[Federal Register Volume 80, Number 2 (Monday, January 5, 2015)]
[Proposed Rules]
[Pages 278-324]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2014-30681]
[[Page 277]]
Vol. 80
Monday,
No. 2
January 5, 2015
Part II
Environmental Protection Agency
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40 CFR Part 50
National Ambient Air Quality Standards for Lead; Proposed Rule
Federal Register / Vol. 80 , No. 2 / Monday, January 5, 2015 /
Proposed Rules
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 50
[EPA-HQ-OAR-2010-0108; FRL-9915-57-OAR]
RIN 2060-AQ44
National Ambient Air Quality Standards for Lead
AGENCY: Environmental Protection Agency.
ACTION: Proposed rule.
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SUMMARY: Based on the Environmental Protection Agency's (EPA's) review
of the air quality criteria and the national ambient air quality
standards (NAAQS) for lead (Pb), the EPA is proposing to retain the
current standards, without revision.
DATES: Comments must be received on or before April 6, 2015.
Public Hearings: If, by January 26, 2015, the EPA receives a
request from a member of the public to speak at a public hearing
concerning the proposed decision, we will hold a public hearing, with
information about the hearing provided in a subsequent notice in the
Federal Register.
ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2010-0108 by one of the following methods:
Federal eRulemaking Portal: http://www.regulations.gov:
Follow the on-line instructions for submitting comments.
Email: [email protected]. Include docket ID No. EPA-
HQ-OAR-2010-0108 in the subject line of the message.
Fax: 202-566-9744.
Mail: Docket No. EPA-HQ-OAR-2010-0108, Environmental
Protection Agency, Mail Code 28221T, 1200 Pennsylvania Ave. NW.,
Washington, DC 20460.
Hand Delivery: Docket No. EPA-HQ-OAR-2010-0108,
Environmental Protection Agency, EPA WJC West Building, Room 3334, 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-
2010-0108. 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 the EPA's public
docket, visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
Public Hearing: To request a public hearing or information
pertaining to a public hearing on this document, contact Ms. Eloise
Shepherd, Health and Environmental Impacts Division, Office of Air
Quality Planning and Standards (C504-02), U.S. Environmental Protection
Agency, Research Triangle Park, NC 27711; telephone number (919) 541-
5507; fax number (919) 541-0804; email address:
[email protected]. See the SUPPLEMENTARY INFORMATION for further
information about a possible public hearing.
Docket: All documents in the docket are listed on the
www.regulations.gov Web site. This includes documents in the rulemaking
docket (Docket ID No. EPA-HQ-OAR-2010-0108) and a separate docket,
established for the Integrated Science Assessment for this review
(Docket ID No. EPA-HQ-ORD-2011-0051) that has been incorporated by
reference into the rulemaking docket. All documents in these dockets
are listed on the www.regulations.gov Web site. 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
Information Center, EPA/DC, 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
Information Center is (202) 566-1742.
FOR FURTHER INFORMATION CONTACT: Dr. Deirdre L. Murphy, 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) 541-0729; fax: (919)
541-0237; email: [email protected]. To request a public hearing or
information pertaining to a public hearing on this document, contact
Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office
of Air Quality Planning and Standards (C504-02), U.S. Environmental
Protection Agency, Research Triangle Park, NC 27711; telephone number
(919) 541-5507; fax number (919) 541-0804; email address:
[email protected].
SUPPLEMENTARY INFORMATION:
General Information
Preparing Comments for the 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 the 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
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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 Information Related to This Action
A number of the documents that are relevant to this action are
available through the EPA's Office of Air Quality Planning and
Standards (OAQPS) Technology Transfer Network (TTN) Web site at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html. These documents
include the Plan for Review of the National Ambient Air Quality
Standards for Lead (USEPA, 2011a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, the Integrated Science Assessment
for Lead (USEPA, 2013a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html, the Review of the National Ambient Air
Quality Standards for Lead: Risk and Exposure Assessment Planning
Document (USEPA, 2011b), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, and the Policy Assessment for the
Review of the Lead National Ambient Air Quality Standards (USEPA,
2014), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pa.html. These and other related documents are also available
for inspection and copying in the EPA docket identified above.
Information About a Possible Public Hearing
To request a public hearing or information pertaining to a public
hearing on this document, contact Ms. Eloise Shepherd, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards (C504-02), U.S. Environmental Protection Agency, Research
Triangle Park, NC 27711; telephone number (919) 541-5507; fax number
(919) 541-0804; email address: [email protected].
Table of Contents
The following topics are discussed in this preamble:
I. Background
A. Legislative Requirements
B. Related Lead Control Programs
C. Review of the Air Quality Criteria and Standards for Lead
D. Multimedia, Multipathway Aspects of Lead
E. Air Quality Monitoring
II. Rationale for Proposed Decision on the Primary Standard
A. General Approach
1. Approach in the Last Review
2. Approach for the Current Review
B. Health Effects Information
1. Array of Effects
2. Critical Periods of Exposure
3. Nervous System Effects in Children
4. At-Risk Populations
5. Potential Impacts on Public Health
C. Blood Lead as a Biomarker of Exposure and Relationships With
Air Lead
D. Summary of Risk and Exposure Assessment Information
1. Overview
2. Summary of Design Aspects
3. Key Limitations and Uncertainties
4. Summary of Risk Estimates and Key Observations
E. Conclusions on Adequacy of the Current Primary Standard
1. Evidence-Based Considerations in the Policy Assessment
2. Exposure/Risk-Based Considerations in the Policy Assessment
3. CASAC Advice
4. Administrator's Proposed Conclusions on the Adequacy of the
Current Primary Standard
III. Rationale for Proposed Decision on the Secondary Standard
A. General Approach
1. Approach in the Last Review
2. Approach for the Current Review
B. Welfare Effects Information
C. Summary of Risk Assessment Information
D. Conclusions on Adequacy of the Current Secondary Standard
1. Evidence- and Risk-Based Considerations in the Policy
Assessment
2. CASAC Advice
3. Administrator's Proposed Conclusions on the Adequacy of the
Current Standard
IV. 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 and 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
K. Determination Under Section 307(d)
References
I. Background
A. Legislative Requirements
Two sections of the Clean Air Act (CAA or the Act) 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\
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\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.''
See 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.''
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The requirement that primary standards provide an adequate margin
of safety was intended to address uncertainties associated with
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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 Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert.
denied, 455 U.S. 1034 (1982); 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
concentration levels, see Lead Industries v. EPA, 647 F.2d at 1156
n.51, 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 involved, the size of sensitive population(s) at risk,\3\ and
the kind and degree of the uncertainties that must be addressed. The
selection of any particular approach to 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.
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\3\ As used here and similarly throughout this notice, the term
population (or group) refers to persons having a quality or
characteristic in common, such as a specific pre-existing illness or
a specific age or life stage. As discussed more fully in section
II.B.4 below, the identification of sensitive groups (called at-risk
groups or at-risk populations) involves consideration of
susceptibility and vulnerability.
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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
1980s, this independent review function has been performed by the Clean
Air Scientific Advisory Committee (CASAC).\4\
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\4\ Lists of CASAC members and of members of the CASAC Lead
Review Panel are available at: http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument.
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B. Related Lead Control Programs
States are primarily responsible for ensuring attainment and
maintenance of the NAAQS. Under section 110 of the Act (42 U.S.C. 7410)
and related provisions, states are to submit, for EPA 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 Prevention of Significant Deterioration
program (42 U.S.C. 7470-7479) for these pollutants.
The NAAQS is only one component of the EPA's programs to address Pb
in the environment. Federal programs additionally provide for
nationwide reductions in air emissions of these and other air
pollutants through the Federal Motor Vehicle Control program under
Title II of the Act (42 U.S.C. 7521-7574), which involves controls for
automobile, truck, bus, motorcycle, nonroad engine, and aircraft
emissions; the new source performance standards under section 111 of
the Act (42 U.S.C. 7411); emissions standards for solid waste
incineration units and the national emission standards for hazardous
air pollutants (NESHAP) under sections 129 (42 U.S.C. 7429) and 112 (42
U.S.C. 7412) of the Act, respectively.
The EPA has taken a number of actions associated with these air
pollution control programs since the last review of the Pb NAAQS,
including completion of several regulations which will result in
reduced Pb emissions from stationary sources regulated under the CAA
sections 112 and 129. For example, in January 2012, the EPA updated the
NESHAP for the secondary lead smelting source category (77 FR 555,
January 5, 2012). These amendments to the original maximum achievable
control technology standards apply to facilities nationwide that use
furnaces to recover Pb from Pb-bearing scrap, mainly from automobile
batteries (15 existing facilities, one under construction). By the
effective date in 2014, this action is estimated to result in a Pb
emissions reduction of 13.6 tons per year (tpy) across the category (a
68% reduction). Somewhat lesser Pb emissions reductions are also
expected from regulations completed in 2013 for commercial and
industrial solid waste incineration units (78 FR 9112, February 7,
2013), as well as several other regulations since 2007 (72 FR 73179,
December 26, 2007; 72 FR 74088, December 28, 2007; 73 FR 225, November
20, 2008; 78 FR 10006, February 12, 2013; 76 FR 15372, March 21, 2011;
78 FR 7138, January 31, 2013; 74 FR 51368, October 6, 2009; Policy
Assessment, Appendix 2A).
The presentation below briefly summarizes additional ongoing
activities that, although not directly pertinent to the review of the
NAAQS, are associated with controlling environmental Pb levels and
human Pb exposures more broadly. Among those identified are the EPA
programs intended to encourage exposure reduction programs in other
countries.
Reducing Pb exposures has long been recognized as a federal
priority as environmental and public health agencies continue to
grapple with soil and dust Pb levels from the historical use of Pb in
paint and gasoline and from other sources (Alliance to End Childhood
Lead Poisoning, 1991; 62 FR 19885, April 23, 1997; 66 FR 52013, October
11, 2001; 68 FR 19931, April 23, 2003). A broad range of federal
programs beyond those that focus on air pollution control provide for
nationwide reductions in environmental releases and human exposures.
For example, pursuant to section 1412 of the Safe Drinking Water Act
(SDWA), the EPA regulates Pb in public drinking water systems through
corrosion control
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and other utility actions which work together to minimize Pb levels at
the tap (40 CFR 141.80-141.91). Under section 1417 of the SDWA, pipes,
fittings and fixtures for potable water applications may not be used or
introduced into commerce unless they are considered ``lead free'' as
defined by that Act (40 CFR 141.43).\5\ Additionally, federal Pb
abatement programs provide for the reduction in human exposures and
environmental releases from in-place materials containing Pb (e.g., Pb-
based paint, urban soil and dust, and contaminated waste sites).
Federal regulations on disposal of Pb-based paint waste help facilitate
the removal of Pb-based paint from residences (68 FR 36487, June 18,
2003).
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\5\ Effective in January 2014, the amount of Pb permitted in
pipes, fittings, and fixtures was lowered (see ``Summary of the
Reduction of Lead in Drinking Water Act and Frequently Asked
Questions'' at http://water.epa.gov/drink/info/lead/index.cfm).
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Federal programs to reduce exposure to Pb in paint, dust, and soil
are specified under the comprehensive federal regulatory framework
developed under the Residential Lead-Based Paint Hazard Reduction Act
(Title X). Under Title X (codified as Title IV of the Toxic Substances
Control Act [TSCA]), the EPA has established regulations and associated
programs in six categories: (1) Training, certification and work
practice requirements for persons engaged in Pb-based paint activities
(abatement, inspection and risk assessment); accreditation of training
providers; and authorization of state and tribal Pb-based paint
programs; (2) training, certification, and work practice requirements
for persons engaged in home renovation, repair and painting (RRP)
activities; accreditation of RRP training providers; and authorization
of state and tribal RRP programs; (3) ensuring that, for most housing
constructed before 1978, information about Pb-based paint and Pb-based
paint hazards flows from sellers to purchasers, from landlords to
tenants, and from renovators to owners and occupants; (4) establishing
standards for identifying dangerous levels of Pb in paint, dust and
soil; (5) providing grant funding to establish and maintain state and
tribal Pb-based paint programs; and (6) providing information on Pb
hazards to the public, including steps that people can take to protect
themselves and their families from Pb-based paint hazards. The most
recent rule issued under Title IV of TSCA is for the Lead Renovation,
Repair and Painting Program (73 FR 21692, April 22, 2008), which became
fully effective in April 2010 and which applies to compensated
renovators and maintenance professionals who perform RRP activities in
housing and child-care facilities built prior to 1978. To foster
adoption of the rule's measures, the EPA has been conducting an
extensive education and outreach campaign to promote awareness of these
new requirements among both the regulated entities and the consumers
who hire them (http://www2.epa.gov/lead/renovation-repair-and-painting-program). In addition, the EPA is investigating whether Pb hazards are
also created by RRP activities in public and commercial buildings, in
which case the EPA plans to issue RRP requirements, where appropriate,
for this class of buildings (79 FR 31072, May 30, 2014).
Programs associated with the Comprehensive Environmental Response,
Compensation, and Liability Act (CERCLA or Superfund) and Resource
Conservation Recovery Act (RCRA) also implement abatement programs,
reducing exposures to Pb and other pollutants. For example, the EPA
determines and implements protective levels for Pb in soil at Superfund
sites and RCRA corrective action facilities. Federal programs,
including those implementing RCRA, provide for management of hazardous
substances in hazardous and municipal solid waste (e.g., 66 FR 58258,
November 20, 2001). Federal regulations concerning batteries in
municipal solid waste facilitate the collection and recycling or proper
disposal of batteries containing Pb.\6\ Similarly, federal programs
provide for the reduction in environmental releases of hazardous
substances such as Pb in the management of wastewater (http://www.epa.gov/owm/).
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\6\ See, e.g., ``Implementation of the Mercury-Containing and
Rechargeable Battery Management Act'' at http://www.epa.gov/epawaste/hazard/recycling/battery.pdf and ``Municipal Solid Waste
Generation, Recycling, and Disposal in the United States: Facts and
Figures for 2005 http://www.epa.gov/epawaste/nonhaz/municipal/pubs/msw-2005.pdf.
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A variety of federal nonregulatory programs also provide for
reduced environmental release of Pb-containing materials by encouraging
pollution prevention, promotion of reuse and recycling, reduction of
priority and toxic chemicals in products and waste, and conservation of
energy and materials. These include the ``Resource Conservation
Challenge'' (http://www.epa.gov/epaoswer/osw/conserve/index.htm), the
``National Waste Minimization Program'' (http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm), ``Plug in to eCycling'' (a partnership
between the EPA and consumer electronics manufacturers and retailers;
http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts),
and activities to reduce the practice of backyard trash burning (http://www.epa.gov/msw/backyard/pubs.htm).
The EPA's research program identifies, encourages and conducts
research needed to locate and assess serious risks and to develop
methods and tools to characterize and help reduce risks related to Pb
exposure. For example, the EPA's Integrated Exposure Uptake Biokinetic
Model for Lead in Children (IEUBK model) is widely used and accepted as
a tool that informs the evaluation of site-specific data. More
recently, in recognition of the need for a single model that predicts
Pb concentrations in tissues for children and adults, the EPA has been
developing the All Ages Lead Model (AALM) to provide researchers and
risk assessors with a pharmacokinetic model capable of estimating
blood, tissue, and bone concentrations of Pb based on estimates of
exposure over the lifetime of the individual (USEPA, 2006a, sections
4.4.5 and 4.4.8; USEPA, 2013a, section 3.6). The EPA's research
activities on substances including Pb, such as those identified here,
focus on improving our characterization of health and environmental
effects, exposure, and control or management of environmental releases
(see http://www.epa.gov/research/).
Other federal agencies also participate in programs intended to
reduce Pb exposures. For example, programs of the Centers for Disease
Control and Prevention (CDC) provide for the tracking of children's
blood Pb levels in the U.S. and provide guidance on levels at which
medical and environmental case management activities should be
implemented (CDC, 2012; ACCLPP, 2012). As a result of coordinated,
intensive efforts at the national, state and local levels, including
those programs described above, blood Pb levels in all segments of the
population have continued to decline from levels observed in the past.
For example, blood Pb levels for the general population of children 1
to 5 years of age have dropped to a geometric mean level of 1.17 [mu]g/
dL in the 2009-2010 National Health and Nutrition Examination Survey
(NHANES) as compared to the geometric mean in 1999-2000 of 2.23
[micro]g/dL and in 1988-1991 of 3.6 [mu]g/dL (USEPA, 2013a, section
3.4.1; USEPA, 2006a, AX4-2). Similarly, blood Pb levels in non-Hispanic
black, Mexican American and lower socioeconomic groups, which are
generally higher than those for the general population, have
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also declined (USEPA, 2013a, sections 3.4.1, 5.2.3 and 5.2.4; Jones et
al., 2009).
The EPA also participates in a broad range of international
programs focused on reducing environmental releases and human exposures
in other countries. For example, the Partnership for Clean Fuels and
Vehicles program engages governments and stakeholders in developing
countries to eliminate Pb in gasoline globally.\7\ From 2007 to 2011,
the number of countries known to still be using leaded gasoline was
reduced from just over 20 to six, with three of the six also offering
unleaded fuel. All six were expected to eliminate Pb from fuel in the
near future (USEPA, 2011c). The EPA is a contributor to the Global
Alliance to Eliminate Lead Paint, a cooperative initiative jointly led
by the World Health Organization and the United Nations Environment
Programme (UNEP) to focus and catalyze the efforts to achieve
international goals to prevent children's Pb exposure from paints
containing Pb and to minimize occupational exposures to Pb paint. This
alliance has the broad objective of promoting a phase-out of the
manufacture and sale of paints containing Pb and eventually to
eliminate the risks that such paints pose. The UNEP is also engaged on
the problem of managing wastes containing Pb, including Pb-containing
batteries. The Governing Council of the UNEP, of which the U.S. is a
member, has adopted decisions focused on promoting the environmentally
sound management of products, wastes and contaminated sites containing
Pb and reducing risks to human health and the environment from Pb and
cadmium throughout the life cycles of those substances (UNEP Governing
Council, 2011, 2013). The EPA is also engaged in the issue of
environmental impacts of spent Pb-acid batteries internationally
through the Commission for Environmental Cooperation (CEC), where the
EPA Administrator along with the cabinet-level or equivalent
representatives of Mexico and Canada comprise the CEC's senior
governing body (CEC Council).\8\
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\7\ International programs in which the U.S. participates,
including those identified here, are described at: http://epa.gov/international/air/pcfv.html, http://www.unep.org/transport/pcfv/,
http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/GAELP/tabid/6176/Default.aspx.
\8\ The CEC was established to support cooperation among the
North American Free Trade Agreement partners to address
environmental issues of continental concern, including the
environmental challenges and opportunities presented by continent-
wide free trade.
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C. Review of the Air Quality Criteria and Standards for Lead
Unlike pollutants such as particulate matter and carbon monoxide,
air quality criteria had not been issued for Pb as of the enactment of
the CAA of 1970, which first set forth the requirement to set NAAQS
based on air quality criteria. In the years just after enactment of the
CAA, the EPA did not list Pb under Section 108 of the Act, having
determined to control Pb air pollution through regulations to phase out
the use of Pb additives in gasoline (See 41 FR 14921, April 8, 1976).
However, the decision not to list Pb under Section 108 was challenged
by environmental and public health groups, and the U.S. District Court
for the Southern District of New York concluded that the EPA was
required to list Pb under Section 108. Natural Resources Defense
Council v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 1976), affirmed, 545
F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA
published a notice in the Federal Register that Pb had been listed
under Section 108 as a criteria pollutant (41 FR 14921, April 8, 1976)
and on October 5, 1978, the EPA promulgated primary and secondary NAAQS
for Pb under Section 109 of the Act (43 FR 46246, October 5, 1978).
Both primary and secondary standards were set at a level of 1.5
micrograms per cubic meter ([mu]g/m\3\), measured as Pb in total
suspended particles (Pb-TSP), not to be exceeded by the maximum
arithmetic mean concentration averaged over a calendar quarter. These
standards were based on the 1977 Air Quality Criteria for Lead (USEPA,
1977).
The first review of the Pb standards was initiated in the mid-
1980s. The scientific assessment for that review is described in the
1986 Air Quality Criteria for Lead (USEPA, 1986a; henceforth referred
to as the 1986 CD), the associated Addendum (USEPA, 1986b) and the 1990
Supplement (USEPA, 1990a). As part of the review, the agency designed
and performed human exposure and health risk analyses (USEPA, 1989),
the results of which were presented in a 1990 Staff Paper (USEPA,
1990b). Based on the scientific assessment and the human exposure and
health risk analyses, the 1990 Staff Paper presented recommendations
for consideration by the Administrator (USEPA, 1990b). After
consideration of the documents developed during the review and the
significantly changed circumstances since Pb was listed in 1976, the
agency did not propose any revisions to the 1978 Pb NAAQS. In a
parallel effort, the agency developed the broad, multi-program,
multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA,
1991). As part of implementing this strategy, the agency focused
efforts primarily on regulatory and remedial clean-up actions aimed at
reducing Pb exposures from a variety of nonair sources judged to pose
more extensive public health risks to U.S. populations, as well as on
actions to reduce Pb emissions to air, such as bringing more areas into
compliance with the existing Pb NAAQS (USEPA, 1991). The EPA continues
this broad, multi-program, multimedia approach to reducing Pb exposures
today, as described in section I.B above.
