in lung function risk estimates.
i. Overview and Summary of Key Results
    In the current review, the HREA estimates risks of lung function 
decrements in school-aged children (ages 5 to 18), asthmatic school-
aged children, and the general adult population for the 15 urban study 
areas. The results presented in the HREA are based on an updated dose-
threshold model that estimates FEV1 responses for 
individuals following short-term exposures to O3 (McDonnell 
et al., 2012), reflecting methodological improvements since the last 
review (II.B.2.a.i, above; U.S. EPA, 2014a, section 6.2.4). The impact 
of the dose threshold is that O3-induced FEV1 
decrements result primarily from exposures on days with average ambient 
O3 concentrations above about 40 ppb (U.S. EPA, 2014a, 
section 6.3.1, Figure 6-9).\76\
---------------------------------------------------------------------------

    \76\ Analysis of this issue in the HREA is based on risk 
estimates in Los Angeles for 2006 unadjusted air quality. The HREA 
shows that more than 90% of daily instances of FEV1 
decrements >=10% occur when 8-hr average ambient concentrations are 
above 40 ppb for this modeled scenario. The HREA notes that the 
distribution of responses will be different for different study 
areas, years, and air quality scenarios (U.S. EPA, 2014c, Chapter 
6).
---------------------------------------------------------------------------

    The HREA estimates risks of moderate to large lung function 
decrements, defined as FEV1 decrements >=10%, 15%, or 20%. 
In evaluating these lung function risk estimates within the context of 
considering the current and alternative O3 standards, the PA 
focuses on the percent of children estimated to experience one or more 
and two or more decrements >=10, 15, and 20%, noting that the 
percentage of asthmatic children estimated to experience such 
decrements is virtually indistinguishable from the percentage estimated 
for all children.\77\ Compared to children, a smaller percentage of 
adults were estimated to experience O3-induced 
FEV1 decrements (U.S. EPA, 2014a, section 6.3.1, Table 6-4). 
As for exposures of concern (see above), the patterns of results across 
urban study areas and over the years evaluated are similar in children 
and adults. Therefore, while the PA highlights estimates in children, 
it notes that these results are also representative of the patterns 
estimated for adult populations.
---------------------------------------------------------------------------

    \77\ Though see below for discussion of uncertainty in lung 
function responses of children and asthmatics.
---------------------------------------------------------------------------

    Table 2 below summarizes key results from the lung function risk 
assessment. Table 2 presents estimates of the percentages of school-
aged children estimated to experience O3-induced 
FEV1 decrements >=10, 15, or 20% when air quality was 
adjusted to just meet the current and alternative 8-hour O3 
standards. Table 2 also presents the numbers of children, including 
children with asthma, estimated to experience such decrements. As shown 
in these tables, the percentage of school-age children in the 15 urban 
study areas estimated to experience O3-induced 
FEV1 decrements declines when comparing just meeting the 
current standard to just meeting alternative

[[Page 75275]]

8-hour O3 standards. Substantial variability is evident 
across years and urban study areas, as indicated by the ranges of 
averaged estimates and estimates for worst-case years and locations.

 Table 2--Summary of Estimated O3-Induced Lung Function Decrements for the Current and Potential Alternative O3
                                       Standards in Urban Case Study Areas
----------------------------------------------------------------------------------------------------------------
                                                                     Number of children (5 to 18    % Children
      Lung function decrement         Alternative      Average %    years)  [number of asthmatic  worst year and
                                    standard level   children \78\         children] \79\              area
----------------------------------------------------------------------------------------------------------------
                                        One or more decrements per season
----------------------------------------------------------------------------------------------------------------
>=10%.............................              75           14-19  3,007,000 [312,000].........              22
                                                70           11-17  2,527,000 [261,000].........              20
                                                65            3-15  1,896,000 [191,000].........              18
                                                60            5-11  1,404,000 [139,000] \80\....              13
>=15%.............................              75             3-5  766,000 [80,000]............               7
                                                70             2-4  562,000 [58,000]............               5
                                                65             0-3  356,000 [36,000]............               4
                                                60             1-2  225,000 [22,000]............               3
>=20%.............................              75             1-2  285,000 [30,000]............             2.8
                                                70             1-2  189,000 [20,000]............             2.1
                                                65             0-1  106,000 [11,000]............             1.4
                                                60             0-1  57,000 [6,000]..............             0.9
----------------------------------------------------------------------------------------------------------------
                                        Two or more decrements per season
----------------------------------------------------------------------------------------------------------------
>=10%.............................              75          7.5-12  1,730,000 [179,000].........              14
                                                70          5.5-11  1,414,000 [145,000].........              13
                                                65         1.3-8.8  1,023,000 [102,000].........              11
                                                60         2.1-6.4  741,000 [73,000]............             7.3
>=15%.............................              75         1.7-2.9  391,000 [40,000]............             3.8
                                                70         0.9-2.4  276,000 [28,000]............             3.1
                                                65         0.1-1.8  168,000 [17,000]............             2.3
                                                60         0.2-1.0  101,000 [10,000]............             1.4
>=20%.............................              75         0.5-1.1  128,000 [13,000]............             1.5
                                                70         0.3-0.8  81,000 [8,000]..............             1.1
                                                65           0-0.5  43,000 [4,000]..............             0.8
                                                60           0-0.2  21,000 [2,000]..............             0.4
----------------------------------------------------------------------------------------------------------------

ii. Key Uncertainties
---------------------------------------------------------------------------

    \78\ Estimates in each urban case study area were averaged for 
the years evaluated in the HREA (2006 to 2010). Ranges reflect the 
ranges across urban study areas.
    \79\ Numbers of children estimated to experience decrements in 
each study urban case study area were averaged over 2006 to 2010. 
These averages were then summed across urban study areas. Numbers 
are rounded to nearest thousand unless otherwise indicated.
    \80\ As discussed in section 4.3.3 of the HREA, the model-based 
air quality adjustment approach used to estimate risks associated 
with the current and alternative standards was unable to estimate 
the distribution of ambient O3 concentrations in New York 
City upon just meeting an alternative standard with a level of 60 
ppb. Therefore, for the 60 ppb standard level the numbers of 
children and asthmatic children reflect all of the urban study areas 
except New York.
---------------------------------------------------------------------------

    As for exposures of concern discussed above, the PA also considers 
important uncertainties in estimates of lung function risk. In addition 
to the uncertainties noted for exposure estimates, the HREA identifies 
several key uncertainties associated with estimates of O3-
induced lung function decrements. An uncertainty with particular 
potential to impact consideration of risk estimates stems from the lack 
of exposure-response information in children. In the near absence of 
controlled human exposure data for children, risk estimates are based 
on the assumption that children exhibit the same lung function response 
following O3 exposures as healthy 18 year olds (i.e., the 
youngest age for which controlled human exposure data is available) 
(U.S. EPA, 2014a, section 6.5.3). This assumption is justified in part 
by the findings of McDonnell et al. (1985), who reported that children 
(8-11 years old) experienced FEV1 responses similar to those 
observed in adults (18-35 years old). In addition, as discussed in the 
ISA (U.S. EPA, 2013a, section 6.2.1), summer camp studies of school-
aged children reported O3-induced lung function decrements 
similar in magnitude to those observed in controlled human exposure 
studies using adults. In extending the risk model to children, the HREA 
fixes the age term in the model at its highest value, the value for age 
18. This approach could result in either over- or underestimates of 
O3-induced lung function decrements in children, depending 
on how children compare to the adults used in controlled human exposure 
studies (U.S. EPA, 2014a, section 6.5.3).
    A related source of uncertainty is that the risk assessment 
estimates O3-induced decrements in asthmatics using the 
exposure-response relationship developed from data collected from 
healthy individuals. Although the evidence has been mixed (U.S. EPA, 
2013a, section 6.2.1.1), several studies have reported larger 
O3-induced lung function decrements in asthmatics than in 
non-asthmatics (Kreit et al., 1989; Horstman et al., 1995; Jorres et 
al., 1996; Alexis et al., 2000). On this issue, CASAC noted that 
``[a]sthmatic subjects appear to be at least as sensitive, if not more 
sensitive, than non-asthmatic subjects in manifesting ozone-induced 
pulmonary function decrements'' (Frey, 2014c, p. 4). To the extent 
asthmatics experience larger O3-induced lung function 
decrements than the healthy adults used to develop exposure-response 
relationships, the HREA could underestimate the impacts of 
O3 exposures on lung function in asthmatics, including 
asthmatic children. The implications of this uncertainty for risk 
estimates remain unknown at this time (U.S. EPA, 2014a,

[[Page 75276]]

section 6.5.4), and could depend on a variety of factors that have not 
been well-evaluated, including the severity of asthma and the 
prevalence of medication use. However, the available evidence shows 
responses to O3 increase with severity of asthma (Horstman 
et al., 1995) and corticosteroid usage does not prevent O3 
effects on lung function decrements or respiratory symptoms in people 
with asthma (Vagaggini et al., 2001, 2007).
b. Mortality and Morbidity Risk Assessments
    As discussed above (II.B.2), epidemiologic studies provide evidence 
for the most serious O3-associated public health outcomes 
(e.g., mortality, hospital admissions, emergency department visits). 
Section II.C.3.b.i below provides an overview of the approach used in 
the HREA to assessing mortality and morbidity risks based on 
information from epidemiologic studies, discusses the approach in the 
PA to considering epidemiology-based risk estimates, and presents a 
summary of key results. Section II.C.3.b.ii summarizes key 
uncertainties in epidemiology-base risk estimates.
i. Overview and Summary of Key Results
    Risk estimates based on epidemiologic studies can provide 
perspective on the most serious O3-associated public health 
outcomes (e.g., mortality, hospital admissions, emergency department 
visits) in populations that often include at-risk groups. The HREA 
estimates O3-associated risks in 12 urban study areas \81\ 
using concentration-response relationships drawn from epidemiologic 
studies. These concentration-response relationships are based on 
``area-wide'' average O3 concentrations.\82\ The HREA 
estimates risks for the years 2007 and 2009 in order to provide 
estimates of risk for a year with generally higher O3 
concentrations (2007) and a year with generally lower O3 
concentrations (2009) (U.S. EPA, 2014a, section 7.1.1).
---------------------------------------------------------------------------

    \81\ The 12 urban areas evaluated are Atlanta, Baltimore, 
Boston, Cleveland, Denver, Detroit, Houston, Los Angeles, New York, 
Philadelphia, Sacramento, and St. Louis.
    \82\ In the epidemiologic studies that provide the health basis 
for HREA risk assessments, concentration-response relationships are 
based on daytime O3 concentrations, averaged across 
multiple monitors within study areas. These daily averages are used 
as surrogates for the spatial and temporal patterns of exposures in 
study populations. Consistent with this approach, the HREA 
epidemiologic-based risk estimates also utilize daytime 
O3 concentrations, averaged across monitors, as 
surrogates for population exposures. In this notice, we refer to 
these averaged concentrations as ``area-wide'' O3 
concentrations. Area-wide concentrations are discussed in more 
detail in section 3.1.4 of the PA (U.S. EPA, 2014c).
---------------------------------------------------------------------------

    As in the last review of the O3 NAAQS (U.S. EPA, 2007, 
pp. 2-48 to 2-54), the PA recognizes that ambient O3 
concentrations, and therefore O3-associated health risks, 
result from precursor emissions from various types of sources. Based on 
the air quality modeling discussed in chapter 2 of the PA (U.S. EPA, 
2014c), approximately 30 to 60% of average daytime O3 during 
the warm season (i.e., daily maximum 8-hour concentrations averaged 
from April to October) is attributable to precursor emissions from U.S. 
anthropogenic sources (U.S. EPA, 2014c, section 2.4.4). The remainder 
is attributable to precursor emissions from international anthropogenic 
sources and natural sources. Because the HREA characterizes health 
risks from all O3, regardless of source, risk estimates 
reflect emissions from U.S. anthropogenic, international anthropogenic, 
and natural sources.
    Compared to the weight given to HREA estimates of exposures of 
concern and lung function risks, and the weight given to the evidence 
(U.S. EPA, 2014c, section 4.4.1), the PA places relatively less weight 
on epidemiologic-based risk estimates. In doing so, the PA notes that 
the overall conclusions from the HREA likewise reflect less confidence 
in estimates of epidemiologic-based risks than in estimates of 
exposures and lung function risks. The determination to attach less 
weight to the epidemiologic-based estimates reflects the uncertainties 
associated with mortality and morbidity risk estimates, including the 
heterogeneity in effect estimates between epidemiologic study areas, 
the potential for epidemiologic-based exposure measurement error, and 
uncertainty in the interpretation of the shape of concentration-
response functions at lower O3 concentrations (discussed 
below). The PA also notes the HREA conclusion that lower confidence 
should be placed in the results of the assessment of respiratory 
mortality risks associated with long-term O3 exposures, 
primarily because that analysis is based on only one study (even though 
that study is well-designed) and because of the uncertainty in that 
study about the existence and level of a potential threshold in the 
concentration-response function (U.S. EPA, 2014a, section 9.6).
    In considering the epidemiology-based risk estimates, the PA 
focuses on mortality risks associated with short-term O3 
concentrations. In doing so, in addition to noting uncertainty in 
estimates of respiratory mortality associated with long-term 
O3, the PA notes that the patterns of estimated respiratory 
morbidity risks across urban study areas, over years, and for different 
standards are similar to the patterns of total mortality risk.
    The PA considers estimates of total risk (i.e., based on the full 
distributions of ambient O3 concentrations) and estimates of 
risk associated with O3 concentrations in the upper portions 
of ambient distributions. A focus on estimates of total risks would 
place greater weight on the possibility that concentration-response 
relationships are linear over the entire distribution of ambient 
O3 concentrations, and thus on the potential for morbidity 
and mortality to be affected by changes in relatively low O3 
concentrations. A focus on risks associated with O3 
concentrations in the upper portions of the ambient distribution would 
place greater weight on the uncertainty associated with the shapes of 
concentration-response curves for O3 concentrations in the 
lower portions of the distribution. Given that both types of risk 
estimates could reasonably inform a decision on standard level, 
depending on the weight placed on uncertainties in the occurrence and 
the estimation of O3-attributable effects at relatively low 
O3 concentrations, the PA considers both types of estimates. 
Key results for O3-associated mortality risk are summarized 
in Table 3 below. Table 3 presents estimates of the number of 
O3-associated deaths in urban study areas, for air quality 
adjusted to just meet the current and alternative standards.

[[Page 75277]]



     Table 3--Estimates of O3-Associated Deaths Attributable to the Full Distribution of 8-Hour Area-Wide O3
                      Concentrations and to Concentrations at or Above 20, 40, or 60 ppb O3
                               [Deaths summed across urban case study areas] \83\
----------------------------------------------------------------------------------------------------------------
                       Number of O3-associated deaths summed across urban case study areas
-----------------------------------------------------------------------------------------------------------------
                 Standard level                      Total O3         20+ ppb         40+ ppb         60+ ppb
----------------------------------------------------------------------------------------------------------------
                                                      2007
----------------------------------------------------------------------------------------------------------------
75 ppb..........................................           7,500           7,500           5,400             500
70 ppb..........................................           7,200           7,200           4,900             240
65 ppb..........................................           6,500           6,500           2,800              90
60 ppb \84\.....................................           6,400           6,400           2,300              10
----------------------------------------------------------------------------------------------------------------
                                                      2009
----------------------------------------------------------------------------------------------------------------
75 ppb..........................................           7,000           7,000           4,700             270
70 ppb..........................................           6,900           6,900           4,300              80
65 ppb..........................................           6,400           6,400           2,600              40
60 ppb..........................................           6,300           6,300           2,100              10
----------------------------------------------------------------------------------------------------------------

ii. Key  Uncertainties
---------------------------------------------------------------------------

    \83\ Table 3 is based on the information in Figures 7-2 and 7-3 
in the HREA (U.S. EPA, 2014a). Estimates of the numbers of 
O3-associated deaths are based on concentration-response 
relationships for total mortality associated with short-term 
O3 from the study by Smith et al. (2009). Estimates of 
the numbers O3-associated deaths are rounded to the 
nearest hundred, unless otherwise indicated.
    \84\ As discussed in section 4.3.3 of the HREA, the model-based 
air quality adjustment approach used to estimate risks associated 
with the current and alternative standards was unable to estimate 
the distribution of ambient O3 concentrations in New York 
City upon just meeting an alternative standard with a level of 60 
ppb. Therefore, the total number of deaths indicated for the 60 ppb 
standard level reflect the 60 ppb estimates for all urban study 
areas except New York City. For New York City, the estimated number 
of O3-associated deaths for the 60 ppb standard level was 
assumed to be equal to the number for the 65 ppb level.
---------------------------------------------------------------------------

    Compared to estimates of O3 exposures of concern and 
estimates of O3-induced lung function decrements (discussed 
above), the HREA conclusions reflect lower confidence in epidemiologic-
based risk estimates (U.S. EPA, 2014a, section 9.6). In particular, the 
HREA highlights the heterogeneity in effect estimates between 
locations, the potential for exposure measurement errors, and 
uncertainty in the interpretation of the shape of concentration-
response functions at lower O3 concentrations (U.S. EPA, 
2014a, section 9.6). The HREA also concludes that lower confidence 
should be placed in the results of the assessment of respiratory 
mortality risks associated with long-term O3, primarily 
because that analysis is based on only one study, though that study is 
well-designed, and because of the uncertainty in that study about the 
existence and identification of a potential threshold in the 
concentration-response function (U.S. EPA, 2014a, section 9.6).\85\ 
\86\ This section further discusses some of the key uncertainties in 
epidemiologic-based risk estimates, as summarized in the PA (U.S. EPA, 
2014c, section 3.2.3.2), with a focus on uncertainties that can have 
particularly important implications for the Administrator's 
consideration of epidemiology-based risk estimates.
---------------------------------------------------------------------------

    \85\ The CASAC also concluded that ``[i]n light of the potential 
nonlinearity of the C-R function for long-term exposure reflecting a 
threshold of the mortality response, the estimated number of 
premature deaths avoidable for long-term exposure reductions for 
several levels need to be viewed with caution'' (Frey, 2014a, p. 3).
    \86\ There is also uncertainty about the extent to which 
mortality estimates based on the long-term metric used in the study 
by Jerrett et al. (2009) (i.e., seasonal average of 1-hour daily 
maximum concentrations) reflects associations with long-term average 
O3 versus repeated occurrences of elevated short-term 
concentrations.
---------------------------------------------------------------------------

    The PA notes that reducing NOX emissions generally 
reduces O3-associated mortality and morbidity risk estimates 
in locations and time periods with relatively high ambient 
O3 concentrations and increases risk estimates in locations 
and time periods with relatively low concentrations (II.C.1, above). 
When evaluating uncertainties in epidemiologic risk estimates, it is 
important to consider (1) The extent to which the O3 
response to reductions in NOX emissions appropriately 
represents the trends observed in ambient O3 following 
actual reductions in NOX emissions; (2) the extent to which 
estimated changes in risks in urban study areas are representative of 
the changes that would be experienced broadly across the U.S. 
population; and (3) the extent to which the O3 response to 
reductions in precursor emissions could differ with emissions reduction 
strategies that are different from those used in HREA to generate risk 
estimates.
    To evaluate the first issue, the HREA conducted a national analysis 
evaluating trends in monitored ambient O3 concentrations 
during a time period when the U.S. experienced large-scale reductions 
in NOX emissions (i.e., 2001 to 2010). Analyses of trends in 
monitored O3 indicate that over such a time period, the 
upper end of the distribution of monitored O3 concentrations 
(i.e., indicated by the 95th percentile) generally decreased in urban 
and non-urban locations across the U.S. (U.S. EPA, 2014a, Figure 8-29). 
During this same time period, median O3 concentrations 
decreased in suburban and rural locations, and in some urban locations. 
However, median concentrations increased in some large urban centers 
(U.S. EPA, 2014a, Figure 8-28). As discussed in the REA, and above 
(II.C.1), these increases in median concentrations likely reflect the 
increases in relatively low O3 concentrations that can occur 
near important sources of NOX upon reductions in 
NOX emissions (U.S. EPA, 2014a, section 8.2.3.1). These 
patterns of monitored O3 during a period when the U.S. 
experienced large reductions in NOX emissions are 
qualitatively consistent with the modeled responses of O3 to 
reductions in NOX emissions.
    To evaluate the second issue, the HREA conducted national air 
quality modeling analyses. These analyses estimated the proportion of 
the U.S. population living in locations where seasonal averages of 
daily O3 concentrations are estimated to decrease in 
response to reductions in NOX emissions, and the proportion 
living in locations where such seasonal averages are estimated to 
increase. Given the close relationship between changes in

[[Page 75278]]

seasonal averages of daily O3 concentrations and changes in 
seasonal mortality and morbidity risk estimates, this analysis informs 
consideration of the extent to which the risk results in urban study 
areas represent the U.S. population as a whole. This representativeness 
analysis indicates that the majority of the U.S. population lives in 
locations where reducing NOX emissions would be expected to 
result in decreases in warm season averages of daily maximum 8-hour 
ambient O3 concentrations. Because the HREA urban study 
areas tend to underrepresent the populations living in such areas 
(e.g., suburban, smaller urban, and rural areas), risk estimates for 
the urban study areas are likely to understate the average reductions 
in O3-associated mortality and morbidity risks that would be 
experienced across the U.S. population as a whole upon reducing 
NOX emissions (U.S. EPA, 2014a, section 8.2.3.2).
    To evaluate the third issue, the HREA assessed the O3 
air quality response to reducing both NOX and VOC emissions 
(i.e., in addition to assessing reductions in NOX emissions 
alone) for a subset of seven urban study areas. As discussed in the PA 
(U.S. EPA, 2014c, section 3.2.1), in most of the urban study areas the 
inclusion of VOC emissions reductions did not alter the NOX 
emissions reductions required to meet the current or alternative 
standards.\87\ However, the addition of VOC reductions generally 
resulted in larger decreases in mid-range O3 concentrations 
(25th to 75th percentiles) (U.S. EPA, 2014a, Appendix 4D, section 
4.7).\88\ In addition, in all seven of the urban study areas evaluated, 
the increases in low O3 concentrations were smaller for the 
NOX/VOC scenarios than the NOX alone scenarios 
(U.S. EPA, 2014a, Appendix 4D, section 4.7). This was most apparent for 
Denver, Houston, Los Angeles, New York, and Philadelphia. Given the 
impacts on total risk estimates of increases in low O3 
concentrations, these results suggest that in some locations optimized 
emissions reduction strategies could result in larger reductions in 
O3-associated mortality and morbidity than indicated by HREA 
estimates.
---------------------------------------------------------------------------

    \87\ The exceptions are Chicago and Denver, for which the HREA 
risk estimates are based on reductions in both NOX and 
VOC (U.S. EPA, 2014a, section 4.3.3.1). Emissions of NOX 
and VOC were reduced by equal percentages, a scenario not likely to 
reflect the optimal combination for reducing risks.
    \88\ This was the case for all of the urban study areas 
evaluated, with the exception of New York (U.S. EPA, 2014a, Appendix 
4-D, section 4.7).
---------------------------------------------------------------------------

    Section 7.4 of the HREA also highlights some additional 
uncertainties associated with epidemiologic-based risk estimates (U.S. 
EPA, 2014a). This section of the HREA identifies and discusses sources 
of uncertainty and presents a qualitative evaluation of key parameters 
that can introduce uncertainty into risk estimates (U.S. EPA, 2014a, 
Table 7-4). For several of these parameters, the HREA also presents 
quantitative sensitivity analyses (U.S. EPA, 2014a, sections 7.4.2 and 
7.5.3). Of the uncertainties discussed in Chapter 7 of the HREA, those 
related to the application of concentration-response functions from 
epidemiologic studies can have particularly important implications for 
consideration of epidemiology-based risk estimates, as discussed below.
    An important uncertainty is the shape of concentration-response 
functions at low ambient O3 concentrations (U.S. EPA, 2014a, 
Table 7-4).\89\ Consistent with the ISA conclusion that there is no 
discernible population threshold in O3-associated health 
effects, the HREA estimates epidemiology-based mortality and morbidity 
risks for entire distributions of ambient O3 concentrations, 
based on the assumption that concentration-response relationships 
remain linear over those distributions. In addition, in recognition of 
the ISA conclusion that certainty in the shape of O3 
concentration-response functions decreases at low ambient 
concentrations, the HREA also estimates total mortality associated with 
various ambient O3 concentrations. The PA considers both 
types of risk estimates, recognizing greater public health concern for 
adverse O3-attributable effects at higher ambient 
O3 concentrations (which drive higher exposure 
concentrations, section 3.2.2 of the PA (U.S. EPA, 2014c)), as compared 
to lower concentrations.
---------------------------------------------------------------------------

    \89\ A related uncertainty is the existence, or not, of a 
threshold. The HREA addresses this issue for long-term O3 
by evaluating risks in models that include potential thresholds 
(II.D.2.c).
---------------------------------------------------------------------------

    A related uncertainty is that associated with the public health 
importance of the increases in relatively low O3 
concentrations following air quality adjustment. This uncertainty 
relates to the assumption that the concentration response function for 
O3 is linear, such that that total risk estimates are 
equally influenced by decreasing high concentrations and increasing low 
concentrations, when the increases and decreases are of equal 
magnitude. Even on days with increases in relatively low area-wide 
average concentrations, resulting in increases in estimated risks, some 
portions of the urban study areas could experience decreases in high 
O3 concentrations. To the extent adverse O3-
attributable effects are more strongly supported for higher ambient 
concentrations (which are consistently reduced upon air quality 
adjustment), the impacts on risk estimates of increasing low 
O3 concentrations reflect an important source of 
uncertainty.
    The HREA also notes important uncertainties associated with using a 
concentration-response relationship developed for a particular 
population in a particular location to estimate health risks in 
different populations and locations (U.S. EPA, 2014a, Table 7-4). As 
discussed above, concentration-response relationships derived from 
epidemiologic studies reflect the spatial and temporal patterns of 
population exposures during the study. The HREA applies concentration-
response relationships from epidemiologic studies to adjusted air 
quality in study areas that are different from, and often larger in 
spatial extent than, the areas used to generate the relationships. This 
approach ensures the inclusion of the actual nonattainment monitors 
that often determine the magnitude of emissions reductions for the air 
quality adjustments throughout the urban study areas. This approach 
also allows the HREA to estimate patterns of health risks more broadly 
across a larger area, including a broader range of air quality 
concentrations and a larger population. The HREA notes that it is not 
possible to quantify the impacts of this uncertainty on risk estimates 
in most urban case study locations, though the HREA notes that 
mortality effect estimates for different portions of the New York City 
core based statistical area (CBSA) vary by a factor of almost 10 (U.S. 
EPA, 2014a, section 7.5.3).
    An additional, related uncertainty is that associated with applying 
concentration-response functions from epidemiologic studies to adjusted 
air quality. Concentration-response functions from the O3 
epidemiologic studies used in the HREA are based on associations 
between day to day variation in ``area-wide'' O3 
concentrations (i.e., averaged across multiple monitors) and variation 
in health effects. Epidemiologic studies use these area-wide 
O3 concentrations, which reflect the particular spatial and 
temporal patterns of ambient O3 present in study locations, 
as surrogates for the pattern of O3 exposures experienced by 
study populations. To the extent adjusting O3 concentrations 
to just meet the current standard results in important alterations in 
the spatial and/

[[Page 75279]]

or temporal patterns of ambient O3, there is uncertainty in 
the appropriateness of applying concentration-response functions from 
epidemiologic studies (which necessarily reflect a different air 
quality distribution than the modelled distribution) to estimate health 
risks associated with adjusted O3 air quality. In 
particular, this uncertainty could be important to the extent that (1) 
factors associated with space modify the effects of O3 on 
health or (2) spatial mobility is a key driver of individual-level 
exposures. Although the impact of this uncertainty on risk estimates 
cannot be quantified (U.S. EPA, 2014a, Table 7-4), it has the potential 
to become more important as model adjustment results in larger changes 
in spatial and temporal patterns of ambient O3 
concentrations across urban study areas.
    The use of a national concentration-response function to estimate 
respiratory mortality associated with long-term O3 is a 
source of uncertainty. Risk estimates generated in sensitivity analyses 
using region-specific effect estimates differ substantially from the 
core estimates based on a single national-level effect estimate (U.S. 
EPA, 2014a; Table 7-14). Furthermore, the risk estimates generated 
using the regional effect estimates display considerable variability 
across urban study areas (U.S. EPA, 2014a; Table 7-14), reflecting the 
substantial variability in the underlying effect estimates (see Jerrett 
et al., 2009, Table 4). While the results of the HREA sensitivity 
analyses evaluating this uncertainty point to the potential for 
regional heterogeneity in the long-term risk estimates, the relatively 
large confidence intervals associated with regional effect estimates 
resulted in the HREA conclusion that staff does not have confidence in 
the regionally based risk estimates themselves.
    Finally, the HREA does not quantify any reductions in risk that 
could be associated with reductions in the ambient concentrations of 
pollutants other than O3, resulting from control of 
NOX. For example, as discussed in chapter 2 of the PA (U.S. 
EPA, 2014c), NOX emissions contribute to ambient 
NO2, and NOX and VOCs can contribute to secondary 
formation of PM2.5 constituents, including ammonium sulfate 
(NH4SO4), ammonium nitrate 
(NH4NO3), and organic carbon (OC). Therefore, at 
some times and in some locations, control strategies that would reduce 
NOX emissions (i.e., to meet an O3 standard) 
could reduce ambient concentrations of NO2 and 
PM2.5, resulting in health benefits beyond those directly 
associated with reducing ambient O3 concentrations. In 
issuing its advice, CASAC likewise noted the potential reductions in 
criteria pollutants other than ozone as a result of NOx reductions, and 
the resulting potential public health benefits (Frey, 2014a, pp. 10 and 
11).

D. Conclusions on the Adequacy of the Current Primary Standard

    The initial issue to be addressed in the current review of the 
primary O3 standard is whether, in view of the advances in 
scientific knowledge and additional information, the existing standard 
should be revised. In evaluating whether it is appropriate to retain or 
revise the current standard, the Administrator's considerations build 
upon those in the 2008 review, including consideration of the broader 
body of scientific evidence and exposure and health risk information 
now available, as summarized above (II.A to II.C).
    In developing conclusions on the adequacy of the current primary 
O3 standard, the Administrator takes into account both 
evidence-based and quantitative exposure- and risk-based 
considerations. Evidence-based considerations include the assessment of 
evidence from controlled human exposure, animal toxicological, and 
epidemiologic studies for a variety of health endpoints. The 
Administrator focuses on health endpoints for which the evidence is 
strong enough to support a ``causal'' or a ``likely to be causal'' 
relationship, based on the ISA's integrative synthesis of the entire 
body of evidence. The Administrator's consideration of quantitative 
exposure and risk information draws from the results of the exposure 
and risk assessments presented in the HREA.
    The Administrator's consideration of the evidence and exposure/risk 
information is informed by the considerations and conclusions presented 
in the PA (U.S. EPA, 2014c). The purpose of the PA is to help ``bridge 
the gap'' between the scientific and technical information assessed in 
the ISA and HREA, and the policy decisions that are required of the 
Administrator (U.S. EPA, 2014c, Chapter 1). The PA's evidence-based and 
exposure-/risk-based considerations and conclusions are summarized 
below in sections II.D.1 to II.D.3. CASAC advice to the Administrator 
and public commenter views are summarized in section II.D.4. Section 
II.D.5 presents the Administrator's proposed conclusions concerning the 
adequacy of the public health protection provided by the current 
standard, and her proposed decision to revise that standard.
1. Summary of Evidence-Based Considerations in the PA
    In considering the available scientific evidence, the PA evaluates 
the O3 concentrations in health effects studies (U.S. EPA, 
2014c, section 3.1.4). Specifically, the PA characterizes the extent to 
which effects have been reported for the O3 exposure 
concentrations evaluated in controlled human exposure studies and over 
the distributions of ambient O3 concentrations in locations 
where epidemiologic studies have been conducted. These considerations, 
as they relate to the adequacy of the current standard, are presented 
in detail in section 3.1.4 of the PA (U.S. EPA, 2014c) and are 
summarized briefly below for controlled human exposure and 
epidemiologic panel studies (II.D.1.a), epidemiologic studies of short-
term O3 exposures (II.D.1.b), and epidemiologic studies of 
long-term O3 exposures (II.D.1.c). Section II.D.1.d 
summarizes the PA conclusions based on consideration of the scientific 
evidence.
a. Concentrations in Controlled Human Exposure and Panel Studies
    The evidence from controlled human exposure studies and panel 
studies is assessed in section 6.2 of the ISA (U.S. EPA, 2013a) and is 
summarized in section 3.1.2 of the PA (U.S. EPA, 2014c). As discussed 
above (II.B), controlled human exposure studies have generally been 
conducted with young, healthy adults, and have evaluated exposure 
durations less than 8 hours. Panel studies have evaluated a wider range 
of study populations, including children, and have generally evaluated 
associations with O3 concentrations averaged over several 
hours (U.S. EPA, 2013a, section 6.2.1.2).\90\
---------------------------------------------------------------------------

    \90\ The PA focuses on panel studies that used on-site 
monitoring, and that are highlighted in the ISA for the extent to 
which monitored ambient O3 concentrations reflect 
exposure concentrations in their study populations (U.S. EPA, 2013a, 
section 6.2.1.2).
---------------------------------------------------------------------------

    As summarized above (II.B), a large number of controlled human 
exposure studies have reported lung function decrements, respiratory 
symptoms, airway inflammation, AHR, and/or impaired lung host defense 
in young, healthy adults engaged in moderate, intermittent exertion, 
following 6.6-hour O3 exposures. These studies have 
consistently reported such effects following exposures to O3 
concentrations of 80 ppb or greater. In addition to lung function 
decrements, available studies have also evaluated respiratory symptoms 
or airway

[[Page 75280]]

inflammation following exposures to O3 concentrations below 
75 ppb. Table 3-1 in the PA highlights the group mean results of 
individual controlled human exposure studies that have evaluated 
exposures of healthy adults to O3 concentrations below 75 
ppb (U.S. EPA, 2014c). The studies included in Table 3-1 of the PA 
indicate a combination of lung function decrements and respiratory 
symptoms following 6.6 hour exposures to O3 concentrations 
as low as 72 ppb, and lung function decrements and airway inflammation 
following 6.6 hour exposures to O3 concentrations as low as 
60 ppb (based on group means).
    The PA also notes consistent results in some panel studies of 
O3-associated lung function decrements. In particular, the 
PA notes that epidemiologic panel studies in children and adults 
consistently indicate O3-associated lung function decrements 
when on-site monitored concentrations were below 75 ppb, although the 
evidence becomes less consistent at lower O3 concentrations 
(U.S. EPA, 2014c, section 3.1.4.1).\91\
---------------------------------------------------------------------------

    \91\ As indicated in the PA (U.S. EPA, 2014c, Table 3-2), key 
O3 panel studies evaluated averaging periods ranging from 
10 minutes to 12 hours.
---------------------------------------------------------------------------

    Thus, controlled human exposure studies and panel studies have 
reported respiratory effects in adults and children following exposures 
to O3 concentrations below 75 ppb (albeit over shorter 
averaging periods than the 8 hour averaging time of the current 
O3 standard). The PA notes that such impairments in 
respiratory function have the potential to be adverse, based on ATS 
guidelines for adversity and based on advice from CASAC (Frey, 2014c, 
pp. 5 and 6) (U.S. EPA, 2014c, section 3.1.3). In addition, the PA 
notes that if they become serious enough, these respiratory effects 
could lead to the types of clearly adverse effects commonly reported in 
O3 epidemiologic studies (e.g., respiratory emergency 
department visits, hospital admissions). Therefore, the PA concludes 
that the respiratory effects experienced following exposures to 
O3 concentrations lower than 75 ppb could be adverse in some 
individuals, particularly if experienced by members of at-risk 
populations (e.g., people with asthma, children).\92\
---------------------------------------------------------------------------

    \92\ These effects were reported in healthy individuals. 
Consistent with CASAC advice (Samet, 2011; Frey, 2014a, p. 14; Frey, 
2014c, p. 7), it is a reasonable inference that the effects would be 
greater in magnitude and potential severity for at-risk groups. See 
National Environmental Development Ass'n Clean Air Project v. EPA, 
686 F. 3d 803, 811 (D.C. Cir. (2012) (making this point).
---------------------------------------------------------------------------

b. Concentrations in Epidemiologic Studies--Short-Term
    The PA also considers distributions of ambient O3 
concentrations in locations where epidemiologic studies have evaluated 
O3-associated hospital admissions, emergency department 
visits, and/or mortality (U.S. EPA, 2014c, section 3.1.4.2). When 
considering epidemiologic studies within the context of the current 
standard, the PA emphasizes those studies conducted in the U.S. and 
Canada. Such studies reflect air quality and exposure patterns that are 
likely more typical of the U.S. population than the air quality and 
exposure patterns reflected in studies conducted outside the U.S. and 
Canada (U.S. EPA, 2014c, section 1.3.1.2).\93\ The PA also emphasizes 
studies reporting associations with effects judged in the ISA to be 
robust to confounding by other factors, including co-occurring air 
pollutants. In addition to these factors, the PA considers the 
statistical precision of study results, the extent to which studies 
report associations in at-risk populations, and the extent to which the 
biological plausibility of associations at various ambient 
O3 concentrations is supported by controlled human exposure 
and/or animal toxicological studies. These considerations help inform 
the range of ambient O3 concentrations over which the 
evidence indicates the most confidence in O3-associated 
health effects, and the range of concentrations over which confidence 
in such associations is appreciably lower.
---------------------------------------------------------------------------

    \93\ Nonetheless, the PA recognizes the importance of all 
studies, including international studies, in the ISA's assessment of 
the weight of the evidence that informs causality determinations.
---------------------------------------------------------------------------

    This section summarizes the PA conclusions regarding the extent to 
which health effect associations have been reported for ambient 
O3 concentrations likely to have met the current 
O3 standard. Section II.D.1.b.i summarizes PA analyses and 
conclusions based on analyses evaluating the extent to which 
epidemiologic studies have reported health effect associations in 
locations that would likely have met the current O3 
standard. Section II.D.1.b.ii summarizes PA conclusions based on 
analyses evaluating the O3 air quality in locations where 
epidemiologic studies have characterized confidence intervals around 
cut point analyses or concentration-response functions. Section 
II.D.1.b.iii summarizes the important uncertainties in these analyses.
i. Associations in Locations Likely Meeting Current Standard
    The PA considers the extent to which U.S. and Canadian 
epidemiologic studies have reported associations with mortality or 
morbidity in locations that would likely have met the current 
O3 standard during the study period (U.S. EPA, 2014c, 
section 3.14.2). Addressing this issue can provide important insights 
into the extent to which O3-health effect associations are 
present for distributions of ambient O3 concentrations that 
would be allowed by the current standard. To the extent associations 
are reported in study areas that would have met the current standard, 
those associations indicate that the current standard could allow the 
types of clearly adverse O3-associated effects reported in 
epidemiologic studies (e.g., mortality, hospital admissions, emergency 
department visits).\94\ In considering these analyses, the PA also 
notes that the lack of such associations in locations meeting the 
current standard indicates increased uncertainty in the extent to which 
O3-associated health effects would persist upon reducing 
O3 precursor emissions in order to meet that standard.
---------------------------------------------------------------------------

    \94\ See ATA III, 283 F.3d at 370 (EPA justified in revising 
NAAQS when health effect associations are observed in epidemiologic 
studies at levels allowed by the NAAQS); State of Mississippi v. 
EPA, 744 F. 3d at 1345 (same).
---------------------------------------------------------------------------

    The PA identifies U.S. and Canadian studies of respiratory hospital 
admissions, respiratory emergency department visits, and mortality 
(total, respiratory, cardiovascular) from the ISA (U.S. EPA, 2013a, 
Tables 6-28, 6-42, and 6-53, and section 6.2.8; U.S. EPA, 2014c, 
Appendix 3D). Analysis of study area air quality indicates that the 
large majority of epidemiologic study areas evaluated would have 
violated the current standard during study periods (U.S. EPA, 2014c, 
Appendix 3D). However, the PA notes that a single-city study conducted 
in Seattle, a location that would have met the current standard over 
the entire study period, reported positive and statistically 
significant associations with respiratory emergency department visits 
in children and adults (Mar and Koenig, 2009). The PA also notes four 
Canadian multicity studies that reported positive and statistically 
significant associations with respiratory morbidity or mortality, and 
for which the majority of study cities would have met the current 
standard over the entire study periods (Cakmak et

[[Page 75281]]

al., 2006; Dales et al., 2006; Katsouyanni et al., 2009; Stieb et al., 
2009).\95\
---------------------------------------------------------------------------

    \95\ In addition, a study by Vedal et al. (2003) was included in 
the 2006 AQCD (U.S. EPA, 2006a). This study reported positive and 
statistically significant associations with mortality in Vancouver 
during a time period when the study area would have met the current 
standard (U.S. EPA, 2007). This study was not assessed in the ISA in 
the current review (U.S. EPA, 2013a).
---------------------------------------------------------------------------

    The PA concludes that the single-city study by Mar and Koenig 
(2009) indicates the presence of associations with mortality and 
morbidity for an ambient distribution of O3 that would have 
met the current standard (U.S. EPA, 2014c, section 3.1.4.2). The PA 
notes that interpretation of the air quality concentrations in the 
multicity study locations evaluated in this review is complicated by 
uncertainties in the extent to which multicity effect estimates can be 
attributed to ambient O3 in the majority of locations, which 
would have met the current standard, versus O3 in the 
smaller number of locations that would have violated the standard. 
While acknowledging this uncertainty in interpreting air quality in 
multicity studies, the PA notes that multicity effect estimates in the 
four studies cited above are largely influenced by locations meeting 
the current standard (i.e., given that most study areas would have met 
this standard). Therefore, the PA concludes that Canadian multicity 
studies, in addition to the single-city study in Seattle, suggest 
confidence in the presence of associations with mortality and morbidity 
for ambient distributions of O3 that would have met the 
current standard (U.S. EPA, 2014c, section 3.1.4.2).
ii. Air Quality Associated With Cut Point Analyses and Concentration-
Response Functions
    The PA also considers the extent to which additional epidemiologic 
studies of mortality or morbidity, specifically those conducted in 
locations that would have violated the current standard, can inform 
consideration of adequacy of the current standard (U.S. EPA, 2014c, 
section 3.1.4.2). In doing so, the PA notes that health effect 
associations reported in epidemiologic studies are influenced by the 
full distributions of ambient O3 concentrations, including 
concentrations below the level of the current standard. The PA focuses 
on studies that have explicitly characterized O3 health 
effect associations, including confidence in those associations, for 
various portions of distributions of ambient O3 
concentrations.
    The U.S. multicity study by Bell et al. (2006) reported health 
effect associations for air quality subsets restricted to ambient 
O3 concentrations below one or more predetermined cut 
points. In these analyses, effect estimates were based only on the 
subsets of days contributing to averaged O3 concentrations 
below cut points ranging from 5 to 60 ppb (Bell et al., 2006, Figure 
2).\96\ The PA notes that such ``cut point'' analyses can provide 
information on the magnitude and statistical precision of effect 
estimates for defined distributions of ambient concentrations, which 
may in some cases include distributions that would meet the current 
standard (U.S. EPA, 2014c, section 3.1.4.2). The cut points below which 
confidence intervals become notably wider depend in large part on data 
density and, therefore, cut point analyses provide insight into the 
ambient concentrations below which the available air quality 
information becomes too sparse to support conclusions about the nature 
of concentration-response relationships with a high degree of 
confidence (U.S. EPA, 2014c, section 3.1.4.2).
---------------------------------------------------------------------------

    \96\ In the published study, 2-day rolling averages of 24-hour 
average O3 concentrations were calculated in each study 
location (based on averaging across monitors in study locations with 
multiple monitors).
---------------------------------------------------------------------------

    The PA considers the extent to which the cut-point analyses 
reported by Bell et al. (2006) indicate health effect associations for 
distributions of ambient O3 concentrations that would likely 
have met the current standard. The PA particularly focuses on the 
lowest cut-point for which the association between O3 and 
mortality was reported to be statistically significant (i.e., 30 ppb, 
based on visual inspection of Figure 2 in the published study). Based 
on the O3 air quality concentrations that met the criteria 
for inclusion in the 30 ppb cut point analysis, 95% of study areas had 
3-year averages of annual 4th highest daily maximum 8-hour 
O3 concentration at or below 75 ppb over the entire study 
period (U.S. EPA, 2014c, section 3.1.4.2, Table 3-6). Though there are 
important uncertainties in this analysis, as discussed below, the PA 
concludes that these results suggest that the large majority of air 
quality distributions that provided the basis for the positive and 
statistically significant association with mortality at the 30 ppb cut 
point would likely have met the current O3 standard.
    The PA also analyzes air quality for studies that have reported 
confidence intervals around concentration-response functions over 
distributions of ambient O3 concentrations (U.S. EPA, 2014c, 
section 3.1.4.2). Confidence intervals around concentration-response 
functions can provide insights into the range of ambient concentrations 
over which the study indicates the most confidence in the reported 
health effect associations (i.e., where confidence intervals are 
narrowest), and into the range of ambient concentrations below which 
the study indicates that uncertainty in the nature of such associations 
becomes notably greater (i.e., where confidence intervals become 
markedly wider). As with cut point analyses, the concentrations below 
which confidence intervals become markedly wider are intrinsically 
related to data density, and do not necessarily indicate the absence of 
an association.
    The PA focuses on two U.S. single-city studies that have reported 
confidence intervals around concentration-response functions (Silverman 
and Ito, 2010; Strickland et al., 2010). Based on the published 
analyses, the PA identifies the ranges of ambient O3 
concentrations over which these studies indicate the highest degree of 
confidence in the reported linear concentration-response functions 
(U.S. EPA, 2014c, section 3.1.4.2). For the lower ends of these ranges, 
air quality analyses in the PA indicate that over 99% of days had 
maximum 8-hour O3 concentrations (i.e., from highest 
monitors in study locations) at or below 75 ppb. For comparison, the 
annual 4th highest daily maximum 8-hour O3 concentration 
generally corresponds to the 98th or 99th percentile of the seasonal 
distribution, depending on the length of the O3 season.
    The PA concludes that these analyses of air quality data from the 
study locations evaluated by Silverman and Ito (2010) and Strickland et 
al. (2010) indicate a relatively high degree of confidence in reported 
statistical associations with respiratory health outcomes on days when 
virtually all monitored 8-hour O3 concentrations were 75 ppb 
or below (U.S. EPA, 2014c, section 3.1.4.2). Though these analyses do 
not identify true design values, the presence of O3-
associated respiratory effects on such days provides insight into the 
types of health effects that could occur in locations with maximum 
ambient O3 concentrations at or below the level of the 
current standard.
iii. Important Uncertainties
    In considering the above evidence within the context of developing 
overall conclusions on the current and potential alternative standards, 
the PA also takes into account important uncertainties in these 
analyses of air quality in locations of epidemiologic study areas. 
These uncertainties are summarized in this

[[Page 75282]]

section. The PA's consideration of the evidence, including the 
associated uncertainties, in reaching conclusions on the current and 
potential alternative standards is summarized in sections II.D.3 
(current standard) and II.E.4.b (potential alternative standards) 
below.
    The PA notes that while multicity studies generally have greater 
statistical power and geographic coverage than single-city studies, 
there is often greater uncertainty in conclusions about the extent to 
which multicity effect estimates reflect associations with air quality 
meeting the current standard (U.S. EPA, 2014c, section 1.3.1.2.1). This 
is particularly the case for the multicity studies evaluated in this 
review with some study locations meeting the current standard and 
others violating that standard. Specifically for the four Canadian 
multicity studies discussed above, the PA notes that interpretation of 
air quality information is complicated by uncertainties in the extent 
to which multicity effect estimates can be attributed to ambient 
O3 in the majority of locations, which would have met the 
current standard, versus O3 in the smaller number of 
locations that would have violated the standard.
    The PA also notes important uncertainties in multicity studies that 
evaluate the potential for thresholds to exist, as was done in the 
study by Bell et al. (2006). Specifically, the ISA highlights the 
regional heterogeneity in O3 health effect associations as a 
factor that could obscure the presence of thresholds, should they 
exist, in multicity studies (U.S. EPA, 2013a, sections 2.5.4.4 and 
2.5.4.5). The ISA notes that community characteristics (e.g., activity 
patterns, housing type, age distribution, prevalence of air 
conditioning) could be important contributors to reported regional 
heterogeneity (U.S. EPA, 2013a, section 2.5.4.5). Given this 
heterogeneity, the ISA concludes that ``a national or combined analysis 
may not be appropriate to identify whether a threshold exists in the 
O3-mortality [concentration-response] relationship'' (U.S. 
EPA, 2013a, p. 2-33). This represents an important source of 
uncertainty when characterizing confidence in reported concentration-
response relationships over distributions of ambient O3 
concentrations, based on multicity studies. The PA notes that this 
uncertainty becomes increasingly important when interpreting 
concentration-response relationships at lower ambient O3 
concentrations, particularly those concentrations corresponding to 
portions of distributions where data density decreases notably (U.S. 
EPA, 2014c, section 3.1.4.2).
    Another important uncertainty, related specifically to the PA 
analysis of cut points by Bell et al. (2006), is that EPA staff was 
unable to obtain the air quality data used to generate the cut-point 
analyses in the published study (U.S. EPA, 2014c, section 3.1.4.2). 
Therefore, the analyses in the PA identified 2-day averages of 24-hour 
O3 concentrations in study locations using the air quality 
data available in AQS, combined with the published description of study 
area definitions. An important uncertainty in this approach is the 
extent to which the PA appropriately recreated the cut-point analyses 
in the published study (U.S. EPA, 2014c, section 3.1.4.2).
    An uncertainty that applies to epidemiologic studies in general is 
the extent to which reported health effects are caused by exposures to 
O3 itself, as opposed to other factors such as co-occurring 
pollutants or pollutant mixtures. The PA notes that this uncertainty 
becomes an increasingly important consideration as health effect 
associations are evaluated at lower ambient O3 
concentrations. In particular, there is increasing uncertainty as to 
whether the observed associations remain plausibly related to exposures 
to ambient O3, rather than to the broader mix of air 
pollutants present in the ambient air. In considering the potential 
importance of this uncertainty at the relatively low ambient 
O3 concentrations that are the focus of the PA analyses, the 
PA notes that Silverman and Ito (2010) and Strickland (2010) reported 
O3 health effect associations in co-pollutant models,\97\ 
providing support for associations with O3 itself (U.S. EPA, 
2014c, section 3.1.4.2). The PA also concludes that air quality 
analyses indicate coherence with the results of experimental studies 
(i.e., in which the study design dictates that exposures to 
O3 itself are responsible for reported effects), and are 
consistent with the occurrence of O3-attributable 
respiratory hospital admissions and emergency department visits, even 
when virtually all monitored concentrations were below the level of the 
current standard (U.S. EPA, 2014c, section 3.1.4.2, Tables 3-4, 3-5).
---------------------------------------------------------------------------

    \97\ In addition, Bell et al. (2006) reported that, based on a 
previous study (Bell et al., 2004), associations with mortality were 
robust to the inclusion of PM10 in the model.
---------------------------------------------------------------------------

c. Concentrations in Epidemiologic Studies--Long-Term
    The PA also considers the extent to which epidemiologic studies 
employing longer-term ambient O3 concentration metrics 
inform our understanding of the air quality conditions associated with 
O3-attributable health effects, and specifically inform 
consideration of the extent to which such effects could occur under air 
quality conditions meeting the current standard (U.S. EPA, 2014c, 
section 3.1.4.3). Unlike for the studies of short-term O3 
discussed above, the available U.S. and Canadian epidemiologic studies 
evaluating long-term ambient O3 concentration metrics have 
not been conducted in locations likely to have met the current 8-hour 
O3 standard during the study period, and have not reported 
concentration-response functions that indicate confidence in health 
effect associations at O3 concentrations meeting the current 
standard (U.S. EPA, 2014c, section 3.1.4.3). Therefore, although these 
studies contribute to understanding of health effects associated with 
long-term or repeated exposures to ambient O3, consideration 
of study area air quality does not inform consideration of the extent 
to which those health effects may be occurring in locations that meet 
the current standard.
d. PA Conclusions Based on Consideration of the Evidence
    As discussed above (II.D.1.a to II.D.1.c), in considering the 
available scientific evidence, including associated uncertainties, as 
it relates to the degree of public health protection provided by the 
current primary O3 standard, the PA evaluates the extent to 
which health effects have been reported for the O3 exposure 
concentrations evaluated in controlled human exposure studies and over 
the distributions of ambient O3 concentrations in locations 
where epidemiologic studies have been conducted. The PA concludes that 
(1) the evidence from controlled human exposure studies provides strong 
support for the occurrence of adverse respiratory effects following 
exposures to O3 concentrations below the level of the 
current standard and that (2) epidemiologic studies provide support for 
the occurrence of adverse respiratory effects and mortality under air 
quality conditions that would likely meet the current standard. In 
further considering the public health protection provided by the 
current standard, the PA next considers the results of exposure and 
health risk assessments.

[[Page 75283]]

2. Summary of Exposure- and Risk-Based Considerations in the PA
    In order to further inform judgments about the potential public 
health implications of the current O3 NAAQS, the PA 
considers the exposure and risk assessments presented in the HREA (U.S. 
EPA, 2014c, section 3.2). Overviews of these exposure and risk 
assessments, including summaries of key results and uncertainties, are 
provided in section II.C above. This section summarizes key 
observations from the PA related to the adequacy of the current 
O3 NAAQS, based on consideration of the HREA exposure 
assessment (II.D.2.a), lung function risk assessment (II.D.2.b), and 
mortality/morbidity risk assessments (II.D.2.c).
a. Exposure Assessment--Key Observations
    As discussed above (II.C.2), the exposure assessment provides 
estimates of the number and percent of people who would experience 
exposures of concern at or above benchmark concentrations of 60, 70, 
and 80 ppb. Benchmarks reflect exposure concentrations at which 
O3-induced respiratory effects are known to occur in some 
healthy adults engaged in moderate, intermittent exertion, based on 
evidence from controlled human exposure studies (U.S. EPA, 2014c, 
section 3.1.2.1; U.S. EPA, 2013a, section 6.2).
    The PA focuses on exposure estimates in children. Compared to 
recent (i.e., unadjusted) air quality, the PA notes that adjusting air 
quality to just meet the current O3 NAAQS consistently 
reduces the estimated occurrence of exposures of concern in children 
(U.S. EPA, 2014a, Appendix 5F). When averaged over the years evaluated 
in the HREA, reductions of up to about 70% were estimated. These 
reductions in estimated exposures of concern, relative to unadjusted 
air quality, reflect the consistent reductions in the highest ambient 
O3 concentrations upon model adjustment to just meet the 
current standard (U.S. EPA, 2014c, section 3.2.1; U.S. EPA, 2014a, 
Chapter 4). Such reductions in estimated exposures of concern are 
evident throughout urban study areas, including in urban cores and in 
surrounding areas (U.S. EPA, 2014a, Appendix 9A).
    Based on Figures 3-7 to 3-10 in the PA (U.S. EPA, 2014c), and the 
associated details described in the HREA (U.S. EPA, 2014a, Chapter 5), 
the PA further highlights key observations with regard to exposures of 
concern in children that are estimated to be allowed by the current 
standard. These key observations are summarized below for exposures of 
concern >=60, 70, and 80 ppb.
    For exposures of concern at or above 60 ppb, the PA highlights the 
following key observations for air quality adjusted to just meet the 
current standard:
    (1) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 10 to 18% of children in urban study 
areas to experience one or more exposures of concern at or above 60 
ppb. Summing across urban study areas, these percentages correspond to 
almost 2.5 million children experiencing approximately 4 million 
exposures of concern at or above 60 ppb during a single O3 
season. Of these children, almost 250,000 are asthmatics.\98\
---------------------------------------------------------------------------

    \98\ As discussed above (II.C.2.b), due to variability in 
responsiveness, only a subset of individuals who experience 
exposures at or above a benchmark concentration can be expected to 
experience adverse health effects.
---------------------------------------------------------------------------

    (2) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 3 to 8% of children in urban study 
areas to experience two or more exposures of concern to O3 
concentrations at or above 60 ppb. Summing across the urban study 
areas, these percentages correspond to almost 900,000 children 
(including almost 90,000 asthmatic children) estimated to experience at 
least two O3 exposure concentrations at or above 60 ppb 
during a single O3 season.
    (3) In the worst-case years (i.e., those with the largest exposure 
estimates), the current standard is estimated to allow approximately 10 
to 25% of children to experience one or more exposures of concern at or 
above 60 ppb, and approximately 4 to 14% to experience two or more 
exposures of concern at or above 60 ppb.
    For exposures of concern at or above 70 ppb, the PA highlights the 
following key observations for air quality adjusted to just meet the 
current standard:
    (1) On average over the years 2006 to 2010, the current standard is 
estimated to allow up to approximately 3% of children in urban study 
areas to experience one or more exposures of concern at or above 70 
ppb. Summing across urban study areas, almost 400,000 children 
(including almost 40,000 asthmatic children) are estimated to 
experience O3 exposure concentrations at or above 70 ppb 
during a single O3 season.\99\
---------------------------------------------------------------------------

    \99\ As discussed above (II.C.2.b), due to variability in 
responsiveness, only a subset of individuals who experience 
exposures at or above a benchmark concentration can be expected to 
experience adverse health effects.
---------------------------------------------------------------------------

    (2) On average over the years 2006 to 2010, the current standard is 
estimated to allow less than 1% of children in urban study areas to 
experience two or more exposures of concern to O3 
concentrations at or above 70 ppb.
    (3) In the worst-case years, the current standard is estimated to 
allow approximately 1 to 8% of children to experience one or more 
exposures of concern at or above 70 ppb, and up to approximately 2% to 
experience two or more exposures of concern, at or above 70 ppb.
    For exposures of concern at or above 80 ppb, the PA highlights the 
observation that the current standard is estimated to allow about 1% or 
fewer children in urban study areas to experience exposures of concern 
at or above 80 ppb, even in years with the highest exposure estimates.
b. Lung Function Risk Assessment--Key Observations
    As discussed above (II.C.3.a), the HREA estimates risks of moderate 
to large lung function decrements (i.e., FEV1 decrements 
>=10%, 15%, or 20%) in school-aged children (ages 5 to 18), asthmatic 
school-aged children, and the general adult population for 15 urban 
study areas. As for exposures of concern, the PA focuses on lung 
function risk estimates in children (including children with asthma).
    Compared to risks associated with recent air quality, risk 
estimates for air quality just meeting the current standard are 
consistently smaller across urban study areas (U.S. EPA, 2014a, 
Appendix 6B). When averaged over the years evaluated in the HREA, risk 
reductions of up to about 40% were estimated compared to recent air 
quality. These reductions reflect the consistent decreases in 
relatively high ambient O3 concentrations upon adjustment to 
just meet the current standard (U.S. EPA, 2014a, Chapter 4). Such 
reductions in estimated lung function risks are evident throughout 
urban study areas, including in urban cores and in surrounding areas 
(U.S. EPA, 2014, Appendix 9A).
    Based on Figures 3-11 to 3-14 in the PA (U.S. EPA, 2014c), and the 
associated details described in the HREA (U.S. EPA, 2014a, chapter 6), 
the PA highlights key observations with regard to lung function risks 
estimated in children for air quality adjusted to just meet the current 
standard. These key observations are presented below for 
FEV1 decrements >=10, 15, and 20%.
    With regard to decrements >=10%, the PA highlights the following 
key observations for air quality adjusted to just meet the current 
standard:

[[Page 75284]]

    (1) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 14 to 19% of children in urban study 
areas to experience one or more lung function decrements >=10%. Summing 
across urban study areas, this corresponds to approximately 3 million 
children experiencing 15 million O3-induced lung function 
decrements >=10% during a single O3 season. Of these 
children, about 300,000 are asthmatics.
    (2) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 7 to 12% of children in urban study 
areas to experience two or more O3-induced lung function 
decrements >=10%. Summing across the urban study areas, this 
corresponds to almost 2 million children (including almost 200,000 
asthmatic children) estimated to experience two or more O3-
induced lung function decrements greater than 10% during a single 
O3 season.
    (3) In the worst-case years, the current standard is estimated to 
allow approximately 17 to 23% of children in urban study areas to 
experience one or more lung function decrements >=10%, and 
approximately 10 to 14% to experience two or more O3-induced 
lung function decrements >=10%.
    With regard to decrements >=15%, the PA highlights the following 
key observations for air quality adjusted to just meet the current 
standard:
    (1) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 3 to 5% of children in urban study 
areas to experience one or more lung function decrements >=15%. Summing 
across urban study areas, this corresponds to approximately 800,000 
children (including approximately 80,000 asthmatic children) estimated 
to experience at least one O3-induced lung function 
decrement >=15% during a single O3 season.
    (2) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 2 to 3% of children in urban study 
areas to experience two or more O3-induced lung function 
decrements >=15%.
    (3) In the worst-case years, the current standard is estimated to 
allow approximately 4 to 6% of children in urban study areas to 
experience one or more lung function decrements >=15%, and 
approximately 2 to 4% to experience two or more O3-induced 
lung function decrements >=15%.
    With regard to decrements >=20%, the PA highlights the following 
key observations for air quality adjusted to just meet the current 
standard:
    (1) On average over the years 2006 to 2010, the current standard is 
estimated to allow approximately 1 to 2% of children in urban study 
areas to experience one or more lung function decrements >=20%. Summing 
across urban study areas, this corresponds to approximately 300,000 
children (including approximately 30,000 asthmatic children) estimated 
to experience at least one O3-induced lung function 
decrement >=20% during a single O3 season.
    (2) On average over the years 2006 to 2010, the current standard is 
estimated to allow less than 1% of children in urban study areas to 
experience two or more O3-induced lung function decrements 
>=20%.
    (3) In the worst-case years, the current standard is estimated to 
allow approximately 2 to 3% of children to experience one or more lung 
function decrements >=20%, and less than 2% to experience two or more 
O3-induced lung function decrements >=20%.
c. Mortality and Morbidity Risk Assessments--Key Observations
    As discussed above (II.C.3.b), risk estimates based on 
epidemiologic studies can provide perspective on the most serious 
O3-associated public health outcomes (e.g., mortality, 
hospital admissions, emergency department visits) in populations that 
often include at-risk groups. The HREA estimates such O3-
associated risks in 12 urban study areas \100\ using concentration-
response relationships drawn from epidemiologic studies. These 
concentration-response relationships are based on ``area-wide'' average 
O3 concentrations.\101\ The HREA estimates risks for the 
years 2007 and 2009 in order to provide estimates of risk for a year 
with generally higher O3 concentrations (2007) and a year 
with generally lower O3 concentrations (2009) (U.S. EPA, 
2014a, section 7.1.1).
---------------------------------------------------------------------------

    \100\ The 12 urban areas evaluated are Atlanta, Baltimore, 
Boston, Cleveland, Denver, Detroit, Houston, Los Angeles, New York, 
Philadelphia, Sacramento, and St. Louis. Morbidity endpoints were 
evaluated in subsets of these areas, based on availability of 
appropriate studies (U.S. EPA, 2014a, Chapter 7).
    \101\ In the epidemiologic studies that provide the health basis 
for HREA risk assessments, concentration-response relationships are 
based on daytime O3 concentrations, averaged across 
multiple monitors within study areas. These daily averages are used 
as surrogates for the spatial and temporal patterns of exposures in 
study populations. Consistent with this approach, the HREA 
epidemiologic-based risk estimates also utilize daytime 
O3 concentrations, averaged across monitors, as 
surrogates for population exposures. In this notice, these averaged 
concentrations are referred to as ``area-wide'' O3 
concentrations. Area-wide concentrations are discussed in more 
detail in section 3.1.4 of the PA (U.S. EPA, 2014c).
---------------------------------------------------------------------------

    In considering these estimates, the PA notes that HREA conclusions 
reflect somewhat lower confidence in epidemiologic-based risk estimates 
than in estimates of O3 exposures of concern and 
O3-induced lung function decrements (U.S. EPA, 2014a, 
section 9.6). In particular, the HREA highlights the unexplained 
heterogeneity in effect estimates between locations, the potential for 
exposure measurement errors, and uncertainty in the interpretation of 
the shape of concentration-response functions at lower O3 
concentrations (U.S. EPA, 2014a, section 9.6). The HREA also concludes 
that lower confidence should be placed in the results of the assessment 
of respiratory mortality risks associated with long-term O3 
exposures, primarily because that analysis is based on only one study, 
though that study is well-designed, and because of the uncertainty in 
that study about the existence and identification of a potential 
threshold in the concentration-response function (U.S. EPA, 2014a, 
section 9.6). These and other uncertainties are considered in the PA in 
reaching conclusions on the current and alternative standards (U.S. 
EPA, 2014c, sections 3.4, 4.6).
    Key observations from the PA are summarized below for mortality and 
morbidity risks associated with air quality adjusted to simulate just 
meeting the current O3 NAAQS. These include key observations 
for estimates of total (nonaccidental) mortality associated with short-
term O3 concentrations, respiratory morbidity associated 
with short-term O3 concentrations, and respiratory mortality 
associated with long-term O3 concentrations (U.S. EPA, 
2014c, section 3.2.3.2).
    With regard to total mortality or morbidity associated with short-
term O3, the PA notes the following for air quality adjusted 
to just meet the current standard:

    (1) When air quality was adjusted to the current standard for 
the 2007 model year (the year with generally ``higher'' 
O3-associated risks), 10 of 12 urban study areas 
exhibited either decreases or virtually no change in estimates of 
the number of O3-associated deaths (U.S. EPA, 2014a, 
Appendix 7B). Increases were estimated in two of the urban

[[Page 75285]]

study areas (Houston, Los Angeles) \102\ (U.S. EPA, 2014a, Appendix 
7B).\103\
---------------------------------------------------------------------------

    \102\ As discussed above (II.C.1), in locations and time periods 
when NOX is predominantly contributing to O3 
formation (e.g., downwind of important NOX sources, where 
the highest O3 concentrations often occur), model-based 
adjustment to the current and alternative standards decreases 
estimated ambient O3 concentrations compared to recent 
monitored concentrations (U.S. EPA, 2014a, section 4.3.3.2). In 
contrast, in locations and time periods when NOX is 
predominantly contributing to O3 titration (e.g., in 
urban centers with high concentrations of NOX emissions, 
where ambient O3 concentrations are often suppressed and 
thus relatively low), model-based adjustment increases ambient 
O3 concentrations compared to recent monitored 
concentrations (U.S. EPA, 2014a, section 4.3.3.2). Changes in 
epidemiology-based risk estimates depend on the balance between the 
daily decreases in high O3 concentrations and increases 
in low O3 concentrations following the model-based air 
quality adjustment. Commenting on this issue, CASAC noted that 
``controls designed to reduce the peak levels of ozone (e.g., the 
4th highest annual MDA8) may not be effective at reducing lower 
levels of ozone on more typical days and may actually increase ozone 
levels on days where ozone concentrations are low'' (Frey 2014a, p. 
2). CASAC further noted that risk results ``suggest that the ozone-
related health risks in the urban cores can increase for some of the 
cities as ozone NAAQS alternatives become more stringent. This is 
because reductions in nitrogen oxides emissions can lead to less 
scavenging of ozone and free radicals, resulting in locally higher 
levels of ozone'' (Frey 2014c, p. 10).
    \103\ For the 2009 adjusted year (i.e., the year with generally 
lower O3 concentrations), changes in risk were generally 
smaller than in 2007 (i.e., most changes about 2% or smaller). 
Increases were estimated for Houston, Los Angeles, and New York 
City.
---------------------------------------------------------------------------

    (2) In focusing on total risk, the current standard is estimated 
to allow thousands of O3-associated deaths per year in 
the urban study areas. In focusing on the risks associated with the 
upper portions of distributions of ambient concentrations (area-wide 
concentrations >=40, 60 ppb), the current standard is estimated to 
allow hundreds to thousands of O3-associated deaths per 
year in the urban study areas.
    (3) The current standard is estimated to allow tens to thousands 
of O3-associated morbidity events per year (i.e., 
respiratory-related hospital admissions, emergency department 
visits, and asthma exacerbations).