The last review of the Pb air quality criteria and standards was
initiated in November 2004 (69 FR 64926, November 9, 2004); the
agency's plans for preparation of the Air Quality Criteria Document and
conduct of the NAAQS review were presented in documents completed in
2005 and early 2006 (USEPA, 2005a; USEPA 2006b).\9\ The schedule for
completion of the review was governed by a judicial order in Missouri
Coalition for the Environment v. EPA (No. 4:04CV00660 ERW, September
14, 2005; and amended on April 29, 2008 and July 1, 2008).
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\9\ In the current review, these two documents have been
combined in the Integrated Review Plan for the National Ambient Air
Quality Standards for Lead (USEPA, 2011a).
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The scientific assessment for the review is described in the 2006
Air Quality Criteria for Lead (USEPA, 2006a; henceforth referred to as
the 2006 CD), multiple drafts of which received review by CASAC and the
public. The EPA also conducted human exposure and health risk
assessments and a pilot ecological risk assessment for the review,
after consultation with CASAC and receiving public comment on a draft
analysis plan (USEPA, 2006c). Drafts of these quantitative assessments
were reviewed by CASAC and the public. The pilot ecological risk
assessment was released in December 2006 (ICF International, 2006), and
the final health risk assessment report was released in November 2007
(USEPA, 2007a). The policy assessment, based on both of these
assessments, air quality analyses and key evidence from the 2006 CD,
was presented in the Staff Paper (USEPA, 2007b), a draft of which also
received CASAC and public review. The final Staff Paper presented OAQPS
staff's evaluation of the public health and welfare policy implications
of the key studies and scientific information contained in the 2006 CD
and presented and interpreted results from the quantitative risk/
exposure analyses
[[Page 283]]
conducted for this review. Based on this evaluation, the Staff Paper
presented OAQPS staff recommendations that the Administrator give
consideration to substantially revising the primary and secondary
standards to a range of levels at or below 0.2 [mu]g/m\3\.
Immediately subsequent to completion of the Staff Paper, the EPA
issued an advance notice of proposed rulemaking (ANPR) that was signed
by the Administrator on December 5, 2007 (72 FR 71488, December 17,
2007).\10\ CASAC provided advice and recommendations to the
Administrator with regard to the Pb NAAQS based on its review of the
ANPR and the previously released final Staff Paper and risk assessment
reports. In 2008, the proposed decision on revisions to the Pb NAAQS
was signed on May 1 and published in the Federal Register on May 20 (73
FR 29184, May 20, 2008). Members of the public provided comments and
the CASAC Pb Panel also provided advice and recommendations to the
Administrator based on its review of the proposal notice. The final
decision on revisions to the Pb NAAQS was signed on October 15, 2008,
and published in the Federal Register on November 12, 2008 (73 FR
66964, November 12, 2008).
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\10\ The ANPR, one of the features of the revised NAAQS review
process that EPA instituted in 2006, was replaced by reinstatement
of the Policy Assessment prepared by OAQPS staff (previously termed
the OAQPS Staff Paper) in 2009 (Jackson, 2009).
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The November 2008 notice described the EPA's decision to revise the
primary and secondary NAAQS for Pb, as discussed more fully in section
II.A.1 below. In consideration of the much-expanded health effects
evidence on neurocognitive effects of Pb in children, the EPA
substantially revised the primary standard from a level of 1.5 [mu]g/
m\3\ to a level of 0.15 [mu]g/m\3\. The averaging time was revised to a
rolling 3-month period with a maximum (not-to-be-exceeded) form,
evaluated over a 3-year period. The indicator of Pb-TSP was retained,
reflecting the evidence that Pb particles of all sizes pose health
risks. The secondary standard was revised to be identical in all
respects to the revised primary standard (40 CFR 50.16). Revisions to
the NAAQS were accompanied by revisions to the data handling
procedures, the treatment of exceptional events and the ambient air
monitoring and reporting requirements, as well as emissions inventory
reporting requirements. One aspect of the revised data handling
requirements is the allowance for the use of monitoring for particulate
matter with mean diameter below 10 microns (Pb-PM10) for Pb
NAAQS attainment purposes in certain limited circumstances at non-
source-oriented sites. Subsequent to the 2008 rulemaking, additional
revisions were made to the monitoring network requirements (75 FR
81126, December 27, 2010). Guidance on the approach for implementation
of the new standards was described in the Federal Register notices for
the proposed and final rules (73 FR 29184, May 20, 2008; 73 FR 66964,
November 12, 2008).
On February 26, 2010, the EPA formally initiated its current review
of the air quality criteria and standards for Pb, requesting the
submission of recent scientific information on specified topics (75 FR
8934, February 26, 2010). Soon after this, the EPA held a workshop to
discuss the policy-relevant science, which informed identification of
key policy issues and questions to frame the review of the Pb NAAQS (75
FR 20843, April 21, 2010). Drawing from the workshop discussions, the
EPA developed the draft Integrated Review Plan (draft IRP, USEPA,
2011d). The draft IRP was made available in late March 2011 for
consultation with the CASAC Pb Review Panel and for public comment (76
FR 20347, April 12, 2011). This document was discussed by the Panel via
a publicly accessible teleconference consultation on May 5, 2011 (76 FR
21346, April 15, 2011; Frey, 2011a). The final Integrated Review Plan
for the National Ambient Air Quality Standards for Lead (IRP),
developed in consideration of the CASAC consultation and public
comment, was released in November 2011 (USEPA, 2011a; 76 FR 76972,
December 9, 2011).
In developing the Integrated Science Assessment (ISA) for this
review, the EPA held a workshop in December 2010 to discuss with
invited scientific experts preliminary draft materials and released the
first external review draft of the document for CASAC review and public
comment in May 2011 (USEPA, 2011e; 76 FR 26284, May 6, 2011; 76 FR
36120, June 21, 2011). The CASAC Pb Review Panel met at a public
meeting on July 20, 2011, to review the draft ISA (76 FR 36120, June
21, 2011). The CASAC provided comments in a December 9, 2011, letter to
the EPA Administrator (Frey and Samet, 2011). The second external
review draft ISA was released for CASAC review and public comment in
February 2012 (USEPA, 2012a; 77 FR 5247, February 2, 2012) and was the
subject of a public meeting on April 10-11, 2012 (77 FR 14783, March
13, 2012). The CASAC provided comments in a July 20, 2012, letter
(Samet and Frey, 2012). The third external review draft was released
for CASAC review and public comment in November 2012 (USEPA, 2012b; 77
FR 70776, November 27, 2012) and was the subject of a public meeting on
February 5-6, 2013 (78 FR 938, January 7, 2013). The CASAC provided
comments in a June 4, 2013, letter (Frey, 2013a). The final ISA was
released in late June 2013 (USEPA, 2013a, henceforth referred to as the
ISA; 78 FR 38318, June 26, 2013).
In June 2011, the EPA developed and released the Risk and Exposure
Assessment Planning Document (REA Planning Document) for consultation
with CASAC and public comment (USEPA, 2011b; 76 FR 58509). This
document presented a critical evaluation of the information related to
Pb human and ecological exposure and risk (e.g., data, modeling
approaches) newly available in this review, with a focus on
consideration of the extent to which new or substantially revised REAs
for health and ecological risk might be warranted by the newly
available evidence. Evaluation of the newly available information with
regard to designing and implementing health and ecological REAs for
this review led us to conclude that the currently available information
did not provide a basis for developing new quantitative risk and
exposure assessments that would have substantially improved utility for
informing the agency's consideration of health and welfare effects and
evaluation of the adequacy of the current primary and secondary
standards, respectively (REA Planning Document, sections 2.3 and 3.3,
respectively). The CASAC Pb Review Panel provided consultative advice
on that document and its conclusions at a public meeting on July 21,
2011 (76 FR 36120, June 21, 2011; Frey, 2011b). Based on their
consideration of the REA Planning Document analysis, the CASAC Pb
Review Panel generally concurred with the conclusion that a new REA was
not warranted in this review (Frey, 2011b; Frey, 2013b). In
consideration of the conclusions reached in the REA Planning Document
and CASAC's consultative advice, the EPA has not developed REAs for
health and ecological risk for this review. Accordingly, we consider
the risk assessment findings from the last review for human exposure
and health risk (USEPA, 2007a, henceforth referred to as the 2007 REA)
and ecological risk (ICF International, 2006; henceforth referred to as
the 2006 REA) with regard to any appropriate further interpretation in
light of the evidence newly available in this review.
A draft of the Policy Assessment (PA) was released for public
comment and review by CASAC in January 2013 (USEPA, 2013b; 77 FR 70776,
November
[[Page 284]]
27, 2012) and was the subject of a public meeting on February 5-6, 2013
(78 FR 938, January 7, 2013). Comments provided by the CASAC in a June
4, 2013 letter (Frey, 2013b), as well as public comments received on
the draft PA were considered in preparing the final PA, which was
released in May 2014 (USEPA, 2014; 79 FR 26751, May 9, 2014).
D. Multimedia, Multipathway Aspects of Lead
Since Pb distributes from air to other media and is persistent, our
review of the NAAQS for Pb considers the protection provided against
such effects associated both with exposures to Pb in ambient air and
with exposures to Pb that makes its way into other media from ambient
air. Additionally, in assessing the adequacy of protection afforded by
the current NAAQS, we are mindful of the long history of greater and
more widespread atmospheric emissions that occurred in previous years
(both before and after establishment of the 1978 NAAQS) and that
contributed to the Pb that exists in human populations and ecosystems
today. Likewise, we also recognize the role of other, nonair sources of
Pb now and in the past that also contribute to the Pb that exists in
human populations and ecosystems today.
Lead emitted to ambient air is transported through the air and is
also distributed from air to other media. This multimedia distribution
of Pb emitted into ambient air (air-related Pb) contributes to multiple
air-related pathways of human and ecosystem exposure (ISA, sections
3.1.1 and 3.7.1). Air-related pathways may also involve media other
than air, including indoor and outdoor dust, soil, surface water and
sediments, vegetation and biota. Air-related Pb exposure pathways for
humans include inhalation of ambient air or ingestion of food, water or
other materials, including dust and soil, that have been contaminated
through a pathway involving Pb deposition from ambient air (ISA,
section 3.1.1.1). Ambient air inhalation pathways include both
inhalation of air outdoors and inhalation of ambient air that has
infiltrated into indoor environments. The air-related ingestion
pathways occur as a result of Pb passing through the ambient air, being
distributed to other environmental media and contributing to human
exposures via contact with and ingestion of indoor and outdoor dusts,
outdoor soil, food and drinking water.
Lead exposures via the various inhalation and ingestion air-related
pathways may vary with regard to the time in which they respond to
changes in air Pb concentrations. For example, exposures resulting from
human exposure pathways most directly involving Pb in ambient air and
exchanges of ambient air with indoor air (e.g., inhalation) can respond
most quickly, while those for pathways involving exposure to Pb
deposited from ambient air into the environment (e.g., diet) may be
expected to respond more slowly. The extent of this will be influenced
by the magnitude of change, as well as--for deposition-related
pathways--the extent of prior deposition and environment
characteristics influencing availability of prior deposited Pb.
Lead currently occurring in nonair media may also derive from
sources other than ambient air (nonair Pb sources) (ISA, sections 2.3
and 3.7.1). For example, Pb in dust inside some houses or outdoors in
some urban areas may derive from the common past usage of leaded paint,
while Pb in drinking water may derive from the use of leaded pipe or
solder in drinking water distribution systems (ISA, section 3.1.3.3).
We also recognize the history of much greater air emissions of Pb in
the past, such as that associated with leaded gasoline usage and higher
industrial emissions which have left a legacy of Pb in other (nonair)
media.
The relative importance of different pathways of human exposure to
Pb, as well as the relative contributions from Pb resulting from recent
and historic air emissions and from nonair sources, vary across the
U.S. population as a result of both extrinsic factors, such as a home's
proximity to industrial Pb sources or its history of leaded paint
usage, and intrinsic factors, such as a person's age and nutritional
status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the
relative contributions from specific pathways is situation specific
(ISA, p. 1-11), although a predominant Pb exposure pathway for very
young children is the incidental ingestion of indoor dust by hand-to-
mouth activity (ISA, section 3.1.1.1). For adults, however, diet may be
the primary Pb exposure pathway (2006 CD, section 3.4). Similarly, the
relative importance of air-related and nonair-related Pb also varies
with the relative magnitudes of exposure by those pathways, which may
vary with different circumstances.
The distribution of Pb from ambient air to other environmental
media also influences the exposure pathways for organisms in
terrestrial and aquatic ecosystems. Exposure of terrestrial animals and
vegetation to air-related Pb can occur by contact with ambient air or
by contact with soil, water or food items that have been contaminated
by Pb from ambient air (ISA, section 6.2). Transport of Pb into aquatic
systems similarly provides for exposure of biota in those systems, and
exposures may vary among systems as a result of differences in sources
and levels of contamination, as well as characteristics of the systems
themselves, such as salinity, pH and turbidity (ISA, section 2.3.2). In
addition to Pb contributed by current atmospheric deposition, Pb may
occur in aquatic systems as a result of nonair sources such as
industrial discharges or mine-related drainage, of historical air Pb
emissions (e.g., contributing to deposition to a water body or via
runoff from soils near historical air sources) or combinations of
different types of sources (e.g., resuspension of sediments
contaminated by urban runoff and surface water discharges).
The persistence of Pb contributes an important temporal aspect to
lead's environmental pathways, and the time (or lag) associated with
realization of the impact of air Pb concentrations on concentrations in
other media can vary with the media (e.g., ISA, section 6.2.2). For
example, exposure pathways most directly involving Pb in ambient air or
surface waters can respond more quickly to changes in ambient air Pb
concentrations while pathways involving exposure to Pb in soil or
sediments generally respond more slowly. An additional influence on the
response time for nonair media is the environmental presence of Pb
associated with past, generally higher, air concentrations. For
example, after a reduction in air Pb concentrations, the time needed
for sediment or surface soil concentrations to indicate a response to
reduced air Pb concentrations might be expected to be longer in areas
of more substantial past contamination than in areas with lesser past
contamination. Thus, considering the Pb concentrations occurring in
nonair environmental media as a result of air quality conditions that
meet the current NAAQS is a complexity of this review, as it also was,
although to a lesser degree, with regard to the prior standard in the
last review.
E. Air Quality Monitoring
Lead emitted to the air is predominantly in particulate form. Once
emitted, particle-bound Pb can be transported long or short distances
depending on particle size, which influences the amount of time spent
in the aerosol phase. In general, larger particles tend to deposit more
quickly, within shorter distances from emissions points, while smaller
particles remain in aerosol phase and travel longer
[[Page 285]]
distances before depositing (ISA, section 1.2.1). Accordingly, airborne
concentrations of Pb near sources are much higher (and the
representation of larger particles generally greater) than at sites not
directly influenced by sources (PA, Figure 2-11; ISA sections 2.3.1 and
2.5.3).
Ambient air monitoring data for Pb, in terms of Pb-TSP, Pb-
PM10 or Pb in particulate matter with mean diameter smaller
than 2.5 microns (Pb-PM2.5), are currently collected in
several national networks. Monitoring conducted for purposes of Pb
NAAQS surveillance is regulated to ensure accurate and comparable data
for determining compliance with the NAAQS. In order to be used in NAAQS
attainment designations, ambient Pb concentration data must be obtained
using either the federal reference method (FRM) or a federal equivalent
method (FEM). The FRMs for sample collection and analysis are specified
in 40 CFR part 50. The procedures for approval of FRMs and FEMs are
specified in 40 CFR part 53. In 2013, after consultation with CASAC's
Ambient Air Monitoring and Methods Subcommittee, the EPA adopted a new
FRM for Pb-TSP, based on inductively coupled plasma-mass spectrometry
(78 FR 40000, July 3, 2013). The previous FRM was retained as an FEM,
and existing FEMs were retained as well.
The Pb monitoring network design requirements (40 CFR part 58,
Appendix D, paragraph 4.5) include two types of monitoring sites--
source-oriented monitoring sites and non-source-oriented monitoring
sites--as well as the collection of a year of Pb-TSP measurements at 15
specific airports. The indicator for the current Pb NAAQS is Pb-TSP,
although in some situations,\11\ ambient Pb-PM10
concentrations may be used in judging nonattainment. Currently,
approximately 260 Pb-TSP monitors are in operation; these are a mixture
of source- and non-source-oriented monitors.
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\11\ The Pb-PM10 measurements may be used for NAAQS
monitoring as an alternative to Pb-TSP measurements in certain
conditions defined in 40 CFR part 58, Appendix C, section 2.10.1.2.
These conditions include where Pb concentrations are not expected to
equal or exceed 0.10 [mu]g/m\3\ as an arithmetic 3-month mean and
where the source of Pb emissions is expected to emit a substantial
majority of its Pb in the size fraction captured by PM10
monitors.
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Since the phase-out of Pb in on-road gasoline, Pb is widely
recognized as a source-oriented air pollutant. Variability in air Pb
concentrations is highest in areas including a Pb source, ``with high
concentrations downwind of the sources and low concentration at areas
far from sources'' (ISA, p. 2-92). The current requirements for source-
oriented monitoring include placement of monitor sites near sources of
air Pb emissions which are expected to or have been shown to contribute
to ambient air Pb concentrations in excess of the NAAQS. At a minimum,
there must be one source-oriented site located to measure the maximum
Pb concentration in ambient air resulting from each non-airport Pb
source which emits 0.50 or more tons of Pb per year and from each
airport which emits 1.0 or more tons of Pb per year.\12\ The EPA
Regional Administrators may require additional monitoring beyond the
minimum requirements where the likelihood of Pb air quality violations
is significant. Such locations may include those near additional
industrial Pb sources, recently closed industrial sources and other
sources of resuspended Pb dust, as well as airports where piston-engine
aircraft emit Pb associated with combustion of leaded aviation fuel (40
CFR part 58, Appendix D, section 4.5(c)). A single year of monitoring
was also required near 15 specific airports \13\ in order to gather
additional information on the likelihood of NAAQS exceedances due to
the combustion of leaded aviation gasoline (75 FR 81126, December 27,
2010; 40 CFR part 58, Appendix D, 4.5(a)(iii)). These airport
monitoring data along with other data gathering and analyses will
inform the EPA's ongoing investigation into the potential for Pb
emissions from piston-engine aircraft to cause or contribute to air
pollution that may reasonably be anticipated to endanger public health
or welfare. This investigation is occurring under section 231 of the
CAA, separate from the Pb NAAQS review. As a whole, the various data
gathering and analyses are expected to improve our understanding of Pb
concentrations in ambient air near airports and conditions influencing
these concentrations.
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\12\ The Regional Administrator may waive this requirement for
monitoring near Pb sources if the state or, where appropriate, local
agency can demonstrate the Pb source will not contribute to a
maximum 3-month average Pb concentration in ambient air in excess of
50 percent of the NAAQS level based on historical monitoring data,
modeling, or other means (40 CFR part 58, Appendix D, section
4.5(a)(ii)).
\13\ These airports were selected based on three criteria:
annual Pb inventory between 0.5 ton/year and 1.0 ton/year, ambient
air within 150 meters of the location of maximum emissions (e.g.,
the end of the runway or run-up location), and airport configuration
and meteorological scenario that leads to a greater frequency of
operations from one runway. These criteria are expected,
collectively, to identify airports with the highest potential to
have ambient air Pb concentrations approaching or exceeding the Pb
NAAQS (75 FR 81126).
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Monitoring agencies are also required, under 40 CFR part 58,
Appendix D, to conduct non-source-oriented Pb monitoring at the NCore
sites \14\ required in metropolitan areas with a population of 500,000
or more (as defined by the U.S. Census Bureau).\15\ Either Pb-TSP or
Pb-PM10 monitoring may be performed at these sites.
Currently, all 50 NCore Pb sites are operational and measuring Pb
concentrations, with 28 measuring Pb in TSP and 24 measuring Pb in
PM10 (2 sites are measuring both Pb in TSP and Pb in
PM10). In a separate action addressing a range of issues
related to monitoring requirements for criteria pollutants, the EPA is
proposing to remove the requirement for Pb monitoring at NCore sites
(79 FR 54395, September 11, 2014). This change is being proposed in
consideration of current information indicating concentrations at these
sites to be well below the Pb NAAQS and of the presence of other
monitoring networks that provide information on Pb concentrations in
urban areas not directly impacted by Pb sources. The data available for
these sites indicate maximum 3-month average concentrations (of Pb-
PM10 or Pb-TSP) well below the level of the Pb NAAQS, with
the vast majority of sites showing concentrations less than 0.01 [mu]g/
m\3\. Additionally, other monitoring networks provide data on Pb in
PM10 or PM2.5, at non-source-oriented urban, and
some rural, sites. These include the National Air Toxics Trends
Stations for PM10 and the Chemical Speciation Network for
PM2.5. Data on Pb in PM2.5 are also provided at
the rural sites of the Interagency Monitoring of Protected Visual
Environments network.
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\14\ The NCore network, that formally began in January 2011, is
a subset of the state and local air monitoring stations network that
is intended to meet multiple monitoring objectives (e.g., long-term
trends analysis, model evaluation, health and ecosystem studies, as
well as NAAQS compliance). The complete NCore network consists of 63
urban and 15 rural stations, with each state containing at least one
NCore station; 46 of the states plus Washington, DC and Puerto Rico
have at least one urban station.
\15\ http://www.census.gov/population/www/metroareas/metroarea.html.