    With regard to respiratory mortality associated with long-term 
O3, the PA notes the following for air quality adjusted to 
just meet the current standard:

    (1) Based on a linear concentration-response function, the 
current standard is estimated to allow thousands of O3-
associated respiratory deaths per year in the urban study areas.
    (2) Based on threshold models, HREA sensitivity analyses 
indicate that the number of respiratory deaths associated with long-
term O3 concentrations could potentially be considerably 
lower (i.e., by more than 75% if a threshold exists at 40 ppb, and 
by about 98% if a threshold exists at 56 ppb) (U.S. EPA, 2014a, 
Figure 7-9).\104\
---------------------------------------------------------------------------

    \104\ Risk estimates for respiratory mortality associated with 
long-term O3 exposures are based on the study by Jerrett 
et al. (2009) (U.S. EPA, 2014a, Chapter 7). As discussed above 
(II.B.2.b.iv) and in the PA (U.S. EPA, 2014c, section 3.1.4.3), 
Jerrett et al. (2009) reported that when seasonal averages of 1-hour 
daily maximum O3 concentrations ranged from 33 to 104 
ppb, there was no statistical deviation from a linear concentration-
response relationship between O3 and respiratory 
mortality across 96 U.S. cities (U.S. EPA, 2013a, section 7.7). 
However, the authors reported ``limited evidence'' for an effect 
threshold at an O3 concentration of 56 ppb (p=0.06). In 
communications with EPA staff (Sasser, 2014), the study authors 
indicated that it is not clear whether a threshold model is a better 
predictor of respiratory mortality than the linear model, and that 
``considerable caution should be exercised in accepting any specific 
threshold.''
---------------------------------------------------------------------------

3. Policy Assessment Conclusions on the Current Standard
    As an initial matter, the PA concludes that reducing precursor 
emissions to achieve O3 concentrations that meet the current 
standard will provide important improvements in public health 
protection. This initial conclusion is based on (1) the strong body of 
scientific evidence indicating a wide range of adverse health outcomes 
attributable to exposures to O3 concentrations commonly 
found in the ambient air and (2) estimates indicating decreased 
occurrences of O3 exposures of concern and decreased health 
risks upon meeting the current standard, compared to recent air 
quality.
    In particular, the PA concludes that strong support for this 
initial conclusion is provided by controlled human exposure studies of 
respiratory effects, and by quantitative estimates of exposures of 
concern and lung function decrements based on information in these 
studies. Analyses in the HREA estimate that the percentages of children 
(i.e., all children and children with asthma) in urban study areas 
experiencing exposures of concern, or experiencing abnormal and 
potentially adverse lung function decrements, are consistently lower 
for air quality that just meets the current O3 standard than 
for recent air quality. The HREA estimates such reductions consistently 
across the urban study areas evaluated and throughout various portions 
of individual urban study areas, including in urban cores and the 
portions of urban study areas surrounding urban cores. These reductions 
in exposures of concern and O3-induced lung function 
decrements reflect the consistent decreases in the highest 
O3 concentrations following reductions in precursor 
emissions to meet the current standard. Thus, populations in both urban 
and non-urban areas would be expected to experience important 
reductions in O3 exposures and O3-induced lung 
function risks upon meeting the current standard.\105\
---------------------------------------------------------------------------

    \105\ As discussed above (II.C.1), CASAC recommended that the 
EPA evaluate how health risks in urban centers, as well as outside 
urban centers, change upon reducing NOX emissions, given 
the varying impacts of NOX emissions reductions on 
ambient O3 concentrations.
---------------------------------------------------------------------------

    The PA further concludes that support for this initial conclusion 
is also provided by estimates of O3-associated mortality and 
morbidity based on application of concentration-response relationships 
from epidemiologic studies to air quality adjusted to just meet the 
current standard. These estimates, which are based on the assumption 
that concentration-response relationships are linear over entire 
distributions of ambient O3 concentrations, are associated 
with uncertainties that complicate their interpretation (II.C.3). 
However, risk estimates for effects associated with short- and long-
term O3 exposures, combined with the HREA's national 
analysis of O3 responsiveness to reductions in precursor 
emissions and the consistent reductions estimated for the highest 
ambient O3 concentrations, suggest that O3-
associated mortality and morbidity would be expected to decrease 
nationwide following reductions in precursor emissions to meet the 
current O3 standard.
    Reductions in O3 precursor emissions (i.e., 
NOX) could also increase public health protection by 
reducing the ambient concentrations of pollutants other than 
O3. For example, in their advice on the second draft HREA 
CASAC acknowledged the potential for ambient NO2 
concentrations to be affected by changes in NOX emissions 
(Frey, 2014a, p. 10). Consistent with this, the PA notes that 
NOX emissions contribute to ambient NO2, and that 
NOX and VOCs can contribute to secondary formation of 
PM2.5 constituents, including ammonium sulfate 
(NH4SO4), ammonium nitrate 
(NH4NO3), and organic carbon (OC). Therefore, at 
some times and in some locations, control strategies that would reduce 
NOX emissions (i.e., to meet an O3 standard) 
could reduce ambient concentrations of NO2 and 
PM2.5, resulting in health benefits beyond those directly 
associated with reducing ambient O3 concentrations.
    After reaching the initial conclusion that meeting the current 
primary O3 standard will provide important improvements in 
public health protection, and that it is not appropriate to consider a 
standard that is less protective than the current standard, the PA 
considers the adequacy of the public health protection that is provided 
by the

[[Page 75286]]

current standard. In considering the available scientific evidence, 
exposure/risk information, advice from CASAC (II.D.4, below), and input 
from the public, the PA reaches the conclusion that the available 
evidence and information clearly call into question the adequacy of 
public health protection provided by the current primary standard. In 
reaching this conclusion, the PA notes that evidence from controlled 
human exposure studies provides strong support for the occurrence of 
adverse respiratory effects following exposures to O3 
concentrations below the level of the current standard. Epidemiologic 
studies provide support for the occurrence of adverse respiratory 
effects and mortality under air quality conditions that would likely 
meet the current standard. In addition, based on the analyses in the 
HREA, the PA concludes that the exposures and risks projected to remain 
upon meeting the current standard are indicative of risks that can 
reasonably be judged to be important from a public health perspective. 
Thus, the PA concludes that the evidence and information provide strong 
support for giving consideration to revising the current primary 
standard in order to provide increased public health protection against 
an array of adverse health effects that range from decreased lung 
function and respiratory symptoms to more serious indicators of 
morbidity (e.g., including emergency department visits and hospital 
admissions), and mortality. In consideration of all of the above, the 
PA draws the conclusion that it is appropriate for the Administrator to 
consider revision of the current primary O3 standard to 
provide increased public health protection.
4. CASAC Advice
    Following the 2008 decision to revise the primary O3 
standard by setting the level at 0.075 ppm (75 ppb), CASAC strongly 
questioned whether the standard met the requirements of the CAA. In 
September 2009, the EPA announced its intention to reconsider the 2008 
standards, issuing a notice of proposed rulemaking in January 2010 (75 
FR 2938). Soon after, the EPA solicited CASAC review of that proposed 
rule and in January 2011, solicited additional advice. This proposal 
was based on the scientific and technical record from the 2008 
rulemaking, including public comments and CASAC advice and 
recommendations. As further described above (I.C), in the fall of 2011, 
the EPA did not revise the standard as part of the reconsideration 
process but decided to defer decisions on revisions to the 
O3 standards to the next periodic review, which was already 
underway. Accordingly, in this section we describe CASAC's advice 
related to the 2008 final decision and the subsequent reconsideration, 
as well as its advice on this current review of the O3 NAAQS 
that was initiated in September 2008.
    In April 2008, the members of the CASAC Ozone Review Panel sent a 
letter to EPA stating ``[I]n our most-recent letters to you on this 
subject--dated October 2006 and March 2007--the CASAC unanimously 
recommended selection of an 8-hour average Ozone NAAQS within the range 
of 0.060 to 0.070 parts per million [60 to 70 ppb] for the primary 
(human health-based) Ozone NAAQS'' (Henderson, 2008). The letter 
continued:

The CASAC now wishes to convey, by means of this letter, its 
additional, unsolicited advice with regard to the primary and 
secondary Ozone NAAQS. In doing so, the participating members of the 
CASAC Ozone Review Panel are unanimous in strongly urging you or 
your successor as EPA Administrator to ensure that these 
recommendations be considered during the next review cycle for the 
Ozone NAAQS that will begin next year . . . numerous medical 
organizations and public health groups have also expressed their 
support of these CASAC recommendations' . . . [The CASAC did] not 
endorse the new primary ozone standard as being sufficiently 
protective of public health. The CASAC--as the EPA's statutorily-
established science advisory committee for advising you on the 
national ambient air quality standards--unanimously recommended 
decreasing the primary standard to within the range of 0.060-0.070 
ppm [60 to 70 ppb]. It is the Committee's consensus scientific 
opinion that your decision to set the primary ozone standard above 
this range fails to satisfy the explicit stipulations of the Clean 
Air Act that you ensure an adequate margin of safety for all 
individuals, including sensitive populations.

    In response to the EPA's solicitation of advice on the EPA's 
proposed rulemaking as part of the reconsideration, CASAC conveyed 
support (Samet, 2010).

CASAC fully supports EPA's proposed range of 0.060-0.070 parts per 
million (ppm) for the 8-hour primary ozone standard. CASAC considers 
this range to be justified by the scientific evidence as presented 
in the Air Quality Criteria for Ozone and Related Photochemical 
Oxidants (March 2006) and Review of the National Ambient Air Quality 
Standards for Ozone: Policy Assessment of Scientific and Technical 
Information, OAQPS Staff Paper (July 2007). As stated in our letters 
of October 24, 2006, March 26, 2007 and April 7, 2008 to former 
Administrator Stephen L. Johnson, CASAC unanimously recommended 
selection of an 8-hour average ozone NAAQS within the range proposed 
by EPA (0.060 to 0.070 ppm). In proposing this range, EPA has 
recognized the large body of data and risk analyses demonstrating 
that retention of the current standard would leave large numbers of 
individuals at risk for respiratory effects and/or other significant 
health impacts including asthma exacerbations, emergency room 
visits, hospital admissions and mortality.

    In response to EPA's request for additional advice on the 
reconsideration in 2011, CASAC reaffirmed their conclusion that ``the 
evidence from controlled human and epidemiological studies strongly 
supports the selection of a new primary ozone standard within the 60-70 
ppb range for an 8-hour averaging time'' (Samet, 2011, p ii). As 
requested by the EPA, CASAC's advice and recommendations were based on 
the scientific and technical record from the 2008 rulemaking. In 
considering the record for the 2008 rulemaking, CASAC stated the 
following to summarize the basis for their conclusions (Samet, 2011, 
pp. ii to iii).
    (1) The evidence available on dose-response for effects of 
O3 shows associations extending to levels within the range 
of concentrations currently experienced in the United States.
    (2) There is scientific certainty that 6.6-hour exposures with 
exercise of young, healthy, non-smoking adult volunteers to 
concentrations >=80 ppb cause clinically relevant decrements of lung 
function.
    (3) Some healthy individuals have been shown to have clinically 
relevant responses, even at 60 ppb.
    (4) Since the majority of clinical studies involve young, healthy 
adult populations, less is known about health effects in such 
potentially ozone sensitive populations as the elderly, children and 
those with cardiopulmonary disease. For these susceptible groups, 
decrements in lung function may be greater than in healthy volunteers 
and are likely to have a greater clinical significance.
    (5) Children and adults with asthma are at increased risk of acute 
exacerbations on or shortly after days when elevated O3 
concentrations occur, even when exposures do not exceed the NAAQS 
concentration of 75 ppb.
    (6) Large segments of the population fall into what the EPA terms a 
``sensitive population group,'' i.e., those at increased risk because 
they are more intrinsically susceptible (children, the elderly, and 
individuals with chronic lung disease) and those who are more 
vulnerable due to increased exposure because they work outside or live 
in areas that are more polluted than the mean levels in their 
communities.
    With respect to evidence from epidemiologic studies, CASAC stated 
``while epidemiological studies are

[[Page 75287]]

inherently more uncertain as exposures and risk estimates decrease (due 
to the greater potential for biases to dominate small effect 
estimates), specific evidence in the literature does not suggest that 
our confidence on the specific attribution of the estimated effects of 
ozone on health outcomes differs over the proposed range of 60-70 ppb'' 
(Samet, 2011, p. 10).
    Following its review of the second draft PA in the current review, 
which considers an updated scientific and technical record since the 
2008 rulemaking, CASAC concluded that ``there is clear scientific 
support for the need to revise the standard'' (Frey, 2014c, p. ii). In 
particular, CASAC noted the following (Frey, 2014c, p. 5):

[T]he scientific evidence provides strong support for the occurrence 
of a range of adverse respiratory effects and mortality under air 
quality conditions that would meet the current standard. Therefore, 
CASAC unanimously recommends that the Administrator revise the 
current primary ozone standard to protect public health.\106\
---------------------------------------------------------------------------

    \106\ CASAC provided similar advice in their letter to the 
Administrator on the REA, stating that ``The CASAC finds that the 
current primary NAAQS for ozone is not protective of human health 
and needs to be revised'' (Frey, 2014a, p. 15).

    In supporting these conclusions, CASAC judged that the strongest 
evidence comes from controlled human exposure studies of respiratory 
effects. The Committee specifically noted that ``the combination of 
decrements in FEV1 together with the statistically 
significant alterations in symptoms in human subjects exposed to 72 ppb 
ozone meets the American Thoracic Society's definition of an adverse 
health effect'' (Frey, 2014c, p. 5). CASAC further judged that ``if 
subjects had been exposed to ozone using the 8-hour averaging period 
used in the standard, adverse effects could have occurred at lower 
concentration'' and that ``the level at which adverse effects might be 
observed would likely be lower for more sensitive subgroups, such as 
those with asthma'' (Frey, 2014c, p. 5).
    With regard to lung function risk estimates based on information 
from controlled human exposure studies, CASAC concluded that 
``estimation of FEV1 decrements of >=15% is appropriate as a 
scientifically relevant surrogate for adverse health outcomes in active 
healthy adults, whereas an FEV1 decrement of >=10% is a scientifically 
relevant surrogate for adverse health outcomes for people with asthma 
and lung disease'' (Frey, 2014c, p. 3). The Committee further concluded 
that ``[a]sthmatic subjects appear to be at least as sensitive, if not 
more sensitive, than non-asthmatic subjects in manifesting 
O3-induced pulmonary function decrements'' (Frey, 2014c, p. 
4). In considering estimates of the occurrence of these decrements in 
urban study areas, CASAC specifically noted that the current standard 
is estimated to allow 11 to 22% of school age children to experience at 
least one day with an FEV1 decrement >=10% (Frey, 2014c, p. 
7).
    Although CASAC judged that controlled human exposure studies of 
respiratory effects provide the strongest evidence supporting their 
conclusion on the current standard, the Committee judged that there is 
also ``sufficient scientific evidence based on epidemiologic studies 
for mortality and morbidity associated with short-term exposure to 
ozone at the level of the current standard'' (Frey, 2014c, p. 5). In 
support of the biological plausibility of the associations reported in 
these epidemiologic studies, CASAC noted that ``[r]ecent animal 
toxicological studies support identification of modes of action and, 
therefore, the biological plausibility associated with the 
epidemiological findings'' (Frey, 2014c, p. 5).
    Consistent with the advice of CASAC, several public commenters 
supported revising the primary O3 standard to provide 
increased public health protection. In considering the available 
evidence as a basis for their views, these commenters generally noted 
that the health evidence is stronger in the current review than in past 
reviews, with new evidence for effects attributable to short- and long-
term exposures, and new evidence for effects at lower O3 
exposure concentrations.
    Other public commenters opposed considering revised standards. 
These commenters discussed a variety of reasons for their views. A 
number of commenters expressed the view that the EPA should not lower 
the level of the standard because a lower level would be closer to 
background O3 concentrations. In addition, several 
commenters challenged the interpretation of the evidence presented in 
the ISA. With respect to the risk assessment, several commenters 
expressed the view that the EPA should only estimate risks above 
O3 background concentrations, or above threshold 
concentrations. Some commenters also expressed the view that, based on 
the mortality and morbidity risk estimates in the HREA, there is little 
to no difference between the risks estimated for the current 
O3 standard and the risks estimated for revised standards 
with lower levels. These commenters concluded that the HREA and PA have 
not shown that the public health improvements likely to be achieved by 
a revised O3 standard would be greater than the improvements 
likely to be achieved by the current standard.
5. Administrator's Proposed Conclusions Concerning the Adequacy of the 
Current Standard
    This section discusses the Administrator's proposed conclusions 
related to the adequacy of the public health protection provided by the 
current primary O3 standard, resulting in her proposed 
decision to revise that standard. These proposed conclusions, and her 
proposed decision, are based on the Administrator's consideration of 
the available scientific evidence, exposure/risk information, the 
comments and advice of CASAC, and public input received thus far, as 
summarized below.
    As an initial matter, the Administrator concludes that reducing 
precursor emissions to achieve O3 concentrations that meet 
the current primary O3 standard will provide important 
improvements in public health protection, compared to recent air 
quality. In reaching this initial conclusion, she notes the discussion 
in section 3.4 of the PA (U.S. EPA, 2014c), summarized above (II.D.3). 
In particular, the Administrator notes that this initial conclusion is 
supported by (1) the strong body of scientific evidence indicating a 
wide range of adverse health outcomes attributable to exposures to 
O3 at concentrations commonly found in the ambient air and 
(2) estimates indicating decreased occurrences of O3 
exposures of concern and decreased O3-associated health 
risks upon meeting the current standard, compared to recent air 
quality. Thus, she concludes that it would not be appropriate in this 
review to consider a standard that is less protective than the current 
standard.\107\
---------------------------------------------------------------------------

    \107\ While not analyzed quantitatively, consistent with CASAC 
advice (Frey, 2014a, p. 10), the Administrator notes that reductions 
in O3 precursor emissions (e.g., NOX; VOC) to 
achieve O3 concentrations that meet the current standard 
could also increase public health protection by reducing the ambient 
concentrations of pollutants other than O3 (i.e., 
PM2.5, NO2).
---------------------------------------------------------------------------

    After reaching the initial conclusion that meeting the current 
primary O3 standard will provide important improvements in 
public health protection, and that it is not appropriate to consider a 
standard that is less protective than the current standard, the 
Administrator next considers the adequacy of the public health 
protection that is provided by the current standard. In doing so, the 
Administrator first notes that studies evaluated since the completion 
of the 2006 O3 AQCD

[[Page 75288]]

support and expand upon the strong body of evidence that, in the last 
review, indicated a causal relationship between short-term 
O3 exposures and respiratory health effects. This is the 
strongest causality finding possible under the ISA's hierarchical 
system for classifying weight of evidence for causation. Together, 
experimental and epidemiologic studies support conclusions regarding a 
continuum of O3 respiratory effects ranging from small 
reversible changes in pulmonary function, and pulmonary inflammation, 
to more serious effects that can result in respiratory-related 
emergency department visits, hospital admissions, and premature 
mortality. Recent animal toxicology studies support descriptions of 
modes of action for these respiratory effects and augment support for 
biological plausibility for the role of O3 in reported 
effects. With regard to mode of action, evidence indicates that 
antioxidant capacity may modify the risk of respiratory morbidity 
associated with O3 exposure, and that the inherent capacity 
to quench (based on individual antioxidant capacity) can be 
overwhelmed, especially with exposure to elevated concentrations of 
O3. In addition, based on the consistency of findings across 
studies and evidence for the coherence of results from different 
scientific disciplines, evidence indicates that certain populations are 
at increased risk of experiencing O3-related effects, 
including the most severe effects. These include populations and 
lifestages identified in previous reviews (i.e., people with asthma, 
children, older adults, outdoor workers) and populations identified 
since the last review (i.e., people with certain genotypes related to 
antioxidant and/or anti-inflammatory status; people with reduced intake 
of certain antioxidant nutrients, such as Vitamins C and E).
    The Administrator further notes that evidence for adverse 
respiratory health effects attributable to long-term, or repeated 
short-term, O3 exposures is much stronger than in previous 
reviews, and the ISA concludes that there is ``likely to be'' a causal 
relationship between such O3 exposures and adverse 
respiratory health effects (the second strongest causality finding). 
Uncertainties related to the extrapolation of data generated by rodent 
toxicology studies to the understanding of health effects in humans 
have been reduced by studies in non-human primates and by recent 
epidemiologic studies. The evidence available in this review includes 
new epidemiologic studies using a variety of designs and analysis 
methods, conducted by different research groups in different locations, 
evaluating the relationships between long-term O3 exposures 
and measures of respiratory morbidity and mortality. New evidence 
supports associations between long-term O3 exposures and the 
development of asthma in children, with several studies reporting 
interactions between genetic variants and such O3 exposures. 
Studies also report associations between long-term O3 
exposures and asthma prevalence, asthma severity and control, 
respiratory symptoms among asthmatics, and respiratory mortality.
    In considering the O3 exposure concentrations reported 
to elicit respiratory effects, the Administrator agrees with the 
conclusions of the PA and with the advice of CASAC (Frey, 2014c) that 
controlled human exposure studies provide the most certain evidence 
indicating the occurrence of health effects in humans following 
exposures to specific O3 concentrations. In particular, as 
discussed further in section II.E.4.d below, she notes that the effects 
reported in controlled human exposure studies are due solely to 
O3 exposures, and interpretation of study results is not 
complicated by the presence of co-occurring pollutants or pollutant 
mixtures (as is the case in epidemiologic studies). Therefore, she 
places the most weight on information from these controlled human 
exposure studies.
    In considering the evidence from controlled human exposure studies, 
the Administrator first notes that these studies have reported a 
variety of respiratory effects in healthy adults following exposures to 
O3 concentrations of 60, 72,\108\ or 80 ppb, and higher. The 
largest respiratory effects, and the broadest range of effects, have 
been studied and reported following exposures of healthy adults to 80 
ppb O3 or higher, with most exposure studies conducted at 
these higher concentrations. She further notes that recent evidence 
includes controlled human exposure studies reporting the combination of 
lung function decrements and respiratory symptoms in healthy adults 
engaged in intermittent, moderate exertion following 6.6 hour exposures 
to concentrations as low as 72 ppb, and lung function decrements and 
pulmonary inflammation following exposures to O3 
concentrations as low as 60 ppb. As discussed below, compared to the 
evidence available in the last review, these studies have strengthened 
support for the occurrence of abnormal and adverse respiratory effects 
attributable to short-term exposures to O3 concentrations 
below the level of the current standard.\109\ The Administrator 
concludes that such exposures to O3 concentrations below the 
level of the current standard are potentially important from a public 
health perspective, given the following:
---------------------------------------------------------------------------

    \108\ As noted above, for the 70 ppb target exposure 
concentration, Schelegle et al. (2009) reported that the actual mean 
exposure concentration was 72 ppb.
    \109\ Cf. State of Misisssippi. 744 F.3d 1350 (``Perhaps more 
studies like the Adams studies will yet reveal that the 0.060 ppm 
level produces significant adverse decrements that simply cannot be 
attributed to normal variation in lung function.'').
---------------------------------------------------------------------------

    (1) The combination of lung function decrements and respiratory 
symptoms reported to occur in healthy adults following exposures to 72 
ppb O3 or higher, while at moderate exertion, meet ATS 
criteria for an adverse response. In specifically considering the 72 
ppb exposure concentration, CASAC noted that ``the combination of 
decrements in FEV1 together with the statistically 
significant alterations in symptoms in human subjects exposed to 72 ppb 
ozone meets the American Thoracic Society's definition of an adverse 
health effect'' (Frey, 2014c, p. 5).
    (2) With regard to 60 ppb O3, CASAC agreed that ``a 
level of 60 ppb corresponds to the lowest exposure concentration 
demonstrated to result in lung function decrements large enough to be 
judged an abnormal response by ATS and that could be adverse in 
individuals with lung disease'' (Frey, 2014c, p. 7). CASAC further 
noted that ``a level of 60 ppb also corresponds to the lowest exposure 
concentration at which pulmonary inflammation has been reported'' 
(Frey, 2014c, p. 7).
    (3) The controlled human exposure studies reporting these 
respiratory effects were conducted in healthy adults, while at-risk 
groups (e.g., children, people with asthma) could experience larger 
and/or more serious effects. In their advice to the Administrator, 
CASAC concurred with this reasoning (Frey, 2014a, p. 14; Frey, 2014c, 
p. 5).
    (4) These respiratory effects are coherent with the serious health 
outcomes that have been reported in epidemiologic studies evaluating 
exposure to O3 (e.g., respiratory-related hospital 
admissions, emergency department visits, and mortality).
    As noted above, the Administrator's proposed conclusions regarding 
the adequacy of the current primary O3 standard place a 
large amount of weight on the results of controlled human exposure 
studies. In particular, given the combination of lung function

[[Page 75289]]

decrements and respiratory symptoms following 6.6 hour exposures to 
O3 concentrations as low as 72 ppb, and given CASAC advice 
regarding effects at 72 ppb along with ATS adversity criteria, she 
concludes that the evidence in this review supports the occurrence of 
adverse respiratory effects following exposures to O3 
concentrations lower than the level of the current standard.\110\ As 
discussed below, the Administrator further considers information from 
the broader body of controlled human exposure studies within the 
context of quantitative estimates of exposures of concern and 
O3-induced FEV1 decrements.
---------------------------------------------------------------------------

    \110\ The use of evidence from controlled human exposure studies 
conducted in healthy adults to characterize the potential for 
adverse effects, including in at-risk groups such as children and 
asthmatics, is discussed in sections II.C.2 and II.C.3.a, above. 
CASAC advice on this issue is discussed in sections II.D.4 and 
II.E.4.c.
---------------------------------------------------------------------------

    In addition to controlled human exposure studies, the Administrator 
also considers what the available epidemiologic evidence indicates with 
regard to the adequacy of the public health protection provided by the 
current primary O3 standard.\111\ She notes that recent 
epidemiologic studies provide support, beyond that available in the 
last review, for associations between short-term O3 
exposures and a wide range of adverse respiratory outcomes (including 
respiratory-related hospital admissions, emergency department visits, 
and mortality) and with total mortality. Associations with morbidity 
and mortality are stronger during the warm or summer months, and remain 
robust after adjustment for copollutants.
---------------------------------------------------------------------------

    \111\ As noted above, she places less weight on information from 
epidemiologic studies than on information from controlled human 
exposure studies.
---------------------------------------------------------------------------

    In considering information from epidemiologic studies within the 
context of her conclusions on the adequacy of the current standard, the 
Administrator considers the extent to which available studies support 
the occurrence of O3 health effect associations with air 
quality likely to be allowed by the current standard. In doing so, she 
places the most weight on air quality analyses in locations of single-
city studies of short-term O3, as discussed in more detail 
in section II.E.4.d below.\112\ In particular, she notes that a U.S. 
single-city study reported associations with respiratory emergency 
department visits in children and adults in a location that would 
likely have met the current O3 standard over the entire 
study period (Mar and Koenig, 2009). In addition, even in some single-
city study locations where the current standard was likely not met 
(i.e., Silverman and Ito, 2010; Strickland et al., 2010), the 
Administrator notes PA analyses indicating that reported concentration-
response functions and available air quality data support the 
occurrence of O3-health effect associations on subsets of 
days with ambient O3 concentrations below the level of the 
current standard (II.D.1). Compared to single-city studies, the 
Administrator notes additional uncertainty in interpreting the 
relationships between air quality in individual study cities and health 
effects based on multicity analyses (discussed further in sections 
II.D.1 and II.E.4.d). While such uncertainties limit the extent to 
which the Administrator bases her conclusions on air quality in 
locations of multicity epidemiologic studies, she does note that 
O3 associations with respiratory morbidity or mortality have 
been reported in several multicity studies when the majority of study 
locations (though not all study locations) would likely have met the 
current O3 standard. When taken together, the Administrator 
reaches the conclusion that single-city epidemiologic studies and 
associated air quality information support the occurrence of 
O3-associated hospital admissions and emergency department 
visits for ambient O3 concentrations likely to have met the 
current standard, and that air quality analyses in locations of 
multicity studies provide some support for this conclusion for a 
broader range of effects (i.e., including mortality).
---------------------------------------------------------------------------

    \112\ As discussed in section II.E.4.d of this preamble, this 
judgment applies specifically to epidemiologic studies of short-term 
O3 concentrations where multicity effect estimates are 
presented, based on combining the effect estimates from multiple 
individual cities, and where individual city effect estimates are 
not presented (as is the case for key multicity studies analyzed in 
the PA). Because these reported multicity effect estimates do not 
allow health effect associations to be disaggregated by individual 
city, it is not possible to assign the health effect association to 
the air quality in any one study location, or to the air quality in 
a subset of locations. In contrast, for epidemiologic studies of 
long-term concentrations, where multicity effect estimates are based 
on comparisons across cities, different judgments have been made 
with regard to the utility of multicity studies (see, e.g. 78 FR 
3086 at 3103/2) (January 15, 2013) (and see discussion below of 
study by Jerrett et al., (2009)).
---------------------------------------------------------------------------

    Beyond her consideration of the scientific evidence, the 
Administrator also considers the results of the HREA exposure and risk 
analyses in reaching initial conclusions regarding the adequacy of the 
current primary O3 standard. In doing so, as noted above, 
she focuses primarily on exposure and risk estimates based on 
information from controlled human exposure studies (i.e., exposures of 
concern and O3-induced lung function decrements). She places 
relatively less weight on epidemiologic-based risk estimates, noting 
that the overall conclusions from the HREA likewise reflect less 
confidence in estimates of epidemiologic-based risks than in estimates 
of exposures and lung function risks (U.S. EPA, 2014, section 9.6). 
Consistent with the conclusions in the PA, her determination to attach 
less weight to the epidemiologic-based risk estimates reflects her 
consideration of key uncertainties, including the heterogeneity in 
effect estimates between locations, the potential for exposure 
measurement errors, and uncertainty in the interpretation of the shape 
of concentration-response functions for O3 concentrations in 
the lower portions of ambient distributions (U.S. EPA, 2014, section 
9.6) (II.D.2). In particular, she concludes that lower confidence 
should be placed in the results of the assessment of respiratory 
mortality risks associated with long-term O3 exposures, 
primarily because that analysis is based on only one study (even though 
that study is well-designed) and because of the uncertainty in that 
study about the existence and level of a potential threshold in the 
concentration-response function (U.S. EPA, 2014a, section 9.6) 
(II.D.2).\113\
---------------------------------------------------------------------------

    \113\ CASAC also called into question the extent to which it is 
appropriate to place confidence in risk estimates for respiratory 
mortality (Frey, 2014a, p. 11).
---------------------------------------------------------------------------

    With regard to estimates of exposures of concern, the Administrator 
considers the extent to which the current standard provides protection 
against exposures to O3 concentrations at or above 60, 70, 
and 80 ppb, noting CASAC advice that 60 ppb ``is an appropriate 
exposure of concern for asthmatic children'' (Frey, 2014c, p. 8). She 
further notes that while single exposures of concern could be adverse 
for some people, particularly for the higher benchmark concentrations 
(70, 80 ppb) where there is stronger evidence for the occurrence of 
adverse effects (discussed further in II.E.4.d, below), she becomes 
increasingly concerned about the potential for adverse responses as the 
frequency of occurrences increases.\114\ In particular,

[[Page 75290]]

she notes that repeated occurrences of the types of effects shown to 
occur following exposures of concern can have potentially adverse 
outcomes. For example, repeated occurrences of airway inflammation 
could potentially result in the induction of a chronic inflammatory 
state; altered pulmonary structure and function, leading to diseases 
such as asthma; altered lung host defense response to inhaled 
microorganisms; and altered lung response to other agents such as 
allergens or toxins (U.S. EPA, 2013a, section 6.2.3). Thus, the 
Administrator notes that the types of lung injury shown to occur 
following exposures to O3 concentrations from 60 to 80 ppb, 
particularly if experienced repeatedly, provide a mode of action by 
which O3 may cause other more serious effects (e.g., asthma 
exacerbations). Therefore, the Administrator places the most weight on 
estimates of two or more exposures of concern (i.e., as a surrogate for 
the occurrence of repeated exposures), though she also considers 
estimates of one or more, particularly for the 70 and 80 ppb 
benchmarks.
---------------------------------------------------------------------------

    \114\ Not all people who experience an exposure of concern will 
experience an adverse effect (even members of at-risk populations). 
For most of the endpoints evaluated in controlled human exposure 
studies (with the exception of O3-induced FEV1 
decrements, as discussed below), the number of those experiencing 
exposures of concern who will experience adverse effects cannot be 
reliably quantified.
---------------------------------------------------------------------------

    Consistent with CASAC advice (Frey, 2014c), the Administrator 
focuses on children in these analyses of O3 exposures, 
noting that estimates for all children and asthmatic children are 
virtually indistinguishable (in terms of the percent estimated to 
experience exposures of concern). Though she focuses on children, she 
also recognizes that exposures to O3 concentrations at or 
above 60 or 70 ppb could be of concern for adults. As discussed in the 
HREA and PA (and II.C.2.a, above), the patterns of exposure estimates 
across urban study areas, across years, and across air quality 
scenarios are similar in adults with asthma, older adults, all 
children, and children with asthma, though smaller percentages of adult 
populations are estimated to experience exposures of concern than 
children and children with asthma. Thus, the Administrator recognizes 
that the exposure patterns for children across years, urban study 
areas, and air quality scenarios are indicative of the exposure 
patterns in a broader group of at-risk populations that also includes 
asthmatic adults and older adults.
    As illustrated in Table 1 (above), the Administrator notes that if 
the 15 urban study areas evaluated in the HREA were to just meet the 
current O3 standard, fewer than 1% of children in those 
areas would be estimated to experience two or more exposures of concern 
at or above 70 ppb, though approximately 3 to 8% of children, including 
approximately 3 to 8% of asthmatic children, would be estimated to 
experience two or more exposures of concern to O3 
concentrations at or above 60 ppb \115\ (based on estimates averaged 
over the years of analysis). To provide some perspective on these 
percentages, the Administrator notes that they correspond to almost 
900,000 children in urban study areas, including about 90,000 asthmatic 
children, estimated to experience two or more exposures of concern at 
or above 60 ppb. Nationally, if the current standard were to be just 
met the number of children experiencing such exposures would be larger. 
In the worst-case year and location (i.e., year and location with the 
largest exposure estimates), the Administrator notes that over 2% of 
children are estimated to experience two or more exposures of concern 
at or above 70 ppb and over 14% are estimated to experience two or more 
exposures of concern at or above 60 ppb.
---------------------------------------------------------------------------

    \115\ Almost no children in those areas would be estimated to 
experience two or more exposures of concern at or above 80 ppb.
---------------------------------------------------------------------------

    Although, as discussed above and in section II.E.4.d, the 
Administrator is less concerned about single occurrences of exposures 
of concern, she notes that even single occurrences can cause adverse 
effects in some people, particularly for the 70 and 80 ppb benchmarks. 
Therefore, she also considers estimates of one or more exposures of 
concern. As illustrated in Table 1 (above), if the 15 urban study areas 
evaluated in the HREA were to just meet the current O3 
standard, fewer than 1% of children in those areas would be estimated 
to experience one or more exposures of concern at or above 80 ppb 
(based on estimates averaged over the years of analysis). However, 
approximately 1 to 3% of children, including 1 to 3% of asthmatic 
children, would be estimated to experience one or more exposures of 
concern to O3 concentrations at or above 70 ppb and 
approximately 10 to 17% would be estimated to experience one or more 
exposures of concern to O3 concentrations at or above 60 
ppb. In the worst-case year and location, the Administrator notes that 
over 1% of children are estimated to experience one or more exposures 
of concern at or above 80 ppb, over 8% are estimated to experience one 
or more exposures of concern at or above 70 ppb, and about 26% are 
estimated to experience one or more exposures of concern at or above 60 
ppb.
    In addition to estimated exposures of concern, the Administrator 
also considers HREA estimates of the occurrence of O3-
induced lung function decrements. In doing so, she particularly notes 
CASAC advice that ``estimation of FEV1 decrements of >=15% 
is appropriate as a scientifically relevant surrogate for adverse 
health outcomes in active healthy adults, whereas an FEV1 
decrement of >=10% is a scientifically relevant surrogate for adverse 
health outcomes for people with asthma and lung disease'' (Frey, 2014c, 
p. 3). The Administrator notes that while single occurrences of 
O3-induced lung function decrements could be adverse for 
some people, as discussed above (II.B.3), a more general consensus view 
of the potential adversity of such decrements emerges as the frequency 
of occurrences increases. Therefore, the Administrator focuses 
primarily on the estimates of two or more O3-induced lung 
function decrements.
    When averaged over the years evaluated in the HREA, the 
Administrator notes that the current standard is estimated to allow 
about 1 to 3% of children in the 15 urban study areas (corresponding to 
almost 400,000 children) to experience two or more O3-
induced lung function decrements >=15%, and to allow about 8 to 12% of 
children (corresponding to about 180,000 asthmatic children \116\) to 
experience two or more O3-induced lung function decrements 
>=10%. Nationally, larger numbers of children would be expected to 
experience such O3-induced decrements if the current 
standard were to be just met. The current standard is also estimated to 
allow about 3 to 5% of children in the urban study areas to experience 
one or more decrements >=15% and about 14 to 19% of children to 
experience one or more decrements >=10%. In the worst-case year and 
location, the current standard is estimated to allow 4% of children in 
the urban study areas to experience two or more decrements >=15% (and 
7% to experience one or more such decrements) and 14% of children to 
experience two or more decrements >=10% (and 22% to experience one or 
more such decrements).
---------------------------------------------------------------------------

    \116\ As noted above, CASAC concluded that ``an FEV1 decrement 
of >=10% is a scientifically relevant surrogate for adverse health 
outcomes for people with asthma and lung disease'' (Frey, 2014c, p. 
3) and that such decrements ``could be adverse for people with lung 
disease'' (Frey, 2014c, p. 7).
---------------------------------------------------------------------------

    In further considering the HREA results, the Administrator 
considers the epidemiology-based risk estimates. As discussed above, 
compared to the weight given to HREA estimates of exposures of concern 
and lung function risks, she places relatively less weight on 
epidemiology-based risk estimates. In giving some consideration to 
these

[[Page 75291]]

risk estimates, the Administrator notes estimates of total risks (i.e., 
based on the full distributions of ambient O3 
concentrations) and risks associated with O3 concentrations 
in the upper portions of ambient distributions. The Administrator notes 
that estimates of total risks are based on the assumption that 
concentration-response relationships remain linear over the entire 
distributions of ambient O3 concentrations. With regard to 
total risks, she notes that the HREA estimates thousands of 
O3-associated hospital admissions, emergency department 
visits, and deaths per year for air quality conditions associated with 
just meeting the current standard in the 12 urban study areas (II.C.3).
    However, the Administrator also notes the increasing uncertainty 
associated with the shapes of concentration-response curves for 
O3 concentrations in the lower portions of ambient 
distributions. She particularly notes that there is less certainty in 
the shape of concentration-response functions for area-wide 
O3 concentrations at the lower ends of warm season 
distributions (i.e., below about 20 to 40 ppb depending on the 
O3 metric, health endpoint, and study population) (U.S. EPA, 
2013a, section 2.5.4.4). The Administrator further notes the evidence 
from controlled human exposure studies, which provide the strongest 
support for O3-induced effects following exposures to 
O3 concentrations corresponding to the upper portions of 
typical ambient distributions (i.e., 60 ppb and above). Therefore, the 
Administrator judges it appropriate to focus on risks associated with 
O3 concentrations in the upper portions of ambient 
distributions. Even when considering only area-wide O3 
concentrations from the upper portions of seasonal distributions, the 
Administrator notes that the current standard is estimated to allow 
hundreds to thousands of O3-associated deaths per year in 
urban study areas (II.C.3).
    Although the Administrator notes the HREA conclusions indicating 
somewhat less confidence in estimates of O3-associated 
mortality and morbidity risks, compared to estimates of exposures of 
concern and risk of lung function decrements, she concludes that the 
general magnitude of mortality and morbidity risk estimates suggests 
the potential for a substantial number of O3-associated 
deaths and adverse respiratory events to occur nationally, even when 
the current standard is met. She especially notes that this is the case 
based on the risks associated with the upper ends of distributions of 
ambient O3 concentrations, where she has the greatest 
confidence in O3-attributable effects.
    In addition to the evidence and exposure/risk information discussed 
above, the Administrator also takes note of the CASAC advice in the 
current review and in the 2010 proposed reconsideration of the 2008 
decision establishing the current standard. As discussed in more detail 
above, the current CASAC ``finds that the current NAAQS for ozone is 
not protective of human health'' and ``unanimously recommends that the 
Administrator revise the current primary ozone standard to protect 
public health'' (Frey, 2014c, p. 5). The prior CASAC O3 
Panel likewise recommended revision of the current standard to one with 
a lower level. This earlier recommendation was based entirely on the 
evidence and information in the record for the 2008 standard decision, 
which, as discussed above, has been substantially strengthened in the 
current review (Samet, 2011; Samet, 2012).
    In consideration of all of the above, the Administrator proposes 
that the current primary O3 standard is not adequate to 
protect public health, and that it should be revised to provide 
increased public health protection. This proposed decision is based on 
the Administrator's initial conclusions that the available evidence and 
exposure and risk information clearly call into question the adequacy 
of public health protection provided by the current primary standard 
and, therefore, that the current standard is not requisite to protect 
public health with an adequate margin of safety. With regard to the 
evidence, she specifically notes that (1) controlled human exposure 
studies provide support for the occurrence of adverse respiratory 
effects following exposures to O3 concentrations below the 
level of the current standard (i.e., as low as 72 ppb), and that (2) 
single-city epidemiologic studies provide support for the occurrence of 
adverse respiratory effects under air quality conditions that would 
likely meet the current standard, with multicity studies providing some 
support for this conclusion for a broader range of effects (i.e., 
including mortality). Courts have repeatedly held that this type of 
evidence justifies an Administrator's conclusion that it is 
``appropriate'' (within the meaning of section 109 (d)(1) of the CAA) 
to revise a primary NAAQS to provide further protection of public 
health.\117\ In addition, based on the analyses in the HREA, the 
Administrator initially concludes that the exposures and risks 
projected to remain upon meeting the current standard can reasonably be 
judged to be important from a public health perspective. Thus, she 
reaches the proposed conclusion that the evidence and information, 
together with CASAC advice based on their consideration of that 
evidence and information, provide strong support for revising the 
current primary standard in order to increase public health protection 
against an array of adverse effects that range from decreased lung 
function and respiratory symptoms to more serious indicators of 
morbidity (e.g., including emergency department visits and hospital 
admissions), and mortality.
---------------------------------------------------------------------------

    \117\ See e.g. State of Mississippi, 744 F. 3d at 1345; American 
Farm Bureau, 559 F. 3d at 525-26.
---------------------------------------------------------------------------

    The Administrator solicits comment on her proposed decision to 
revise the current primary O3 NAAQS, including on her 
considerations and proposed conclusions based on the scientific 
evidence, exposure/risk information, and CASAC advice. In doing so, she 
recognizes that some have expressed alternative approaches to viewing 
the evidence and information, including alternative approaches to 
viewing, evaluating, and weighing important uncertainties. In some 
cases, these alternative approaches have led some public commenters to 
recommend retaining the current standard. Given these alternative 
views, in addition to proposing to revise the current primary 
O3 standard, the Administrator solicits comment on the 
option of retaining that standard. In doing so, she also solicits 
comment on the potential approaches to viewing the scientific evidence 
and exposure/risk information that could support a conclusion that the 
current standard is requisite to protect public health with an adequate 
margin of safety.

E. Conclusions on the Elements of the Primary Standard

    Having reached the proposed conclusion that the currently available 
scientific evidence and exposure/risk information call into question 
the adequacy of the current O3 standard, the Administrator 
next considers the range of alternative standards supported by that 
evidence and information. Consistent with her consideration of the 
adequacy of the current standard, the Administrator's proposed 
conclusions on alternative standards are informed by the available 
scientific evidence assessed in the ISA, exposure/risk information 
presented and assessed in the HREA, the evidence-based and exposure-/
risk-based considerations and conclusions in the PA, CASAC advice, and 
input from members of the public. The sections below discuss the 
evidence

[[Page 75292]]

and exposure/risk information, CASAC advice and public input, and the 
Administrator's proposed conclusions, for the major elements of the 
NAAQS: indicator (II.E.1), averaging time (II.E.2), form (II.E.3), and 
level (II.E.4).
1. Indicator
    In the last review, the EPA focused on O3 as the most 
appropriate indicator for a standard meant to provide protection 
against ambient photochemical oxidants. In this review, while the 
complex atmospheric chemistry in which O3 plays a key role 
has been highlighted, no alternatives to O3 have been 
advanced as being a more appropriate indicator for ambient 
photochemical oxidants. More specifically, the ISA noted that 
O3 is the only photochemical oxidant (other than 
NO2) that is routinely monitored and for which a 
comprehensive database exists (U.S. EPA, 2013a, section 3.6). Data for 
other photochemical oxidants (e.g., PAN, H2O2, 
etc.) typically have been obtained only as part of special field 
studies. Consequently, no data on nationwide patterns of occurrence are 
available for these other oxidants; nor are extensive data available on 
the relationships of concentrations and patterns of these oxidants to 
those of O3 (U.S. EPA, 2013a, section 3.6). In its review of 
the second draft PA, CASAC stated ``The indicator of ozone is 
appropriate based on its causal or likely causal associations with 
multiple adverse health outcomes and its representation of a class of 
pollutants known as photochemical oxidants'' (Frey, 2014c, p. ii).
    In addition, the PA notes that meeting an O3 standard 
can be expected to provide some degree of protection against potential 
health effects that may be independently associated with other 
photochemical oxidants, even though such effects are not discernible 
from currently available studies indexed by O3 alone (U.S. 
EPA, 2014c, section 4.1). That is, since the precursor emissions that 
lead to the formation of O3 generally also lead to the 
formation of other photochemical oxidants, measures leading to 
reductions in population exposures to O3 can generally be 
expected to lead to reductions in population exposures to other 
photochemical oxidants. In considering this information, and CASAC's 
advice, the Administrator reaches the proposed conclusion that 
O3 remains the most appropriate indicator for a standard 
meant to provide protection against photochemical oxidants.\118\
---------------------------------------------------------------------------

    \118\ The DC Circuit upheld the use of O3 as the 
indicator for photochemical oxidants based on these same 
considerations. American Petroleum Inst. v. Costle, 665 F. 2d 1176, 
1186 (D.C. Cir. 1981).
---------------------------------------------------------------------------

2. Averaging Time
    The EPA established the current 8-hour averaging time \119\ for the 
primary O3 NAAQS in 1997 (62 FR 38856). The decision on 
averaging time in that review was based on numerous controlled human 
exposure and epidemiologic studies reporting associations between 6 to 
8 hour O3 concentrations and adverse respiratory effects (62 
FR 38861). It was also noted that a standard with a max 8-hour 
averaging time is likely to provide substantial protection against 
respiratory effects associated with 1-hour peak O3 
concentrations. Similar conclusions were reached in the last 
O3 NAAQS review and thus, the 8-hour averaging time was 
retained in 2008.
---------------------------------------------------------------------------

    \119\ This 8-hour averaging time reflects daily max 8-hour 
average O3 concentrations.
---------------------------------------------------------------------------

    In reaching a proposed conclusion on averaging time in the current 
review, the Administrator considers the extent to which the available 
evidence continues to support the appropriateness of a standard with an 
8-hour averaging time. Specifically, the Administrator considers the 
extent to which the available information indicates that a standard 
with the current 8-hour averaging time provides appropriate protection 
against short- and long-term O3 exposures.
a. Short-Term
    As an initial consideration with respect to the most appropriate 
averaging time for the O3 NAAQS, the Administrator notes 
that the strongest evidence for O3-associated health effects 
is for respiratory effects following short-term exposures. More 
specifically, the Administrator notes the ISA conclusion that the 
evidence is ``sufficient to infer a causal relationship'' between 
short-term O3 exposures and respiratory effects. The ISA 
also judges that for short-term O3 exposures, the evidence 
indicates ``likely to be causal'' relationships with both 
cardiovascular effects and mortality (U.S. EPA, 2013a, section 2.5.2). 
Therefore, as in past reviews, the strength of the available scientific 
evidence provides strong support for a standard that protects the 
public health against short-term exposures to O3.
    In first considering the level of support available for specific 
short-term averaging times, the Administrator notes the evidence 
available from controlled human exposure studies. As discussed in more 
detail in chapter 3 of the PA, substantial health effects evidence from 
controlled human exposure studies demonstrates that a wide range of 
respiratory effects (e.g., pulmonary function decrements, increases in 
respiratory symptoms, lung inflammation, lung permeability, decreased 
lung host defense, and AHR) occur in healthy adults following 6.6 hour 
exposures to O3 (U.S. EPA, 2013a, section 6.2.1.1). Compared 
to studies evaluating shorter exposure durations (e.g., 1-hour), 
studies evaluating 6.6 hour exposures in healthy adults have reported 
respiratory effects at lower O3 exposure concentrations and 
at more moderate levels of exertion.
    The Administrator also notes the strength of evidence from 
epidemiologic studies that have evaluated a wide variety of populations 
(e.g., including at-risk lifestages and populations, such as children 
and people with asthma, respectively). A number of different averaging 
times are used in O3 epidemiologic studies, with the most 
common being the max 1-hour concentration within a 24-hour period (1-
hour max), the max 8-hour average concentration within a 24-hour period 
(8-hr max), and the 24-hour average. These studies are summarized above 
and assessed in detail in chapter 6 of the ISA (U.S. EPA, 2013a). 
Limited evidence from time-series and panel epidemiologic studies 
comparing risk estimates across averaging times does not indicate that 
one exposure metric is more consistently or strongly associated with 
respiratory health effects or mortality, though the ISA notes some 
evidence for ``smaller O3 risk estimates when using a 24-
hour average exposure metric'' (U.S. EPA, 2013a, section 2.5.4.2; p. 2-
31). For single- and multi-day average O3 concentrations, 
lung function decrements were associated with 1-hour max, 8-hour max, 
and 24-hour average ambient O3 concentrations, with no 
strong difference in the consistency or magnitude of association among 
the averaging times (U.S. EPA, 2013a, p. 6-71). Similarly, in studies 
of short-term exposure to O3 and mortality, Smith et al. 
(2009) and Darrow et al. (2011) have reported high correlations between 
risk estimates calculated using 24-hour average, 8-hour max, and 1-hour 
max averaging times (U.S. EPA, 2013a, p. 6-253). Thus, the 
Administrator notes that the epidemiologic evidence alone does not 
provide a strong basis for distinguishing between the appropriateness 
of 1-hour, 8-hour, and 24-hour averaging times.
    Considering the health information discussed above, the 
Administrator concludes that an 8-hour averaging time remains 
appropriate for addressing health effects associated with short-term 
exposures to ambient O3. An 8-hour

[[Page 75293]]

averaging time is similar to the exposure periods evaluated in 
controlled human exposure studies, including recent studies that 
provide evidence for respiratory effects following exposures to 
O3 concentrations below the level of the current standard. 
In addition, epidemiologic studies provide evidence for health effect 
associations with 8-hour O3 concentrations, as well as with 
1-hour and 24-hour concentrations. As in previous reviews, the 
Administrator notes that a standard with an 8-hour averaging time 
(combined with an appropriate standard form and level) would also be 
expected to provide substantial protection against health effects 
attributable to 1-hour and 24-hour exposures (e.g., 62 FR 38861, July 
18, 1997). This conclusion is consistent with the advice received from 
CASAC that ``the current 8-hour averaging time is justified by the 
combined evidence from epidemiologic and clinical studies'' (Frey, 
2014c, p. 6).
b. Long-Term
    The ISA concludes that the evidence for long-term O3 
exposures indicates that there is ``likely to be a causal 
relationship'' with respiratory effects (U.S. EPA, 2013a, chapter 7). 
Thus, in this review the Administrator also considers the extent to 
which currently available evidence and exposure/risk information 
suggests that a standard with an 8-hour averaging time can provide 
protection against respiratory effects associated with longer term 
exposures to ambient O3.
    In considering this issue in the last review of the O3 
NAAQS, the Staff Paper noted that ``because long-term air quality 
patterns would be improved in areas coming into attainment with an 8-hr 
standard, the potential risk of health effects associated with long-
term exposures would be reduced in any area meeting an 8-hr standard'' 
(U.S. EPA, 2007, p. 6-57). In the current review, the PA further 
evaluates this issue, with a focus on the long-term O3 
metrics reported to be associated with mortality or morbidity in recent 
epidemiologic studies. As discussed in section 3.1.3 of the PA (U.S. 
EPA, 2014c, section 4.2), much of the recent evidence for such 
associations is based on studies that defined long-term O3 
in terms of seasonal averages of daily maximum 1-hour or 8-hour 
concentrations.
    As an initial consideration, the Administrator notes the risk 
results from the HREA for respiratory mortality associated with long-
term O3 concentrations. These HREA analyses indicate that as 
air quality is adjusted to just meet the current 8-hour standard, most 
urban study areas are estimated to experience reductions in respiratory 
mortality associated with long-term O3 concentrations based 
on the seasonal averages of 1-hour daily maximum O3 
concentrations evaluated in the study by Jerrett et al. (2009) (U.S. 
EPA, 2014a, chapter 7).\120\ As air quality is adjusted to meet lower 
alternative standard levels, for standards based on 3-year averages of 
the annual fourth-highest daily maximum 8-hour O3 
concentrations, respiratory mortality risks are estimated to be reduced 
further in urban study areas. This analysis indicates that an 
O3 standard with an 8-hour averaging time, when coupled with 
an appropriate form and level, can reduce respiratory mortality 
reported to be associated with long-term O3 concentrations.
---------------------------------------------------------------------------

    \120\ Though the Administrator also notes important 
uncertainties associated with these risk estimates, as discussed 
above (II.C.3.b).
---------------------------------------------------------------------------

    In further considering the study by Jerrett et al. (2009), the 
Administrator notes the PA comparison of long-term O3 
concentrations following model adjustment in urban study areas (i.e., 
adjusted to meet the current and alternative 8-hour standards) to the 
concentrations present in study cities that provided the basis for the 
positive and statistically significant association with respiratory 
mortality. As indicated in Table 4-3 of the PA (U.S. EPA, 2014c, 
section 4.2), this comparison suggests that a standard with an 8-hour 
averaging time can decrease seasonal averages of 1-hour daily maximum 
O3 concentrations, and can maintain those O3 
concentrations below the seasonal average concentration where the study 
indicates the most confidence in the reported concentration-response 
relationship with respiratory mortality (U.S. EPA, 2014c, sections 4.2 
and 4.4.1).
    The Administrator also notes that the HREA conducted analyses 
evaluating the impacts of reducing regional NOX emissions on 
the seasonal averages of daily maximum 8-hour O3 
concentrations. Seasonal averages of 8-hour daily max O3 
concentrations reflect long-term metrics that have been reported to be 
associated with respiratory morbidity effects in several recent 
O3 epidemiologic studies (e.g., Islam et al., 2008; Lin et 
al., 2008; Salam et al., 2009). The HREA analyses indicate that the 
large majority of the U.S. population lives in locations where reducing 
NOX emissions would be expected to result in decreases in 
seasonal averages of daily max 8-hour ambient O3 
concentrations (U.S. EPA, 2014a, chapter 8). Thus, consistent with the 
respiratory mortality risk estimates noted above, these analyses 
suggest that reductions in O3 precursor emissions in order 
to meet a standard with an 8-hour averaging time would also be expected 
to reduce the long-term O3 concentrations that have been 
reported in recent epidemiologic studies to be associated with 
respiratory morbidity.
c. Administrator's Proposed Conclusion on Averaging Time
    Taken together, the Administrator notes that the analyses 
summarized above indicate that a standard with an 8-hour averaging 
time, coupled with the current 4th high form and an appropriate level, 
would be expected to provide appropriate protection against the short- 
and long-term O3 concentrations that have been reported to 
be associated with respiratory morbidity and mortality. The CASAC 
agreed with this conclusion, stating that ``[t]he current 8-hour 
averaging time is justified by the combined evidence from epidemiologic 
and clinical studies'' and that ``[t]he 8-hour averaging window also 
provides protection against the adverse impacts of long-term ozone 
exposures, which were found to be ``likely causal'' for respiratory 
effects and premature mortality'' (Frey, 2014c, p. 6). Therefore, 
considering the available evidence and exposure risk information, and 
CASAC's advice, the Administrator proposes to retain the current 8-hour 
averaging time, and not to set an additional standard with a different 
averaging time.
3. Form
    The ``form'' of a standard defines the air quality statistic that 
is to be compared to the level of the standard in determining whether 
an area attains that standard. The foremost consideration in selecting 
a form is the adequacy of the public health protection provided by the 
combination of the form and the other elements of the standard. In this 
review, the Administrator considers the extent to which the available 
evidence and/or information continue to support the appropriateness of 
a standard with the current form, defined by the 3-year average of 
annual 4th-highest 8-hour daily maximum O3 concentrations.
    The EPA established the current form of the primary O3 
NAAQS in 1997 (62 FR 38856). Prior to that time, the standard had a 
``1-expected-exceedance'' form.\121\ An advantage of the current 
concentration-based form recognized in the 1997 review is that

[[Page 75294]]

such a form better reflects the continuum of health effects associated 
with increasing ambient O3 concentrations. Unlike an 
expected exceedance form, a concentration-based form gives 
proportionally more weight to years when 8-hour O3 
concentrations are well above the level of the standard than years when 
8-hour O3 concentrations are just above the level of the 
standard.\122\ It was judged appropriate to give more weight to higher 
O3 concentrations, given that available health evidence 
indicated a continuum of effects associated with exposures to varying 
concentrations of O3, and given that the extent to which 
public health is affected by exposure to ambient O3 is 
related to the actual magnitude of the O3 concentration, not 
just whether the concentration is above a specified level.
---------------------------------------------------------------------------

    \121\ For a standard with a 1-expected-exceedance form to be met 
at an air quality monitoring site, the fourth-highest air quality 
value in 3 years, given adjustments for missing data, must be less 
than or equal to the level of the standard.
    \122\ As discussed (61 FR 65731), this is because with an 
exceedance-based form, days on which the ambient O3 
concentration is well above the level of the standard are given 
equal weight to those days on which the O3 concentration 
is just above the standard (i.e., each day is counted as one 
exceedance), even though the public health impact of such days would 
be very different. With a concentration-based form, days on which 
higher O3 concentrations occur would weigh proportionally 
more than days with lower O3 concentrations since the 
actual concentrations are used directly to calculate whether the 
standard is met or violated.
---------------------------------------------------------------------------

    During the 1997 review, the EPA considered a range of alternative 
``concentration-based'' forms, including the second-, third-, fourth- 
and fifth-highest daily maximum 8-hour concentrations in an 
O3 season. The fourth-highest daily maximum was selected, 
recognizing that a less restrictive form (e.g., fifth highest) would 
allow a larger percentage of sites to experience O3 peaks 
above the level of the standard, and would allow more days on which the 
level of the standard may be exceeded when the site attains the 
standard (62 FR 38856). Consideration was also given to setting a 
standard with a form that would provide a margin of safety against 
possible but uncertain chronic effects, and would provide greater 
stability to ongoing control programs.\123\ A more restrictive form was 
not selected, recognizing that the differences in the degree of 
protection afforded by the alternatives were not well enough understood 
to use any such differences as a basis for choosing the most 
restrictive forms (62 FR 38856).
---------------------------------------------------------------------------

    \123\ See American Trucking Assn's v. EPA, 283 F. 3d at 374-75 
(less stable implementation programs may be less effective, and 
therefore the EPA can consider programmatic stability in determining 
the form of a NAAQS).
---------------------------------------------------------------------------

    In the 2008 review, the EPA additionally considered the potential 
value of a percentile-based form. In doing so, the EPA recognized that 
such a statistic is useful for comparing datasets of varying length 
because it samples approximately the same place in the distribution of 
air quality values, whether the dataset is several months or several 
years long. However, the EPA concluded that a percentile-based 
statistic would not be effective in ensuring the same degree of public 
health protection across the country. Specifically, a percentile-based 
form would allow more days with higher air quality values in locations 
with longer O3 seasons relative to places with shorter 
O3 seasons. Thus, in the 2008 review, the EPA concluded that 
a form based on the nth-highest maximum O3 concentration 
would more effectively ensure that people who live in areas with 
different length O3 seasons receive the same degree of 
public health protection.
    Based on analyses of forms specified in terms of an nth-highest 
concentration (n ranged from 3 to 5), advice from CASAC, and public 
comment,\124\ the Administrator concluded that a 4th-highest daily 
maximum should be retained (73 FR 16465, March 27, 2008). In reaching 
this decision, the Administrator recognized that ``there is not a clear 
health-based threshold for selecting a particular nth-highest daily 
maximum form of the standard'' and that ``the adequacy of the public 
health protection provided by the combination of the level and form is 
a foremost consideration'' (73 FR 16475, March 27, 2008). Based on 
this, the Administrator judged that the existing form (4th-highest 
daily maximum 8-hour average concentration) should be retained, 
recognizing the increase in public health protection provided by 
combining this form with a lower standard level (i.e., 75 ppb).
---------------------------------------------------------------------------

    \124\ In the 2008 review, one group of commenters expressed the 
view that the standard was not adequate and supported a more health-
protective form (e.g., a second- or third-highest daily max form). 
Another group of commenters expressed the view that the standard was 
adequate and did not provide any views on alternative forms that 
would be appropriate should the Administrator consider revisions to 
the standard. The Administrator considered the protection afforded 
by the combination of level and form in revising the standard in 
2008 to 75 ppb, as a 3-year average of the annual fourth-highest 
daily max 8-hour concentrations (73 FR 16475, March 27, 2008).
---------------------------------------------------------------------------

    The Administrator also recognized that it is important to have a 
form that provides stability with regard to implementation of the 
standard. In the case of O3, for example, he noted the 
importance of a form insulated from the impacts of the meteorological 
events that are conducive to O3 formation. Such events could 
have the effect of reducing public health protection, to the extent 
they result in frequent shifts in and out of attainment due to 
meteorological conditions. The Administrator noted that such frequent 
shifting could disrupt an area's ongoing implementation plans and 
associated control programs (73 FR 16474, March 27, 2008). In his final 
decision, the Administrator judged that a 4th high form ``provides a 
stable target for implementing programs to improve air quality'' (73 FR 
16475, March 27, 2008).
    In the current review, the Administrator considers the extent to 
which newly available information provides support for the current 
form. In so doing, she takes note of the conclusions of prior reviews 
summarized above. She recognizes the value of an nth-high statistic 
over that of an expected exceedance or percentile-based form in the 
case of the O3 standard, for the reasons summarized above. 
The Administrator additionally takes note of the importance of 
stability in implementation to achieving the level of protection 
specified by the NAAQS. Specifically, she notes that to the extent 
areas engaged in implementing the O3 NAAQS frequently shift 
from meeting the standard to violating the standard, it is possible 
that ongoing implementation plans and associated control programs could 
be disrupted, thereby reducing public health protection.
    In light of this, while giving foremost consideration to the 
adequacy of public health protection provided by the combination of all 
elements of the standard, including the form, the Administrator 
considers particularly findings from prior reviews with regard to the 
use of the nth-high metric. As noted above, the 4th-highest daily 
maximum was selected in recognition of the public health protection 
provided by this form, when coupled with an appropriate averaging time 
and level, and recognizing that such a form can provide stability for 
implementation programs. The Administrator concludes that the currently 
available evidence and information do not call into question these 
conclusions from previous reviews. In reaching this conclusion, the 
Administrator notes that CASAC concurred that the O3 
standard should be based on the fourth highest, daily maximum 8-hour 
average value (averaged over 3 years), stating that this form 
``provides health protection while allowing for atypical meteorological 
conditions that can lead to abnormally high ambient ozone 
concentrations which, in turn, provides programmatic stability'' (Frey, 
2014c, p. 6). Thus, a standard with the current 4th high form, coupled 
with a level lower than 75 ppb

[[Page 75295]]

as discussed below, would be expected to increase public health 
protection relative to the current standard while continuing to provide 
stability for implementation programs. Therefore, the Administrator 
proposes to retain the current 4th-highest daily maximum form for an 
O3 standard with an 8-hour averaging time and a revised 
level, as discussed below.
4. Level
    The Administrator next considers the extent to which alternative 
levels below 75 ppb could provide greater protection than the current 
primary standard against short- and long- term exposures to 
O3 in ambient air, for a standard based on the 3-year 
average of the annual 4th highest daily maximum 8-hour O3 
concentration. In doing so, she particularly notes the evidence-based 
and exposure-/risk-based considerations in the PA, which take into 
account the experimental and epidemiologic evidence as assessed in the 
ISA; quantitative estimates of O3 exposures and health risks 
in at-risk populations provided by the HREA; uncertainties and 
limitations associated with this evidence and information; CASAC 
advice; and public input (U.S. EPA, 2014c, sections 4.4 and 4.5). 
Section II.E.4.a below summarizes the PA's approach to considering the 
scientific evidence and the exposure/risk information related to level 
of the primary standard. Section II.E.4.b presents the PA's conclusions 
on alternative primary O3 standard levels. Section II.E.4.c 
summarizes CASAC advice on the level of the primary standard, and 
public input received thus far. Section II.E.4.d presents the 
Administrator's proposed conclusions on primary O3 standard 
levels.
a. PA Approach to Considering the Evidence and Information Related to 
Alternative Levels of the Primary Standard
    The PA's approach to reaching conclusions on alternative standard 
levels focuses on the evidence from controlled human exposure and 
epidemiologic studies, as assessed in the ISA (U.S. EPA, 2013a), and 
the exposure and health risk analyses presented in the HREA (U.S. EPA, 
2014a). This approach is discussed in detail in Chapters 1 and 4 of the 
PA (U.S. EPA, 2014c, sections 1.3, 4.6), and is summarized below.
    As an initial matter, the PA notes that controlled human exposure 
studies provide the most certain evidence indicating the occurrence of 
health effects in humans following exposures to specific O3 
concentrations. Consistent with this, CASAC concluded that ``the 
scientific evidence supporting the finding that the current standard is 
inadequate to protect public health is strongest based on the 
controlled human exposure studies of respiratory effects'' (Frey, 
2014c, p. 5). As discussed above and in section 3.1.2.1 of the PA (U.S. 
EPA, 2014c), controlled human exposure studies have reported a variety 
of respiratory effects in healthy adults following exposures to 
O3 concentrations of 60, 72,\125\ or 80 ppb, and higher.
---------------------------------------------------------------------------

    \125\ As noted above, for the 70 ppb exposure concentration 
Schelegle et al. (2009) reported that the actual 6.6-hour mean 
exposure concentration was 72 ppb.
---------------------------------------------------------------------------

    Given the evidence for respiratory effects from controlled human 
exposure studies, the PA considers the extent to which standards with 
revised levels would be estimated to protect at-risk populations 
against exposures of concern to O3 concentrations at or 
above the health benchmark concentrations of 60, 70, and 80 ppb (i.e., 
based on HREA estimates of one or more and two or more exposures of 
concern). In doing so, the PA notes the CASAC conclusion that (Frey, 
2014c, p. 6):

The 80 ppb-8hr benchmark level represents an exposure level for 
which there is substantial clinical evidence demonstrating a range 
of ozone-related effects including lung inflammation and airway 
responsiveness in healthy individuals. The 70 ppb-8hr benchmark 
level reflects the fact that in healthy subjects, decreases in lung 
function and respiratory symptoms occur at concentrations as low as 
72 ppb and that these effects almost certainly occur in some people, 
including asthmatics and others with low lung function who are less 
tolerant of such effects, at levels of 70 ppb and below. The 60 ppb-
8hr benchmark level represents the lowest exposure level at which 
ozone-related effects have been observed in clinical studies of 
healthy individuals.