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The long-term record of Pb monitoring data documents the dramatic
decline in atmospheric Pb concentrations that has occurred since the
1970s in response to reduced emissions (PA, Figures 2-1 and 2-7).
Currently, the highest concentrations occur near some metals industries
where some individual locations have concentrations that exceed the
NAAQS (PA, Figure 2-10). Concentrations at non-source-oriented
monitoring sites are much lower than those at source-oriented sites and
well below the standard (PA, Figure 2-11).
[[Page 286]]
II. Rationale for Proposed Decision on the Primary Standard
This section presents the rationale for the Administrator's
proposed decision to retain the existing Pb primary standard. As
discussed more fully below, this rationale is based on a thorough
review, in the ISA, of the latest scientific information, generally
published through September 2011,\16\ on human health effects
associated with Pb and pertaining to the presence of Pb in the ambient
air. This proposal also takes into account: (1) The PA's staff
assessments of the most policy-relevant information in the ISA and
staff analyses of air quality, human exposure and health risks, upon
which staff conclusions regarding appropriate considerations in this
review are based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the ISA and PA at public meetings, in separate
written comments, and in CASAC's letters to the Administrator; and (3)
public comments received during the development of these documents,
either in connection with CASAC meetings or separately.
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\16\ In addition to the review's opening ``call for
information'' (75 FR 8934), ``literature searches were conducted
routinely to identify studies published since the last review,
focusing on studies published from 2006 (close of the previous
scientific assessment) through September 2011,'' and references
``that were considered for inclusion or actually cited in this ISA
can be found at http://hero.epa.gov/lead'' (ISA, p. 1-2).
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In presenting the rationale and its foundations, section II.A
provides background on the general approach for review of the primary
NAAQS for Pb, including a summary of the approach used in the last
review (section II.A.1) and the general approach for the current review
(section II.A.2). Sections II.B and II.C summarize the body of evidence
supporting this rationale, focusing on consideration of key policy-
relevant questions, and section II.D summarizes the exposure/risk
information for this review. Section II.E presents the Administrator's
proposed conclusions on adequacy of the current standard, drawing on
both evidence-based and exposure/risk-based considerations (sections
II.E.1 and II.E.2), and advice from CASAC (section II.E.3).
A. General Approach
The past and current approaches described below are both based,
most fundamentally, on using the EPA's assessment of the current
scientific evidence and associated quantitative analyses to inform the
Administrator's judgment regarding a primary standard for Pb that
protects public health with an adequate margin of safety. We note that
in drawing conclusions with regard to the primary standard, the final
decision on the adequacy of the current standard is largely a public
health policy judgment to be made by the Administrator. The
Administrator's final decision must draw upon scientific information
and analyses about health effects, population exposure and risks, as
well as judgments about how to consider the range and magnitude of
uncertainties that are inherent in the scientific evidence and
analyses. Our approach to informing these judgments, discussed more
fully below, is based on the recognition that the available health
effects evidence generally reflects a continuum, consisting of levels
at which scientists generally agree that health effects are likely to
occur, through lower levels at which the likelihood and magnitude of
the response become increasingly uncertain. This approach is consistent
with the requirements of the NAAQS provisions of the Act and with how
the EPA and the courts have historically interpreted the Act. These
provisions require the Administrator to establish primary standards
that, in the judgment of the Administrator, are requisite to protect
public health with an adequate margin of safety. In so doing, the
Administrator seeks to establish standards that are neither more nor
less stringent than necessary for this purpose. The Act does not
require that primary standards be set at a zero-risk level, but rather
at a level that avoids unacceptable risks to public health including
the health of sensitive groups.\17\ The four basic elements of the
NAAQS (indicator, averaging time, level, and form) are considered
collectively in evaluating the health protection afforded by the
current standard.
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\17\ The at-risk population groups identified in a NAAQS review
may include low-income or minority groups. Where low-income/minority
groups are among the at-risk populations, the rulemaking decision
will be based on providing protection for these and other at-risk
populations and lifestages (e.g., children, older adults, persons
with pre-existing heart and lung disease). To the extent that low-
income/minority groups are not among the at-risk populations
identified in the ISA, a decision based on providing protection of
the at-risk lifestages and populations would be expected to provide
protection for the low-income/minority groups.
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1. Approach in the Last Review
The last review of the NAAQS for Pb was completed in 2008 (73 FR
66964, November 12, 2008). The 2008 decision to substantially revise
the primary standard was based on the extensive body of scientific
evidence published over almost three decades, from the time the
standard was originally set in 1978 through 2005-2006. In so doing, the
2008 decision considered the body of evidence as assessed in the 2006
CD (USEPA, 2006a), as well as the 2007 Staff Paper assessment of the
policy-relevant information contained in the CD and the quantitative
risk/exposure assessment (USEPA, 2007a, 2007b), the advice and
recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and
public comment. While recognizing that Pb has been demonstrated to
exert ``a broad array of deleterious effects on multiple organ
systems,'' the review focused on the effects most pertinent to ambient
air exposures, which given ambient air Pb reductions over the past 30
years, are those associated with relatively lower exposures and
associated blood Pb levels (73 FR 66975, November 12, 2008). In so
doing, the EPA recognized the general consensus that the developing
nervous system in children is among the most sensitive health endpoints
associated with Pb exposure, if not the most sensitive one. Thus,
primary attention was given to consideration of nervous system effects,
including neurocognitive and neurobehavioral effects, in children (73
FR 66976, November 12, 2008). The body of evidence included
associations of such effects in study populations of variously aged
children with mean blood Pb levels below 10 [micro]g/dL, extending from
8 down to 2 [micro]g/dL (73 FR 66976, November 12, 2008). The public
health implications of effects of air-related Pb on cognitive function
(e.g., IQ) in young children were given particular focus in the review.
The conclusions reached by the Administrator in the last review
were based primarily on the scientific evidence, with the risk- and
exposure-based information providing support for various aspects of the
decision. In reaching his conclusion on the adequacy of the then-
current standard, which was set in 1978, the Administrator placed
primary consideration on the large body of scientific evidence
available in the review including significant new evidence concerning
effects at blood Pb concentrations substantially below those identified
when the standard was initially set (73 FR 66987, November 12, 2008; 43
FR 46246, October 5, 1978). Given particular attention was the robust
evidence of neurotoxic effects of Pb exposure in children, recognizing:
(1) That while blood Pb levels in U.S. children had decreased notably
since the late 1970s, newer epidemiological studies had investigated
and reported
[[Page 287]]
associations of effects on the neurodevelopment of children with those
more recent lower blood Pb levels and (2) that the toxicological
evidence included extensive experimental laboratory animal evidence
substantiating well the plausibility of the epidemiological findings
observed in human children and expanding our understanding of likely
mechanisms underlying the neurotoxic effects (73 FR 66987, November 12,
2008). Additionally, within the range of blood Pb levels investigated
in the available evidence base, a threshold level for neurocognitive
effects was not identified (73 FR 66984, November 12, 2008; 2006 CD, p.
8-67). Further, the evidence indicated a steeper concentration-response
(C-R) relationship for effects on cognitive function at those lower
blood Pb levels than at higher blood Pb levels that were more common in
the past, ``indicating the potential for greater incremental impact
associated with exposure at these lower levels'' (73 FR 66987, November
12, 2008). As at the time when the standard was initially set in 1978,
the health effects evidence and exposure/risk assessment available in
the last review supported the conclusion that air-related Pb exposure
pathways contribute to blood Pb levels in young children by inhalation
and ingestion (73 FR 66987, November 12, 2008). The available
information in the last review also indicated, however, a likely
greater change in blood Pb per unit of air Pb than was estimated when
the standard was initially set (73 FR 66987, November 12, 2008).
In the Administrator's decision on the adequacy of the 1978
standard, the Administrator considered the evidence using a very
specifically defined framework, referred to as an air-related IQ loss
evidence-based framework. This framework integrates evidence for the
relationship between Pb in air and Pb in young children's blood with
evidence for the relationship between Pb in young children's blood and
IQ loss (73 FR 66987, November 12, 2008). This evidence-based approach
considers air-related effects on neurocognitive function (using the
quantitative metric of IQ loss) associated with exposure in those areas
with elevated air concentrations equal to potential alternative levels
for the Pb standard. In simplest terms, the framework focuses on
children exposed to air-related Pb in those areas with elevated air Pb
concentrations equal to specific potential standard levels, providing
for estimation of a mean air-related IQ decrement for young children in
the high end of the national distribution of air-related exposures.
Thus, the conceptual context for the framework is that it provides
estimates of air-related IQ loss for the subset of U.S. children living
in close proximity to air Pb sources that contribute to such elevated
air Pb concentrations. In such cases, when a standard of a particular
level is just met at a monitor sited to record the highest source-
oriented concentration in an area, the large majority of children in
the larger surrounding area would likely experience exposures to
concentrations well below that level.
The two primary inputs to the evidence-based air-related IQ loss
framework are air-to-blood ratios and C-R functions for the
relationship between blood Pb and IQ response in young children.
Additionally taken into consideration in applying and drawing
conclusions from the framework were the uncertainties inherent in these
inputs. Application of the framework also entailed consideration of an
appropriate level of protection from air-related IQ loss to be used in
conjunction with the framework. The framework estimates of mean air-
related IQ loss are derived through multiplication of the following
factors: standard level ([micro]g/m\3\), air-to-blood ratio (albeit in
terms of [micro]g/dL blood Pb per [micro]g/m\3\ air concentration), and
slope for the C-R function in terms of points IQ decrement per
[micro]g/dL blood Pb.
Based on the application of the air-related IQ loss framework to
the evidence, the Administrator concluded that, for exposures projected
for air Pb concentrations at the level of the 1978 standard, the
quantitative estimates of IQ loss associated with air-related Pb
indicated risk of a magnitude that, in his judgment, was significant
from a public health perspective, and that the evidence-based framework
supported a conclusion that the 1978 standard did not protect public
health with an adequate margin of safety (73 FR 66987, November 12,
2008). The Administrator further concluded that the evidence indicated
the need for a substantially lower standard level to provide increased
public health protection, especially for at-risk groups (most notably
children), against an array of effects, most importantly including
effects on the developing nervous system (73 FR 66987, November 12,
2008). In addition to giving primary consideration to the much expanded
evidence base since the standard was set, the Administrator also took
into consideration the exposure/risk assessments. In so doing, he
observed that, while taking into consideration their inherent
uncertainties and limitations, the quantitative estimates of IQ loss
associated with air-related Pb in air quality scenarios just meeting
the then-current standard also indicated risk of a magnitude that, in
his judgment, was significant from a public health perspective. Thus,
the Administrator concluded the exposure/risk estimates provided
additional support to the evidence-based conclusion that the standard
needed revision (73 FR 66987, November 12, 2008).
In considering appropriate revisions to the prior standard in the
review completed in 2008, each of the four basic elements of the NAAQS
(indicator, averaging time, form and level) was evaluated. The
rationale for decisions on those elements is summarized below.
With regard to indicator, consideration was given to replacing Pb-
TSP with Pb-PM10. The EPA recognized, however, that Pb in
all particle sizes contributes to Pb in blood and associated health
effects, additionally noting that the difference in particulate Pb
captured by TSP and PM10 monitors may be on the order of a
factor of two in some areas (73 FR 66991, November 12, 2008). Further,
the Administrator recognized uncertainty with regard to whether a Pb-
PM10-based standard would also effectively control ultra-
coarse \18\ Pb particles, which may have a greater presence in areas
near sources where Pb concentrations are highest (73 FR 66991, November
12, 2008). The Administrator decided to retain Pb-TSP as the indicator
to provide sufficient public health protection from the range of
particle sizes of ambient air Pb, including ultra-coarse particles (73
FR 66991, November 12, 2008). Additionally, a role was provided for Pb-
PM10 in the monitoring required for a Pb-TSP standard (73 FR
66991, November 12, 2008) based on the conclusion that use of Pb-
PM10 measurements at sites not influenced by sources of
ultra-coarse Pb, and where Pb concentrations are well below the
standard, would take advantage of the increased precision of these
measurements and decreased spatial variation of Pb-PM10
concentrations, without raising the same concerns over a lack of
protection against health risks from all particulate Pb emitted to the
ambient air that
[[Page 288]]
support retention of Pb-TSP as the indicator (versus revision to Pb-
PM10) (73 FR 66991, November 12, 2008). Accordingly,
allowance was made for the use of Pb-PM10 monitoring for Pb
NAAQS attainment purposes in certain limited circumstances, at non-
source-oriented sites, where the Pb concentrations are expected to be
substantially below the standard and ultra-coarse particles are not
expected to be present (73 FR 66991, November 12, 2008).
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\18\ The term ``ultra-coarse'' refers to particles collected by
a TSP sampler but not by a PM10 sampler. This terminology
is consistent with the traditional usage of ``fine'' to refer to
particles collected by a PM2.5 sampler, and ``coarse'' to
refer to particles collected by a PM10 sampler but not by
a PM2.5 sampler, recognizing that there will be some
overlap in the particle sizes in the three types of collected
material.
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With regard to averaging time and form for the revised standard,
consideration was given to a monthly averaging time, with a form of
second maximum, and to 3-month and calendar quarter averaging times,
with not-to-be exceeded forms. While the Administrator recognized that
there were some factors that might imply support for a period as short
as a month for averaging time, he also noted other factors supporting
use of a longer time. He additionally took note of the complexity
inherent in this consideration for the primary Pb standard, which is
greater than in the case of other criteria pollutants due to the
multimedia nature of Pb and its multiple pathways of human exposure. In
this situation for Pb, the Administrator emphasized the importance of
considering all of the relevant factors, both those pertaining to the
human physiological response to changes in Pb exposures and those
pertaining to the response of air-related Pb exposure pathways to
changes in airborne Pb, in an integrated manner.
As discussed further in the PA, the evidence on human physiological
response to changes in Pb exposure available in the last review
indicated that children's blood Pb levels respond quickly to increased
Pb exposure, particularly during the time of leaded gasoline usage but
likely with lessened immediacy since that time as children's exposure
pathways have changed (PA, section 4.1.1.2). The Administrator also
recognized limitations and uncertainties in the evidence and
variability with regard to the information regarding the response time
of indoor dust Pb to ambient airborne Pb. In consideration of the
uncertainty associated with the evidence, the Administrator noted that
the two changes in form for the standard (to a rolling 3-month average
and to providing equal weighting to each month in deriving the 3-month
average) both afford greater weight to each individual month than did
the calendar quarter form of the 1978 standard, tending to control both
the likelihood that any month will exceed the level of the standard and
the magnitude of any such exceedance. Thus, based on an integrated
consideration of the range of relevant factors, the averaging time was
revised to a rolling 3-month period with a maximum (not-to-be-exceeded)
form, evaluated over a 3-year period. As compared to the previous
averaging time and form of calendar quarter (not-to-be exceeded), this
revision was considered to be more scientifically appropriate and more
health protective (73 FR 66996, November 12, 2008). The rolling average
gives equal weight to all 3-month periods, and the new calculation
method gives equal weight to each month within each 3-month period (73
FR 66996, November 12, 2008). Further, the rolling average yields
twelve 3-month averages each year to be compared to the NAAQS versus
four averages in each year for the block calendar quarters pertaining
to the previous standard (73 FR 66996, November 12, 2008).
Lastly, based on the body of scientific evidence and information
available, as well as CASAC recommendations and public comment, the
Administrator decided on a standard level that, in combination with the
specified choice of indicator, averaging time, and form, he judged
requisite to protect public health, including the health of sensitive
groups, with an adequate margin of safety (73 FR 67006, November 12,
2008). In reaching the decision on level for the revised standard, the
Administrator considered as a useful guide the evidence-based framework
developed in that review. As described above, that framework integrates
evidence for the relationship between Pb in air and Pb in children's
blood and the relationship between Pb in children's blood and IQ loss.
Application of the air-related IQ loss evidence-based framework was
recognized, however, to provide ``no evidence- or risk-based bright
line that indicates a single appropriate level'' for the standard (73
FR 67006, November 12, 2008). Rather, the framework was seen as a
useful guide for consideration of health risks from exposure to ambient
levels of Pb in the air, in the context of a specified averaging time
and form, with regard to the Administrator's decision on a level for a
revised NAAQS that provides public health protection that is sufficient
but not more than necessary under the Act (73 FR 67004, November 12,
2008).
As noted above, use of the evidence-based air-related IQ loss
framework to inform selection of a standard level involved
consideration of the evidence with regard to two input parameters. The
two input parameters are an air-to-blood ratio and a C-R function for
population IQ response associated with blood Pb level (73 FR 67004,
November 12, 2008). The evidence at the time of the last review
indicated a broad range of air-to-blood ratio estimates,\19\ each with
limitations and associated uncertainties. Based on the then-available
evidence, the Administrator concluded that 1:5 to 1:10 represented a
reasonable range to consider and identified 1:7 as a generally central
value on which to focus (73 FR 67004, November 12, 2008). With regard
to C-R functions, in light of the evidence of nonlinearity and of
steeper slopes at lower blood Pb levels, the Administrator concluded it
was appropriate to focus on C-R analyses based on blood Pb levels that
most closely reflected the then-current population of children in the
U.S.,\20\ recognizing the EPA's identification of four such analyses
and giving weight to the central estimate or median of the resultant C-
R functions (73 FR 67003, November 12, 2008, Table 3; 73 FR 67004,
November 12, 2008). The median estimate for the four C-R slopes of -
1.75 IQ points decrement per [micro]g/dL blood Pb was selected for use
with the framework. With the framework, potential alternative standard
levels ([micro]g/m\3\) are multiplied by estimates of air-to-blood
ratio ([micro]g/dL blood Pb per [micro]g/m\3\ air Pb) and the median
slope for the C-R function (points IQ decrement per [micro]g/dL blood
Pb), yielding estimates of a mean air-related IQ decrement for a
specific subset of young children (i.e., those children exposed to air-
related Pb in areas with elevated air Pb concentrations equal to
specified alternative levels). As such, the application of the
framework yields estimates for the mean air-related IQ decrements of
the subset of children expected to experience air-related Pb exposures
at the high end of the distribution of such exposures. The associated
mean IQ loss estimate is the average for this highly exposed subset and
is not the average air-related IQ loss projected for the entire U.S.
population of children. Uncertainties and limitations were recognized
in the use
[[Page 289]]
of the framework and in the resultant estimates (73 FR 67000, November
12, 2008).
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\19\ The term ``air-to-blood ratio'' describes the increase in
blood Pb (in [micro]g/dL) estimated to be associated with each unit
increase of air Pb (in [micro]g/m\3\). Ratios are presented in the
form of 1:x, with the 1 representing air Pb (in [micro]g/m\3\) and x
representing blood Pb (in [micro]g/dL). Description of ratios as
higher or lower refers to the values for x (i.e., the change in
blood Pb per unit of air Pb).
\20\ The geometric mean blood Pb level for U.S. children aged 5
years and below, reported for NHANES in 2003-04 (the most recent
years for which such an estimate was available at the time of the
2008 decision) was 1.8 [micro]g/dL and the 5th and 95th percentiles
were 0.7 [micro]g/dL and 5.1 [micro]g/dL, respectively (73 FR
67002).
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In considering the use of the evidence-based air-related IQ loss
framework to inform his judgment as to the appropriate degree of public
health protection that should be afforded by the NAAQS to provide
requisite protection against risk of neurocognitive effects in
sensitive populations, such as IQ loss in children, the Administrator
recognized in the 2008 review that there were no commonly accepted
guidelines or criteria within the public health community that would
provide a clear basis for such a judgment. During the 2008 review,
CASAC commented regarding the significance from a public health
perspective of a 1-2 point IQ loss in the entire population of children
and along with some commenters, emphasized that the NAAQS should
prevent air-related IQ loss of a significant magnitude, such as on the
order of 1-2 IQ points, in all but a small percentile of the
population. Similarly, the Administrator stated that ``ideally air-
related (as well as other) exposures to environmental Pb would be
reduced to the point that no IQ impact in children would occur'' (73 FR
66998, November 12, 2008). The Administrator further recognized that,
in the case of setting a NAAQS, he was required to make a judgment as
to what degree of protection is requisite to protect public health with
an adequate margin of safety (73 FR 66998, November 12, 2008). The
NAAQS must be sufficient but not more stringent than necessary to
achieve that result, and the Act does not require a zero-risk standard
(73 FR 66998, November 12, 2008). The Administrator additionally
recognized that the evidence-based air-related IQ loss framework did
not provide estimates pertaining to the U.S. population of children as
a whole. Rather, the framework provided estimates (with associated
uncertainties and limitations) for the mean of a subset of that
population, the subset of children assumed to be exposed to the level
of the standard. As described in the final decision ``[t]he framework
in effect focuses on the sensitive subpopulation that is the group of
children living near sources and more likely to be exposed at the level
of the standard'' (73 FR 67000, November 12, 2008). As further noted in
the final decision (73 FR 67000, November 12, 2008):
EPA is unable to quantify the percentile of the U.S. population
of children that corresponds to the mean of this sensitive
subpopulation. Nor is EPA confident in its ability to develop
quantified estimates of air-related IQ loss for higher percentiles
than the mean of this subpopulation. EPA expects that the mean of
this subpopulation represents a high, but not quantifiable,
percentile of the U.S. population of children. As a result, EPA
expects that a standard based on consideration of this framework
would provide the same or greater protection from estimated air-
related IQ loss for a high, albeit unquantifiable, percentage of the
entire population of U.S. children.