    The PA also notes that, due to individual variability in 
responsiveness, only a subset of people who experience exposures at or 
above the three benchmark concentrations can be expected to experience 
associated health effects, and that available data are not sufficient 
to quantify that subset of people for most of the endpoints that have 
been evaluated in controlled human exposure studies (i.e., with the 
exception of FEV1 decrements). The PA views the health 
effects evidence as a continuum with greater confidence and less 
uncertainty about the occurrence of adverse health effects at higher 
O3 exposure concentrations, and less confidence and greater 
uncertainty as one considers lower exposure concentrations (U.S. EPA, 
2014c, section 3.2.2, p. 3-101).
    While there is greater uncertainty regarding the occurrence of 
adverse health effects at lower concentrations, the PA also notes that 
the controlled human exposure studies that provided the basis for 
benchmark concentrations have not evaluated responses in populations at 
the greatest risk from exposures to O3 (e.g., children, 
people with asthma). Compared to the healthy people included in most 
controlled human exposure studies, members of at-risk populations and 
lifestages are at greater risk of experiencing adverse effects. Thus, 
the effects reported in healthy adults at each of the benchmark 
concentrations may underestimate effects in these at-risk groups. In 
considering the health evidence within the context of drawing 
conclusions on alternative standard levels, the PA balances concerns 
about the potential for adverse health effects, especially in at-risk 
populations, with the increasing uncertainty regarding the likelihood 
of such effects following exposures to lower O3 
concentrations.
    With respect to the lung function decrements that have been 
evaluated in controlled human exposure studies, the PA considers the 
extent to which standards with revised levels would be estimated to 
protect healthy and at-risk populations against O3-induced 
lung function decrements large enough to be adverse in some people 
(based on quantitative risk estimates in the HREA). As discussed in 
section 3.1.3 of the PA (U.S. EPA, 2014c) and section II.B.3 above, 
although some experts would judge single occurrences of moderate 
responses to be a nuisance, especially for healthy individuals, a more 
general consensus view of the adversity of moderate lung function 
decrements emerges as the frequency of occurrence increases. Repeated 
occurrences of moderate responses, even in otherwise healthy 
individuals, may be considered to be adverse, since they could well set 
the stage for more serious illness (73 FR 16448). In reaching 
conclusions on alternative standard levels, the PA considers the extent 
to which standards with revised levels would be estimated to protect 
healthy and at-risk populations against one or more, and two or more, 
moderate (i.e., FEV1 decrements >=10% and >=15%) and large 
(i.e., FEV1 decrements >=20%) lung function decrements.
    In evaluating the epidemiologic evidence within the context of 
drawing conclusions on alternative standard levels, the PA considers 
the extent to which available studies have reported associations with 
emergency

[[Page 75296]]

department visits, hospital admissions, and/or mortality in locations 
that would likely have met alternative standards with levels below 75 
ppb. In evaluating the epidemiologic evidence in this way, the PA 
considers both multicity and single-city studies, recognizing the 
strengths and limitations of each. In particular, while single-city 
studies are more limited than multicity studies in terms of statistical 
power and geographic coverage, conclusions linking air quality in a 
specific area with health effect associations in that same area can be 
made with greater certainty for single-city studies (i.e., compared to 
multicity studies reporting only multicity effect estimates).
    The PA also considers the epidemiologic evidence within the context 
of epidemiology-based risk estimates. Compared to the weight given to 
HREA estimates of exposures of concern and lung function risks, and the 
weight given to the evidence, the PA places relatively less weight on 
epidemiologic-based risk estimates. In doing so, the PA notes that the 
overall conclusions from the HREA likewise reflect less confidence in 
estimates of epidemiologic-based risks than in estimates of exposures 
and lung function risks. The determination to attach less weight to the 
epidemiologic-based estimates reflects the uncertainties associated 
with mortality and morbidity risk estimates, including the 
heterogeneity in effect estimates between locations, the potential for 
exposure measurement errors, and uncertainty in the interpretation of 
the shape of concentration-response functions at lower O3 
concentrations (U.S. EPA, 2014a, section 9.6). The HREA also concludes 
that lower confidence should be placed in the results of the assessment 
of respiratory mortality risks associated with long-term O3 
exposures, primarily because that analysis is based on only one study 
(even though that study is well-designed) and because of the 
uncertainty in that study about the existence and level of a potential 
threshold in the concentration-response function (U.S. EPA, 2014a, 
section 9.6).
    In considering the epidemiology-based risk estimates, the PA 
focuses on the extent to which potential alternative O3 
standards with levels below 75 ppb are estimated to reduce the risk of 
O3-associated mortality.\126\ As discussed for the current 
standard (II.D.2.c), the PA considers estimates of total risk (i.e., 
based on the full distributions of ambient O3 
concentrations) and estimates of risk associated with O3 
concentrations in the upper portions of ambient distributions.
---------------------------------------------------------------------------

    \126\ Differences in estimated respiratory morbidity risks 
between alternative standard levels are similar to the differences 
estimated for total mortality associated with short-term 
O3 concentrations.
---------------------------------------------------------------------------

b. PA Conclusions on Alternative O3 Standard Levels
    Using the approach discussed above to consider the scientific 
evidence and exposure/risk information, CASAC advice (II.E.4.c, below), 
and public comments, the PA reaches the conclusion that it is 
appropriate for the Administrator to consider alternative primary 
O3 standard levels from 70 to 60 ppb. The basis for this 
conclusion is discussed in detail in sections 4.4.1 and 4.4.2 of the PA 
(U.S. EPA, 2014c), and is summarized below.
    With regard to controlled human exposure studies, the PA considers 
the lowest O3 exposure concentrations at which various 
effects have been evaluated and statistically significant effects 
reported. The PA also considers the potential for reported effects to 
be adverse, including in at-risk populations and lifestages. As 
discussed in section 3.1.2.1 of the PA (U.S. EPA, 2014c), controlled 
human exposure studies provide evidence of respiratory symptoms 
combined with lung function decrements (an adverse response based on 
ATS criteria) in healthy adults following 6.6 hour exposures to 
O3 concentrations as low as 72 ppb, and evidence of 
potentially adverse lung function decrements and airway inflammation 
following 6.6 hour exposures to O3 concentrations as low as 
60 ppb.
    Although some studies show that respiratory symptoms also develop 
during exposures to 60 ppb O3, the increase in symptoms has 
not been reported to reach statistical significance by the end of the 
6.6 hour exposure period (Adams, 2006; Schelegle et al., 2009). Thus, 
while significant increases in respiratory symptoms combined with lung 
function decrements have not been reported following exposures to 60 
ppb O3, this combination of effects is likely to occur to 
some degree in healthy adults with 6.6-hour exposures to concentrations 
below 72 ppb, and also are more likely to occur with longer (i.e., 8-
hour) exposures.\127\ In addition, pulmonary inflammation, particularly 
if experienced repeatedly, provides a mechanism by which O3 
may cause other more serious respiratory morbidity effects (e.g., 
asthma exacerbations) and possibly extrapulmonary effects. As discussed 
in section 3.1.2.1 of the PA (U.S. EPA, 2014c), the physiological 
effects reported in controlled human exposure studies down to 60 ppb 
O3 have been linked to aggravation of asthma and increased 
susceptibility to respiratory infection, potentially leading to 
increased medication use, increased school and work absences, increased 
visits to doctors' offices and emergency departments, and increased 
hospital admissions.
---------------------------------------------------------------------------

    \127\ In addition, CASAC observed that, ``adverse health effects 
in young healthy adults occur with exposures to 72 ppb of ozone for 
6.6 hours'' and that ``[i]t is the judgment of CASAC that if 
subjects had been exposed to ozone using the 8-hour averaging period 
used in the standard, adverse effects could have occurred at [a] 
lower concentration. Further, in our judgment, the level at which 
adverse effects might be observed would likely be lower for more 
sensitive subgroups, such as those with asthma'' (Frey, 2014c, p. 
5).
---------------------------------------------------------------------------

    With regard to the lowest exposure concentration shown to cause 
respiratory effects (i.e., 60 ppb),\128\ the PA notes that most 
controlled human exposure studies have not evaluated O3 
concentrations below 60 ppb. Therefore, 60 ppb does not necessarily 
reflect an exposure concentration below which effects such as lung 
function decrements and airway inflammation no longer occur. This is 
particularly the case given that controlled human exposure studies were 
conducted in healthy adults, while people with asthma, including 
asthmatic children, are likely to be more sensitive to O3-
induced respiratory effects.
---------------------------------------------------------------------------

    \128\ As discussed above (II.B.2), prolonged 6.6 exposure to 40 
ppb O3 has been shown to result in a small decrease in 
group mean FEV1 that is not statistically different from 
responses following exposure to filtered air (Adams, 2002; Adams, 
2006).
---------------------------------------------------------------------------

    With regard to other O3-induced effects, the PA notes 
that AHR and impaired lung host defense capabilities have been reported 
in healthy adults engaged in moderate exertion following exposures to 
O3 concentrations as low as 80 ppb, the lowest concentration 
evaluated for these effects. As discussed in section 3.1.2.1 of the PA 
(U.S. EPA, 2014c), these physiological effects have been linked to 
aggravation of asthma and increased susceptibility to respiratory 
infection, potentially leading to increased medication use, increased 
school and work absences, increased visits to doctors' offices and 
emergency departments, and increased hospital admissions. These are all 
indicators of adverse O3-related morbidity effects, which 
are consistent with, and provide plausibility for, the adverse 
morbidity effects and mortality effects observed in epidemiologic 
studies.
    Based on consideration of the above evidence, the PA concludes that 
available controlled human exposure studies support considering 
alternative O3 standard levels from 70 to 60 ppb in

[[Page 75297]]

the current review. In reaching this conclusion, the PA notes that 70 
ppb is just below the O3 exposure concentration reported to 
result in lung function decrements and respiratory symptoms in healthy 
adults (i.e., 72 ppb), a combination of effects that meet ATS criteria 
for an adverse response. In addition, while 70 ppb is well below the 80 
ppb exposure concentration shown to cause potentially adverse 
respiratory effects such as AHR and impaired host-defense capabilities, 
these effects have not been evaluated at exposure concentrations below 
80 ppb and there is no reason to believe that 80 ppb represents a 
threshold for such effects. In addition, potentially adverse lung 
function decrements and pulmonary inflammation have been demonstrated 
to occur in healthy adults at 60 ppb. Thus, 60 ppb is a short-term 
exposure concentration that may be reasonably concluded to elicit 
adverse effects in at-risk groups.
    The PA further notes that the range of alternative levels from 70 
to 60 ppb is supported by evidence from epidemiologic studies and by 
exposure and risk estimates from the HREA. This evidence and exposure/
risk information indicate that a level from anywhere in the range of 70 
to 60 ppb would be expected to result in important public health 
improvements over the current standard. In particular, compared to the 
current standard a revised standard with a level from 70 to 60 ppb 
would be expected to (1) more effectively maintain short- and long-term 
O3 concentrations below those present in the epidemiologic 
studies that reported significant O3 health effect 
associations in locations likely to have met the current standard; (2) 
reduce the occurrence of exposures of concern to O3 
concentrations that result in respiratory effects in healthy adults (at 
or above 60, 70, and 80 ppb); (3) reduce the occurrence of moderate-to-
large O3-induced lung function decrements; and (4) reduce 
the risk of O3-associated mortality and morbidity, 
particularly the risk associated with the upper portions of the 
distributions of ambient O3 concentrations. The PA also 
notes that the range of levels from 70 to 60 ppb corresponds to the 
range of levels recommended for consideration by CASAC, based on the 
available evidence and information (Frey, 2014a; Frey, 2014c).
    In reaching a conclusion on whether it is appropriate to consider 
alternative standard levels below 60 ppb, the PA notes the following:

    (1) While controlled human exposure studies provide evidence for 
O3-induced respiratory effects following exposures to 
O3 concentrations as low as 60 ppb, they do not provide 
evidence for adverse effects following exposures to lower 
concentrations. On this issue, CASAC concurred that 60 ppb 
O3 is an appropriate and justifiable scientifically based 
lower bound for a revised primary standard, based upon findings of 
``adverse effects, including clinically significant lung function 
decrements and airway inflammation, after exposures to 60 ppb ozone 
in healthy adults with moderate exertion (Adams, 2006; Schelegle et 
al., 2009; Brown et al., 2008; Kim et al., 2011), with limited 
evidence of adverse effects below 60 ppb'' (Frey, 2014c, p. 7).
    (2) Based on the HREA results, meeting an O3 standard 
with a level of 60 ppb would be expected to almost eliminate 
exposures of concern to O3 concentrations at or above 60 
ppb. To the extent lower exposure concentrations may result in 
adverse health effects in some people, a standard level of 60 ppb 
would be expected to also reduce exposures to O3 
concentrations below 60 ppb.
    (3) U.S. and Canadian epidemiologic studies have not reported 
O3 health effect associations based primarily on study 
locations likely to have met a standard with a level of 60 ppb.
    (4) In all of the urban study areas evaluated, a standard with a 
level of 60 ppb would be expected to maintain long-term 
O3 concentrations below those where a key study indicates 
the most confidence in a linear concentration-response relationship 
with respiratory mortality.

    Given all of the above considerations the PA concludes that, 
compared to standards with levels from 70 to 60 ppb, the extent to 
which standards with levels below 60 ppb could result in further public 
health improvements becomes notably less certain. Therefore, the PA 
concludes that it is not appropriate in this review to consider 
standard levels below 60 ppb.
    The following sections summarize the PA's consideration of the 
scientific evidence and exposure/risk information specifically related 
to potential alternative O3 standards with levels from the 
upper (70 ppb) (II.E.4.c.i), middle (65 ppb) (II.E.4.c.ii), and lower 
(60 ppb) (II.E.4.c.iii) portions of the range of 70 to 60 ppb. Key 
exposure/risk information considered in the PA is summarized in Tables 
4 and 5, below (from U.S. EPA, 2014c, Tables 4-4 and 4-5).
---------------------------------------------------------------------------

    \129\ All alternative standard levels evaluated in the HREA were 
effective at limiting exposures of concern at or above 80 ppb (U.S. 
EPA, 2014c, Figures 4-1 to 4-4). Therefore, Table 4 focuses on 
exposures of concern at or above the 70 and 60 ppb benchmark 
concentrations.
    \130\ Estimates for each urban case study area were averaged for 
the years evaluated in the HREA (2006 to 2010). Ranges reflect the 
ranges across urban study areas.
    \131\ Numbers of children exposed in each urban case study area 
were averaged over the years 2006 to 2010. These averages were then 
summed across urban study areas. Numbers are rounded to nearest 
thousand unless otherwise indicated.
    \132\ As noted in section II.C.3.a.ii, the responsiveness of 
asthmatics to O3 exposures could depend on factors that 
have not been well-evaluated such as asthma severity, the 
effectiveness of asthma control, or the prevalence of medication 
use.
    \133\ Percent reductions in each urban study area were 
calculated and averaged across areas.
    \134\ Estimates smaller than 0.05% were rounded to zero.
    \135\ As discussed in section 4.3.3 of the HREA (U.S. EPA, 
2014a), the model-based air quality adjustment approach used to 
estimate risks associated with the current and alternative standards 
was unable to estimate the distribution of ambient O3 
concentrations in New York City upon just meeting an alternative 
standard with a level of 60 ppb. Therefore, for the 60 ppb standard 
level the numbers of children and asthmatic children reflect all of 
the urban study areas except New York.

  Table 4--Summary of Estimated Exposures of Concern for Potential Alternative O3 Standard Levels of 70, 65, 60
                                       ppb in Urban Case Study Areas \129\
----------------------------------------------------------------------------------------------------------------
                                                            Number of children
                             Alternative      Average %       (5 to 18 years)       Average %      % Children--
     Benchmark level       standard level     children     [number of asthmatic  reduction from   worst year and
                                (ppb)       exposed \130\     children] \131\        current        worst area
                                                                   \132\         standard \133\
----------------------------------------------------------------------------------------------------------------
                                   One or more exposures of concern per season
----------------------------------------------------------------------------------------------------------------
>=70 ppb.................              70         0.1-1.2  94,000 [10,000].....              73              3.2
                                       65           0-0.2  14,000 [2,000]......              95              0.5
                                       60         \134\ 0  1,400 [200] \135\...             100              0.1
>=60 ppb.................              70        3.3-10.2  1,176,000 [126,000].              46             18.9
                                       65           0-4.2  392,000 [42,000]....              80              9.5

[[Page 75298]]

 
                                       60           0-1.2  70,000 [8,000]......              96              2.2
----------------------------------------------------------------------------------------------------------------
                                   Two or more exposures of concern per season
----------------------------------------------------------------------------------------------------------------
>=70 ppb.................              70           0-0.1  5,400 [600].........              95              0.4
                                       65               0  300 [100]...........             100                0
                                       60               0  0 [0]...............             100                0
>=60 ppb.................              70         0.5-3.5  320,000 [35,000]....              61              9.2
                                       65           0-0.8  67,000 [7,500]......              92              2.8
                                       60           0-0.2  5,100 [700].........             100              0.3
----------------------------------------------------------------------------------------------------------------

     
---------------------------------------------------------------------------

    \136\ Estimates in each urban case study area were averaged for 
the years evaluated in the HREA (2006 to 2010). Ranges reflect the 
ranges across urban study areas.
    \137\ Numbers of children estimated to experience decrements in 
each urban case study area were averaged over 2006 to 2010. These 
averages were then summed across urban study areas. Numbers are 
rounded to nearest thousand unless otherwise indicated.
    \138\ As noted in section II.C.3.a.ii, the responsiveness of 
asthmatics to O3 exposures could depend on factors that 
have not been well-evaluated such as asthma severity, the 
effectiveness of asthma control, or the prevalence of medication 
use.
    \139\ As discussed in section 4.3.3 of the HREA (U.S. EPA, 
2014a), the model-based air quality adjustment approach used to 
estimate risks associated with the current and alternative standards 
was unable to estimate the distribution of ambient O3 
concentrations in New York City upon just meeting an alternative 
standard with a level of 60 ppb. Therefore, for the 60 ppb standard 
level the numbers of children and asthmatic children reflect all of 
the urban study areas except New York.

 Table 5--Summary of Estimated Lung Function Decrements for Potential Alternative O3 Standard Levels of 70, 65,
                                      and 60 ppb in Urban Case Study Areas
----------------------------------------------------------------------------------------------------------------
                                                             Number of children
                                                               (5 to 18 years)       Average %      % Children
  Lung function decrement     Alternative      Average %    [number of asthmatic  reduction from  worst year and
                            standard level  children \136\     children] \137\        current          area
                                                                    \138\            standard
----------------------------------------------------------------------------------------------------------------
                                        One or more decrements per season
----------------------------------------------------------------------------------------------------------------
>=10%.....................              70           11-17  2,527,000 [261,000].              15              20
                                        65            3-15  1,896,000 [191,000].              31              18
                                        60            5-11  1,404,000 [139,000]               45              13
                                                             \139\.
>=15%.....................              70             2-4  562,000 [58,000]....              26               5
                                        65             0-3  356,000 [36,000]....              50               4
                                        60             1-2  225,000 [22,000]....              67               3
>=20%.....................              70             1-2  189,000 [20,000]....              32             2.1
                                        65             0-1  106,000 [11,000]....              59             1.4
                                        60             0-1  57,000 [6,000]......              77             0.7
----------------------------------------------------------------------------------------------------------------
                                        Two or more decrements per season
----------------------------------------------------------------------------------------------------------------
>=10%.....................              70          5.5-11  1,414,000 [145,000].              17              13
                                        65         1.3-8.8  1,023,000 [102,000].              37              11
                                        60         2.1-6.4  741,000 [73,000]....              51             7.3
>=15%.....................              70         0.9-2.4  276,000 [28,000]....              29             3.1
                                        65         0.1-1.8  168,000 [17,000]....              54             2.3
                                        60         0.2-1.0  101,000 [10,000]....              71             1.4
>=20%.....................              70         0.3-0.8  81,000 [8,000]......              34             1.1
                                        65           0-0.5  43,000 [4,000]......              66             0.8
                                        60           0-0.2  21,000 [2,000]......              83             0.4
----------------------------------------------------------------------------------------------------------------

i. PA Consideration of an O3 Standard Level of 70 ppb
    The PA notes that a level of 70 ppb is below the lowest 
O3 exposure concentration that has been reported to elicit a 
range of respiratory effects that includes AHR and decreased lung host 
defense, in addition to lung function decrements, airway inflammation, 
and respiratory symptoms (i.e., 80 ppb). A level of 70 ppb is also 
below the lowest exposure concentration at which the combined 
occurrence of respiratory symptoms and lung function decrements have 
been reported (i.e., 72 ppb), a combination judged adverse by the ATS 
(U.S. EPA, 2014c, section 3.1.3). A level of 70 ppb is above the lowest 
exposure concentration demonstrated to result in lung function 
decrements large enough to be judged an abnormal response by ATS and 
above the lowest exposure concentration demonstrated to result in 
pulmonary inflammation (i.e., 60 ppb).
    Compared to the current standard, the HREA estimates that a revised 
O3

[[Page 75299]]

standard with a level of 70 ppb would reduce exposures of concern to 
O3 concentrations of 60, 70, and 80 ppb in urban study 
areas, with such a standard level estimated to be most effective at 
limiting exposures at or above the higher health benchmark 
concentrations and at limiting multiple occurrences of such exposures. 
On average over the years 2006 to 2010, for a standard with a level of 
70 ppb, up to about 1% of children (i.e., ages 5 to 18) are estimated 
to experience exposures of concern at or above 70 ppb (73% reduction, 
compared to current standard), and far less than 1% are estimated to 
experience two or more such exposures (95% reduction, compared to 
current standard). In the worst-case location and year (i.e., location 
and year with the largest exposure estimate), about 3% of children are 
estimated to experience one or more exposures of concern at or above 70 
ppb, and less than 1% are estimated to experience two or more. Far less 
than 1% of children are estimated to experience exposures of concern at 
or above the 80 ppb benchmark concentration, even in the worst-case 
year (Table 4, above).\140\
---------------------------------------------------------------------------

    \140\ As noted above, due to interindividual variability, 
children (or adults) exposed at these levels will not necessarily 
experience health effects; the information available for some health 
effects is not sufficient to quantify the numbers of children in the 
urban study areas who might experience these effects.
---------------------------------------------------------------------------

    As noted above, CASAC advised the EPA that 60 ppb is an appropriate 
exposure of concern with respect to adverse effects on people with 
asthma, including children (Frey, 2014c, pp. 6 and 8). For an 
O3 standard with a level of 70 ppb, about 3 to 10% of 
children, including asthmatic children, are estimated to experience one 
or more exposures of concern at or above 60 ppb in a single 
O3 season. Compared to the current standard, this reflects 
about a 46% reduction, on average across the urban study areas. About 
1% to 4% of children are estimated to experience two or more exposures 
of concern at or above 60 ppb (approximately 60% reduction, compared to 
current standard). In the worst-case location and year, for a standard 
set at 70 ppb, about 19% of children are estimated to experience one or 
more exposures of concern at or above 60 ppb, and 9% are estimated to 
experience two or more such exposures (Table 4, above).
    Compared to the current standard, the HREA estimates that a revised 
O3 standard with a level of 70 ppb would also reduce 
O3-induced lung function decrements in children. A level of 
70 ppb is estimated to be most effective at limiting the occurrences of 
moderate and large lung function decrements (i.e., FEV1 
decrements >=15% and >=20%, respectively), and at limiting multiple 
occurrences of O3-induced decrements. On average over the 
years 2006 to 2010, for a standard with a level of 70 ppb, about 2 to 
4% of children in the urban study areas are estimated to experience one 
or more moderate O3-induced lung function decrements (i.e., 
FEV1 decrement >=15%), which would be of concern for healthy 
people, and about 1 to 2.5% of children are estimated to experience two 
or more such decrements (approximately 30% reduction, compared to the 
current standard). In the worst-case location and year, up to 5% of 
children are estimated to experience one or more O3-induced 
lung function decrements >=15%, and up to 3% are estimated to 
experience two or more such decrements. For a standard set at 70 ppb, 
about 2% or fewer children are estimated to experience large 
O3-induced lung function decrements (i.e., FEV1 
decrement >=20%), and about 1% or fewer children are estimated to 
experience two or more such decrements, even in the worst-case years 
and locations (Table 5, above).
    On average over the years 2006 to 2010, for an O3 
standard set at 70 ppb, about 11 to 17% of children in the urban study 
areas are estimated to experience one or more moderate O3-
induced lung function decrements (i.e., FEV1 decrement 
>=10%), which could be adverse for people with lung disease. This 
reflects an average reduction of about 15%, compared to the current 
standard. About 6 to 11% of children are estimated to experience two or 
more such decrements (17% reduction, compared to current standard). In 
the worst-case location and year, for a standard set at 70 ppb, about 
20% of children in the urban study areas are estimated to experience 
one or more O3-induced lung function decrements >=10%, and 
13% are estimated to experience two or more such decrements (Table 5, 
above).
    Compared to the current standard, a revised standard with a level 
of 70 ppb would also more effectively maintain short-term ambient 
O3 concentrations below those present in the epidemiologic 
studies that reported significant O3 health effect 
associations in locations likely to have met the current standard. In 
particular, the single-city study by Mar and Koenig (2009) reported 
positive and statistically significant associations with respiratory 
emergency department visits in children and adults in a location that 
likely would have met the current O3 standard over the 
entire study period but violated a revised standard with a level of 70 
ppb or below. None of the single-city studies evaluated in section 
4.4.1 of the PA (U.S. EPA, 2014c) provide evidence for O3 
health effect associations in locations meeting a standard with a level 
of 70 ppb or below. While this analysis does not provide information on 
the extent to which the reported O3-associated emergency 
department visits would persist upon meeting an O3 standard 
with a level of 70 ppb, or on the extent to which standard levels below 
70 ppb could further reduce the incidence of such emergency department 
visits,\141\ it suggests that a revised O3 standard with a 
level at or below 70 ppb would require reductions in the ambient 
O3 concentrations that provided the basis for the health 
effect associations reported by Mar and Koenig (2009).
---------------------------------------------------------------------------

    \141\ Put another way, one cannot infer from this analysis the 
extent to which effects would occur at O3 concentrations 
below those observed in the study.
---------------------------------------------------------------------------

    As discussed above, compared to single-city studies, there is 
greater uncertainty in linking air quality concentrations from 
individual study cities to multicity effect estimates. With regard to 
the multicity studies in this review, the PA notes that Dales et al. 
(2006) reported significant associations with respiratory hospital 
admissions based on air quality in 11 Canadian cities, most of which 
would likely have met the current standard over the entire study 
period, but violated a revised standard with a level of 70 ppb or below 
over at least part of that period (Table 4-1). This analysis suggests 
that although the current standard would allow the ambient 
O3 concentrations in most of the study locations that 
provided the basis for the association with hospital admissions, a 
revised O3 standard with a level at or below 70 ppb would 
require reductions in those ambient O3 concentrations. As 
with the study by Mar and Koenig (2009), this analysis does not provide 
information on the extent to which the reported O3-
associated hospital admissions would persist upon meeting an 
O3 standard with a level of 70 ppb, or on the extent to 
which standard levels below 70 ppb could further reduce the incidence 
of such hospital admissions.\142\
---------------------------------------------------------------------------

    \142\ In addition, for the other multicity studies identified in 
Table 4-1 of the PA (Cakmak et al., 2006; Stieb et al., 2009; 
Katsouyanni et al., 2009), and for the study by Bell et al. (2006) 
(for the 30 ppb cut point) (Table 4-2 of the PA), the majority of 
study locations would likely have met a standard with a level of 70 
ppb (U.S. EPA, 2014c).
---------------------------------------------------------------------------

    With regard to long-term O3 concentrations, the PA 
evaluates the long-term O3 metrics reported to be associated 
with mortality or morbidity in recent epidemiologic studies (e.g.,

[[Page 75300]]

seasonal averages of 1-hour or 8-hour daily max concentrations). 
Compared to the current standard, a revised standard with a level of 70 
ppb would be expected to reduce the risk of respiratory mortality 
associated with long-term O3 concentrations, based on 
information from the study by Jerrett et al. (2009), though the PA 
notes the HREA conclusion, discussed above, that lower confidence 
should be placed in respiratory mortality risk estimates based on this 
study (U.S. EPA, 2014a, section 9.6). In addition, a standard with a 
level of 70 ppb would be expected to more effectively maintain long-
term O3 concentrations below those where the study by 
Jerrett et al. (2009) indicates the most confidence in the reported 
association with respiratory mortality.\143\ Specifically, air quality 
analyses indicate this to be the case in 9 out of the 12 urban study 
areas for a level of 70 ppb, compared to 6 out of 12 areas for the 
current standard. Finally, a revised standard with a level of 70 ppb 
would be expected to reduce long-term O3 concentrations 
based on the types of metrics that have been reported in recent 
epidemiologic studies to be associated with respiratory morbidity 
(i.e., seasonal averages of daily maximum 8-hour concentrations).
---------------------------------------------------------------------------

    \143\ As discussed in section 3.1.4.3 of the PA (U.S. EPA, 
2014c), the study by Jerrett et al. (2009) suggests notably 
decreased confidence in the reported linear concentration-response 
function for long-term O3 concentrations in the first 
quartile (i.e., at or below about 53 ppb), given the widening in 
confidence intervals for lower concentrations; the fact that most 
study cities contributing to the linear function had O3 
concentrations in the highest three quartiles, accounting for 
approximately 72% of the respiratory deaths in the cohort (based on 
Table 2 in the published study); and the limited evidence presented 
in the published study for a threshold at or near 56 ppb.
---------------------------------------------------------------------------

    In further considering the potential implications of epidemiology 
studies for alternative standard levels, the PA notes estimates of 
total mortality associated with short-term O3 
concentrations.\144\ As discussed above, the PA considers estimates of 
total risk (i.e., based on the full distributions of ambient 
O3 concentrations) and estimates of risk associated with 
O3 concentrations in the upper portions of ambient 
distributions. With regard to total risk the PA notes that, when summed 
across urban study areas, a standard with a level of 70 ppb is 
estimated to reduce the number of deaths associated with short-term 
O3 concentrations by about 4% (2007) and 2% (2009), compared 
to the current standard.\145\ Based on a national modeling analysis, 
the majority of the U.S. population would be expected to experience 
reductions in such risks upon reducing precursor emissions.
---------------------------------------------------------------------------

    \144\ As discussed above, compared to the weight given to the 
evidence and to HREA estimates of exposures of concern and lung 
function risks, the PA places relatively less weight on 
epidemiologic-based risk estimates.
    \145\ A standard with a level of 70 ppb is also estimated to 
reduce respiratory mortality associated with long-term O3 
concentrations in urban study areas. However, given uncertainties 
associated with these risk estimates, as discussed above, the PA 
gives them limited weight.
---------------------------------------------------------------------------

    Compared to the total risk estimates noted above, an O3 
standard with a level of 70 ppb is estimated to be more effective at 
reducing the number of deaths associated with short-term O3 
concentrations at the upper ends of ambient distributions. 
Specifically, for area-wide O3 concentrations at or above 40 
ppb, a standard with a level of 70 ppb is estimated to reduce the 
number of deaths associated with short-term O3 
concentrations by about 10% compared to the current standard. In 
addition, for area-wide concentrations at or above 60 ppb, a standard 
with a level of 70 ppb is estimated to reduce O3-associated 
deaths by about 50% to 70% (U.S. EPA, 2014c, Figure 4-13).
    The PA noted that in providing the advice that 70 ppb is an 
appropriate upper bound for consideration, CASAC advised that a level 
of 70 ppb would provide little margin of safety for protection of 
public health, particularly for sensitive subpopulations (Frey, 2014c, 
p. 8). In particular, CASAC stated that:

At 70 ppb, there is substantial scientific certainty of a variety of 
adverse effects, including decrease in lung function, increase in 
respiratory symptoms, and increase in airway inflammation. Although 
a level of 70 ppb is more protective of public health than the 
current standard, it may not meet the statutory requirement to 
protect public health with an adequate margin of safety (Frey, 
2014c, p. 8).\146\
---------------------------------------------------------------------------

    \146\ Also see Frey (2014c, p. ii).

However, the committee also acknowledged that ``the choice of a level 
within the range recommended based on scientific evidence [i.e., 70 to 
60 ppb] is a policy judgment under the statutory mandate of the Clean 
Air Act'' (Frey, 2014c, pp. ii and 8).
    In summary, compared to the current standard, the PA concludes that 
a revised O3 standard with a level of 70 ppb would be 
expected to (1) reduce the occurrence of exposures of concern to 
O3 concentrations that result in respiratory effects in 
healthy adults (at or above 60 and 70 ppb) by about 45 to 95%, almost 
eliminating the occurrence of multiple exposures at or above 70 ppb; 
(2) reduce the occurrence of moderate-to-large O3-induced 
lung function decrements (FEV1 decrements >=10, 15, 20%) by 
about 15 to 35%, most effectively limiting the occurrence of multiple 
decrements and decrements >=15, 20%; (3) more effectively maintain 
short- and long-term O3 concentrations below those present 
in the epidemiologic studies that reported significant O3 
health effect associations in locations likely to have met the current 
standard; \147\ and (4) reduce the risk of O3-associated 
mortality and morbidity, particularly the risk associated with the 
upper portions of the distributions of ambient O3 
concentrations.
---------------------------------------------------------------------------

    \147\ Epidemiologic studies also provide some evidence for 
O3 health effect associations in locations likely to have 
met a standard with a level of 70 ppb, as discussed below for lower 
standard levels.
---------------------------------------------------------------------------

ii. PA Consideration of an O3 Standard Level of 65 ppb
    The PA also considers a standard with a level of 65 ppb. A level of 
65 ppb is well below 80 ppb, an O3 exposure concentration 
that has been reported to elicit a range of respiratory effects that 
includes airway hyperresponsiveness and decreased lung host defense, in 
addition to lung function decrements, airway inflammation, and 
respiratory symptoms. A standard level of 65 ppb is also below the 
lowest exposure concentration at which the combined occurrence of 
respiratory symptoms and lung function decrements has been reported 
(i.e., 72 ppb), a combination judged adverse by the ATS (U.S. EPA, 
2014c, section 3.1.3). A level of 65 ppb is above the lowest exposure 
concentration demonstrated to result in lung function decrements large 
enough to be judged an abnormal response by ATS, where statistically 
significant changes in group mean responses would be judged to be 
adverse by ATS, and which the CASAC has indicated could be adverse in 
people with lung disease (i.e., 60 ppb). A level of 65 ppb is also 
above the lowest exposure concentration at which pulmonary inflammation 
has been reported in healthy adults (i.e., 60 ppb).
    Compared to the current standard and a revised standard with a 
level of 70 ppb, the HREA estimates that a standard with a level of 65 
ppb would reduce exposures of concern to the range of O3 
benchmark concentrations analyzed (i.e., 60, 70, and 80 ppb). The HREA 
estimates that meeting a standard with a level of 65 ppb would 
eliminate exposures of concern at or above 80 ppb in the urban study 
areas. Such a standard is estimated to allow far less than 1% of 
children in the urban study areas to experience one or more exposures 
of concern at or above the 70

[[Page 75301]]

ppb benchmark level, even in the worst-case years and locations, and is 
estimated to eliminate the occurrence of two or more exposures at or 
above 70 ppb (Table 4, above).
    In addition, for a standard with a level of 65 ppb, between 0 and 
about 4% of children (including asthmatic children) in urban study 
areas are estimated to experience exposures of concern at or above 60 
ppb, which CASAC has indicated is an appropriate exposure of concern 
for people with asthma, including children. This reflects an 80% 
reduction (on average across areas), relative to the current standard. 
Less than 1% of children are estimated to experience two or more 
exposures of concern at or above 60 ppb (> 90% reduction, compared to 
current standard). In the worst-case location and year, about 10% of 
children are estimated to experience one or more exposures of concern 
at or above 60 ppb, with about 3% estimated to experience two or more 
such exposures (Table 4, above).
    Compared to the current standard and a revised standard with a 
level of 70 ppb, the HREA estimates that a standard with a level of 65 
ppb would also further reduce the occurrence of O3-induced 
lung function decrements. For a level of 65 ppb, about 4% of children, 
or less, are estimated to experience moderate O3-induced 
FEV1 decrements >=15% (50% reduction, compared to current 
standard), even considering the worst-case location and year. About 2% 
of children, or less, are estimated to experience two or more such 
decrements. Only about 1% of children, or less, are estimated to 
experience large O3-induced lung function decrements (i.e., 
FEV1 decrement >=20%), even in the worst-case year and 
location.
    In addition, for a standard with a level of 65 ppb, about 3 to 15% 
of children are estimated to experience one or more moderate 
O3-induced lung function decrements (i.e., FEV1 
decrement >=10%), which CASAC has indicated could be adverse for people 
with lung disease. This reflects an average reduction of about 30%, 
relative to the current standard. About 1 to 9% of children in the 
urban study areas are estimated to experience two or more such 
decrements (37% reduction, compared to current standard). In the worst-
case location and year, for a standard set at 65 ppb, up to about 18% 
of these children are estimated to experience one or more moderate 
O3-induced lung function decrements >=10%, and up to 11% are 
estimated to experience two or more such decrements.
    With regard to O3 epidemiologic studies, the PA notes 
that a revised standard with a level of 65 ppb would be expected to 
maintain short-term ambient O3 concentrations below those 
present in some of the study locations that provided the basis for 
reported O3 health effect associations and that were likely 
to have met a revised standard with a level of 70 ppb. In particular, 
Katsouyanni et al. (2009) reported statistically significant 
associations with mortality based on air quality in 12 Canadian cities, 
most of which would likely have met a standard with a level of 70 ppb 
over the entire study period but violated a revised standard with a 
level of 65 ppb or below over at least part of that period (U.S. EPA, 
2014c, Table 4-1). This analysis suggests that although the current 
standard or a standard with a level of 70 ppb would allow the ambient 
O3 concentrations in most of the study locations that 
provided the basis for the association with mortality in this study, a 
revised O3 standard with a level at or below 65 ppb would 
require reductions in those ambient O3 concentrations. As 
discussed above for a level of 70 ppb, this analysis does not provide 
information on the extent to which O3-associated mortality 
would persist upon meeting an O3 standard with a level of 65 
ppb, or on the extent to which standard levels below 65 ppb could 
further reduce the incidence of this mortality.\148\
---------------------------------------------------------------------------

    \148\ For the other multicity studies identified in Table 4-1 of 
the PA (Cakmak et al., 2006; Stieb et al., 2009; Katsouyanni et al., 
2009 (for hospital admissions)), and for the study by Bell et al. 
(2006) (for the 30 ppb cut point) (Table 4-2 of the PA), the 
majority of study locations would have met a standard with a level 
of 65 ppb (U.S. EPA, 2014c).
---------------------------------------------------------------------------

    With regard to long-term O3 concentrations, as for 70 
ppb (above) the PA evaluates the long-term O3 metrics 
reported to be associated with mortality or morbidity in recent 
epidemiologic studies (e.g., seasonal averages of 1-hour or 8-hour 
daily max concentrations). Compared to the current standard or a 
revised O3 standard with a level of 70 ppb, a revised 
standard with a level of 65 ppb would be expected to further reduce the 
risk of respiratory mortality associated with long-term O3 
concentrations, based on information from the study by Jerrett et al. 
(2009).\149\ In addition, a standard with a level of 65 ppb would be 
expected to more effectively maintain long-term O3 
concentrations below those where the study by Jerrett et al. (2009) 
indicates the most confidence in the reported association with 
respiratory mortality. Specifically, air quality analyses indicate this 
to be the case in 10 out of the 12 urban study areas for a level of 65 
ppb, compared to 6 out of 12 areas for the current standard and 9 out 
of 12 for a standard with a level of 70 ppb (U.S. EPA, 2014c, Table 4-
3). Finally, a revised standard with a level of 65 ppb would be 
expected to further reduce long-term O3 concentrations based 
on the types of metrics that have been reported in recent epidemiologic 
studies to be associated with respiratory morbidity (i.e., seasonal 
averages of daily maximum 8-hour concentrations).
---------------------------------------------------------------------------

    \149\ Though as discussed above, the PA notes the lower 
confidence placed in these risk results (U.S. EPA, 2014a, section 
9.6).
---------------------------------------------------------------------------

    In further considering the potential implications of epidemiology 
studies for alternative standard levels, the PA notes estimates of 
total mortality associated with short-term O3.\150\ As 
discussed above, the PA considers estimates of total risk (i.e., based 
on the full distributions of ambient O3 concentrations) and 
estimates of risk associated with O3 concentrations in the 
upper portions of ambient distributions. With regard to total risk the 
PA notes that, when summed across urban study areas, a standard with a 
level of 65 ppb is estimated to reduce the number of deaths associated 
with short-term O3 exposures by about 13% (2007) and 9% 
(2009), compared to the current standard.\151\ For area-wide 
concentrations at or above 40 ppb, a standard level of 65 ppb is 
estimated to reduce O3-associated deaths by almost 50% 
compared to the current standard, when summed across urban study areas. 
For area-wide concentrations at or above 60 ppb, a standard level of 65 
ppb is estimated to reduce O3-associated deaths by more than 
80% (U.S. EPA, 2014c, Figure 4-13).
---------------------------------------------------------------------------

    \150\ As discussed above, compared to the weight given to the 
evidence and to HREA estimates of exposures of concern and lung 
function risks, the PA places relatively less weight on 
epidemiologic-based risk estimates.
    \151\ A standard with a level of 65 ppb is also estimated to 
reduce respiratory mortality associated with long-term O3 
concentrations in urban study areas. However, given uncertainties 
associated with these risk estimates, as discussed above, we give 
them limited weight.
---------------------------------------------------------------------------

    In summarizing CASAC's advice regarding a standard with a level of 
65, the PA noted CASAC's conclusion that an alternative standard with a 
level of 65 ppb would further reduce, though not eliminate, the 
frequency of lung function decrements >=15% and would lead to lower 
frequency of short-term premature mortality (i.e., compared to a 
standard with a level of 70 ppb) (Frey, 2014c, p. 8).
    In summary, compared to a standard with a level of 70 ppb, the PA 
concludes that a revised standard with a level of

[[Page 75302]]

65 ppb would be expected to further reduce O3 exposures and 
health risks. In particular, a standard with a level of 65 ppb is 
estimated to (1) reduce the occurrence of exposures of concern by about 
80 to 100%, compared to the current standard, decreasing exposures at 
or above 60 ppb and almost eliminating exposures at or above 70 and 80 
ppb; (2) reduce the occurrence of FEV1 decrements >=10, 15, 
and 20% by about 30 to 65%, compared to the current standard; (3) more 
effectively maintain short- and long-term O3 concentrations 
below those present in the epidemiologic studies that reported 
significant O3 health effect associations in locations 
likely to have met the current standard; \152\ and (4) further reduce 
the risk of O3-associated mortality and morbidity, 
particularly the risk associated with the upper portion of the 
distribution of ambient O3 concentrations.
---------------------------------------------------------------------------

    \152\ Though epidemiologic studies also provide evidence for 
O3 health effect associations in locations likely to have 
met a standard with a level of 65 ppb, as discussed below for a 
level of 60 ppb.
---------------------------------------------------------------------------

iii. PA Consideration of an O3 Standard Level of 60 ppb
    The PA also considers a standard with a level of 60 ppb. A level of 
60 ppb is well below the O3 exposure concentration that has 
been reported to elicit a wide range of potentially adverse respiratory 
effects in healthy adults (i.e., 80 ppb). A level of 60 ppb is also 
below the lowest concentration where the combined occurrence of 
respiratory symptoms and lung function decrements was observed, a 
combination judged adverse by the ATS (i.e., 72 ppb). A level of 60 ppb 
corresponds to the lowest exposure concentration demonstrated to result 
in lung function decrements that are large enough to be judged an 
abnormal response by ATS, that meet ATS criteria for adversity based on 
a downward shift in the distribution of FEV1, and that the CASAC 
indicated could be adverse in people with lung disease. A level of 60 
ppb also corresponds to the lowest exposure concentration at which 
pulmonary inflammation has been reported in a single controlled human 
exposure study.
    Based on the HREA analyses of O3 exposures of concern, a 
standard with a level of 60 ppb is estimated to eliminate exposures of 
concern at or above the 70 and 80 ppb benchmark concentrations and to 
be more effective than the higher standard levels at limiting exposures 
of concern at or above 60 ppb. On average over the years 2006 to 2010, 
for a standard with a level of 60 ppb, between 0 and about 1% of 
children, including asthmatic children, in urban study areas are 
estimated to experience exposures of concern at or above 60 ppb, which 
CASAC indicated is an appropriate exposure of concern for asthmatic 
children. This reflects a 96% reduction (on average across areas), 
compared to the current standard. Virtually no children are estimated 
to experience two or more exposures of concern at or above 60 ppb. In 
the worst-case location and year, about 2% of children are estimated to 
experience exposures of concern at or above 60 ppb, with far less than 
1% estimated to experience two or more such exposures (Table 4, above).
    Based on the HREA analyses of O3-induced lung function 
decrements, a standard with a level of 60 ppb would be expected to be 
more effective than a level of 65 or 70 ppb at limiting the occurrence 
of O3-induced lung function decrements. For a standard with 
a level of 60 ppb, about 2% of children, or less, in the urban study 
areas are estimated to experience one or more moderate O3-
induced FEV1 decrements >=15% (almost 70% reduction, 
compared to current standard), and about 1% or less are estimated to 
experience two or more such decrements (3% in the location and year 
with the largest estimates). About 1% of children, or less, are 
estimated to experience large O3-induced lung function 
decrements (i.e., FEV1 decrement >=20%), even in the worst-
case locations and year (Table 5, above).
    In addition, for a standard with a level of 60 ppb, about 5 to 11% 
of children in the urban study areas are estimated to experience one or 
more moderate O3-induced lung function decrements that CASAC 
indicated could be adverse for people with lung disease (i.e., 
FEV1 decrements >=10%). This reflects an average reduction 
of about 45%, compared to the current standard. About 2 to 6% of 
children in these areas are estimated to experience two or more such 
decrements (51% reduction, compared to current standard). In the worst-
case location and year, for a standard set at 60 ppb, up to about 13% 
of children are estimated to experience one or more moderate 
O3-induced FEV1 decrements >=10%, and 7% are 
estimated to experience two or more such decrements (Table 5, above).
    With regard to O3 epidemiologic studies, the PA notes 
that a revised standard with a level of 60 ppb would be expected to 
maintain short-term ambient O3 concentrations below those 
present in some of the study locations that provided the basis for 
reported O3 health effect associations and that were likely 
to have met a revised standard with a level of 70 or 65 ppb. 
Specifically, in all of the U.S. and Canadian epidemiologic studies 
evaluated, the majority of study cities had ambient O3 
concentrations that would likely have violated a standard with a level 
of 60 ppb. Thus, none of the U.S. and Canadian epidemiologic studies 
analyzed provide evidence for O3 health effect associations 
when the majority of study locations would likely have met a standard 
with a level of 60 ppb (U.S. EPA, 2014c, Tables 4-1 and 4-2). As 
discussed above, while this analysis does not provide information on 
the extent to which the O3-associated morbidity or mortality 
would persist upon meeting an O3 standard with a level of 60 
ppb, it suggests that a revised O3 standard with a level of 
60 ppb would require reductions in the ambient O3 
concentrations that provided the basis for those health effect 
associations.
    With regard to long-term O3 concentrations, compared to 
the current standard or a revised O3 standard with a level 
of 65 or 70 ppb, a revised standard with a level of 60 ppb would be 
expected to further reduce the risk of respiratory mortality associated 
with long-term O3 concentrations, based on information from 
the study by Jerrett et al. (2009).\153\ In addition, a standard with a 
level of 60 ppb would be expected to more effectively maintain long-
term O3 concentrations below those where the study by 
Jerrett et al. (2009) indicates the most confidence in the reported 
association with respiratory mortality. Specifically, air quality 
analyses indicate this to be the case in all of the urban study areas 
evaluated at a level of 60 ppb, compared to 6 out of 12 areas for the 
current standard, 9 out of 12 for a standard with a level of 70 ppb, 
and 10 out of 12 for a standard with a level of 65 ppb (U.S. EPA, 
2014c, Table 4-3). Finally, a revised standard with a level of 60 ppb 
would be expected to further reduce long-term O3 
concentrations based on the types of metrics that have been reported in 
recent epidemiologic studies to be associated with respiratory 
morbidity (i.e., seasonal averages of daily maximum 8-hour 
concentrations).
---------------------------------------------------------------------------

    \153\ Though as discussed above, the PA notes the lower 
confidence we place in these risk results (U.S. EPA, 2014a, section 
9.6).
---------------------------------------------------------------------------

    In further considering the potential implications of epidemiology 
studies for alternative standard levels, the PA notes estimates of 
total mortality associated with short-term O3 
concentrations.\154\

[[Page 75303]]

As discussed above, the PA considers estimates of total risk (i.e., 
based on the full distributions of ambient O3 
concentrations) and estimates of risk associated with O3 
concentrations in the upper portions of ambient distributions. With 
regard to total risk the PA notes that, when summed across urban study 
areas, a standard with a level of 60 ppb is estimated to reduce the 
number of deaths associated with short-term O3 exposures by 
about 15% (2007) and 11% (2009), compared to the current standard (U.S. 
EPA, 2014c, Figure 4-13).\155\ For area-wide concentrations at or above 
40 ppb, a standard with a level set at 60 ppb is estimated to reduce 
O3-associated deaths by almost 60% compared to the current 
standard. For area-wide concentrations at or above 60 ppb, a standard 
level of 60 ppb is estimated to reduce O3-associated deaths 
by over 95% compared to the current standard.
---------------------------------------------------------------------------

    \154\ As discussed above, compared to the weight given to the 
evidence and to HREA estimates of exposures of concern and lung 
function risks, we place relatively less weight on epidemiologic-
based risk estimates.
    \155\ A standard with a level of 60 ppb is also estimated to 
reduce respiratory mortality associated with long-term O3 
concentrations in urban study areas. However, given uncertainties 
associated with these risk estimates, as discussed above, the PA 
gives them limited weight.
---------------------------------------------------------------------------

    In summary, compared to a standard with a level of 65 or 70 ppb, 
the PA concludes that a revised standard with a level of 60 ppb would 
be expected to further reduce O3 exposures and health risks. 
In particular, a standard with a level of 60 ppb is estimated to (1) 
reduce the occurrence of exposures of concern by about 95 to 100%, 
compared to the current standard, almost eliminating exposures at or 
above 60 ppb; (2) reduce the occurrence of FEV1 decrements 
>=10, 15, and 20% by about 45 to 85%, compared to the current standard; 
(3) more effectively maintain short- and long-term O3 
concentrations below those present in the epidemiologic studies that 
reported significant O3 health effect associations in 
locations likely to have met the current standard; \156\ and (4) 
further reduce the risk of O3-associated mortality and 
morbidity, particularly the risk associated with the upper portion of 
the distribution of ambient O3 concentrations.
---------------------------------------------------------------------------

    \156\ As discussed above, these studies do not provide 
information on the extent to which O3 health effect 
associations would persist following reductions in ambient 
O3 concentrations in order to meet a standard with a 
level of 60 ppb.
---------------------------------------------------------------------------

c. CASAC Advice
    The PA recognizes that decisions regarding the weight to place on 
various types of evidence, exposure/risk information, and associated 
uncertainties reflect public health policy judgments that are 
ultimately left to the Administrator. To help inform those judgments 
with regard to the range of alternative primary O3 standard 
levels appropriate for consideration, CASAC has provided advice to the 
Administrator based on their reviews of draft versions of the 
O3 ISA, HREA, and PA. This section summarizes the advice 
provided by CASAC regarding alternative standard levels, as well as the 
views expressed at the CASAC meetings by public commenters. This 
section includes CASAC advice from the reconsideration of the 2008 
final decision on the level of the standard, as well as CASAC advice 
received during the current review as it pertains to alternative 
standards.
    Consistent with its advice in 2008, CASAC reiterated during the 
reconsideration its support for an 8-hour primary O3 
standard with a level ranging from 60 to 70 ppb, combined with the 
current indicator, averaging time, and form. Specifically, in response 
to the EPA's solicitation of CASAC advice during the reconsideration, 
the CASAC letter (Samet, 2010) to the Administrator stated:

CASAC fully supports EPA's proposed range of 0.060-0.070 parts per 
million (ppm) for the 8-hour primary ozone standard. CASAC considers 
this range to be justified by the scientific evidence as presented 
in the Air Quality Criteria for Ozone and Related Photochemical 
Oxidants (March 2006) and Review of the National Ambient Air Quality 
Standards for Ozone: Policy Assessment of Scientific and Technical 
Information, OAQPS Staff Paper (July 2007).

    Similarly, in response to the EPA's request for additional advice 
on the reconsideration in 2011, CASAC reaffirmed its conclusion that 
``the evidence from controlled human and epidemiologic studies strongly 
supports the selection of a new primary ozone standard within the 60-70 
ppb range for an 8-hour averaging time'' (Samet, 2011). CASAC further 
concluded that this range ``would provide little margin of safety at 
its upper end'' (Samet, 2011, p. 2).
    In the current review of the Second Draft PA, CASAC concurred with 
staff's conclusions that it is appropriate to consider retaining the 
current indicator (O3), averaging time (8-hour average) and 
form (3-year average of the 4th highest maximum daily 8-hour average. 
With regard to level, CASAC stated the following (Frey, 2014c, pp. ii 
to iii):

The CASAC further concludes that there is adequate scientific 
evidence to recommend a range of levels for a revised primary ozone 
standard from 70 ppb to 60 ppb. The CASAC reached this conclusion 
based on the scientific evidence from clinical studies, 
epidemiologic studies, and animal toxicology studies, as summarized 
in the Integrated Science Assessment (ISA), the findings from the 
exposure and risk assessments as summarized in the HREA, and the 
interpretation of the implications of these sources of information 
as given in the Second Draft PA.
    The CASAC acknowledges that the choice of a level within the 
range recommended based on scientific evidence [i.e., 70 to 60 ppb] 
is a policy judgment under the statutory mandate of the Clean Air 
Act. The CASAC advises that, based on the scientific evidence, a 
level of 70 ppb provides little margin of safety for the protection 
of public health, particularly for sensitive subpopulations.
    Thus, our policy advice is to set the level of the standard 
lower than 70 ppb within a range down to 60 ppb, taking into account 
your judgment regarding the desired margin of safety to protect 
public health, and taking into account that lower levels will 
provide incrementally greater margins of safety.

    The public commenters who expressed the view that the current 
primary O3 standard is not adequate (II.D.3) also submitted 
comments that supported revising the level of the primary O3 
standard. Several of these commenters expressed the view that the level 
should be revised to the lower end of the range of 70 to 60 ppb, or in 
some cases to a level below 60 ppb. These commenters often placed a 
large amount of emphasis on evidence from controlled human exposure 
studies for respiratory effects following exposures to 60 ppb 
O3.
    In addition, as discussed above (II.D.3), some public commenters 
expressed the view that revision of the current standard is not 
necessary. Consistent with their view that it would not be appropriate 
to revise the current standard, these commenters did not provide any 
provisional views on alternative levels below 75 ppb that would be 
appropriate for consideration.
d. Administrator's Proposed Conclusions on Level
    This section discusses the Administrator's proposed conclusions on 
the level of the primary O3 standard. In conjunction with 
her proposed decisions to retain the current indicator, averaging time, 
and form (II.E.1 to II.E.3, above), the Administrator proposes to 
revise the level of the primary O3 standard to within the 
range of 65 to 70 ppb. In doing so, she is mindful that the selection 
of a primary O3 standard that is requisite to protect public 
health with an adequate margin of safety requires judgments based on an 
interpretation of the scientific evidence and exposure/risk information 
that neither overstates nor understates the strengths and limitations 
of that evidence and information, nor the appropriate

[[Page 75304]]

inferences to be drawn therefrom.\157\ The rationale supporting the 
Administrator's proposed conclusions on alternative standard levels is 
discussed below.
---------------------------------------------------------------------------

    \157\ As discussed above (I.B), in addressing the requirement 
for an adequate margin of safety the EPA considers such factors as 
the nature and severity of the health effects, the size of sensitive 
population(s) at risk, and the kind and degree of the uncertainties 
that must be addressed. The selection of any particular approach for 
providing an adequate margin of safety is a policy choice left 
specifically to the Administrator's judgment. See Lead Industries 
Association v. EPA, 647 F. 2d at 1161-62; State of Mississippi, 744 
F. 3d at 1353.
---------------------------------------------------------------------------

    The Administrator's proposed conclusions on alternative standard 
levels build upon her proposed conclusion that the overall body of 
scientific evidence and exposure/risk information call into question 
the adequacy of public health protection afforded by the current 
primary O3 standard, particularly for at-risk populations 
and lifestages (II.D.5). These proposed conclusions are based on 
consideration of the scientific evidence assessed in the ISA (U.S. EPA, 
2013a); the results of the exposure and risk assessments in the HREA 
(U.S. EPA, 2014a); the evidence-based and exposure-/risk-based 
considerations and conclusions in the PA (U.S. EPA, 2014c); CASAC 
advice and recommendations, as reflected in CASAC's letters to the 
Administrator and in public discussions of drafts of the ISA, HREA, and 
PA; and public input received during the development of these 
documents.
    In reaching proposed conclusions on alternative levels for the 
primary O3 standard, the Administrator considers the extent 
to which various alternatives would be expected to protect the public, 
including at-risk populations, against the wide range of adverse health 
effects that have been linked with short- or long-term O3 
exposures. At-risk populations include people with asthma; children and 
older adults; people who are active outdoors, including outdoor 
workers; people with certain genetic variants; and people with reduced 
intake of certain nutrients.
    As was the case for her consideration of the adequacy of the 
current primary O3 standard (II.D.5), the Administrator 
places the greatest weight on the results of controlled human exposure 
studies and on exposure and risk analyses based on information from 
these studies. In doing so, she notes that controlled human exposure 
studies provide the most certain evidence indicating the occurrence of 
health effects in humans following exposures to specific O3 
concentrations. The effects reported in these studies are due solely to 
O3 exposures, and interpretation of study results is not 
complicated by the presence of co-occurring pollutants or pollutant 
mixtures (as is the case in epidemiologic studies). She further notes 
the CASAC judgment that ``the scientific evidence supporting the 
finding that the current standard is inadequate to protect public 
health is strongest based on the controlled human exposure studies of 
respiratory effects'' (Frey, 2014c, p. 5). Consistent with this 
emphasis, the HREA conclusions reflect relatively greater confidence in 
the results of the exposure and risk analyses based on information from 
controlled human exposure studies (i.e., exposures of concern and risk 
of lung function decrements) than the results of epidemiology-based 
risk analyses, given the greater uncertainties in the epidemiology-
based risk estimates (U.S. EPA, 2014a, section 9.6). For all of these 
reasons, the Administrator has the most confidence in using the 
information from controlled human exposure studies to reach proposed 
conclusions on alternative standard levels.
    In considering the evidence from controlled human exposure studies, 
the Administrator first notes that these studies have reported a 
variety of respiratory effects in healthy adults following exposures to 
O3 concentrations of 60,\158\ 72,\159\ or 80 ppb, and 
higher. The largest respiratory effects, and the broadest range of 
effects, have been studied and reported following exposures of healthy 
adults to 80 ppb O3 or higher, with most exposure studies 
conducted at these higher concentrations. Exposures of healthy adults 
to O3 concentrations of 80 ppb or higher have been reported 
to decrease lung function, increase airway inflammation, increase 
respiratory symptoms, result in airway hyperresponsiveness, and 
decrease lung host defenses (II.B.2).
---------------------------------------------------------------------------

    \158\ As discussed above (II.B.2), exposures to 60 ppb 
O3 have been evaluated in studies by Adams (2002, 2006), 
Schelegle et al. (2009), and Kim et al. (2011). In the study by 
Schelegle, for the 60 ppb target exposure concentration, study 
authors reported that the actual mean exposure concentration was 63 
ppb.
    \159\ As noted above, for the 70 ppb target exposure 
concentration, Schelegle et al. (2009) reported that the actual mean 
exposure concentration was 72 ppb.
---------------------------------------------------------------------------

    The Administrator notes that O3 exposure concentrations 
as low as 72 ppb have been shown to both decrease lung function and 
increase respiratory symptoms (Schelegle et al., 2009), a combination 
that meets the ATS criteria for an adverse response. In considering 
effects at 72 ppb, CASAC likewise noted that ``the combination of 
decrements in FEV1 together with the statistically 
significant alterations in symptoms in human subjects exposed to 72 ppb 
ozone meets the American Thoracic Society's definition of an adverse 
health effect'' (Frey, 2014c, p. 5).
    With regard to lower exposure concentrations, the Administrator 
notes that the combination of statistically significant increases in 
respiratory symptoms and decrements in lung function has not been 
reported. More specifically, she notes that respiratory symptoms have 
been evaluated following 6.6-hour exposures to average O3 
concentrations of 60 ppb (Adams, 2006; Kim et al., 2011) and 63 ppb 
(Schelegle et al., 2009) and that none of these studies reported a 
statistically significant increase in respiratory symptoms, compared to 
filtered air controls.\160\
---------------------------------------------------------------------------

    \160\ However, following exposures to 60 ppb O3, 
several studies have observed decreases in lung function and one 
study (Kim et al., 2011) observed an increase in airway inflammation 
(II.B.2).
---------------------------------------------------------------------------

    Based on this evidence, the Administrator reaches the initial 
conclusion that the results of controlled human exposure studies 
strongly support setting the level of a revised O3 standard 
no higher than 70 ppb. In reaching this initial conclusion, the 
Administrator places a large amount of weight on the importance of 
setting the level of the standard well below 80 ppb, the O3 
exposure concentration shown in healthy adults to result in the 
broadest range of respiratory effects, and below 72 ppb, the lowest 
O3 exposure concentration shown in healthy adults to result 
in the adverse combination of respiratory symptoms and lung function 
decrements.
    In further considering the potential public health implications of 
a standard with a level of 70 ppb, the Administrator also considers the 
extent to which such a standard would be expected to limit population 
exposures to the broader range of O3 concentrations reported 
in controlled human exposure studies to cause respiratory effects. 
Given the range of effects reported following exposures to 80 ppb 
O3, and the evidence for the adverse combination of lung 
function decrements and respiratory symptoms in healthy adults 
following exposures as low as 72 ppb, the Administrator concludes that 
the evidence in this review supports the occurrence of adverse 
respiratory effects for exposures to O3 concentrations at or 
above 72 ppb.
    The Administrator has decreasing confidence that adverse effects 
will occur following exposures to O3 concentrations below 72 
ppb. In particular, compared to O3 exposure

[[Page 75305]]

concentrations at or above 72 ppb, she has less confidence that adverse 
effects will occur following exposures to O3 concentrations 
as low as 60 ppb. In reaching this conclusion, she notes that, as 
discussed above, statistically significant increases in respiratory 
symptoms, combined with lung function decrements, have not been 
reported following exposures to 60 or 63 ppb O3, though 
several studies have evaluated the potential for such effects.
    Although she has decreasing confidence in the occurrence of adverse 
effects following exposures to O3 concentrations below 72 
ppb, the Administrator notes the CASAC judgment that the adverse 
combination of lung function decrements and respiratory symptoms 
``almost certainly occur in some people'' following exposures to lower 
concentrations (Frey, 2014c, p. 6). In particular, when commenting on 
the extent to which the study by Schelegle et al. (2009) suggests the 
potential for adverse effects following O3 exposures below 
72 ppb, CASAC judged that:

[I]f subjects had been exposed to ozone using the 8-hour averaging 
period used in the standard [i.e., rather than the 6.6 hour 
exposures evaluated in the study], adverse effects could have 
occurred at lower concentration. Further, in our judgment, the level 
at which adverse effects might be observed would likely be lower for 
more sensitive subgroups, such as those with asthma [i.e., compared 
to the healthy adults evaluated in the study] (Frey, 2014c, p. 5).

Though CASAC did not provide advice as to how far below 72 ppb adverse 
effects would likely occur, the Administrator agrees that such effects 
could occur following exposures at least somewhat below 72 ppb.
    Based on the evidence and CASAC advice noted above, when 
considering the extent to which a standard with a level of 70 ppb would 
be expected to limit population exposures to the broader range of 
O3 concentrations shown to cause respiratory effects, the 
Administrator considers the extent to which such a standard would be 
expected to limit the occurrence of O3 exposures of concern 
at or above 60, 70, and 80 ppb.\161\ In doing so, she notes that an 
O3 standard established at a particular level can provide 
protection against a range of exposure concentrations, including 
concentrations below the standard level. This is because the degree of 
protection provided by any NAAQS is due to the combination of all of 
the elements of the standard (i.e., indicator, averaging time, form, 
level). In the case of the 4th maximum form of the O3 NAAQS, 
which the Administrator is proposing to retain in the current review 
(II.E.3), the large majority of days in areas that meet the standard 
will have 8-hour O3 concentrations below the level of the 
standard.
---------------------------------------------------------------------------

    \161\ As with her consideration of the current standard 
(II.D.5), the Administrator focuses on estimated exposures of 
concern in children, including asthmatic children, noting the HREA 
analyses indicating that exposures of concern occur in a larger 
percentage of children than adults (given that a larger percentage 
of children are estimated to spend an extended period of time being 
physically active outdoors when O3 concentrations are 
elevated) (II.C.2). To the extent alternative standards provide an 
appropriate degree of protection for children, she judges that those 
standards will also protect adult populations (including at-risk 
adult populations).
---------------------------------------------------------------------------

    In considering exposures of concern at or above 60, 70, and 80 ppb, 
the Administrator judges that the evidence supporting the occurrence of 
adverse respiratory effects is strongest for exposures at or above the 
70 and 80 ppb benchmarks. While the Administrator has less confidence 
that adverse effects will occur following exposures to O3 
concentrations as low as 60 ppb, she notes the possibility for adverse 
effects following such exposures given that (1) CASAC has indicated the 
moderate lung function decrements (i.e., FEV1 decrements 
>=10%) that occur in some healthy adults following exposures to 60 ppb 
O3, which are large enough to be judged an abnormal response 
by ATS, could be adverse to people with lung disease (II.B.3), and that 
(2) airway inflammation has been reported following exposures as low as 
60 ppb O3. She also takes note of CASAC advice that the 
occurrence of exposures of concern at or above 60 ppb is an appropriate 
consideration for people (including children) with asthma (Frey, 2014c, 
p. 6).
    Due to interindividual variability in responsiveness, the 
Administrator further notes that not every occurrence of an exposure of 
concern will result in an adverse effect.\162\ Repeated occurrences of 
some of the effects demonstrated following exposures of concern could 
increase the likelihood of adversity. For example, as discussed in the 
ISA (U.S. EPA, 2013a, Section 6.2.3), repeated occurrences of airway 
inflammation could lead to the induction of a chronic inflammatory 
state; altered pulmonary structure and function, leading to diseases 
such as asthma; altered lung host defense response to inhaled 
microorganisms, particularly in potentially at-risk populations such as 
the very young and old; and altered lung response to other agents such 
as allergens or toxins. The Administrator notes that the types of lung 
injury that can occur following exposures of concern, particularly if 
experienced repeatedly, provide a plausible mode of action by which 
O3 may cause other more serious effects. Therefore, the 
Administrator is most concerned about protecting at-risk populations 
against repeated occurrences of exposures of concern.
---------------------------------------------------------------------------

    \162\ For most of the effects demonstrated in controlled human 
exposure studies (e.g., airway inflammation, AHR, decreased lung 
host defense, respiratory symptoms) the available data are not 
sufficient to quantify the number of people who would experience 
adverse effects due to O3 exposures.
---------------------------------------------------------------------------

    Based on the above considerations, the Administrator focuses on the 
extent to which a revised standard would be expected to protect 
populations from experiencing two or more O3 exposures of 
concern (i.e., as a surrogate for repeated exposures). While she 
emphasizes the importance of limiting two or more exposures and 
reducing their occurrence, compared to the current standard, she 
balances this emphasis by noting that (1) not all exposures of concern 
will result in adverse effects; (2) she has less confidence in the 
occurrence of adverse effects at the 60 ppb benchmark than at the 70 or 
80 ppb benchmarks; and (3) the NAAQS are not meant to be zero-risk 
standards.\163\ Therefore, in using estimates of exposures of concern 
to inform her decisions on alternative standard levels, the 
Administrator judges that it would not be appropriate to set a standard 
intended to eliminate all exposures of concern for all benchmarks, 
particularly the 60 ppb benchmark. Her consideration of specific 
estimates of exposures of concern is discussed below.
---------------------------------------------------------------------------

    \163\ State of Mississippi, 744 F. 3d at 1343.
---------------------------------------------------------------------------

    As illustrated in Table 1 (above), the Administrator notes that, in 
urban study areas, a revised standard with a level of 70 ppb would be 
expected to eliminate the occurrence of two or more exposures of 
concern to O3 concentrations at and above 80 ppb and to 
virtually eliminate the occurrence of two or more exposures of concern 
to O3 concentrations at and above 70 ppb, even in the worst-
case urban study area and year. For the 70 ppb benchmark, this reflects 
about a 95% reduction in the occurrence of two or more exposures of 
concern, compared to the current standard (Table 4).
    Though the Administrator acknowledges greater uncertainty with 
regard to the occurrence of adverse effects following exposures of 
concern at or above 60 ppb, she notes that a revised standard with a 
level of 70 ppb would also be expected to protect the large majority of 
children in the urban study areas (i.e., about 96% to more

[[Page 75306]]

than 99% of children in individual urban study areas) from experiencing 
two or more exposures of concern at or above 60 ppb. Compared to the 
current standard, this represents a reduction of more than 60% in the 
occurrence of two or more exposures of concern (Tables 1 and 4).
    Based on the above information, the Administrator concludes that a 
revised O3 standard with a level of 70 ppb would be expected 
to virtually eliminate the occurrence of two or more O3 
exposures of concern for the 70 and 80 ppb benchmarks, and to 
substantially reduce the occurrence of two or more O3 
exposures of concern for the 60 ppb benchmark, compared to the current 
standard.
    Although the Administrator is less concerned about single 
occurrences of exposures of concern, she acknowledges that even single 
exposures to O3 concentrations at or above benchmark 
concentrations (particularly for the 70 and 80 ppb benchmarks) could 
potentially result in adverse effects. To the extent this may be the 
case, the Administrator notes that a standard with a level of 70 ppb 
would also be expected to (1) virtually eliminate all occurrences of 
exposures of concern at or above 80 ppb, even in the worst-case year 
and location and (2) achieve important reductions, compared to the 
current standard, in the occurrence of one or more exposures of concern 
at or above 70 and 60 ppb (i.e., about a 70% reduction for the 70 ppb 
benchmark and almost a 50% reduction for the 60 ppb benchmark) (Tables 
1 and 4).
    In further evaluating the potential public health impacts of a 
standard with a level of 70 ppb, the Administrator also considers the 
HREA estimates of O3-induced lung function decrements. To 
inform her consideration of these decrements, the Administrator takes 
note of CASAC advice that ``estimation of FEV1 decrements of 
>=15% is appropriate as a scientifically relevant surrogate for adverse 
health outcomes in active healthy adults, whereas an FEV1 
decrement of >=10% is a scientifically relevant surrogate for adverse 
health outcomes for people with asthma and lung disease'' (Frey, 2014c, 
p. 3). Consistent with this advice, she considers estimates of the 
occurrence of O3-induced FEV1 decrements >=10 and 
15% as surrogates for the occurrence of adverse health outcomes.
    While these surrogates provide perspective on the potential for the 
occurrence of adverse respiratory effects following O3 
exposures, the Administrator agrees with the conclusion in past reviews 
that a more general consensus view of the adversity of moderate 
responses emerges as the frequency of occurrence increases (61 FR 
65722-3) (Dec. 13, 1996). Specifically, she concludes that not every 
estimated occurrence of an O3-induced FEV1 
decrement will be adverse and that repeated occurrences of moderate 
responses, even in otherwise healthy individuals, may be considered to 
be adverse since they could set the stage for more serious illness. 
Therefore, the Administrator becomes increasingly concerned about the 
potential for adversity as the frequency of occurrences increases and, 
as a result, she focuses primarily on estimates of two or more 
O3-induced FEV1 decrements (i.e., as a surrogate 
for repeated exposures).
    Given the above considerations, the Administrator does not believe 
it would be appropriate to set a standard that is intended to eliminate 
all O3-induced FEV1 decrements. She notes that 
this is consistent with CASAC advice, which did not include a 
recommendation to set the standard level low enough to eliminate all 
O3-induced FEV1 decrements >=10 or 15% (Frey, 
2014c). Rather, the Administrator considers the extent to which a 
standard with a level of 70 ppb would be expected to protect the 
population from experiencing O3-induced FEV1 
decrements >=10 and 15%, including the extent to which such a standard 
would be expected to achieve reductions in the occurrence of 
O3-induced FEV1 decrements, relative to the 
current standard.\164\
---------------------------------------------------------------------------

    \164\ The Administrator additionally notes that, unlike 
exposures of concern, the variability in lung function risk 
estimates across urban study areas is often greater than the 
differences in risk estimates between various standard levels (Table 
2, above). Given this, and the resulting considerable overlap 
between the ranges of lung function risk estimates for different 
standard levels, although the Administrator has confidence in the 
lung function risk estimates themselves, she views them as providing 
a more limited basis than exposures of concern for distinguishing 
between the degree of public health protection provided by 
alternative standard levels.
---------------------------------------------------------------------------

    The Administrator notes that a revised O3 standard with 
a level of 70 ppb is estimated to protect about 98 to 99% of children 
in urban study areas from experiencing two or more O3-
induced FEV1 decrements >=15%, and about 89 to 94% from 
experiencing two or more decrements >=10%.\165\ Compared to the current 
standard, these estimates represent decreases in the occurrence of two 
or more O3-induced decrements of about 29 and 17%, 
respectively (Tables 2 and 5). Although the Administrator is less 
concerned about the public health implications of single O3-
induced lung function decrements, she also gives some consideration to 
estimates of one or more O3-induced FEV1 
decrements. In particular, she notes that a revised standard with a 
level of 70 ppb is estimated to reduce the occurrence of one or more 
O3-induced decrements, compared to the current standard, by 
about 26% (for decrements >=15%) and 15% (for decrements >=10%) (Tables 
2 and 5).
---------------------------------------------------------------------------

    \165\ In the worst-case year and location, a standard with a 
level of 70 ppb is estimated to protect about 97% of children in 
urban study areas from experiencing two or more O3-
induced FEV1 decrements >=15%, and about 87% from 
experiencing two or more decrements >=10%.
---------------------------------------------------------------------------

    Given all of the above information, the Administrator concludes 
that a revised standard with a level of 70 ppb would be expected to 
provide substantial protection against O3 exposures of 
concern (for benchmark concentrations of 60, 70, 80 ppb) and 
O3-induced lung function decrements, and would be expected 
to result in important reductions in the occurrence of such exposures 
and decrements, compared to the current standard. This is particularly 
the case for estimates of two or more occurrences of exposures of 
concern and lung function decrements.
    In next considering the additional protection that would be 
expected from standard levels below 70 ppb, the Administrator evaluates 
the extent to which a standard with a level of 65 ppb would be expected 
to further limit O3 exposures of concern and O3-
induced lung function decrements.
    In addition to eliminating almost all exposures of concern to 
O3 concentrations at or above 80 and 70 ppb, even in the 
worst-case years and locations, the Administrator notes that a revised 
standard with a level of 65 ppb would be expected to protect more than 
99% of children in urban study areas (and 100% of children in some 
urban study areas) from experiencing two or more exposures of concern 
at or above 60 ppb. Compared to the current standard, this represents 
about a 95% reduction in the occurrence of two or more exposures of 
concern for the 60 ppb benchmark (Tables 1 and 4). In addition, the 
Administrator notes that a revised standard with a level of 65 ppb is 
estimated to reduce the occurrence of one or more exposures of concern 
for the 60 ppb benchmark by about 80%, compared to the current standard 
(Tables 1 and 4).
    With regard to O3-induced lung function decrements, the 
Administrator notes that an O3 standard with a level of 65 
ppb is estimated to protect about 98% to more than 99% of children from 
experiencing two or more O3-induced FEV1 
decrements >=15%, even considering the worst-case year and location, 
and about 91 to 99% from