In reaching a judgment as to the appropriate degree of protection,
the Administrator considered advice and recommendations from CASAC and
public comments and recognized the uncertainties in the health effects
evidence and related information as well as the role of, and context
for, a selected air-related IQ loss in the application of the
framework, as described above. Based on these considerations, the
Administrator identified an air-related IQ loss of 2 points for use
with the framework, as a tool for considering the evidence with regard
to the level for the standard (73 FR 67005, November 12, 2008). In so
doing, the Administrator was not determining that such an IQ decrement
value was appropriate in other contexts (73 FR 67005, November 12,
2008). Given the various uncertainties associated with the framework
and the scientific evidence base, and the focus of the framework on the
sensitive subpopulation of children that are more highly exposed to
air-related Pb, a standard level selected in this way, in combination
with the selected averaging time and form, was expected to
significantly reduce and limit for a high percentage of U.S. children
the risk of experiencing an air-related IQ loss of that magnitude (73
FR 67005, November 12, 2008). At the standard level of 0.15 [micro]g/
m\3\, with the combination of the generally central estimate of air-to-
blood ratio of 1:7 and the median of the four C-R functions (-1.75 IQ
point decrement per [micro]g/dL blood Pb), the framework estimates of
air-related IQ loss were below 2 IQ points (73 FR 67005, November 12,
2008, Table 4).
In reaching the decision in 2008 on a level for the revised
standard, the Administrator also considered the results of the
quantitative risk assessment to provide a useful perspective on risk
from air-related Pb. In light of important uncertainties and
limitations for purposes of evaluating potential standard levels,
however, the Administrator placed less weight on the risk estimates
than on the evidence-based assessment. Nevertheless, in recognition of
the general comparability of quantitative risk estimates for the case
studies considered most conceptually similar to the scenario
represented by the evidence-based framework, he judged the quantitative
risk estimates to be ``roughly consistent with and generally
supportive'' of the evidence-based framework estimates (73 FR 67006,
November 12, 2008).
Based on consideration of the entire body of evidence and
information available in the review, as well as the recommendations of
CASAC and public comments, the Administrator decided that a level for
the primary Pb standard of 0.15 [micro]g/m\3\, in combination with the
specified choice of indicator, averaging time and form, was requisite
to protect public health, including the health of sensitive groups,
with an adequate margin of safety (73 FR 67006, November 12, 2008). In
reaching decisions on level as well as the other elements of the
revised standard, the Administrator took note of the complexity
associated with consideration of health effects caused by different
ambient air concentrations of Pb and with uncertainties with regard to
the relationships between air concentrations, exposures, and health
effects. For example, selection of a maximum, not to be exceeded, form
in conjunction with a rolling 3-month averaging time over a 3-year span
was expected to have the effect that the at-risk population of children
would be exposed below the standard most of the time (73 FR 67005,
November 12, 2008). The Administrator additionally considered the
provision of an adequate margin of safety in making decisions on each
of the elements of the standard, including, for example ``selection of
TSP as the indicator and the rejection of the use of PM10
scaling factors; selection of a maximum, not to be exceeded form, in
conjunction with a 3-month averaging time that employs a rolling
average, with the requirement that each month in the 3-month period be
weighted equally (rather than being averaged by individual data) and
that a 3-year span be used for comparison to the standard; and the use
of a range of inputs for the evidence-based framework, that includes a
focus on higher air-to-blood ratios than the lowest ratio considered to
be supportable, and steeper rather than shallower C-R functions, and
the consideration of these inputs in selection of 0.15 [mu]g/m\3\ as
the level of the standard'' (73 FR 67007, November 12, 2008).
The Administrator additionally noted that a standard with this
level would reduce the risk of a variety of health effects associated
with exposure to Pb, including effects indicated in the epidemiological
studies at lower blood Pb levels, particularly including
[[Page 290]]
neurological effects in children, and the potential for cardiovascular
and renal effects in adults (73 FR 67006, November 12, 2008). The
Administrator additionally considered higher and lower levels for the
standard, concluding that a level of 0.15 [micro]g/m\3\ provided for a
standard that was neither more or less stringent than necessary for
this purpose, recognizing that the Act does not require that primary
standards be set at a zero-risk level, but rather at a level that
reduces risk sufficiently so as to protect public health with an
adequate margin of safety (73 FR 67007, November 12, 2008). For
example, the Administrator additionally considered potential public
health protection provided by standard levels above 0.15 [micro]g/m\3\,
which he concluded were insufficient to protect public health with an
adequate margin of safety. The Administrator also noted that in light
of all of the evidence, including the evidence-based framework, the
degree of public health protection likely afforded by standard levels
below 0.15 [micro]g/m\3\ would be greater than what is necessary to
protect public safety with an adequate margin of safety.
The Administrator concluded, based on review of all of the evidence
(including the evidence-based framework), that when taken as a whole
the selected standard, including the indicator, averaging time, form,
and level, would be ``sufficient but not more than necessary to protect
public health, including the health of sensitive subpopulations, with
an adequate margin of safety'' (73 FR 67007, November 12, 2008).
2. Approach for the Current Review
The approach in this review of the current primary standard takes
into consideration the approach used in the last Pb NAAQS review,
addressing key policy-relevant questions in light of currently
available scientific and technical information. To evaluate whether it
is appropriate to consider retaining the current primary Pb standard,
or whether consideration of revision is appropriate, the EPA has
adopted an approach in this review that builds upon the general
approach used in the last review and reflects the broader body of
evidence and information now available. As summarized above, the
Administrator's decisions in the prior review were based on an
integration of information on health effects associated with exposure
to Pb with that on relationships between ambient air Pb and blood Pb;
expert judgments on the adversity and public health significance of key
health effects; and policy judgments as to when the standard is
requisite to protect public health with an adequate margin of safety.
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.
Similarly in this review, as described in the PA, we draw on the
current evidence and quantitative assessments of exposure pertaining to
the public health risk of Pb in ambient air. In considering the
scientific and technical information here as in the PA, we consider
both the information available at the time of the last review and
information newly available since the last review, including most
particularly that which has been critically analyzed and characterized
in the current ISA. We additionally consider the quantitative exposure/
risk assessments from the last review that estimated Pb-related IQ
decrements associated with different air quality conditions in
simulated at-risk populations in multiple case studies (PA, section
3.4; 2007 REA). The evidence-based discussions presented below draw
upon evidence from epidemiological studies and experimental animal
studies evaluating health effects related to exposures to Pb, as
discussed in the ISA. The exposure/risk-based discussions have drawn
from the quantitative health risk analyses for Pb performed in the last
Pb NAAQS review in light of the currently available evidence (PA,
section 3.4; 2007 REA; REA Planning Document). Sections II.B through
II.D below summarize the current health effects and exposure/risk
information with a focus on the specific policy-relevant questions
identified for these categories of information in the PA (PA, chapter
3).
B. Health Effects Information
1. Array of Effects
Lead has been demonstrated to exert a broad array of deleterious
effects on multiple organ systems as described in the assessment of the
evidence available in this review and consistent with conclusions of
past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable number
of studies on Pb health effects are newly available in this review and
are critically assessed in the ISA as part of the full body of
evidence. The newly available evidence reaffirms conclusions on the
broad array of effects recognized for Pb in the last review (see ISA,
section 1.10).\21\ Consistent with those conclusions, in the context of
pollutant exposures considered relevant to the Pb NAAQS review,\22\ the
ISA determines that causal relationships \23\ exist for Pb with effects
on the nervous system in children (cognitive function decrements and
the group of externalizing behaviors comprising attention, impulsivity
and hyperactivity), the hematological system (altered heme synthesis
and decreased red blood cell survival and function), and the
cardiovascular system (hypertension and coronary heart disease), and on
reproduction and development (postnatal development and male
reproductive function) (ISA, Table 1-2). Additionally, the ISA
describes relationships between Pb and effects on the nervous system in
adults, on immune system function and with cancer \24\ as likely to be
causal \25\ (ISA, Table 1-2, sections 1.6.4 and 1.6.7).
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\21\ Since the last Pb NAAQS review, the ISAs which have
replaced CDs in documenting each review of the scientific evidence
(or air quality criteria) employ a systematic framework for weighing
the evidence and describing associated conclusions with regard to
causality using established descriptors: ``causal'' relationship
with relevant exposure, ``likely'' to be a causal relationship,
evidence is ``suggestive'' of a causal relationship, ``inadequate''
evidence to infer a causal relationship, and ``not likely'' to be a
causal relationship (ISA, Preamble).
\22\ In drawing judgments regarding causality for the criteria
air pollutants, the ISA places emphasis ``on evidence of effects at
doses (e.g., blood Pb concentration) or exposures (e.g., air
concentrations) that are relevant to, or somewhat above, those
currently experienced by the population. The extent to which studies
of higher concentrations are considered varies . . . but generally
includes those with doses or exposures in the range of one to two
orders of magnitude above current or ambient conditions. Studies
that use higher doses or exposures may also be considered . . .
[t]hus, a causality determination is based on weight of evidence
evaluation . . ., focusing on the evidence from exposures or doses
generally ranging from current levels to one or two orders of
magnitude above current levels'' (ISA, pp. lx-lxi).
\23\ In determining a causal relationship to exist for Pb with
specific health effects, the EPA concludes that ``[e]vidence is
sufficient to conclude that there is a causal relationship with
relevant pollutant exposures (i.e., doses or exposures generally
within one to two orders of magnitude of current levels)'' (ISA, p.
lxii).
\24\ The EPA concludes that a causal relationship is likely to
exist between Pb exposure and cancer, based primarily on consistent,
strong evidence from experimental animal studies, but inconsistent
epidemiological evidence (ISA, section 4.10.5). Lead has also been
classified as a probable human carcinogen by the International
Agency for Research on Cancer, based mainly on sufficient animal
evidence, and as reasonably anticipated to be a human carcinogen by
the U.S. National Toxicology Program (ISA, section 4.10).
\25\ In determining that there is likely to be a causal
relationship for Pb 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'' (ISA, p. lxii).
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In some categories of health effects, there is newly available
evidence regarding some aspects of the effects described in the last
review or that strengthens our conclusions regarding aspects of Pb
toxicity on a particular
[[Page 291]]
physiological system. Among the nervous system effects of Pb, the newly
available evidence is consistent with conclusions in the previous
review which recognized that ``[t]he neurotoxic effects of Pb exposure
are among those most studied and most extensively documented among
human population groups'' (2006 CD, p. 8-25) and took note of the
diversity of studies in which such effects of Pb exposure early in
development (from fetal to postnatal childhood periods) have been
observed (2006 CD, p. E-9). Nervous system effects that receive
prominence in the current review, as in previous reviews, include those
affecting cognitive function and behavior in children (ISA, section
4.3), with conclusions that are consistent with findings of the last
review.
Across the broad array of Pb effects for systems and processes
other than the nervous system, the evidence base has been augmented
with additional epidemiological investigations in a number of areas,
including developmental outcomes, such as puberty onset, and adult
outcomes related to cardiovascular function, for which several large
cohorts have been analyzed (ISA, Table 1-8 and sections 4.4 and 4.8).
Conclusions on these other systems and processes are generally
consistent with conclusions reached in the last review, while also
extending our conclusions on some aspects of these effects (ISA,
section 4.4 and Table 1-8).
Based on the extensive assessment of the full body of evidence
available in this review, the major conclusions drawn by the ISA
regarding health effects of Pb in children include the following (ISA,
p. lxxxvii).
Multiple epidemiologic studies conducted in diverse populations
of children consistently demonstrate the harmful effects of Pb
exposure on cognitive function (as measured by IQ decrements,
decreased academic performance and poorer performance on tests of
executive function). . . . Evidence suggests that some Pb-related
cognitive effects may be irreversible and that the
neurodevelopmental effects of Pb exposure may persist into adulthood
(Section 1.9.4). Epidemiologic studies also demonstrate that Pb
exposure is associated with decreased attention, and increased
impulsivity and hyperactivity in children (externalizing behaviors).
This is supported by findings in animal studies demonstrating both
analogous effects and biological plausibility at relevant exposure
levels. Pb exposure can also exert harmful effects on blood cells
and blood producing organs, and is likely to cause an increased risk
of symptoms of depression and anxiety and withdrawn behavior
(internalizing behaviors),decreases in auditory and motor function,
asthma and allergy, as well as conduct disorders in children and
young adults. There is some uncertainty about the Pb exposures
contributing to the effects and blood Pb levels observed in
epidemiologic studies; however, these uncertainties are greater in
studies of older children and adults than in studies of young
children (Section 1.9.5).
Based on the extensive assessment of the full body of evidence
available in this review, the major conclusions drawn by the ISA
regarding health effects of Pb in adults include the following (ISA, p.
lxxxviii).
A large body of evidence from both epidemiologic studies of
adults and experimental studies in animals demonstrates the effect
of long-term Pb exposure on increased blood pressure (BP) and
hypertension (Section 1.6.2). In addition to its effect on BP, Pb
exposure can also lead to coronary heart disease and death from
cardiovascular causes and is associated with cognitive function
decrements, symptoms of depression and anxiety, and immune effects
in adult humans. The extent to which the effects of Pb on the
cardiovascular system are reversible is not well-characterized.
Additionally, the frequency, timing, level, and duration of Pb
exposure causing the effects observed in adults has not been
pinpointed, and higher past exposures may contribute to the
development of health effects measured later in life.
As in prior reviews of the Pb NAAQS, this review is focused on
those effects most pertinent to ambient air Pb exposures. Given the
reductions in ambient air Pb concentrations over the past decades,
these effects are generally those associated with the lowest levels of
Pb exposure that have been evaluated. Additionally, we recognize the
limitations on our ability to draw conclusions regarding the exposure
conditions contributing to the findings from epidemiological analyses
of blood Pb levels in populations of older children and adults,
particularly in light of their history of higher Pb exposures. Evidence
available in future reviews may better inform this issue. In the last
review, while recognizing the range of health effects in variously aged
populations related to Pb exposure, we focused on the health effects
for which the evidence was strongest with regard to relationships with
the lowest exposure levels, neurocognitive effects in young children.
As is the case for studies of nervous system effects in children
(discussed in more detail in section II.B.3 below), newly available
studies of other effects in child and adult cohorts include cohorts
with similar or somewhat lower mean blood Pb levels than in previously
available studies. Categories of effects for which a causal
relationship has been concluded in the ISA and for which there are a
few newly available epidemiological studies indicating blood Pb
associations with effects in study groups with somewhat lower blood Pb
levels than previously available for these effects include effects on
development (delayed puberty onset) and reproduction (male reproductive
function) and on the cardiovascular system (hypertension) (ISA,
sections 4.4 and 4.8; 2006 CD, sections 6.5 and 6.6). With regard to
the former category, study groups in the newly available studies
include groups composed of older children ranging up to age 18 years,
for which there is increased uncertainty regarding historical exposures
and their role in the observed effects.\26\ An additional factor that
handicaps our consideration of exposure levels associated with these
findings is the appreciable uncertainty associated with our
understanding of Pb biokinetics during this lifestage (ISA, sections
3.2, 3.3, and 4.8.6). The evidence newly available for Pb relationships
with cardiovascular effects in adults include some studies with
somewhat lower blood Pb levels than in the last review. The long
exposure histories of these cohorts, as well as the generally higher Pb
exposures of the past, complicate conclusions regarding exposure levels
that may be eliciting observed effects (ISA, sections 4.4.2.4 and
4.4.7).\27\ Accordingly, as discussed further below, we focus in this
review, as in the last, on neurocognitive effects in young children.
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\26\ Several of these studies involve NHANES III cohorts for
which early childhood exposures were generally much higher than
those common in the U.S. today (ISA, section 4.8.5).
\27\ Studies from the late 1960s and 1970s suggest that adult
blood Pb levels during that period ranged from roughly 13 to 16
[mu]g/dL and from 15 to 30 [mu]g/dL in children aged 6 and younger
(ISA, section 4.4.1).
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2. Critical Periods of Exposure
As in the last review, we base our current understanding of health
effects associated with different Pb exposure circumstances at various
stages of life or in different populations on the full body of
available evidence and primarily on epidemiological studies of health
effects associated with population Pb biomarker levels (discussed
further in section II.B.3 below). The epidemiological evidence is
overwhelmingly composed of studies that rely on blood Pb for the
exposure metric, with the remainder largely including a focus on bone
Pb. Because these metrics reflect Pb in the body (e.g., as compared to
Pb exposure concentrations) and, in the case of blood Pb, reflect Pb
available for distribution to target sites, they strengthen the
[[Page 292]]
evidence base for purposes of drawing causal conclusions with regard to
Pb generally. The complexity of Pb exposure pathways and internal
dosimetry, however, tends to limit the extent to which these types of
studies inform our more specific understanding of the Pb exposure
circumstances (e.g., timing within lifetime, duration, frequency and
magnitude) eliciting the various effects.
As at the time of the last review (and discussed more fully in
section II.B.3 below), assessment of the full evidence base, including
evidence newly available in this review, demonstrates that Pb exposure
prenatally and also in early childhood can contribute to neurocognitive
impacts in childhood, with evidence also indicating the potential for
effects persisting into adulthood (ISA, sections 1.9.4, 1.9.5, and
1.10). In addition to the observed associations of prenatal and
childhood blood Pb with effects at various ages in childhood, there is
also evidence of Pb-related cognitive function effects in non-
occupationally exposed adults (ISA, section 4.3.11). This includes
evidence of associations of such effects in adulthood with childhood
blood Pb levels and in other cohorts, with concurrent (adult) blood Pb
levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies
finding associations of adult effects with childhood blood Pb levels
did not examine adult blood Pb levels, the relative influence of adult
Pb exposure cannot be ascertained, and a corresponding lack of early
life exposure or biomarker measurements for the latter studies limits
our ability to draw conclusions regarding specific Pb exposure
circumstances eliciting the observed effects (4.3.11). Findings of
stronger associations for adult neurocognitive effects with bone Pb,
however, indicate the role of historical or cumulative exposures for
those effects (ISA, section 4.3).
A critical aspect of much of the epidemiological evidence,
particularly studies focused on adults (and older children) in the U.S.
today, is the backdrop of generally declining environmental Pb exposure
(from higher exposures during their younger years) that is common
across many study populations (ISA, p. 4-2).\28\ An additional factor
complicating the interpretation of health effect associations with
blood Pb measurements in older children and younger adults is the
common behaviors of younger children (e.g., hand-to-mouth contact) that
generally contribute to relatively greater exposures earlier in life
(ISA, sections 3.1.1, 4.2.1). Such exposure histories for adults and
older children complicate our ability to draw conclusions regarding
critical time periods and lifestages for Pb exposures eliciting the
effects for which associations with Pb biomarkers have been observed in
these populations (e.g., ISA, section 1.9.6).\29\ Thus, our confidence
is greatest in the role of early childhood exposure in contributing to
Pb-related neurocognitive effects that have been associated with blood
Pb levels in young children. This is due, in part, to the relatively
short exposure histories of young children (ISA, sections 1.9.4, 1.9.6
and 4.3.11).
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\28\ The declines in Pb exposure concentrations occurring from
the 1970s through the early 1990s (and experienced by middle aged
and older adults of today), as indicated by NHANES blood Pb
information, were particularly dramatic (ISA, section 3.4.1).
\29\ The evidence from experimental animal studies can be
informative with regard to key aspects of exposure circumstances in
eliciting specific effects, thus informing our interpretation of
epidemiological evidence. For example, the animal evidence base with
regard to Pb effects on blood pressure demonstrates the
etiologically-relevant role of long-term exposure (ISA, section
4.4.1). This finding then informs consideration of epidemiological
studies of adult populations for whom historical exposures were
likely more substantial than concurrent ones, suggesting that the
observed effects may be related to the past exposure (ISA, section
4.4.1). For other health effects, the animal evidence base may or
may not be informative in this manner.
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Epidemiological analyses evaluating risk of neurocognitive impacts
(e.g., reduced IQ) associated with different blood Pb metrics in
cohorts with differing exposure patterns (including those for which
blood Pb levels at different ages were not highly correlated) also
indicate associations with blood Pb measurements concurrent with full
scale IQ (FSIQ) tests at ages of approximately 6-7 years. The analyses
did not, however, conclusively demonstrate stronger findings for early
(e.g., age 2 years) or concurrent blood Pb (ISA, section 4.3.11).\30\
The experimental animal evidence additionally indicates early life
susceptibility (ISA, section 4.3.15 and p. 5-21). Thus, while
uncertainties remain with regard to the role of Pb exposures during a
particular age of life in eliciting nervous system effects, such as
cognitive function decrements, the full evidence base continues to
indicate prenatal and early childhood lifestages as periods of
increased Pb-related risk (ISA, sections 4.3.11 and 4.3.15). We
recognize increasing uncertainty, however, in our understanding of the
relative impact on neurocognitive function of additional Pb exposure of
children by school age or later that is associated with limitations of
the currently available evidence, including epidemiological cohorts
with generally similar temporal patterns of exposure.
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\30\ In the collective body of evidence of nervous system
effects in children, it is difficult to distinguish exposure in
later lifestages (e.g., school age) and its associated risk from
risks resulting from exposure in prenatal and early childhood (ISA,
section 4.3.11). While early childhood is recognized as a time of
increased susceptibility, a difficulty in identifying a discrete
period of susceptibility from epidemiological studies has been that
the period of peak exposure, reflected in peak blood Pb levels, is
around 18-27 months when hand-to-mouth activity is at its maximum
(ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is
additionally complicated by the role of maternal exposure history in
contributing Pb to the developing fetus (ISA, section 3.2.2.4.).
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As in the last review, there is also substantial evidence of other
neurobehavioral effects in children, including effects on externalizing
behaviors (reduced attention span, increased impulsivity,
hyperactivity, and conduct disorders) and on internalizing behaviors.
The evidence for many of these endpoints, as with neurocognitive
effects, also includes associations of effects at various ages in
childhood and for some effects, into adulthood, with blood Pb levels
reflective of several different lifestages (e.g., prenatal and several
different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is
similar or relatively less extensive evidence to inform our
understanding of such effects associated with specific time periods of
exposure at specific lifestages than is the case for effects on
cognitive function.
Across the range of Pb effects on physiological systems and
processes other than the nervous system, the evidence base for blood
pressure and hypertension is somewhat more informative with regard to
the circumstances of Pb exposure eliciting the observed effects than
are the evidence bases for many other effects. In the case of Pb-
induced increases in blood pressure, the evidence indicates an
importance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1). The
greater uncertainties regarding the time, duration and magnitude of
exposure contributing to these observed health effects complicate
identification of sensitive lifestages and associated exposure patterns
that might be compared with our understanding of the sensitivity of
young children to neurocognitive impacts of Pb. Thus, while augmenting
the evidence base on these additional endpoints, the newly available
evidence does not lead us to identify a health endpoint expected to be
more sensitive to Pb exposure than neurocognitive endpoints in
children, leading us to continue to conclude that the appropriate
primary focus for our review is on neurocognitive endpoints in
children.
[[Page 293]]
In summary, as in the last review, we continue to recognize a
number of uncertainties regarding the circumstances of Pb exposure,
including timing or lifestages, eliciting specific health effects.
Consideration of the evidence newly available in this review has not
appreciably changed our understanding on this topic. The relationship
of long-term exposure to Pb with hypertension and increased blood
pressure in adults is substantiated despite some uncertainty regarding
the exposures circumstances (e.g., magnitude and timing) contributing
to blood Pb levels measured in epidemiological studies. Across the full
evidence base, the effects for which our understanding of relevant
exposure circumstances is greatest are neurocognitive effects in young
children. Moreover, available evidence does not suggest a more
sensitive endpoint. Thus, we continue to recognize and give particular
attention to the role of Pb exposures relatively early in childhood in
contributing to neurocognitive effects, some of which may persist into
adulthood.
3. Nervous System Effects in Children
In considering the question of levels of Pb exposure at which
health effects occur, we recognize, as discussed in sections II.B.1 and
II.B.2 above, that the epidemiological evidence base for our
consideration in this review, as in the past, includes substantial
focus on internal biomarkers of exposure, such as blood Pb, with
relatively less information specific to exposure levels, including
those derived from air-related pathways. Given that blood and bone Pb
are integrated markers of aggregate exposure across all sources and
exposure pathways, our interpretation of studies relying on them is
informed by what is known regarding the historical context and exposure
circumstances of the study populations. For example, a critical aspect
of much of the epidemiological evidence is the backdrop of generally
declining Pb exposure over the past several decades (e.g., ISA,
sections 2.5 and 3.4.1; 2006 CD, section 3.4). Thus, as a generality,
recent epidemiological studies of populations with similar
characteristics as those studied in the past tend to involve lower
overall Pb exposures and accordingly lower blood Pb levels. This has
been of particular note in the evidence of blood Pb associations with
nervous system effects, particularly impacts on cognitive function in
children, for which we have seen associations with progressively lower
childhood blood Pb levels across past reviews (ISA, section 4.3.12;
1986 CD; USEPA, 1990a; 2006 CD; 73 FR 66976, November 12, 2008).
The evidence currently available with regard to the magnitude of
blood Pb levels associated with neurocognitive effects in children is
generally consistent with that available in the review completed in
2008. Nervous system effects in children, specifically effects on
cognitive function, continue to be the effects that are best
substantiated as occurring at the lowest blood Pb concentrations (ISA,
pp. lxxxvii-lxxxviii). Associations of blood Pb with effects on
cognitive function measures in children have been reported in many
studies across a range of childhood blood Pb levels, including study
group (mean/median) levels ranging down to 2 [mu]g/dL (e.g., ISA, p.
lxxxvii and section 4.3.2).\31\
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\31\ The value of 2 [mu]g/dL refers to the regression analysis
of blood Pb and end-of-grade test scores, in which blood Pb was
represented by categories for integer values of blood Pb from 1
[mu]g/dL to 9 and >10 [mu]g/dL from large statewide database. A
significant effect estimate was reported for test scores with all
blood Pb categories in comparison to the reference category (1
[mu]g/dL), which included results at and below the limit of
detection. Mean levels are not provided for any of the categories
(Miranda et al., 2009).
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Among the analyses of lowest study group blood Pb levels at the
youngest ages are analyses available in the last review of Pb
associations with neurocognitive function decrement in study groups
with mean levels on the order of 3-4 [mu]g/dL in children aged 24
months or ranging from 5 to 7 years (73 FR 66978-66979, November 12,
2008; ISA, sections 4.3.2.1 and 4.3.2.2; Bellinger and Needleman, 2003;
Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006;
Bellinger, 2008; Canfield, 2008; Tellez-Rojo, 2008; Kirrane and Patel,
2014).\32\ Newly available in this review are two studies reporting
association of blood Pb levels prior to 3 years of age with academic
performance on standardized tests in primary school; mean blood Pb
levels in these studies were 4.2 and 4.8 [mu]g/dL (ISA, section
4.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these
two studies, which represented integer blood Pb levels as categorical
variables, indicated a small effect on end-of-grade reading score of
blood Pb levels as low as 2 [mu]g/dL, after adjustment for age of
measurement, race, sex, enrollment in free or reduced lunch program,
parental education, and school type (Miranda et al., 2009).
---------------------------------------------------------------------------
\32\ The tests for cognitive function in these studies include
age-appropriate Wechsler intelligence tests (Lanphear et al., 2005;
Bellinger and Needleman, 2003), the Stanford-Binet intelligence test
(Canfield et al., 2003), and the Bayley Scales of Infant Development
(Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests
are widely used to assess neurocognitive function in children and
adults. These tests, however, are not appropriate for children under
age 3. For such children, studies generally use the age-appropriate
Bayley Scales of Infant Development as a measure of cognitive
development.
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In a newly available study of blood Pb levels at primary school
age, a significant association of blood Pb in children aged 8-11 years
and concurrently measured FSIQ was reported for a cross-sectional
cohort in Korea with a mean blood Pb level of 1.7 [mu]g/dL and range of
0.43-4.91 [mu]g/dL (Kim et al., 2009).\33\ In considering the blood Pb
levels in this study, we note that blood Pb levels in children aged 8-
11 are generally lower than those in pre-school children, for reasons
related to behavioral and other factors (ISA, sections 3.3.5, 3.4.1 and
5.2.1.1). It is likely that the blood Pb levels of this study group at
earlier ages, e.g., prior to school entry, were higher and the
available information does not provide a basis to judge whether the
blood Pb levels in this study represent lower exposure levels than
those experienced by the younger study groups. In still older children,
a large cross-sectional investigation of blood Pb association with
effects on memory and learning that was available in the last review
was focused on children aged 6-16 years, born during 1972-1988, with a
mean blood Pb of 1.9 [mu]g/dL (Lanphear et al., 2000). A study newly
available in this review, focused on a subset of the earlier study
cohort (ages 12-16, born during 1975-1982), also reports a significant
negative association of blood Pb with learning and memory test results
with mean blood Pb levels of approximately 2 [mu]g/dL (ISA, section
4.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering
these study findings with regard to the question of exposure levels
eliciting effects, we recognize, however, that blood Pb levels are, in
general, lower among teenagers than young children and also that, for
these subjects specifically, the magnitude of blood Pb levels during
the earlier childhood (e.g., pre-school ages) was much higher. For
example, the mean blood Pb levels for the 1-5 year old age group in the
NHANES 1976-80 sample was 15 [mu]g/dL, declining to 3.6 [mu]g/dL in the
NHANES 1988-1991 sample (Pirkle et al., 1994; ISA, section 3.4.1). In
summary, the available information is for population groups of ages for
which the NHANES samples indicate exposure levels were higher earlier
in childhood. Thus, in light of the NHANES information, although the
[[Page 294]]
blood Pb levels in the studies of cognitive effects in older child
population groups are lower (at the time of the study) than the younger
child study levels, the studies of older children do not provide a
basis for concluding a role for lower Pb exposure levels than those
experienced by the younger study groups.
---------------------------------------------------------------------------
\33\ Limitations of this study included a lack of consideration
of potential confounding by parental caregiving quality or IQ (ISA,
Table 4-3).
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With regard to other nervous system effects in children, the
evidence base at lower blood Pb levels is somewhat extended since the
last review with regard to the evidence on Pb and effects on
externalizing behaviors, such as attention, impulsivity, hyperactivity
and conduct disorders (ISA, section 4.3.3 and Table 4-17). Several
newly available studies investigating the role of blood Pb levels in
older children (primary school age and older) have reported significant
associations for these effects with concurrent blood Pb levels, with
mean levels generally on the order of 5 [mu]g/dL or higher (ISA,
section 4.3.3). One exception is the newly available cross-sectional,
categorical analysis of the NHANES 2001-2004 sample of children aged 8-
15 years, which found higher prevalence of conduct disorder in the
subgroup with concurrent blood Pb levels of 0.8-1.0 [mu]g/dL as
compared to the <0.8 [mu]g/dL group (ISA, section 4.3.4 and Table 4-
12). As noted above, we recognize that many of these children, born
between 1986 and 1996, are likely to have had much higher Pb exposures
(and associated blood Pb levels) in their earlier years than those
commonly experienced by young children today, thus making this study
relatively uninformative with regard to evidence of effects associated
with lower exposure levels than provided by evidence previously
available.
In summary, our conclusions regarding exposure levels at which Pb
health effects occur, particularly with regard to such levels that
might be common in the U.S. today, are complicated now, as in the last
review, by several factors. These factors include the scarcity of
information in epidemiological studies on cohort exposure histories, as
well as by the backdrop of higher past exposure levels which frame the
history of most, if not all, older study cohorts. Recognizing the
complexity, as well as the potential role of higher exposure levels in
the past, we continue to focus our consideration of this question on
the evidence of effects in young children for which our understanding
of exposure history is less uncertain.\34\ Within this evidence base,
we recognize the lowest study group blood Pb levels to be associated
with effects on cognitive function measures, indicating that to be the
most sensitive endpoint. As described above, the evidence available in
this review is generally consistent with that available in the last
review with regard to blood Pb levels at which such effects had been
reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-
66979, November 12, 2008). As blood Pb levels are a reflection of
exposure history, particularly in early childhood (ISA, section 3.3.2),
we conclude, by extension, that the currently available evidence does
not indicate Pb effects at exposure levels appreciably lower than
recognized in the last review.
---------------------------------------------------------------------------
\34\ In focusing on effects associated with blood Pb levels in
early childhood, however, we additionally recognize the evidence
across categories of effects that relate to blood Pb levels in older
child study groups (for which early childhood exposure may have had
an influence) which provides additional support to an emphasis on
nervous system effects (ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8).
---------------------------------------------------------------------------
We additionally note that, as in the last review, a threshold blood
Pb level with which nervous system effects, and specifically cognitive
effects, occur in young children cannot be discerned from the currently
available studies (ISA, sections 1.9.3 and 4.3.12). Epidemiological
analyses have reported blood Pb associations with cognitive effects
(FSIQ or BSID MDI \35\) for young child population subgroups (age 5
years or younger) with individual blood Pb measurements as low as
approximately 1 [mu]g/dL and mean concentrations as low as 2.9 to 3.8
[mu]g/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003;
Bellinger, 2008; Canfield et al., 2003; Canfield, 2008; Tellez-Rojo et
al., 2006; Tellez-Rojo, 2008). As concluded in the ISA, however, ``the
current evidence does not preclude the possibility of a threshold for
neurodevelopmental effects in children existing with lower blood levels
than those currently examined'' (ISA, section 4.3.13).
---------------------------------------------------------------------------
\35\ The Bayley Scales of Infant Development, Mental Development
Index is a well-standardized and widely used assessment measure of
infant cognitive development. Scores earlier than 24 months are not
necessarily strongly correlated with later FSIQ scores in children
with normal development (ISA, section 4.3.15.1).
---------------------------------------------------------------------------
Important uncertainties associated with the evidence of effects at
low exposure levels are similar to those recognized in the last review,
including the shape of the concentration-response relationship for
effects on neurocognitive function at low blood Pb levels in today's
young children. Also of note is our interpretation of associations
between blood Pb levels and effects in epidemiological studies, with
which we recognize uncertainty with regard to the specific exposure
circumstances (timing, duration, magnitude and frequency) that have
elicited the observed effects, as well as uncertainties in relating
ambient air concentrations (and associated air-related exposures) to
blood Pb levels in early childhood, as discussed in section II.B.2
above. We additionally recognize uncertainties associated with
conclusions drawn with regard to the nature of the epidemiological
associations with blood Pb (e.g., ISA, section 4.3.13), but note that,
based on consideration of the full body of evidence for neurocognitive
effects, the EPA has determined a causal relationship to exist between
relevant blood Pb levels and neurocognitive impacts in children (ISA,
section 4.3.15.1).
Based primarily on studies of FSIQ, the assessment of the currently
available studies, as was the case in the last review, continues to
recognize a nonlinear relationship between blood Pb and effects on
cognitive function, with a greater incremental effect (greater slope)
at lower relative to higher blood Pb levels within the range thus far
studied, extending from well above 10 [mu]g/dL to below 5 [mu]g/dL
(ISA, section 4.3.12). This was supported by the evidence available in
the last review, including the analysis of the large pooled
international dataset comprised of blood Pb measurements and IQ test
results from seven prospective cohorts (Lanphear et al., 2005;
Rothenberg and Rothenberg, 2005; ISA, section 4.3.12). The blood Pb
measurements in this pooled dataset that were concurrent with the IQ
tests ranged from 2.5 [mu]g/dL to 33.2 [mu]g/dL. The study by Lanphear
et al. (2005) additionally presented analyses that stratified the
dataset based on peak blood Pb levels (e.g., with cutpoints of 7.5
[mu]g/dL and 10 [mu]g/dL peak blood Pb) and found that the coefficients
from linear models of the association for IQ with concurrent blood Pb
were higher in the lower peak blood Pb level subsets than the higher
groups (ISA, section 4.3.12; Lanphear et al., 2005).
We note that since the completion of the ISA, two errors have been
identified with the pooled dataset analyzed by Lanphear et al. (2005)
(Kirrane and Patel, 2014). A recent publication and the EPA have
separately recalculated the statistics and mathematical model
parameters of Lanphear et al. (2005) using the corrected pooled dataset
(see Kirrane and Patel, 2014). While the magnitude of the loglinear and
linear regression coefficients are modified slightly based on the
corrections, the conclusions drawn from these coefficients, including
the finding of a steeper slope at lower (as compared to
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higher) blood Pb concentrations, are not affected (Kirrane and Patel,
2014).
In other publications, stratified analyses of several individual
cohorts also observed higher coefficients for blood Pb relationships
with measures of neurocognitive function in lower as compared to higher
blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003;
Bellinger and Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al.,
2006). Of these subgroup analyses, those involving the lowest mean
blood Pb levels and closest to the current mean for U.S. preschool
children are listed in Table 1 (drawn from Table 3 of the 2008 final
rulemaking notice [73 FR 67003, November 12, 2008], and Kirrane and
Patel, 2014).\36\ These analyses were important inputs for the
evidence-based, air-related IQ loss framework which informed decisions
on a revised standard in the last review (73 FR 67005, November 12,
2008), discussed in section II.A.1 above. As the framework focused on
the median of the four slopes in Table 1, the change to the one from
Lanphear et al. (2005) based on the recent recalculation described
above has no impact on conclusions drawn from the framework.
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\36\ One of these four is from the analysis of the lowest blood
Pb subset of the pooled international study by Lanphear et al.
(2005). The nonlinear model developed from the full pooled dataset
is the basis of the C-R functions used in the 2007 REA, in which
risk was estimated over a large range of blood Pb levels (PA,
section 3.4.3.3). Given the narrower focus of the evidence-based
framework on IQ response at the end of studied blood Pb levels
(closer to U.S. mean level), the C-R functions in Table 1 are from
linear analyses (each from separate publications) for the study
group subsets with blood Pb levels closest to mean for children in
the U.S. today.
Table 1--Summary of Quantitative Relationships of IQ and Blood Pb for Analyses With Blood Pb Levels Closest to
Those of Young Children in the U.S. Today
----------------------------------------------------------------------------------------------------------------
Blood Pb levels ([mu]g/dL) Average linear
--------------------------------------------------------------- slope \A\ (IQ
Range (min- Study/analysis \B\ points per
Geometric mean max) [mu]g/dL)
----------------------------------------------------------------------------------------------------------------
2.9........................................... 0.8-4.9 Tellez-Rojo et al. (2006)\B\, -1.71
subgroup w. concurrent blood Pb
<5 [mu]g/dL.
3.3........................................... 0.9-7.4 Lanphear et al. (2005)\C\, -2.53
subgroup w. peak blood Pb <7.5
[mu]g/dL.
3.32.......................................... 0.5-8.4 Canfield et al. (2003) \C\ \D\, -1.79
subgroup w. peak blood Pb <10
[mu]g/dL.
3.8........................................... 1-9.3 Bellinger and Needleman (2003) -1.56
\C\ \E\, subgroup w. peak blood
Pb <10 [mu]g/dL.
Median value.............................. .............. ................................ -1.75
----------------------------------------------------------------------------------------------------------------
A--Average linear slope estimates here are generally for relationship with IQ assessed concurrently with blood
Pb measurement. As exceptions, Bellinger & Needleman (2003) slope is relationship for 10 year old IQ with
blood Pb levels at 24 months, and the data for Boston cohort included in Lanphear et al. (2005) slope are
relationship for 10 year old IQ with blood Pb levels at 5 years.
B--The slope for Tellez-Rojo et al. (2006) is for BSID (MDI), a measure of cognitive development appropriate to
study population age (24-mos). The blood Pb levels for this subgroup are from Tellez-Rojo (2008).
C--The Lanphear et al. (2005) pooled international study also includes blood Pb data from the Rochester and
Boston cohorts, although for different ages (6 and 5 years, respectively) than the ages analyzed in Canfield
et al. (2003) and Bellinger and Needleman (2003). Thus, the ages at the blood Pb measurements used in
derivation of the linear slope for the Lanphear et al. (2005) subgroup shown here are 5 to 7 years. The blood
Pb levels and coefficient presented here for Lanphear et al. (2005) study group reflect the recalculation
using the corrected pooled dataset (Kirrane and Patel, 2014).
D--Blood Pb levels for this subgroup are from Canfield (2008).
E--Blood Pb levels for this subgroup are from Bellinger (2008).
Several studies newly available in the current review have, in all
but one instance, also found a nonlinear blood Pb-cognitive function
relationship in nonparametric regression analyses of the cohort blood
Pb levels analyzed (ISA, section 4.3.12). These studies, however, used
statistical approaches that did not produce quantitative results for
each blood Pb group (ISA, section 4.3.12). Thus, newly available
studies have not extended the range of observation for quantitative
estimates of this relationship to lower blood Pb levels than those of
the previous review. The ISA further notes that the potential for
nonlinearity has not been examined in detail within a lower, narrower
range of blood Pb levels than those of the full cohorts thus far
studied in the currently available evidence base (ISA, section 4.3.12).
Such an observation in the last review supported the consideration of
linear slopes with regard to blood Pb levels at and below those
represented in Table 1. In summary, the newly available evidence does
not substantively alter our understanding of the C-R relationship
(including quantitative aspects) for neurocognitive impact, such as IQ
with blood Pb in young children.
4. At-Risk Populations
In this section, we use the term ``at-risk populations'' \37\ to
recognize populations that have a greater likelihood of experiencing
Pb-related health effects, i.e., groups with characteristics that
contribute to an increased risk of Pb-related health effects. These
populations are also sometimes referred to as sensitive groups (as in
section I.A above). In identifying factors that increase risk of Pb-
related health effects, the EPA has considered evidence regarding
factors contributing to increased susceptibility, generally including
physiological or intrinsic factors contributing to a greater response
for the same exposure, and those contributing to increased exposure,
including that resulting from behavior leading to increased contact
with contaminated media (ISA, Chapter 5). Physiological risk factors
include both conditions contributing to a group's increased risk of
effects at a given blood Pb level, and those that contribute to blood
Pb levels higher than those otherwise associated with a
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given Pb exposure (e.g., ISA, sections 5.3 and 5.1, respectively).
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\37\ In the context of ``at-risk populations,'' the term
``population'' refers to persons having one or more qualities or
characteristics including, for example, a specific pre-existing
illness or a specific age or lifestage, with lifestage referring to
a distinguishable time frame in an individual's life characterized
by unique and relatively stable behavioral and/or physiological
characteristics that are associated with development and growth.