[[Page 75307]]

experiencing two or more decrements >=10% (89% in worst-case year and 
location). These estimates reflect reductions, compared to the current 
standard, of about 54 and 37%, respectively. A revised standard with a 
level of 65 ppb is also estimated to reduce the occurrence of one or 
more lung function decrements >=15 and 10%, compared to the current 
standard, by about 50 and 31%, respectively.
    Taken together, the Administrator initially concludes that the 
evidence from controlled human exposure studies, and the information 
from quantitative analyses that draw upon these studies (i.e., 
exposures of concern, O3-induced FEV1 
decrements), provide strong support for standard levels from 65 to 70 
ppb. In particular, she bases this conclusion on the fact that such 
standard levels would be well below the O3 exposure 
concentration shown to result in the widest range of respiratory 
effects (i.e., 80 ppb), and below the lowest O3 exposure 
concentration shown to result in the adverse combination of lung 
function decrements and respiratory symptoms (i.e., 72 ppb). A standard 
with a level from 65 to 70 ppb would also be expected to result in 
important reductions, compared to the current standard, in the 
occurrence of O3 exposures of concern for all of the 
benchmarks evaluated (i.e., 60, 70, and 80 ppb) and in the risk of 
O3-induced lung function decrements >=10 and 15%.
    In further considering the evidence and exposure/risk information, 
the Administrator considers the extent to which the epidemiologic 
evidence, and the quantitative risk estimates based on information from 
epidemiologic studies, also provide support for standard levels from 65 
to 70 ppb. In doing so, as in her consideration of the adequacy of the 
current O3 standard, the Administrator focuses on 
epidemiologic studies of respiratory-related hospital admissions, 
emergency department visits, and mortality. These considerations are 
discussed below.
    The Administrator first considers the extent to which available 
epidemiologic studies have reported associations between short-term 
O3 concentrations and emergency department visits, hospital 
admissions, and/or mortality in locations that would likely have met 
alternative standards with levels from 65 to 70 ppb (U.S. EPA, 2014c, 
section 4.4.1). In evaluating the epidemiologic evidence in this way, 
the Administrator places the most weight on single-city studies of 
short-term O3 concentrations, recognizing that there were no 
multicity studies for which air quality data indicated that all cities 
included in the analyses would likely have met alternative standard 
levels. In particular, she notes that while single-city studies are 
more limited than multicity studies in terms of statistical power and 
geographic coverage, conclusions linking air quality in a given city 
with health effect associations in that same city can be made with 
greater certainty for single-city studies of short-term O3, 
compared to health effect associations aggregated across multiple 
cities in multicity studies. In particular, the Administrator notes 
considerable uncertainty in linking multicity effect estimates 
(aggregated across multiple cities) for short-term O3 with 
the air quality for subsets of study locations (rather than all 
locations) likely to have met an alternative standard.\166\
---------------------------------------------------------------------------

    \166\ In recognizing that multicity studies are often emphasized 
over single-city studies for purposes of making weight of evidence 
judgments (U.S. EPA, 2013a), the Administrator's judgment in this 
case applies specifically to interpreting air quality analyses for 
epidemiologic studies of short-term O3 concentrations 
where multicity effect estimates are aggregated across cities, and 
where individual city effect estimates are not presented (as is the 
case for the key O3 studies analyzed in the PA, with the 
exception of the study by Stieb et al. (2009) where none of the 
city-specific effect estimates for asthma emergency department 
visits were statistically significant). Because reported multicity 
effect estimates do not allow health effect associations to be 
disaggregated by individual city, it is not possible to assign the 
multicity health effect association to the air quality in any one 
study location, or to the air quality in a particular subset of 
locations. In contrast, for epidemiologic studies of long-term 
concentrations, where multicity effect estimates are based on 
comparisons across cities, different judgments have been made by EPA 
with regard to the utility of multicity studies (see, e.g. 78 FR 
3086 at 3103/2, January 15, 2013) (and see discussion below of study 
by Jerrett et al., 2009).
---------------------------------------------------------------------------

    Given the above, the Administrator notes analyses in the PA (U.S. 
EPA, 2014c, section 4.4.1) indicating that a revised standard with a 
level of 65 or 70 ppb would be expected to maintain short-term ambient 
O3 concentrations below those present in the locations of 
all of the single-city studies analyzed. As discussed in the PA (U.S. 
EPA, 2014c, section 4.4.1), this includes several single-city studies 
conducted in locations that would have violated the current standard, 
and the single-city study by Mar and Koenig (2009) that reported 
positive and statistically significant associations with respiratory 
emergency department visits with children and adults in a location that 
likely would have met the current standard over the entire study period 
but that would likely not have met a revised standard with a level of 
70 ppb or below. Thus, the Administrator notes that, while the current 
standard would allow the ambient O3 concentrations that 
provided the basis for the health effect associations reported by Mar 
and Koenig (2009), a revised O3 standard with a level at or 
below 70 ppb would require reductions in those ambient O3 
concentrations. While the Administrator acknowledges uncertainty in the 
extent to which the reported O3-associated emergency 
department visits could be further reduced by standard levels below 65 
or 70 ppb, she concludes that this analysis indicates that a revised 
standard with a level at least as low as 70 ppb would result in 
improvements in public health, beyond the protection provided by the 
current standard, in the locations of the single-city epidemiologic 
studies that reported significant health effect associations.
    As discussed above, the Administrator notes the greater uncertainty 
in interpreting air quality in locations of multicity epidemiologic 
studies of short-term O3 for the purpose of evaluating 
alternative standard levels (II.D.1 and U.S. EPA, 2014c, section 
4.4.1). Therefore, she places less weight on these studies than on the 
single-city studies noted above. Despite this uncertainty, she notes 
that PA analyses suggest that standard levels of 65 or 70 ppb would 
require additional reductions, beyond those required by the current 
standard, in ambient O3 concentrations in several of the 
epidemiologic study locations that provided the basis for statistically 
significant O3 health effect associations. For example, she 
notes that Dales et al. (2006) reported significant associations with 
respiratory hospital admissions based on air quality in 11 Canadian 
cities, most of which would likely have met the current standard over 
the entire study period (i.e., seven cities) but would have violated a 
standard with a level of 70 ppb or below over at least part of that 
period (U.S. EPA, 2014c, Table 4-1). She further notes that Katsouyanni 
et al. (2009) reported statistically significant associations with 
mortality based on air quality in 12 Canadian cities, most of which 
would likely have met the current standard (i.e., eight study cities) 
and a standard with a level of 70 ppb (i.e., seven study cities) over 
the entire study period, but would have violated a standard with a 
level of 65 ppb over at least part of that period (U.S. EPA, 2014c, 
Table 4-1). While most of the other multicity epidemiologic studies 
evaluated also suggest that a level from 65 to 70 ppb would result in 
public health improvements, compared to the current standard, the 
Administrator acknowledges that several multicity epidemiologic studies 
reported O3 health effect associations when the majority of 
study cities would likely

[[Page 75308]]

have met standards with levels from 65 to 70 ppb. However, given the 
important uncertainties in interpreting the air quality in these 
multicity studies, the Administrator places limited weight on them 
overall, relative to the single-city studies noted above (and relative 
to the information based on controlled human exposure studies).
    With regard to long-term O3 concentrations, the 
Administrator considers the long-term O3 metrics reported to 
be associated with mortality or morbidity in recent epidemiologic 
studies (e.g., seasonal averages of 1-hour or 8-hour daily max 
concentrations). Compared to the current standard, she notes that 
analyses in the PA (U.S. EPA, 2014c, section 4.4.1) suggest a revised 
standard with a level of 65 or 70 ppb would more effectively maintain 
long-term O3 concentrations below those where the multicity 
study by Jerrett et al. (2009) indicates the most confidence in the 
reported association with respiratory mortality (II.B.2, II.D.1). Based 
on additional information from the study by Jerrett et al. (2009), the 
Administrator also notes HREA analyses indicating that a revised 
standard with a level of 65 or 70 ppb would be expected to reduce the 
risk of respiratory mortality associated with long-term O3 
concentrations (though she also notes important uncertainties with 
these risk estimates, as described below). Finally, she notes analyses 
in the HREA suggesting that a revised standard with a level of 65 or 70 
ppb would be expected to reduce long-term O3 concentrations, 
defined in terms of O3 metrics similar to the long-term 
metrics that have been reported in recent epidemiologic studies to be 
associated with respiratory morbidity (i.e., seasonal averages of daily 
maximum 8-hour concentrations). Given the above evidence and 
information, the Administrator concludes that a revised 8-hour standard 
with a level from 70 to 65 ppb could increase public health protection, 
compared to the current standard, against effects associated with long-
term O3 exposures.
    In further evaluating information from epidemiologic studies, the 
Administrator also considers the HREA's epidemiology-based risk 
estimates of morbidity and mortality associated with short-term 
O3 (U.S. EPA, 2014a). Compared to the weight given to the 
evidence from controlled human exposure studies, and to HREA estimates 
of exposures of concern and lung function risks, she places relatively 
less weight on epidemiology-based risk estimates. In doing so, she 
notes that the overall conclusions from the HREA likewise reflect 
relatively less confidence in estimates of epidemiology-based risks 
than in estimates of exposures of concern and lung function risks. As 
discussed above (II.C.3.b), this is based on the greater uncertainties 
associated with mortality and morbidity risk estimates, including the 
heterogeneity in effect estimates between locations, the potential for 
exposure measurement errors, and uncertainty in the interpretation of 
the shape of concentration-response functions at lower O3 
concentrations. The Administrator further notes the HREA conclusion 
that lower confidence should be placed in the results of the assessment 
of respiratory mortality risks associated with long-term O3 
exposures, primarily because that analysis is based on only one study 
(even though that study is well-designed) and because of the 
uncertainty in that study regarding the existence and identification of 
a potential threshold in the concentration-response function (U.S. EPA, 
2014a, section 9.6).
    In considering epidemiology-based risk estimates, the Administrator 
focuses on the extent to which potential alternative O3 
standards are estimated to reduce the risk of mortality associated with 
short-term exposures to O3, noting the similar patterns of 
risk across urban study areas and air quality scenarios for respiratory 
morbidity endpoints (II.C.3). Given the uncertainties in epidemiology-
based risk estimates, the Administrator focuses on the general 
magnitudes of risk changes estimated for standard levels of 65 and 70 
ppb, compared to the current standard, rather than placing a large 
amount of weight on the absolute estimates of O3-associated 
deaths. In doing so, she notes the CASAC conclusion that ``[a]lthough 
the estimates for short-term exposure impacts are subject to 
uncertainty, the data supports a conclusion that there are meaningful 
reductions in mean premature mortality associated with ozone levels 
lower than the current standard'' (Frey, 2014a, p. 10). She further 
notes that, as discussed above (II.C.3.b), the HREA risk estimates for 
urban study areas are likely to understate the average reductions in 
O3-associated mortality and morbidity risks that would be 
experienced across the U.S. population as a whole upon meeting 
standards with lower levels.
    The Administrator's primary focus is on risks associated with 
O3 concentrations in the upper portions of ambient 
distributions, given the greater uncertainty associated with the shapes 
of concentration-response curves for O3 concentrations in 
the lower portions of ambient distributions.\167\ The Administrator 
further notes that experimental studies provide the strongest evidence 
for O3-induced effects following exposures to O3 
concentrations corresponding to the upper portions of typical ambient 
distributions. In particular, as discussed above, she notes controlled 
human exposure studies showing respiratory effects following exposures 
to O3 concentrations at or above 60 ppb (II.B).
---------------------------------------------------------------------------

    \167\ The ISA concludes that there is less certainty in the 
shape of concentration-response functions for area-wide 
O3 concentrations at the lower ends of warm season 
distributions (i.e., below about 20 to 40 ppb) (U.S. EPA, 2013a, 
section 2.5.4.4).
---------------------------------------------------------------------------

    In considering risks associated with O3 concentrations 
in the upper portions of ambient distributions, the Administrator 
focuses on area-wide O3 concentrations at or above 40 ppb 
and 60 ppb. For area-wide O3 concentrations at or above 40 
ppb, the Administrator notes that revised standards with levels of 70 
or 65 ppb are estimated to reduce the number of premature deaths 
associated with short-term O3 concentrations by about 10% 
and almost 50%, respectively, compared to the current standard.\168\ In 
addition, for area-wide concentrations at or above 60 ppb, revised 
standards are estimated to reduce O3-associated premature 
deaths by about 50% to 70% for a standard level of 70 ppb, and by more 
than 80% for a standard level of 65 ppb.\169\ Risk reductions are 
smaller when total risks are considered (II.C.3.b).
---------------------------------------------------------------------------

    \168\ For area-wide O3 concentrations at or above 40 
ppb, reductions in estimated premature deaths are disproportionately 
larger with the 65 ppb standard level than with the 70 ppb standard 
level. This results from the larger air quality adjustments required 
to meet the 65 ppb level. Across urban study areas, the additional 
reductions required to meet 65 ppb result in many fewer days with 
area-wide O3 concentrations at or above 40 ppb and, 
therefore, many fewer O3-associated deaths for area-wide 
concentrations at or above 40 ppb (U.S. EPA, 2014a, Figures 7-2 and 
7-3).
    \169\ Though only a relatively small number of days in urban 
study areas had area-wide O3 concentrations at or above 
60 ppb.
---------------------------------------------------------------------------

    Given all of the above evidence, exposure/risk information, and 
advice from CASAC, the Administrator proposes to revise the level of 
the current primary O3 standard to within the range of 65 to 
70 ppb. She concludes that a standard with a level from within this 
range could reasonably be judged to be requisite to protect public 
health with an adequate margin of safety, based on her consideration of 
the evidence and information discussed above. In reaching this 
conclusion, she particularly notes that a level from anywhere within 
this range would be below the lowest O3 exposure 
concentration shown to result in the

[[Page 75309]]

adverse combination of respiratory symptoms and lung function 
decrements (i.e., 72 ppb), would be expected to maintain ambient 
O3 concentrations below those in locations where single-city 
studies assessed in the ISA have reported statistically significant 
O3 health effect associations, and would be expected to 
result in important reductions in O3 exposures and health 
risks, compared to the current standard.
    The Administrator notes that the determination of what constitutes 
an adequate margin of safety is expressly left to the judgment of the 
EPA Administrator. She further notes that in evaluating how particular 
standards address the requirement to provide an adequate margin of 
safety, the Administrator must consider such factors as the nature and 
severity of the health effects, the size of sensitive population(s) at 
risk, and the kind and degree of the uncertainties that must be 
addressed (I.B, above). Consistent with past practice and long-standing 
judicial precedent, she takes the need for an adequate margin of safety 
into account as an integral part of her decision-making on the 
appropriate level, averaging time, form, and indicator of the 
standard.\170\
---------------------------------------------------------------------------

    \170\ See, e.g., NRDC v. EPA, 902 F. 2d 962, 973-74 (D.C. Cir. 
1990).
---------------------------------------------------------------------------

    The Administrator notes that the NAAQS are not designed to be zero-
risk or background standards, and that the sizeable risk reductions 
that are estimated in the HREA to be associated with standard levels of 
65 or 70 ppb represent substantial improvements in public health for 
important segments of the population, including at-risk groups such as 
children and people with asthma. Although any rationale supporting a 
decision to set a specific level within the range of 65 to 70 ppb would 
discuss the full body of evidence and information, the Administrator 
notes that certain aspects of this evidence and information could be 
particularly important in distinguishing between the appropriateness of 
a level closer to 65 ppb versus a level closer to 70 ppb.\171\
---------------------------------------------------------------------------

    \171\ Although this discussion refers to supporting rationale 
for a level of 65 ppb or 70 ppb, the Administrator is proposing the 
entire range between 65 and 70 ppb. The Administrator notes that 
although neither the PA nor CASAC reached conclusions or provided 
advice on a standard set at a specific level between 65 ppb and 70 
ppb, there is nothing in either the evidence, exposure/risk 
information, or CASAC advice that would preclude such a standard 
level.
---------------------------------------------------------------------------

    For example, a level at or near 65 ppb could be judged requisite to 
protect public health with an adequate margin of safety to the extent 
the Administrator places greater weight on the importance of: (1) 
Eliminating almost all exposures of concern (even single occurrences) 
at or above 70 and 80 ppb, even in worst-case years and locations; (2) 
almost eliminating the occurrence of two or more exposures of concern 
at or above 60 ppb; (3) achieving additional reductions in 
O3-induced FEV1 decrements, beyond those achieved 
with a level of 70 ppb (4) maintaining ambient concentrations below 
those in locations of single-city studies and more effectively doing so 
for multicity studies (i.e., more effectively than 70 ppb); and (5) 
achieving substantial reductions, compared to a standard with a level 
of 70 ppb, in mortality associated with the upper portion of the 
distribution of ambient O3 concentrations, despite 
uncertainties in risk estimates.
    In contrast, a level at or near 70 ppb could be judged requisite to 
protect public health with an adequate margin of safety to the extent 
the Administrator places a greater amount of weight (i.e., greater than 
for 65 ppb) on the importance of: (1) Almost eliminating the occurrence 
of two or more exposures of concern at or above 70 and 80 ppb, even in 
the worst-case year and location; (2) substantially reducing, but not 
eliminating, the occurrence of two or more exposures of concern at or 
above 60 ppb, noting conclusions regarding increasing uncertainty in 
adverse effects for the 60 ppb benchmark; (3) reducing, but not 
eliminating, the occurrence of one or more exposures of concern, noting 
that not all exposures of concern result in adverse effects; (4) 
maintaining ambient O3 concentrations below those in 
locations of single-city epidemiologic studies, and uncertainties in 
analyses of air quality in multicity study locations; and (5) 
recognizing uncertainties in epidemiology-based risk estimates.
    In considering CASAC advice on the range of standard levels, the 
Administrator first notes CASAC's conclusion that there is adequate 
scientific evidence to consider a range of levels for a primary 
standard that includes an upper end at 70 ppb. For the reasons 
discussed above, she agrees with this advice. She also notes that while 
CASAC concluded that a standard with a level of 70 ppb ``may not meet 
the statutory requirement to protect public health with an adequate 
margin of safety'' (Frey, 2014c, p. 8), it further acknowledged that 
``the choice of a level within the range recommended based on 
scientific evidence is a policy judgment under the statutory mandate of 
the Clean Air Act'' (Frey, 2014c, p. ii). While she agrees with CASAC 
that it is appropriate to consider levels below 70 ppb, as reflected in 
her range of proposed levels from 65 to 70 ppb, for the reasons 
discussed above she also concludes that a standard level as high as 70 
ppb, which CASAC concluded could be supported by the scientific 
evidence, could reasonably be judged to be requisite to protect public 
health with an adequate margin of safety.
    The Administrator has also considered the appropriateness of 
standard levels below 65 ppb. In doing so, she notes the conclusions of 
the PA and the advice of CASAC that it would be appropriate for her to 
consider standard levels as low as 60 ppb. In particular, she notes 
that a decision to set the primary O3 standard level at 60 
ppb would place a large amount of weight on the potential public health 
importance of virtually eliminating even single occurrences of 
exposures of concern at and above 60 ppb, though controlled human 
exposure studies have not reported the adverse combination of 
respiratory symptoms and decrements in lung function following 
exposures to 60 ppb O3; on the potential public health 
importance of further reducing the occurrence of O3-induced 
lung function decrements >=10 and 15%; on analyses of ambient 
O3 concentrations in locations of multicity epidemiologic 
studies, despite uncertainties in linking multicity effect estimates 
for short-term O3 with air quality in individual study 
cities; and on epidemiology-based risk estimates, despite the important 
uncertainties in those estimates. However, as discussed more fully 
above, given the uncertainties associated with the adversity of 
exposures to 60 ppb O3, particularly single occurrence of 
such exposures; uncertainties associated with air quality analyses in 
locations of multicity epidemiologic studies; and uncertainties in 
epidemiology-based risk estimates, particularly uncertainties in the 
shape of the concentration-response functions at lower O3 
concentrations and uncertainties associated with the heterogeneity in 
O3 effect estimates across locations, the Administrator does 
not agree that it is appropriate to place significant weight on these 
factors or to use them to support the appropriateness of standard 
levels below 65 ppb. Compared to O3 standard levels from 65 
to 70 ppb, the Administrator concludes that the extent to which 
standard levels below 65 ppb could result in further public health 
improvements becomes notably less certain. Therefore, she concludes 
that it

[[Page 75310]]

is not appropriate to propose standard levels below 65 ppb.\172\
---------------------------------------------------------------------------

    \172\ Although, as discussed below, she solicits comment on 
standard levels as low as 60 ppb.
---------------------------------------------------------------------------

    The Administrator acknowledges that her proposed range of 65 to 70 
ppb does not include the lower portion of the range supported by CASAC. 
In reaching the conclusion that this is appropriate, she focuses on 
CASAC's rationale for levels as low as 60 ppb. In particular, she notes 
the following CASAC advice (Frey, 2014c, p. 7):

    The CASAC concurs that 60 ppb is an appropriate and justifiable 
scientifically based lower bound for a revised primary standard. 
This is based upon findings of adverse effects, including clinically 
significant lung function decrements and airway inflammation, after 
exposures to 60 ppb ozone in healthy adults with moderate exertion 
(Adams 2006; Schelegle et al., 2009; Brown et al., 2008; Kim et al., 
2011), with limited evidence of adverse effects below 60 ppb.

    In considering this advice, the Administrator notes that CASAC 
focused on the importance of limiting exposures to O3 
concentrations as low as 60 ppb. As discussed above, the Administrator 
agrees with this advice. In particular, she notes that standards within 
the proposed range of 65 to 70 ppb would be expected to substantially 
limit the occurrence of exposures of concern to O3 
concentrations at or above 60 ppb, particularly the occurrence of two 
or more exposures.\173\ When she further considers that not all 
exposures of concern lead to adverse effects, and that the NAAQS are 
not meant to be zero-risk or background standards, the Administrator 
judges that alternative standard levels below 65 ppb are not needed to 
further reduce such exposures. Therefore, the Administrator's initial 
conclusion is that standard levels below 65 ppb would be more than 
requisite to protect public health with an adequate margin of safety.
---------------------------------------------------------------------------

    \173\ In fact, as noted above (Table 4), a standard with a level 
of 70 ppb would be expected to limit multiple occurrences of 
exposures of concern at or above the 60 ppb benchmark to as low as 
0.5% in urban case study areas (and as low as 0% for a standard with 
a level of 65 ppb).
---------------------------------------------------------------------------

    In reaching this initial conclusion, the Administrator acknowledges 
that alternative approaches to viewing the available scientific 
evidence and exposure/risk information, and to viewing the 
uncertainties inherent in that evidence and information, could lead one 
to reach a different conclusion. In particular, as noted above, she 
recognizes that levels as low as 60 ppb could potentially be supported, 
to the extent substantial weight is placed on the public health 
importance of estimates of one or more occurrences of exposures of 
concern at or above 60 ppb and O3-induced lung function 
decrements >=10%; analyses of ambient O3 concentrations in 
locations of multicity epidemiologic studies; and epidemiology-based 
estimates of total risk. This approach would also place a large amount 
of weight on the possibility that at-risk groups would experience 
adverse effects at lower levels than the benchmarks derived from 
clinical studies conducted using healthy adult subjects, despite the 
fact that these studies have not reported a statistically significant 
increase in respiratory symptoms, combined with lung function 
decrements, following exposures to 60 ppb.\174\ Such an approach to 
viewing the evidence and exposure/risk information would place very 
little weight on the uncertainties in these estimates and analyses. In 
some cases, elements of this approach have been supported by public 
commenters, leading some commenters to recommend setting the level of 
the primary O3 standard at least as low as 60 ppb. In 
recognition of such an alternative approach to viewing the evidence and 
information, in addition to proposing to set the level of the 
O3 standard from 65 to 70 ppb, the Administrator solicits 
comment on alternative standard levels below 65 ppb, and as low as 60 
ppb. In doing so, the Administrator reiterates that the CAA does not 
require the establishment of a primary NAAQS at a zero-risk level or at 
background concentration levels, but rather at a level that reduces 
risk sufficiently so as to protect public health with an adequate 
margin of safety (I.A).
---------------------------------------------------------------------------

    \174\ More specifically, as discussed above, respiratory 
symptoms have been evaluated following 6.6-hour exposures to average 
O3 concentrations of 60 ppb (Adams, 2006; Kim et al., 
2011) and 63 ppb (Schelegle et al., 2009). None of these studies 
reported a statistically significant increase in respiratory 
symptoms, compared to filtered air controls.
---------------------------------------------------------------------------

F. Proposed Decision on the Primary Standard

    For the reasons discussed above, and taking into account 
information and assessments presented in the 2013 ISA, 2014 HREA and 
integration of this information and assessments into staff conclusions 
in the 2014 PA, the advice and recommendations of CASAC, and public 
comments received during the development of these documents, the 
Administrator proposes to retain the current indicator, averaging time 
and form of the primary O3 standard, and to set a new level 
for the 8-hour primary O3 standard. Specifically, the 
Administrator proposes to set the level of the 8-hour primary 
O3 standard to within the range of 65 to 70 ppb. The 
proposed 8-hour primary standard would be met at an ambient air 
monitoring site when the 3-year average of the annual fourth-highest 
daily maximum 8-hour average O3 concentration is less than 
or equal to the level of the revised standard that is promulgated. 
Thus, the Administrator proposes to set a standard with a level within 
this range. For the reasons discussed above, the Administrator also 
solicits comment on setting the level of the primary O3 
standard below 65 ppb, and as low as 60 ppb.

III. Communication of Public Health Information

    Information on the public health implications of ambient 
concentrations of criteria pollutants is currently made available 
primarily through EPA's Air Quality Index (AQI) program. The AQI has 
been in use since its inception in 1999 (64 FR 42530). It provides 
accurate, timely, and easily understandable information about daily 
levels of pollution (40 CFR 58.50). It is designed to tell individual 
members of the public how clean or unhealthy their air is, whether 
health effects might be a concern, and, if so, measures individuals can 
take to reduce their exposure to air pollution. The AQI focuses on 
health effects individuals may experience within a few hours or days 
after breathing unhealthy air. The AQI establishes a nationally uniform 
system of indexing pollution concentrations for O3, carbon 
monoxide, nitrogen dioxide, particulate matter and sulfur dioxide. The 
AQI converts pollutant concentrations in a community's air to a number 
on a scale from 0 to 500. Reported AQI values enable the public to know 
whether air pollution concentrations in a particular location are 
characterized as good (0-50), moderate (51-100), unhealthy for 
sensitive groups (101-150), unhealthy (151-200), very unhealthy (201-
300), or hazardous (301-500). The AQI index value of 100 typically 
corresponds to the level of the short-term NAAQS for each pollutant. 
For the O3 NAAQS, an 8-hour average concentration of 75 ppb 
corresponds to an AQI value of 100. An AQI value greater than 100 means 
that a pollutant is in one of the unhealthy categories (i.e., unhealthy 
for sensitive groups, unhealthy, very unhealthy, or hazardous) on a 
given day; an AQI value at or below 100 means that a pollutant 
concentration is in one of the satisfactory categories (i.e., moderate 
or good). An additional consideration in

[[Page 75311]]

selecting breakpoints is for each category to span at least a 15 ppb 
range to allow for more accurate forecasting. Decisions about the 
pollutant concentrations at which to set the various AQI breakpoints, 
that delineate the various AQI categories, draw directly from the 
underlying health information that supports the NAAQS review.
    The Agency recognizes the importance of revising the AQI in a 
timely manner to be consistent with any revisions to the NAAQS. 
Therefore EPA is proposing conforming changes to the AQI, in connection 
with the Agency's proposed decision on revisions to the O3 
NAAQS if revisions to the primary standard are promulgated. These 
conforming changes would include setting the 100 level of the AQI at 
the same level as the revised primary O3 NAAQS and also 
making adjustments based on health information from this NAAQS review 
to AQI breakpoints at the lower end of each range (i.e., AQI values of 
50, 150, 200 and 300). The EPA does not propose to change the level at 
the top of the index (i.e., AQI value of 500) that typically is set 
equal to the Significant Harm Level (40 CFR 51.16), which would apply 
to state contingency plans.
    The EPA is proposing to revise the AQI for O3 by setting 
an AQI value of 100 equal to the level of the revised O3 
standard (65-70 ppb). The EPA is also proposing to revise the following 
breakpoints: An AQI value of 50 to within a range from 49-54 ppb; an 
AQI value of 150 to 85 ppb; an AQI value of 200 to 105 ppb, and an AQI 
value of 300 to 200 ppb. All these levels are averaged over 8 hours. 
The EPA is proposing to set an AQI value of 50, the breakpoint between 
the good and moderate categories, at 15 ppb below the value of the 
proposed standard, i.e. to within a range from 49 to 54 ppb. The EPA is 
taking comment on what level within this range to select, recognizing 
that there is no health message for either at-risk or healthy 
populations in the good category. Thus, the level selected should be 
below the lowest concentration (i.e., 60 ppb) that has been shown in 
controlled human exposure studies of healthy adults \175\ to cause 
moderate lung function decrements (i.e., FEV1 decrements 
>=10%, which could be adverse to people with lung disease), large lung 
function decrements (i.e., FEV1 decrements >=20%) in a small 
proportion of people, and airway inflammation.\176\ The EPA is 
proposing to set an AQI value of 150, the breakpoint between the 
unhealthy for sensitive groups and unhealthy categories, at 85 ppb. At 
this level, controlled human exposure studies of healthy adults 
indicate that up to 25% of exposed people are likely to have moderate 
lung function decrements (i.e., 25% have FEV1 decrements 
>=10%; 12% have FEV1 decrements >=15%) and up to 7% are 
likely to have large lung function decrements (i.e., FEV1 
decrements >=20%) (McDonnell et al., 2012; Figure 7). Large lung 
function decrements would likely interfere with normal activity for 
many healthy people. For people with lung disease, large lung function 
decrements would likely interfere with normal activity for most people 
and would increase the likelihood that they would seek medical 
treatment (72 FR 37850, July 11, 2007). The EPA is proposing to set an 
AQI value of 200, the breakpoint between the unhealthy and very 
unhealthy categories, at 105 ppb. At this level, controlled human 
exposure studies of healthy adults indicate that up to 38% of exposed 
people are likely to have moderate lung function decrements (i.e., 38% 
have FEV1 decrements >=10%; 22% have FEV1 
decrements >=15%) and up to 13% are likely to have large lung function 
decrements (i.e., FEV1 decrements >=20%). The EPA is 
proposing to set an AQI value of 300, the breakpoint between the very 
unhealthy and hazardous categories, at 200 ppb. At this level, 
controlled human exposure studies of healthy adults indicate that up to 
25% of exposed individuals are likely to have large lung function 
decrements (i.e., FEV1 decrements >=20%), which would 
interfere with daily activities for many of them. Large lung function 
decrements would interfere with daily activities for most people with 
lung disease, and likely cause them to seek medical attention.
---------------------------------------------------------------------------

    \175\ Effects would likely be greater in people with asthma.
    \176\ Exposures to 50 ppb have not been evaluated 
experimentally, but are estimated to potentially affect only a small 
proportion of healthy adults and with only a half to a third of the 
moderate to large lung function decrements observed at 60 ppb 
(McDonnell et al., 2012; Figure 7).

                                        Table 6--Proposed AQI Breakpoints
----------------------------------------------------------------------------------------------------------------
                                                                   Existing
                                                                  breakpoints    Proposed breakpoints  (ppb, 8-
                 AQI category                    Index values    (ppb, 8-hour             hour average)
                                                                   average)
----------------------------------------------------------------------------------------------------------------
Good..........................................            0-50            0-59  0-(49 to 54).
Moderate......................................          51-100           60-75  (50 to 55)-(65 to 70).
Unhealthy for Sensitive Groups................         101-150           76-95  (66 to 71)-85.
Unhealthy.....................................         151-200          96-115  86-105.
Very Unhealthy................................         201-300         116-374  106-200.
Hazardous.....................................         301-400            375-  201-.
                                                       401-500
----------------------------------------------------------------------------------------------------------------

    EPA believes that the proposed breakpoints reflect an appropriate 
balance between reflecting the health evidence that is the basis for 
the proposed primary O3 standard and providing category 
ranges that are large enough to be forecasted accurately, so that the 
new AQI for O3 can be implemented more easily in the public 
forum for which the AQI ultimately exists. However, the EPA recognizes 
that some have expressed alternative approaches to viewing the evidence 
and information and solicits comment on these proposed revisions to the 
AQI.
    With respect to reporting requirements (40 CFR part 58, Sec.  
58.50), EPA proposes to revise 40 CFR part 58, Sec.  58.50 (c) to 
require the AQI reporting requirements to be based on the latest 
available census figures, rather than the most recent decennial U.S. 
census. This change is consistent with our current practice of using 
the latest population figures to make monitoring requirements more 
responsive to changes in population.

[[Page 75312]]

IV. Rationale for Proposed Decision on the Secondary Standard

    This section presents the rationale for the Administrator's 
proposed decisions regarding the need to revise the current secondary 
O3 NAAQS and the appropriate revisions to the standard, 
including her proposed decisions that the current secondary standard is 
not requisite to protect public welfare and should be revised to 
provide additional public welfare protection. Based on her 
consideration of the full body of welfare effects evidence and related 
analyses, the Administrator proposes to conclude that ambient 
O3 concentrations in terms of a W126 index value, averaged 
across three consecutive years, within the range from 13 ppm-hrs to 17 
ppm-hrs would provide the requisite protection against known or 
anticipated adverse effects to the public welfare. In considering 
policy options for achieving that level of air quality, the 
Administrator has further considered the full body of information, 
including air quality analyses that relate ambient O3 
concentrations in terms of a three-year average W-126-based metric and 
in terms of the form and averaging time for the current standard. Based 
on this consideration, the Administrator proposes to revise the level 
of the current secondary standard to within the range of 0.065 to 0.070 
ppm to achieve the appropriate air quality.
    As discussed more fully below, this proposal is based on a thorough 
review, in the ISA, of the latest scientific information on 
O3-induced environmental effects. This proposed decision 
also takes into account: (1) Staff assessments in the PA of the most 
policy-relevant information in the ISA and WREA analyses of air 
quality, exposure, and ecological risks and associated ecosystem 
services; (2) CASAC advice and recommendations; and, (3) public 
comments received during the development of these documents, either in 
connection with CASAC meetings or separately.
    This proposed decision draws on the ISA's integrative synthesis of 
the entire body of evidence, published through July 2011, on 
environmental effects associated with the presence of O3 and 
related photochemical oxidants in the ambient air. As summarized in 
section IV.B below, this body of evidence addresses the range of 
environmental responses associated with exposure to ambient levels of 
O3 (U.S. EPA, 2013a, ISA chapters 9-10), and includes more 
than four hundred new studies that build on the extensive evidence base 
from the last review. This rationale also draws upon the results of 
quantitative exposure and risk assessments, summarized in section IV.C 
below. Section IV.D presents the Administrator's proposed decisions on 
the adequacy of the current secondary standard (section IV.D.3) drawing 
on both evidence-based and exposure/risk-based considerations in the PA 
(section IV.D.1) and advice from CASAC (section IV.D.2). Proposed 
conclusions on alternative standards are summarized in section IV.E.

A. Approach

    In evaluating whether it is appropriate to retain or revise the 
current secondary O3 standard, the Administrator adopts an 
approach in this review that builds upon the general approach used in 
the 2008 review \177\ and reflects the broader body of scientific 
evidence now available, updated exposure/risk information, advances in 
O3 air quality modeling, and air monitoring information. 
This review of the standard also considers the July 2013 remand of the 
secondary standard by the U.S. Court of Appeals for the D.C. Circuit, 
such that the proposed decision described herein incorporates the EPA's 
response to this remand.
---------------------------------------------------------------------------

    \177\ The 2008 revision of the O3 secondary standard, 
the proposed reconsideration of the 2008 decision, and the 2013 
court decision on the 2008 revision of the secondary standard are 
summarized in section I.C above.
---------------------------------------------------------------------------

    The Administrator's decisions in the 2008 review were based on an 
integration of information on welfare effects associated with exposure 
to O3, judgments on the adversity and public welfare 
significance of key effects, and judgments as to what standard would be 
requisite to protect public welfare. These considerations were informed 
by air quality and related analyses, quantitative exposure and risk 
assessments, and qualitative assessment of impacts that could not be 
quantified. As a result of the 2008 review, the Administrator concluded 
the then-current secondary standard did not provide the requisite 
public welfare protection and it was revised. The current secondary 
standard is 75 ppb based on the annual fourth-highest daily maximum 8-
hour average concentration, averaged over three consecutive years, 
which is identical to the current primary standard. In 2008, the 
Administrator considered the then-available monitoring data with regard 
to relationships between the revised primary standard and degree of 
protection of public welfare from cumulative seasonal O3 
exposures, expressed in terms of the W126 exposure index (described in 
section IV.B.1 below), and decided to revise the secondary standard to 
be equal to the revised primary standard (73 FR 16499-16500, March 27, 
2008). In remanding the 2008 decision on the secondary standard back to 
the EPA (described in section I.C above), the U.S. Court of Appeals for 
the D.C. Circuit determined that EPA did not specify what level of air 
quality was requisite to protect public welfare from adverse public 
welfare effects or explain why any such level would be requisite. 
Mississippi, 744 F.3d at 272-73.
    In addition to reviewing the most recent scientific information as 
required by the CAA, this rulemaking responds to the remand and fully 
explains the Administrator's proposed conclusions as to the level of 
air quality requisite to protect public welfare from known or 
anticipated effects. Our general approach in considering the scientific 
information available in this review involves consideration of the 
integrative synthesis of the entire body of available scientific 
evidence in the ISA (U.S. EPA, 2013a), including information on 
biologically relevant exposure indices, exposure/risk and air quality 
modeling analyses presented in the WREA (U.S. EPA, 2014b), staff 
analyses in the PA; advice and recommendations from CASAC (Frey, 2014b, 
c), and public comments. We note that in drawing conclusions on the 
secondary standard, the final decision to retain or revise the standard 
is a public welfare policy judgment to be made by the Administrator. 
The Administrator's final decision will draw upon the available 
scientific evidence for O3-attributable welfare effects and 
on analyses of exposures and public welfare risks based on impacts to 
vegetation, ecosystems and their associated services, as well as 
judgments about the appropriate weight to place on the range of 
uncertainties inherent in the evidence and analyses. Such judgments in 
the context of this review include: The weight to place on the evidence 
of specific vegetation-related effects estimated to result across a 
range of cumulative seasonal concentration-weighted O3 
exposures; the weight to give associated uncertainties, including those 
related to the variability in occurrence of such effects in areas of 
the U.S., especially areas of particular public welfare significance; 
and, judgments on the extent to which such effects in such areas may be 
considered adverse to public welfare.
    As provided in the CAA, section 109(b)(2), the secondary standard 
is to ``specify a level of air quality the attainment and maintenance 
of which in the judgment of the Administrator . . .

[[Page 75313]]

is requisite to protect the public welfare from any known or 
anticipated adverse effects associated with the presence of such air 
pollutant in the ambient air.'' Effects on welfare include, but are not 
limited to, ``effects on soils, water, crops, vegetation, man-made 
materials, animals, wildlife, weather, visibility, and climate, damage 
to and deterioration of property, and hazards to transportation, as 
well as effects on economic values and on personal comfort and well-
being'' (CAA section 302(h)). As recognized in the last review, the 
secondary standard is not meant to protect against all known or 
anticipated O3-related effects, but rather those that are 
judged to be adverse to the public welfare (73 FR 16496, March 27, 
2008). Thus, the level of protection from known or anticipated adverse 
effects to public welfare that is requisite for the secondary standard 
is a public welfare policy judgment to be made by the Administrator. In 
the current review, the Administrator's judgment is informed by 
conclusions drawn with regard to adversity of effects to public welfare 
in decisions on secondary O3 standards in past reviews.
    In the 2008 decision, the Administrator concluded that the degree 
to which O3 effects on vegetation should be considered to be 
adverse to the public welfare depends on the intended use of the 
vegetation and the significance of the vegetation to the public 
welfare, and also applied this concept beyond the species level to the 
ecosystem level (73 FR 16496, March 27, 2008). In so doing, the 
Administrator took note of ``a number of actions taken by Congress to 
establish public lands that are set aside for specific uses that are 
intended to provide benefits to the public welfare, including lands 
that are to be protected so as to conserve the scenic value and the 
natural vegetation and wildlife within such areas, and to leave them 
unimpaired for the enjoyment of future generations'' (73 FR 16496, 
March 27, 2008). The notice for the 2008 decision further noted that 
[s]uch public lands that are protected areas of national interest 
include national parks and forests, wildlife refuges, and wilderness 
areas'' (73 FR 16496, March 27, 2008).178 179 The 
Administrator additionally recognized that ``States, Tribes and public 
interest groups also set aside areas that are intended to provide 
similar benefits to the public welfare, for residents on State and 
Tribal lands, as well as for visitors to those areas'' (73 FR 16496, 
March 27, 2008). The Administrator took note of the ``clear public 
interest in and value of maintaining these areas in a condition that 
does not impair their intended use and the fact that many of these 
lands contain O3-sensitive species'' (73 FR 16496, March 27, 
2008). Similarly, in judgments of adversity to public welfare in the 
2010 proposed reconsideration, the Administrator proposed to place the 
highest priority and significance on vegetation and ecosystem effects 
to sensitive species that are known to or are likely to occur in 
federally protected areas such as national parks and other Class I 
areas,\180\ or on lands set aside by states, tribes and public interest 
groups to provide similar benefits to the public welfare (75 FR 3023-
24, January 19, 2010).
---------------------------------------------------------------------------

    \178\ For example, the National Park Service Organic Act of 1916 
established the National Park Service (NPS) and, in describing the 
role of the NPS with regard to ``Federal areas known as national 
parks, monuments, and reservations'', stated that the ``fundamental 
purpose'' for these Federal areas ``is to conserve the scenery and 
the natural and historic objects and the wild life therein and to 
provide for the enjoyment of the same in such manner and by such 
means as will leave them unimpaired for the enjoyment of future 
generations.'' 16 U.S.C. 1.
    \179\ As a second example, the Wilderness Act of 1964 defines 
designated ``wilderness areas'' in part as areas ``protected and 
managed so as to preserve [their] natural conditions'' and requires 
that these areas ``shall be administered for the use and enjoyment 
of the American people in such manner as will leave them unimpaired 
for future use and enjoyment as wilderness, and so as to provide for 
the protection of these areas, [and] the preservation of their 
wilderness character . . .'' 16 U.S.C. 1131 (a).
    \180\ As defined by section 162 of the CAA, Class I areas 
include all international parks, national wilderness areas which 
exceed 5,000 acres in size, national memorial parks which exceed 
5,000 acres in size, and national parks which exceed six thousand 
acres in size, provided the park or wilderness area was in existence 
on August 7, 1977, as well as other areas designated as Class I 
consistent with that section of the Act. The current Class I areas 
are specified at 40 CFR part 81.
---------------------------------------------------------------------------

    In the current review, our consideration of the scientific evidence 
for effects on vegetation is based fundamentally on using information 
from controlled chamber studies, free air methodologies, and field-
based observational, survey and gradient studies. Such evidence, 
discussed below, informs consideration of welfare endpoints and at-risk 
species and ecosystems on which to focus the current review, and 
consideration of the ambient O3 conditions under which 
various welfare effects are known or anticipated to occur. As in past 
reviews, we recognize that the available evidence has not provided 
identification of a threshold in exposure or ambient O3 
concentrations below which it can be concluded with confidence that 
O3-attributable effects on vegetation do not occur, when 
considering the broad range of O3-sensitive plant species 
growing within the U.S and the array of effects. This is due in part to 
the fact that research shows that there is variability in sensitivity 
between and within species and that numerous factors, i.e., chemical, 
physical, biological, and genetic, can influence the direction and 
magnitude of the studied effect (U.S. EPA, 2013a, section 9.4.8). In 
the absence of evidence for a discernible threshold, the general 
approach to considering the available O3 welfare effects 
evidence involves characterizing the confidence in conclusions 
regarding O3-attributable vegetation effects over the ranges 
of cumulative seasonal O3 exposure values evaluated in 
chamber studies and in field studies in areas where O3-
sensitive vegetation are known to occur, as well as characterizing the 
extent to which these effects can be considered adverse at the plant 
level and beyond. With this approach, we consider the evidence for 
O3 affecting other ecosystem components (such as soils, 
water, and wildlife) and their associated goods and services, through 
its effects on vegetation, as well as the associated uncertainties.
    Our general approach further recognizes the complexity of judgments 
to be made regarding the identification of particular vegetation 
effects as welfare effects and regarding the point that known or 
anticipated vegetation-related effects become adverse to the public 
welfare. For example, in addition to the magnitude of the ambient 
concentrations, the species present, their sensitivity to 
O3, and their public welfare importance are also essential 
considerations in drawing conclusions regarding the significance of 
public welfare impact. Taking this into account, we recognize the 
existence of a continuum from relatively higher ambient O3 
concentrations and conditions, in areas with sensitive species and 
public welfare significance, for which there might be general agreement 
that effects on public welfare are likely to occur, through lower 
concentrations at which the degree to which public welfare might be 
expected to be affected becomes increasingly uncertain.
    The evidence base for this review, summarized in section IV.B 
below, includes quantitative information across a broad array of 
vegetation effects (e.g., growth impairment during seedling, sapling 
and mature tree growth stages, visible foliar injury, and yield loss in 
annual crops) and across a diverse set of exposure methods from 
laboratory and field studies. While considering the full breadth of 
information available, we place greater weight on U.S. studies due to 
the often species-, site-, and climate-

[[Page 75314]]

specific nature of O3-related vegetation responses, and 
particularly emphasize those studies that include O3 
exposures that fall within the range of those likely to occur in the 
ambient air. We additionally recognize differences across different 
study types in what information they provide (U.S. EPA, 2013a, section 
9.2.6). For example, because conditions can be controlled in laboratory 
studies, responses in such studies may be less variable and smaller 
differences may be easier to detect. However, the controlled conditions 
may limit the range of responses or incompletely reflect pollutant 
bioavailability, so they may not reflect responses that would occur in 
the natural environment. Alternatively, field data can provide 
important information for assessments of multiple stressors or where 
site-specific factors significantly influence exposure. They are also 
often useful for analyses of larger geographic scales and higher levels 
of biological organization. However, depending on the type of field 
study, many field study conditions may not be controlled, which can 
make variability higher and differences harder to detect. In some field 
studies (e.g., gradient studies), the presence of confounding factors 
can also make it difficult to attribute observed effects to specific 
stressors.
    In developing quantitative exposure and risk assessments for this 
review, summarized in section IV.C below, we have placed greatest 
emphasis on studies that have evaluated plant response over multiple 
exposure levels and developed exposure-response (E-R) relationships 
that allow the estimation of plant responses over the range of 
O3 exposures pertinent to judgments on the current and 
potential alternative standards. In considering the information from 
these assessments, we focus particularly on the quantitative risks 
related to three types of O3 effects on vegetation and 
associated ecosystem services: visible foliar injury, biomass loss in 
trees, and crop yield loss. These risks were assessed in a range of 
analyses primarily involving national-scale air quality scenarios 
developed using model adjustments and interpolation methods. We 
consider particularly the national scale assessments for these 
scenarios, while recognizing the uncertainties with regard to the 
conditions they represent.
    With regard to the appropriate characterization of exposures 
associated with ambient O3 concentrations, as in the 2008 
and 1997 reviews, we continue to recognize the relevance of cumulative, 
seasonal, concentration-weighted exposures for assessing vegetation 
effects. More specifically, in the 2008 review, the EPA concluded and 
the CASAC agreed that the W126 cumulative exposure metric was the most 
appropriate to use to evaluate both the adequacy of the current 
secondary standard and the appropriateness of any potential revisions. 
As discussed in section IV.B.1 below, the information available in this 
review continues to support the use of such a metric and it is used in 
considering potential public welfare impacts in the sections below.

B. Welfare Effects Information

1. Nature of Effects and Biologically Relevant Exposure Metric
    This section describes the nature of O3-induced welfare 
effects, including the nature of the exposures that drive the 
biological and ecological responses (U.S. EPA, 2013a, chapter 9).
    Ozone's phytotoxic effects were first identified on grape leaves in 
a study published in 1958 (Richards et al., 1958). In the almost fifty 
years that have followed, extensive research has been conducted both in 
and outside of the U.S. to examine the impacts of O3 on 
plants and their associated ecosystems, since ``of the phytotoxic 
compounds commonly found in the ambient air, O3 is the most 
prevalent, impairing crop production and injuring native vegetation and 
ecosystems more than any other air pollutant'' (U.S. EPA, 1989, 1996a). 
As was established in prior reviews, O3 can interfere with 
carbon gain (photosynthesis) and allocation of carbon within the plant. 
As a result of decreased carbohydrate availability, fewer carbohydrates 
are available for plant growth, reproduction, and/or yield. For seed-
bearing plants, these reproductive effects will culminate in reduced 
seed production or yield (U.S. EPA, 1996a, pp. 5-28 and 5-29). Recent 
studies, assessed in the ISA, together with this longstanding and well-
established literature on O3-related vegetation effects, 
further contribute to the coherence and consistency of the vegetation 
effects evidence. As described in the ISA, a variety of factors in 
natural environments can either mitigate or exacerbate predicted 
O3-plant interactions and are recognized sources of 
uncertainty and variability. These include: (1) Multiple genetically 
influenced determinants of O3 sensitivity; (2) changing 
sensitivity to O3 across vegetative growth stages; (3) co-
occurring stressors and/or modifying environmental factors (U.S. EPA, 
2013a, section 9.4.8).
    Among the studies of vegetation effects, the ISA recognizes 
controlled chamber studies as the best method for isolating or 
characterizing the role of O3 in inducing the observed plant 
effects, and in assessing plant response to O3 at the finer 
scales (U.S. EPA, 2013a, sections 9.2 and 9.3). Recent controlled 
studies have focused on a variety of plant responses to O3 
including the underlying mechanisms governing such responses. These 
mechanisms include: (1) Reduced carbon dioxide uptake due to stomatal 
closure (U.S. EPA, 2013a, section 9.3.2.1); (2) the upregulation of 
genes associated with plant defense, signaling, hormone synthesis and 
secondary metabolism (U.S. EPA, 2013a, section 9.3.3.2); (3) the down 
regulation of genes related to photosynthesis and general metabolism 
(U.S. EPA, 2013a, section 9.3.3.2); (4) the loss of carbon assimilation 
capacity due to declines in the quantity and activity of key proteins 
and enzymes (U.S. EPA, 2013a, section 9.3.5.1); and (5) the negative 
impacts on the efficiency of the photosynthetic light reactions (U.S. 
EPA, 2013a, section 9.3.5.1). As described in the ISA, these new 
studies ``have increased knowledge of the molecular, biochemical and 
cellular mechanisms occurring in plants in response to O3'', 
adding ``to the understanding of the basic biology of how plants are 
affected by oxidative stress . . .'' (U.S. EPA, 2013a, p. 9-11). The 
ISA further concludes that controlled studies ``have clearly shown that 
exposure to O3 is causally linked to visible foliar injury, 
decreased photosynthesis, changes in reproduction, and decreased 
growth'' in many species of vegetation (U.S. EPA, 2013a, p. 1-15).
    Such effects at the plant scale can also be linked to an array of 
effects at larger spatial scales. For example, recent field studies at 
larger spatial scales, together with previously available evidence, 
support the controlled exposure study results and indicate that 
``ambient O3 exposures can affect ecosystem productivity, 
crop yield, water cycling, and ecosystem community composition'' (U.S. 
EPA, 2013a, p. 1-15; Chapter 9, section 9.4). The current body of 
O3 welfare effects evidence confirms the conclusions reached 
in the last review on the nature of O3-induced welfare 
effects and is summarized in the ISA as follows (U.S. EPA, 2013a, p. 1-
8).

    The welfare effects of O3 can be observed across 
spatial scales, starting at the subcellular and cellular level, then 
the whole plant and finally, ecosystem-level processes. Ozone 
effects at small spatial scales, such as the leaf of an individual 
plant, can result in effects along a continuum of larger spatial 
scales. These effects include altered rates of leaf gas exchange, 
growth, and reproduction at the individual plant level, and can 
result

[[Page 75315]]

in broad changes in ecosystems, such as productivity, carbon 
storage, water cycling, nutrient cycling, and community composition.

    Based on its assessment of this extensive body of science, the ISA 
determines that, with respect to vegetation and ecosystems, a causal 
relationship exists between exposure to O3 in ambient air 
and visible foliar injury effects on vegetation, reduced vegetation 
growth, reduced productivity in terrestrial ecosystems, reduced yield 
and quality of agricultural crops and alteration of below-ground 
biogeochemical cycles \181\ (U.S. EPA, 2013a, Table 1-2). In 
consideration of the evidence of O3 exposure and alterations 
in stomatal performance, ``which may affect plant and stand 
transpiration and therefore possibly affecting hydrological cycling,'' 
the ISA concludes that ``[a]lthough the direction of the response 
differed among studies,'' the evidence is sufficient to conclude a 
likely causal relationship between O3 exposure and the 
alteration of ecosystem water cycling (U.S. EPA, 2013a, section 2.6.3). 
The ISA also concludes that the evidence is sufficient to conclude a 
likely causal relationship between O3 exposure and the 
alteration of community composition of some terrestrial ecosystems 
(U.S. EPA, 2013a, section 2.6.5). Related to the effects on vegetation 
growth, productivity and, to some extent, below-ground biogeochemical 
cycles, the ISA additionally determines that a likely causal 
relationship exists between exposures to O3 in ambient air 
and reduced carbon sequestration (also termed carbon storage) \182\ in 
terrestrial ecosystems (U.S. EPA, 2013a, p. 1-10 and section 2.6.2). 
Modeling studies available in this review consistently found negative 
impacts of O3 on carbon sequestration, although the severity 
of impact was influenced by ``multiple interactions of biological and 
environmental factors'' (U.S. EPA, 2013a, p. 2-39).
---------------------------------------------------------------------------

    \181\ Based on studies focused on O3-associated 
alterations in quality and quantity of carbon input to soil, 
microbial community composition, and carbon and nutrient cycling, 
the ISA concludes that the evidence is sufficient ``to infer that 
there is a causal relationship between O3 exposure and 
the alteration of below-ground biogeochemical cycles'' (U.S. EPA, 
2013a, pp. 2-41 to 2-42).
    \182\ The terms sequestration and storage are used somewhat 
interchangeably in the ISA and other documents in this review.
---------------------------------------------------------------------------

    The ISA notes that ``[t]he suppression of ecosystem [carbon] sinks 
results in more [carbon dioxide] accumulation in the atmosphere'' and 
that a recent study has suggested that ``the indirect radiative forcing 
caused by O3 exposure through lowering the ecosystem 
[carbon] sink could have an even greater impact on global warming than 
the direct radiative forcing of O3'' (U.S. EPA, 2013a, p. 2-
39). With regard to direct radiative forcing, however, the ISA makes a 
stronger causality conclusion that the evidence supports a causal 
relationship between changes in tropospheric O3 
concentrations and radiative forcing \183\ (U.S. EPA, 2013a, section 
2.7.1). There are, however, ``large uncertainties in the magnitude of 
the radiative forcing estimate attributed to tropospheric 
O3, making the impact of tropospheric O3 on 
climate more uncertain than the effect of the longer-lived greenhouse 
gases'' (U.S. EPA, 2013a, p. 2-47). In this regard, the ISA observes 
that ``radiative forcing does not take into account the climate 
feedbacks that could amplify or dampen the actual surface temperature 
response,'' that ``[q]uantifying the change in surface temperature 
requires a complex climate simulation in which all important feedbacks 
and interactions are accounted for'' and that ``[t]he modeled surface 
temperature response to a given radiative forcing is highly uncertain 
and can vary greatly among models and from region to region within the 
same model'' (U.S. EPA, 2013a, p. 2-47). Even with these uncertainties, 
the ISA notes that ``global climate models indicate that tropospheric 
O3 has contributed to observed changes in global mean and 
regional surface temperatures'' and as a result of such evidence 
presented in climate modeling studies, concludes that there is likely 
to be a causal relationship between changes in tropospheric 
O3 concentrations and effects on climate (U.S. EPA, 2013a, 
p. 2-47). The ISA additionally notes, however, that ``[i]mportant 
uncertainties remain regarding the effect of tropospheric O3 
on future climate change'' (U.S. EPA, 2013a, p. 10-31).
---------------------------------------------------------------------------

    \183\ Radiative forcing by a greenhouse gas or aerosol is a 
metric used to quantify the change in balance between radiation 
coming into and going out of the atmosphere caused by the presence 
of that substance. For example, a reduction in outgoing infrared 
radiation has been associated with O3 by satellite data 
(U.S. EPA, 2013a, p. 2-47).
---------------------------------------------------------------------------

    Given the strong evidence base, and findings of causal or likely 
causal relationships with O3 in ambient air, including the 
quantitative assessments of relationships between O3 
exposure and occurrence and magnitude of effects, we give a primary 
focus to three main areas of effects. The three main areas, for which 
the evidence is summarized in more detail below, are: 1) impacts on 
tree growth, productivity and carbon storage (section IV.B.1.b); 2) 
crop yield loss (section IV.B.1.c); and 3) visible foliar injury 
(section IV.B.1.a). Consideration of these three areas includes, as 
appropriate, consideration of evidence of associated effects at larger 
scales, including ecosystems, and on associated ecosystem services.
    With regard to biologically based indices of exposure pertinent to 
O3 effects on vegetation, the ISA states the following (U.S. 
EPA, 2013a, p. 2-44).

    The main conclusions from the 1996 and 2006 O3 AQCDs 
[Air Quality Criteria Documents] regarding indices based on ambient 
exposure remain valid. These key conclusions can be restated as 
follows: ozone effects in plants are cumulative; higher 
O3 concentrations appear to be more important than lower 
concentrations in eliciting a response; plant sensitivity to 
O3 varies with time of day and plant development stage; 
[and] quantifying exposure with indices that cumulate hourly 
O3 concentrations and preferentially weight the higher 
concentrations improves the explanatory power of exposure/response 
models for growth and yield, over using indices based on mean and 
peak exposure values.

    The long-standing body of available evidence upon which these 
conclusions are based provides a wealth of information on aspects of 
O3 exposure that are important in influencing plant 
response. Specifically, a variety of ``factors with known or suspected 
bearing on the exposure-response relationship, including concentration, 
time of day, respite time, frequency of peak occurrence, plant 
phenology, predisposition, etc.,'' have been identified (U.S. EPA, 
2013a, section 9.5.2). In addition, the importance of the duration of 
the exposure and the relatively greater importance of higher 
concentrations over lower concentrations in determining plant response 
to O3 have been consistently well documented (U.S. EPA, 
2013a, section 9.5.3). Much of this evidence was assessed in the 1996 
AQCD (U.S. EPA, 1996a), while more recent work substantiating this 
evidence is assessed in the subsequent 2006 AQCD and 2013 ISA.
    Understanding of the biological basis for plant response to 
O3 exposure led to the development of a large number of 
``mathematical approaches for summarizing ambient air quality 
information in biologically meaningful forms for O3 
vegetation effects assessment purposes'' (U.S. EPA, 2013a, section 
9.5.3), including those that cumulate exposures over some specified 
period while weighting higher concentrations more than lower (U.S. EPA, 
2013a, section 9.5.2). As with any summary statistic, these exposure 
indices retain information on some, but not all, characteristics of the 
original observations. The 1996 AQCD contained an extensive review of 
the published

[[Page 75316]]

literature on different types of exposure-response metrics, including 
comparisons between metrics, from which the 1996 Staff Paper built its 
assessment of forms appropriate to consider in the context of the 
secondary NAAQS review. The result of these assessments was a decision 
by the EPA to focus on cumulative, concentration-weighted indices, 
which were recognized as the most appropriate biologically based 
metrics to consider in this context, with attention given primarily to 
two cumulative, concentration-weighted index forms: SUM06 and 
W126.\184\
---------------------------------------------------------------------------

    \184\ The SUM06 index is a threshold-based approach described as 
the sum of all hourly O3 concentrations greater or equal 
to 0.06 ppm observed during a specified daily and seasonal time 
window (U.S. EPA, 2013a, section 9.5.2). The W126 index is a non-
threshold approach described as the sigmoidally weighted sum of all 
hourly O3 concentrations observed during a specified 
daily and seasonal time window, where each hourly O3 
concentration is given a weight that increases from zero to one with 
increasing concentration (U.S. EPA, 2013a, section 9.5.2).
---------------------------------------------------------------------------

    In both the 1997 and 2008 reviews, the EPA concluded that the risk 
to vegetation comes primarily from cumulative exposures to 
O3 over a season or seasons \185\ and focused on metrics 
intended to characterize such exposures: SUM06 (61 FR 65716, December 
13, 1996) and W126 (72 FR 37818, July 11, 2007) in the 1997 and 2008 
reviews, respectively. Although in both reviews the policy decision was 
made to set the secondary standard to be identical to a revised primary 
standard (with an 8-hour averaging time), the Administrator, in both 
cases, also concluded, consistent with CASAC advice, that a cumulative, 
seasonal index was the most biologically relevant way to relate 
exposure to plant growth response (62 FR 38856, July 18, 1997; 73 FR 
16436, March 27, 2008; 75 FR 2938, January 19, 2010). This approach for 
characterizing O3 exposure concentrations that are 
biologically relevant with regard to potential vegetation effects 
received strong support from CASAC in the last review and again in this 
review, including strong support for use of such a metric as the form 
for the secondary standard (Henderson, 2006, 2008; Samet, 2010; Frey, 
2014c).
---------------------------------------------------------------------------

    \185\ In describing the form as ``seasonal'', the EPA is 
referring generally to the growing season of O3-sensitive 
vegetation, not to the seasons of the year (i.e., spring, summer, 
fall, winter).
---------------------------------------------------------------------------

    An alternative to using ambient exposure durations and 
concentrations to predict plant response has been developed in recent 
years, primarily in Europe, i.e., flux models. While ``some researchers 
have claimed that using flux models can be used {sic{time}  to better 
predict vegetation responses to O3 than exposure-based 
approaches'' because flux models estimate the ambient O3 
concentration that actually enters the leaf (i.e., flux or deposition) 
(U.S. EPA, 2013a, p. 9-114), it is important to note that ``[f]lux 
calculations are data intensive and must be carefully implemented'' 
(U.S. EPA, 2013a, p. 9-114). Further, the ISA states, ``[t]his uptake-
based approach to quantify the vegetation impact of O3 
requires inclusion of those factors that control the diurnal and 
seasonal O3 flux to vegetation (e.g., climate patterns, 
species and/or vegetation-type factors and site-specific factors)'' 
(U.S. EPA, 2013a, p. 9-114). In addition to these data requirements, 
each species has different amounts of internal detoxification potential 
that may protect species to differing degrees. The lack of detailed 
species- and site-specific data required for flux modeling in the U.S. 
and the lack of understanding of detoxification processes have 
continued to make this technique less viable for use in vulnerability 
and risk assessments at the national scale in the U.S. (U.S. EPA, 
2013a, section 9.5.4).
    Therefore, consistent with the ISA conclusions regarding the 
appropriateness of considering cumulative exposure indices that 
preferentially weight higher concentrations over lower for predicting 
O3 effects of concern based on the long-established 
conclusions and long-standing supporting evidence described above, and 
in light of continued CASAC support, we continue to focus on cumulative 
concentration-weighted indices as the most biologically relevant 
metrics for consideration of O3 exposures eliciting 
vegetation-related effects. Such a metric has an ``explanatory power'' 
that is improved ``over using indices based on mean and peak exposure 
values'' (U.S. EPA, 2013a, section 2.6.6.1, p. 2-44). In this review as 
in the last review, we use the W126 cumulative, seasonal metric (U.S. 
EPA, 2013a, sections 2.6.6.1 and 9.5.2) for consideration of the 
effects evidence and in the exposure and risk analyses in the WREA.
    The subsections below summarize key aspects of the welfare effects 
information for O3-elicited visible foliar injury (section 
IV.B.1.a), effects on forest tree growth, productivity and carbon 
storage (section IV.B.1.b) and reductions in crop yield (section 
IV.B.1.c), as well as associated effects.
a. Visible Foliar Injury
    Visible foliar injury resulting from exposure to O3 has 
been well characterized and documented over several decades of research 
on many tree, shrub, herbaceous, and crop species (U.S. EPA, 2013a, p. 
1-10; U.S. EPA, 2006a, 1996a, 1986, 1978). Additionally, O3-
induced visible foliar injury symptoms on certain plant species, such 
as black cherry, yellow-poplar and common milkweed, are considered 
diagnostic of exposure to O3 based on the consistent 
association established with experimental evidence (U.S. EPA, 2013a, p. 
1-10). The significance of O3 injury at the leaf and whole 
plant levels depends on an array of factors, and therefore, it is 
difficult to quantitatively relate visible foliar injury symptoms to 
vegetation effects such as individual tree growth, or effects at 
population or ecosystem levels (U.S. EPA, 2013a, p. 9-39). The ISA 
notes that visible foliar injury ``is not always a reliable indicator 
of other negative effects on vegetation'' (U.S. EPA, 2013a, p. 9-39). 
Factors that influence the significance to the leaf and whole plant 
include the amount of total leaf area affected, age of plant, size, 
developmental stage, and degree of functional redundancy among the 
existing leaf area (U.S. EPA, 2013a, section 9.4.2). Visible foliar 
injury by itself is an indication of phytotoxicity due to O3 
exposure, which occurs only when sensitive plants are exposed to 
elevated O3 concentrations in a predisposing environment, a 
major aspect of which is the lack of drought conditions during the year 
such injury is assessed (U.S. EPA, 2013a, section 9.4.2).
    Recent research is consistent with previous conclusions and that 
O3-induced visible foliar injury symptoms are well 
characterized and considered diagnostic on certain bioindicator plant 
species. Diagnostic usage for these plants has been verified 
experimentally in exposure-response studies, using exposure 
methodologies such as continuous stirred tank reactors, open-top 
chambers (OTCs), and free-air carbon dioxide (and ozone) enrichment 
(FACE). Although there remains a lack of robust exposure-response 
functions that would allow prediction of visible foliar injury severity 
and incidence under varying air quality and environmental conditions, 
``experimental evidence has clearly established a consistent 
association of the presence of visible foliar injury symptoms with 
O3 exposure, with greater exposure often resulting in 
greater and more prevalent injury'' (U.S. EPA, 2013a, section 9.4.2, p. 
9-41). The research newly available in this review includes: 1) 
controlled exposure studies conducted to test and verify the 
O3

[[Page 75317]]

sensitivity and response of potential new bioindicator plant species; 
2) multi-year field surveys in several National Wildlife Refuges (NWR) 
documenting the presence of foliar injury in valued areas; and 3) 
ongoing data collection and assessment by the U.S. Forest Service's 
Forest Health Monitoring Forest Inventory and Analysis (USFS FHM/FIA) 
program, including multi-year trend analysis (U.S. EPA, 2013a, section 
9.4.2). These recent studies, in combination with the entire body of 
available evidence, thus form the basis for the ISA determinations of a 
causal relationship between ambient O3 exposure and the 
occurrence of O3-induced visible foliar injury on sensitive 
vegetation across the U.S. (U.S. EPA, 2013a, p. 9-42).
    Recently available evidence confirms the evidence available in 
previous reviews that visible foliar injury can occur when sensitive 
plants are exposed to elevated O3 concentrations in a 
predisposing environment (i.e., adequate soil moisture) (U.S. EPA, 
2013a, section 9.4.2). Recent evidence also continues to support 
previous findings that indicated the occurrence of visible foliar 
injury at cumulative ambient O3 exposures previously 
examined.
    With regard to evidence from controlled exposure studies, a recent 
study, using continuously stirred tank reactor chambers, evaluated the 
occurrence of O3 characteristic visible foliar injury 
symptoms on 28 species of plants that were suspected of being 
O3 sensitive and most of which grow naturally throughout the 
northeast and midwest U.S., including in national parks and wilderness 
areas (U.S. EPA, 2013a, section 9.4.2.1; Kline et al., 2008). Across 
the 28 tested species, the study reported O3-induced 
responses in 12, 20, 28 and 28 species at the 30, 60, 90 and 120 ppb 
exposure concentrations,\186\ respectively; the plants were exposed for 
7 hours per each weekday over 21 to 29 summer days (Kline et al., 
2008).
---------------------------------------------------------------------------

    \186\ Two of the target exposure levels, 30 and 60 ppb, fall 
below the level of the current standard (75 ppb), although the 
exposures were average concentrations for 7-hour exposures across 
durations shorter than a month. Because the form of the current 
standard targets peak concentrations in a season, an area that just 
meets the current standard can be expected to have mean 
concentrations well below that level due to variability in ambient 
O3 concentrations.
---------------------------------------------------------------------------

    A string of recently published multi-year field studies provide a 
complementary line of field-based evidence by documenting the incidence 
of visible foliar injury symptoms on a variety of O3-
sensitive species over multiple years and across a range of cumulative, 
seasonal exposure values in several eastern and midwestern NWRs (U.S. 
EPA, 2013a, section 9.4.2.1; Davis and Orendovici, 2006; Davis, 2007a, 
b; Davis, 2009). Some of these studies also included information 
regarding soil moisture stress using the Palmer Drought Severity Index 
(PDSI). While environmental conditions and species varied across the 
four NWRs, visible foliar injury was documented to a varying degree at 
each site.
    By far the most extensive field-based dataset of visible foliar 
injury incidence is that obtained by the USFS FHM/FIA biomonitoring 
network program. A trend analysis of data from the sites located in the 
Northeast and North Central U.S. for the 16 year period from 1994 
through 2009 (Smith, 2012) describes evidence of visible foliar injury 
occurrence in the field as well as some insight into the influence of 
changes in air quality and soil moisture on visible foliar injury and 
the difficulty inherent in predicting foliar injury response under 
different air quality/soil moisture scenarios (Smith, 2012; U.S. EPA, 
2013a, section 9.2.4.1). Study results showed that incidence and 
severity of foliar injury were dependent on local site conditions for 
soil moisture availability and O3 exposure. Overall, there 
was a declining trend in the incidence of visible foliar injury as peak 
O3 concentrations declined, although the study additionally 
indicated that moderate O3 exposures continued to cause 
visible foliar injury at sites throughout the region (U.S. EPA, 2013a, 
p. 9-40). In a similar assessment of the USFS FHM/FIA data in the West, 
six years (2000 to 2005) of biomonitoring data, during a period where a 
large proportion of California sites did not meet the current standard, 
indicated O3-related visible foliar injury in 25-37% of 
biosites in California (Campbell et al., 2007; U.S. EPA, 2013a, section 
9.4.2.1).\187\ These recent studies provide additional evidence of 
O3-induced visible foliar injury in many areas across the 
U.S. and augment the EPA's understanding of O3-related 
visible foliar injury and of factors, such as soil moisture, that 
influence associations between O3 exposures or 
concentrations and visible foliar injury.
---------------------------------------------------------------------------