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The information newly available in this review has not
substantially altered our previous understanding of at-risk populations
for Pb in ambient air. As in the last review, the factor most
prominently recognized to contribute to increased risk of Pb effects is
childhood (ISA, section 1.9.6). As noted in section II.B.2 above,
although the specific ages or lifestages of greatest susceptibility
\38\ or risk have not been established (e.g., ISA, section 4.3.11), the
at-risk status of young children to the neurodevelopmental effects of
Pb is well recognized (e.g., ISA, sections 1.9.6, 4.3, 5.2.1, 5.3.1,
and 5.4). The evidence indicates that prenatal blood Pb levels are
associated with nervous system effects, including mental development in
very young children and can also be associated with cognitive
decrements in older children (ISA, section 4.3). Additionally, the
coincidence during early childhood of behaviors that increase exposure,
such as hand-to-mouth contact by which children transfer Pb in settled
particles to their mouths, and the development of the nervous system
also contributes increased risk during this time (ISA, sections 3.7.1,
4.3.2.6, 5.2.1.1, 5.3.1.1 and 5.4). Collectively, however, the evidence
indicates both the susceptibility of the developing fetus and early
postnatal years, as well as the potential for continued susceptibility
through childhood as the human central nervous system continues to
mature and be vulnerable to neurotoxicants (ISA, sections 1.9.5 and
4.3.15; 2006 CD, section 6.2.12). As discussed in section II.B.2 above,
while uncertainties remain with regard to the role of Pb exposures
during a particular age of life in eliciting nervous system effects,
such as cognitive function decrements, the full evidence base continues
to indicate prenatal and early childhood lifestages as periods of
increased Pb-related risk (ISA, sections 4.3.11 and 4.3.15).
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\38\ As noted in the ISA, ``in most instances, `susceptibility'
refers to biological or intrinsic factors (e.g., age and sex) while
`vulnerability' refers to nonbiological or extrinsic factors (e.g.,
socioeconomic status [SES])'' and the terms ``at-risk'' and
``sensitive'' populations have in various instances been used to
encompass these concepts more generally (ISA, p. 5-1). In providing
detail regarding factors contributing to an ``at-risk'' status in
this section, we have used the other terms in particular instances,
with our usage consistent with these common definitions.
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Several physiological factors increase the risk of Pb-related
health effects by contributing to increased blood Pb levels over those
otherwise associated with a given Pb exposure (ISA, sections 3.2, 3.3
and 5.1). These include nutritional status, which plays a role in Pb
absorption from the gastrointestinal tract (ISA, sections 3.2.1.2, 5.1,
5.3.10 and 5.4). For example, diets deficient in iron, calcium or zinc
can contribute to increased Pb absorption and associated higher blood
Pb levels (ISA, sections 3.2.1.2, and 5.1). Evidence is suggestive of
some genetic characteristics as potential risk factors, such as
presence of the [delta]-aminolevulinic acid dehydratase-2 (ALAD-2)
allele which has been indicated to increase blood Pb levels or Pb-
related risk of health effects in some studies (ISA, sections 3.3.2 and
5.1).
Risk factors based on increased exposure include spending time in
proximity to sources of Pb to ambient air or other environmental media
(e.g., large active metals industries or locations of historical Pb
contamination) (ISA, sections 1.9.6, 3.7.1, 5.2.5 and 5.4). Residential
factors associated with other sources of Pb exposure (e.g., leaded
paint or plumbing with Pb pipes or solder) are another exposure-related
risk factor (ISA, sections 3.7.1, 5.2.6 and 5.4). Additionally, some
races or ethnicities have been associated with higher blood Pb levels,
with differential exposure indicated in some cases as the cause (ISA,
sections 5.2.3 and 5.4). Lower socioeconomic status (SES) has been
associated with higher Pb exposure and higher blood Pb concentration,
leading the ISA to conclude the evidence is suggestive for low SES as a
risk factor (ISA, sections 5.3.16, 5.2.4 and 5.4). Although the
differences in blood Pb levels between children of lower and higher
income levels (as well as among some races or ethnicities) have
lessened, blood Pb levels continue to be higher among lower-income
children indicating higher exposure and/or greater influence of factors
independent of exposure, such as nutritional factors (ISA, sections
1.9.6, 5.2.1.1 and 5.4).
In considering risk factors associated with increased Pb exposure
or increased blood Pb levels, we note that the currently available
evidence continues to support a nonlinear relationship between
neurocognitive effects and blood Pb that indicates incrementally
greater impacts at lower as compared to higher blood Pb levels (ISA,
section 4.3.12), as described in section II.B.3 above. An important
implication of this finding is that while children with higher blood Pb
levels are at greater risk of Pb-related effects than children with
lower blood Pb levels, on an incremental basis (e.g., per [micro]g/dL),
the risk is greater for children at lower blood Pb levels. This was
given particular attention in the last review of the Pb NAAQS, in which
the standard was revised with consideration of the incremental impact
of air-related Pb on young children in the U.S. and the recognition of
greater impact for those children with lower absolute blood Pb levels
(73 FR 67002, November 12, 2008). Such consideration included a focus
on those C-R studies involving the lowest blood Pb levels, as described
in section II.A.1 above.
In summary, the information newly available in this review has not
appreciably altered our understanding of human populations that are
particularly sensitive to Pb exposures. In the current review, as at
the time of the last review of the Pb NAAQS, we recognize young
children as an important at-risk population, with sensitivity extending
to prenatal exposures and into childhood development. Additional risk
factors for increased blood Pb levels include deficiencies in dietary
minerals (iron, calcium and zinc), some racial or ethnic
backgrounds,\39\ and spending time in proximity to environmental
sources of Pb or residing in older houses with Pb exposure related to
paint or plumbing.\40\ The currently available evidence continues to
additionally suggest a potential for increased risk associated with
several other factors, including older adulthood,\41\ pre-existing
disease
[[Page 297]]
(e.g., hypertension), variants for certain genes and increased stress
(ISA, section 5.3.4). As discussed above, we recognize the sensitivity
of the prenatal period and several lifestages of childhood to an array
of neurocognitive and behavioral effects, and we particularly recognize
young children as an important at-risk population in light of current
environmental exposure levels. Age or lifestage was used to distinguish
potential groups on which to focus in the last review in recognition of
its role in exposure and susceptibility, and young children were the
focus of the REA in consideration of the health effects evidence
regarding endpoints of greatest public health concern and in
recognition of effects on the developing nervous system as a sentinel
endpoint for public health impacts of Pb. This identification continues
to be supported by the evidence available in the current review.
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\39\ The ISA concludes that studies of race/ethnicity provide
adequate evidence that race/ethnicity is an at-risk factor based on
the higher exposure observed among non-white populations and some
modification observed in studies of associations between Pb levels
and some health effects, such as hypertension (ISA, section 6.4).
\40\ The evidence for SES continues to indicate increased blood
Pb levels in lower income children, although its role with regard to
an increased health risk for the same blood Pb level is unclear and
its role generally with regard to Pb-related risk is somewhat
complicated. SES often serves as a marker term for one or a
combination of unspecified or unknown environmental or behavioral
variables. Further, it is independently associated with an adverse
impact on neurocognitive development, and a few studies have
examined SES as a potential modifier of the association of childhood
Pb exposure with cognitive function with inconsistent findings
regarding low SES as a potential risk factor. The ISA concludes the
evidence for SES as a Pb risk factor is suggestive, based on the
greater exposures or blood Pb levels in some low SES groups (ISA,
section 5.4).
\41\ The ISA identifies older adulthood as a lifestage of
potentially greater risk of Pb-related health effects based
primarily on the evidence of increases in blood Pb levels during
this lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4), as well as
observed associations of some cardiovascular and nervous system
effects with bone and blood Pb in older populations, with biological
plausibility for the role of Pb provided by experimental animal
studies (ISA, sections 4.3.5, 4.3.7 and 4.4). Exposure histories of
older adult study populations, which included younger years during
the time of leaded gasoline usage and other sources of Pb exposures
which were more prevalent in the past than today, are likely
contributors to their blood Pb levels (ISA, pp. lx-lxi; Figure 2-1
and sections 2.5.2, 3.3.5 and 5.2.1.2).
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5. Potential Impacts on Public Health
There are several potential public health impacts associated with
Pb exposure in the current U.S. population. In recognition of effects
causally related to blood Pb levels somewhat near those most recently
reported for today's population and for which the weight of the
evidence is greatest, the potential public health impacts most
prominently recognized in the ISA are population IQ impacts associated
with childhood Pb exposure and prevalence of cardiovascular effects in
adults (ISA, section 1.9.1). With regard to the latter category, as
discussed above, the full body of evidence indicates a role of long-
term cumulative exposure, with uncertainty regarding the specific
exposure circumstances contributing to the effects in the
epidemiological studies of adult populations, for whom historical Pb
exposures were likely much higher than exposures that commonly occur
today (ISA, section 4.4). There is less uncertainty regarding the
exposure patterns contributing to the blood Pb levels reported in
studies of younger populations (ISA, sections 1.9.4 and 1.10).
Accordingly, the discussion of public health implications relevant to
this review is focused predominantly on nervous system effects,
including IQ decrements, in children.
The magnitude of a public health impact is dependent upon the type
or severity of the effect, as well as the size of populations affected.
Intelligence quotient is a well-established, widely recognized and
rigorously standardized measure of neurocognitive function, as well as
a global measure reflecting the integration of numerous processes (ISA,
section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). Examples of other
measures of cognitive function negatively associated with Pb exposure
include other measures of intelligence and cognitive development and
measures of other cognitive abilities, such as learning, memory, and
executive functions, as well as academic performance and achievement
(ISA, section 4.3.2). Although some neurocognitive effects of Pb in
children may be transient, some may persist into adulthood (ISA,
section 1.9.5).\42\ We also note that deficits in neurodevelopment
early in life may have lifetime consequences as ``[n]eurodevelopmental
deficits measured in childhood may set affected children on
trajectories more prone toward lower educational attainment and
financial well-being'' (ISA, section 4.3.14). Thus, population groups
for which neurodevelopment is affected by Pb exposure in early
childhood are at risk of related impacts on their success later in
life. Further, in considering population risk, the ISA notes that
``[s]mall shifts in the population mean IQ can be highly significant
from a public health perspective'' (ISA, p. xciii). For example, if Pb-
related decrements are manifested uniformly across the range of IQ
scores in a population, ``a small shift in the population mean IQ may
be significant from a public health perspective because such a shift
could yield a larger proportion of individuals functioning in the low
range of the IQ distribution, which is associated with increased risk
of educational, vocational, and social failure'' as well as a decrease
in the proportion with high IQ scores (ISA, section 1.9.1).
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\42\ The ISA states that the ``persistence of effects appears to
depend on the duration and window of exposure as well as other
factors that may affect an individual's ability to recover from an
insult,'' with some evidence of greater recovery in children reared
in households with more optimal caregiving characteristics and low
concurrent blood Pb levels (ISA, p. 1-77; Bellinger et al., 1990).
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As summarized above, young children are the at-risk population that
may be most at risk of health effects associated with exposure to Pb
and children at greatest risk from air-related Pb are those children
with highest air-related Pb exposure which we consider to be those
living in areas of higher ambient air Pb concentrations. To inform our
understanding of the extent of this population potentially at risk from
air-related Pb, the PA includes two analyses. The first analysis is
based on consideration of the available air Pb monitoring information.
As the air quality data set available for the first analysis may not be
inclusive of all of the newly sited monitors (as discussed in section
2.2.1 of the PA) and there may be other areas with elevated Pb
concentrations, a second analysis was performed in consideration of
emissions estimates from the National Emissions Inventory (NEI),
although with recognition of uncertainties associated with inferences
drawn from such estimates with regard to ambient air Pb concentrations
and exposures (PA, pp. 3-36 to 3-38).\43\
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\43\ Such uncertainties include those with regard to specific
source characteristics and meteorology, not explicitly considered in
the analysis. In light of such uncertainties, the PA interprets the
emissions-based analysis to provide a bounding estimate below which
the true value is expected to fall (PA, p. 3-37).
---------------------------------------------------------------------------
The first PA analysis indicates that approximately one hundredth of
one percent of the full population of children aged 5 or under in the
U.S. reside within 0.5 km of monitors exceeding or within 10 percent of
the level of the current standard (PA, section 2.2.2.2, pp. 3-36 to 3-
37, 4-25 and Table 3-4). In the second analysis, the size of young
child populations residing in areas near large Pb sources was
approximately four hundredths of one percent of the full U.S.
population of children aged 5 years or younger (PA, pp. 3-37 to 3-38,
4-25). The PA recognized uncertainties and potential limitations
associated with the use of the emissions estimates in the second
analysis to make inferences regarding ambient air Pb exposures,
uncertainties both with regard to the accuracy of such estimates and
also with regard to the role of specific source characteristics and
meteorology, not explicitly considered here, in influencing ambient air
Pb concentrations and contributing to substantial variation in air Pb
concentrations at source locations (e.g., PA, Figure 2-11).
Accordingly, while the second analysis is considered informative with
regard to the potential prevalence of airborne Pb emissions and
potential exposure of human populations, it is limited with regard to
its ability to identify populations living in areas of elevated ambient
air Pb concentrations. The PA interprets the two analyses together to
indicate that well below one tenth of one percent of the full
population of children aged 5 years or younger in the U.S. today live
in areas with air Pb concentrations near or above the current standard,
with the current monitoring data indicating the size of this population
to be approximately one hundredth of a percent of the full population
of children aged 5 or younger (PA, pp. 3-36 to 3-38, 4-25, 4-32).
[[Page 298]]
C. Blood Lead as a Biomarker of Exposure and Relationships With Air
Lead
Blood Pb is well established as a biomarker of Pb exposure and of
internal dose, with relationships between air Pb concentrations and
blood Pb concentrations informing consideration of the NAAQS for Pb
since its initial establishment in 1978. Lead associated with inhaled
particles may, depending on particle size and Pb solubility, be
absorbed into the systemic circulation or transported with particles to
the gastrointestinal tract (ISA, section 3.2.1.1), where its absorption
is influenced by a range of factors (ISA, section 3.2.1.2). Lead in the
blood stream is quickly distributed throughout the body (e.g., within
days), available for exchange with the soft and skeletal tissues, the
latter of which serves as the largest storage compartment (ISA, section
3.2.2.2). Given the association with exposure and the relative ease of
collection, blood Pb levels are extensively used as an index or
biomarker of exposure by national and international health agencies, as
well as in epidemiological and toxicological studies of Pb health
effects and dose-response relationships (ISA, sections 3.3.2, 3.4.1,
4.3, 4.4, 4.5, 4.6, 4.7, and 4.8). While bone Pb measurements are also
used in epidemiological studies as an indicator of cumulative Pb
exposure, blood Pb measurements remain the predominant, well-
established and well-characterized exposure approach.
Since 1976, the CDC has been monitoring blood Pb levels nationally
through the NHANES. This survey has documented the dramatic decline in
mean blood Pb levels in all ages of the U.S. population that has
occurred since the 1970s (PA, Figure 3-1), and that coincides with
actions on leaded fuels, leaded paint, Pb in food packaging, and Pb-
containing plumbing materials that have reduced Pb exposure in the U.S.
(ISA, section 3.4.1; Pirkle et al., 1994; Schwemberger et al., 2005).
This decline has continued over the more recent past. For example, the
2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 years
is 1.17 [mu]g/dL, as compared to 1.51 [mu]g/dL in 2007-2008 (ISA,
section 3.4.1) and 1.8 [mu]g/dL in 2003-2004, the most recent data
available at the time of the last review (73 FR 67002, November 12,
2008). Somewhat less dramatic declines have been reported in the upper
tails of the distribution and in different groups with higher blood Pb
levels than the general child population (ISA, Figures 3-17 and 3-19).
The blood Pb concentration in childhood (particularly early
childhood) can more quickly (than in adulthood) reflect changes in
total body burden (associated with the shorter exposure history) and
can also reflect changes in recent exposures (ISA, section 3.3.5). The
relationship of children's blood Pb to recent exposure may reflect
their labile bone pool, with their rapid bone turnover in response to
rapid childhood growth rates (ISA, section 3.3.5). The relatively
smaller skeletal compartment of Pb in children (particularly very young
children) compared to adults is subject to more rapid turnover. The
distribution of Pb in the body is dynamic throughout life, with Pb in
the body being exchanged between blood and bone and between blood and
soft tissues (ISA, sections 3.3.5 and 3.2.2; 2006 CD, section 4.3.2).
The rates of these exchanges vary with age, exposure and various
physiological variables. For example, resorption of bone, which results
in the mobilization of Pb from bone into the blood, is a somewhat rapid
and ongoing process during childhood and a more gradual process in
later adulthood (ISA, sections 3.2.2.2, 3.3.5 and 3.7.2; PA, pp. 3-2 to
3-3).
Lead in ambient air contributes to Pb in blood by multiple exposure
pathways by both inhalation and ingestion exposure routes (ISA, section
3.1.1). Multiple studies have demonstrated young children's blood Pb
levels to reflect Pb exposures, including exposures to Pb in surface
dust (e.g., Lanphear and Roghmann, 1997; Lanphear et al., 1998). These
and studies of child populations near sources of air Pb emissions, such
as metal smelters, have further demonstrated the effect of airborne Pb
on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3;
Hilts, 2003; Gulson et al., 2004).
As blood Pb is an integrated marker of aggregate Pb exposure across
all pathways, the blood Pb C-R relationships described in
epidemiological studies of Pb-exposed populations do not distinguish
among different sources of Pb or pathways of Pb exposure (e.g.,
inhalation, ingestion of indoor dust, ingestion of dust containing
leaded paint). Thus, our interpretation of the health effects evidence
for purposes of this review necessitates characterization of the
relationships between Pb from those sources and pathways of interest in
this review (i.e., those related to Pb emitted into the air) and blood
Pb.
The evidence for air-to-blood relationships derives from analyses
of datasets for populations residing in areas with differing air Pb
concentrations, including datasets for circumstances in which blood Pb
levels have changed in response to changes in air Pb. The control for
variables other than air Pb that can affect blood Pb varies across
these analyses. At the conclusion of the last review in 2008, the EPA
interpreted the evidence as providing support for use (in informing the
Administrator's decision on standard level) of a range of air-to-blood
ratios \44\ ``inclusive at the upper end of estimates on the order of
1:10 and at the lower end on the order of 1:5'' (73 FR 67002, November
12, 2008). This conclusion reflected consideration of the air-to-blood
ratios presented in the 1986 CD \45\ and associated observations
regarding factors contributing to variation in such ratios, ratios
reported subsequently and ratios estimated based on modeling performed
in the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-
67002, November 12, 2008). The information available in this review,
which is assessed in the ISA and largely, although not completely,
comprises studies that were available in the last review, does not
alter the primary scientific conclusions drawn in the last review
regarding the relationships between Pb in ambient air and Pb in
children's blood. The ratios summarized in the ISA in this review span
a range generally consistent with the range concluded in 2008 (ISA,
section 3.5.1).
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\44\ The quantitative relationship between ambient air Pb and
blood Pb, often termed a slope or ratio, describes the increase in
blood Pb (in [mu]g/dL) estimated to be associated with each unit
increase of air Pb (in [micro]g/m\3\). Ratios are presented in the
form of 1:x, with the 1 representing air Pb (in [mu]g/m\3\) and x
representing blood Pb (in [mu]g/dL). Description of ratios as higher
or lower refers to the values for x (i.e., the change in blood Pb
per unit of air Pb). Slopes are presented as simply the value of x.
\45\ The 2006 CD did not include an assessment of then-current
evidence on air-to-blood ratios.
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The evidence pertaining to the quantitative relationship between
air Pb and children's blood Pb is now, as in the past, limited by the
circumstances in which the data are collected. These estimates are
generally developed from studies of populations in a variety of Pb
exposure circumstances. Accordingly, there is significant variability
in air-to-blood ratios among the different study populations exposed to
Pb through different air-related exposure pathways and at different
exposure levels. This variability in air-to-blood estimates can relate
to the representation of air-related pathways and study populations,
including, for example, relatively narrow age ranges for the population
in order to reduce age-related variability in blood Pb, or including
populations with narrowly specified dietary sources. It
[[Page 299]]
can relate to the study population exposure and blood Pb levels (ISA,
section 3.7.4). It can also relate to the precision of air and blood
measurements and of the study circumstances, such as with regard to
spatial and temporal aspects. Additionally, in situations where
exposure to nonair sources covaries with air-related exposures that are
not accounted for in deriving ratio estimates, uncertainties may relate
to the potential for confounding by nonair exposure covariance (ISA,
section 3.5). Most of the studies assessed in the ISA and PA have
reported ratios for which the relationship is linear, while a subset
are derived from nonlinear models (PA, Table 3-1; ISA, section 3.7.4).
As was noted in the last review, age is an important influence on
the magnitude of air-to-blood ratio estimates derived. Ratios for
children are generally higher than those for adults, and higher for
young children than older children, perhaps due to behavioral
differences between the age groups, as well as their shorter exposure
history. Similarly, given the common pattern of higher blood Pb levels
in pre-school-aged children than during the rest of childhood, related
to behaviors that increase environmental exposures (e.g., hand-to-mouth
activity), ratios would be expected to be highest in earlier childhood.
Additionally, estimates of air-to-blood ratios that include air-related
ingestion pathways in addition to the inhalation pathway are
``necessarily higher,'' in terms of blood Pb response, than those
estimates based on inhalation alone (1986 CD, p. 11-106). Thus, the
extent to which studies account for the full set of air-related
inhalation and ingestion exposure pathways affects the magnitude of the
resultant air-to-blood estimates, such that including fewer pathways as
``air-related'' yields lower ratios. Estimates of air-to-blood ratios
can also be influenced by population characteristics that may influence
blood Pb; accordingly, some analyses include adjustments.