    \187\ See: http://www.epa.gov/airtrends/values.html.
---------------------------------------------------------------------------

b. Effects on Forest Tree Growth, Productivity and Carbon Storage
    Ozone has been shown to affect a number of important U.S. tree 
species with respect to growth, productivity, and carbon storage. 
Ambient O3 concentrations have long been known to cause 
decreases in photosynthetic rates and plant growth. As discussed in the 
ISA, research published since the 2006 AQCD substantiates prior 
conclusions regarding O3-related effects on forest tree 
growth, productivity and carbon storage. The ISA states, ``previous 
O3 AQCDs concluded that there is strong evidence that 
exposure to O3 decreases photosynthesis and growth in 
numerous plant species'' and that ``[s]tudies published since the 2008 
review support those conclusions'' (U.S. EPA, 2013a, p. 9-42). The 
available studies come from a variety of different study types that 
cover an array of different species, effects endpoints, levels of 
biological organization and exposure methods and durations. The 
O3-induced effects at the plant scale may translate to the 
ecosystem scale, with changes in productivity and carbon storage. As 
stated in the ISA, ``[s]tudies conducted during the past four decades 
have demonstrated unequivocally that O3 alters biomass 
allocation and plant reproduction'' (U.S. EPA, 2013a, p. 1-10).
    The previously available strong evidence for trees includes robust 
E-R functions for seedling relative biomass loss (RBL) \188\ in 11 
species developed under the National Health and Environmental Effects 
Research Laboratory-Western Ecology Division program. This series of 
experiments used OTCs to study seedling growth response for a single 
growing season under a variety of O3 exposures (ranging from 
near background to well above current ambient concentrations) and 
growing conditions (U.S. EPA, 2013a, section 9.6.2; Lee and Hogsett, 
1996). The evidence from these studies shows that there is a wide range 
in sensitivity across the studied species in the seedling growth stage 
over the course of a single growing season, with some species being 
extremely sensitive and others being very insensitive over the range of 
cumulative O3 exposures studied (U.S. EPA, 2014c, Figure 5-
1). At the other end of the organizational spectrum, field-based 
studies of species growing in natural stands have compared observed 
plant response across a number of different sites and/or years when 
exposed to varying ambient O3 exposure conditions. For 
example, a study conducted in forest stands in the southern Appalachian 
Mountains during a period when O3 concentrations exceeded 
the current standard found that the cumulative

[[Page 75318]]

effects of O3 decreased seasonal stem growth (measured as a 
change in circumference) by 30-50 percent for most of the examined tree 
species (i.e., tulip poplar, black cherry, red maple, sugar maple) in a 
high O3 year in comparison to a low O3 year (U.S. 
EPA, 2013a, section 9.4.3.1; McLaughlin et al., 2007a). The study also 
reported that high ambient O3 concentrations can increase 
whole-tree water use and in turn reduce late-season streamflow 
(McLaughlin et al., 2007b; U.S. EPA, 2013a, p. 9-43).
---------------------------------------------------------------------------

    \188\ These functions for RBL estimate reduction in a year's 
growth as a percentage of that expected in the absence of 
O3 (U.S. EPA, 2013a, section 9.6.2; U.S. EPA, 2014b, 
section 6.2).
---------------------------------------------------------------------------

    The magnitude of O3 impact on ecosystem productivity and 
on forest composition can vary among plant communities based on several 
factors including: the type of stand or community in which the 
sensitive species occurs (e.g., single species versus mixed canopy), 
the role or position of the species in the stand (e.g., dominant, sub-
dominant, canopy, understory), the sensitivity of co-occurring species 
and environmental factors (e.g., drought and other factors). For 
example, O3 has been found to have little impact on white 
fir, but to greatly reduce growth of ponderosa pine in southern 
California, and cause decreased net primary production of most forest 
types in the Mid-Atlantic region, although only small impacts on 
spruce-fir forest (U.S. EPA, 2013a, section 9.4.3.4).
    As noted above, long-standing evidence has demonstrated that 
O3 alters biomass allocation and plant reproduction (U.S. 
EPA, 2013a, section 9.4.3). Several studies published since the 2006 
O3 AQCD further demonstrate that O3 can alter 
reproductive processes in herbaceous and woody plant species, such as 
the timing of flowering and the number of flowers, fruits and seeds 
(U.S. EPA, 2013a, section 9.4.3.3). Further, limited evidence in 
previous reviews reported that vegetation effects from a single year of 
exposure to elevated O3 could be observed in the following 
year. For example, growth affected by a reduction in carbohydrate 
storage in one year may result in the limitation of growth in the 
following year. Such ``carry-over'' effects have been documented in the 
growth of some tree seedlings and in roots (U.S. EPA, 2013a, section 
9.4.8; Andersen, et al., 1997). In the current review, additional 
field-based evidence expands the EPA's understanding of the 
consequences of single and multi-year O3 exposures in 
subsequent years. A number of studies were conducted at a planted 
forest at the Aspen FACE site in Wisconsin. These studies, which 
occurred in a field setting (more similar to natural forest stands than 
OTC studies), observed tree growth responses when grown in single or 
two species stands within 30-m diameter rings and exposed over a period 
of ten years to existing ambient conditions and elevated O3 
concentrations. Some studies indicate the potential for carry-over 
effects, such as those showing that the effects of O3 on 
birch seeds (reduced weight, germination, and starch levels) could lead 
to a negative impact on species regeneration in subsequent years, and 
that the effect of reduced aspen bud size might have been related to 
the observed delay in spring leaf development. These effects suggest 
that elevated O3 exposures have the potential to alter 
carbon metabolism of overwintering buds, which may have subsequent 
effects in the following year (Darbah, et al., 2008, 2007; Riikonen et 
al., 2008; U.S. EPA, 2013a, section 9.4.3). Other studies found that, 
in addition to affecting tree heights, diameters, and main stem volumes 
in the aspen community, elevated O3 over a 7-year study 
period was reported to increase the rate of conversion from a mixed 
aspen-birch community to a community dominated by the more tolerant 
birch, leading the authors to conclude that elevated O3 may 
alter intra- and inter-species competition within a forest stand (U.S. 
EPA, 2013a, section 9.4.3; Kubiske et al., 2006; Kubiske et al., 2007). 
These studies confirm earlier FACE results of aspen growth reductions 
from a 6-7 year exposure to elevated O3 and of cumulative 
biomass impacts associated with changes in annual production in studied 
tree communities (U.S. EPA, 2013a, section 9.4.3; King et al., 2005).
    In addition to individual studies, recent meta-analyses have 
quantitatively analyzed the effect of O3 on trees across 
large numbers of studies. In particular, a recent meta-analysis of 55 
peer reviewed studies from the past 40 years indicates a negative 
relationship between O3 concentrations in the northern 
hemisphere during that period and stomatal conductance and 
photosynthesis, which decreases growth (U.S. EPA, 2013a, section 
9.4.3.1; Wittig et al., 2007). In this analysis, younger trees (less 
than 4 years) were affected less by O3 than older trees 
(U.S. EPA, 2013a, section 9.4.3.1; Wittig, et al., 2007). A second 
meta-analysis that quantitatively compiled 263 peer-reviewed studies 
``demonstrates the coherence of O3 effects across numerous 
studies and species that used a variety of experimental techniques, and 
these results support the conclusion of the previous AQCD that exposure 
to O3 decreases plant growth'' (U.S. EPA, 2013a, p. 9-43). 
Other meta-analyses have examined the effect of O3 exposure 
on root growth and generally found that O3 exposure reduced 
carbon allocated to roots (U.S. EPA, 2013a, pp. 9-45 to 9-46).
    As noted above, robust E-R functions have been developed for 11 
tree species (black cherry, Douglas fir, loblolly pine, ponderosa pine, 
quaking aspen, red alder, red maple, sugar maple, tulip poplar, 
Virginia pine, white pine) from the extensive evidence base of 
O3-induced growth effects that was also available and relied 
upon in the previous review. While the species for which robust E-R 
functions have been developed represent only a small fraction (0.8 
percent) of the total number of native tree species in the contiguous 
U.S. (1,497), this small subset includes eastern and western species, 
deciduous and coniferous species, and species that grow in a variety of 
ecosystems and represent a range of tolerance to O3 (U.S. 
EPA, 2013a, section 9.6.2; U.S. EPA, 2014b, section 6.2, Figure 6-2, 
Table 6-1). Each of these species were studied in OTCs, with most 
species studied multiple times under a wide range of exposure and/or 
growing conditions, with separate E-R functions developed for each 
combination of species, exposure condition and growing condition 
scenario. These species-specific composite E-R functions have been 
successfully used to predict the biomass loss response from tree 
seedling species over a range of cumulative exposure conditions (U.S. 
EPA, 2013a, section 9.6.2). The 11 robust composite E-R functions 
available in the last review, as well as the E-R for eastern cottonwood 
(derived from a field study in which O3 and climate 
conditions were not controlled), are described in the ISA and graphed 
in the WREA to illustrate the predicted responses of these species over 
a wide range of cumulative exposures (U.S. EPA, 2014b, section 6.2, 
Table 6-1 and Figure 6-2; U.S. EPA, 2013a, section 9.6.2). For some of 
these species, the E-R function is based on a single study (e.g., red 
maple), while for other species there were as many as 11 studies 
available (ponderosa pine). In total, the E-R functions developed for 
these 12 species (the 11 with robust composite E-R functions plus 
eastern cottonwood) reflect 52 tree seedling studies. A stochastic 
analysis in WREA, summarized in section IV.C below, indicates the 
potential for within species variability to contribute appreciably to 
estimates for each species. Consideration of biomass loss estimates in 
the PA and in discussions

[[Page 75319]]

below, however, is based on conventional method and focuses on 
estimates for the 11 species for which the robust datasets from OTC 
experiments are available, in consideration of CASAC advice.\189\
---------------------------------------------------------------------------

    \189\ The CASAC cautioned EPA against placing too much emphasis 
on the eastern cottonwood data, stating that while the cottonwood 
data are important results, they are not as strong as those from 
other experiments that developed E-R functions based on controlled 
O3 exposure in OTCs; they are from a single gradient 
study that did not control for O3 and climatic conditions 
and they show extreme sensitivity to O3 compared to other 
studies (Frey, 2014c, p. 10).
---------------------------------------------------------------------------

c. Crop Yield Loss
    The ``detrimental effect of O3 on crop production has 
been recognized since the 1960s'' (U.S. EPA, 2013a, p. 1-10, section 
9.4.4). On the whole, the newly available evidence supports previous 
conclusions that exposure to O3 decreases growth and yield 
of crops. The ISA describes average crop yield loss reported across a 
number of recently published meta-analyses and identifies several new 
exposure studies that support prior findings for a variety of crops of 
decreased yield and biomass with increased O3 exposure (U.S. 
EPA, 2013a, section 9.4.4.1, Table 9-17). Studies have also ``linked 
increasing O3 concentration to decreased photosynthetic 
rates and accelerated aging in leaves, which are related to yield'' and 
described effects of O3 on crop quality, such as nutritive 
quality of grasses, macro- and micronutrient concentrations in fruits 
and vegetable crops and cotton fiber quality (U.S. EPA, 2013a, p. 1-10, 
section 9.4.4). The findings of the newly available studies do not 
change the basic understanding of O3-related crop yield loss 
since the last review and little additional information is available in 
this review on factors that influence associations between 
O3 levels and crop yield loss (U.S. EPA, 2013a, section 
9.4.4.).
    The new evidence has strengthened support for previously 
established E-R functions for 10 crops (barley, field corn, cotton, 
kidney bean, lettuce, peanut, potato, grain sorghum, soybean and winter 
wheat), reducing two important areas of uncertainty, especially for 
soybean. The established E-R functions were developed from OTC-type 
experiments (U.S. EPA, 2013a, section 9.6.3; U.S. EPA, 2014b, section 
6.2; U.S. EPA, 2014c, Figure 5-4). In this review, the ISA included an 
analysis comparing OTC data for soybean from the National Crop Loss 
Assessment Network (NCLAN) with field-based data from SoyFACE (Soybean 
Free Air Concentration Enrichment) studies (U.S. EPA, 2013a, section 
9.6.3.1).\190\ Yield loss in soybean from O3 exposure at the 
SoyFACE field experiment was reliably predicted by soybean E-R 
functions developed from NCLAN data, demonstrating a robustness of the 
E-R functions developed with NCLAN data to predict relative yield loss 
from O3 exposure. A second area of uncertainty that was 
reduced is that regarding the application of the NCLAN E-R functions, 
developed in the 1980s, to more recent cultivars currently growing in 
the field. Recent studies, especially those focused on soybean, provide 
little evidence that crops are becoming more tolerant of O3 
(U.S. EPA, 2006a; U.S. EPA, 2013a). A meta-analysis of 53 studies found 
consistent deleterious effects of O3 exposures on soybean 
from studies published between 1973 and 2001 (Morgan et al., 2003). 
Further, Betzelberger et al. (2010) utilized the SoyFACE facility to 
compare the impact of elevated O3 concentrations across 10 
soybean cultivars to investigate intraspecific variability of the 
O3 response, finding that the E-R functions derived for 
these 10 current cultivars were similar to the response functions 
derived from the NCLAN studies conducted in the 1980s (Heagle, 1989), 
``suggesting there has not been any selection for increased tolerance 
to O3 in more recent cultivars'' (U.S. EPA, 2013a, p. 9-59). 
Additionally, the ISA comparisons of NCLAN and SoyFACE data referenced 
above ``confirm that the response of soybean yield to O3 
exposure has not changed in current cultivars'' (U.S. EPA, 2013a, p. 9-
59; section 9.6.3.1). Thus, the evidence available in the current 
review has reduced uncertainties in two areas with regard to the use of 
E-R functions for soybean crop yield loss.
---------------------------------------------------------------------------

    \190\ The NCLAN program, which was undertaken in the early to 
mid-1980s, assessed multiple U.S. crops, locations, and 
O3 exposure levels, using consistent methods, to provide 
the largest, most uniform database on the effects of O3 
on agricultural crop yields (U.S. EPA 1996a; U.S. EPA, 2006a; U.S. 
EPA, 2013a, sections 9.2, 9.4, and 9.6, Frey, 2014c, p. 9). The 
SoyFACE experiment was a chamberless (or free-air) field-based 
exposure study conducted in Illinois from 2001-2009 (U.S. EPA, 
2013a, section 9.2.4).
---------------------------------------------------------------------------

    During past O3 NAAQS reviews, there were very few 
studies that estimated O3 impacts on crop yields at large 
geographical scales (i.e., regional, national or global). Recent 
modeling studies of the impact of O3 concentrations 
historically found that increased O3 in the past generally 
reduced crop yield, but the impacts varied across regions and crop 
species, with the largest O3-induced crop yield losses 
estimated to have occurred in high-production areas that had been 
exposed to elevated O3 concentrations, such as the Midwest 
and the Mississippi Valley regions of the U.S. (U.S. EPA, 2013a, 
Section 9.4.4.1). Among affected crop species, the estimated yield loss 
for wheat and soybean were higher than rice and maize (i.e., field 
corn). Additionally, satellite and ground-based O3 
measurements have assessed soybean yield loss estimated to result from 
O3 over the continuous area of Illinois, Iowa, and 
Wisconsin, finding a relationship which correlates well with the 
previous results from FACE- and OTC-type experiments (U.S. EPA, 2013a, 
section 9.4.4.1).
    Thus, consistent with the conclusions of the 1996 and 2006 CDs, the 
current ISA concludes that O3 concentrations in ambient air 
can reduce the yield of major commodity crops in the U.S. and focuses 
on use of crop E-R functions based on OTC experiments to characterize 
the quantitative relationship between ambient O3 
concentrations and yield loss (U.S. EPA, 2013a, section 9.4.4). In the 
PA, as summarized in sections IV.D and IV.E below, relative yield loss 
(RYL) is estimated for 10 different crops using the individual E-R 
functions described in the WREA \191\ (U.S. EPA, 2014b, section 6.2; 
U.S. EPA, 2014c, section 6.3).
---------------------------------------------------------------------------

    \191\ These functions for RYL estimate reduction in a year's 
growth as a percentage of that expected in the absence of 
O3 (U.S. EPA, 2013a, section 9.6.2; U.S. EPA, 2014b, 
section 6.2).
---------------------------------------------------------------------------

2. Potential Impacts on Public Welfare
    The magnitude of a public welfare impact or the degree to which it 
may be considered adverse is dependent upon the nature and severity of 
the specific welfare or ecological effect, the use or service (and 
value) of the affected ecosystem and the relevance and significance of 
that use \192\ to the public welfare. In the preamble of the 2012 final 
notice of rulemaking on the secondary standards for oxides of nitrogen 
and sulfur (NOx/SOx), the EPA stated that ``[a]n evaluation of 
adversity to the public welfare might consider the likelihood, type, 
magnitude, and spatial scale of the effect, as well as the potential 
for recovery and any uncertainties relating to these conditions'' (77 
FR 20232, April 3,

[[Page 75320]]

2012). The EPA additionally stated that ``[c]onceptually, changes in 
ecosystem services may be used to aid in characterizing a known or 
anticipated adverse effect to public welfare'' (77 FR 20232, April 3, 
2012).\193\
---------------------------------------------------------------------------

    \192\ Ecosystem services have been defined as ``the benefits 
that people obtain from ecosystems'' (U.S. EPA, 2013a, Preamble, p. 
1xxii; UNEP, 2003) and thus are an aspect of the use of a type of 
vegetation or ecosystem. Similarly, a definition used for the 
purposes of EPA benefits assessments states that ecological goods 
and services are the ``outputs of ecological functions or processes 
that directly or indirectly contribute to social welfare or have the 
potential to do so in the future'' and that ``[s]ome outputs may be 
bought and sold, but most are not marketed'' (U.S. EPA, 2006b).
    \193\ Ecosystem services analyses were one of the tools used in 
that review to inform the decisions made with regard to adequacy and 
as such, were used in conjunction with other considerations in the 
discussion of adversity to public welfare (77 FR 20241).
---------------------------------------------------------------------------

    Potential public welfare impacts associated with ecosystems and 
associated services have a range of dimensions, including spatial, 
temporal, and social, and these likely will vary depending on the type 
of effect being characterized. For example, ecosystems can cover a 
range of spatial scales, and the services they provide can accrue 
locally or be distributed more broadly, such as when crops are sold and 
eaten locally and/or also sold in regional, national and world markets. 
Accordingly, impacts can be localized or more widely distributed. 
Further, ecosystem services can be realized over a range of temporal 
scales from immediate up to longer term. The size of the societal unit 
receiving benefits from ecosystem services can also vary dramatically. 
For example, a national park can provide direct recreational services 
to the thousands of visitors that come each year, but also provide an 
indirect value to the millions who may not visit but receive 
satisfaction from knowing it exists and is preserved for the future 
(U.S. EPA, 2014b, chapter 5, section 5.5.1).
    As recognized in the last review, judgments regarding adverse 
effects to the public welfare depend on the intended use for and 
significance of the affected vegetation, ecological receptors, 
ecosystems and resources to the public welfare (73 FR 16496, March 27, 
2008).\194\ For example, a number of different types of locations 
provide services of special significance to the public welfare. As 
emphasized in previous O3 NAAQS decisions, and summarized in 
section IV.A above, Class I areas and other parks have been afforded 
special federal protection to preserve services that provide for the 
enjoyment of these resources for current and future generations. 
Surveys have indicated that Americans rank as very important the 
existence of the resource, the option or availability of the resource 
and the ability to bequest or pass on to future generations (Cordell et 
al., 2008). These and other services provided by Class I areas and 
other areas that have been afforded special protection can flow in part 
or entirely from the vegetation that grows there. Aesthetic value and 
outdoor recreation depend on the perceived scenic beauty of the 
environment. Many outdoor recreation activities directly depend on the 
scenic value of the area, in particular scenic viewing, wildlife-
watching, hiking, and camping (U.S. EPA, 2014b, chapters 5 and 7). 
Further, analyses have reported that the American public values--in 
monetary as well as nonmonetary ways--the protection of forests from 
air pollution damage. In fact, studies that have assessed willingness-
to-pay for spruce-fir forest protection in the southeastern U.S. from 
air pollution and insect damage have found that values held by the 
survey respondents for the more abstract services (existence, option 
and bequest) were greater than those for recreation or other services 
(U.S. EPA, 2014b, Table 5-6; Haefele et al., 1991; Holmes and Kramer, 
1995).
---------------------------------------------------------------------------

    \194\ As noted in section IV.A above, in judgments regarding 
public welfare significance in the last review, emphasis was placed 
on vegetation and ecosystem effects to sensitive species that are 
known to or are likely to occur in federally protected areas such as 
national parks and other Class I areas, or on lands set aside by 
states, tribes and public interest groups to provide similar 
benefits to the public welfare (73 FR 16496, March 27, 2008; 75 FR 
3023-24, January 19, 2010).
---------------------------------------------------------------------------

    There are several potential public welfare impacts related to the 
three main categories of O3 effects on vegetation (i.e., 
effects on tree growth, productivity and carbon storage; crop yield 
loss; and, visible foliar injury, as described in section IV.B.1 above) 
and their associated ecosystem services. At the same time, these three 
categories of effects differ with regard to aspects important to 
judging their public welfare significance. Judgments regarding crop 
yield loss, for example, depend on considerations related to the heavy 
management of agriculture in the U.S., while judgments regarding the 
other categories of effects generally relate to considerations 
regarding forested areas. For example, while both tree growth-related 
effects and visible foliar injury have the potential to be significant 
to the public welfare through impacts in Class I and other protected 
areas, they differ in how they might be significant and with regard to 
the clarity of the data which describes the relationship between the 
effect and the services potentially affected.
    With regard to effects on tree growth, reduced growth is associated 
with effects on an array of ecosystem services including reduced 
productivity, altered forest and forest community (plant, insect and 
microbe) composition, reduced carbon storage and altered water cycling 
(U.S. EPA, 2013a, Figure 9-1, sections 9.4.1.1 and 9.4.1.2; U.S. EPA, 
2014b, section 6.1). For example, forest or forest community 
composition can be affected through O3 effects on growth and 
reproductive success of sensitive species in the community, with the 
extent of compositional changes dependent on factors such as 
competitive interactions (U.S. EPA, 2013a, sections 9.4.3 and 9.4.3.1). 
Depending on the type and location of the affected ecosystem, services 
benefitting the public in other ways can be affected as well. For 
example, other services valued by people that can be affected by 
reduced tree growth, productivity and carbon storage include aesthetic 
value, food, fiber, timber, other forest products, habitat, 
recreational opportunities, climate and water regulation, erosion 
control, air pollution removal, hydrologic and fire regime 
stabilization (U.S. EPA 2013a, sections 9.4.1.1 and 9.4.1.2; U.S. EPA, 
2014b, section 6.1, Figure 6-1, section 6.4, Table 6-13). Further, 
impacts on some of these services (e.g., forest or forest community 
composition) may be considered of greater public welfare significance 
when occurring in Class I or other protected areas.
    Consideration of the magnitude of tree seedling growth effects that 
might cause or contribute to adverse effects for trees, forests, 
forested ecosystems or the public welfare is complicated by aspects of, 
or limitations in, the available information. For example, the evidence 
on tree seedling growth effects, deriving from the E-R functions for 11 
species, provides no clear threshold or breakpoint in the response to 
O3 exposure. Additionally, there are no established 
relationships between magnitude of tree seedling growth reduction and 
forest ecosystem impacts and, as noted in section IV.B.1.b above, other 
factors can influence the degree to which O3-induced growth 
effects in a sensitive species affect forest and forest community 
composition and other ecosystem service flows from forested ecosystems. 
These include: 1) the type of stand or community in which the sensitive 
species is found (i.e., single species versus mixed canopy); 2) the 
role or position the species has in the stand (i.e., dominant, sub-
dominant, canopy, understory); 3) the O3 sensitivity of the 
other co-occurring species (O3 sensitive or tolerant); and 
4) environmental factors, such as soil moisture and others. The lack of 
such established relationships complicates judgments as to the extent 
to which different amounts of tree seedling growth would be significant 
to the public welfare and thus an important consideration in the level 
of protection for the secondary standard.
    During the 1997 review of the secondary standard, views related to

[[Page 75321]]

this issue were provided by a 1996 workshop of 16 then-leading 
scientists in the context of discussing their views for a secondary 
O3 standard (Heck and Cowling, 1997). In their consideration 
of tree growth effects as an indicator for forest ecosystems and crop 
yield reduction as an indicator of agricultural systems, the workshop 
participants identified annual percentages, of RBL for forest tree 
seedlings and RYL for agricultural crops, considered important to their 
judgments on the standard. With regard to forest ecosystems and 
seedling growth effects as an indicator, the participants selected a 
range of 1-2% RBL per year ``to avoid cumulative effects of yearly 
reductions of 2%.'' With regard to crops, they indicated an interest in 
protecting against crop yield reductions of 5% RYL yet noted 
uncertainties surrounding such a percentage which led them to 
identifying 10% RYL for the crop yield endpoint (Heck and Cowling, 
1997). The workshop report provides no explicit rationale for the 
percentages identified (2% RBL and 5% or 10% RYL); nor does it describe 
their connection to ecosystem impacts of a specific magnitude or type 
and judgments on significance of the effects for public welfare, e.g., 
taking into consideration the intended use and significance of the 
affected vegetation (Heck and Cowling, 1997). In recognition of the 
complexity of assessing the adversity of tree growth effects and 
effects on crop yield in the broader context of public welfare, the 
EPA's consideration of those effects in both the 1997 and 2008 reviews 
extended beyond the consideration of various benchmark responses for 
the studied species, and with regard to crops, additionally took note 
of their extensive management (62 FR 38856, July 18, 1997; 73 FR 16436, 
March 27, 2008).
    While, as noted above, public welfare benefits of forested lands 
can be particular to the type of area in which the forest occurs, some 
of the potential public welfare benefits associated with forest 
ecosystems are not location dependent. A potentially extremely valuable 
ecosystem service provided by forested lands and for which the ISA 
concludes a likely causal relationship with O3 in ambient 
air is carbon storage, a regulating service that is ``of paramount 
importance for human society'' (U.S. EPA, 2013a, section 2.6.2.1 and p. 
9-37). The service of carbon storage is potentially important to the 
public welfare no matter in what location the sensitive trees are 
growing, or what their intended current or future use. In other words, 
the benefit exists as long as the tree is growing, regardless of what 
additional functions and services it provides.
    Another example of locations potentially vulnerable to 
O3-related impacts but not necessarily identified for such 
protection might be forested lands, both public and private, where 
trees are grown for timber production, particularly where they are 
dominated by a single timber species stand that is sensitive to 
O3, such as ponderosa pine. Further, forests in urbanized 
areas provide a number of services that are important to the public in 
those areas, including air pollution removal, cooling of the heat 
island effect, and beautification (U.S. EPA, 2014b, section 6.6.2 and 
Appendix 6D; Akbari, 2002).\195\ The presence of O3-
sensitive trees in such areas may place them at risk from elevated 
O3 exposures, contributing to potential impacts on important 
services provided by urban forests (U.S. EPA, 2014b, sections 6.6.2 and 
6.7). There are many other tree species, such as species used in the 
USFS biomonitoring network, and various ornamental and agricultural 
species (i.e., Christmas trees, fruit and nut trees) that provide 
ecosystem services that may be judged important to the public welfare 
but whose vulnerability to impacts from O3 on tree growth, 
productivity and carbon storage has not been quantitatively 
characterized (U.S. EPA, 2014b, Chapter 6; Abt Associates, 1995).
---------------------------------------------------------------------------

    \195\ For example, see http://www.fs.fed.us/research/urban/environmental-justice.php.
---------------------------------------------------------------------------

    As noted above, in addition to tree growth-related effects, 
O3-induced visible foliar injury also has the potential to 
be significant to the public welfare through impacts in Class I and 
other similarly protected areas. Visible foliar injury is a visible 
bioindicator of O3 exposure in species sensitive to this 
effect, with the injury affecting the physical appearance of the plant. 
Accordingly visible foliar injury surveys are used by federal land 
managers as tools in assessing potential air quality impacts in Class I 
areas. These surveys may focus on plant species that have been 
identified as potentially sensitive air quality related values (AQRVs) 
due to their sensitivity to O3-induced foliar injury (USFS, 
NPS, FWS, 2010). An AQRV is defined by the National Park Services as a 
``resource, as identified by the FLM for one or more Federal areas that 
may be adversely affected by a change in air quality'' and the resource 
``may include visibility or a specific scenic, cultural, physical, 
biological, ecological, or recreational resource identified by the FLM 
for a particular area'' (USFS, NPS, USFWS, 2010).\196\ No criteria have 
been established, however, regarding a level or prevalence of visible 
foliar injury considered to be adverse to the affected vegetation, and, 
as noted in section IV.B.1.a above, there is not a clear relationship 
between visible foliar injury and other effects, such as reduced growth 
and productivity. Thus, key considerations with regard to public 
welfare significance of this endpoint have related to qualitative 
consideration of the plant's aesthetic value in protected forested 
areas. Depending on the extent and severity, O3-induced 
visible foliar injury might be expected to have the potential to impact 
the public welfare in scenic and/or recreational areas during the 
growing season, particularly in areas with special protection, such as 
Class I areas.
---------------------------------------------------------------------------

    \196\ The identification, monitoring and assessment of AQRVs 
with regard to an adverse effect is an approach used for assessing 
the potential for air pollution impacts from pending permit actions 
in Class I areas (USFS, NPS, USFWS, 2010). An adverse impact is 
recognized by the National Park Service as one that results in 
diminishment of the Class I areas's national significance or the 
impairment of the ecosystem structure or functioning, as well as 
impairment of the quality of the visitor experience (USFS, NPS, 
USFWS, 2010). Federal land managers (FLMs) make such adverse impact 
determinations on a case-by-case basis, using technical and other 
information which they provide for consideration by permitting 
authorities. The National Park Services has developed is a document 
describing an overview of approaches related to assessing projects 
under the National Environmental Policy Act and other planning 
initiatives affecting the National Park System (http://www.nature.nps.gov/air/Pubs/pdf/AQGuidance_2011-01-14.pdf).
---------------------------------------------------------------------------

    The ecosystem services most likely to be affected by O3-
induced visible foliar injury (some of which are also recognized above 
for tree growth-related effects) are cultural services, including 
aesthetic value and outdoor recreation. In addition, several tribes 
have indicated that many of the species identified as O3-
sensitive (including bioindicator species) are culturally significant 
(U.S. EPA, 2014c, Table 5-1). The geographic extent of protected areas 
that may be vulnerable to such public welfare effects of O3 
is potentially appreciable. Sixty six species that occur on U.S. 
National Park Service (NPS) and U.S. Fish and Wildlife Service lands 
\197\ have been identified as sensitive to O3-induced 
visible foliar injury and some also have particular cultural importance 
to some tribes (U.S. EPA, 2014c, Table 5-1 and Appendix 5-A; U.S. EPA, 
2014b, section 6.4.2). Not all species are equally sensitive to 
O3, however, and quantitative relationships between 
O3 exposure and other important effects, such as seedling 
growth reduction, are

[[Page 75322]]

only available for a subset of the 66, as described in section IV.B.1. 
above. A diverse array of ecosystem services has been identified for 
these twelve species (U.S. EPA, 2014c, Table 5-1). Two of the species 
in this group that are relatively more sensitive with regard to effects 
on growth are the ponderosa pine and quaking aspen (U.S. EPA, 2014b, 
section 6.2), the ranges for which overlap with many lands that are 
protected or preserved for enjoyment of current and future generations 
(consistent with the discussion above on Class I and other protected 
areas), including such lands located in the west and southwest regions 
of the U.S. where ambient O3 concentrations and associated 
cumulative seasonal exposures can be highest (U.S. EPA, 2014c, Appendix 
2B).\198\
---------------------------------------------------------------------------

    \197\ See http://www2.nature.nps.gov/air/Pubs/pdf/flag/NPSozonesensppFLAG06.pdf.
    \198\ Basal area for resident species in national forests and 
parks are available in files accessible at: http://www.fs.fed.us/foresthealth/technology/nidrm2012.shtml.
---------------------------------------------------------------------------

    With regard to agriculture-related effects, the EPA has recognized 
other complexities, stating that the degree to which O3 
impacts on vegetation that could occur in areas and on species that are 
already heavily managed to obtain a particular output (such as 
commodity crops or commercial timber production) would impair the 
intended use at a level that might be judged adverse to the public 
welfare has been less clear (73 FR 16497, March 27, 2008; 75 FR 3024; 
January 19, 2010). We note that while having sufficient crop yields is 
of high public welfare value, important commodity crops are typically 
heavily managed to produce optimum yields. In light of all of the 
inputs that go into achieving these yields, such as fertilizer, 
herbicides, pesticides, and irrigation, it is difficult to determine at 
what point O3-induced yield loss creates an adverse impact 
for the producer in the way of requiring increased inputs in order to 
maintain the desired yields. Moreover, based on the economic theory of 
supply and demand, increases in crop yields would be expected to result 
in lower prices for affected crops and their associated goods, which 
would primarily benefit consumers. Given these competing impacts on 
producers and consumers, it is unclear how to consider these effects in 
terms of potential adversity to the public welfare (U.S. EPA, 2014c, 
sections 5.3.2 and 5.7).
    When agricultural impacts or vegetation effects in other areas are 
contrasted with the emphasis on forest ecosystem effects in Class I and 
similarly protected areas, it can be seen that the Administrator has in 
past reviews judged the significance to the public welfare of 
O3-induced effects on sensitive vegetation growing within 
the U.S. to differ depending on the nature of the effect, the intended 
use of the sensitive plants or ecosystems, and the types of 
environments in which the sensitive vegetation and ecosystems are 
located, with greater significance ascribed to areas identified for 
specific uses and benefits to the public welfare, such as Class I 
areas, than to areas for which such uses have not been established. In 
summary, several considerations are recognized as important to 
judgments on the public welfare significance of the array of effects of 
different O3 exposure conditions on vegetation. While there 
are complexities associated with the consideration of the magnitude of 
key vegetation effects that might be concluded to be adverse to 
ecosystems and associated services, there are numerous locations where 
O3-sensitive tree species are present that may be vulnerable 
to impacts from O3 on tree growth, productivity and carbon 
storage and their associated ecosystems and services. It is not 
possible to generalize across all studied species regarding which 
cumulative exposures are of greatest concern, however, as this can vary 
by situation due to differences in exposed species sensitivity, the 
importance of the observed or predicted O3-induced effect, 
the role that the species plays in the ecosystem, the intended use of 
the affected species and its associated ecosystem and services, the 
presence of other co-occurring predisposing or mitigating factors, and 
associated uncertainties and limitations. These factors contribute to 
the complexity of the Administrator's judgments regarding the adversity 
of known and anticipated effects to the public welfare.

C. Exposure and Risk Assessment Information

    The WREA characterized ambient O3 exposure and its 
relationship to tree biomass loss, crop yield loss, and visible foliar 
injury and the associated ecosystem services \199\ in national-scale 
and case study analyses. The WREA also qualitatively assessed impacts 
to some ecosystem services, including impacts on the hydrologic cycle, 
pollination regulation, and fire regulation; commercial non-timber 
forest products and insect damage; and aesthetic and non-use values. In 
the quantitative analyses, the WREA characterized effects associated 
with exposures to O3 in ambient air using the W126 metric.
---------------------------------------------------------------------------

    \199\ In its review of drafts of the WREA and PA, the CASAC 
conveyed support for analyses and considerations of ecosystem 
services that may be affected by O3 exposures (Frey, 
2014b, 2014c).
---------------------------------------------------------------------------

    The following sections summarize the analyses and adjustment 
approach used to develop the O3 concentrations used as 
inputs to the vegetation risk analyses for tree biomass and crop yield 
loss, and the analyses, including key results and uncertainties, for 
tree seedling growth, productivity, carbon storage and associated 
ecosystem services (section IV.C.2); crop yield loss (section IV.C.3); 
and visible foliar injury (section IV.C.4).
1. Air Quality Analyses
    The WREA evaluated O3 exposure and risks for several 
national-scale air quality scenarios: recent conditions (2006 to 
2008),\200\ the current secondary standard, and W126 index values of 15 
ppm-hrs, 11 ppm-hrs, and 7 ppm-hrs, using three-year averages (U.S. 
EPA, 2014b, chapter 4). For each of these scenarios, three-year average 
W126 index values were estimated at each 12 km by 12 km grid cell in a 
national-scale spatial surface. Additionally, some analyses were based 
on single-year surfaces.\201\ The method for creating the five 
scenarios generally involved two steps (summarized in Table 5-4 of the 
PA). The first is derivation of the average W126 index value (across 
the three years) at each monitor location. This value is based on 
unadjusted O3 concentrations from monitoring data for recent 
conditions and adjusted concentrations for the four other scenarios. 
Concentrations were adjusted based on model predicted relationships 
between O3 and U.S.-wide emissions reductions in oxides of 
nitrogen (NOx). The adjusted air quality does not represent an 
optimized control scenario that just meets the current standard (or 
target W126 index values for other scenarios), but rather characterizes 
one potential distribution of air quality across a region when all 
monitor locations meet the standard (U.S. EPA, 2014b, section 4.3.4.2). 
The development of adjusted concentrations was done for each of nine 
regions independently (see U.S. EPA, 2014b, section 4.3.4.1). In the 
second step, national-scale spatial surfaces (W126 index values for 
each 12 km x 12 km

[[Page 75323]]

grid cell used in the air quality model) were created using the 
monitor-location values and the Voronoi Neighbor Averaging (VNA) 
spatial interpolation technique (details on the VNA technique are 
presented in U.S. EPA, 2014b, Appendix 4A).
---------------------------------------------------------------------------

    \200\ Certain visible foliar injury analyses assessed recent 
conditions from 2006 to 2010 on an annual basis.
    \201\ An analysis using data from USFS FHM/FIA O3 
biomonitoring sampling sites (``biosites'') and a screening-level 
assessment in 214 national parks were done using national-scale 
spatial surfaces of unadjusted O3 concentrations (in 
terms of the W126 index) created for each year from 2006 through 
2010 using the VNA interpolation technique (U.S. EPA, 2014b, section 
4.3.2, Appendix 4A).
---------------------------------------------------------------------------

    In the dataset used to create the recent conditions scenario, the 
three-year average W126 index values at the monitor locations (before 
application of the VNA technique) ranged from below 5 ppm-hrs to 48.6 
ppm-hrs (U.S. EPA, 2014b, Figure 4-4 and Table 4-3). In the nine 
modeling regions, the maximum three-year average W126 index values at 
monitor locations ranged from 48.6 ppm-hrs in the West region down to 
6.6 ppm-hrs in the Northwest region.\202\ After adjustment of the 
monitor location concentrations to just meet the current standard in 
each region (using relationships described above), the region-specific 
maximum three-year average W126 values ranged from 18.9 ppm-hrs in the 
West region to 2.6 ppm-hrs in the Northeast region (U.S. EPA, 2014b, 
Table 4-3). With the next step, creation of the national surface of air 
quality values at grid cell centroids, the highest values were reduced, 
such that all the three-year average W126 index values were below 15 
ppm-hrs across the national surface with the exception of a very small 
area of the Southwest region (near Phoenix) where average W126 index 
values were just above 15 ppm-hrs. Thus, it can be seen that 
application of the VNA interpolation method to estimate W126 index 
values at the centroid of every 12 x 12 km \2\ grid cell rather than 
only at each monitor location results in a lowering of the highest 
values.
---------------------------------------------------------------------------

    \202\ The regions referenced here and also with regard to 
monitoring data analyses described in section IV.D.4 below are NOAA 
climate regions, as shown in Figure 2B-1 of the PA.
---------------------------------------------------------------------------

    Because the W126 estimates generated for the different air quality 
scenarios assessed are inputs to the vegetation risk analyses for tree 
biomass and crop yield loss, and also used in the foliar injury 
analyses, any uncertainties in the air quality analyses are propagated 
into the those analyses (U.S. EPA, 2014b, section 8.5). The WREA 
identified sources of uncertainty for the W126 estimates for each air 
quality scenario and qualitatively characterized the magnitude of 
uncertainty and potential for directional bias (U.S. EPA, 2014b, Table 
4-5). As discussed in Chapter 4 and 8 of the WREA, an important large 
uncertainty in the analyses is the assumed response of the W126 
concentrations to emissions reductions needed to meet the existing 
standard (U.S. EPA, 2014b, section 8.5.1). Any approach to 
characterizing O3 air quality over broad geographic areas 
based on concentrations at monitor locations will convey inherent 
uncertainty. The model-based adjustments are based on U.S.-wide 
emissions reductions in NOx and characterize only one potential 
distribution of air quality across a region when all monitor locations 
meet the standard (U.S. EPA, 2014b, section 4.3.4.2).\203\ 
Additionally, the surface is created from the three-year average at the 
monitor locations, rather than creating a surface for each year and 
then averaging across years at each grid cell; the potential impact of 
this on the resultant estimates is considered in the WREA (U.S. EPA, 
2014b, Appendix 4A).
---------------------------------------------------------------------------

    \203\ The WREA analyses used U.S.-wide NOx emissions reductions 
to simulate air quality that independently in each region would just 
meet the existing standard and the three W126 scenarios. The NOx 
emissions reductions were determined such that the highest monitor 
within each region would just meet the target level. In this way, 
the adjustment results in broad regional reductions in O3 
and includes reductions in O3 at some monitors that were 
already meeting or below the target level. Thus, the adjustments 
performed to develop a scenario meeting a target level at the 
highest monitor in each region did result in substantial reduction 
below the target level in some areas of the region. This result at 
the monitors already well below the target indicates an uncertainty 
with regard to air quality expected from specific control strategies 
that might be implemented to meet a particular target level.
---------------------------------------------------------------------------

    An additional uncertainty related to the W126 index value estimates 
for each air quality scenario comes from the creation of a national 
W126 surface using the VNA technique to interpolate recent air quality 
measurements of O3. In general, spatial interpolation 
techniques perform better in areas where the O3 monitoring 
network is denser. Therefore, the W126 index values estimated in the 
rural areas in the West, Northwest, Southwest, and West North Central 
with few or no monitors (U.S. EPA, 2014b, Figure 2-1) are more 
uncertain than those estimated for areas with denser monitoring. 
Further, this interpolation method generally underpredicts higher 12-
hour W126 exposures. Due to the important influence of higher exposures 
in determining risks to plants, the potential for the VNA interpolation 
approach to underpredict higher W126 exposures could result in an 
underestimation of risks to vegetation in some areas. Underestimation 
of the highest W126 index values for the current standard scenario is 
an additional impact of the interpolation method that is important to 
consider.
2. Tree Seedling Growth, Productivity, Carbon Storage and Associated 
Ecosystem Services
    For the WREA assessments related to tree growth, productivity, 
carbon storage and associated ecosystem services, the sections below 
provide an overview of the analyses along with the key results (section 
IV.C.2.a) and summarize the key uncertainties (section IV.C.2.b).
    a. Overview and Summary of Key Results
    The assessments to estimate the exposures and risks for tree 
seedling growth, productivity, and carbon storage reflect a range of 
spatial scales ranging from the county scale up to the national park, 
urban area, and national scales. For the air quality scenarios 
described above, the WREA applied the species-specific E-R functions to 
develop estimates of O3-associated RBL, productivity, carbon 
storage and associated ecosystem services (U.S. EPA, 2014b, Chapter 6). 
Some analyses also apply the median across species E-R functions.
    The WREA examined multiple approaches for characterizing the median 
tree response to O3 exposure based on the 11 robust E-R 
functions for tree seedlings from the OTC research and the E-R function 
for eastern cottonwood (U.S. EPA, 2014b, section 6.2.1.2 and Figure 6-
5). For some species, only one study was available (e.g., red maple), 
and for other species there were as many as 11 studies available (e.g., 
ponderosa pine). To illustrate the effect of within-species variability 
associated with the E-R data available on estimates for a median 
response across the 12 species, the WREA performed a stochastic 
sampling analysis involving multiple iterations of random selection of 
E-R functions from the studies available for each of the 12 species. 
This analysis produced median values at each cumulative exposure level 
that were higher than medians derived by two conventional, 
deterministic methods (U.S. EPA, 2014b, section 6.2.1.2 and Figure 6-
5).\204\ For example, the median seasonal W126 index value for which a 
two percent biomass loss is estimated in seedlings for the studied 
species ranges from approximately 7 ppm-hrs using the conventional 
methods up to 14 ppm-hrs when derived by the stochastic method. 
Although the stochastic method provides some illustration of the effect 
of within-species variability, we focus on the conventional approach 
that gives equal weight to each studied species,

[[Page 75324]]

calculating the median response based on the composite E-R functions, 
consistent with CASAC advice (Frey, 2014b).
---------------------------------------------------------------------------

    \204\ These methods were calculating a median using the 
composite functions and calculating a median using all tree seedling 
studies available.
---------------------------------------------------------------------------

    The WREA estimates indicate substantial heterogeneity in plant 
responses to O3, both within species, between species, and 
across regions of the U.S. The tree species known to be O3-
sensitive are different in the eastern and western U.S. and the eastern 
U.S. has far more such species. Ozone exposure and risk is somewhat 
easier to assess in the eastern U.S. because of the availability of 
more data and the greater number of species to analyze. In addition, 
there are more O3 monitors in the eastern U.S. but fewer 
national parks (U.S. EPA, 2014b, chapter 8). In consideration of CASAC 
advice, the WREA derived RBL and weighted RBL (wRBL) estimates 
separately with and without the eastern cottonwood. The results 
summarized here are for the analyses that exclude cottonwood.\205\ The 
WREA reported RBL estimates relative to a benchmark of 2% RBL for tree 
seedlings, as well as relative to other percent RBL values. The 2% RBL 
benchmark was considered based on CASAC advice that stated that ``focus 
on a 2% loss level for trees . . . is appropriate.'' (Frey, 2014b, p. 
6). The main WREA analyses for effects related to tree growth, 
productivity and carbon storage are summarized below, with the key 
findings for each.
---------------------------------------------------------------------------

    \205\ The CASAC advised that the eastern cottonwood response 
data ``receive too much emphasis'' in a draft version of the PA, 
explaining that these ``results are from a gradient study that did 
not control for ozone and climatic conditions and show extreme 
sensitivity to ozone compared to other studies'' and that 
``[a]lthough they are important results, they are not as strong as 
those from other experiments that developed E-R functions based on 
controlled ozone exposure'' (Frey, 2014b, p. 10).
---------------------------------------------------------------------------

    Relative biomass loss nationally was estimated for each of the 12 
studied species from the composite E-R functions for each species 
described above and information on the distribution of those species 
across the U.S. (U.S. EPA, 2014b, section 6.2.1.3 and Appendix 6A). As 
one example of a tree species near the median of the studied species, 
relative biomass loss estimates (reduced growth) for ponderosa pine in 
the current standard air quality scenario are below two percent for 
most areas where this species is found but estimates of RBL for this 
species in some areas of the southwest fall above two percent biomass 
loss (U.S. EPA, 2014b, Figure 6-8). Maximum estimates of RBL for all 
areas where ponderosa pine is found decrease to just over three percent 
and just over two percent for the 15 and 7 ppm-hrs scenarios, 
respectively (U.S. EPA, 2014b, Table 6-6).
    To provide an indication of ecosystem-level impacts, weighted 
estimates of RBL (wRBL) were also developed for each grid cell 
nationwide. This is estimated from the species-specific E-R functions 
and a weighting approach based on information on prevalence of the 
studied species across the U.S. (i.e., the proportion of the total 
basal area modeled by USFS across all species for which data were 
available). An overall wRBL value for each grid cell is generated by 
summing the wRBL values for each studied tree species found within that 
grid cell. The wRBL is intended to be an indication of the potential 
magnitude of the ecological effect that could occur in some ecosystems. 
In general, the higher the wRBL is in a given ecosystem, the larger the 
potential ecological effect. (U.S. EPA, 2014b, section 6.8, Table 6-
25).
    For the national-scale analysis, the WREA presents the percent of 
total basal area with wRBL greater than 2%. The estimates for the 
weighted biomass loss analysis reflecting the 11 tree species with 
robust E-R functions are as follows (U.S. EPA, 2014b, Table 6-25):
     For the current standard scenario, the percent of total 
basal area that exceeds a two percent wRBL is 0.2 percent.
     For the W126 scenarios of 15, 11 and 7 ppm-hrs, the 
percent of total basal area that exceeds a two percent wRBL is 0.2 
percent, 0.1 percent, and less than 0.1 percent respectively (U.S. EPA, 
2014b, Table 6-25).
    In the wRBL analysis for Class I areas, the number of Class I areas 
with wRBL greater than 2% is estimated for the grid cells located in 
the 145 of the 156 Class I areas for which data were available (U.S. 
EPA, 2014b, Table 6-26).
     For the current standard scenario, two of the 145 assessed 
Class I areas have weighted RBL values above two percent (U.S. EPA, 
2014b, Table 6-26).
     For the W126 scenarios of 15, 11 and 7 ppm-hrs, there are 
two, two and one Class I area with wRBL above two percent, 
respectively.
    In the county analysis, the WREA estimated the number of U.S. 
counties in which any of the studied tree species is estimated to 
experience more than two percent RBL, the number of species affected, 
and the number of counties for which the median of the species-specific 
functions exceeds two percent RBL. In addition to the estimates based 
on all 12 studied species and also the 11 species with the exclusion of 
eastern cottonwood (in response to CASAC advice), additional estimates 
were developed without black cherry to show contribution of that 
sensitive species to the multi-species estimates (U.S. EPA, 2014b, 
Table 6-7).
     In the current standard scenarios, 66% of the 3,109 
assessed counties are estimated to have at least one of the 11 species 
(excluding cottonwood) with an RBL greater than two percent, with three 
counties having three species exceeding two percent. The median RBL 
(across the species present) is above two percent in 239 counties. The 
maximum number of species in any one county with an RBL greater than 
two percent is three (excluding cottonwood). (U.S. EPA, 2014b, Table 6-
7).
     For the 15, 11 and 7 ppm-hrs scenarios, the proportion of 
3,109 counties with one or more species with an RBL above two percent 
decreases to 61 percent, 59 percent, and 58 percent, respectively. For 
the 7 ppm-hrs scenario, the median RBL is above two percent in six 
percent of the counties (U.S. EPA, 2014b, Table 6-7).
     The county RBL estimates are appreciably influenced by 
black cherry, a very sensitive species that is widespread in the 
Eastern U.S. For 1,805 of the 1,929 counties estimated to have at least 
one species with an RBL greater than two percent when air quality is 
meeting the current standard, only black cherry exceeds this level of 
RBL. If black cherry is excluded, the median RBL for the 10 remaining 
species decreases. For the median RBL values, 203 of the 239 counties 
estimated to have a median RBL above two percent when air quality is 
meeting the current standard are because of the presence of black 
cherry (U.S. EPA, 2014b, Table 6-7).
    Additionally, the WREA estimated relative yield loss in timber 
production and associated changes in consumer and producer/farmer 
economic surplus using E-R functions for tree seedlings to calculate 
relative yield loss (equivalent to relative biomass loss) across full 
tree lifespans and through modeling of the resulting market-based 
welfare effects. Because the forestry and agriculture sectors are 
related and trade-offs occur between the sectors, the WREA calculated 
the resulting market-based welfare effects of O3 exposure in 
the forestry and agriculture sectors on consumer and producer 
surplus.\206\

[[Page 75325]]

Because demand for most forestry and agricultural commodities is not 
highly responsive to changes in price, producer surplus (i.e., producer 
gains) often declines. These declines can be more than offset by 
changes in consumer surplus gains from lower prices, but, in some 
cases, lower prices reduce producer gains more than can be offset by 
consumer surplus (U.S. EPA, 2014b, Appendix 6B, Table and B-9).
---------------------------------------------------------------------------

    \206\ The WREA used the Forest and Agricultural Sector 
Optimization Model with Greenhouse Gases (FASOMGHG). FASOMGHG is a 
national-scale model that provides a complete representation of the 
impacts of meeting alternative standards on the U.S. forest and 
agricultural sectors. FASOMGHG simulates the allocation of land over 
time to competing activities in both the forest and agricultural 
sectors. FASOMGHG results include multi-period, multi-commodity 
results over 60 to 100 years in 5-year time intervals when running 
the combined forest-agriculture version of the model.
---------------------------------------------------------------------------

     In the current standard scenario, estimates of the 
relative yield loss for timber production are below one percent other 
than in the Southwest, Southeast, Central, and South regions (U.S. EPA, 
2014b, section 6.3, Table 6-9) (see U.S. EPA, 2014b, Table 6-8 for 
clarification on region names). The highest yield loss occurs in upland 
hardwood forests in the South Central and Southeast regions at over 
three percent per year and in Corn Belt hardwoods at just over two 
percent loss per year (U.S. EPA, 2014b, section 6.3, Table 6-9).
     For the 15 and 11 ppm-hrs scenarios, relative yield loss 
estimates for timber production are above one percent in parts of the 
Southeast, Central, and South regions and above two percent in parts of 
the Southeast and Central U.S.
     For the 7 ppm-hrs scenario, relative yield loss estimates 
for timber production are above one percent in the Southeast and South 
regions (U.S. EPA, 2014b, section 6.3, Table 6-9).
    The WREA also estimated impacts on tree growth and two ecosystem 
services provided by urban trees: removal of air pollutants and carbon 
storage. The estimates of the tons of carbon monoxide, nitrogen 
dioxide, ozone and sulfur dioxide removed are for a 25-year period in 
five urban case study areas: Baltimore, Syracuse, the Chicago region, 
Atlanta, and the urban areas of Tennessee (U.S. EPA, 2014b, section 
6.7).\207\
---------------------------------------------------------------------------

    \207\ The WREA used the i-Tree model for the urban case studies. 
i-Tree is a peer-reviewed suite of software tools provided by USFS.
---------------------------------------------------------------------------

     Estimates for all five urban case study areas indicate 
increased pollutant removal of O3, nitrogen dioxide, carbon 
monoxide, and sulfur dioxide in the current standard scenario (U.S. 
EPA, 2014b, sections 6.7). The results for the 15 ppm-hrs scenario were 
very similar to those for meeting the current standard. For the 11 and 
7 ppm-hrs scenarios, all five case study areas indicate smaller 
additional increases in air pollutant removal beyond moving from 
current conditions to the current standard (U.S. EPA, 2014b, sections 
6.7).
    The WREA estimated carbon storage related to O3-induced 
biomass loss in forests and agricultural crops nationally and also in 
forests in five urban areas using the FASOMGHG and i-Tree models noted 
above (U.S. EPA, 2014b, section 6.6). Ozone effects on tree growth 
affects the climate regulation service provided by ecosystems by 
reducing carbon sequestration and storage (U.S. EPA, 2013a, section 
9.4.3.4; U.S. EPA, 2014b, chapter 6, section 6.6). Because 
O3 exposure affects photosynthesis and CO2 uptake 
by trees, forests sequester less carbon and thus more carbon stays in 
the atmosphere. In the model used to calculate national-level impacts 
to forests and agriculture from O3-related biomass loss, 
carbon sequestration reflects carbon in standing (live and dead) trees, 
forest soils, the forest understory vegetation, forest floor including 
litter and large woody debris, and wood products both in use and in 
landfills (U.S. EPA, 2014b, chapter 6, Appendix 6B, section 2.7.1).
     Over 30 years for the national-scale analysis, carbon 
storage in the forestry sector estimated for the current standard 
scenario is just over 89,000 million metric tons of CO2 
equivalents (MMtCO2e); this is 11,840 more 
MMtCO2e storage associated with the reduced O3-
related growth impact from meeting the current standard as compared 
with recent conditions.\208\ The estimates of carbon storage in the 
agricultural sector are much smaller (i.e., 8,469 MMtCO2e 
for the current standard scenario which is 606 MMtCO2e more 
than the recent conditions scenario) (U.S. EPA, 2014b, section 6.6.1 
and Appendix 6B). The forestry sector carbon storage estimated for each 
of the three W126 scenarios is just slightly greater than that 
estimated for the current standard. As a percentage of the current 
standard estimate, the three scenario estimates are less than 0.1% (13 
MMtCO2e), just under 1% (593 MMtCO2e) and under 
2% (1,600 MMtCO2e) for the 15, 11 and 7 ppm-hrs scenarios, 
respectively (U.S. EPA, 2014b, Tables 6-19 and B-10).
---------------------------------------------------------------------------

    \208\ One MMtCO2e is equivalent to 208,000 passenger 
vehicles or the electricity to run 138,000 homes for 1 year as 
calculated by the EPA Greenhouse Gas Equivalencies Calculator 
(updated September 2013 and available at http://www.epa.gov/cleanenergy/energy-resources/calculator.html).
---------------------------------------------------------------------------

     Estimates of the effects of avoided O3-related 
biomass loss on carbon sequestration in forests in the five urban area 
case studies indicate the potential for an increase in carbon 
sequestration of somewhat more than one MMtCO2e for the 
current standard scenario compared to the recent conditions estimate 
(U.S. EPA, 2014b, section 6.6.2 and Appendix 6D). The additional 
increases in O3-related carbon sequestration estimated 
across the five case studies for the three W126 scenarios are 
relatively small (U.S. EPA, 2014b, section 6.6.2 and Appendix 6D).
    Although not discussed in detail here, the WREA also describes 
qualitative assessments for some ecosystem services that may be 
affected by O3 effects on tree growth and productivity, such 
as commercial non-timber forest products and recreation (U.S. EPA, 
2014b, section 6.4), aesthetic and non-use values (U.S. EPA, 2014b, 
section 6.4), increased susceptibility to insect attack and fire damage 
(U.S. EPA, 2014b, sections 5.3 and 5.4, respectively). Other ecological 
effects that are causally or likely causally associated with 
O3 exposure, such as effects on terrestrial productivity, 
the water cycle, the biogeochemical cycle, and community composition 
(U.S. EPA, 2013a, Table 9-19), were not quantitatively addressed in the 
WREA due to a lack of sufficient quantitative information.
b. Key Uncertainties
    The WREA identified several key limitations and uncertainties in 
the biomass loss assessments for trees, which may have a large impact 
on both overall confidence and confidence in individual analyses. Key 
uncertainties that affect the assessment of impacts on ecosystem 
services at the national and case-study scales, as well as across 
species, U.S. geographic regions and future years, include those 
associated with the interpolated and adjusted O3 
concentrations used to estimate W126 exposures in the air quality 
scenarios, the available seedling E-R functions, combining effects 
across sensitive species, the effects of compounding over time, and 
modeling impacts of biomass loss on timber harvesting and urban air 
pollutant removal.
    With regard to the robust seedling E-R functions, the WREA provided 
some characterization of the variability of individual study results 
and the impact of that on estimates of W126 index values that might 
elicit different percentages of biomass loss in tree seedlings (U.S. 
EPA, 2014b, section 6.2.1.2). Even though the evidence shows that there 
are additional species affected by O3-related biomass loss, 
the WREA only has E-R functions available to quantify this loss for 12 
tree species. This limited information only allows a partial 
characterization of the O3-related biomass loss impacts in 
trees associated

[[Page 75326]]

with recent O3 index values and with just meeting the 
existing and potential alternative secondary standards. In addition, 
there are uncertainties inherent in these E-R functions, including the 
extrapolation of relative biomass loss rates from tree seedlings to 
adult trees and information regarding within-species variability. The 
overall confidence in the E-R function varies by species based on the 
number of studies available for that species. Some species have low 
within-species variability (e.g., many agricultural crops) and high 
seedling/adult comparability (e.g., aspen), while other species do not 
(e.g., black cherry). The uncertainties in the E-R functions for 
biomass loss and in the air quality analyses are propagated into the 
analysis of the impact of biomass loss on ecosystem services, including 
provisioning and regulating services (U.S. EPA, 2014b, Table 6-27). The 
WREA characterizes the direction of potential influence of E-R function 
uncertainty as unknown, yet its magnitude as high, concluding that 
further studies are needed to determine how accurately the assessed 
species reflect the larger suite of O3-sensitive tree 
species in the U.S. (U.S. EPA, 2014b, Table 6-27).
    Another uncertainty associated with interpretation of the WREA 
biomass loss-related estimates concerns the potential for 
underestimation of compounding of growth effects across multiple years 
of varying concentrations. Though tree biomass loss impacts were 
estimated using air quality scenarios of three-year average W126 index 
values, the WREA also conducted an analysis to compare the impact of 
using a variable compounding rate based on yearly variations in W126 
exposures to that of using a W126 index value averaged across three 
years. The WREA compared the compounded values for an example species 
occurring in the eastern U.S. and another example species occurring in 
the western U.S. In both examples, one species (tulip polar and 
ponderosa pine, respectively) and one climate region where that species 
occurred (Southeast and Southwest regions, respectively) were chosen 
and air quality values associated with just meeting the existing 
standard of 75 ppb were used. Within each region, the WREA analysis 
used both the W126 index value at each monitor in the region for each 
year and the three-year average W126 index value using the method 
described in Chapter 4 of the WREA. The results show that the use of 
the three-year average W126 index value may underestimate RBL values 
slightly (U.S. EPA, 2014b, section 6.2.1.4 and Figure 6-14). In both 
regions, the three-year average W126 index value is sometimes above and 
sometimes below the individual year W126 index value.
    The WREA recognizes uncertainty regarding the extent to which the 
subset of studied tree species encompass the O3 sensitive 
species in the U.S. and the extent to which it represents U.S. 
vegetation as a whole (U.S. EPA, 2013a, pp. 9-123 to 9-125; U.S. EPA, 
2014b, Table 6-27). There are also uncertainties associated with 
estimating the national scale ecosystem-level impacts using wRBL. For 
example the wRBL estimates are likely biased low as there may be other 
unstudied O3-sensitive tree species in some areas that are 
also being affected at those levels, although this analysis does not 
take into account the effects of competition, which could further 
affect forest biomass loss.
    Uncertainties are recognized in the national-scale analyses of 
timber production, agricultural harvesting, and carbon sequestration, 
for which the WREA used the FASOMGHG model. These uncertainties include 
those associated with the functions for carbon sequestration, the 
assumptions made regarding proxy species where there are insufficient 
data, and the non-W126 E-R functions for three crops. The FASOMGHG 
model does not include agriculture and forestry on public lands, 
changes in exports due to O3 into international trade 
projections, or forest adaptation. Despite the inherent limitations and 
uncertainties, the WREA concludes that the FASOMGHG model reflects 
reasonable and appropriate assumptions for a national-scale assessment 
of changes in the agricultural and forestry sectors due to changes in 
vegetation biomass associated with O3 exposure (U.S. EPA, 
2014b, sections 6.3, 6.5, 6.6, and 8.5.2, and Table 6-27).
    In the case study analyses of five urban areas, the WREA used the 
i-Tree model, which includes an urban tree inventory for each area and 
species-specific pollution removal and carbon sequestration functions. 
However, i-Tree does not account for the potential additional VOC 
emissions from tree growth, which could contribute to O3 
formation. Uncertainties are also recognized with regard to the base 
inventory of city trees, the functions used for air pollutant removal 
and for carbon storage (U.S. EPA, 2014b, sections 6.6.2 and 6.7, and 
Table 6-27). Despite the inherent limitations and uncertainties, the 
WREA concludes that the i-Tree model reflects reasonable and 
appropriate assumptions for a case study assessment of pollution 
removal and carbon sequestration for changes in biomass associated with 
O3 exposure (U.S. EPA, 2014b, sections 6.6.2, 6.7, and 
8.5.2).
3. Crop Yield
    Section IV.C.3.a below provides an overview of the assessments 
performed in the WREA to estimate the exposures and risks for crop 
yield, as well as the key results. Section IV.C.3.b summarizes the key 
uncertainties.
a. Overview and Summary of Key Results
    The WREA conducted two analyses to estimate O3 impacts 
related to crop yield, including annual yield losses estimated for 10 
commodity crops grown in the U.S. with E-R functions and how these 
losses affect producer and consumer economic surpluses (U.S. EPA, 
2014b, sections 6.2, 6.5). Summary estimates for crop yield loss 
related effects in the WREA are presented relative to a 5% yield loss 
benchmark based on consideration of CASAC's recommendation to consider 
a benchmark of 5% for median crop yield loss and to consider 5% yield 
loss for individual crop species. In addition, other benchmarks levels 
are considered in the WREA (e.g. 10% and 20%).
    The WREA derived estimates of crop RYL estimates nationally and in 
a county-specific analysis. Crop-specific estimates of O3-
related RYL nationally were derived for each of the air quality 
scenarios from the 10 E-R functions for crops described above combined 
with information regarding crop distribution (U.S. EPA, 2014b, section 
6.5). The WREA also reported crop RYL results at the county-level, as 
well as the number of crop-producing counties with greater than five 
percent RYL (U.S. EPA, 2014b, section 6.5.1, Appendix 6B).
     The largest reduction in O3-induced crop yield 
loss and yield changes occurs when moving from the recent conditions 
scenario to the current standard scenario (U.S. EPA, 2014b, section 
6.5). Among the major commercial crops, winter wheat and soybeans are 
more sensitive to ambient O3 levels than other crops.
     In the current standard scenario, no counties have RYL 
estimates at or above 5% (U.S. EPA, 2014b, section 6.5).\209\
---------------------------------------------------------------------------

    \209\ In the air quality scenario for the current standard, a 
monitor that already met the current standard but was located within 
the same region as another monitor that was above the current 
standard would have had its concentration adjusted downward. This is 
due to the fact that concentrations were adjusted independently for 
each region, applying reductions to all monitors within the region, 
such that all monitors located within a region meet the standard 
(U.S. EPA, 2014b, section 4.3.4.2).

---------------------------------------------------------------------------

[[Page 75327]]

    The WREA also estimated O3-related crop impacts on 
producer and consumer surplus.\210\ These are national-scale estimates 
of the effects of yield loss on agricultural harvesting, which supply 
provisioning services of food and fiber for each of the air quality 
scenarios. Overall effect on agricultural yields and producer and 
consumer surplus depends on (1) the ability of producers/farmers to 
substitute other crops that are less O3 sensitive, and (2) 
the responsiveness, or elasticity, of demand and supply (U.S. EPA, 
2014b, section 6.5).
---------------------------------------------------------------------------

    \210\ Welfare economics focuses on the optimal allocation of 
resources and goods and how those allocations affect total social 
welfare. Total welfare is also referred to as economic surplus, 
which is the overall benefit a society, composed of consumers and 
producers, receives when a good or service is bought or sold, given 
a quantity provided and a market price. Economic surplus is divided 
into two parts: Consumer and producer surplus (U.S. EPA, 2014b, p. 
ES-6).
---------------------------------------------------------------------------

     Estimates of consumer surplus, or consumer gains, were 
generally higher in the current standard scenario in the agricultural 
sector because higher productivity under lower O3 
concentrations increased total yields and reduced market prices (U.S. 
EPA, 2014b, Tables 6-17 and 6-18). Combined gains in producer and 
consumer surplus for forestry and agriculture were essentially 
unchanged for the 15 ppm-hrs scenario, but annualized gains increased 
by $21 million beyond the current standard scenario for the 11 ppm-hrs 
scenario and $231 million for the 7 ppm-hrs scenario. In some cases, 
lower prices reduce producer gains more than can be offset by higher 
yields (U.S. EPA, 2014b, Table 6-18).
     Because demand for most agricultural commodities is not 
highly responsive to changes in price, producer surplus or producer 
gains often declined. For agricultural welfare, annualized combined 
consumer and producer surplus gains were estimated to be $2.6 trillion 
in 2010 for the current standard scenario (U.S. EPA, 2014b, Table 6-
17).
b. Key Uncertainties
    The WREA discusses multiple areas of uncertainty associated with 
the crop yield loss estimates, including those associated with the 
model-based adjustment methodology as well as those associated with the 
projection of yield loss using the FASOMGHG model at the estimated 
O3 concentrations (U.S. EPA, 2014b, Table 6-27, section 
8.5). Because the W126 estimates generated in the air quality analyses 
are inputs to the vegetation risk analyses for crop yield loss, any 
uncertainties in the air quality analyses are propagated into the those 
analyses (U.S. EPA, 2014b, Table 6-27, section 8.5). Therefore, the air 
quality scenarios in the crop yield analyses have the same 
uncertainties and limitations as in the biomass loss analyses 
(summarized above), including those associated with the model-based 
adjustment methodology (U.S. EPA, 2014b, section 8.5).
4. Visible Foliar Injury
    Section IV.C.4.a below provides an overview of the assessment in 
the WREA of O3-related visible foliar injury and associated 
ecosystem services impacts, as well as the key results. Section 
IV.C.4.b summarizes the key uncertainties.
a. Overview and Summary of Key Results
    The WREA presents a number of analyses of O3-related 
visible foliar injury and associated ecosystem services impacts (U.S. 
EPA, 2014b, Chapter 7). An initial analysis using USFS FHM/FIA biosite 
data included the development of benchmark criteria reflecting 
different prevalences of visible foliar injury at different W126 
exposures and soil moisture conditions. These criteria were then used 
in a screening-level characterization of the potential risk of foliar 
injury incidence in 214 national parks and a case study assessment of 
three national parks, which also provides limited characterization of 
the associated ecosystem services.
    In the biosite data analysis, the WREA used the biomonitoring site 
data from the USFS FHM/FIA Network (USFS, 2011),\211\ associated soil 
moisture data during the sample years, and national surfaces of ambient 
air O3 concentrations based on spatial interpolation of 
monitoring data from 2006 to 2010 to calculate the proportion of 
biosites with any visible foliar injury. The proportion of biosites 
metric is derived by first ordering the data (across biosites and 
sample years) by W126 index value estimated for that biosite and year. 
Then for each W126 index value, the proportion of biosites is 
calculated with any foliar injury for all observations at or below that 
W126 index value. (U.S. EPA, 2014b, section 7.2). This analysis 
indicates that the proportion of biosites showing the presence of any 
foliar injury increases rapidly from zero to about 20 percent at 
relatively low W126 index values. Specifically: (1) the proportion of 
biosites exhibiting foliar injury rises rapidly with increasing W126 
index values below approximately 10 ppm-hrs (W126 <10.46 ppm-hrs), and 
(2) there is relatively little change in this proportion with 
increasing W126 index values above approximately 10 ppm-hrs (W126 
>10.46 ppm-hrs). The data for biosites during normal moisture years are 
very similar to the dataset as a whole, with an overall proportion of 
close to 18 percent for presence of any foliar injury. Among the 
biosites with a relatively wet season, the proportion of biosites 
showing injury is much higher and the relationship with annual W126 
index value is much steeper. Much lower proportions of biosites show 
injury with relatively dry seasons (U.S. EPA, 2014b, section 7.2.3, 
Figures 7-10), consistent with the ISA finding that many studies have 
shown that dry periods tend to decrease the incidence and severity of 
O3-induced visible foliar injury (U.S. EPA, 2013a, section 
9.4.2). While these analyses indicate the potential for foliar injury 
to occur under conditions that meet the current standard, the extent of 
foliar injury that might be expected under such conditions is unclear 
from these analyses.
---------------------------------------------------------------------------

    \211\ Data were not available for several western states 
(Montana, Idaho, Wyoming, Nevada, Utah, Colorado, Arizona, New 
Mexico, Oklahoma, and portions of Texas).
---------------------------------------------------------------------------

    The national-scale screening-level assessment in 214 parks employed 
benchmark criteria developed from the above analysis.212 213 
For example, annual O3 concentrations corresponding to a 
W126 index value of 10.46 ppm-hrs represents the O3 exposure 
concentration where the slope of exposure-response relationship changes 
for FHM biosites, with the percentage of biosites showing injury 
remaining relatively constant for higher W126 index values. The WREA 
refers to this as the ``base scenario'' benchmark. The

[[Page 75328]]

W126 benchmarks across this and the other four scenarios range from 
3.05 ppm-hrs (foliar injury observed at five percent of biosites, 
normal moisture) up to 24.61 ppm-hrs (foliar injury observed at 10 
percent of biosites, dry). For the scenario of 10 percent biosites with 
injury, W126 index values were approximately 4, 6, and 25 ppm-hrs for 
wet, normal and dry years, respectively. The national-scale screening-
level assessment applied these benchmarks to 42 parks with 
O3 monitors and a total of 214 parks with O3 
exposure estimated from the interpolated national O3 
surfaces for individual years from 2006 to 2010 (U.S. EPA, 2014b, 
Appendix 7A and section 7.3).
---------------------------------------------------------------------------

    \212\ The parks assessed in the WREA include lands managed by 
the NPS in the continental U.S., which includes National Parks, 
Monuments, Seashores, Scenic Rivers, Historic Parks, Battlefields, 
Reservations, Recreation Areas, Memorials, Parkways, Military Parks, 
Preserves, and Scenic Trails.
    \213\ This analysis considered the approach in Kohut (2007), 
which assessed the risk of O3-induced visible foliar 
injury on O3 bioindicators (i.e., O3-sensitive 
vegetation) in 244 parks managed by the NPS. Consistent with advice 
from CASAC (Frey and Samet, 2012a), however, the WREA modified the 
approach used by Kohut (2007) to apply the W126 metric alone. The 
WREA applied different foliar injury benchmarks in this assessment 
after further investigation into the benchmarks applied in Kohut 
(2007), which were derived from biomass loss rather than visible 
foliar injury. Kohut cited a threshold of 5.9 ppm-hrs for highly 
sensitive species from Lefohn (1997), which was based on the lowest 
W126 estimate corresponding to a 10 percent growth loss for black 
cherry. For soil moisture, Kohut (2007) qualitatively assessed 
whether there appeared to be an inverse relationship between soil 
moisture and high O3 exposure.
---------------------------------------------------------------------------

     Based on NPS lists, 95 percent of the 214 parks in this 
screening-level assessment contain at least one vegetation species 
sensitive to O3-induced foliar injury (U.S. NPS, 2003, 
2006).
     In the current standard scenario, none of the 214 parks 
had O3 concentrations estimated to exceed the annual 
benchmark of a W126 index value above 10.46 ppm-hrs (U.S. EPA, 2014b, 
section 7.3.3.3).
    The case study analyses focused on Great Smoky Mountains National 
Park (GRSM), Rocky Mountain National Park (ROMO), and Sequoia and Kings 
Canyon National Parks (SEKI). Information on visitation patterns, 
recreational activities and visitor expenditures was considered. For 
example, visitor spending in 2011 exceeded $800 million, $170 million 
and $97 million dollars in GRSM, ROMO and SEKI, respectively. In each 
park, the percent cover of species sensitive to foliar injury was 
estimated and the overlap between recreation areas within the park and 
elevated W126 concentrations was described. (U.S. EPA, 2014b, section 
7.4).
     In the current standard scenario, the three-year average 
W126 index values were at or below 7 ppm-hrs in all areas of two of the 
three parks (GRSM and SEKI). Three-year average W126 index values were 
below 7 ppm-hrs in a little more than half of the area of the third 
park (ROMO) and between 7 and 11 ppm-hrs in the remainder of the park 
(U.S. EPA, 2014b, section 7.4).
     For the 15, 11 and 7 ppm-hrs scenarios, all areas of the 
three specific national parks evaluated (GRSM, SEKI, and ROMO) had 
three-year average W126 index values at or below 7 ppm-hrs, well below 
the 10.46 ppm-hrs benchmark. However, the extent of foliar injury that 
might be expected under these scenarios is unclear from these analyses.
    Although not discussed in detail here, the WREA also describes 
qualitative assessments for some of the ecosystem services most likely 
to be affected by O3-induced foliar injury such as cultural 
services, including aesthetic value and outdoor recreation. Aesthetic 
value and outdoor recreation depend on the perceived scenic beauty of 
the environment. Many outdoor recreation activities directly depend on 
the scenic value of the area, in particular scenic viewing, wildlife-
watching, hiking, and camping. These activities and services are of 
significant importance to public welfare as they are enjoyed by 
millions of Americans every year and generate millions of dollars in 
economic value (U.S. EPA, 2014b, Chapters 5 and 7). Although data are 
not available to explicitly quantify O3 effects on ecosystem 
services, the WREA includes several qualitative analyses.
b. Key Uncertainties
    Uncertainties associated with these analyses are discussed in the 
WREA, sections 7.5 and 8.5.3, and in WREA Table 7-24, and also 
summarized in the PA (e.g., U.S. EPA, 2014c, section 6.3). As discussed 
in the WREA (section 8.5.3), evaluating soil moisture is more 
subjective than evaluating O3 exposure because of its high 
spatial and temporal variability within the O3 season, and 
there is considerable subjectivity in the categorization of relative 
drought. The WREA generally concludes that the spatial and temporal 
resolution for the soil moisture data is likely to underestimate the 
potential for foliar injury to occur in some areas. In addition, there 
is lack of a clear threshold for drought below which visible foliar 
injury would not occur. In general, low soil moisture reduces the 
potential for foliar injury, but injury could still occur, and the 
degree of drought necessary to reduce potential injury is not clear. 
Studies in the ISA provide additional information regarding the role of 
soil moisture in influencing visible foliar injury response, (U.S. EPA, 
2013a, section 9.4.2). These studies confirm that adequate soil 
moisture creates an environment conducive to greater visible foliar 
injury in the presence of O3 than drier conditions. As 
stated in the ISA, ``[a] major modifying factor for O3-
induced visible foliar injury is the amount of soil moisture available 
to a plant during the year that the visible foliar injury is being 
assessed . . . because lack of soil moisture generally decreases 
stomatal conductance of plants and, therefore, limits the amount of 
O3 entering the leaf that can cause injury'' (U.S. EPA, 
2013a, p. 9-39). As a result, ``many studies have shown that dry 
periods in local areas tend to decrease the incidence and severity of 
O3-induced visible foliar injury; therefore, the incidence 
of visible foliar injury is not always higher in years and areas with 
higher O3, especially with co-occurring drought (Smith, 
2012; Smith et al., 2003)'' (U.S. EPA, 2013a, p. 9-39). This ``. . . 
partial `protection' against the effects of O3 afforded by 
drought has been observed in field experiments (Low et al., 2006) and 
modeled in computer simulations (Broadmeadow and Jackson, 2000)'' (U.S. 
EPA, 2013a, p. 9-87). In considering the extent of any protective role 
of drought conditions, however, the ISA also notes that other studies 
have shown that ``drought may exacerbate the effects of O3 
on plants (Pollastrini et al., 2010; Grulke et al., 2003)'' and that 
``[t]here is also some evidence that O3 can predispose 
plants to drought stress (Maier-Maercker, 1998)''. Accordingly, the ISA 
concludes that ``the nature of the response is largely species-specific 
and will depend to some extent upon the sequence in which the stressors 
occur'' (U.S. EPA, 2013a, p. 9-87).
    Due to the absence of biosite injury data in the Southwest region 
and limited biosite data in the West and West North Central regions, 
the W126 benchmarks for foliar injury that the WREA developed and 
applied in the national park screening assessment may not be applicable 
to these regions. The WREA applied the benchmarks from the national-
scale analysis to a screening-level assessment of 214 national parks 
and case studies of three national parks. Therefore, uncertainties in 
the foliar injury benchmarks are propagated into these analyses.
    Other uncertainties associated with these analyses include 
uncertainty associated with our understanding of the number and 
sensitivity of O3 sensitive species, uncertainties 
associated with spatial assignment of foliar injury biosite data to 12 
km x 12 km grid cells, and uncertainties associated with O3 
exposure data of vegetation and recreational areas within parks (U.S. 
EPA, 2014b, Table 7-22).
    There are also important uncertainties in the estimated 
O3 concentrations for the different air quality scenarios 
evaluated (U.S. EPA, 2014b, section 8.5), as discussed earlier in this 
section. These uncertainties only apply to the national park case 
studies because these are the only foliar injury analyses that rely on 
the air quality scenarios, but any uncertainties in the air quality 
analyses are propagated into those analyses. The WREA identifies 
additional uncertainties that are associated with

[[Page 75329]]

the national park case studies. Specifically, there is uncertainty 
inherent in survey estimates of participation rates, visitor spending/
economic impacts, and willingness-to-pay. These surveys potentially 
double-count impacts based on the allocation of expenditures across 
activities but also potentially exclude other activities with economic 
value. In general, the national level surveys apply standard 
approaches, which minimize potential bias. Other sources of uncertainty 
are associated with the mapping, including park boundaries, vegetation 
species cover, and park amenities, such as scenic overlooks and trails. 
In general, the WREA concludes that there is high confidence in the 
park mapping (U.S. EPA, 2014b, Table 7-24).

D. Conclusions on Adequacy of the Current Secondary Standard

    The initial issue to be addressed in the current review of the 
secondary O3 standard is whether, in view of the currently 
available scientific evidence, exposure and risk information and air 
quality analyses, discussed in the PA, the existing standard should be 
revised. In drawing conclusions on adequacy of the current 
O3 secondary standard, the Administrator has taken into 
account both evidence-based and quantitative exposure- and risk-based 
considerations, and advice from CASAC. Evidence-based considerations 
draw upon the EPA's assessment and integrated synthesis of the 
scientific evidence from experimental and field studies evaluating 
welfare effects related to O3 exposure, with a focus on 
policy-relevant considerations, as discussed in the PA. Air quality 
analyses inform these considerations with regard to cumulative, 
seasonal exposures occurring in areas of the U.S. that meet the current 
standard. Exposure- and risk-based considerations draw upon EPA 
assessments of risk of key welfare effects, including O3 
effects on forest growth, productivity, carbon storage, crop yield and 
visible foliar injury, expected to occur in model-based scenarios for 
the current standard, with appropriate consideration of associated 
uncertainties.
    The following sections describe consideration of the evidence and 
the exposure/risk information in the PA and advice received from CASAC, 
as well as the comments received from various parties, and the 
Administrator's proposed conclusions regarding the adequacy of the 
current secondary standard.
1. Evidence- and Exposure/Risk-Based Considerations in the Policy 
Assessment
    Staff assessments in the PA focus on the policy-relevant aspects of 
the assessment and integrative synthesis of the currently available 
welfare effects evidence in the ISA, analyses of air quality 
relationships with exposure metrics of interest, the exposure and risk 
assessments in the WREA, comments and advice of CASAC and public 
comment on drafts of the PA, ISA and WREA. The PA describes evidence- 
and exposure/risk-based considerations and presents staff conclusions 
for the Administrator to consider in reaching her proposed decision on 
the current standard. The focus of the initial PA conclusions is 
consideration of the question: Does the currently available scientific 
evidence and exposure/risk information, as reflected in the ISA and 
WREA, support or call into question the adequacy and/or appropriateness 
of the protection afforded by the current secondary O3 
standard?
    The PA's general approach to informing judgments by the 
Administrator recognizes that the available welfare effects evidence 
demonstrates a range of O3 sensitivity across studied plant 
species and documents an array of O3-induced effects that 
extend from lower to higher levels of biological organization. These 
effects range from those affecting cell processes and individual plant 
leaves to effects on the physiology of whole plants, as well as the 
range from species effects and effects on plant communities to effects 
on related ecosystem processes and services. Given this evidence, the 
PA notes that it is not possible to generalize across all studied 
species regarding which cumulative exposures are of greatest concern, 
as this can vary by situation due to differences in exposed species 
sensitivity, the importance of the observed or predicted O3-
induced effect, the role that the species plays in the ecosystem, the 
intended use of the affected species and its associated ecosystem and 
services, the presence of other co-occurring predisposing or mitigating 
factors, and associated uncertainties and limitations. Therefore, in 
developing conclusions in the PA, staff takes note of the complexity of 
judgments to be made by the Administrator regarding the adversity of 
known and anticipated effects to the public welfare and are mindful 
that the Administrator's ultimate judgments on the secondary standard 
will most appropriately reflect an interpretation of the available 
scientific evidence and exposure/risk information that neither 
overstates nor understates the strengths and limitations of that 
evidence and information (U.S. EPA, 2014c, section 5.7).
    In considering the estimates of exposures and risks for air quality 
scenarios assessed in the WREA, the PA: (1) Evaluates the weight of the 
scientific evidence concerning vegetation effects associated with those 
O3 exposures; (2) considers the importance, from a public 
welfare perspective, of the O3-induced effects on sensitive 
vegetation and associated ecosystem services that are known or 
anticipated to occur as a result of exposures in the assessed air 
quality scenarios; and, (3) recognizes that predictions of effects 
associated with any given O3 exposure may be mitigated or 
exacerbated by actual conditions in the environment (i.e., co-occurring 
modifying environmental and genetic factors). When considering WREA 
analyses that involve discrete exposure levels or varying levels of 
severity of effects, the PA's approach recognizes that the available 
welfare effects evidence demonstrates a wide range in O3 
sensitivities across studied plant species. The PA additionally 
considers the uncertainties associated with this information.
    As an initial matter, the PA recognizes that the CAA does not 
require that a secondary standard be protective of all effects 
associated with a pollutant in the ambient air, but rather those 
considered adverse to the public welfare (as described in section 
IV.B.2 above). In considering the extent to which it may be appropriate 
to consider particular welfare effects adverse, the PA applies a 
paradigm used in past reviews. As discussed in section IV.B.2 above, 
this paradigm recognizes that the significance to the public welfare of 
O3-induced effects on sensitive vegetation growing within 
the U.S. can vary depending on the nature of the effect, the intended 
use of the sensitive plants or ecosystems, and the types of 
environments in which the sensitive vegetation and ecosystems are 
located. Accordingly, any given O3-related effect on 
vegetation and ecosystems (e.g., biomass loss, crop yield loss, visible 
foliar injury) may be judged to have a different degree of impact on 
the public welfare depending, for example, on whether that effect 
occurs in a Class I area, a city park, or commercial cropland. In the 
last review, the Administrator took note of actions taken by Congress 
to establish public lands that are set aside for specific uses that are 
intended to provide benefits to the public welfare, including lands 
that are to be protected so as to conserve the scenic value and the 
natural vegetation

[[Page 75330]]

and wildlife within such areas for the enjoyment of future generations 
(73 FR 16497, March 27, 2008). Such public lands that are protected 
areas of national interest include national parks and forests, wildlife 
refuges, and wilderness areas (73 FR 16497, March 27, 2008). The PA 
notes that effects occurring in such areas would likely have the 
highest potential for being classified as adverse to the public 
welfare, given the expectation of preserving these areas to ensure 
their intended use is met (U.S. EPA, 2014c, section 5.1). In 
considering uses of vegetation and forested lands, the paradigm also 
includes consideration of impacts to ecosystem goods and services. In 
summary, the paradigm considered in the PA, consistent with the 
discussion in section IV.B.2 above, integrates the concepts of: (1) 
Variability in public welfare significance given intended use and value 
of the affected entity, such as individual species; (2) relevance of 
associated ecosystem services to public welfare; and (3) variability in 
spatial, temporal, and social distribution of ecosystem services 
associated with known and anticipated welfare effects. Further, the PA 
recognizes that there is no bright-line rule delineating the set of 
conditions or scales at which known or anticipated effects become 
adverse to public welfare.
    With respect to the scientific evidence, the PA takes note of the 
longstanding evidence base that demonstrates O3-induced 
effects that occur across a range of biological and ecological scales 
of organization, as described in the ISA and summarized in section 
IV.B.1 above (U.S. EPA, 2013a, p. 1-8). Many of the recent studies 
evaluated in this review have focused on and further increased our 
understanding of the molecular, biochemical and physiological 
mechanisms that explain how plants are affected by O3 in the 
absence of other stressors (U.S. EPA, 2013a, section 9.3). These recent 
studies, in combination with the extensive and long-standing evidence, 
have further strengthened the coherence and consistency of the entire 
body of research since the last review. Consistent with conclusions in 
the 2006 AQCD, the ISA determined that a causal relationship exists 
between O3 exposure and visible foliar injury on sensitive 
vegetation, reduced plant growth, reduced productivity in terrestrial 
ecosystems, reduced yield and quality of agricultural crops and 
alteration of below-ground biogeochemical cycles (U.S. EPA, 2013a, 
Table 1-2 and section 2.6). The relationship between O3 
exposures and reduced carbon sequestration in terrestrial ecosystems, 
alteration of terrestrial ecosystem water cycling and alteration of 
terrestrial community composition was concluded to be likely causal 
(U.S. EPA, 2013a, Table 1-2).
    The PA recognizes that consistent with conclusions drawn in the 
last review, the currently available evidence base also strongly 
supports that effects on vegetation are attributable to cumulative 
seasonal O3 exposures. Moreover, on the basis of the entire 
body of evidence in this regard, the ISA concludes that ``quantifying 
exposure with indices that cumulate hourly O3 concentrations 
and preferentially weight the higher concentrations improves the 
explanatory power of exposure/response models for growth and yield, 
over using indices based on mean and peak exposure values'' (U.S. EPA, 
2013a, p. 2-44). Accordingly, as in other recent reviews, the evidence 
continues to provide a strong basis for concluding that it is 
appropriate to judge impacts of O3 on vegetation, related 
effects and services, and the level of public welfare protection 
achieved, using a cumulative, seasonal exposure metric, such as the 
W126-based metric. In this review, as in the last review, the CASAC 
concurs with this conclusion (Frey, 2014c, p. iii). Thus, based on the 
consistent and well-established evidence described above, the PA 
concludes that the most appropriate and biologically relevant way to 
relate O3 exposure to plant growth, and to determine what 
would be adequate protection for public welfare effects attributable to 
the presence of O3 in the ambient air is to characterize 
exposures in terms of a cumulative seasonal form, and in particular the 
W126 metric.
    In considering the current standard with regard to protection from 
the array of O3-related effects recognized in this review, 
the PA first considers effects related to forest tree growth, 
productivity and carbon storage, effects for which the ISA concludes 
the evidence supports a causal or likely causal relationship with 
exposures to O3 in ambient air (U.S. EPA, 2014c, sections 
5.2 and 5.7). In so doing, the PA notes that while changes in biomass 
affect individual tree species, the overall effect on forest ecosystem 
productivity depends on the composition of forest stands and the 
relative sensitivity of trees within those stands. In considering the 
evidence for these effects and the extent to which they might be 
expected to occur under conditions that meet the current secondary 
standard, the PA focused particularly on RBL estimates for the 11 
species for which robust E-R functions have been developed. The PA 
recognized that recent studies, such as multiple-year exposures of 
aspen and birch, have provided additional evidence on tree biomass or 
growth effects associated with multiple year exposures in the field, 
including the potential for cumulative and carry-over effects. For 
example, findings from these studies indicate that effects of 
O3 on birch seeds (reduced weight, germination, and starch 
levels) could lead to a negative impact on species regeneration in 
subsequent years and may have the potential to alter carbon metabolism 
of overwintering buds, potentially affecting growth in the following 
year. Other studies have reported that multiple-year exposures reduced 
tree size parameters in an aspen community, and increased the rate of 
conversion from a mixed aspen-birch community to a community dominated 
by the more tolerant birch, such that elevated O3 may alter 
intra- and inter-species competition within a forest stand (U.S. EPA, 
2013a, section 9.4.3; U.S. EPA, 2014c, section 5.2). In giving 
particular attention to tree seedling biomass loss estimates, the PA 
notes that CASAC ``concurs that biomass loss in trees is a relevant 
surrogate for damage to tree growth that affects ecosystem services 
such as habitat provision for wildlife, carbon storage, provision of 
food and fiber, and pollution removal'' (Frey, 2014c, p. 10).
    In evaluating the current evidence and exposure/risk information 
associated with tree growth, productivity and carbon storage, with 
regard to the adequacy of public welfare protection afforded by the 
current standard, the PA considers the evidence of vegetation and 
welfare impacts in areas of the U.S. likely to have met the current 
standard. With regard to O3 effects on tree growth, 
productivity and carbon storage and associated ecosystems and services, 
the PA focuses on relative biomass loss estimates based on the OTC-
based E-R functions, noting that analyses newly performed in this 
review have reduced the uncertainty associated with using OTC E-R 
functions to predict tree growth effects in the field (U.S. EPA, 2014c, 
section 5.2.1; U.S. EPA, 2013a, section 9.6.3.2).
    In focusing on RBL estimates, the PA recognized that comparison to 
an array of benchmarks would be informative to considerations of 
significance to public welfare. Included in this array were RBL values 
of 2% and 6% given emphasis by CASAC (Frey, 2014c). In considering the 
RBL estimates for different O3 conditions associated with 
the current standard, the PA focused first on the median of the 
species-specific (composite) E-R functions. In so doing,

[[Page 75331]]

the PA takes note of CASAC's comments that a 6% median RBL is 
``unacceptably high'', and that the 2% median RBL is an important 
benchmark to consider (Frey, 2014c).\214\ Based on the summary of RBL 
estimates in the PA, the PA notes that the median species RBL estimate 
is at or below 2% for W126 exposure index values less than or equal to 
7 ppm-hrs (U.S. EPA, 2014c, Table 6-1 and Appendix 5C). The median 
species RBL is at or above 6% for W126 index values of 19 ppm-hrs and 
higher.
---------------------------------------------------------------------------

    \214\ The CASAC provided several comments related to 2% RBL for 
tree seedlings both with regard to its use in summarizing WREA 
results and with regard to consideration of the potential 
significance of vegetation effects, as summarized in sections IV.D.2 
and IV.E.3. In identifying 2% as an important benchmark, CASAC 
referenced the 1996 workshop sponsored by the Southern Oxidants 
Study group at which, as noted in section IV.B.2 above, participants 
identified annual percentages of tree seedling growth reduction and 
crop yield loss they considered important to their judgments on a 
secondary standard. The workshop report provides no explicit 
rationale for the percentages identified or specification with 
regard to number or proportion of species for which such percentages 
should be met (Heck and Cowling, 1997).
---------------------------------------------------------------------------

    In recognition of the significance of welfare effects in Class I 
areas, the PA gives appreciable weight to consideration of the 
occurrence of O3 concentrations associated with the 
potential for RBL estimates above benchmarks of interest in Class I 
areas that meet the current standard. Based on air quality data for the 
period from 1998 to 2012, the PA focused consideration on 22 Class I 
areas, in which during one or more three-year periods the air quality 
met the current standard and the three-year average W126 index value 
was at or above 15 ppm-hrs (see Table 7 below, drawn from U.S. EPA, 
2014c, Table 5-2). Across these 22 Class I areas, the highest single-
year W126 index values for these three-year periods ranged from 17.4 to 
29.0 ppm-hrs. In 20 of the areas, distributed across eight states (AZ, 
CA, CO, KY, NM, SD, UT, WY) and four regions (West, Southwest, West 
North Central and Central), this range was 19.1 to 29.0 ppm-hrs, 
exposure values for which the corresponding median species RBL 
estimates equal or exceed 6%, which CASAC has termed ``unacceptably 
high''. Recognizing that in any given year, other environmental factors 
can influence the extent to which O3 may have the impact 
predicted by the E-R functions, the PA looked beyond single year 
occurrences of such magnitudes of W126 index values. For example, 
focusing on the highest three-year periods that include these highest 
annual values for 21 areas, the PA notes that in 10 areas (across five 
states in the West and Southwest regions), the three-year average W126 
values (for the highest three-year period that includes these annual 
values) are at or above 19 ppm-hrs, ranging up to 22.5 ppm-hrs (for 
which the median species RBL estimate is above 7%). This indicates that 
the W126 value above 19 ppm-hrs is not simply a single year in a period 
of lower years, but that in these cases there were sustained higher 
values that contributed to a three-year W126 also above 19 ppm-hrs. In 
terms of the highest three-year values observed (regardless of single-
year values), the PA additionally notes that the highest three-year 
average W126 index value (during periods meeting the current standard) 
was at or above 19 (ranging up to 22.5 ppm-hrs) in 11 areas, 
distributed among five states in the West and Southwest regions (U.S. 
EPA, 2014c, Table 5-2, Appendix 5B).

 Table 7--O3 Concentrations in Class I Areas During Period From 1998 to 2012 that Met the Current Standard and Where Three-year Average W126 Index Value
                                                               was at or Above 15 ppm-hrs
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                      3-year Average W126 (ppm-
             Class I Area                       State/county           Design value    hrs)* (# >=19 ppm-hrs,    Annual W126 (ppm-hrs)*    Number of 3-
                                                                          (ppb)*               range)            (# >=19 ppm-hrs, range)   year periods
--------------------------------------------------------------------------------------------------------------------------------------------------------
Bandelier Wilderness Area QA, DF, PP.  NM/Sandoval..................           70-74  15.8-20.8 (2, 20.0-20.8)  12.1-25.3 (4, 19.2-25.3)               8
Bridger Wilderness Area QA, DF.......  WY/Sublette..................           69-72  15.1-17.4...............  9.9-19.2 (1, 19.2)......               5
Canyonlands National Park QA, DF, PP.  UT/San Juan..................           69-73  15.0-20.5 (2, 19.8-20.5)  9.9-24.8 (5, 19.3-24.8).               9
Carlsbad Caverns National Park PP....  NM/Eddy......................              69  15.0-15.3...............  8.6-26.7 (1, 26.7)......               3
Chiricahua National Monument DF, PP..  AZ/Cochise...................           69-73  15.7-18.0...............  13.2-21.6 (2, 19.3-21.6)               7
Grand Canyon National Park QA, DF, PP  AZ/Coconino..................           68-74  15.3-22.2 (7, 19.2-22.2)  11.3-26.7 (7, 19.8-26.7)              12
John Muir Wilderness Area QA, DF, PP.  CA/Inyo......................           71-72  16.5-18.6...............  10.1-25.8 (2, 23.9-25.8)               3
Lassen Volcanic National Park DF, PP.  CA/Shasta....................              75  15.3....................  13.6-18.7...............               1
Mammoth Cave National Park BC, C, LP,  KY/Edmonson..................              74  15.9....................  12.5-22.5 (1, 22.5).....               1
 RM, SM, VP, YP.
Mesa Verde National Park DF..........  CO/Montezuma.................           67-73  15.5-21.0 (2, 19.0-21.0)  10.7-23.6 (4, 19.7-23.6)              10
Mokelumne Wilderness Area DF, PP.....  CA/Amador....................              74  17.6....................  14.8-22.6 (1, 22.6).....               1
Petrified Forest National Park.......  AZ/Navajo....................              70  15.7....................  12.9-19.2 (1, 19.2).....               1
Pinnacles National Monument..........  CA/San Benito................              74  15.1....................  13.1-17.4...............               1
Rocky Mountain National Park QA, DF,   CO/Boulder...................           73-75  15.1-19.3 (1, 19.3).....  9.5-25.1 (5, 20.7-25.1).               6
 PP.
                                       CO/Larimer...................              74  15.0-18.3...............  8.1-25.8 (3, 19.1-25.8).               3
Saguaro National Park DF, PP.........  AZ/Pima......................           69-74  15.4-18.9...............  11.0-23.1 (3, 20.0-23.1)               6
Sierra Ancha Wilderness Area DF, PP..  AZ/Gila......................           72-75  17.9-22.4 (3, 20.2-22.4)  14.8-27.5 (4, 20.3-27.5)               4

[[Page 75332]]

 
Superstition Wilderness Area PP......
                                       AZ/Maricopa..................              75  22.4 (1, 22.4)..........  14.5-28.6 (2, 27.4-28.6)               1
                                       AZ/Pinal.....................           73-75  18.7-22.5 (2, 20.8-22.5)  14.8-29.0 (3, 22.6-29.0)               3
Weminuche Wilderness Area QA, DF, PP.  CO/La Plata..................           70-74  15.0-19.1 (1, 19.1).....  10.9-21.0 (2, 20.8-21.0)               5
West Elk Wilderness Area QA, DF......  CO/Gunnison..................           68-73  15.6-20.1 (1, 20.1).....  12.9-23.9 (3, 21.1-23.9)               8
Wind Cave National Park QA, PP.......  SD/Custer....................              70  15.4....................  12.2-20.6 (1, 20.6).....               1
Yosemite National Park QA, DF, PP....  CA/Tuolumne..................           73-74  20.7-20.8 (2, 20.7-20.8)  19.7-22.1 (4, 19.7-22.1)               2
Zion National Park QA, DF, PP........  UT/Washington................           70-73  17.8-21.1 (2, 20.3-21.1)  14.9-24.2 (5, 19.3-24.2)               4
--------------------------------------------------------------------------------------------------------------------------------------------------------
* Based on data from http://www.epa.gov/ttn/airs/airsaqs/detaildata/downloadaqsdata.htm. W126 values are truncated after first decimal place.
  Superscript letters refer to species present for which E-R functions have been developed. QA=Quaking Aspen, BC=Black Cherry, C=Cottonwood, DF=Douglas
  Fir, LP=Loblolly Pine, PP=Ponderosa Pine, RM=Red Maple, SM=Sugar Maple, VP=Virginia Pine, YP=Yellow (Tulip) Poplar. Sources include USDA-NRCS
  (2014,http://plants.usda.gov), USDA-FS (2014, http://www.fs.fed.us/foresthealth/technology/nidrm2012.shtml) UM-CFCWI (2014, http://www.wilderness.net/printFactSheet.cfm?WID=583) and Phillips and Comus (2000).

    In considering the data analysis for 22 Class I areas described 
above, the PA additionally considers the species-specific RBL estimates 
for quaking aspen and ponderosa pine, two tree species that are found 
in many of these 22 areas and have a sensitivity to O3 
exposure that places them near the middle of the group for which E-R 
functions have been established (U.S. EPA, 2014c, sections 5.2 and 
5.7). In the Class I areas where ponderosa pine is present, the highest 
single year W126 index values ranged from 18.7 to 29.0 ppm-hrs and the 
highest three-year average W126 values in which these single year 
values were represented ranged from 15 to 22.5 ppm-hrs, with these 
three-year values above 19 ppm-hrs in eight areas across five states. 
The ponderosa pine RBL estimates for 29 and 22.5 ppm-hrs are 
approximately 12% and 9%, respectively (U.S. EPA, 2014c, Appendix 5C). 
In Class I areas where quaking aspen is present, the highest single 
year W126 index values ranged from 19.2 to 26.7 ppm-hrs and the highest 
three-year average W126 values in which these single year values were 
represented ranged from 15.0 to 22.2 ppm-hrs, with these three-year 
values above 19 ppm-hrs in eight areas across five states. The quaking 
aspen RBL estimates for 26.7 and 22.2 ppm-hrs are approximately 16% and 
13%, respectively (U.S. EPA, 2014c, Appendix 5C).
    The PA describes the above observations, particularly in light of 
advice from CASAC, summarized in section IV.D.2 below, as evidence of 
the occurrence in Class I areas during periods where the current 
standard is met of cumulative seasonal O3 exposures of a 
magnitude for which the tree growth impacts indicated by the estimated 
median species RBL might reasonably be concluded to be important to 
public welfare (U.S. EPA, 2014c, sections 5.2.1 and 5.7).
    In considering the WREA analyses of effects on tree growth and 
associated ecosystem services in the air quality scenario for the 
current standard, the PA first takes note of the potential for the 
interpolation method used in creating the national surface of 
O3 concentrations for the air quality scenarios to 
underestimate the higher W126 values such that W126-based exposures 
would be expected to be somewhat higher than those included in each 
scenario (U.S. EPA, 2014b, pp. 5-31 to 5-32). While recognizing this, 
the PA considers results of the WREA analyses for the current standard 
scenario and the 11 species of trees, for which robust E-R functions 
are available. These results indicate that O3 can impact 
growth of these species across the U.S., as well as an array of 
associated ecosystem services provided by forests, including timber 
production, carbon storage and air pollution removal (U.S. EPA, 2014b, 
sections 6.2-6.8; U.S. EPA, 2014c, section 5.2).
    With regard to WREA analyses of ecosystem services, the PA notes 
that the national-scale analysis of O3 impacts on carbon 
storage indicates appreciably more storage in the air quality scenario 
for the current standard (approximately 11,000 MMtCO2e, over 
30 years) compared to the scenario for recent, higher O3 
conditions (U.S. EPA, 2014b, Appendix 6B, Table B-10). The PA 
additionally considers the WREA estimates of tree growth and ecosystem 
services provided by urban trees over a 25-year period for five urban 
areas based on case-study scale analyses that quantified the effects of 
biomass loss on carbon storage and pollution removal (U.S. EPA, 2014b, 
sections 6.6.2 and 6.7; U.S. EPA, 2014c, sections 5.2 and 5.7). The 
urban areas included in this analysis represent diverse geography in 
the Northeast, Southeast, and Central regions, although they do not 
include an urban area in the western U.S. Estimates of the effects of 
O3-related biomass loss on carbon sequestration indicate the 
potential for an increase of somewhat more than a MMtCO2e 
for the current standard scenario as compared to the recent conditions 
scenario (U.S. EPA, 2014b, section 6.6.2 and Appendix 6D; U.S. EPA, 
2014c, sections 5.2 and 5.7). The PA also notes the WREA estimates of 
increased pollution removal in the current standard scenario as 
compared to the scenario for recent conditions (U.S. EPA, 2014b, 
section 6.6.2; U.S. EPA, 2014c, section 5.2.2).
    In considering the significance of these WREA analyses of risks for 
the associated ecosystem services for timber production, air pollution 
removal, and carbon sequestration, the PA takes note of the large 
uncertainties associated with these analyses (see U.S. EPA, 2014b, 
Table 6-27), and the potential for these findings to underestimate the 
response at the national scale. While noting the potential usefulness 
of considering predicted and anticipated impacts to these services in 
assessing the extent to which the current information supports or calls 
into question the adequacy of the protection afforded by the current 
standard, the PA also notes that staff places limited

[[Page 75333]]

weight on the absolute magnitude of the risk results for these 
ecosystem service endpoints due to the identification of significant 
associated uncertainties (U.S. EPA, 2014c, sections 5.2 and 5.7).
    In reaching conclusions regarding support for the adequacy of the 
current secondary standard provided by the currently available 
information on O3-induced effects on trees and associated 
services, the PA takes note of: (1) the robust evidence supporting the 
causal relationship between cumulative O3 exposures and 
effects on tree growth and productivity, and information from model 
simulations supporting the determination of a likely causal 
relationships for carbon storage in terrestrial ecosystems (U.S. EPA, 
2013a, sections 2.6.2.1 and 9.4.3); (2) the tree seedling E-R functions 
evidence, which has been strengthened and demonstrates variability in 
sensitivity to O3 across species; (3) estimates of median 
species RBL at or above 6% associated with W126-based exposure levels 
in several areas when O3 concentrations were at or below the 
current standard; (4) growth effects estimates associated with exposure 
concentrations in several Class I areas based on O3 
concentrations from 1998-2012 that were at or below the current 
standard; (5) evidence that impacts from single year exposures can 
carry over to the subsequent year and/or cumulate over multiple years 
with repeated annual exposures; (6) evidence from recent mechanistic 
studies and field based studies that support earlier findings from OTC 
studies; and (7) WREA analyses indicating that O3-induced 
biomass loss can impact ecosystem services provided by forests, 
including timber production, carbon storage, and air pollution removal, 
even when air quality is adjusted to just meet the current standard. 
Given the above, and noting CASAC views (described in section IV.D.2 
below), the PA concludes that the current evidence and exposure/risk 
information call into question the adequacy of public welfare 
protection afforded by the current standard from the known and 
anticipated adverse effects associated with O3-induced 
impacts on tree growth, productivity and carbon storage, including the 
associated ecosystem services assessed in this review. Therefore, the 
PA concludes that it is appropriate to consider revision of the 
secondary standard to provide increased protection.
    With respect to crops, the PA takes note of the extensive and long-
standing evidence on the detrimental effect of O3 on crop 
production, which continues to be confirmed by newly available evidence 
(U.S. EPA, 2013a, section 9.4.4; U.S. EPA, 2014c, sections 5.3 and 
5.7). The PA additionally notes that recent studies have highlighted 
the effects of O3 on crop quality, such as through decreases 
in the nutritive quality of grasses, and in the macro- and micro-
nutrient concentrations in fruits and vegetable crops (U.S. EPA, 2013a, 
section 9.4.4; U.S. EPA, 2014c, section 5.3). Further, the PA notes 
that there has been little published evidence that crops are becoming 
more tolerant of O3, taking note particularly of the ISA 
analyses of data from cultivars used in NCLAN studies, and yield data 
for modern cultivars from SoyFACE which confirm that the average 
response of soybean yield to O3 exposure has not changed in 
current cultivars (U.S. EPA, 2006a; U.S. EPA, 2013a, section 9.6.3; 
U.S. EPA, 2014c, section 5.3). In consideration of the currently 
available evidence for O3 effects on crops, the PA concludes 
that the recently available evidence, as assessed in the ISA, continues 
to support the conclusions of the 1996 and 2006 CDs that ambient 
O3 concentrations can reduce the yield of major commodity 
crops in the U.S, and that the currently available evidence continues 
to support the use of the E-R functions developed for 10 crops from OTC 
experiment data. Further, the PA recognizes that important 
uncertainties have been reduced regarding the exposure-response 
functions for crop yield loss, especially for soybean, the second-most 
planted field crop in the U.S.,\215\ with the ISA generally reporting 
consistent results across exposure techniques and across crop varieties 
(U.S. EPA, 2013a, section 9.6.3.2).
---------------------------------------------------------------------------

    \215\ See http://www.ers.usda.gov/topics/crops/soybeans-oil-crops/background.aspx
---------------------------------------------------------------------------

    With regard to consideration of the quantitative impacts of 
O3 on crop yield, the PA considers RYL estimates for 
O3 conditions associated with the current standard. As in 
the case of the PA considerations of RBL estimates for tree seedlings, 
the PA recognized CASAC comments, which described greater than 5% RYL 
for the median crop species as ``unacceptably high'' and 5% RYL for the 
median crop species as adverse, while noting the opportunities to alter 
management of annual crops (Frey, 2014c, pp. iii and 14). The PA notes 
that staff analyses of recent monitoring data (2009-2011) indicate that 
O3 concentrations in multiple agricultural areas in the U.S. 
that meet the current standard correspond to W126 index levels above 12 
ppm-hrs, a value for which soybean RYL estimates are greater than 5%. 
In particular, the PA notes that while the design values for two 
counties in the Midwest met the current standard in 2009-2011, both had 
a maximum annual W126 of 19 ppm-hrs (in 2011) for which the soybean 
annual RYL estimate, based on the E-R function, is 9%.\216\
---------------------------------------------------------------------------

    \216\ The monitoring data reflect observations in locations that 
meet the current standard. The WREA analysis that assessed crop 
yield loss used a model-developed air quality scenario to reflect 
air quality associated with the current standard (as described in 
section IV.C.1 above). In so doing, adjustments are made to create 
air quality that meets the standard and when the highest monitor in 
an area is adjusted downward to meet the standard, concentrations at 
nearby monitors that already meet the standard are also reduced.
---------------------------------------------------------------------------

    In considering the evidence and exposure/risk-based information for 
effects on crops, the PA notes the CASAC comments regarding the use of 
crop yields as a surrogate for consideration of public welfare impacts, 
in which it noted that ``[c]rops provide food and fiber services to 
humans'' and that ``[e]valuation of market-based welfare effects of 
O3 exposure in forestry and agricultural sectors is an 
appropriate approach to take into account damage that is adverse to 
public welfare'' (Frey, 2014c, p. 10; U.S. EPA, 2014c, section 5.7). 
The PA additionally notes, however, as recognized in section IV.B.2 
above that the determination of the point at which O3-
induced crop yield loss becomes adverse to the public welfare is still 
unclear, given that crops are heavily managed with additional inputs 
that have their own associated markets and that benefits can be 
unevenly distributed between producers and consumers. The PA further 
notes that to the extent protection is provided by the current standard 
with regard to impacts on trees, protection may also be provided for 
commodity crops (U.S. EPA, 2014c, sections 5.3 and 5.7).
    In reaching conclusions regarding support provided for the adequacy 
of the current secondary standard by the currently available 
information on O3-related crop effects, the PA notes: (1) 
the support for a causal relationship between cumulative O3 
exposures and effects on crop yields and quality (U.S. EPA, 2013a, 
section 9.4.4); (2) the evidence supporting E-R functions for 10 crops, 
which has been strengthened in this review and which demonstrates 
variability in sensitivity to O3 across species; (3) 
evidence from recent mechanistic studies and field based studies 
supporting earlier findings from OTC studies; (4) evidence that crops, 
and in particular soybean, have not become more tolerant of 
O3 (U.S. EPA, 2013a, section 9.6.3, 9.4.4.1); and, (5) WREA 
analysis results indicating that O3-induced crop yield loss 
can impact producer and consumer surpluses and

[[Page 75334]]

the interaction between agriculture and timber production.
    With regard to visible foliar injury, the PA recognizes the long-
standing evidence that has established that O3 causes 
diagnostic visible injury symptoms on studied bioindicator species and 
that soil moisture is a major confounding effect that can decrease the 
incidence and severity of visible foliar injury under dry conditions 
and vice versa (U.S. EPA, 2014c, sections 5.4 and 5.7). As at the time 
of the last review, the most extensive dataset regarding visible foliar 
injury incidence across the U.S. is that collected by the U.S. Forest 
Service (USFS) Forest Health Monitoring/Forest Inventory and Analysis 
(FHM/FIA) Program, which has documented incidence of visible foliar 
injury in both the eastern and western U.S. Evidence available in the 
current review includes studies using controlled exposures as well as 
multi-year field surveys. In addition to supporting prior conclusions, 
the newly available studies also address some uncertainties identified 
in the last review, such as the influence of soil moisture on visible 
injury development (U.S. EPA, 2013a, section 9.4.2). As stated in the 
ISA, ``many studies have shown that dry periods in local areas tend to 
decrease the incidence and severity of O3-induced visible 
foliar injury; therefore, the incidence of visible foliar injury is not 
always higher in years and areas with higher O3, especially 
with co-occurring drought'' (U.S. EPA, 2013a, p. 9-39). The ISA 
additionally concludes, however, that ``the nature of the response is 
largely species-specific and will depend to some extent upon the 
sequence in which the stressors occur'' (U.S. EPA, 2013a, p. 9-87). As 
recognized in the PA, this area of uncertainty complicates 
characterization of the potential for visible foliar injury and its 
severity or extent of occurrence for any given air quality conditions 
and thus complicates identification of air quality conditions that 
might be expected to provide a specific level of protection from this 
effect (U.S. EPA, 2014c, sections 5.4 and 5.7).
    Information available in this review indicates the occurrence of 
visible foliar injury in some Class I areas during times when 
O3 concentrations met or would be expected to meet the 
current standard (U.S. EPA, 2014c, sections 5.4.1 and 5.7). In noting 
this occurrence in Class I areas, the PA notes it has particular public 
welfare significance in light of direction from Congress that these 
areas merit a high level of protection (U.S. EPA, 2014c, sections 5.1, 
5.4.1 and 5.7). The PA also notes that visible foliar injury surveys 
are used by the federal land managers to assess potential O3 
impacts in Class I areas (USFS, NPS, FWS, 2010). Given this focus on 
visible foliar injury, the PA concludes that such O3-induced 
impacts have the potential to impact the public welfare in scenic and/
or recreational areas on an annual basis. Visible foliar injury is 
associated with important cultural and recreational ecosystem services 
to the public, such as scenic viewing, wildlife-watching, hiking, and 
camping, that are of significance to the public welfare and enjoyed by 
millions of Americans every year, generating millions of dollars in 
economic value (U.S. EPA, 2014b, section 7.1). In addition, several 
tribes have indicated that many of the O3-sensitive species 
(including bioindicator species) are culturally significant (U.S. EPA, 
2014c, Table 5-1). With respect to agricultural species, such visible 
effects of O3 exposure can affect the market value of 
certain crops and ornamentals for which leaves are the product, such as 
spinach (U.S. EPA, 2006a, p. AX-9-189). The PA additionally notes CASAC 
comments that ``visible foliar injury can impact public welfare by 
damaging or impairing the intended use or service of a resource'', 
including through ``visible damage to ornamental or leafy crops that 
affects their economic value, yield, or usability; visible damage to 
plants with special cultural significance; and visible damage to 
species occurring in natural settings valued for scenic beauty or 
recreational appeal'' (Frey, 2014c, p. 10).
    With regard to the exposure and risk-based information, the PA 
takes note of the WREA analyses of the nationwide dataset (2006-2010) 
for USFS/FHM biosites, including the observation that the proportion of 
biosites with injury varies with soil moisture conditions and 
O3 W126 index values (U.S. EPA, 2014b, Chapter 7, Figure 7-
10; U.S. EPA, 2014c, section 5.4.2). These analyses indicate that the 
proportion of biosites showing visible foliar injury incidence 
increases steeply with W126 index values up to approximately 10 ppm-
hrs, with little difference in incidence across higher W126 index 
levels. The screening-level assessment of national parks indicated that 
risk of visible foliar injury is likely to be lower in most national 
parks after simulating just meeting the current standard, although 
visible foliar injury would likely continue to occur at lower 
O3 exposures, including some sensitive species growing in 
National Parks and other Class I areas that may provide important 
cultural ecosystem services to the public. The PA also notes the WREA 
recognition that many of the outdoor recreational activities which 
directly depend on the scenic value of the area are of significant 
importance to public welfare as they are enjoyed by millions of 
Americans every year and generate millions of dollars in economic value 
(U.S. EPA, 2014b, Chapter 5, Chapter 7).
    In reaching conclusions regarding support for the adequacy of the 
current secondary standard provided by the currently available 
information on O3-induced visible foliar injury, the PA took 
note of: (1) The evidence for many species of native plants, including 
trees, that have been observed to have visible foliar injury symptoms 
in both OTC and field settings, some of which have also been identified 
as bioindicators of O3 exposure by the USFS; (2) the finding 
that visible foliar injury incidence can occur at very low cumulative 
exposures, but due to confounding by soil moisture and other factors, 
it is difficult to predictively relate a given O3 exposure 
to plant response; (3) information indicating the occurrence of visible 
foliar injury in some Class I areas under air quality conditions 
expected to meet the current standard; and, (4) WREA analyses, based on 
USFS biosite data, indicating a relationship of the proportion of 
biosites showing visible foliar injury incidence with W126 index values 
below approximately 10 ppm-hrs (U.S. EPA, 2014c, section 5.7).
    The PA additionally recognizes a lack of guidance for federal land 
managers regarding what spatial scale or degree of severity of visible 
foliar injury is considered sufficient to trigger protective action for 
O3 sensitive AQRVs. Further, there does not appear to be any 
consensus in the literature in this regard, and CASAC, while 
identifying benchmarks to consider for percent biomass loss and yield 
loss for tree seedlings and commodity crops, respectively, did not 
provide a similar recommendation for this endpoint. Likewise, as in 
previous reviews, the ISA notes the difficulty in relating visible 
foliar injury symptoms to other vegetation effects such as individual 
plant growth, stand growth, or ecosystem characteristics (U.S. EPA, 
2013a, section 9.4.2, p. 9-39) and further notes that the full body of 
evidence indicates that there is wide variability in this endpoint, 
such that although evidence shows visible foliar injury can occur under 
very low cumulative O3 concentrations, ``. . .the degree and 
extent of visible foliar injury development varies from year to year 
and site to site . . ., even among co-members of a population exposed 
to similar O3 levels, due to the influence

[[Page 75335]]

of co-occurring environmental and genetic factors'' (U.S. EPA, 2013a, 
section 9.4.2, p. 9-38).
    Given the above, and taking note of CASAC views, the PA recognizes 
visible foliar injury as an important O3 effect which, 
depending on severity and spatial extent, may reasonably be concluded 
to be of public welfare significance, especially when occurring in 
nationally protected areas. While noting the uncertainties associated 
with describing the potential for visible foliar injury and its 
severity or extent of occurrence for any given air quality conditions, 
the PA notes the occurrence of O3-induced visible foliar 
injury in areas, including federally protected Class I areas that meet 
the current standard, and suggests it may be appropriate to consider 
revising the standard to achieve greater protection, while recognizing 
that the degree to which O3-induced visible foliar injury 
would be judged important and potentially adverse to public welfare is 
uncertain (U.S. EPA, 2014c, section 5.7).
    With regard to other welfare effects, for which the ISA determined 
a causal or likely causal relationships with O3 in ambient 
air, such as alteration of ecosystem water cycling and changes in 
climate, the PA concludes there are limitations in the available 
information which affect our ability to consider potential impacts of 
air quality conditions associated with the current standard.
    In reaching conclusions on options for the Administrator's 
consideration, the PA indicates that the final decision to retain or 
revise the current secondary O3 standard is a public welfare 
policy judgment to be made by the Administrator, based on her judgment 
as to what level of air quality would be requisite (i.e., neither more 
nor less stringent than necessary) to protect the public welfare from 
any known or anticipated adverse effects. This final decision will draw 
upon the available scientific evidence for O3-attributable 
welfare effects and on quantitative analyses of vegetation and 
ecosystem exposures and associated risks to vegetation, ecosystems and 
their associated services, and judgments about the appropriate weight 
to place on the range of uncertainties inherent in the evidence and 
analyses. In making this decision, the Administrator will need to weigh 
the importance of these effects and their associated ecosystem services 
in the overall context of public welfare protection.
    Based on the considerations described in the PA and summarized 
here, the PA concludes that the currently available evidence and 
exposure/risk information call into question the adequacy of the public 
welfare protection provided by the current standard and provides 
support for considering potential alternative standards to achieve 
increased public welfare protection, especially for sensitive 
vegetation and ecosystems in federally protected Class I and similarly 
protected areas. In this conclusion, staff gives particular weight to 
the evidence indicating the occurrence in Class I areas that meet the 
current standard of cumulative seasonal O3 exposures 
associated with estimates of tree growth impacts of a magnitude that 
may reasonably be considered important to public welfare.
2. CASAC Advice
    Beyond the evidence- and exposure/risk-based considerations in the 
PA discussed above, the EPA's consideration of the adequacy of the 
current secondary standard also takes into account the advice and 
recommendations of CASAC.
    In its advice offered in the current review, based on the updated 
scientific and technical record since the 2008 rulemaking, the CASAC 
stated that they ``support the conclusion in the Second Draft PA that 
the current secondary standard is not adequate to protect against 
current and anticipated welfare effects of ozone on vegetation'' (Frey, 
2014c, p. iii) and that the PA ``clearly demonstrates that ozone-
induced injury may occur in areas that meet the current standard'' 
(Frey, 2014c, p. 12). The Panel further stated ``[w]e support EPA's 
continued emphasis on Class I and other protected areas'' (Frey, 2014c, 
p. 9). Additionally, the CASAC indicated support for the concept of 
ecosystem services ``as part of the scope of characterizing damage that 
is adverse to public welfare'' and ``concurs that trees are important 
from a public welfare perspective because they provide valued services 
to humans, including aesthetic value, food, fiber, timber, other forest 
products, habitat, recreational opportunities, climate regulation, 
erosion control, air pollution removal, and hydrologic and fire regime 
stabilization'' (Frey, 2014c, p. 9). Similar to comments from CASAC in 
the last review, including comments on the proposed reconsideration, 
the current CASAC also endorsed the PA discussions and conclusions on 
biologically relevant exposure metrics and the focus on the W126 index 
accumulated over a 12-hour period (8am-8pm) over the three-month 
summation period of a year resulting in the maximum value (Frey, 2014c, 
p. iii).
    In addition, CASAC stated that ``relative biomass loss for tree 
species, crop yield loss, and visible foliar injury are appropriate 
surrogates for a wide range of damage that is adverse to public 
welfare'' (Frey, 2014c, p. 10). With respect to relative biomass loss 
for tree species, CASAC states that it is appropriate to ``include 
levels that aim for not greater than 2% RBL for the median tree 
species'' and that a median tree species RBL of 6% is ``unacceptably 
high.'' With respect to crop yield loss, CASAC points to a benchmark of 
5%, stating that a crop RYL for median species over 5% is 
``unacceptably high'' (Frey, 2014c, p. 13).
3. Administrator's Proposed Conclusions on Adequacy of the Current 
Standard
    In considering the adequacy of the current secondary O3 
standard, the Administrator has considered the assessment of the 
current evidence in the ISA, findings of the WREA, including associated 
limitations and uncertainties, considerations and staff conclusions and 
associated rationales presented in the PA, views expressed by CASAC, 
and public comments. In taking into account the information discussed 
above with regard to the nature of O3-related effects on 
vegetation, the Administrator has taken particular note of: the PA 
analysis of the magnitude of tree seedling growth effects (biomass 
loss) estimated for different cumulative, seasonal, concentration-
weighted exposures in terms of the W126 metric; the monitoring analysis 
in the PA of W126 exposures occurring in locations where the current 
standard is met, including those locations in Class I areas, and 
associated estimates of tree seedling growth effects; the analyses in 
the WREA illustrating the geographic distribution of tree species for 
which E-R functions are available and relative differences estimated 
for O3-related growth impacts across areas of the U.S. for 
the air quality scenarios, taking into account the identified potential 
for the WREA's scenario for the current standard to underestimate the 
highest W126-based O3 values that would be expected to 
occur.
    As an initial matter, the Administrator recognizes the 
appropriateness and usefulness of the W126 metric, as described in 
sections IV.B.1 and IV.D.1 above, in evaluating O3 exposures 
of potential concern for vegetation effects. In so doing, the 
Administrator additionally notes support conveyed by CASAC for such a 
use for this metric.
    With regard to considering the adequacy of public welfare 
protection provided by the current secondary standard, the 
Administrator focuses first on welfare effects related to reduced

[[Page 75336]]

native plant growth and productivity in terrestrial ecosystems, taking 
note of the ISA conclusion of a causal relationship between 
O3 in the ambient air and these effects. In considering the 
assessment of the information available in this review with regard to 
O3 effects on vegetation growth and productivity, the 
Administrator takes note of the evidence from OTC studies of the 
effects of O3 exposure on tree seedling growth that support 
robust E-R functions for 11 tree seedling species, and the 
characterization of growth effects across these species for different 
cumulative seasonal concentration-weighted exposures using the W126 
metric. Reductions in growth of sensitive species, as recognized in 
section IV.B above, have the potential to result in effects on 
ecosystem productivity, as well as, on forest and forest community 
composition. The Administrator takes particular note of the evidence, 
described in section IV.D.1 above, of the occurrence in Class I areas 
during periods where the current standard is met of cumulative seasonal 
O3 exposures for which median species RBL estimates are of a 
magnitude that CASAC has termed ``unacceptably high.'' In so doing, the 
Administrator also takes note of a number of actions taken by Congress 
to establish public lands that are set aside for specific uses intended 
to provide benefits to the public welfare, including lands that are to 
be protected so as to conserve the scenic value and the natural 
vegetation and wildlife within such areas for the enjoyment of future 
generations. Such public lands that are protected areas of national 
interest include national parks and forests, wildlife refuges, and 
wilderness areas (many of which have been designated Class I 
areas).\217\
---------------------------------------------------------------------------

    \217\ As noted in section IV.A above, Congress has established 
areas such as national parks and wilderness areas with specific 
purposes including the preservation of the areas for future 
generations, and has identified many of those areas as Class I 
areas.
---------------------------------------------------------------------------

    While recognizing the variability in the various environmental 
factors that can influence the occurrence and severity of the effect of 
ambient O3 concentrations on vegetation in different 
locations, the Administrator concludes that the information referenced 
above including the currently available, extensive evidence base and 
also factors affecting the significance of impacts to public welfare, 
as well as WREA estimates regarding the potential for occurrence of 
impacts important to public welfare, provides an appropriate basis to 
inform a conclusion as to whether the current standards provide 
adequate protection against O3-related vegetation effects on 
public welfare. With regard to the results of the monitoring analysis, 
the Administrator takes note of the PA conclusions that the impacts on 
tree growth (and the potential for associated ecosystem effects) 
estimated for W126 values found to occur in Class I areas when meeting 
the current standard are reasonably concluded to be important from a 
public welfare standpoint in terms of both the magnitude of the 
vegetation effects and the significance to public welfare of such 
effects in such areas, calling into question the adequacy of the 
current secondary standard.
    The Administrator also recognizes the causal relationships between 
O3 in the ambient air and visible foliar injury, reduced 
yield and quality of agricultural crops and alteration of below-ground 
biogeochemical cycles associated with effects on growth and 
productivity. As to visible foliar injury, the Administrator takes note 
of the complexities and limitations in the evidence base regarding 
characterizing air quality conditions with respect to the magnitude and 
extent of risk for visible foliar injury. She additionally recognizes 
the challenges of associated judgments with regard to adversity of such 
effects to public welfare. In taking note of the conclusions with 
regard to crops, she recognizes the complexity of considering adverse 
O3 impacts to public welfare due to the heavy management 
common for achieving optimum yields and market factors that influence 
associated services and additionally takes note of the PA conclusions 
that placing emphasis on the protection afforded to trees inherently 
also recognizes a level of protection afforded for crops.
    Based on her consideration of the conclusions in the PA, and with 
particular weight given to PA findings pertaining to tree growth-
related effects, as well as with consideration of CASAC's conclusion 
that the current standard is not adequate, the Administrator proposes 
to conclude that the current standard is not requisite to protect 
public welfare from known or anticipated effects and that revision is 
needed to provide increased public welfare protection, especially for 
sensitive vegetation and ecosystems in federally protected Class I 
areas and in other areas providing similar public welfare benefits. The 
Administrator further concludes that the scientific evidence and 
quantitative analyses on tree growth-related effects provide strong 
support for consideration of alternative standards that would provide 
increased public welfare protection beyond that afforded by the current 
O3 secondary standard. She further notes that a revised 
standard would provide increased protection for other growth-related 
effects, including for carbon storage and for areas for which it is 
more difficult to determine public welfare significance, as recognized 
in section IV.B.2 above, as well other welfare effects of 
O3, including visible foliar injury and crop yield loss.
    In giving particular focus to tree growth-related effects of 
O3 on public welfare, the Administrator additionally 
recognizes that there are alternative approaches to viewing the 
evidence and information, including alternative approaches to viewing, 
evaluating, and weighing important uncertainties. In some cases, these 
alternative approaches have been expressed by public commenters, 
leading some public commenters to recommend retaining the current 
standard. Given these alternative views, in addition to proposing to 
revise the current secondary standard, the Administrator also solicits 
comment on the option of retaining the standard without revision.

E. Consideration of Alternative Secondary Standards

    Given her proposed conclusion that the current secondary standard 
is inadequate, the Administrator has then considered what revisions to 
the standard may be appropriate, focusing on revisions to the key 
standard elements of indicator, form, averaging time, and level. On the 
basis of the strength and coherence of the vegetation effects evidence 
indicating a cumulative, seasonal, concentration-weighted metric as the 
most appropriate approach for judging potential impacts of and 
protection from O3 in ambient air, the Administrator judges 
that it is appropriate to consider revisions to the secondary standard 
that reflect this understanding and to use such a metric in identifying 
an appropriate level of protection and considering the protection 
afforded by potential alternative standards. The Administrator also 
judges that the current averaging time and form may also provide 
protection to vegetation when set at an appropriate level. Therefore, 
the Administrator considered whether revision to the level of the 
current secondary standard might provide sufficient protection to also 
achieve the level of air quality that is determined requisite to 
protect the public welfare.
    The sections below address the indicator for the secondary standard 
(section IV.E.1), consideration of a cumulative, seasonal exposure-
based

[[Page 75337]]

standard in the PA (section IV.E.2), CASAC advice and public input 
(section IV.E.3), analyses of air quality in the PA and subsequent to 
the PA (section IV.E.4) and the Administrator's proposed conclusions 
regarding an alternative secondary standard (section IV.E.5)
1. Indicator
    In the last review of the air quality for O3 and other 
photochemical oxidants and of the O3 standard, as in other 
prior reviews, the EPA focused on a standard for O3 as the 
most appropriate surrogate for ambient photochemical oxidants. Ozone is 
a long-established surrogate for ambient photochemical oxidants, among 
which it is by far the most widely studied with regard to effects on 
welfare and specifically on vegetation. The information available in 
this review adds to the understanding of the atmospheric chemistry for 
photochemical oxidants and O3 in particular (as described in 
the ISA, sections 3.2 and 3.6, and summarized in section 2.2 in the 
PA). The 1996 Staff Paper noted that the database on vegetation effects 
is generally considered to raise concern at levels found in the ambient 
air for O3 and, therefore, control of ambient O3 
levels has previously been concluded to provide the best means of 
controlling other photochemical oxidants of potential welfare concern 
(U.S. EPA, 1996b, p. 277). In the current review, while the complex 
atmospheric chemistry in which O3 plays a key role has been 
highlighted, no alternatives to O3 have been advanced as 
being a more appropriate surrogate for ambient photochemical oxidants. 
Ozone continues to be the only photochemical oxidant (other than 
nitrogen dioxide) that is routinely monitored and for which a 
comprehensive database exists (U.S. EPA, 2013a, section 3.6).
    Thus, the Administrator concludes that ozone is the appropriate 
indicator and proposes to continue to use O3 as indicator 
for a secondary standard that is intended to address effects associated 
with exposure to O3, alone and in combination with related 
photochemical oxidants. In so doing, the Administrator recognizes that 
measures leading to reductions in ecosystem exposures to O3 
will also reduce exposures to other photochemical oxidants.
2. Consideration of a Cumulative, Seasonal Exposure-based Standard in 
the Policy Assessment
    In recognition of the extensive evidence supporting a cumulative, 
seasonal exposure index as a biologically relevant metric for assessing 
potential for O3 effects on vegetation, discussed in 
sections IV.B.1 above, as well as advice from CASAC in the current and 
last O3 NAAQS reviews, summarized in sections IV.D.3 above 
and IV.E.3 below, the PA focused its consideration of alternative 
standards on a revised secondary standard based on a cumulative, 
seasonal, concentration-weighted form. The PA considered the currently 
available information that has been critically analyzed and 
characterized in the ISA, the risk and exposure information presented 
in the WREA, and CASAC advice and public comment with regard to support 
for consideration of options for alternative standards that might be 
expected to provide increased protection from ambient O3 
exposures over the current standard.
a. Form and Averaging Time
    In considering potential forms for a revised secondary standard, 
the PA considers the characterization of the evidence in the ISA, 
summarized in section IV.B.1 above, including the ISA conclusion that 
exposure indices that cumulate and differentially weight the higher 
hourly average concentrations over a season and also include the mid-
level values, such as the W126 index, offer the most scientifically 
defensible approach for characterizing vegetation response to ambient 
O3 and comparing study findings, as well as for defining 
indices for vegetation protection (U.S. EPA, 2013a, section 2.6.6.1). 
The PA additionally considers CASAC advice in the current review, as 
well as that from the last review, all of which provided support for 
such a form. Thus, in considering alternative forms of a revised 
standard, the PA concludes that it is reasonable and appropriate to 
consider a cumulative, concentration-weighted form to provide 
protection against cumulative, seasonal exposures to O3 that 
are known or anticipated to harm sensitive vegetation or ecosystems. 
The PA recognizes that such a metric is specifically designed to focus 
on the kind of O3 exposures that have been shown to cause 
harm to vegetation and states that it would have a distinct advantage 
over the form of the current standard in characterizing air quality 
conditions potentially of concern for vegetation and in more directly 
demonstrating that the desired degree of protection against those 
conditions was being achieved (U.S. EPA, 2014c, sections 6.2 and 6.6).
    With regard to the appropriate index for a cumulative seasonal 
form, the PA considers the evidence and background for a number of 
different cumulative concentration weighted indices that have been 
developed and evaluated in the scientific literature and in past NAAQS 
reviews in terms of their ability to predict vegetation response and 
their usefulness in the NAAQS context (U.S. EPA, 2006a, pp. 9-11 to 9-
15 and pp. AX9-159 to AX9-187; U.S. EPA, 2007, pp. 7-15 to 7-16). While 
these various forms have different strengths and limitations, the PA 
notes the ISA conclusion that the W126 index, described in section 
IV.B.1 above, has some important advantages over other non-sigmoidally 
weighted cumulative indices, including its lack of a cut-off in its 
weighting scheme which allows for cumulation of lower O3 
concentrations (U.S. EPA, 2013a, section 9.5; U.S. EPA, 2014c, sections 
6.2 and 6.6). Additionally, the W126 metric adds increasing weight to 
hourly concentrations from about 40 ppb to about 100 ppb, which is an 
important feature because ``as hourly concentrations become higher, 
they become increasingly likely to overwhelm plant defenses and are 
known to be more detrimental to vegetation'' (U.S. EPA, 2013a, p. 9-
104). The PA additionally takes note of CASAC advice in the current and 
last review that concurred with a focus on the W126 form (Frey, 2014c, 
p. iii; Henderson, 2006; Samet, 2010). Based on the considerations 
summarized here, the PA concludes that the W126 index is the most 
appropriate cumulative seasonal form to consider in the context of the 
secondary O3 NAAQS review.
    The PA next considers the exposure periods--diurnal and seasonal--
over which the W126 index would be summed in any given year. The 
currently available information continues to provide support for a 
definition of the diurnal period of interest as the 12-hour period from 
8:00 a.m. to 8:00 p.m., which the EPA identified in past reviews as 
appropriately capturing the diurnal window with most relevance to the 
photosynthetic process (U.S. EPA, 2013a, section 9.5.3; 72 FR 37900, 
July 11, 2007). The CASAC has generally supported this 12-hour daylight 
period as well (Frey, 2014c; Henderson, 2006, 2007). Based on these 
considerations, the PA concludes that the 12-hour daylight window (8:00 
a.m. to 8:00 p.m.) represents the portion of the diurnal exposure 
period that is most relevant to predicting or inducing plant effects 
related to photosynthesis and growth and thus is an appropriate diurnal 
period to use in conjunction with a W126 cumulative metric (U.S. EPA, 
2014c, sections 6.2 and 6.6). With regard

[[Page 75338]]

to a seasonal period of interest, the current evidence base continues 
to provide support for a seasonal period with a minimum duration of 
three months, as described more fully in the ISA and considered in the 
PA (U.S. EPA, 2013a, section 9.5.3; U.S. EPA, 2014c, sections 6.2 and 
6.6). The CASAC has also indicated support for such a three month 
period (Frey, 2014c; Samet, 2010; Henderson, 2006). The PA thus 
concludes that it is appropriate to identify the seasonal W126 index 
value as that derived from the consecutive 3-month period within the 
O3 season with the highest W126 index value.
    The PA additionally considers the period of time over which a 
cumulative seasonal W126-based standard should be evaluated, 
considering the support for both a single year form and a form averaged 
over three years (U.S. EPA, 2014c, pp. 6-29 through 6-33). The PA 
considers the evidence of effects associated with single year and 
multiple year exposures as well as their potential public welfare 
significance. The PA also considers comments from CASAC, including 
their comment in the current review that ``[t]he CASAC does not 
recommend the use of a three-year averaging period'' and that they 
``favor a single-year period for determining the highest three-month 
summation which will provide more protection for annual crops and for 
the anticipated cumulative effects on perennial species'' (Frey, 2014c, 
p. iii).
    The PA considered O3-induced effects that can occur with 
a single year's exposure, including visible foliar injury, growth 
reduction in annual and perennial species and yield loss in annual 
crops (U.S. EPA, 2014c, section 6.3). While recognizing that there are 
a number of O3-induced effects that have the potential for 
public welfare significance within the annual timeframe, the PA also 
notes the uncertainties associated with these effects that complicate 
consideration of the level of appropriate protection on an annual basis 
for such effects in order to protect the public welfare from known or 
anticipated adverse effects, and thus recognizes the possibility that a 
multiple-year form could be considered to provide a more consistent 
target level of protection for certain effects (U.S. EPA, 2014c, pp. 6-
29 to 6-31). With regard to visible foliar injury, the ISA notes that 
``the degree and extent of visible foliar injury development varies 
from year to year and site to site . . . even among co-members of a 
population exposed to similar O3 levels, due to the 
influence of co-occurring environmental and genetic factors'' (U.S. 
EPA, 2013a, p. 9-38; U.S. EPA, 2014c, p. 6-30). Additionally, the PA 
takes note of the difficulty and complexity shown by the WREA analyses 
with regard to identifying W126 index values that would provide 
consistent protection on an annual basis given likely fluctuations in 
annual O3 and soil moisture conditions (U.S. EPA, 2014c, p. 
6-30).
    The PA additionally notes evidence of some O3 effects on 
perennial species that may result from a single season's elevated 
O3 exposures, such as reduced bud size or starch content, 
which may have the potential for some ``carry over'' of effects on 
plant growth or reproduction in the subsequent season. Another effect 
where such potential for ``carry over'' has been noted with elevated 
O3 exposure is reduction in below-ground carbohydrate 
reserves which can impair growth in subsequent seasons (U.S. EPA, 
2014c, pp. 6-30 to 6-31; U.S. EPA, 2013a, pp. 9-43 to 9-44 and p. 9-
86). The PA notes that the occurrence of such annual effects of 
elevated O3 exposures over multiple years may contribute to 
a potential to be compounded, increasing the potential for effects at 
larger scales (e.g., population, ecosystem). In the PA, staff notes 
that multiple consecutive years of critical O3 exposures 
might be expected to result in larger impacts on forested areas than 
intermittent occurrences of such exposures due to the potential for 
compounding or carry-over effects on tree growth (U.S. EPA, 2014c, pp. 
6-29 to 6-31).
    In light of the above summarized considerations for potential 
compounding of carry-over effects, the PA concludes that the public 
welfare significance of the effects that can occur as a result of 
three-year O3 exposures are potentially greater than those 
associated with a single year of such exposure. Thus, to the extent 
that the focus for public welfare protection to be afforded by the 
secondary O3 standard is on long-term effects that occur in 
sensitive tree species in natural forested ecosystems, including 
federally protected areas such as Class I areas or on lands set aside 
by States, Tribes and public interest groups to provide similar 
benefits to the public welfare, the PA concludes that a standard with a 
form that evaluates the cumulative seasonal index across multiple years 
might be considered to provide a more appropriate match to the nature 
of O3-related effects on vegetation upon which the secondary 
O3 standard is focused. In considering such forms, the PA 
focuses on one that averages the W126 index values across three years 
(U.S. EPA, 2014c, section 6.2).
    With regard to single-year and three-year forms, the PA considers a 
WREA analysis that examined the extent to which cumulative RBL across a 
three-year period might be underestimated when each year's RBL is 
derived from the three-year average W126 index value versus each 
single-year W126 index value for each of three years (in which no other 
influence on plant growth is presumed to change). This analysis 
indicates that use of the three-year average may lead to an 
underestimation, although of relatively small magnitude (U.S. EPA, 
2014b, section 6.2.1.4). The PA notes that this limited analysis does 
not account for moisture levels and other environmental factors that 
could affect plant growth and that vary from year to year. When 
considering an appropriate level for a form that averages W126 index 
values across three years, the PA also recognizes the importance of 
considering the extent to which the cumulative effect of different 
average W126 exposures across the three-year period would be judged 
adverse (U.S. EPA, 2014c, p. 6-31).
    Although single-year W126 index values were not separately analyzed 
in the PA analysis of recent monitoring data, the data indicate 
appreciable variation in cumulative, seasonal O3 
concentrations among monitor locations meeting different levels of a 
standard of the current form (U.S. EPA 2014c, section 6. Appendix 
2B).Therefore, a standard with an annual form would have the cumulative 
seasonal index values be at or lower than the level of the standard in 
all years and, noting the inter-annual observed variability in seasonal 
W126 index values, could be appreciably below the standard level in 
some years. For a standard with a form that averages the cumulative 
seasonal index values across three consecutive years, the annual 
seasonal index value could be above the level in some years, but would 
have to be below it in others within the same three-year period, thus 
restricting the air quality for a given area to have no more than two 
years out of three with a W126 index value above the standard level, 
and depending on magnitude of each year's index, potentially having no 
more than one.
    In its consideration of one year as compared to three year forms, 
the PA also considers implications with regard to stability of air 
quality programs that implement the NAAQS (U.S. EPA, 2014c, pp. 6-31 to 
6-32). The PA notes that a standard based on a single year W126 index 
would be expected to have a less stability relative to a standard based 
on a form that averages seasonal indices across three consecutive 
years, given the potential for large year-to-year variability in annual 
W126 index values in areas across the country. Thus, a

[[Page 75339]]

three-year evaluation period can contribute to greater public welfare 
protection by limiting year-to-year disruptions in ongoing control 
programs that would occur if an area was frequently shifting in and out 
of attainment due to extreme year-to-year variations in meteorological 
conditions. This greater stability in air quality management programs 
would thus facilitate achievement of the protection intended by a 
standard. Such considerations of stability often receive particular 
weight in NAAQS reviews, such as those resulting in selection of the 
form for the current O3 primary and secondary standards (62 
FR 38856, July 18, 1997), as well as the primary standards for nitrogen 
dioxide (75 FR 6474, February 9, 2010) and sulfur dioxide (75 FR 35520, 
June 22, 2010). See also ATA III, 283 F. 3d at 374-75 (recognizing 
programmatic stability as a legitimate consideration in the NAAQS 
standard-setting process).
    Thus, to the extent that emphasis continues to be placed on 
protecting against effects associated with multi-year exposures and 
maintaining more year-to-year stability of public welfare protection, 
the PA concludes that it is appropriate to consider a secondary 
standard form that is an average of the seasonal W126 index values 
across three consecutive years. The PA concludes that such a form might 
be appropriate for a standard intended to achieve the desired level of 
protection from longer-term effects, including those associated with 
potential compounding, and that such a form might be concluded to 
contribute to greater stability in air quality management programs, and 
thus, greater effectiveness in achieving the desired level of public 
welfare protection, than that might result from a single year form 
(U.S. EPA, 2014c, section 6.6).
    The PA additionally recognized that to the extent the Administrator 
finds it useful to consider the public welfare protection that might be 
afforded by a revised primary standard, this is appropriately judged by 
evaluating the impact of attainment of such a revised primary standard 
on O3 exposures in terms of the cumulative seasonal W126-
based exposure index.
b. Level
    In considering an appropriate range of levels to consider for a 
W126-based standard, the PA notes that, due to the variability in the 
importance of the associated ecosystem services provided by different 
species at different exposures and in different locations, as well as 
differences in associated uncertainties and limitations, both the 
species present and their public welfare significance, in addition to 
the magnitude of the ambient concentrations, are essential 
considerations in drawing conclusions regarding the significance or 
magnitude of public welfare impact. Therefore, in development of the PA 
conclusions, staff took note of the complexity of judgments to be made 
by the Administrator regarding the adversity of known and anticipated 
effects to the public welfare and recognized that the Administrator's 
ultimate judgments on the secondary standard will most appropriately 
reflect an interpretation of the available scientific evidence and 
exposure/risk information that neither overstates nor understates the 
strengths and limitations of that evidence and information.
    As described in section IV.D.1 above, the PA employed a paradigm, 
which has evolved over the course of the O3 and other 
secondary NAAQS reviews, to assist in putting the available science and 
exposure/risk information into the public welfare context (U.S. EPA, 
2014c, section 5.1). This paradigm recognizes that the significance to 
the public welfare of O3-induced effects on sensitive 
vegetation growing within the U.S. can vary depending on the nature of 
the effect, the intended use of the sensitive plants or ecosystems, and 
the types of environments in which the sensitive vegetation and 
ecosystems are located. Accordingly, any given O3-related 
effect on vegetation and ecosystems (e.g., biomass loss, crop yield 
loss, visible foliar injury) may be judged to have a different degree 
of impact on or significance to the public welfare depending, for 
example, on whether that effect occurs in a Class I area, a city park, 
or commercial cropland. This approach also includes consideration of 
impacts to ecosystem goods and services, which are an important 
category of public welfare effects with an obvious relationship to 
consideration of intended use (73 FR 16492, March 27, 2008).
    In considering potential levels for an alternative standard based 
on the W126 metric, the PA focused primarily on impacts on tree growth, 
crop yield loss, and visible foliar injury, as well as impacts on the 
associated ecosystem services, while taking note of the uncertainties 
and limitations associated with several key aspects of this 
information. In addition to uncertainties related to the WREA air 
quality scenarios and assessments summarized in section IV.C above, the 
PA also recognized uncertainties associated with the evidence 
underlying the tree seedling and crop E-R functions (U.S. EPA, 2014c, 
section 6.3). These include uncertainties regarding intra-species 
variability due to the different numbers of studies that exist for 
different species so that the weight of evidence is not the same for 
each species. Those species with more than one study show variability 
in response and E-R functions. The potential variability in less well-
studied species is, however, unknown (U.S. EPA, 2013a, pp. 9-123 to 9-
125; U.S. EPA, 2014b, section 6.2.1.2, and Table 6-27). The PA also 
recognizes uncertainty regarding the extent to which tree seedling E-R 
functions can be used to represent mature trees since seedling 
sensitivity has been shown in some cases to not reflect mature tree 
O3 sensitivity in the same species and uncertainty in the 
relationship of O3 effects on tree seedlings (e.g., relative 
biomass loss) in one or a few growing seasons to effects that might be 
expected to accrue over the life of the trees extending into adulthood 
(U.S. EPA, 2013a, section 9.6 and pp. 9-52 to 9-53; U.S. EPA, 2014b, 
sections 6.2.1.1, 6.2.1.4 and Tables 6-5 and 6-27).
    With respect to tree growth, the PA gave primary consideration to 
relative biomass loss estimates derived from the E-R functions, 
described in section IV.B.1.b above and in the PA, while also 
considering WREA risk/exposure estimates related to this effect (U.S. 
EPA, 2014c, section 6.4). The PA takes note of the different index 
value estimates presented in Table 6-1 of PA (Table 8 below) with 
regard to the number of studied species below different response 
benchmarks, as well as with regard to the median response. The PA 
additionally considers the WREA estimates regarding: (1) percent of 
assessed geographic area exceeding 2% weighted relative biomass (U.S. 
EPA, 2014c, Table 6-2); (2) number of assessed Class I areas with tree 
seedling weighted relative biomass loss estimates below 2% (U.S. EPA, 
2014c, Table 6-3); and (3) the percent median biomass loss across 
counties for different air quality scenarios (U.S. EPA, 2014c, Table 5-
5). The PA further notes other WREA estimates for effects on ecosystem 
services related to public welfare, such as carbon sequestration and 
air pollutant removal. With respect to crop yield loss, the PA notes 
the summary of RYL estimates for individual crop species and for the 
median across species (Table 8), and the WREA risk/exposure estimates 
(U.S. EPA, 2014b, Section 6.3). The PA also notes information available 
on visible foliar damage to species occurring in areas preserved for 
their natural character,

[[Page 75340]]

such as federal Class I areas, and the analyses in the WREA evaluating 
biosite data and several benchmarks of injury (U.S. EPA, 2014b, section 
5.4.2).