Given the recognition of young children as a key at-risk population
in this review, as in the last (as discussed in section II.B.3 above),
as well as the influence of age on blood Pb levels, we have considered
the available studies in groups based on the extent of their inclusion
of children younger than or barely school age (less than or equal to 5
years of age). Among the first group of studies, focused exclusively on
young children, only one study dates from the end of or after the
phase-out of leaded gasoline usage (Hilts, 2003). This study reports
changes in children's blood Pb levels associated with reduced Pb
emissions and associated air concentrations near a Pb smelter in Canada
(for children through age 5). Given the timing of this study, after the
leaded gasoline phase-out, and its setting near a smelter, the ambient
air Pb in this study may be somewhat more comparable to that near
sources in the U.S. today than other studies discussed herein. The
study authors report an air-to-blood ratio of 1:6.\46\ An EPA analysis
of the air and blood data reported for 1996, 1999 and 2001 results in a
ratio of 1:6.5, and an analysis focused only on the 1996 and 1999 data
(pre- and post- the new technology) yields a ratio of 1:7 (ISA, section
3.5.1; Hilts, 2003).\47\ The two other studies that focused on children
of age 5 or younger analyzed variations in air Pb as a result of
variations in leaded gasoline usage in Chicago, Illinois and reported
somewhat higher ratios of 1:8 and 1:8.6 (Hayes et al., 1994; Schwartz
and Pitcher, 1989). We note, however, the blood Pb concentrations in
the two leaded gasoline studies are appreciably higher (a factor of two
or more) than those in the study near the smelter (Hilts, 2003), and
also than those commonly reported in the U.S. today.
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\46\ Sources of uncertainty include the role of factors other
than ambient air Pb reduction in influencing decreases in blood Pb
(ISA, section 3.5.1). The author cited remedial programs (e.g.,
community and home-based dust control and education) as potentially
responsible for some of the blood Pb reduction seen during the study
period (1997 to 2001), although the author notes that these programs
were in place in 1992, suggesting they are unlikely to have
contributed to the sudden drop in blood Pb levels occurring after
1997 (Hilts, 2003). Other aspects with potential implications for
ratios include the potential for children with lower blood Pb levels
not to return for subsequent testing, and the age range of 6 to 36
months in the 2001 blood screening compared to ages up to 60 months
in earlier years of the study (Hilts, 2003).
\47\ This study considered changes in ambient air Pb levels and
associated blood Pb levels over a 5-year period which included
closure of an older Pb smelter and subsequent opening of a newer
facility in 1997 and a temporary (3-month) shutdown of all smelting
activity in the summer of 2001. The author observed that the air-to-
blood ratio for children in the area over the full period was
approximately 1:6. The author noted limitations in the dataset
associated with exposures in the second time period, after the
temporary shutdown of the facility in 2001, including sampling of a
different age group at that time and a shorter time period (3
months) at these lower ambient air Pb levels prior to collection of
blood Pb levels. Consequently, the EPA calculated an alternate air-
to-blood Pb ratio based on ambient air Pb and blood Pb reductions in
the first time period, after opening of the new facility in 1997
(ISA, section 3.5.1).
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The second group of studies includes but is not limited to children
less than or equal to 5 years of age. This group includes a complex
statistical analysis and associated dataset for a cohort of children
born in Mexico City from 1987 through 1992 (Schnaas et al., 2004).
Although this study, which was not assessed in the last review,
encompasses the period of leaded gasoline usage, it further informs our
understanding of factors influencing the quantitative relationship
between air Pb and children's blood Pb. Air-to-blood ratios developed
from this study are influenced by a number of factors and appear to
range from roughly 1:2 to 1:6, in addition to an estimate of 1:9 (ISA,
section 3.5.1), although the latter is derived from a data set
restricted to the latter years of the study when little change in air
Pb concentration occurred, such that the role of air Pb may be more
uncertain. Estimates associated with the developmental period of
highest exposure (e.g., age 2 years) range up to approximately 1:6,
illustrating the influence of age on the ratio (ISA, section 3.5.1).
Also in the second group of studies are two much older studies of
populations with age ranges extending well beyond 6 years. The first is
the review and meta-analysis by Brunekreef (1984) using datasets
available at the time for variously aged children as old as 18 years
with identified air monitoring methods and reliable blood Pb data for
18 locations in the U.S. and internationally.\48\ Two air-to-blood
ratio estimates derived from this study based on log-log models both
round to 1:5 (for air concentrations corresponding to the geometric
means of the two sets of data pairs [1.5 and 0.54 [mu]g/m\3\]). A ratio
on the order of 1:9 was derived based on the study by Schwartz and
Pitcher (1989) of the relationship between U.S. NHANES II blood Pb
levels for white subjects, aged <=74 years, and national usage of
leaded gasoline, adjusted for age and other covariates (Henderson,
2007a, pp. D-2 to D-3; ISA, Table 3-12).
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\48\ In the dataset reviewed by Brunekreef (1984), air-to-blood
ratios from the subset of those studies that used quality control
protocols and presented adjusted slopes include values of 3.6,
(Zielhuis et al., 1979), 5.2 (Billick et al., 1979, 1980); 2.9
(Billick, 1983), and 8.5 (Brunekreef et al., 1983). The studies
cited here adjusted for parental education (Zielhuis et al., 1979),
age and race (Billick et al., 1979, 1980) and air Pb monitor height
(Billick, 1983); Brunekreef (1984) used multiple regression to
control for several confounders (73 FR 66974).
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The last two studies are focused on older children, ages 6-11 in
India and Germany (Tripathi et al., 2001; Ranft et al., 2008) and
employed methods to characterize media Pb concentrations that differed
from the other studies assessed (PA, p. 3-11). The location-specific
geometric mean blood Pb levels in the Indian study (8.6-14.4 [micro]g/
dL) indicate blood Pb distributions in this age group much higher than
those pertinent to similarly aged children in the U.S. today and the
air-to-blood ratio
[[Page 300]]
estimate reported was 1:3.6 (Tripathi et al., 2001). The more recent
German study by Ranft et al. (2008) analyzed data from a nearly 20-year
period associated with the leaded gasoline phase-out, during which
average blood Pb levels declined from 9 [micro]g/dL in 1983 (345
children, average age of 9 years) to 3 [micro]g/dL in 2000 (162
children, average of 6 years).\49\ Average air Pb concentration
declined from 0.45 [micro]g/m\3\ to 0.06 [micro]g/m\3\ over the same
period, with the largest reduction occurring between the first study
year (derived from two monitoring sites for full study area) and the
second study year, 1991, for which air concentrations were derived from
a combination of dispersion modeling and the two monitoring sites.\50\
For a mean air Pb concentration of 0.1 [micro]g/m\3\, the study's
multivariate loglinear regression model predicted air-to-blood ratios
of 3.2 and 6.4 for ``background'' blood Pb concentrations of 1.5 and 3
[micro]g/dL, respectively. In this study, background referred to Pb in
blood from other sources; the blood Pb distribution over the study
period, including levels when air Pb concentrations are lowest,
indicates 3 [micro]g/dL may be the better estimate of background for
this study population. Inclusion of soil Pb as a variable in the model
may have contributed to an underestimation of the blood Pb-air Pb
ratios for this study because some of the Pb in soil likely originated
in air and the blood Pb-air Pb slope does not include the portion of
the soil/dust Pb ingestion pathway that derives from air Pb. Using
univariate linear, log-log and loglinear models on the median air and
blood Pb concentrations reported for the 5 years included in this
study, the ISA also derived air-to-blood ratio estimates for data from
this study ranging from 9 to 17 (ISA, p. 3-126; Ranft et al., 2008,
Table 2). Uncertainties related to this study's estimates include those
related to the bulk of air concentration reduction occurring between
the first two time points (1983 and 1991) and the difference among the
year's air datasets (e.g., two data sources [air monitors] in 1983 and
multiple geographical points from a combination of the monitors and
modeling in subsequent years).
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\49\ Blood Pb measurements were available on a total of 843
children across five time periods, in the first of which the average
child age was 9 years while it was approximately 6 years in each of
the latter years: 1983 (n=356), 1991 (n=147), 1994 (n=122), 1997
(n=56), and 2000 (n=162) (Ranft et al., 2008).
\50\ The 1983 air Pb concentrations were based on two monitoring
stations, while a combination of dispersion modeling and monitoring
data was used in the later years. Surface soil Pb measurements were
from 2000-2001, but geo-matched to blood Pb measurements across full
study period (Ranft et al., 2008).
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In this review, as in the 2008 Pb NAAQS review, in addition to
considering the evidence presented in the published literature and that
reviewed in the 1986 CD, we also consider air-to-blood ratios derived
from the exposure assessment (PA, p. 3-14; 73 FR 66974, November 12,
2008; 2007 REA, section 5.2.5.2). In the exposure assessment
(summarized in section II.D below), current modeling tools and
information on children's activity patterns, behavior and physiology
were used to estimate blood Pb levels associated with multimedia and
multipathway Pb exposure. The results from the various case studies
assessed, with consideration of the context in which they were derived
(e.g., the extent to which the range of air-related pathways was
simulated, and the limitations associated with those simulations), and
the multiple sources of uncertainty are also informative to our
understanding of air-to-blood ratios. Estimates of air-to-blood ratios
for the two REA case studies that represent localized population
exposures exhibited an increasing trend across air quality scenarios
representing decreasing air concentrations. For example, across the
alternative standard levels assessed, which ranged from a calendar
quarter average of 1.5 [micro]g/m\3\ down to a monthly average of 0.02
[micro]g/m\3\, the ratios ranged from 1:2 to 1:9 for the generalized
(local) urban case study, with a similar trend, although of generally
higher ratio, for the primary smelter case study subarea. This pattern
of model-derived ratios is generally consistent with the range of
ratios obtained from the literature, briefly discussed above. We
continue to recognize a number of sources of uncertainty associated
with these model-derived ratios which may contribute to high or low
biases (as discussed further in section 3.1 of the PA).
The evidence on the quantitative relationship between air Pb and
air-related Pb in blood is now, as in the past, limited by the
circumstances (such as those related to Pb exposure) in which the data
were collected. Previous reviews have recognized the significant
variability in air-to-blood ratios for different populations exposed to
Pb through different air-related exposure pathways and at different air
and blood levels, with the 1986 CD noting that ratios derived from
studies involving the higher blood and air Pb levels pertaining to
occupationally exposed workers are generally smaller than ratios from
studies involving lower blood and air Pb levels (ISA, p. 3-132; 1986
CD, p. 11-99). Consistent with this observation, slopes in the range of
3 to 5 were estimated for child population datasets assessed in the
1986 CD (ISA, p. 3-132; 1986 CD p. 11-100; Brunekreef, 1984).
Additional studies considered in the last review and those assessed in
the ISA provide evidence of ratios above this older range (ISA, p. 3-
133). For example, a ratio of 1:6.5-1:7 is indicated by the study by
Hilts (2003), one of the few studies that evaluate the air Pb-blood Pb
relationship in conditions that are closer to the current state in the
U.S. (ISA, p. 3-132). We additionally note the variety of factors
identified in the ISA that may potentially affect estimates of various
ratios (including potentially coincident reductions in nonair Pb
sources during the course of the studies), and for which a lack of
complete information may preclude any adjustment of estimates to
account for their role (ISA, section 3.5).
In summary, as at the time of the last review of the NAAQS for Pb,
the currently available evidence includes estimates of air-to-blood
ratios, both empirical and model-derived, with associated limitations
and related uncertainties. These limitations and uncertainties, which
are summarized here and also noted in the ISA, usually include
uncertainty associated with reductions in other Pb sources during the
study period. The limited amount of new information available in this
review has not appreciably altered the scientific conclusions reached
in the last review regarding relationships between Pb in ambient air
and Pb in children's blood or with regard to the range of ratios. The
currently available evidence continues to indicate ratios relevant to
the population of young children in the U.S. today, reflecting multiple
air-related pathways in addition to inhalation, to be generally
consistent with the approximate range of 1:5 to 1:10 given particular
attention in the 2008 NAAQS decision, including the ``generally central
estimate'' of 1:7 (73 FR 67002, 67004, November 12, 2008; ISA, pp. 3-
132 to 3-133).
D. Summary of Risk and Exposure Assessment Information
The risk information available for this review and summarized here
is based primarily on the exposure and risk assessment developed in the
last review of the Pb NAAQS, described in the 2007 REA, the 2007 Staff
Paper and the 2008 notice of final decision (USEPA, 2007a; USEPA,
2007b; 73 FR 66964, November 12, 2008), as considered in the context of
the evidence newly available in this review (PA, section 3.4). As
described in
[[Page 301]]
the REA Planning Document, careful consideration of the information
newly available in this review, with regard to designing and
implementing a full REA for this review, led to the conclusion that
performance of a new REA for this review was not warranted. We did not
find the information newly available in this review to provide the
means by which to develop an updated or enhanced risk model that would
substantially improve the utility of risk estimates in informing the
current Pb NAAQS review (REA Planning Document, section 2.3). Based on
their consideration of the REA Planning Document analysis, the CASAC Pb
Review Panel generally concurred with the conclusion that a new REA was
not warranted in this review (Frey, 2011b).\51\ Accordingly, the risk/
exposure information considered in this review is drawn primarily from
the 2007 REA, augmented by a limited new computation for one case study
focused on risk associated with the current standard, as described
below (PA, section 3.4 and Appendix 3A).
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\51\ In their review of the draft PA, the CASAC Pb Review Panel
reinforced their concurrence with the EPA's decision not to develop
a new REA (Frey, 2013).
---------------------------------------------------------------------------
1. Overview
The focus for the risk assessment and associated estimates is on Pb
derived from sources emitting Pb to ambient air. As discussed in
section I.D above, the multimedia and persistent nature of Pb, the role
of multiple exposure pathways, and the contributions of nonair sources
of Pb to human exposure media all present challenges and contribute
significant additional complexity to the health risk assessment that
goes far beyond the situation for similar assessments typically
performed for other NAAQS pollutants (e.g., that focus only on the
inhalation pathway). The conceptual model that informed planning for
the 2007 REA identified sources, pathways, routes, exposed populations,
and health endpoints, focusing on those aspects of Pb exposure most
relevant to the review, while also recognizing the role of Pb exposure
pathways unrelated to Pb in ambient air (2007 REA, section 2.1).
Limitations in the available data and models affected our
characterization of the various complexities associated with exposure
to ambient air Pb. As a result, the assessment included a number of
simplifying assumptions in a number of areas and the estimates of air-
related Pb risk produced are approximate and are characterized by upper
and lower bounds.
As recognized in I.D above, sources of human Pb exposure include
current and historical air emissions sources, as well as miscellaneous
nonair sources, which can contribute to multiple exposure media and
associated pathways (e.g., inhalation of ambient air, ingestion of
indoor dust, outdoor soil/dust and diet or drinking water). In addition
to airborne emissions (recent or those in the past), sources of Pb to
these pathways also include old leaded paint, including Pb mobilized
indoors during renovation/repair activities, and contaminated soils.
Lead in diet and drinking water may have air pathway-related
contributions as well as contributions from nonair sources (e.g., Pb
solder on water distribution pipes and Pb in materials used in food
processing). Limitations in our data and modeling tools handicapped our
ability to fully separate the nonair contributions to Pb exposure from
estimates of air-related Pb exposure and risk. As a result, we have
developed bounds within which we estimate air-related Pb risk to fall.
The lower bound is based on a combination of pathway-specific estimates
that do not completely represent all air-related pathways, while the
upper bound is based on a combination of pathway-specific estimates
that includes pathways that are not air-related but the separating out
of which is precluded by modeling and data limitations.
Inclusion of exposure populations, exposure/dose metric, health
effects endpoint and risk metric in the 2007 REA were based on
consideration of the then-currently available evidence as assessed in
detail in the 2006 CD. As discussed in the REA Planning Document
(USEPA, 2011b), these selections continue to be supported by the
evidence now available in this review as described in the ISA. The REA
focused on risk to the central nervous system in childhood as the most
sensitive effect that could be quantitatively assessed, with decrement
in IQ used as the risk metric. Exposure and biokinetic modeling was
used to estimate blood Pb concentrations in children exposed to Pb up
to age 7 years.\52\ This focus reflected the evidence for young
children with regard to air-related exposure pathways and
susceptibility to Pb health impacts (e.g., ISA, sections 3.1.1, 4.3,
5.2.1.1, 5.3.1.1, and 5.4). For example, the hand-to-mouth activity of
young children contributes to their Pb exposure (i.e., incidental soil
and indoor dust ingestion) and ambient air-related Pb has been shown to
contribute to Pb in outdoor soil and indoor house dust (ISA, sections
3.1.1 and 3.4.1; 2006 CD, section 3.2.3).
---------------------------------------------------------------------------
\52\ The pathways represented in this modeling included
childhood inhalation and ingestion pathways, as well as maternal
contributions to newborn body burden (2007 REA, Appendix H, Exhibit
H-6).
---------------------------------------------------------------------------
The 2007 REA relied on a case study approach to provide estimates
that inform our understanding of air-related exposure and risk in
different types of air Pb exposure situations. Lead exposure and
associated risk were estimated for multiple case studies that generally
represent two types of residential population exposures to air-related
Pb: (1) Location-specific urban populations of children with a broad
range of air-related exposures, reflecting existence of urban
concentration gradients; and (2) children residing in localized areas
with air-related exposures representing air concentrations specifically
reflecting the standard level being evaluated (see PA, Table 3-6).
Thus, the two types of case studies differed with regard to the extent
to which they represented population variability in air-related Pb
exposure.
In drawing on the 2007 REA for our purposes in this review, we
focused on two case studies, one from each of these two categories: (1)
The location-specific urban case study for Chicago and (2) the
generalized (local) urban case study (PA, Table 3-6). Accordingly, our
summary of analysis details below focuses on details particular to
these two case studies. The generalized (local) urban case study (also
referred to as general urban case study) was not based on a specific
geographic location and reflected several simplifying assumptions in
representing exposure including uniform ambient air Pb levels
associated with the standard of interest across the hypothetical study
area and a uniform study population. Based on the nature of the
population exposures represented by the two categories of case study,
the generalized (local) urban case study includes populations that are
relatively more highly exposed by way of air pathways to air Pb
concentrations near the standard level evaluated, compared with the
populations in the location-specific urban case. The location-specific
urban case studies provided representations of urban populations with a
broad range of air-related exposures due to spatial gradients in both
ambient air Pb levels and population density. For example, the highest
air concentrations in these case studies (i.e., those closest to the
standard being assessed) were found in very small parts of the study
areas, while a large majority of the case study
[[Page 302]]
populations resided in areas with much lower air concentrations.
2. Summary of Design Aspects
The approach to assessing exposure and risk for the two categories
of case studies was comprised of four main analytical steps: (1)
Estimation of ambient air Pb concentrations, (2) estimation of Pb
concentrations in other key exposure media, including outdoor soil and
indoor dust, (3) use of exposure media Pb concentrations, with other
pathway Pb intake rates (e.g., diet), to estimate blood Pb levels in
children using biokinetic modeling, and (4) use of C-R functions
derived from epidemiological studies to estimate IQ loss associated
with the blood Pb levels.
Concentrations of Pb were estimated in ambient media and indoor
dust using a combination of empirical data and modeling projections.
The use of empirical data brings with it uncertainty related to the
potential inclusion of nonair source signals in these measurements
(e.g., house paint contributions to indoor dust and outdoor soil Pb).
Conversely, the use of modeling tools introduces other uncertainties
(e.g., model and parameter uncertainties).
Characterization of Pb in ambient air relied on (1) the use of
ambient monitor data for the location-specific urban case studies and
(2) an assumption of uniform ambient air Pb levels (matching the
standard level being considered) for the generalized (local) urban case
study. For the location-specific urban case studies, we used Pb
monitors within each study area to characterize spatial gradients. By
contrast, the generalized (local) urban case study is designed to
assess exposure and risk for a smaller group of residents (e.g.,
neighborhood) exposed at the level of the standard and, therefore, did
not rely on monitor data; rather, ambient air Pb concentration was
fixed at the standard being assessed. For the generalized (local) urban
case study, which has a single exposure zone in which air Pb
concentrations do not vary spatially, we derived a single air Pb
concentration estimate to meet the standard assessed. Concentrations in
the location-specific urban study areas, which relied on empirical
(monitor-based) data to define ambient air Pb concentrations, reflected
contributions from all sources affecting the concentrations in those
locations, be they currently active stationary or mobile sources,
resuspension of previously deposited Pb or other.\53\
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\53\ Additional detail on estimation of ambient (outdoor) and
indoor air concentrations is presented in section 5.2.2 and
Appendices A through D of the 2007 REA.
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The air quality scenarios assessed in the 2007 REA included
conditions just meeting the NAAQS that was current at the time of the
last review (1.5 [micro]g/m\3\, as a calendar quarter average),
conditions meeting several alternative, lower standards,\54\ and
current conditions in the three location-specific urban case studies
(PA, section 3.4.3.2). The full impact of changes in air Pb conditions
associated with attainment of lower standards was not simulated,
however, due to limitations in the available data and modeling tools
that precluded simulation of linkages between some media and air Pb.