         Table 8--Tree Seedling Biomass Loss and Crop Yield Loss Estimated for O3 Exposure Over a Season
----------------------------------------------------------------------------------------------------------------
                                      Tree seedling RBL \a\                           Crop RYL \c\
 W126 value for exposure  --------------------------------------------------------------------------------------
          period               Median value       Individual species       Median value       Individual species
----------------------------------------------------------------------------------------------------------------
21 ppm-hrs...............  Median species w.     <= 2% loss: 3/11      Median species w.     <=5% loss: 4/10
                            6.8% loss \b\.        species.              7.7% loss \d\.        species.
                                                 <=5% loss: 5/11                             >5, <10% loss: 3/10
                                                  species.                                    species.
                                                 <=10% loss: 7/11                            >10, <20% loss: 3/
                                                  species.                                    10 species.
                                                 <=15% loss: 10/11
                                                  species.
                                                 >40% loss: 1/11
                                                  species.
19 ppm-hrs...............  Median species w.     <=2% loss: 3/11       Median species w.     <=5% loss: 5/10
                            6.0% loss \b\.        species.              6.4% loss \d\.        species.
                                                 <5% loss: 5/11                              >5, <10% loss: 3/10
                                                  species.                                    species.
                                                 <=10% loss: 7/11                            >10, <20% loss: 2/
                                                  species.                                    10 species.
                                                 <=15% loss: 10/11
                                                  species.
                                                 >30% loss: 1/11
                                                  species.
17 ppm-hrs...............  Median species w.     <=2% loss: 5/11       Median species w.     <=5% loss: 5/10
                            5.3% loss \b\.        species.              5.1% loss \d\.        species.
                                                 <5% loss: 5/11                              >5, <10% loss: 3/10
                                                  species.                                    species.
                                                 <=10% loss: 9/11                            >10, <20% loss: 2/
                                                  species.                                    10 species.
                                                 15% loss: 10/11
                                                  species.
                                                 >30% loss: 1/11
                                                  species.
15 ppm-hrs...............  Median species w.     <=2% loss: 5/11       Median species w.     <=5% loss: 6/10
                            4.5% loss \b\.        species.              <=5% loss \d\.        species.
                                                 <=5% loss: 6/11                             >5, <10% loss: 4/10
                                                  species.                                    species.
                                                 <=10% loss: 10/11
                                                  species.
                                                 >30% loss: 1/11
                                                  species.
13 ppm-hrs...............  Median species w.     <=2% loss: 5/11       Median species w.     <=5% loss: 6/10
                            3.8% loss \b\.        species.              <=5% loss \d\.        species.
                                                 <5% loss: 7/11                              >5, <10% loss: 4/10
                                                  species.                                    species.
                                                 <10% loss: 10/11
                                                  species.
                                                 >20% loss: 1/11
                                                  species.
11 ppm-hrs...............  Median species w.     <=2% loss: 5/11       Median species w.     <=5% loss: 9/10
                            3.1% loss \b\.        species.              <=5% loss \d\.        species.
                                                 <=5% loss: 8/11                             >5, <10% loss: 1/10
                                                  species.                                    species.
                                                 <=10% loss: 10/11
                                                  species.
                                                 >20% loss: 1/11
                                                  species.
9 ppm-hrs................  Median species w.     <=2% loss: 5/11       Median species w.     <=5% loss: all
                            2.4% loss \b\.        species.              <=5% loss \d\.        species.
                                                 <=5% loss: 10/11
                                                  species.
                                                 >20% loss: 1/11
                                                  species.
7 ppm-hrs................  Median species w.     <=2% loss: 7/11       Median species w.     <=5% loss: all
                            <=2% loss \b\.        species.              <=5% loss \d\.        species.
                                                 <=5% loss: 10/11
                                                  species.
                                                 >15% loss: 1/11
                                                  species.
----------------------------------------------------------------------------------------------------------------
\a\ Estimates are based on the 11 E-R functions for tree seedlings described in WREA, Appendix 6F and discussed
  in the PA, section 5.2.1, with the exclusion of cottonwood in consideration of CASAC comments on differences
  of that study from the other controlled E-R studies (Frey, 2014b, 2014c).
\b\ This is the median of the composite E-R functions for 11 tree species from the WREA, Appendix 6F (discussed
  in the PA, section 5.2.1).
\c\ Estimates here are based on the 10 E-R functions for crops (from the PA, Appendix 6F and section 5.3.1).
\d\ This median value is the median of the composite E-R functions for 10 crops from WREA, Appendix 6F (also
  discussed in the PA, section 5.3.1).

    Given the wide variation in sensitivity of studied tree species to 
O3-induced relative biomass loss, the PA focused 
consideration on both median species values and individual species 
responses and RBL estimates for a given range of W126 index values. In 
this consideration, the PA took note of CASAC's advice regarding RBL 
levels, specifically their emphasis on a benchmark of median relative 
tree biomass loss at or below 2% and their view that a 6% median 
relative biomass loss is ``unacceptably high.'' The median tree species 
RBL estimate is at or below 2% only at the lowest W126 level assessed, 
7 ppm-hrs. At incrementally higher W126 index levels, the median RBL is 
also incrementally higher, so that at W126 index values of 9, 11, 13, 
15, 17 and 19 ppm-hrs, the median RBL increases to 2.4%, 3.1%, 3.8%, 
4.5%, 5.3% and 6.0%, respectively. Thus, the median species biomass 
loss is below 6%, the level characterized by the CASAC as unacceptably 
high, across the W126 range of 7 to 17 ppm-hrs, for which it varies 
from approximately 2% to approximately 5%. Given this finding, the PA 
discussion of a range of levels appropriate to consider focuses on this 
range. In focusing on this range, the PA considers the full array of 
CASAC advice with regard to interpretation of the evidence and 
exposure/risk information on vegetation-related effects of 
O3, as well as the role of the Administrator's judgments in 
identifying the level of air quality that is requisite to protect 
public welfare from adverse effects, as noted in section IV.A 
above.\218\
---------------------------------------------------------------------------

    \218\ In the context of the O3 standard, such 
judgments include: The weight to give the evidence of specific 
vegetation-related effects estimated to result across a range of 
cumulative seasonal concentration-weighted O3 exposures; 
the weight to give associated uncertainties, including those related 
to the variability in occurrence of such effects in specific areas 
of U.S., such as those of particular public welfare significance; 
and, judgments on the extent to which such effects in such areas may 
be considered adverse to public welfare.
---------------------------------------------------------------------------

    The PA recognizes that public welfare judgments may reasonably be 
informed by a range of biomass loss benchmarks, in contexts of 
considering both median RBL estimates and RBL estimates for individual 
species. Accordingly, in considering individual tree species estimates, 
the PA notes the value of additionally characterizing the RBL

[[Page 75341]]

estimates in comparison to higher loss levels such as 10% or 15%.
    For every W126 value over the full range from 7 to 17 ppm-hrs, the 
RBLs for each of five species is less than 2% (Table 8), which is the 
lower benchmark that CASAC identified for tree species. Accordingly, 
the PA focused attention on the remaining six more sensitive studied 
species (i.e., eastern white pine, aspen, tulip poplar, ponderosa pine, 
red alder, and black cherry) to evaluate the protection against tree 
seedling biomass loss at different W126 levels within the range from 17 
to 7 ppm-hrs. At a W126 index value of 17 ppm-hrs, one of these six 
species (red alder) has a RBL estimate below 6%, while at the W126 
index value of 7 ppm-hrs, five of these six species have RBLs below 6% 
(eastern white pine, aspen, tulip poplar, ponderosa pine, red alder). 
Taken together with the more tolerant species, the proportion of the 
studied tree species with RBLs below 6% are 6 of 11, 7 of 11, 8 of 11, 
and 10 of 11 at W126 index values of 17, 15, 13, and 11 ppm-hrs, 
respectively.
    With regard to other, higher, RBL benchmark levels and estimates 
for all 11 species, the PA notes that 9 of 11 studied tree species have 
a predicted RBL below 10% at the W126 level of 17 ppm-hrs, while 10 of 
11 species have a predicted RBL below 10% for W126 levels of 15 to 7 
ppm-hrs. In addition, 10 of 11 studied tree species have a predicted 
RBL below 15% for W126 levels of 17 to 7 ppm-hrs. The PA notes that the 
RBL estimates for black cherry, the most sensitive of the 11 species, 
remain above 15% for W126 index values across the range from 17 to 7 
ppm-hrs, making unclear the extent to which black cherry estimates 
might inform consideration of different W126 exposures within this 
range (U.S. EPA, 2014c, section 6.6 and Table 6-1; U.S. EPA, 2014b, 
section 6.2 and Appendix 6A).
    While recognizing the limitations and uncertainties associated with 
the WREA air quality scenarios with regard to their representation of 
conditions just meeting different three-year average W126 index values 
(as summarized in section IV.C.1 above), including the potential 
underestimation of the highest O3 concentrations, the PA 
additionally considers several WREA RBL analyses (U.S. EPA, 2014c, 
section 6.3). In the WREA characterization of the number of counties 
where the median RBLs were greater than 2%, 7% of the counties have 
median RBLs greater than 2% in the 15 and 11 ppm-hrs W126 scenarios, as 
compared to 8% for the current standard (U.S. EPA, 2014c, Table 5-5; 
U.S. EPA, 2014b, Table 6-7). The percentage is 6% in the 7 ppm-hrs W126 
scenario. Of the 221 counties (7% of counties) estimated to have a 
median RBL above 2% for the 15 ppm-hrs scenario, 203 of those counties 
have a RBL greater than 2% because of the presence of black cherry 
(U.S. EPA, 2014c, section 6.3).
    In considering the potential magnitude of the ecosystem impact of 
O3-related biomass effects on tree growth, the PA 
additionally focused on the WREA estimates of weighted RBL for the W126 
air quality scenarios (U.S. EPA, 2014b, section 6.8). For the current 
standard and the three W126 scenarios, the percent of total assessed 
area having weighted RBL greater than 2% was 0.2%, 0.2%, 0.1% and 
<0.1%, respectively (U.S. EPA, 2014c, Table 6-2; U.S. EPA 2014b, Table 
6-25). In giving particular attention to estimates for Class I areas, 
the PA notes that for all four scenarios, the WREA estimates indicate 
weighted RBL greater than 2% in one or two of the 145 assessed 
nationally protected Class I areas (U.S. EPA, 2014c, sections 6.3 and 
6.6).
    In considering potential impacts on ecosystem services related to 
reductions in O3 effects on tree growth, the PA particularly 
recognizes that impacts on climate regulation can reasonably be 
concluded to be potentially significant from a public welfare 
perspective. In additionally recognizing that carbon sequestration has 
been identified as a potentially important tool for managing 
anthropogenic impacts on climate, the PA considers the WREA estimates 
of potential increases in forestry carbon storage for ambient 
O3 reductions in the three W126 air quality scenarios (U.S. 
EPA, 2014c, sections 6.3 and 6.6; U.S. EPA, 2014b, section 6.6.1). The 
WREA estimates additional forestry carbon storage potential of 13, 593 
and 1,600 MMtCO2e (over 30 years) for the W126 scenarios of 
15, 11 and 7 ppm-hrs, respectively, as compared to the current standard 
(U.S. EPA, 2014b, Table 6-18). Compared to the absolute estimate for 
the current standard scenario (approximately 89,000 MMtCO2e, 
over 30 years), these amounts represent additional storage of less than 
0.1%, just under 1% and under 2% for the 15, 11 and 7 ppm-hrs 
scenarios, respectively (U.S. EPA, 2014b, section 6.6.1 and Appendix 
6B).
    The PA additionally considers the WREA estimates for five urban 
areas of how reduced growth of O3-sensitive trees in urban 
forests may affect air pollutant removal (U.S. EPA, 2014b, sections 
6.6.2 and 6.7 and Appendix 6D). As with the national estimates, 
estimates for all five case study areas indicate generally small 
differences between the current standard and the three W126 scenarios 
(U.S. EPA, 2014c, Table 6-5). The PA additionally notes significant 
uncertainties and limitations associated with WREA estimates related to 
carbon sequestration and air pollution removal (U.S. EPA, 2014b, Table 
6-27; U.S. EPA, 2014c, sections 6.3 and 6.6), some of which are 
summarized in section IV.C.2.b above. The PA recognizes that, as with 
consideration of other pertinent evidence and exposure/risk 
information, the Administrator's consideration of WREA estimates for 
these ecosystem services will involve judgments regarding the 
appropriate weight to place on such uncertainties as well as the 
potential impacts to the public welfare of the estimates.
    The PA additionally considers the biomass effects of O3 
on crops estimated for different W126 index values across the range 
identified above. For this consideration, the PA focuses on the 10 
crops for which robust E-R functions have been established, as 
described in section IV.B.1 above: Barley, lettuce, field corn, grain 
sorghum, peanut, winter wheat, field cotton, soybean, potato and kidney 
bean (U.S. EPA, 2013a; U.S. EPA, 2014b, section 6.5 and Figure 6-3). In 
evaluating this information, the PA takes note of CASAC's comment 
regarding significance of 5% for median crop relative yield loss (RYL). 
The PA finds that the median crop RYL is at or below 5% for all W126 
index values from 7 to 17 ppm-hrs and observes that this finding makes 
it unclear to what extent this information informs consideration of 
levels within this range. The RBL estimates for half of the ten 
individual species are below 5% RYL at 17 ppm-hrs. The number of the 
ten individual crops with RYL below 5% is six for W126 values of 15 and 
13 ppm-hrs, nine for a W126 value of 11 ppm-hrs and ten for W126 levels 
of 9 and 7 ppm-hrs. Recognizing that different crops are likely to have 
different values or importance to public welfare, the PA also considers 
the RYL estimates across the W126 range for individual species.
    In considering these RYL estimates, the PA recognizes that they do 
not reflect the influence of the heavy management of agricultural crops 
that is common in the U.S. and so cannot be easily interpreted with 
regard to potential public welfare significance. In light of the median 
RYL estimates of approximately 5% or lower for W126 index values at and 
below 17 ppm-hrs, the PA gives less emphasis to consideration of crop 
RYL, while noting that this information indicates that a secondary 
standard revised to provide

[[Page 75342]]

additional protection for vegetation with attention to tree growth, 
would be expected to also provide additional protection to crops over 
that provided by the current standard (U.S. EPA, 2014c, section 6.6).
    The PA also considers the evidence and exposure/risk information 
with regard to visible foliar injury and the extent to which that might 
inform consideration of potential alternative secondary standards 
appropriate for the Administrator to consider. Specifically, the PA 
notes the findings of the WREA analyses of the nationwide USFS/FHM 
biosite dataset (2006-2010) that while soil moisture conditions 
influence the proportion of biosites with O3-related visible 
foliar injury, as described in section IV.B.1.a above, the proportion 
of such sites increases appreciably with increasing W126 index values 
up to approximately 10 ppm-hrs, while relatively little or no change in 
incidence of injury is seen with O3 exposures at higher W126 
index values (U.S. EPA 2014b, Chapter 7, Figure 7-10). The PA 
additionally notes that visible foliar injury has been identified by 
the federal land managers as a diagnostic tool for informing 
conclusions regarding potential O3 impacts on potentially 
sensitive AQRVs (USFS, NPS, FWS, 2010), which the PA concludes 
indicates that such O3-induced impacts might be considered 
to have the potential to impact the public welfare in scenic and/or 
recreational areas during years they occur.
    The PA was unable, however, to identify any guidance for federal 
land managers regarding at what spatial scale or what degree of 
severity visible foliar injury might be sufficient to trigger 
protective action based on this potential impact on AQRVs. The PA 
states that there does not appear to be consensus in the literature 
regarding severity of visible foliar injury and risks to plant 
functions or services, additionally noting that CASAC, while 
identifying percent biomass loss and yield loss benchmarks for tree 
seedlings and commodity crops, respectively, did not provide any 
benchmark or criteria for consideration of O3 impacts 
related to this endpoint. Further, as in previous reviews, the ISA 
concludes visible foliar injury is not always a reliable indicator of 
other negative effects on vegetation, making it difficult to relate 
visible foliar injury symptoms to other vegetation effects such as 
individual plant growth, stand growth, or ecosystem characteristics 
(U.S. EPA, 2013a, section 9.4.2, p. 9-39). Additionally, although 
evidence shows visible foliar injury can occur under very low 
cumulative O3 exposures, ``. . . the degree and extent of 
visible foliar injury development varies from year to year and site to 
site . . ., even among co-members of a population exposed to similar 
O3 levels, due to the influence of co-occurring 
environmental and genetic factors'' (U.S. EPA 2013a, section 9.4.2, p. 
9-38). Thus, while the PA recognizes visible foliar injury as an 
important O3 effect which, depending on severity and spatial 
extent may reasonably be concluded to be of public welfare 
significance, most particularly in nationally protected areas such as 
Class I areas, it additionally recognizes the appreciable variability 
in this endpoint, which poses challenges to giving it primary emphasis 
in identifying potential alternative standard levels.
    On the basis of all the considerations described above, including 
the evidence and exposure/risk analyses, and advice from CASAC, the PA 
concludes that a range of W126 index values appropriate for the 
Administrator to consider in identifying a secondary standard that 
might be expected to provide the requisite protection to the public 
welfare from any known or anticipated adverse effects, extends from 7 
to 17 ppm-hrs. The PA notes, however, the role of judgments by the 
Administrator in such decisions, as recognized above. In selecting this 
range, the PA primarily considers the evidence- and exposure/risk-based 
information for cumulative seasonal O3 exposures represented 
by W126 index values (including those represented by the WREA average 
W126 scenarios) associated with biomass loss in studied tree species, 
both in and outside areas that have been afforded special protections. 
The PA recognizes that tree biomass loss can be an indicator of more 
significant ecosystem-wide effects which might reasonably be concluded 
to be significant to public welfare. For example, when biomass loss 
occurs over multiple years at a sufficient magnitude, it is linked to 
some level of effects on an array of ecosystem-level processes, such as 
nutrient and water cycles, changes in above and below ground 
communities, carbon storage and air pollution removal, that benefit the 
public welfare (U.S. EPA, 2014c, Figure 5-1). In focusing on tree 
biomass effects, the PA gave emphasis to CASAC's judgment that a 6% 
median RBL is unacceptably high, and that the 2% median RBL is an 
important benchmark to consider. The PA notes that for the lower W126 
value of 7 ppm-hrs that the median tree species biomass loss is at or 
below 2% and that for the upper value of 17 ppm-hrs that the median 
tree biomass loss is below 6%.\219\
---------------------------------------------------------------------------

    \219\ We note that a W126 index value of 19 ppm-hrs is estimated 
to result in a median RBL value of 6%, as shown in Table 2 above.
---------------------------------------------------------------------------

    In considering the stability and potential for associated greater 
public welfare protection offered by a three-year form, as well as 
based on the recognition that in any given year in the environment, 
other environmental factors can influence the extent to which 
O3 may have the impact predicted by the E-R functions on 
which much of the range discussion above focuses, the PA gave careful 
consideration to the support for consideration of potential alternative 
W126 based standards with levels in the range identified above (17 ppm-
hrs to 7 ppm-hrs) with a three-year average form.
    Thus, the PA concludes that in staff's view, the evidence- and 
exposure/risk-based information relevant to tree biomass loss and the 
associated ecosystem services important to the public welfare support 
consideration of a W126-based secondary standard with index values 
within the range of 7 to 17 ppm-hrs, and a form averaged over three 
years. In reaching this conclusion, the PA gave particular 
consideration to the importance of considering the lasting or carry-
over effects that can derive from single year exposures of perennial 
plants, recognizing the importance of considering the available 
evidence and exposure/risk based information related to such effects, 
as well as associated uncertainties. The PA additionally recognized 
that there is limited information to discern differences in the level 
of protection afforded for cumulative growth-related effects by 
potential alternative W126-based standards of a single year form as 
compared to a three-year average form. Lastly, the PA recognizes the 
role of policy judgments required of the Administrator with regard to 
the public welfare significance of identified effects, the appropriate 
weight to assign the range of uncertainties inherent in the evidence 
and analyses, and, ultimately, in identifying the requisite protection 
for the secondary O3 standard. Examples of areas where the 
Administrator's judgments would be expected include those stemming from 
consideration of the effects associated with longer-term conditions and 
the role that year-to-year exposure variability may play in associated 
public welfare impacts, as well as the objectives for consideration of 
tree species biomass loss estimates in relationship to identified 
benchmarks (e.g., 2% or greater).

[[Page 75343]]

    The PA also concludes that, to the extent the Administrator finds 
it useful to consider the public welfare protection that might be 
afforded by a revised primary standard, this is appropriately judged 
through the use of a cumulative seasonal W126-based exposure metric, a 
metric considered appropriate for evaluating impacts on vegetation. For 
example, comparison of the air quality conditions (expressed in terms 
of W126 exposures) expected to result from a revised primary standard 
to the W126-based exposures concluded to provide requisite public 
welfare protection would thus inform a judgment of whether a secondary 
standard set identical to a revised primary standard would be expected 
to achieve the appropriate level of air quality. The PA notes that such 
a comparison would be in terms of a metric considered appropriate for 
evaluating impacts on vegetation which inform conclusions on public 
welfare impacts. The PA further concludes that the drawing of 
conclusions with regard to the public welfare protection afforded by 
such a standard should entail consideration of the air quality 
conditions likely to be achieved in terms of the cumulative seasonal 
W126-based metric described above.
    Accordingly, the PA describes several analyses of air quality data 
that might inform such consideration (U.S. EPA, 2014c, section 6.4), 
and notes the importance of taking into account associated 
uncertainties, including those associated with the limited monitor 
coverage in many rural areas, such as those in the West and Southwest 
regions and at high elevation sites. Additional such analyses, based on 
more recent O3 monitoring data, have been developed since 
the completion of the PA. All of these analyses are summarized in 
section IV.E.4 below. In reaching conclusions on appropriate policy 
options for a revised secondary standard the Administrator has 
considered the findings of these analyses, as described in section 
IV.E.5 below.
3. CASAC Advice
    Beyond the evidence- and exposure/risk-based considerations in the 
PA discussed above, the EPA's consideration of a revised secondary 
standard also takes into account the advice and recommendations of 
CASAC. The EPA also considered public comments received to date, some 
of which urged the consideration of a secondary standard with a 
cumulative seasonal form using the W126 metric and a level within the 
range of 7 to 15 ppm-hrs or in the low end of this range,\220\ while 
others have urged retaining the existing form and averaging time due to 
their view of a lack of new information to support a distinct secondary 
standard.
---------------------------------------------------------------------------

    \220\ Public comment received thus far in this review are in the 
docket EPA-HQ-OAR-2008-0699, accessible at www.regulations.gov
---------------------------------------------------------------------------

    In advice offered on a revised secondary standard in the current 
review, similar to advice in the last review, including advice offered 
on the 2010 proposed reconsideration, the CASAC recommended ``retaining 
the current indicator (ozone) but establishing a revised form of the 
secondary standard to be the biologically relevant W126 index 
accumulated over a 12-hour period (8 a.m.-8 p.m.) over the 3-month 
summation period of a single year resulting in the maximum value of 
W126'' (Frey, 2014c, p. iii). With regard to the level, the CASAC 
recommended that ``that the level associated with this form be within 
the range of 7 ppm-hrs to 15 ppm-hrs to protect against current and 
anticipated welfare effects of ozone'' and that ``CASAC does not 
support a level higher than 15 ppm-hrs'' (Frey, 2014c, p. iii). The 
CASAC additionally stated that ``[i]n reaching its scientific judgment 
regarding the indicator, form, summation time, and range of levels for 
a revised secondary standard, the CASAC has focused on the scientific 
evidence for the identification of the kind and extent of adverse 
effects on public welfare,'' while also acknowledging ``that the choice 
of a level within the range recommended based on scientific evidence is 
a policy judgment under the statutory mandate of the Clean Air Act'' 
(Frey, 2014c, p. iii).
    In providing advice on a range for the secondary standard, the 
CASAC noted a W126 index value for which the median tree species RBL 
estimate was 6 percent, and the median crop species RBL estimate was 
over 5 percent, stating that ``[t]hese levels are unacceptably high'' 
(Frey, 2014c, p. iii).\221\ In addition, regarding consideration of 
relative biomass loss benchmarks for tree seedlings, the CASAC stated 
that ``[a] 2% biomass loss is an appropriate scientifically based value 
to consider as a benchmark of adverse impact for long-lived perennial 
species such as trees, because effects are cumulative over multiple 
years'' (Frey, 2014c, p. 14). In so stating, the CASAC referenced 
findings for biomass loss in aspen exposed to elevated O3 
over seven years, citing Wittig et al., 2009.\222\ The CASAC 
additionally pointed to the report of the 1996 workshop sponsored by 
the Southern Oxidants Study group (Heck and Cowling, 1997, noted in 
section IV.B.2 above) which described a general consideration of 1-2% 
per year growth reduction in making judgments the group identified as 
appropriate for the endpoint of growth effects in trees, without 
providing an explicit rationale for the identified percentages (Frey, 
2014c, p. 14). The CASAC also commented that ``it is appropriate to 
identify a range of levels of alternative W126-based standards that 
includes levels that aim for not greater than 2% RBL for the median 
tree species'' (Frey, 2014c, p. 14). The CASAC noted that the ``level 
of 7 ppm-hrs is the only level analyzed for which the relative biomass 
loss for the median tree species is less than or equal to 2 percent'' 
indicating that 7 ppm was appropriate lower bound for the recommended 
range (Frey, 2014c, p. 14).
---------------------------------------------------------------------------

    \221\ The CASAC made this comment while focusing on Table 6-1 in 
the second draft PA and the entry for 17 ppm-hrs. That table was 
revised for inclusion in the final PA in consideration of CASAC 
comments on the E-R function for eastern cottonwood, such that the 
RBL estimates for 17 ppm-hrs in the final table (see Table 2 above) 
are below the values CASAC viewed as ``unacceptably high''.
    \222\ The way in which the statement pointing to the aspen 
seven-year biomass loss value from Wittig et al (2009) relates to 
CASAC's view with regard to 2%, however, is unclear as the original 
source for this finding (cited in Wittig et al., 2009) indicates 
yearly relative biomass loss values during this seven year exposure 
that are each well above 2%, and, in fact, are all above 20% (King, 
et al., 2005).
---------------------------------------------------------------------------

    With regard to consideration of effects on crops, the CASAC, as 
noted above, described median species RYL over 5% yield loss as 
``unacceptably high.'' The CASAC further noted that ``[c]rop loss 
appears to be less sensitive than these other indicators, largely 
because of the CASAC judgment that a 5% yield loss represents an 
adverse impact, and in part due to more opportunities to alter 
management of annual crops'' (Frey, 2014c, p. 14).
    The CASAC acknowledged that ``the choice of a level within the 
range recommended based on scientific evidence is a policy judgment 
under the statutory mandate of the Clean Air Act'', while further 
providing its own policy recommendations, including the following 
(Frey, 2014c, p. iii).

    [T]he CASAC advises that a level of 15 ppm-hrs for the highest 
3-month sum in a single year is requisite to protect crop yield 
loss, but that lower levels provide additional protection against 
crop yield loss. Furthermore, there are specific economically 
significant crops, such as soybeans, that may not be protected at 15 
ppm-hrs but would be protected at lower levels. A level below 10 
ppm-hrs is required to reduce foliar injury. A level of 7 ppm-hrs is 
protective of relative biomass loss for trees and offers additional

[[Page 75344]]

protection against crop yield loss and foliar injury. Therefore, 7 
ppm-hrs is protective of ecosystem services. Thus, lower levels 
within the recommended range offer a greater degree of protection of 
more endpoints than do higher levels within the range.

    Additionally, in regard to consideration of form, the CASAC noted 
that ``[i]f, as a policy matter, the Administrator prefers to base the 
secondary standard on a three-year averaging period for the purpose of 
program stability, then the level of the standard should be revised 
downward such that the level for the highest three-month summation in 
any given year of the three-year period would not exceed the 
scientifically recommended range of 7 ppm-hrs to 15 ppm-hrs'' (Frey, 
2014c, pp. iii and iv). In related manner, the CASAC noted that a 
three-year average W126 level of 13 ppm-hrs may be appropriate 
depending on consideration of year-to-year variability and such policy 
considerations (Frey, 2014c, p. iv).
    Lastly, in comments recognizing uncertainties associated with the 
evidence and exposure and risk analyses, the CASAC stated that ``there 
is sufficient scientific evidence, and sufficient confidence in the 
available research results, to support the advice we have given above 
for this review cycle of the primary and secondary standards'' (Frey, 
2014c, p. iv).
4. Air Quality Analyses
    As described in section II.D. above, the PA concludes with regard 
to the primary standard that it is appropriate for the Administrator to 
consider revision of the level to within the range of 60 to 70 ppb. In 
consideration of this conclusion for the primary standard, although the 
PA also concludes it is appropriate to consider a revised secondary 
standard with a cumulative, seasonal, concentration-weighted form, the 
PA recognized that, it may be practical to consider the extent to which 
a revised secondary standard in the form of the current secondary 
standard might be expected to also reduce and provide protection from 
cumulative seasonal exposures of concern, noting that, for example, if 
a clear and robust relationship was found to exist between 8-hour daily 
peak O3 concentrations and cumulative, seasonal exposures, 
the averaging time and form of the current standard might be concluded 
to have the potential to be effective as a surrogate (U.S. EPA, 2014c, 
section 6.4).
    Therefore, the PA evaluated what the available information 
indicated with regard to control of cumulative O3 exposures 
that might be afforded by alternative secondary standards with the 
averaging time and form of the current standard (a three-year average 
of 4th highest 8-hour average concentrations). The available 
information addressing this point includes a ``focus study'' in the 
ISA, and several air quality analyses described in the PA, chapters 2, 
5 and 6 and Appendix 2b.\223\ Additionally, a similar air quality 
analysis performed with more recent monitoring data is now available 
and is also described here.
---------------------------------------------------------------------------

    \223\ This information and analyses were included in the second 
draft PA (U.S. EPA, 2014j), reviewed by CASAC in early 2014, and 
drafts of the ISA, reviewed by CASAC earlier in the review.
---------------------------------------------------------------------------

    The focus study described in the ISA examined the diel variability 
in O3 concentrations in six rural areas between 2007 and 
2009 (U.S. EPA, 2013a, pp. 3-131 to 3-133). The ISA reported that 
``[t]here was considerable variability in the diel patterns observed in 
the six rural focus areas'' with the three mountainous eastern sites 
exhibiting a ``generally flat profile with little hourly variability in 
the median concentration and the upper percentiles,'' while the three 
western rural areas demonstrated a ``clear diel pattern to the hourly 
O3 data with a peak in concentration in the afternoon 
similar to those seen in the urban areas,'' which was especially 
obvious at the San Bernardino National Forest site, 90 km east of Los 
Angeles at an elevation of 1,384 meters (U.S. EPA, 2013a, p. 3-132). 
Thus, while the western sites that are influenced by upwind urban 
plumes may have increased cumulative seasonal values coincident with 
increased daily 8-hour peak O3 concentrations, this analysis 
indicates that, in sites without such an urban influence (the eastern 
sites in this analysis), such a relationship does not occur (U.S. EPA, 
2013a, section 3.6.3.2). Thus, the lack of such a relationship 
indicates that in some locations, O3 air quality patterns 
can lead to elevated cumulative, seasonal O3 exposures 
without the occurrence of elevated daily maximum 8-hour average 
O3 concentrations (U.S. EPA, 2013a, section 3.6.3.2). 
Further, staff notes that the prevalence and geographic extent of such 
locations is unclear, since as in the last review, there continue to be 
relatively fewer monitors in the western U.S., including in high 
elevation remote sites. In considering the findings of this analysis, 
the PA additionally recognized, however, that the cumulative seasonal 
values for the eastern rural sites, where cumulative seasonal 
O3 concentrations appear to be relatively less related to 
daily maximum 8-hour concentrations, are lower in general than those of 
the western, urban-influenced sites.
    In addition to the focus study described in the ISA (U.S. EPA, 
2013a, section 3.6.3.2), the PA considers additional analyses of air 
quality monitoring data. For example, Chapter 2 of the PA characterized 
recent monitoring data of O3 air quality in rural areas. 
While approximately 80 percent of the O3 monitoring network 
is urban focused, about 120 rural monitors are divided among CASTNET, 
NCore, and portable O3 monitors (POMs) sites (U.S. EPA, 
2014c, Chapter 2, pp. 2-2 to 2-3, Figure 2.1). Specifically, as stated 
in Chapter 2 of the PA, ``[a]lthough rural monitoring sites tend to be 
less directly affected by anthropogenic pollution sources than urban 
sites, rural sites can be affected by transport of O3 or 
O3 precursors from upwind urban areas and by local 
anthropogenic sources such as motor vehicles, power generation, biomass 
combustion, or oil and gas operations'' (U.S. EPA, 2013a, section 
3.6.2.2). In addition, O3 tends to persist longer in rural 
than in urban areas due to lower rates of chemical scavenging in non-
urban environments. At higher elevations, increased O3 
concentrations can also result from stratospheric intrusions (U.S. EPA, 
2013a, sections 3.4, 3.6.2.2). As a result, O3 
concentrations measured in some rural sites can be higher than those 
measured in nearby urban areas (U.S. EPA, 2013a, section 3.6.2.2) and 
the ISA concludes that ``cumulative exposures for humans and vegetation 
in rural areas can be substantial, and often higher than cumulative 
exposures in urban areas'' (U.S. EPA, 2013a, p. 3-120). These known 
differences between urban and rural sites suggest that there is the 
potential for an inconsistent relationship between 8-hour daily peak 
O3 concentrations and cumulative, seasonal exposures in 
those areas. However, the PA also notes that reductions in NOx 
emissions that occur in urban areas to attain primary standards would 
also have the effect of reducing downwind, rural concentrations over 
the season (U.S. EPA, 2014c, section 6.4).
    In addition, as was done in both the 1997 and 2008 reviews, the PA 
analyzed relationships between O3 levels in terms of the 
current averaging time and form and a W126 cumulative form, based on 
recent air quality data. One analysis in the PA describes the W126 
index values and current standard design values at each monitor for two 
periods: 2001-2003 and 2009-2011 (e.g., U.S. EPA, 2014c, Appendix 2B, 
Figures 2B-2 and 2B-3). This shows that between the two periods, during 
which broad scale O3

[[Page 75345]]

precursor emission reductions occurred, O3 concentrations in 
terms of both metrics were reduced. There is a fairly strong, positive 
degree of correlation between the two metrics (U.S. EPA, 2014c, 
Appendix 2B).\224\ Focusing only on the latter dataset (2009-2011), it 
can be seen that at monitors just meeting the current standard (three-
year average fourth-highest daily maximum 8-hour average concentration 
equal to 0.075 ppm), W126 index values (in this case three-year 
averages) varied from less than 3 ppm-hrs to approximately 20 ppm-hrs 
(U.S. EPA, 2014c, Appendix 2B, Figure 2B-3b). At sites with a three-
year average fourth-highest daily maximum 8-hour average concentration 
at or below a potential alternative primary standard level of 70 ppb, 
three-year W126 index values were above 17 ppm-hrs at no monitors, 
above 15 ppm-hrs at one monitor, and above 13 ppm-hrs at 8 monitors in 
the West and Southwest NOAA climate regions. At sites with a three-year 
average fourth-highest daily maximum 8-hour average concentration at or 
below a potential alternative primary standard level of 65 ppb, three-
year W126 index values were above 11 ppm-hrs at no monitors, above 9 
ppm-hrs at three monitors, and above 7 ppm-hrs at 9 monitors 
(distributed across five regions). The majority of these nine 
monitoring sites are located in the West and Southwest regions and 
include the states of Arizona, California, Colorado, Nevada, New 
Mexico, and Utah. At sites with a three-year average fourth-highest 
daily maximum 8-hour average concentration at or below a potential 
alternative primary standard level of 60 ppb, three-year W126 index 
values were at or below 7 ppm-hrs at all monitors (U.S. EPA, 2014c, 
Figure 2B-3b).
---------------------------------------------------------------------------

    \224\ Appendix 2B in the PA additionally observes that the 
program implemented for reducing precursor emissions, especially 
NOx, appears to have been an effective strategy for lowering both 
design values and W126 index values.
---------------------------------------------------------------------------

    Another analysis in Chapter 2 of the PA presents the data for sets 
of recent three-year periods back to 2006-2008 and indicates that among 
the counties with O3 concentrations that met the current 
standard, the number of counties with three-year W126 index values 
above 15 ppm-hrs ranges from fewer than 10 to 24 (U.S. EPA, 2014c, 
Appendix 2B, Figure 2B-9). In general during this longer period, W126 
index values above 15 ppm-hrs and meeting the current standard were 
predominantly in Southwest region. As the first analysis in Appendix 2B 
of the PA (for the 2001-2003 and 2009-2011 periods) indicates, monitors 
in the West and Southwest tend to have higher W126 index values 
relative to their design values than do monitors in other regions. This 
pattern is noteworthy because the Southwest region has a less dense 
monitoring network than regions in the eastern U.S. (see U.S. EPA, 
2014c, Figure 2-1), so that the extent to which this pattern occurs 
throughout these regions is uncertain.
    An additional air quality analysis was performed for this review 
that is documented in a technical memorandum (Wells, 2014). This 
analysis examines the relationships between O3 levels in 
terms of the form and averaging time for the current standard (the 
``4th max'' metric) and a three-year average, W126-based metric. The 
first part of the analyses focus on the air quality values for the most 
recent three-year period, 2011-2013. Based on this information, it can 
be seen that at monitors just meeting the current standard (three-year 
average fourth-highest daily maximum 8-hour average concentration equal 
to 0.075 ppm), W126 index values (in this case three-year averages) 
varied from less than 3 ppm-hrs to up to 23 ppm-hrs (Figure 5a). At 
sites with a three-year average fourth-highest daily maximum 8-hour 
average concentration at or below a level of 70 ppb (566 monitors 
distributed across all regions of the U.S.), three-year W126 index 
values were above 17 ppm-hrs at no monitors, above 15 ppm-hrs at 4 
monitors, and above 13 ppm-hrs at 16 monitors (1% of the monitors in 
full dataset and less than 3% in this group). These 16 monitors are 
located in the Southwest (15 monitors) and West North Central NOAA 
climate regions and include the states of Arizona, Colorado, New 
Mexico, Utah and Wyoming. At sites with a three-year average fourth-
highest daily maximum 8-hour average concentration at or below a level 
of 65 ppb (220 monitors distributed across all regions of the 
U.S.\225\), three-year W126 index values were above 11 ppm-hrs at no 
monitors, above 7 ppm-hrs at 15 monitors. These 15 monitoring sites are 
predominantly located in the West North Central and Southwest regions. 
At all sites with a three-year average fourth-highest daily maximum 8-
hour average concentration at or below a level of 60 ppb, three-year 
W126 index values were at or below 7 ppm-hrs (Wells, 2014, Figure 5b).
---------------------------------------------------------------------------

    \225\ This memo utilizes the same regional specifications as are 
used in the PA and WREA (e.g., U.S. EPA, 2014c, Appendix 2B, Figure 
2B-1).
---------------------------------------------------------------------------

    Further analysis in the technical memorandum focused on a 
comparison of monitors with a three-year average fourth-highest daily 
maximum 8-hour average concentration at or below a level of 70 ppb and 
a three-year W126 index values above 13 ppm-hrs for sets of three-year 
periods between 2001-2003 and 2011-2013 (Wells, 2014, Figure 8). This 
analysis found that the number of sites meeting 70 ppb while exceeding 
13 ppm-hrs has remained relatively constant over the past decade, with 
these sites consistently being limited to a small number in the West 
and Southwest. In addition, the number of sites meeting both 70 ppb and 
13 ppm-hrs has increased over time, while the number of sites exceeding 
both 70 ppb and 13 ppm-hrs has decreased by a similar amount.
    The second part of the analysis in the technical memorandum focused 
on trends in the relationships between O3 levels in terms of 
the 4th high metric and a three-year average W126 metric, starting with 
the 2001-2003 period and ending with the 2011-2013 period. Based on 
analysis of 729 monitors, trends in both the 4th high metric and the 
three-year average, W126 metric showed decreasing values between 2001-
2003 and 2011-2013. In addition, the amount of year-to-year variability 
in the two metrics tended to decrease over time with decreasing 
O3 concentrations, especially for the W126 metric. Most 
sites in the eastern U.S. and California saw large, widespread 
decreases in both the 4th high metric and the three-year average W126 
metrics over the past decade as a result of regional NOX 
control programs. In the inter-mountain west, where control programs 
have been more localized, the decreases observed in the 4th high metric 
and three-year average W126 metrics were typically much smaller in 
magnitude, with a small number of sites showing significant increases.
    As part of this analysis, regional comparisons were included on the 
relative changes in the relationships between O3 levels in 
terms of the 4th high metric and a three-year average W126 metric 
between the periods of 2001-2003 and 2011-2013. Figure 12 in the 
technical memorandum shows that a positive, linear relationship 
persists within each region between the changes in 4th high and three-
year average W126 metrics. Nationally, the three-year average W126 
metric decreased by approximately 0.7 ppm-hrs per unit ppb decrease in 
the 4th high metric. In addition, the Southwest and West regions, which 
have the greatest potential for sites to measure elevated cumulative, 
seasonal O3 exposures without the occurrence of elevated 
daily maximum 8-hour average O3 concentrations, exhibited 
the greatest

[[Page 75346]]

response in W126 value change per unit change in 4th high metric 
(Wells, 2014, Table 6).
    The technical memorandum concludes that the 4th high metric and a 
three-year average W126 metric are highly correlated, as are the 
relative changes in these two metrics over the past decade. In this 
way, the technical memorandum concludes that that future control 
programs designed to help meet a revised primary O3 standard 
based on the three-year average of the 4th highest daily maximum 8-hour 
concentration are expected to also result in decreases in the values of 
a three-year average W126 metric.
    The above information suggests that depending on the level for a 
standard of the current averaging time and form, the current form and 
averaging time of the secondary standard can be expected to achieve 
control of cumulative seasonal O3 exposures, providing air 
quality that may meet specific three-year average W126 index values. As 
discussed above, we recognize limitations in the dataset and associated 
analyses, including those related to monitor coverage, which may 
contribute uncertainties to conclusions related to the relationships 
described. With respect to monitor coverage, the current O3 
monitoring network is urban focused, with fewer monitors in some parts 
of the country, particular rural areas of the southwestern and western 
U.S. Because of this, there are potential uncertainties in the extent 
to which the monitoring information discussed above represents air 
quality patterns and relationships that would occur in areas without 
monitors. There is some information suggesting that there is a 
potential for inconsistencies in the relationship between W126 measures 
of seasonal O3 concentrations and the fourth highest peak 
O3 concentrations assessed by the current standard averaging 
time and form, but the available data suggest that air quality in areas 
meeting a standard of the current form and averaging time with a level 
in the range of 65 to 70 ppb would also meet a three-year W126 index 
value falling in the range of 13 to 17 ppm-hrs, and that to the extent 
areas need to take action to attain a primary standard in the range of 
65 to 70 ppb, those actions would also improve air quality as measured 
by the W126 metric.\226\ To the extent to which the monitoring data can 
be expected to describe future relationships in air quality, we 
acknowledge potential uncertainties in specifying future air quality 
but note that these uncertainties are limited by the fact that the data 
analysis includes over a decade of O3 measurements, with 
similar patterns and trends observed in air quality over this period of 
time.
---------------------------------------------------------------------------

    \226\ EPA notes that areas can be expected to have air quality 
at least as good as that specified by the primary standard, so to 
the extent there are inconsistencies between fourth highest peak 
concentrations and W126 values such that some areas meeting a 
standard of 0.065 to 0.070 ppm might be well below the range of 13 
to 17 ppm-hours, those inconsistencies are less relevant to 
consideration of the appropriate form and level for the secondary 
standard.
---------------------------------------------------------------------------

5. Administrator's Proposed Conclusions
    In considering what revisions to the secondary standard are 
appropriate, the Administrator has drawn on the ISA conclusions 
regarding the weight of the evidence for a range of welfare effects 
associated with O3 in ambient air, and associated areas of 
uncertainty; quantitative risk and exposure analyses in the WREA for 
different adjusted air quality scenarios and associated limitations and 
uncertainties; staff evaluations of the evidence, exposure/risk 
information and air quality information in the PA; additional air 
quality analyses of relationships between air quality metrics based on 
form and averaging time of the current standards and a cumulative 
seasonal exposure index; and CASAC advice; and, public comments 
received thus far in the review.
    As described in section IV.E.1 above, the Administrator concludes 
it is appropriate to continue to use O3 as the indicator for 
a secondary standard intended to address adverse effects to public 
welfare associated with exposure to O3 alone and in 
combination with related photochemical oxidants. In this review, no 
alternatives to O3 have been advanced as being a more 
appropriate surrogate for ambient photochemical oxidants. Thus, as is 
the case for the primary standard (discussed above in section II.E.1), 
the Administrator proposes to continue to use O3 as the 
indicator for a standard that is intended to address effects associated 
with exposure to O3 alone and in combination with related 
photochemical oxidants. In so doing, the Administrator recognizes that 
measures leading to reductions in ecosystem exposures to O3 
would also be expected to reduce exposures to other photochemical 
oxidants.
    The Administrator has next considered the array of information with 
regard to identifying policy options for a revised secondary standard 
for O3 that in her judgment would provide appropriate 
protection for public welfare effects associated with O3 in 
ambient air. This information includes ISA conclusions, WREA analysis 
findings, staff considerations and conclusions in the PA and CASAC 
advice, as well as the Administrator's conclusions in the last review, 
with regard to a biologically relevant exposure metric for 
O3 vegetation-related effects. The information also includes 
PA conclusions and CASAC advice with regard to key aspects of the 
definition of such a metric, as summarized in section IV.E.2 and IV.E.3 
above. Additionally, the Administrator has considered findings of staff 
evaluations in the PA with regard to potential impacts on vegetation 
and forested ecosystems associated with a range of values for such a 
metric and identified uncertainties and limitations of such 
information, as summarized in section IV.E.2 above. Additionally 
important to her deliberations here are findings of air quality 
analyses of relationships between the W126-based exposure metric and 
levels of a standard of the same form and averaging time as the current 
standards, as described in section IV.E.4 above. Based on consideration 
of this array of information, as described below, the Administrator has 
drawn conclusions with regard to policy options for a revised secondary 
standard. In drawing conclusions on such options, she recognizes that 
the Act does not require that NAAQS be set at zero-risk or background 
levels, but rather at levels that reduce risk sufficiently to protect 
public welfare from adverse effects.
    As an initial matter, the Administrator recognizes the longstanding 
evidence, described in the ISA, of O3 effects on vegetation 
and associated terrestrial ecosystems. Further, in reaching a proposed 
conclusion on the appropriate form and averaging time for a revised 
secondary standard that would provide increased protection against 
vegetation-related effects on public welfare, the Administrator takes 
note of the conclusions drawn in the ISA, the PA and by CASAC in this 
review that the scientific evidence continues to demonstrate the 
cumulative nature of O3-induced plant effects and the need 
to give greater weight to higher concentrations, as summarized in 
sections IV.B.1, IV.D.1, IV.D.2, IV.E.2.a and IV.E.3 above. Based on 
these considerations, the Administrator concurs with the CASAC that a 
cumulative, seasonal, concentration-weighted exposure-based form and 
averaging time provides the most direct link between O3 in 
ambient air and O3-related effects on vegetation. The 
Administrator further concludes that in judging the extent of public 
welfare protection that might be afforded by a revised standard, it is 
appropriate to use

[[Page 75347]]

a cumulative, seasonal concentration-weighted metric.
    In identifying a cumulative, seasonal, concentration-weighted 
metric for use in judging public welfare protection, the Administrator 
gives weight to the PA conclusions regarding consideration of a revised 
secondary standard in terms of the cumulative, seasonal, concentration-
weighted form, the W126 index. As described in section IV.B.1 above, 
the ISA has recognized the strength of the W126 index in its weighting 
of potentially damaging O3 concentrations that contributes 
to the advantages it offers over other weighted cumulative indices. The 
Administrator notes the PA conclusions regarding the W126 metric, 
specifically use of the three consecutive month period within the 
O3 season with the maximum index value as the seasonal 
period over which to cumulate hourly O3 exposures and the 
cumulation of daily exposures for the 12-hour period from 8:00 a.m. to 
8:00 p.m. The Administrator additionally takes note of CASAC support 
for consideration of the W126 index defined in this way and concludes 
it is appropriate to use the cumulative seasonal W126-based metric 
derived in this way.
    In further considering the PA conclusions regarding a revised 
secondary standard in terms of the W126 index, the Administrator takes 
note of considerations in the PA of a three-year or single-year 
evaluation period. Such considerations include the variability in 
ambient air O3 concentrations from year to year, as well as 
variability and uncertainties related to environmental factors that 
influence the occurrence and magnitude of O3-related 
effects. The Administrator additionally notes the PA observation of 
greater significance for effects associated with multiple-year 
exposures. Based on these and related considerations described in the 
PA (and summarized in section IV.E.2 above), the Administrator, in 
identifying a metric for use in judging public welfare protection 
afforded, agrees with the PA conclusion that it is appropriate to 
consider a form that averages W126 index values across three 
consecutive years, and to do so in conjunction with identification of 
levels for such a form that might be judged to provide the appropriate 
degree of public welfare protection from O3 effects across 
multiple years. In so doing, the Administrator takes note of the ISA 
conclusions regarding the role of environmental factors in variability 
associated with effects of ambient air O3 and the year-to-
year variability commonly observed in such environmental factors. 
Further, the Administrator also recognizes uncertainties associated 
with determining the degree of vegetation impacts for annual effects 
that would be adverse to public welfare. Even in the case of annual 
crops, the assessment of public welfare significance is unclear for the 
reasons discussed below related to agricultural practices. The 
considerations identified here lead the Administrator to conclude it is 
appropriate to use an index averaged across three years.
    In reaching this conclusion regarding a three-year average metric, 
the Administrator has considered CASAC comments that it favors a W126-
based secondary standard with a single year form and that its 
recommended range of levels relates to such a form. The Administrator 
concurs with CASAC that it is important to consider impacts associated 
with a single year that may be of a magnitude concluded to represent an 
adverse effect on public welfare. The Administrator further concludes 
that such an occurrence can be addressed through use of a three-year 
average metric, chosen with consideration of the relevant factors. As 
noted above, the Administrator gives consideration to the 
variabilities, as well as the uncertainties, associated with single 
year and multiple year impacts. Based on all of these considerations, 
the Administrator recognizes greater confidence in judgments related to 
public welfare impacts based on a three-year average metric.
    Thus, based on all of the above, the Administrator proposes, for 
purposes of judging the extent of public welfare protection that might 
be afforded by a revised standard and whether it meets the appropriate 
level of protection, to use the average W126 index value across three 
years, with each year's value identified as that for the three-month 
period yielding the highest seasonal value and with daily O3 
exposures within a three-month period cumulated for the 12-hour period 
from 8:00 a.m. to 8:00 p.m.
    In reaching a conclusion on the appropriate range of W126 index 
values that describe the O3 conditions expected to provide 
the requisite protection of public welfare, the Administrator has given 
careful consideration to the following: (1) The nature and degree of 
effects of O3 to the public welfare, including what 
constitutes an adverse effect; (2) the strengths and limitations of the 
evidence that is available regarding known or anticipated adverse 
effects from cumulative, seasonal exposures, and its usefulness in 
informing selection of a proposed range; and (3) CASAC's views 
regarding a range of W126 levels appropriate to consider, as well as on 
the strength of the evidence and its adequacy to inform a range of 
levels. In this consideration, the Administrator recognizes that the 
choice of a range of W126 index values (and the form of the W126 index) 
that might be expected to provide protection of the public welfare from 
any known or anticipated adverse effects requires judgments about the 
interpretation of the evidence and other information, such as the 
quantitative analyses of air quality monitoring, exposure and risk, 
that neither overstates nor understates the strengths and limitations 
of the evidence and information nor the appropriate inferences to be 
drawn as to risks to public welfare. The CAA does not require that a 
secondary standard be protective of all effects associated with a 
pollutant in the ambient air but rather those considered adverse to the 
public welfare (as described in section IV.B.2 above). The 
Administrator additionally recognizes that there is not a bright line 
clearly directing the choice of a range of W126 index values and that 
the choice of what is appropriate is a public welfare policy judgment 
entrusted to the Administrator.
    In determining the range of three-year average W126 index values 
that might be expected to provide the appropriate level of public 
welfare protection, the Administrator first considers the nature and 
degree of effects of O3 on the public welfare. The 
Administrator recognizes that the significance to the public welfare of 
O3-induced effects on sensitive vegetation growing within 
the U.S. can vary, depending on the nature of the effect, the intended 
use of the sensitive plants or ecosystems, and the types of 
environments in which the sensitive vegetation and ecosystems are 
located. Any given O3-related effect on vegetation and 
ecosystems (e.g., biomass loss, visible foliar injury), therefore, may 
be judged to have a different degree of impact on the public depending, 
for example, on whether that effect occurs in a Class I area, or a 
residential or commercial setting. The Administrator notes that such a 
distinction is supported by CASAC advice in this review. In her 
judgment, like those of the Administrator in the last review, it is 
appropriate that this variation in the significance of O3-
related vegetation effects should be taken into consideration in making 
judgments with regard to the level of ambient O3 
concentrations that is requisite to protect the public welfare from any 
known or anticipated adverse effects. As a result, the Administrator 
concludes that of those known and anticipated O3-related 
vegetation and ecosystem effects

[[Page 75348]]

identified and discussed in this notice, particular significance should 
be ascribed to those that occur on sensitive species that are known to 
or are likely to occur in federally protected areas such as Class I 
areas \227\ or on lands set aside by States, Tribes and public interest 
groups to provide similar benefits to the public welfare, for residents 
on those lands, as well as visitors to those areas.
---------------------------------------------------------------------------

    \227\ For example, the Wilderness Act of 1964 defines designated 
``wilderness areas'' in part as areas ``protected and managed so as 
to preserve [their] natural conditions'' and requires that these 
areas ``shall be administered for the use and enjoyment of the 
American people in such manner as will leave them unimpaired for 
future use and enjoyment as wilderness, and so as to provide for the 
protection of these areas [and] the preservation of their wilderness 
character.''16 U.S.C. 1131(a).
---------------------------------------------------------------------------

    Likewise, the Administrator also notes that the same known or 
anticipated O3-induced effects occurring in other areas may 
call for less protection. For example, the maintenance of adequate 
agricultural crop yields is extremely important to the public welfare 
and is currently achieved through the application of intensive 
management practices. With respect to commercial production of 
commodities, the Administrator notes that judgments about the extent to 
which O3-related effects on commercially managed vegetation 
are adverse from a public welfare perspective are particularly 
difficult to reach, given that the extensive management of such 
vegetation (which, as CASAC noted, may reduce yield variability) may 
also to some degree mitigate potential O3-related effects. 
The management practices used on these lands are highly variable and 
are designed to achieve optimal yields, taking into consideration 
various environmental conditions. In addition, changes in yield of 
commercial crops and timber may affect producers and consumers 
differently, further complicating the question of assessing overall 
public welfare impacts. Thus, the Administrator concludes that 
agricultural crops do not have same need for additional protection from 
the NAAQS as forested ecosystems and, while research on agricultural 
crop species remains useful in illuminating mechanisms of action and 
physiological processes, information from this sector on O3-
induced effects is considered less useful in informing judgments on 
what level(s) would be sufficient but not more than necessary to 
protect the public welfare. The CASAC identified a crop RYL benchmark 
of 5% for the median species and indicated they found higher 
percentages unacceptably high. Although the Administrator has not drawn 
a conclusion with regard to this specific benchmark, the Administrator 
finds the public welfare impacts associated with crop yield loss to be 
a less important consideration in this review for the reasons discussed 
here, including the extensive management of crop yields and the 
dynamics of agricultural markets, and thus is not focusing on crop 
yield loss in selecting a revised standard. She notes, however, the PA 
finding that median species crop RYL estimates for W126 index values in 
the PA identified range (17 to 7 ppm-hrs) fall below the 5% benchmark 
emphasized by CASAC for this endpoint. The Administrator also notes 
that a standard revised to increase protection for forested ecosystems 
would also be expected to provide some increased protection for 
agricultural crops.
    The Administrator also recognizes that O3-related 
effects on sensitive vegetation can occur in other areas that have not 
been afforded special federal protections, ranging from effects on 
vegetation growing in managed city parks and residential or commercial 
settings, such as ornamentals used in urban/suburban landscaping or 
vegetation grown in land use categories that are heavily managed for 
commercial production of commodities such as timber. For vegetation 
used for residential or commercial ornamental purposes, the 
Administrator believes that there is not adequate information at this 
time to establish a secondary standard based specifically on impairment 
of these categories of vegetation, but notes that a secondary standard 
revised to provide protection for sensitive natural vegetation and 
ecosystems would likely also provide some degree of protection for such 
vegetation.
    Based on the above, the Administrator finds that the type of 
information most useful in informing the selection of an appropriate 
range of protective levels is appropriately focused on information 
regarding exposures and responses of sensitive trees and other native 
species known or anticipated to occur in protected areas such as Class 
I areas or on lands set aside by States, Tribes and public interest 
groups to provide similar benefits to the public welfare, for residents 
on those lands, as well as visitors to those areas.
    With regard to the available evidence, the Administrator finds the 
coherence and strength of the weight of evidence from the large body of 
available literature compelling. This evidence addresses a broad array 
of O3-induced effects on a variety of tree species across a 
range of growth stages (i.e., seedlings, saplings and mature trees) 
using diverse field-based (e.g., free air, gradient and ambient) and 
OTC exposure methods. The Administrator gives particular attention to 
the effects related to native tree growth and productivity, recognizing 
their relationship to a range of ecosystem services, including forest 
and forest community composition.
    With regard to selection of the values for use with the W126 index 
for the purpose of identifying a range of O3 conditions 
expected to provide the appropriate level of protection from vegetation 
effects of particular concern, the Administrator, as an initial matter, 
takes note of the PA conclusion that, with regard to a target level of 
protection for a revised standard, it is appropriate to give 
consideration to a range of levels from 17 ppm-hrs to 7 ppm-hrs, 
expressed in terms of the W126 index averaged across three consecutive 
years. As summarized in section IV.E.2.b above, this PA conclusion 
draws heavily on considerations related to estimates of tree seedling 
growth impacts (in terms of relative biomass loss) associated with a 
range of W126-based index values developed from the robust E-R 
functions for 11 tree species. This conclusion also gives weight to 
CASAC comments as to an unacceptably high magnitude of relative biomass 
loss (6%) for the median species and a magnitude of median relative 
biomass loss on which to focus considerations (2%). The Administrator 
takes particular note of the CASAC view of a median species RBL of 6% 
as unacceptably high.
    In considering the basis for the range of W126 index levels 
identified by the PA, for which 17 ppm-hrs is the upper end, the 
Administrator considers the CASAC advice, including their view that a 
6% median tree seedling species RBL is unacceptably high, their 
consideration of Table 6-1 in the second draft PA which indicated such 
a RBL estimate for a W126 index value of 17 ppm-hrs, and their 
consequent lack of support for levels higher than 15 ppm-hrs (Frey, 
2014c, p. iii; U.S. EPA 2014j, Table 6-1). As noted in section IV.E.3 
above, revisions to this table in the final PA, made in consideration 
of CASAC comments have resulted in changes to the median species RBL 
estimates such that the median species RBL estimate for a W126 index 
value of 17 ppm-hrs in this table in the final PA (5.3%) is nearly 
identical to the median species estimate for 15 ppm-hrs (the value 
corresponding to the upper end of the CASAC-identified range) in the 
second draft PA (5.2%) (U.S. EPA, 2014c, Table 6-1; U.S. EPA, 2014j, 
Table 6-1).

[[Page 75349]]

    The Administrator additionally takes note of the PA observations 
that the number and proportion of individual species with RBL estimates 
at or below 2%, a benchmark given emphasis by CASAC, do not vary across 
W126 index values from 17 ppm-hrs down to 9 ppm-hrs (as seen in Table 8 
above), providing little distinction with regard to the significance of 
growth impacts for exposures across this large portion of the PA range. 
The Administrator also notes the CASAC recommendation regarding a 
lowering of the level with consideration of a three-year average index; 
however, the Administrator's judgments on a three-year average index, 
as described above, focus on confidence in conclusions that might be 
drawn with regard to single as compared to multiple year impacts. For 
example, the Administrator, while recognizing the strength of the 
evidence with regard to quantitative characterization of O3 
effects on growth of tree seedlings and crops, in addition to noting 
the additional difficulties for assessing welfare impacts of crops, 
takes note of the uncertainty associated with drawing conclusions with 
regard to the extent to which small percent reductions in annual growth 
contribute to adverse effects on public welfare and the role of annual 
variability in environmental factors that affect plant responses to 
O3. Moreover, as explained above, the Administrator 
concludes that concerns related to the possibility of a singly 
unusually damaging year can be addressed through use of a three-year 
average metric, chosen with consideration of the relevant factors. 
Accordingly, she judges it appropriate to include 17 ppm-hrs, without 
adjustment, in the range of three-year average W126 index values 
appropriate to consider in determining what secondary standard will 
provide air quality associated with the appropriate level of public 
welfare protection. She thus judges it appropriate to focus on a range 
for three-year average W126 levels with 17 ppm-hrs at the upper end. In 
so doing, she additionally notes CASAC's recognition that, within a 
scientifically appropriate range, the choice of levels is a public 
policy judgment by the Administrator.
    In turning to consideration of the low end for the W126 index 
range, the Administrator considers the full range of W126 levels 
identified in the PA with regard to the evidence and exposure/risk-
based information, and associated uncertainties, identified in the PA, 
as well as CASAC advice. The Administrator notes the CASAC policy view 
regarding protection provided for trees and associated ecosystem 
services from a W126 index value of 7 ppm-hrs, which is based on the 
W126 index value for which the median species estimate falls below 2% 
RBL. The Administrator recognizes, however, as noted above, the greater 
uncertainty associated with the extent to which estimates of benefits 
in terms of ecosystem services and reduced effects on vegetation at 
lower O3 exposures might be judged significant to the public 
welfare.
    The Administrator additionally notes the results of the EPA's 
quantitative exposure and risk assessments for the air quality 
scenarios for W126 levels at and below 11 ppm-hrs, including the 
relatively small additional benefits and increased uncertainty with the 
ecosystem services estimates in these lower W126 scenarios. With regard 
to the PA evaluation of RBL estimates, the Administrator, while noting 
the PA observations of similarity in the number of species with less 
than 2% RBL across the W126 range from 17 to 9 ppm-hrs, as stated 
above, additionally notes PA observations of a similar number of 
studied species with RBL estimates below 5% for W126 index values of 13 
and 11 ppm-hrs. Thus, to the extent that weight is given to the 
importance of 5% RBL for individual species, both W126 index values are 
observed to provide RBL estimates below this benchmark.
    With regard to considerations of O3 effects beyond 
biomass loss in tree seedlings, the Administrator takes note of the 
lack of new quantitative E-R relationships for larger trees growing in 
the field that would help inform consideration of a standard level 
within the lower part of PA range. Thus, the Administrator recognizes 
that important uncertainties remain in interpreting the quantitative 
O3-related growth effects for tree seedlings assessed in OTC 
studies for the purpose of characterizing long-term growth effects, and 
other more subtle but important effects on sensitive tree species, 
natural forests, and forested ecosystems in the broader context of 
protection of public welfare. Additionally, while the Administrator 
notes that there is evidence that O3-related visible foliar 
injury can occur at such lower levels (below a W126 index value of 13 
ppm-hrs), she recognizes, as summarized in sections IV.C.3.c and IV.D.1 
above, the significant challenges in judging the extent to which such 
effects should be considered adverse to public welfare, in light of the 
variability and the lack of clear quantitative relationship with other 
effects on vegetation, as well as the lack of established criteria or 
objectives that might inform consideration of potential public welfare 
impacts related to this vegetation effect.
    Thus, in the Administrator's judgment, focus on a three-year 
average W126 index value below 13 ppm-hrs would not give sufficient 
attention to the important uncertainties and limitations inherent in 
the currently available scientific evidence and in the quantitative 
assessments conducted for the current review. Taking into account the 
uncertainties that remain in interpreting the evidence, the 
Administrator observes that the likelihood of obtaining benefits to 
public welfare decreases with a standard set below a level of 13 ppm-
hrs, while the likelihood of requiring reductions in ambient 
concentrations that go beyond those that are needed to reduce adverse 
impacts to public welfare increases.
    Based on the above considerations and based on the entire body of 
evidence and information currently available, the Administrator 
identifies the range of three-year average W126 index values extending 
from 13 to 17 ppm-hrs as appropriate to consider in identifying the 
ambient O3 concentrations that would provide the appropriate 
level of public welfare protection. In so doing, the Administrator 
notes CASAC recognition that a three-year average W126 level of 13 ppm-
hrs may be appropriate depending on consideration of year-to-year 
variability and policy considerations. Thus, based on the discussion 
above, and with consideration of CASAC advice on these issues, the 
Administrator proposes that ambient O3 concentrations 
resulting in cumulative seasonal O3 exposures of a level 
within the range from 13 ppm-hrs to 17 ppm-hrs, in terms of a W126 
index averaged across three consecutive years, would provide the 
requisite protection against known or anticipated adverse effects to 
the public welfare. The EPA solicits comments on levels within this 
range.
    The Administrator next turns to consideration of policy options for 
a revised secondary standard that would provide this level of 
protection. The Administrator takes note of staff conclusions that it 
is appropriate to consider a revised secondary standard in terms of the 
cumulative, seasonal, concentration-weighted form, the W126 index. 
Further, she gives extensive consideration to CASAC advice to set such 
a secondary standard. Such a standard, as mentioned above, would be 
directly linked to O3 exposures to which vegetation are most 
responsive and thus might be expected to provide some

[[Page 75350]]

confidence that such exposures of concern would be controlled.
    In considering different policy options for a revised secondary 
standard, the Administrator finds it useful to consider what can be 
concluded from the available information with regard to relationships 
between air quality characterized in terms of the current form and 
averaging time and also in terms of the W126 metric. She has considered 
particularly what such analyses and relationships indicate with regard 
to the extent to which W126-based O3 concentrations may be 
controlled by a revised secondary standard set identical to a revised 
primary standard (in the range identified in section II.F above). In so 
doing, she considers the air quality analyses in the PA and also the 
analyses of more recent air quality data summarized in the EPA 
technical memo (described in section IV.E.4 above), focusing 
particularly on analyses examining the W126-based O3 
exposure achieved in locations found to meet potential alternative 
standards within the range of primary standards proposed in section 
II.F above.
    Findings from these analyses of recent O3 measurements 
and trends in the relationship between the current standard and the 
W126 metrics were substantially similar for the various time periods 
examined over the past decade. There is some information suggesting 
that there is a potential for inconsistencies in the relationship 
between W126 measures of seasonal O3 concentrations and the 
fourth highest peak O3 concentrations assessed by the 
current standard averaging time and form, but the available data 
suggest that air quality in areas meeting a primary standard in the 
range of 65 to 70 ppb would also meet a three-year W126 index value 
falling in the range of 13 to 17 ppm-hrs, and that to the extent areas 
need to take action to attain a standard in the range of 0.065 to 0.070 
ppm, those actions would also improve air quality as measured by the 
W126 metric. The Administrator also recognizes that the relatively 
lesser density of monitors in rural areas, including in areas of the 
West and Southwest NOAA climatic regions currently meeting the current 
standard where O3 W126 index values are generally higher, 
makes uncertain the degree to which a revised level for the current 
standard would provide the appropriate degree of protection for 
vegetation-related effects on public welfare in these areas. The 
Administrator takes note of the PA finding, referenced in section 
IV.D.3 above, that reductions in NOX emissions that occur in 
urban areas to attain primary standards would also have the effect of 
reducing downwind, rural concentrations over the season. Thus, while 
the potential for underprotection may exist, depending on the specific 
levels chosen, the extent of such areas and of such a risk is not 
clear.
    Based on the most recent period of monitoring data, the 
Administrator notes that in all areas in which the O3 
concentrations would have met a primary standard with a revised level 
of 70 ppb (which includes over 500 monitors distributed across all 
regions of U.S), the three-year average W126 index values are at or 
below 17 ppm-hrs. In the same areas, only 16 monitors (or less than 3% 
of all monitors in this group, all but one of which is located in the 
Southwest region) had three-year average W126 index values above 13 
ppm-hrs. She further notes that in all areas in which the O3 
concentrations would have met a primary standard with a revised level 
of 65 ppb (which includes 220 monitors distributed across all regions 
of U.S), the three-year average W126 index values are at or below 13 
ppm-hrs.
    In considering these findings regarding cumulative seasonal 
O3 exposures in areas that would have met a primary standard 
with a revised level within the proposed range, the Administrator also 
takes note of the high correlation observed between the design value 
for the current secondary (and primary) standard and values for the 
three-year average, W126 metric, as well as the high correlation in the 
relative changes in these two metrics based on air quality analyses of 
O3 measurements from over the past decade. This finding 
supports a conclusion that the air quality analyses indicate that 
future control programs designed to reduce O3 concentrations 
to help meet a revised primary O3 standard that retains the 
current form and averaging time (three-year average of the 4th highest 
daily maximum 8-hour concentration) would also be expected to result in 
reductions in three-year average, W126 index values. Further, she notes 
the conclusion from the air quality analysis that the Southwest and 
West regions, which have the greatest potential for sites to measure 
elevated cumulative, seasonal O3 exposures without the 
occurrence of elevated daily maximum 8-hour average O3 
concentrations, exhibited the greatest response in W126 index value 
change per unit change in metric based on the current standard form and 
averaging time. While recognizing the limitations of such analyses in 
projections of future air quality patterns, the Administrator also 
notes that the time period over which the analyses focused involved 
emissions control programs to achieve O3 reductions such 
that their findings would be expected to be informative of further 
similar control activities, such as those to meet a revised standard 
with a lower level, in the future.
    Based on the findings from these analyses, the Administrator finds 
it appropriate to consider the policy option of retaining the form and 
averaging time of the current secondary standard and revising the level 
to within the range of 65 to 70 ppb. In such consideration, the 
Administrator first notes her proposed conclusion that the requisite 
protection from known or anticipated adverse effects to public welfare 
may be achieved by cumulative, seasonal, concentration-weighted 
O3 concentrations characterized in terms of a W126 index 
value that falls within the range from 13 to 17 ppm-hrs. Her final 
decision on the W126 index value in this range that affords the 
requisite protection will be based on a series of judgments, as 
described above. Given the focus on tree seedling growth effects in 
identifying this range, such judgments will include the weight to give 
the evidence of specific vegetation-related effects estimated to result 
from W126 index values within this range, including the objectives for 
consideration of tree species biomass loss estimates in relationship to 
identified benchmarks (e.g., median species RBL of 2% and greater), the 
weight to give associated uncertainties, including those related to the 
variability in occurrence of such effects in forested areas, the 
associated ecosystem services including those of particular public 
welfare significance, and judgments on the extent to which such effects 
in forested areas may be considered adverse to public welfare. This 
final decision will also take into account judgments with regard to the 
weight to give the evidence and quantitative analyses, and associated 
uncertainties, related to other effects of O3 (summarized in 
sections IV.C, IV.D.1 and IV.E.2 above), particularly including those 
for which the ISA concludes causal or likely causal relationships with 
O3 exposures. As noted above, a standard that provides the 
appropriate level of protection for growth effects would also be 
expected to provide additional protection for other effects including 
visible foliar injury, crops and carbon storage.
    The Administrator notes that based on the above analyses, the 
proposed range of levels for a revised primary standard provide air 
quality, in terms of three-year average W126 index values, of a

[[Page 75351]]

range at or below the range which the Administrator has identified for 
consideration with regard to the requisite public welfare protection. 
Thus, depending on final judgments on revisions to the primary standard 
and the requisite protection for the secondary standard, a revised 
secondary standard identical to the revised primary standard may 
provide sufficient protection for public welfare. Therefore, the 
Administrator proposes to retain the current averaging time and form of 
the secondary standard and revise the level to within the range of 65 
to 70 ppb.
    In reaching such a conclusion, the Administrator recognizes that 
such a strengthening of the secondary standard would be expected to 
provide significant additional protection for public welfare, including 
effects related to vegetation and associated ecosystem services (and 
others discussed above), over that afforded by the current secondary 
standard.
    Thus, based on her consideration of the full range of information 
as described above, the Administrator judges that ambient O3 
concentrations in terms of a three-year average W126 index value within 
the range extending from 13 ppm-hrs to 17 ppm-hrs would provide 
requisite public welfare protection. She further judges that it would 
be appropriate to achieve that level of air quality by retaining the 
existing averaging time and form, and revising the level to within the 
range of 65 to 70 ppb. In recognition of CASAC's recommendation and the 
PA conclusion with regard to a distinct secondary standard, the 
Administrator additionally solicits comment on the policy option of 
revising the form and averaging time for the secondary standard to a 
W126 index value, averaged across three years, with each year's value 
identified as that for the three-month period yielding the highest 
seasonal value and with daily O3 exposures within a three-
month period cumulated for the 12-hour period from 8:00 a.m. to 8:00 
p.m., and a level within the range from 13 ppm-hrs to 17 ppm-hrs.

F. Proposed Decision on the Secondary Standard

    The Administrator proposes to revise the level of the current 
secondary standard within the range of 0.065 to 0.070 ppm. The EPA 
solicits comments on this proposed revision of the secondary standard. 
Further, the EPA solicits comments on the proposed conclusion that air 
quality in terms of a W126 index value, averaged across three 
consecutive years, within the range of 13 ppm-hrs to 17 ppm-hrs would 
provide requisite protection against known or anticipated adverse 
effects to the public welfare. Additionally, the EPA solicits comments 
on alternative values for a three-year average W126 index for such a 
purpose within the range extending below 13 ppm-hrs down to 7 ppm-hrs.
    The EPA also solicits comments on the alternative approach of 
revising the secondary standard to a cumulative, seasonal, 
concentration-weighted form, the W126 index based on the three 
consecutive month period within the O3 season with the 
maximum index value, with daily exposures cumulated for the 12-hour 
period from 8:00am to 8:00pm and with a form that averages seasonal 
W126 values across three consecutive years and a level within the range 
of 13 to 17 ppm-hrs. The EPA additionally solicits comments on such a 
distinct secondary standard with a level within the range extending 
below 13 ppm-hrs down to 7 ppm-hrs. Further, the EPA solicits comments 
on retaining the current secondary standard without revision, along 
with the alternative views of the evidence that would support retaining 
the current standard.

V. Appendix U: Interpretation of the Primary and Secondary NAAQS for 
O3

A. Background

    The EPA is proposing to create Appendix U to 40 CFR part 50 to 
reflect the proposed revisions to the primary and secondary NAAQS for 
O3 discussed in previous sections of this preamble. The 
proposed Appendix U explains the computations necessary for determining 
when the proposed primary and secondary O3 NAAQS are met at 
an ambient air quality monitoring site, similar to Appendix P to 40 CFR 
part 50 which deals with interpretation of the O3 NAAQS 
promulgated in 2008. Specifically, the proposed Appendix U addresses 
data selection requirements (section V.B), data reporting and data 
handling requirements (section V.C), and data completeness 
requirements. The EPA is proposing to maintain the data completeness 
requirements from the previous O3 NAAQS.
    Given that the EPA is soliciting public comment on a distinct 
secondary standard based on the W126 metric, section V.D of this 
preamble contains a discussion of additional data handling requirements 
that would be adopted in Appendix U in the event that the Administrator 
decides to set a distinct secondary standard based on public comments 
received.
    The proposed Appendix U also provides specific requirements for the 
handling of data affected by exceptional events in accordance with 40 
CFR 50.14. Section V.E of this preamble addresses O3-
specific deadlines related to the flagging and submission of 
demonstrations for exceptional event data for the proposed 
O3 NAAQS.

B. Data Selection Requirements

    The EPA is proposing to clarify which data are to be used in 
comparisons with the NAAQS. First, the EPA proposes to maintain the 
existing regulatory requirements that only O3 data collected 
by a federal reference method specified in Appendix D to 40 CFR part 
50, or an equivalent method designated in accordance with 40 CFR part 
53, and meeting all applicable monitoring requirements listed in 40 CFR 
part 58, are eligible for comparison to the proposed O3 
NAAQS.
    Second, the EPA is proposing in Appendix U that O3 
design values are to be calculated on a site-level basis. Past practice 
has been to calculate a design value for each individual O3 
monitor. However, this practice could be viewed as inconsistent with 
the stated purpose of the previous O3 data handling 
appendix, which is to determine ``whether the national 8-hour primary 
and secondary ambient air quality standards for ozone (O3) 
specified in Sec.  50.15 are met at an ambient O3 air 
quality monitoring site.'' (40 CFR part 50, Appendix P, section 1 
(emphasis added)). Given the level of consistency in the measurement 
data obtained across the various federal reference and equivalent 
O3 monitoring instruments currently in operation (U.S. EPA, 
2013a, section 3.5.2.1), the EPA believes that it would be appropriate 
to combine data across O3 monitors operating at the same 
site. Therefore, the EPA is proposing an analytic approach for 
combining data collected from multiple O3 monitors at a site 
in order to obtain a single set of hourly O3 concentration 
data for each site.
    The proposed approach allows the monitoring agencies to designate 
one monitor as the ``primary monitor'' for each site. In the absence of 
a primary monitor designation, the primary monitor would default to the 
monitor with the most complete hourly dataset in each year. Once a 
primary monitor has been determined for the site, missing hourly 
O3 concentrations for the primary monitor would be 
substituted from any other monitors at the site. In the event of three 
or more monitors operating at the same site, missing hourly 
O3 concentrations for the primary monitor would be 
substituted with hourly values averaged across the other monitors. The 
EPA notes that at the time of this proposal, there were approximately 
20 sites operating two

[[Page 75352]]

monitors simultaneously, and no O3 sites operating three or 
more monitors simultaneously. This proposed approach for combining data 
across monitors at a site is consistent with the existing approach 
described in Appendix N to Part 50 for the PM2.5 NAAQS. The 
EPA invites public comment on the scientific validity of combining data 
across O3 monitors, and the merits of the proposed approach 
for combining data across multiple O3 monitors at a site.
    Third, the EPA proposes to maintain the existing practice of 
combining data from nearby monitoring sites in order to determine a 
valid design value, known as a ``site combination''. Site combinations 
typically involve situations where sites have been replaced or 
relocated a short distance away, and the monitoring agency wishes to 
combine the data from the two sites in order to maintain a continuous 
data record. The EPA regional offices have approved over 100 site 
combinations for O3 since the promulgation of the 1997 
O3 NAAQS. The EPA has maintained records of approved site 
combinations, but these records are not easily accessible by the 
public.
    The EPA proposes to replace the current procedure for approving 
O3 site combinations with a more formal procedure in 
Appendix U, which would allow states to submit site combination 
requests to the appropriate Regional Administrator. Site combinations 
may be approved by the Regional Administrator, after he or she has 
determined that the measured air quality concentrations do not differ 
substantially between the two sites. In order to make this 
determination, the Regional Administrator may request additional 
information from the states, including detailed information on the 
locations and distance between the two sites, levels of ambient 
concentrations measured at the two sites, and local emissions or 
meteorology data.
    In order to improve transparency, the EPA will make records of all 
approved site combinations available in their Air Quality System (AQS) 
database, and will update design value calculations in AQS so that 
approved site combinations are implemented. The EPA invites public 
comment on the merits of the proposed process for approving site 
combinations in order to obtain valid design values for the 
O3 NAAQS.

C. Data Reporting and Data Handling Requirements

    The EPA is proposing to maintain the requirement that hourly 
O3 concentration data be reported in parts per million (ppm) 
to three decimal places. Any decimal digits reported beyond three 
decimal digits will be truncated, consistent with past practice (40 CFR 
part 50, Appendix P, section 2.1) and the typical measurement 
uncertainty associated with most O3 monitoring instruments. 
The proposed Appendix U clarifies that hourly O3 
concentrations are to be reported in Local Standard Time (LST), 
consistent with how the values are currently stored in AQS.
    The EPA is proposing to maintain the existing procedures for 
calculating moving 8-hour averages from the hourly O3 data 
(40 CFR part 50, Appendix P, section 2.1), with one minor exception. In 
instances where fewer than six hourly O3 concentrations are 
available during an 8-hour period (i.e. less than 75% completeness), 
the EPA is proposing to substitute zero (i.e. 0.000 ppm) instead of one 
half of the O3 monitoring instrument's minimum detectable 
limit (MDL) for the missing concentration values to determine if the 
resulting 8-hour average is greater than the level of the NAAQS. The 
purpose of this ``data substitution test'' is to identify any 8-hour 
periods that do not meet the requirements for a valid 8-hour average, 
but have reported concentrations that are so high that the NAAQS is 
exceeded even when substituting low values for the missing 
concentrations. The EPA believes that a constant substitution value of 
zero is preferable to 1/2 MDL, which may vary across O3 
monitoring instruments. The MDL value for most O3 monitoring 
instruments is 0.005 ppm, and the 1/2 MDL value is 0.002 ppm (with 
truncation); thus, in practice, the difference is slight. The EPA notes 
that a value of zero micrograms per cubic meter (ug/m\3\) is used in 
data substitution tests for 24-hour average PM2.5 
concentrations, as specified in Appendix N to 40 CFR part 50. The EPA 
invites public comment on the merits of using zero instead of 1/2 MDL 
for the 8-hour average data substitution test.
    The EPA is proposing new procedures for determining daily maximum 
8-hour average O3 concentrations. Past practice allows for 
daily maximum 8-hour average O3 concentrations from two 
consecutive days to have some hours in common (40 CFR part 50, Appendix 
P, section 2.1). One implication of this is that an O3 site 
may be counted as having exceeded the NAAQS on two distinct days based 
on two 8-hour periods having up to 7 hours in common. Theoretically, 
this could result in an annual fourth-highest value greater than the 
NAAQS based on high overnight O3 concentrations occurring 
only twice during the year.
    The EPA performed an analysis based on ambient O3 
concentration data from 2004 to 2013 (Wells, 2014b), which showed that 
at least one instance of overlapping daily maximum 8-hour averages 
occurred at 99.5% of O3 sites during that time period. 
Overlapping daily maximum 8-hour averages were infrequent at most 
sites, but in some cases, these values occurred quite regularly (up to 
60 times per year). Overlapping daily maximum 8-hour averages 
contributed to additional exceedances of the proposed O3 
NAAQS at 14% of sites for a level of 0.070 ppm, and at 23% of sites for 
a level of 0.065 ppm. In addition, 8% of sites had overlapping daily 
maximum 8-hour averages which contributed to a higher annual fourth-
highest daily maximum value in one or more years. Finally, the analysis 
showed that O3 sites located in non-urban areas affected by 
long-range transport, especially those sites at higher elevations, were 
most likely to have additional exceedances of the proposed 
O3 NAAQS due to the occurrence of overlapping daily maximum 
8-hour averages.
    Based on this analysis, the EPA initially concludes that 
overlapping daily maximum 8-hour averages are more likely to contribute 
to additional exceedances of the O3 NAAQS as the level of 
the standard is lowered. Therefore, the EPA is proposing a new 
procedure for determining daily maximum 8-hour average O3 
concentrations for the proposed NAAQS that is based on 17 consecutive 
8-hour periods in each day, beginning with the 8-hour period from 7:00 
a.m. to 3:00 p.m., and ending with the 8-hour period from 11:00 p.m. to 
7:00 a.m. Given that 8-hour averages are stored in the beginning hour 
of each period, this corresponds to the 8-hour averages from 7:00 a.m. 
to 11:00 p.m.
    The rationale for the proposed approach is twofold. First, it 
avoids any possibility of ``double counting'' exceedances of the NAAQS 
based on 8-hour periods with one or more hours in common, while 
continuing to make use of all of the hourly concentration data, and 
keeping the calculations simple and straightforward. Second, it is more 
consistent with the physical processes involved in the formation and 
transport of ground-level O3. Specifically, the chemical 
reactions involved in the formation of new ground-level O3 
require sunlight. Therefore, it is appropriate to begin the 
``O3 day'' at sunrise, which for simplicity is assumed to be 
7:00 a.m. LST. Similarly, any daily maximum 8-hour averages occurring 
after sunset are assumed to be caused by transport of O3 
molecules which

[[Page 75353]]

originated before sunset. Therefore, it is appropriate to end the 
``O3 day'' with the 8-hour period beginning at 11:00 p.m. 
and ending at 7:00 a.m.
    In order to accommodate the above proposed approach to the hours 
considered in an ``O3 day'', the EPA is also proposing to 
modify the requirement for determining whether a daily maximum 8-hour 
average O3 concentration is valid for assessing compliance 
with the NAAQS (40 CFR part 50, Appendix P, section 2.1). The proposed 
Appendix U requires valid 8-hour averages for 13 of the 17 8-hour 
periods in a day in order to determine a valid daily maximum value. The 
requirement of 13 valid 8-hour averages was chosen because 13/17 is the 
smallest ratio greater than 75%, which is consistent with the long 
standing requirement of 75% data completeness for daily and annual 
NAAQS-related statistics. In addition, the EPA is proposing to maintain 
the existing provision allowing daily maximum 8-hour averages greater 
than the level of the NAAQS to be considered valid (40 CFR part 50, 
Appendix P, section 2.1). The EPA invites public comment on the merits 
of the proposed procedure for determining daily maximum 8-hour average 
O3 concentrations, and the merits of the proposed daily 
validity criteria.
    Finally, the EPA has included additional language in the proposed 
Appendix U codifying existing data handling procedures for the previous 
O3 NAAQS. First, the proposed Appendix U maintains the 
provision that hourly O3 concentrations approved under 40 
CFR 50.14 as having been affected by exceptional events are to be 
counted as missing or unavailable when calculating 8-hour averages, and 
that these concentrations are to be included when determining whether 
the daily validity criteria have been met for a given day. Effectively, 
this means that it is possible for an 8-hour period affected by 
exceptional events to lack sufficient data to determine an 8-hour 
average, yet the 8-hour period may still be counted toward meeting the 
daily validity criteria. Second, the proposed Appendix U maintains the 
existing practice of including monitored days outside of the 
O3 monitoring season when determining the annual fourth-
highest daily maximum value. Finally, the proposed Appendix U maintains 
the existing practice of using only daily maximum 8-hour average values 
for days where the daily validity criteria have been met when 
determining the annual fourth-highest daily maximum value.

D. Considerations for the Possibility of a Distinct Secondary Standard

    Given that the EPA is soliciting public comment on setting a 
distinct secondary O3 NAAQS based on the W126 index, the EPA 
is including a discussion on the data handling requirements for a 
distinct secondary standard. In the event that the Administrator 
decides to set a distinct secondary O3 standard based on the 
W126 index, the EPA will adopt data handling requirements for the 
secondary standard similar to those proposed during the reconsideration 
of the 2008 O3 NAAQS in 2010 (see 75 FR 3049-3052, January 
19, 2010).
    Two changes would need to be made to the data handling provisions 
for the secondary standard proposed in 2010 in order to provide 
consistency with what the EPA is proposing for the primary standard in 
Appendix U. First, the secondary standard design value (i.e. the 3-year 
average of the annual W126 index) would be truncated after the decimal 
point, instead of being rounded to the nearest whole number. Second, 
paragraph 4(c)(ii) would be modified to read:
    ``If one or more months during the ozone monitoring seasons of 
three consecutive years has less than 75% data completeness, the three 
years shall nevertheless be used in the computation of a valid design 
value for the site, if, after adjusting the monthly W126 index values 
for the months with less than 75% data completeness by a factor of 4/3, 
the resulting design value is greater than the level of the standard.''

E. Exceptional Events Information Submission Schedule

    States \228\ are responsible for identifying air quality data that 
they believe warrant special consideration, including data affected by 
exceptional events. States identify such data by flagging (making a 
notation in a designated field in the electronic data record) specific 
values in the AQS database. States flag the data and submit supporting 
documentation showing that the data have been affected by exceptional 
events if they wish the EPA to consider excluding the data in 
regulatory decisions, including determining whether or not an area is 
attaining the proposed revised O3 NAAQS, if a different 
standard is finalized.
---------------------------------------------------------------------------

    \228\ References to ``state'' are meant to include state, local 
and tribal agencies responsible for preparing and submitting 
exceptional event documentation as identified in the Exceptional 
Events Rule (72 FR 13560, March 22, 2007).
---------------------------------------------------------------------------

    All states and areas of Indian country that include areas that 
could exceed or contribute to an exceedance of any revised 
O3 NAAQS in a nearby area and could therefore be designated 
as nonattainment have the potential to be affected by this rulemaking. 
Therefore, this action applies to all states; to local air quality 
agencies to which a state has delegated relevant responsibilities for 
air quality management including air quality monitoring and data 
analysis; and to tribal air quality agencies, where appropriate.
    The ``Treatment of Data Influenced by Exceptional Events; Final 
Rule'' (72 FR 13560, March 22, 2007), known as the Exceptional Events 
Rule and codified at 40 CFR 50.1, 50.14 and 51.930, contains generic 
deadlines for a state to submit to the EPA specified information about 
exceptional events and associated air pollutant concentration data. 
Under this generic flagging schedule in 40 CFR 50.14(c)(2)(iii), a 
state must initially notify the EPA that data have been affected by an 
event by July 1 of the calendar year following the year in which the 
event occurred. This is done by flagging the data in AQS and providing 
an initial event description. According to the generic demonstration 
schedule in 40 CFR 50.14(c)(3)(i), the state must also, after notice 
and opportunity for public comment, submit a demonstration to justify 
any claim within 3 years after the quarter in which the data were 
collected. This section of the regulation also states that if the EPA 
must make a regulatory decision based on the data, the state must 
submit all information to the EPA no later than 1 year before the 
decision is to be made.
    These generic deadlines in the Exceptional Events Rule apply to 
data influencing redesignation efforts or other regulatory decisions 
made by the EPA after the EPA promulgates initial area designations for 
a new or revised NAAQS. However, these same generic deadlines in the 
Exceptional Events Rule may not work well with the timing of the 
initial area designation process and schedule under a new or revised 
NAAQS. Until the EPA promulgates the level and form of the NAAQS, a 
state does not know whether the criteria for excluding data (which are 
tied to the level and form of the NAAQS) were met for a given event. In 
some cases, the generic deadlines, especially the deadlines for 
flagging some relevant data, may have already passed by the time the 
EPA promulgates the new or revised NAAQS. This scheduling constraint 
could result in the EPA's being unable to consider whether an 
exceptional event has affected the data relied on for initial area 
designations and further result in an area being designated 
nonattainment based on data

[[Page 75354]]

that might have been excluded as having been influenced by an 
exceptional event if the EPA had been able to consider it during the 
designation process. For this reason, the EPA has historically 
undertaken rulemaking as part of the NAAQS promulgation process to 
adjust the generic deadlines in sections 50.14(c)(2)(iii) and 
50.14(c)(3)(i) of the Exceptional Events Rule to accommodate the 
initial area designation process and schedule under a new or revised 
NAAQS.
    The Exceptional Events Rule at section 50.14(c)(2)(vi) indicates 
``when EPA sets a NAAQS for a new pollutant or revises the NAAQS for an 
existing pollutant, it may revise or set a new schedule for flagging 
exceptional event data, providing initial data descriptions and 
providing detailed data documentation in AQS for the initial 
designations of areas for those NAAQS.'' The EPA intends to issue its 
final action promulgating a revised O3 NAAQS or determine 
that it is not necessary to do so in October 2015.
    The CAA provides requirements regarding the schedule for initial 
area designations. Section 107(d)(1) of the CAA states that, ``By such 
date as the Administrator may reasonably require, but not later than 1 
year after promulgation of a new or revised national ambient air 
quality standard for any pollutant under section 109, the Governor of 
each state shall . . . submit to the Administrator a list of all areas 
(or portions thereof) in the State, designating . . . '' those areas as 
nonattainment, attainment, or unclassifiable.\229\ No later than 120 
days prior to promulgating designations, the EPA is required to notify 
states of any intended modifications to their designation 
recommendations as the EPA may deem necessary. Section 107(d)(1)(B)(i) 
further provides, ``Upon promulgation or revision of a NAAQS, the 
Administrator shall promulgate the designations of all areas (or 
portions thereof) . . . as expeditiously as practicable, but in no case 
later than 2 years from the date of promulgation. Such period may be 
extended for up to one year in the event the Administrator has 
insufficient information to promulgate the designations.'' As described 
in more detail in section VII.C of this proposal, the EPA intends to 
complete designations for any revised O3 NAAQS promulgated 
in 2015 following the standard 2-year process. The EPA is required by 
Court Order to take final action for this O3 NAAQS review no 
later than October 1, 2015. The EPA does not intend to establish a date 
earlier than the 1 year submission period provided in CAA section 
107(d)(4); thus, state Governors (and tribes, if they choose) would be 
required to submit their initial designation recommendations for any 
revised NAAQS no later than 1 year after promulgation (i.e., by October 
1, 2016, if the EPA promulgates a revised NAAQS on October 1, 2015). 
State Governors (and tribes, if they choose) would likely use air 
quality data from the years 2013 to 2015 as the basis for their 
recommendations. The EPA would notify states and tribes of intended 
modifications to their recommendations no later than June 2017 and the 
EPA would promulgate initial designations for any revised NAAQS in 
October 2017. We anticipate that the EPA's notification of intended 
modifications and the final designations would be based on air quality 
data from the years 2014 to 2016, because air quality data from 2016 is 
required to be certified by the state no later than May 1, 2017, and 
thus would be available for consideration for purposes of initial area 
designations by October 2017.
---------------------------------------------------------------------------

    \229\ While the CAA says ``designating'' with respect to the 
Governor's letter, in the full context of the CAA section it is 
clear that the Governor actually makes a recommendation.
---------------------------------------------------------------------------

    As indicated above, and as explained in additional detail in 
section VII.C of this preamble, section 107(d)(1)(B) of the CAA allows 
the Administrator to extend the designations schedule for up to 1 year 
in the event the Administrator has insufficient information to 
promulgate the designations for a newly promulgated NAAQS. If the EPA 
were to determine that it is necessary to extend the schedule for 
designating areas for a revised O3 NAAQS (promulgation in 
October 2015) from 2017 to 2018, then it is possible that air quality 
data from 2017 could be considered for designations. This could raise 
concerns about whether influences from exceptional events in 2017 could 
be investigated and submitted by the state and reviewed by the EPA in 
sufficient time for consideration during the designation process.
    For purposes of initial designations, where the EPA considers the 
most recent air quality monitoring data in a relatively quick 
timeframe, the EPA is proposing revisions to the flagging and data 
submission schedule in 40 CFR 50.14 applicable to the initial area 
designations process. The proposed exceptional events schedule is based 
on following a standard 2 year designation process. However, because 
the CAA also provides for a 3-year process in the event the 
Administrator has insufficient information to promulgate the 
designations for a newly promulgated NAAQS within 2 years and provides 
for the promulgation of designations as ``expeditiously as 
practicable,'' which could include accelerating the designations 
schedule ahead of the 2-year schedule, the proposed exceptional event 
schedule also includes provisions for both an accelerated designations 
process and a 3-year process. If the EPA were to pursue a designations 
schedule other than a 2- or 3-year process, the EPA would notify the 
state Governors of the intended date for final designations through 
notification letters, guidance and/or Federal Register notices.
    These proposed revised exceptional event scheduling provisions 
would, if promulgated, apply to submission of information supporting 
claimed exceptional events affecting pollutant data for initial area 
designations under any new or revised NAAQS, including any revised 
O3 NAAQS promulgated in October 2015. The general data 
flagging deadlines in the Exceptional Events Rule at 40 CFR 
50.14(c)(2)(iii) and the general schedule for submission of 
demonstrations at 40 CFR 50.14(c)(3)(i) would continue to apply to 
regulatory decisions other than those related to the initial area 
designations process under a new or revised NAAQS. The EPA believes 
these proposed revisions to the exceptional events scheduling 
provisions will provide adequate time for states to determine whether 
data have been influenced by an exceptional event, to notify the EPA by 
flagging the relevant data and providing an initial description in AQS, 
and to submit documentation to support claims for exceptional events.
    Therefore, using the authority provided in CAA section 319(b)(2), 
the EPA proposes to modify the schedule for data flagging and 
submission of demonstrations for exceptional events data considered for 
initial area designations by replacing the deadlines and information in 
Table 1 in 40 CFR 50.14 with the deadlines and information presented in 
Table 9. The EPA is also providing Table 10 to illustrate how the 
proposed schedule might apply to the designations process for any 
revised O3 NAAQS promulgated in October 2015 or to 
designations processes for future new or revised NAAQS. The EPA invites 
comment on these proposed changes, shown in Table 9, to the exceptional 
event data flagging and documentation submission deadlines for future 
new or revised

[[Page 75355]]

NAAQS, including any revised O3 NAAQS promulgated in 2015.

      Table 9--Proposed Schedule for Exceptional Event Flagging and
      Documentation Submission for Data To Be Used in Initial Area
                              Designations
------------------------------------------------------------------------
                                                      Exceptional event
        Exceptional event/regulatory action           deadline schedule
                                                             \d\
------------------------------------------------------------------------
Exceptional event data flagging and initial         If state and tribal
 description deadline for data years 1, 2 and 3      initial designation
 \a\.                                                recommendations for
                                                     the new/revised
                                                     NAAQS are due
                                                     August through
                                                     January, then the
                                                     flagging and
                                                     initial description
                                                     deadline will be
                                                     the July 1 prior to
                                                     the recommendation
                                                     deadline. If state
                                                     and tribal
                                                     recommendations for
                                                     the new/revised
                                                     NAAQS are due
                                                     February through
                                                     July, then the
                                                     flagging and
                                                     initial description
                                                     deadline will be
                                                     the January 1 prior
                                                     to the
                                                     recommendation
                                                     deadline.
Exceptional event demonstration submittal deadline  No later than the
 for data years 1, 2 and 3 \a\.                      date that state and
                                                     tribal
                                                     recommendations are
                                                     due to EPA.
Exceptional event data flagging, initial            By the last day of
 description, and exceptional event demonstration    the month that is 1
 submittal deadline for data year 4 \b\ and          year and 7 months
 potential data year 5 \c\.                          after promulgation
                                                     of a new or revised
                                                     NAAQS, unless
                                                     either option a or
                                                     b applies.
                                                    a. If the EPA
                                                     follows a 3-year
                                                     designation
                                                     schedule, the
                                                     deadline is 2 years
                                                     and 7 months after
                                                     promulgation of a
                                                     new or revised
                                                     NAAQS.
                                                    b. If the EPA
                                                     notifies the state/
                                                     tribe via Federal
                                                     Register notice,
                                                     letter or guidance
                                                     that it intends to
                                                     complete the
                                                     initial area
                                                     designations
                                                     process according
                                                     to a schedule other
                                                     than a 2-year or 3-
                                                     year timeline, the
                                                     deadline is 5
                                                     months prior to the
                                                     date specified for
                                                     final designations
                                                     decisions in such
                                                     EPA notification.
------------------------------------------------------------------------
\a\ Where data years 1, 2, and 3 are those years expected to be
  considered in state and tribal recommendations.
\b\ Where data year 4 is the additional year of data that the EPA may
  consider when it makes final area designations for the new/revised
  NAAQS under the standard designations schedule.
\c\ Where data year 5 is the additional year of data that the EPA may
  consider when it makes final area designations for the new/revised
  NAAQS under an extended designations schedule.
\d\ The date by which air agencies must certify their ambient air
  quality monitoring data in AQS is annually on May 1 of the year
  following the year of data collection. The EPA cannot require air
  agencies to certify data prior to this date. In some cases, however,
  air agencies may choose to certify a prior year's data in advance of
  May 1 of the following year, particularly if the EPA has indicated its
  intent to promulgate final designations in the months of May, June,
  July or August. Exceptional event flagging, initial description, and
  demonstration deadlines for ``early certified'' data will follow the
  deadlines for ``year 4'' and ``year 5'' data.


[[Page 75356]]

[GRAPHIC] [TIFF OMITTED] TP17DE14.000


[[Page 75357]]

[GRAPHIC] [TIFF OMITTED] TP17DE14.001

    Additionally, in conjunction with proposing exceptional event 
schedules related to implementing any revised O3 standards, 
the EPA is also proposing to remove obsolete regulatory language 
associated with exceptional event

[[Page 75358]]

schedules for historical standards. The EPA expects to propose 
additional revisions to the Exceptional Events Rule in a future notice 
and comment rulemaking effort and will solicit public comment on other, 
non-schedule related, aspects of the Exceptional Events Rule at that 
time.

VI. Ambient Monitoring Related to Proposed O3 Standards

A. Background

    The EPA is proposing to: Revise the state-by-state O3 
monitoring seasons; revise the PAMS monitoring requirements; revise the 
FRM for measuring O3; and revise the FEM testing 
requirements. The EPA is also proposing to make additional minor 
changes to the FEM testing requirements for NO2 and 
particulate matter in part 53 as discussed below.
    The EPA is proposing to extend the length of the required 
O3 monitoring season in some states to be appropriate for 
the O3 NAAQS revision finalized in 2008, as well as a final 
revised O3 standard, if a revision is finalized in 2015.
    The EPA is proposing to make changes to the PAMS monitoring 
requirements in 40 CFR part 58, Appendix D section 5. Section VI.C of 
this preamble provides background on the current PAMS monitoring 
requirements, recent efforts to re-evaluate the current PAMS 
requirements, and a summary of the proposed PAMS requirement revisions.
    The EPA is proposing to revise the FRM to establish a new, 
additional technique for measuring O3 in the ambient air. 
This new technique is based on nitric oxide-chemiluminescence (NO-CL) 
methodology. Because of the similarity of this new chemiluminescence 
technique to the existing ethylene-chemiluminescence (ET-CL) 
methodology, the EPA proposes that it be incorporated into the existing 
O3 FRM, using the same calibration procedure. Appendix D of 
40 CFR part 50 would be revised to include both the original ET-CL as 
well as the new NO-CL methodology. A minor change is proposed to the 
existing O3 FRM calibration procedure, which would be 
applicable to both of the chemiluminescence FRM methodologies. The 
proposed change in section 4.5.2.3 of the calibration procedure in 
appendix D provides for more flexibility in the range of the linearity 
test.
    The only substantial changes proposed to the requirements of 40 CFR 
part 53 are in Tables B-1 and B-3 of subpart B. Table B-1 has been 
updated in recent years with regard to FRM and FEM methods for 
SO2 (74 FR 64877, December 8, 2009) and CO (76 FR 54294, 
August 31, 2011) to be more consistent with current analyzer 
performance capabilities. Similar changes to Table B-1 are proposed 
here for methods for O3. Modest changes to Table B-3 would 
add new interferent test concentrations specifically for NO-CL 
analyzers, adding a test for NO2. Also, the table would 
clarify that the existing test concentrations apply to ET-CL 
O3 analyzers.
    In addition, the EPA is making minor additional changes to Part 53 
including: conforming changes to the FEM testing requirements in Table 
B-1 and Figure B-5 for NO2; extending the period of time for 
the Administrator to take action on a request for modification of a FRM 
or FEM from 30 days to 90 days; and removing an obsolete provision for 
manufacturers to submit Product Manufacturing Checklists for certain PM 
monitors.

B. Revisions to the Length of the Required O3 Monitoring 
Seasons

    Unlike the ambient monitoring requirements for other criteria 
pollutants that mandate year-round monitoring, O3 monitoring 
is only required during the seasons of the year that are conducive to 
O3 formation. These seasons vary in length from place to 
place as the conditions conducive to the formation of O3 
(i.e., seasonally-dependent factors such as ambient temperature, 
strength of solar insolation, and length of day) differ by 
location.\230\ In some locations, conditions conducive to O3 
formation are limited to the summer months of the year. For example, in 
states with colder climates such as Montana and South Dakota, the 
currently required O3 monitoring season is four months long. 
However, in other states with warmer climates such as California, 
Nevada, and Arizona, the currently required O3 monitoring 
season is year-round.\231\
---------------------------------------------------------------------------

    \230\ See 40 CFR part 58 Appendix D, section 4.1, Table D-3 for 
a table of required O3 seasons.
    \231\ Certain states, such as California and Arizona, have 
approved shorter seasons for a subset of O3 sites, based 
on Regional Administrator review and approval (see 40 CFR part 58, 
Appendix D, section 4.1(i) for the waiver authority).
---------------------------------------------------------------------------

    Based on the O3 NAAQS revision that was finalized in 
2008, as well as the proposed NAAQS revisions discussed in this 
rulemaking, the EPA has determined that lengthening the O3 
monitoring seasons may be appropriate. Ambient O3 
concentrations could approach or exceed the level of the 2008 NAAQS, as 
well as the proposed NAAQS, more frequently and during more months of 
the year. The EPA has done an analysis to address the issue of whether 
extensions of currently required monitoring seasons are appropriate 
(Rice, 2014). In this analysis, we determined the number of days where 
one or more monitors had a daily maximum 8-hour O3 average 
equal to or above 0.060 ppm in the months outside the currently-
required state O3 monitoring season using data from monitors 
that collected O3 data year-round in 2010-2013.\232\ We find 
that this level, taking into consideration reasonable uncertainty, 
serves as an appropriate indicator of ambient conditions that may be 
conducive to the formation of O3 concentrations that 
approach or exceed the 2008 NAAQS or the proposed 8-hour average range 
of 0.065 to 0.070 ppm. Although we refer to these days as ``exceedance 
days'' in the analysis, this 0.060 ppm threshold is simply a 
conservative benchmark that is below the levels proposed for the 
revised NAAQS. Proposals for revising each state's required monitoring 
season are based on the observed ``exceedance days'' where the 8-hour 
average daily maximum was >=0.060 ppm in and surrounding the state. The 
EPA considered a number of factors including out-of-season ``exceedance 
days'' either before or after the current O3 monitoring 
season, the pattern of ``exceedance days'' in the out-of-season months, 
and regional consistency. We note that seasonal O3 patterns 
vary year-to-year due primarily to highly variable meteorological 
conditions conducive to the formation of early or late season elevated 
O3 concentrations in some years and not others. The EPA 
believes it is important that O3 monitors operate during all 
periods when there is a reasonable possibility of ambient levels 
approaching the level of the proposed NAAQS.
---------------------------------------------------------------------------

    \232\ Approximately 800 O3 monitors are currently 
operated year-round, representing greater than 50% of the total 
O3 monitoring network of about 1500 monitors. They 
include monitors that are mandated to operate year-round due to the 
required O3 season and other monitors that are 
voluntarily operated year-round by states and other organizations 
including EPA-operated monitors at Clean Air Status and Trends 
Network (CASTNET) sites.
---------------------------------------------------------------------------

    The EPA reviewed the year-round, O3 data for 2010 
through 2013. A year-round monitor was identified as ``year-round'' if 
it had at least 20 daily observations in all 12 months, for at least 1 
year of the 4 year period. During the 2010-2013 data period, all states 
operated a portion of their monitoring network outside of their 
required O3 monitoring season and reported the data to the 
EPA Air Quality System (AQS).

[[Page 75359]]

The EPA's analysis found the frequency of observed ``exceedance days'' 
of daily maximum 8-hour average O3 readings of >=0.060 ppm 
to be quite high in several states across the country in months outside 
of the currently required monitoring season. A total of 43 states 
experienced at least one ``exceedance day'' outside of their current 
O3 season; 21 states had ``exceedance days'' only before the 
required monitoring season; 4 states had ``exceedance days'' only after 
the required monitoring season; and 18 states had ``exceedance days'' 
both before and after the required monitoring season. In some cases, 
the frequency of ``exceedance days'' before the current O3 
season was high, with four states (South Dakota, Colorado, Wyoming, and 
Utah) experiencing between 31 and 230 out-of-season ``exceedance days'' 
from 2010 to 2013 at monitors operating year-round.
    Basing O3 monitoring season requirements on the goal of 
ensuring monitoring when ambient O3 levels approach or 
exceed the level of the proposed NAAQS supports established monitoring 
network objectives described in Appendix D of Part 58, including the 
requirement to provide air pollution data to the general public in a 
timely manner \233\ and to support comparisons of an area's air 
pollution levels against the NAAQS. The EPA believes that frequency of 
``exceedance days'' in which daily maximum of 8-hour O3 
levels are observed to be greater than or equal to a threshold level of 
0.060 ppm in months outside the currently required O3 
monitoring season supports the proposed lengthening of the 
O3 monitoring season requirements for certain states.
---------------------------------------------------------------------------

    \233\ Public reporting requirements are detailed in 40 CFR part 
58 Appendix G, Uniform Air Quality Index (AQI) and Daily Reporting.
---------------------------------------------------------------------------

    The operation of O3 monitors during periods of time when 
ambient levels approach or exceed the level of the proposed NAAQS 
ensures that persons unusually sensitive to O3 are alerted 
to potential levels of health concern allowing them to take 
precautionary measures. The majority of O3 monitors in the 
U.S. report to AIRNOW,\234\ as well as to state-operated Web sites and 
automated phone reporting systems. These programs support many 
objectives including real-time air quality reporting to the public, 
O3 forecasting programs, and the verification of real-time 
air quality forecast models.
---------------------------------------------------------------------------

    \234\ See http://airnow.gov/.
---------------------------------------------------------------------------

    The specific proposed changes to the required state O3 
monitoring seasons are detailed in the proposed changes to Table D-3 of 
40 CFR part 58, Appendix D (O3 Monitoring Season by State). 
Although 43 states had at least one exceedance day outside the current 
monitoring season, changes are proposed for only 33 of those states. 
These proposed changes would entail an increase of 1 month for 23 
states (Connecticut, Delaware, District of Columbia, Idaho, Illinois, 
Iowa, Kansas, Maryland, Massachusetts, Minnesota, Missouri, Nebraska, 
New Hampshire, New Jersey, New York, North Carolina, Ohio, 
Pennsylvania, Rhode Island, South Carolina, Northern Texas, Virginia, 
and West Virginia), an increase of one and one half months for 
Wisconsin, an increase of two months for four states (Indiana, 
Michigan, Montana, and North Dakota), an increase of four months for 
Florida and South Dakota, an increase of five months for Colorado, and 
an increase of seven months for Utah. For Wyoming, we are proposing to 
add three months at the beginning of the season and remove one month at 
the end of the season, resulting in a net increase of two months. Ozone 
season requirements are currently split by Air Quality Control Region 
(AQCR) in Louisiana and Texas. Included in the state-by-state 
accounting is the proposal to lengthen the required season in the 
northern part of Texas (AQCR 022, 210, 211, 212, 215, 217, and 218) by 
one month. Southern Texas O3 monitors in AQCRs 106, 153, 
213, 214, and 216 would remain on a year-round schedule. In some states 
with limited available data and few exceedance days outside the current 
season, proposed changes were made by considering regional consistency 
and using supporting information from the surrounding states; these 
changes were all minor, involving the proposed addition of 1 month to 
the current required season in Iowa, Missouri, and West Virginia.
    The EPA solicits comment on the proposed changes to the required 
O3 monitoring seasons. We note that EPA Regional 
Administrators have previously approved certain deviations from the 
required O3 monitoring seasons through rulemakings (64 FR 
3028, January 20, 1999; 67 FR 57332, September 10, 2002; and 69 FR 
52836, August 30, 2004). The current ambient monitoring rule, in 
paragraph 4.1(i) of 40 CFR part 58 Appendix D (71 FR 61319, October 17, 
2006), allows the EPA Regional Administrators to approve changes to the 
O3 monitoring season without rulemaking. The EPA is 
retaining the rule language allowing such deviations from the required 
O3 monitoring seasons in the proposed revision to paragraph 
4.1(i) of 40 CFR part 58, Appendix D. The proposed changes to 
O3 monitoring season requirements, if finalized, will revoke 
previous Regional Administrator-granted waiver approvals. As 
appropriate, monitoring agencies could seek new waivers. Post-final 
rule requests submitted along with relevant supporting information by 
states for monitoring season waivers from the revised requirements will 
be reviewed by Regional Administrators using, at a minimum, occurrences 
of the moderate AQI level, the frequency of out-of-season O3 
NAAQS exceedances, and regional consistency. Any deviations based on 
the Regional Administrator's waiver of requirements must be described 
in the state's annual monitoring network plan and updated in the AQS.
    Current regulations permit O3 monitors located at NCore 
multi-pollutant stations to be counted toward meeting minimum network 
monitoring requirements. The NCore network requirements were 
promulgated in the October 17, 2006 (71 FR 61317) revisions to ambient 
monitoring regulations in order to build a long-term, nationwide 
network that supports multiple objectives including air quality trends 
analyses, model evaluation, ecosystem studies, and assessment of 
transport between urban and rural areas. In the 2006 rulemaking, the 
EPA did not propose a different O3 monitoring season for 
NCore stations.
    NCore stations are required to operate a full suite of gaseous and 
particulate matter monitors as well as basic meteorology to support the 
objectives. Given the potential value of NCore data to support year-
round scientific studies, the EPA believes that it is appropriate to 
require O3 monitors at NCore stations to be operated year-
round. Accordingly, the EPA proposes that the required monitoring 
season for NCore stations be January through December regardless of the 
length of the required O3 monitoring season for the 
remainder of the SLAMS (State and Local Air Monitoring Stations) 
monitors within a state.
    The EPA has estimated the cost of the proposed changes to the 
O3 seasons. The results are detailed in the EPA ICR #2313.03 
and summarized in Section VIII.B., ``Paperwork Reduction Act''. The 
estimated cost is $1,668,433 which is about 7% of the total average 
annual cost of $24,115,182 for the national O3 monitoring 
network. This estimate is based on the current requirements in 40 CFR 
part 58 and the proposed requirements in this rule. We note however, 
that greater than 50% of the monitors are currently operated year-round 
due to existing requirements, as

[[Page 75360]]

well as other monitors that are voluntarily operated year-round by the 
states. Taking into consideration the number of year-round 
O3 monitors that are operated due to existing requirements, 
as well as on a discretionary basis by states, the incremental cost of 
these proposed changes is reduced from $1,668,433 to approximately 
$230,000, which is less than 1% of the total average annual cost of the 
national O3 monitoring network.
    Considering the timing of this proposal and the final rulemaking 
(court ordered deadline of October 1, 2015) and associated burden on 
state/local monitoring agencies, we propose that implementation of the 
revised O3 seasons become effective at SLAMS (including 
NCore sites) on January 1, 2017. The EPA is proposing to add paragraph 
58.13 (g) of 40 CFR part 58 to require that monitors operating under 
the requirements of section 4.1 of 40 CFR part 58, Appendix D operate 
on the applicable required O3 monitoring seasons effective 
January 1, 2017 as listed in Table D-3 of appendix D to this part. We 
solicit comment on whether the revised seasons could be implemented 
beginning January 1, 2016 for all monitors or for a subset of monitors, 
such as those currently operating year-round or on a schedule that 
corresponds to the proposed O3 season. If we determine, 
based on any such comments that implementation could occur earlier in 
such cases, we could proceed to final action requiring earlier 
implementation.

C. Revisions to the Photochemical Assessment Monitoring Stations (PAMS)

    Section 182 (c)(1) of the CAA required the EPA to promulgate rules 
for enhanced monitoring of O3, oxides of nitrogen, and VOCs 
for nonattainment areas classified as serious (or above) to obtain more 
comprehensive and representative data on O3 air pollution. 
In addition, Section 185B of the CAA required the EPA to work with the 
National Academy of Sciences (NAS) to conduct a study on the role of 
O3 precursors in tropospheric O3 formation and 
control. In 1992, the NAS issued the report entitled, ``Rethinking the 
Ozone Problem in Urban and Regional Air Pollution'', (NAS, 1991).
    In response to the CAA requirements and the recommendations of the 
NAS report, on February 12, 1993 (58 FR 8452), the EPA revised the 
ambient air quality surveillance regulations to require PAMS in each 
O3 nonattainment area classified as serious, severe, or 
extreme (``PAMS areas'').\235\ As noted in EPA's Technical Assistance 
Document (TAD) for Sampling and Analysis of Ozone Precursors (U.S. EPA, 
1998), the objectives of the PAMS program are to: (1) Provide a 
speciated ambient air database which is both representative and useful 
in evaluating control strategies and understanding the mechanisms of 
pollutant transport by ascertaining ambient profiles and distinguishing 
among various individual VOCs; (2) provide local, current 
meteorological and ambient data to serve as initial and boundary 
condition information for photochemical grid models; (3) provide a 
representative, speciated ambient air database which is characteristic 
of source emission impacts to be used in analyzing emissions inventory 
issues and corroborating progress toward attainment; (4) provide 
ambient data measurements which would allow later preparation of 
unadjusted and adjusted pollutant trends reports; (5) provide 
additional measurements of selected criteria pollutants for attainment/
nonattainment decisions and to construct NAAQS maintenance plans; and 
(6) provide additional measurements of selected criteria and non-
criteria pollutants to be used for evaluating population exposure to 
air toxics as well as criteria pollutants.
---------------------------------------------------------------------------

    \235\ Additional information on the O3 designation 
process can be obtained at EPA's O3 designations Web page 
at http://www.epa.gov/groundlevelozone/designations/.
---------------------------------------------------------------------------

    The original PAMS requirements called for two to five sites per 
area depending on the area's population. Four types of PAMS sites were 
identified including upwind (Type 1), maximum precursor emission rate 
(Type 2), maximum O3 (Type 3), and extreme downwind (Type 4) 
sites. Each PAMS site was required to measure O3, NO, 
NO2, speciated VOCs, selected carbonyl compounds, and 
selected meteorological parameters. In addition, upper air 
meteorological monitoring was required at one site in each PAMS area.
    In the October 17, 2006 monitoring rule (71 FR 61267), the EPA 
revised the PAMS requirements to only require two PAMS sites per PAMS 
area.\236\ The intent of the revision was to ``allow PAMS monitoring to 
be more customized to local data needs rather than meeting so many 
specific requirements common to all subject O3 nonattainment 
areas; the PAMS changes would also give states the flexibility to 
reduce the overall size of their PAMS programs--within limits--and to 
use the associated resources for other types of monitoring they 
consider more useful.'' In addition to reducing the number of required 
sites per PAMS area, the 2006 revisions also limited the requirement 
for carbonyl measurements (specifically formaldehyde, acetaldehyde, and 
acetone) to areas classified as serious or above for the 8-hour 
O3 standard. This change was made in recognition of carbonyl 
sampling issues which were believed to cause significant uncertainty in 
the measured concentrations.
---------------------------------------------------------------------------

    \236\ One Type 2 site and either a Type 1 or a Type 3 site are 
currently required.
---------------------------------------------------------------------------

    Twenty-two areas were classified as serious or above O3 
nonattainment at the time the PAMS requirements were promulgated in 
1993. On July 18, 1997 (62 FR 38856), the EPA revised the averaging 
time of the O3 NAAQS from a 1-hour averaging period to an 8-
hour averaging period. On June 15, 2005 (70 FR 44470), the EPA revoked 
the 1-hour standard in most areas of the country; however, PAMS 
requirements were identified as requirements that had to be retained in 
the anti-backsliding provisions\237\ included in that action. 
Therefore, PAMS requirements continue to be applicable to areas that 
were classified as serious or above nonattainment for the 1-hour 
O3 standard as of June 15, 2004. Currently, 25 areas are 
subject to the PAMS requirements with a total of 75 sites. As will be 
discussed in detail later, the current PAMS sites are concentrated in 
the North East and California with relatively limited coverage in the 
rest of the country (Cavender, 2014).
---------------------------------------------------------------------------

    \237\ Refer to 40 CFR part 51.905
---------------------------------------------------------------------------

    As discussed above, the first PAMS sites began operation in 1994, 
and have been in operation for over 20 years. Many changes have 
occurred during that time that have changed the O3 problem 
in the U.S. as well as our understanding of it. The O3 
standard has been revised multiple times since the PAMS program was 
first implemented. On July 18, 1997, the EPA revised the O3 
NAAQS to a level of 0.08 ppm, with a form based on the 3-year average 
of the annual fourth-highest daily maximum 8-hour average O3 
concentration. On March 28, 2008 (73 FR 16436), the EPA revised the 
O3 standard to a level of 0.075 ppm, with a form based on 
the 3-year average of the annual fourth-highest daily maximum 8-hour 
average O3 concentration. These changes in the level and 
form of the O3 NAAQS, along with notable decreases in 
O3 levels in most parts of the U.S., have changed the 
landscape of the O3 problem in the U.S. At the time of the 
first round of designations for the 8-hour standard

[[Page 75361]]

(June 15, 2005), only five areas were classified as serious or above 
for the 8-hour standard as compared to 22 areas that were classified as 
serious or above for the 1-hour standard.\238\ While the number of 
serious and above areas decreased, the number of nonattainment areas 
remained nearly the same. In addition, much of the equipment used at 
PAMS sites is old and in need of replacement. New technologies have 
been developed since the inception of the PAMS program that should be 
considered for use in the network. For these reasons, the EPA 
determined that it would be appropriate to re-evaluate the PAMS program 
and associated requirements in light of current O3 issues.
---------------------------------------------------------------------------

    \238\ PAMS requirements continue to apply to all areas 
classified as serious or above as of June 15, 2005 due to anti-
backsliding provisions of 40 CFR 51.905.
---------------------------------------------------------------------------

    In 2011 (U.S. EPA, 2011c), the EPA initiated an effort to re-
evaluate the PAMS requirements in light of changes in the needs of PAMS 
data users and the improvements in monitoring technology. The EPA 
consulted with CASAC's, Air Monitoring and Methods Subcommittee (AMMS) 
to seek advice on potential revisions to the technical and regulatory 
aspects of the PAMS program; including changes to required measurements 
and associated network design requirements. The EPA also requested 
advice on appropriate technology, sampling frequency, and overall 
program objectives in the context of the most recently revised 
O3 NAAQS and changes to atmospheric chemistry that have 
occurred over the past 10-15 years in the significantly impacted areas. 
The CASAC AMMS met on May 16 and May 17, 2011, and provided a report 
with their advice on the PAMS program on September 28, 2011 (U.S. EPA, 
2011c). In addition, the EPA met multiple times with the National 
Association of Clean Air Agencies (NACAA) Monitoring Steering Committee 
(MSC) to seek advice on the PAMS program. The MSC includes monitoring 
experts from various state and local agencies actively engaged in 
ambient air monitoring and many members of the MSC have direct 
experience with running PAMS sites. As discussed in more detail in the 
appropriate sections below, the EPA took into consideration advice from 
the CASAC AMMS and the MSC in proposing changes to the PAMS 
requirements.
    Based on the findings of the PAMS evaluation and the consultations 
with the CASAC AMMS and NACAA MSC, the EPA is proposing to revise 
several aspects of the PAMS monitoring requirements including changes 
in 1) network design, 2) VOC sampling, 3) carbonyl sampling, 4) 
nitrogen oxides sampling, and 5) upper air meteorology measurements. 
The following paragraphs describe the changes being proposed including 
the rationale for the proposed changes. Timing and other implementation 
issues associated with these proposed changes are discussed at the end 
of this section.
1. Network Design
    As discussed above, the current PAMS network design calls for two 
sites (a Type 2, and a Type 1 or Type 3) per PAMS area. In their report 
(U.S EPA, 2011c), the CASAC AMMS found ``that the existing uniform 
national network design model for PAMS is outdated and too resource 
intensive,'' and recommended ``that greater flexibility for network 
design and implementation of the PAMS program be transferred to state 
and local monitoring agencies to allow monitoring, research and data 
analysis to be better tailored to the specific needs of each 
O3 problem area.'' While stating that the current PAMS 
objectives were appropriate, the AMMS report also stated that 
``objectives may need to be revised to include both a national and 
regional focus because national objectives may be different from 
regional objectives.'' The NACAA MSC also advised the EPA that the 
existing PAMS requirements were too prescriptive and may hinder state 
efforts to collect other types of data that were more useful in 
understanding their local O3 problems.
    The EPA agrees with CASAC that the PAMS objectives include both 
local and national objectives, and believes that the current PAMS 
network design is no longer suited for meeting either sets of 
objectives. As part of the PAMS evaluation, it was determined that at 
the national level the primary use of the PAMS data has been to 
evaluate photochemical model performance. Due to the locations of the 
current PAMS areas and the current network design, existing PAMS sites 
are clustered along the northeast and west coasts leading to 
significant redundancy in these areas and very limited coverage 
throughout the remainder of the country (Cavender, 2014). The resulting 
uneven spatial coverage greatly limits the value of the PAMS data for 
evaluation of model performance. CASAC (U.S. EPA, 2011c) noted the 
spatial coverage issue and advised that EPA should consider requiring 
PAMS measurements in areas in addition to ``areas classified as serious 
and above for the O3 NAAQS to improve spatial coverage.'' 
The EPA also agrees with CASAC and the NACAA that the PAMS requirements 
should be revised to provide monitoring agencies greater flexibility in 
meeting local objectives.
    The EPA is proposing changes to the network design requirements 
that we believe will better serve both national and local objectives. 
The EPA is proposing a two part network design. The first part of the 
design includes a network of fixed sites (required PAMS sites) intended 
to support O3 model development and the tracking of trends 
of important O3 precursor concentrations. The second part of 
the network design includes monitoring agency directed Enhanced 
Monitoring Plans which allow monitoring agencies the needed flexibility 
to implement additional monitoring capabilities to suit the needs of 
their area.
    The EPA considered a number of options to revise the fixed site 
portion of the network design (Cavender, 2014). An initial option 
considered was to require all NCore sites to make PAMS measurements 
regardless of O3 attainment status. This option would take 
advantage of the existing NCore infrastructure and would result in a 
relatively wide geographic distribution of sites. However, it was noted 
that this option would place some PAMS measurements in areas with 
relatively low O3 levels and would also result in a network 
of approximately 80 required sites, which would strain existing 
resources with a somewhat larger network than the current situation, 
and could make it difficult to also implement the desired state-
directed Enhanced Monitoring Plans. The second option considered was to 
require only NCore sites in O3 nonattainment areas to 
collect PAMS measurements. This option would provide the benefits 
discussed above for collecting PAMS measurements at existing NCore 
sites. This option would also reduce the total number of sites required 
and focus efforts in areas with higher, non-attaining, levels of 
O3. The final option considered would add a population limit 
in addition to the consideration of O3 attainment status at 
NCore sites. An illustration of this example would be a PAMS 
requirement that applied only to NCore sites in O3 
nonattainment areas with a population greater than a given threshold, 
for example, Core Based Statistical Areas with 1,000,000 people or 
more. This approach would continue the current practice of focusing 
PAMS resources in areas of elevated O3 readings with an 
additional consideration that measurements in these larger population 
areas would be

[[Page 75362]]

sufficient to characterize O3 formation on a national basis.
    After considering the above options as well as the comments of 
CASAC and NACAA, the EPA believes that an approach focused primarily on 
the use of the existing NCore sites in O3 nonattainment 
areas provides an appropriate balance to the consideration of 
O3 levels as well as population, noting that a majority of 
NCore sites are already located in the larger urban areas of each 
state. Accordingly, the EPA is proposing to require PAMS measurements 
at any existing NCore site in an O3 nonattainment area 
(either based on the 2008 O3 NAAQS or the 2015 O3 
NAAQS if finalized) in lieu of the current PAMS network design 
requirements.\239\ The NCore network is a multi-pollutant monitoring 
network consisting of 80 sites (63 urban, 17 rural) and is intended to 
support multiple air quality objectives including the development and 
model evaluation of photochemical models (including both 
PM2.5 and O3 models), and the tracking of 
regional precursor trends. NCore sites are sited in typical 
neighborhood scale locations which are more suitable than source 
impacted locations for evaluation of grid models typical of current 
photochemical models and tracking of trends in pre-cursor 
concentrations. The EPA believes NCore sites are well suited for 
O3 model development and evaluation.
---------------------------------------------------------------------------

    \239\ Although enhanced monitoring for O3, oxides of 
nitrogen, and VOCs is specifically required for areas classified at 
least serious for the O3 NAAQS by section 182(c)(1) of 
the CAA, the EPA has concluded that requiring enhanced monitoring 
for all O3 nonattainment areas is appropriate for the 
purposes of monitoring ambient air quality and better understanding 
O3 pollution.
---------------------------------------------------------------------------

    The proposal to require PAMS measurements at existing NCore sites 
in O3 nonattainment areas would replace the existing PAMS 
network design.\240\ This change would keep roughly the same number of 
required PAMS sites while improving spatial coverage (Cavender, 2014). 
Based on the range of the O3 NAAQS being proposed today and 
current O3 design value estimates (based on 2011-2013 air 
quality data), the number of required sites is estimated to be between 
48 and 65, which compares to 50 currently required sites, and 75 
currently operating sites. Potential redundancy in the existing network 
would be reduced while important network coverage in the Southeast and 
Midwest would be added. The improved spatial coverage will also improve 
the EPA's ability to track trends in precursor concentrations 
regionally. The EPA notes that in limited situations, an O3 
nonattainment area may not have an NCore site and in those cases, the 
area would only be subject to the requirement for an Enhanced 
Monitoring Plan as discussed in more detail below. The EPA believes 
that the network coverage provided by existing NCore sites in 
O3 nonattainment areas would be adequate for the national 
PAMS objectives discussed above, and that requiring PAMS sites, in 
addition to Enhanced Monitoring Plans, in those O3 
nonattainment areas without NCore sites would not substantially improve 
the network coverage.
---------------------------------------------------------------------------

    \240\ While the EPA is proposing to replace the multi-site 
design, monitoring agencies would be encouraged to identify the type 
of PAMS site the NCore site represents. In most cases, NCore sites 
would likely be classified as either a Type 2 or Type 3 site. In 
limited situations, rural NCore sites might be subject to these 
proposed requirements, in which case, these sites would likely be 
either Type 1 or Type 4 sites.
---------------------------------------------------------------------------

    The EPA notes that the proposed network design change would provide 
significant cost efficiencies. By adding PAMS measurements to existing 
NCore sites, the PAMS network would be taking advantage of existing 
infrastructure and measurements currently being collected at NCore 
sites. NCore sites already have the larger, climate-controlled shelters 
that are necessary to operate the automated gas chromatographs (``auto-
GCs'') used to collect speciated VOCs. In addition, existing NCore 
sites currently collect data on many of the required PAMS measurements 
including O3, CO, total reactive nitrogen (NOy), 
and meteorological measurements including wind speed and direction, 
temperature, and relative humidity.
    While the EPA believes these proposed changes will result in fixed 
network cost savings for the overall network on a national basis, 
individual monitoring agencies may see either an increase or a decrease 
in burden as a result of these proposed changes. Monitoring agencies in 
O3 nonattainment areas who are not currently affected by the 
existing PAMS requirements would be required to add PAMS measurements 
to their existing NCore sites, while several monitoring agencies with 
existing PAMS sites would not be required to continue PAMS monitoring 
if these proposed requirements are promulgated.\241\ As discussed later 
in this preamble, the EPA is proposing a staggered compliance schedule 
for the proposed PAMS requirements in recognition of the need for 
capital investment and staff training at these sites.
---------------------------------------------------------------------------

    \241\ Monitoring agencies would be ab