Specifically, while Pb concentrations in indoor dust were simulated to
change with the different air quality scenarios for which there were
differing ambient air Pb concentrations (outdoors and indoors), dietary
and drinking water Pb concentrations, as well as soil Pb
concentrations, were not varied across the air quality scenarios in any
case study (see PA, Table 3-7).\55\
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\54\ The alternatives lower than the NAAQS at the time of the
last review for which air quality scenarios were assessed were a
maximum calendar quarter average of 0.2 [micro]g/m\3\ and maximum
monthly averages of 0.5, 0.2, 0.05 and 0.02 [micro]g/m\3\ (PA, Table
3-8).
\55\ Characterization of Pb concentrations in outdoor surface
soil/dust for the generalized (local) and location-specific urban
cases studies was based on the use of nationally representative
residential soil measurements obtained from the literature (2007
REA, sections 3.1.3 and 5.2.2.2 and Appendix F). Diet and drinking
water intake and concentrations, as well as other model inputs, were
based on the most current information (2007 REA, Appendix H).
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In estimating blood Pb levels using the IEUBK model, Pb
concentrations in exposure media (e.g., ambient air, diet, water,
indoor dust) were held constant throughout the 7-year simulation
period, while behavioral and physiological variables were changed with
age of child (2007 REA, sections 3.2.1.1 and 5.2.4). Detail on methods
used to characterize media Pb concentrations and all IEUBK inputs for
each case study are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and
5.2.4, and appendices C through H. Population variability in Pb intake
and uptake was simulated through use of the IEUBK model to first
generate a central-tendency estimate of the blood Pb levels for the
group of children within a given exposure zone of a study area, coupled
with use of a geometric standard deviation (GSD) and for the location-
specific case studies, Monte Carlo-based population sampling (PA,
section 3.4; 2007 REA, Appendix H). The risk characterization step
employed in the 2007 REA generated a distribution of IQ loss estimates
for the set of children simulated in the assessment.
Specifically, blood Pb estimates for the concurrent blood Pb metric
\56\ were combined with four C-R functions for blood Pb concentration
with IQ loss based on the analysis by Lanphear et al. (2005) of a
pooled international dataset of blood Pb and IQ (see the 2007 REA,
section 5.3.1.1). We used the four different C-R functions to provide
different characterizations of behavior at low exposures in recognition
of uncertainty related to modeling this endpoint, particularly at lower
blood Pb levels for which there is limited representation in the
Lanphear et al. (2005) pooled dataset.\57\ In considering the risk
estimates here (as in the last review), we focus on estimates for one
of the four functions (referred to as the loglinear with low-exposure
linearization C-R function [PA, section 3.4.3.3]). The range of risk
estimates reflecting all four C-R functions provide perspective on the
impact of uncertainty in this key modeling step. Additional detail on
the C-R functions is provided in the PA and the 2007 Pb Staff Paper
(PA, section 3.4.3.3; USEPA, 2007b, section 4.2.1).\58\ We focus on the
median IQ loss estimates, as in the last review, due to increased
confidence in these estimates relative to the higher percentile
estimates, for which we recognize significant uncertainty (PA,
[[Page 303]]
sections 3.4.5, 3.4.6 and 3.4.7; 2007 Staff Paper, p. 4-20).
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\56\ As in the last review, we give primary emphasis to
estimates based on the concurrent blood Pb metric, consistent with
CASAC advice in the last review (Henderson, 2007b).
\57\ The 5th percentile for the concurrent blood Pb measurements
in that dataset is 2.5 [micro]g/dL, and the median is 9.7 [micro]g/
dL (Lanphear et al., 2005).
\58\ As noted in section II.B.3 above, since the completion of
the ISA in the current review, two errors have been identified with
the pooled dataset analyzed by Lanphear et al., (2005) (Kirrane and
Patel, 2014). The EPA and a recent publication have separately
recalculated the statistics and mathematical models of Lanphear et
al., (2005) using the corrected pooled dataset (Kirrane and Patel,
2014). While the conclusions drawn from these coefficients,
including the finding of a steeper slope at lower (as compared to
higher) blood Pb concentrations, are unaffected, the magnitude of
the loglinear and linear regression coefficients are somewhat lower
based on the corrections. For example, the loglinear model
coefficient used for the C-R function, on which the EPA focused in
the last review and also focuses on here, changed only negligibly
from -2.7 to -2.65 when recalculated using the corrected pooled
dataset (Kirrane and Patel, 2014). As a result, the risk estimates
for this function would be expected to be very similar although
slightly lower if derived using the recalculated loglinear model
coefficient for the corrected dataset. Since the loglinear model
coefficient calculated from the corrected dataset is unchanged at
two significant figures from that original reported, any change to
the risk estimates would be very small and, particularly in light of
other uncertainties in the analysis, does not materially affect
staff's consideration of the results.
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As the 2007 REA did not include an air quality scenario simulated
to just meet the standard selected by the 2008 decision,\59\ we
employed two different approaches to estimate risk pertaining to
conditions just meeting the current Pb standard (set in 2008) for our
purposes in this review. First, given the similarity to the current
standard of the then-current conditions scenario for the Chicago case
study (among all the 2007 REA scenarios), we consider the risk
estimates for that scenario as informative with regard to risk
associated with the current standard.\60\ To augment the risk
information available in this current review and in recognition of the
variation among specific locations and urban areas with regard to air
quality patterns and exposed population, we have also newly developed
estimates for an air quality scenario just meeting the current Pb NAAQS
in the context of the generalized (local) urban case study. These
estimates were derived based on interpolation from the risk estimates
available for scenarios previously assessed for the generalized (local)
urban case study. Such interpolated estimates were only developed for
the generalized urban case study due to its use of a single exposure
zone which greatly simplified the method employed.\61\
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\59\ The 2008 decision on the level for the revised NAAQS was
based primarily on consideration of the evidence-based air-related
IQ loss framework; risk estimates available for scenarios simulated
in the 2007 REA were concluded to be roughly consistent with and
generally supportive of the evidence-based air-related IQ loss
estimates (see section II.A.1 above).
\60\ In the Chicago urban case study, the maximum monthly
average concentration was 0.31 [micro]g/m\3\, and the maximum
calendar quarter average concentration was 0.14 [micro]g/m\3\ (2003-
2005 data; 2007 REA, Appendix O).
\61\ We did not interpolate risk estimates for the current
standard for the other case studies (i.e., the primary Pb smelter
and location-specific urban case studies) because those case studies
utilized a more complex, spatially-differentiated and population-
based approach (see 2007 REA) which precludes application of the
simple linear interpolation approach described, without introduction
of substantial added uncertainty (relative to the other estimates
for the same case study). The simplicity of the generalized (local)
urban study area, however, with its single exposure zone, is
amenable to the linear interpolation of risk described here.
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The general approach we followed to newly develop estimates for the
current standard in the generalized (local) urban case study was to
identify the two alternative standard scenarios simulated in the 2007
REA which represented air quality conditions bracketing those for the
current standard and then linearly interpolate an estimate of risk for
the current standard based on the slope created from the two bracketing
estimates (PA, section 3.4.3.3.2 and Appendix 3A). By this method, the
air quality scenario for the current standard (0.15 [micro]g/m\3\, as a
not-to-be-exceeded 3-month average) was found to be bracketed by the
scenarios for alternative standards of 0.20 [micro]g/m\3\ (maximum
calendar quarter average) and 0.20 [micro]g/m\3\ (maximum monthly
average). Using interpolation between the risk estimates for these two
scenarios, we developed median risk estimates for the current standard
(PA, Appendix 3A).
3. Key Limitations and Uncertainties
In characterizing risk associated with Pb from air-related exposure
pathways, we faced a variety of challenges and employed a number of
methods. The challenges related to significant data and modeling
limitations which affected our ability to parse out the portion of
total (all-pathway) blood Pb and IQ loss attributable to air-related
pathways, as well as our representation of key sources of variability
and characterization of uncertainty. Although we separated total
estimates into risk estimates for diet/drinking water and two air-
related categories (``recent air'' and ``past air''), significant
limitations in our modeling tools and data resulted in an inability to
parse risk estimates specific to the air-related pathways. For example,
we recognize that Pb in diet and drinking water sources may include
some Pb derived from Pb in the ambient air, as well as Pb from nonair
sources, but limitations precluded explicit modeling of the
contribution from air pathways to these exposure pathways, such that
the air-related component of these exposures was not estimated. Rather,
we focused on estimates from the two air-related categories, which we
considered to under- and over-estimate air-related risk, respectively,
to create bounds within which we consider air-related risk to fall.
The first air-related category (``recent'') included Pb exposure
pathways tied most directly to ambient air, which consequently have the
potential to respond relatively more quickly to changes in air Pb
(i.e., inhalation and ingestion of indoor dust Pb derived from the
infiltration of ambient air Pb indoors). Importantly, media
concentrations associated with the pathways in this category were
simulated to change in response to air concentrations (as noted in
section II.D.2 above and described in section 3.4.3.1 of the PA). The
air-related Pb exposure pathways in the second air-related category
(``past air''), all of which are associated with atmospheric
deposition, included ingestion of Pb in outdoor dust/soil and ingestion
of the portion of Pb in indoor dust that after deposition from ambient
air outdoors is carried indoors with humans. While there is the
potential for these other air-related exposures to be affected (over
some time frame) by changes in air Pb concentrations (associated with
an adjustment to the Pb standard), limitations in our data and tools
precluded simulation of that relationship. Consequently, risk estimated
for this category reflects media measurements available for the 2007
REA and is identical for all air quality scenarios. Further, although
paint is not an air-related source of Pb exposure, it may be reflected
somewhat in estimates developed for the ``past air'' category, due to
modeling constraints (2007 Staff Paper, section 4.2.4). Thus, as
exposures included in the first air-related category (``recent'') do
not completely capture all air-related pathways, we consider risk for
this category an underestimate of air-related risk. Yet, as exposures
included in the second air-related category include pathways that are
not air-related, we consider the summed risk across both categories to
include a slight over-estimate of air-related risk.
In summary, because of limitations in the assessment design, data
and modeling tools, we consider our estimates of risk attributable to
air-related exposure pathways to be approximate and to be bounded on
the low end by the risk estimated for the ``recent air'' category and
on the upper end by the risk estimated for the ``recent air'' plus
``past air'' categories. With regard to the latter, we are additionally
cognizant of the modeling and data limitations which reduce the extent
to which the upper end of these bounds reflects impacts of alternative
air quality conditions simulated. We note that this limitation will
tend to contribute to estimates for the ``past air'' category
representing relatively greater overestimates with relatively lower air
Pb air quality scenarios.
We recognize several important sources of variability in air-
related Pb exposures and associated risk, for which the approaches by
which they were addressed in the 2007 REA are summarized here (PA,
section 3.4.6).
Variation in distributions of potential urban residential
exposure and risk across U.S. urban residential areas is addressed by
the inclusion of location-specific urban study areas that reflect a
diverse set of urban areas in the U.S.
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Representation of a more highly exposed subset of urban
residents potentially exposed at the level of the standard is addressed
by the inclusion of the generalized (local) urban study area.
Variation in residential exposure to ambient air Pb within
an urban area of the location-specific case studies is addressed
through the partitioning of these study areas into exposure zones to
provide some representation of spatial gradients in ambient air Pb and
their interaction with population distribution and demographics.
Inter-individual variability in blood Pb levels is
addressed through the use of empirically derived GSDs to develop blood
Pb distribution for the child population in each exposure zone, with
GSDs selected particular to each case study population.
Inter-individual variability in IQ response to blood Pb is
addressed through the use of C-R functions for IQ loss based on a
pooled analysis reflecting studies of diverse populations.
With regard to uncertainties, we recognize one overarching area
concerning the precision of our estimation of the neurocognitive risk
(as represented by IQ loss) associated with ambient air Pb. For reasons
related to the evidence of nonlinear responses of blood Pb to Pb
exposure and of Pb-associated IQ response to blood Pb, the 2007 REA
first estimated blood Pb levels and associated risk for total Pb
exposure (i.e., including Pb from air-related and nonair exposure
pathways) and then separated out estimates for pathways of interest
(PA, section 3.4.4). However, as described above, significant
limitations in our modeling tools affected our ability to develop
precise estimates for air-related exposure pathways. We believe these
limitations led to a slight overestimation of the risks for the ``past
air'' category and to an under-representation of air-related pathways
for the ``recent air'' category. Thus, we characterized the risk
attributable to air-related exposure pathways to be bounded by the
estimates developed for the ``past air'' category and the sum of
estimates for the ``recent air'' and ``past air'' categories. For air
quality scenarios other than those for the previous NAAQS, this upper
bound is recognized as having a potential upward bias with regard to
its reflection of the simulated air quality conditions because modeling
and data limitations precluded simulation of the influence of lower air
Pb concentrations on the outdoor dust and soil exposure pathways (PA,
section 3.4.4).
We recognize a range of additional uncertainties, limitations, and
assumptions that are reflected in various ways in the 2007 REA and
associated results (PA, section 3.4.7), which include the following.
Temporal Aspects: During the 7-year exposure period, media
concentrations remain fixed and the simulated child resides at the same
residence (although exposure factors, including behavioral and
physiological parameters, are adjusted to match the aging of the
child). These aspects introduce uncertainty into the risk estimates,
although the existence of a directional bias is unclear.
Generalized (local) Urban Case Study: The design for this
case study employs assumptions regarding uniformity that are reasonable
in the context of a general description of a small neighborhood
population but would contribute significant uncertainty to
extrapolation of these estimates to a specific urban location,
particularly a relatively large one. An additional area of uncertainty
concerns the representation of variability in air quality. Given the
relatively greater variability common in areas of high Pb
concentrations, the approach used to reflect variability may bias the
estimates high.
Location-specific Urban Case Studies: Limitations in the
spatial density of ambient air monitors in the simulated areas limit
our characterization of spatial gradients of ambient air Pb levels in
these case studies. This factor introduces uncertainty into the risk
estimates for this category of case study; the existence of a
directional bias is unclear.
Air Quality Simulation: Focus on only then-current
conditions (2003-2005) scenario for the Chicago urban case study in
this review precludes uncertainty associated with simulations of
alternative air quality scenarios in the 2007 REA.
Outdoor Soil/Dust Pb Concentrations: Limitations in
datasets on Pb levels in surface soil/dust Pb in urban areas and in our
ability to simulate the impact of reduced air Pb levels related to
lowering the NAAQS in the 2007 REA contribute uncertainty to air-
related risk estimates for the current standard in the generalized
(local) urban case study. The likely impact is a high bias on these
risk estimates (related to low bias on estimating risk reduction for
lower standard levels in the 2007 REA) given lack of simulated changes
in soil Pb related to changes in ambient air Pb.
Indoor Dust Pb Concentrations: Limitations and uncertainty
in modeling of indoor dust Pb levels, including the impact of
reductions in ambient air Pb levels, contributes uncertainty to air-
related risk estimates. Although the indoor dust modeling does link
changes in ambient air Pb to changes in indoor dust Pb, it does not
include a link between ambient air Pb, outdoor soil Pb and subsequent
changes in the level of Pb carried (or ``tracked'') into the house.
This could introduce low bias into the total estimates of air-related
Pb exposure and risk.
Interindividual Variability in Blood Pb Levels:
Uncertainty related to population variability in blood Pb levels
related to interindividual variability in factors other than media
concentration and limitations in modeling of this introduces
significant uncertainty into blood Pb and IQ loss estimates for the
95th percentile of the population. The extent of any systematic bias
from this source of uncertainty is unknown.
Pathway Apportionment for Higher Percentile Blood Pb and
Risks: Limitations, primarily in data, prevented us from characterizing
the degree of correlation among high-end Pb exposures for the various
pathways (e.g., the degree to which an individual experiencing high
drinking water Pb exposure would also experience high Pb paint exposure
and high ambient air-related Pb exposure). Our inability to
characterize potential correlations between exposure pathways
(particularly at the higher percentile exposure levels) limited our
ability to (1) effectively model high-end Pb risk and (2) apportion
that risk between different exposure pathways, including ambient air-
related pathways.
IQ Loss C-R Functions: Specification of the quantitative
relationship between blood Pb level and IQ loss is subject to greater
uncertainty at lower blood Pb levels. The use of four C-R functions
models (which each treat the response at low blood Pb levels in a
different manner) is considered to provide a reasonable
characterization of this source of uncertainty and its impact on risk
estimates. Comparison of risk estimates from the four models indicates
this source of uncertainty to have a potentially significant impact on
risk.
4. Summary of Risk Estimates and Key Observations
In this summary of risk estimates, drawn from the PA, we focus on
the estimates of air-related IQ loss derived using the C-R function in
which we have greatest confidence (see PA, sections 3.4.3.3.1 and
3.4.7) for the median child in a given case study (exposure modeled
through age 7 years), given the substantially greater uncertainty
associated with air-related
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risk estimates for extremes of the risk distribution, such as the 95th
percentile (PA, section 3.4). Estimates for other risk metrics and the
full range of case studies and air quality scenarios are described
elsewhere in detail (e.g., 2007 REA, sections 4.2 and 5.3.2 and
appendices; 2007 Staff Paper, chapter 4; 73 FR 66964, November 12,
2008). Based on results from the 2007 REA for a location-specific urban
study area (Chicago case study) and on those newly derived in this
review based on interpolation from the 2007 REA results (for the
generalized [local] urban case study), median air-related IQ loss for
the current standard is estimated, with rounding, to generally fall
near or somewhat above a rough lower bound of 1 point IQ loss and below
a rough upper bound of 3 points IQ loss. As would be expected by the
use of interpolation, the newly derived estimates are consistent with
the estimates for similar air quality scenarios that were available in
the last review (PA, section 3.4.5). For example, the generalized
(local) urban case study current standard scenario estimates for median
air-related IQ loss are identical to those for the scenario of just
meeting a potential alternative of 0.2 [mu]g/m\3\ maximum calendar
quarter average for that case study (PA, Table 3-11). Further, the
upper bound below which the median IQ loss is estimated to fall is also
approximately 3 IQ points in the generalized (local) urban case study
scenarios for just meeting potential alternatives of 0.2 [mu]g/m\3\,
0.05 and 0.02 [mu]g/m\3\ maximum monthly average, providing an
indication of the limitations associated with estimating air-related Pb
exposures and risk for lower air Pb scenarios (PA, sections 3.4.4 and
3.4.5).
As summarized in section II.D.3 above, a range of limitations and
areas of uncertainty were associated with the information available in
the last review (PA, sections 3.4.4, 3.4.6 and 3.4.7). In this review,
the REA Planning Document concluded that none of the primary sources of
uncertainty identified to have the greatest impact on risk estimates
would be substantially reduced through the use of newly available
information (USEPA, 2011b). Thus, the key observations regarding air-
related Pb risk modeled for the set of standard levels assessed in the
2007 REA, as well as the risk estimates interpolated for the current
standard, are not significantly affected by the new information.
Further, our overall characterization of uncertainty and variability
associated with those estimates (as summarized above and in sections
3.4.6 and 3.4.7 of the PA) is not appreciably affected by new
information. As recognized at the time of the last review, exposure and
risk modeling conducted for this analysis was complex and subject to
significant uncertainties due to limitations in the data and models,
among other aspects. Of particular note, limitations in the assessment
design, data and modeling tools handicapped us from sharply separating
Pb linked to ambient air from Pb that is not air related.
In summary, the estimates of risk attributable to air-related
exposures, with which we recognize a variety of sources of uncertainty,
are considered to be approximate, falling within upper and lower
bounds. These bounds for scenarios just meeting the current standard
are roughly estimated, with rounding, as 3 and 1 IQ points, which over-
and underestimate risk, respectively. In characterizing the magnitude
of air-related risk associated with the current standard, we focus on
median estimates, for which we have appreciably greater confidence than
estimates for outer ends of the risk distribution (see PA, section
3.4.7) and on risks derived using the C-R function in which we have
greatest confidence (see PA, sections 3.4.3.3.1 and 3.4.7). These risk
results for the current standard, both those estimated in the last
review for one of the location-specific urban study area populations
and those newly derived in this review using interpolation of the
estimates from the last review for the generalized (local) urban case
study, which is recognized to reflect a generalized high end of air-
related exposure for localized populations, provide approximate bounds
for air-related risk, with attendant uncertainties described above.
Focusing on the results for the generalized (local) urban case study,
the interpolated estimates for the scenario representing the current
standard are very similar to estimates for the two 0.2 [mu]g/m\3\
scenarios (maximum monthly and calendar quarter averages) simulated in
the 2007 REA \62\ and are appreciably lower than those associated with
the previous standard. For this case study, across the two 0.2 [mu]g/
m\3\ scenarios, the current standard scenario and the more restrictive
air quality scenarios, the upper bound below which air-related risk is
estimated to fall rounds to the same value, reflecting the significant
limitations associated with developing precise estimates of air-related
risk, particularly for the lower air Pb scenarios (PA, sections 3.4.4,
3.4.5, and 3.4.7).
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\62\ There is uncertainty associated with judging differences
between the current standard and these potential alternative
standards due to the difference in air quality datasets used to
estimate air concentration variability of the 2007 REA estimates
versus the interpolated risk estimate.
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E. Conclusions on Adequacy of the Current Primary Standard
In evaluating whether, in view of the advances in scientific
knowledge and additional information now available, it is appropriate
to retain or revise the current standard, the Administrator builds upon
the last review and reflects upon the body of evidence and information
now available. The Administrator has taken into account both evidence-
based and quantitative exposure- and risk-based considerations in
developing conclusions on the adequacy of the current primary Pb
standard. Evidence-based considerations draw upon the EPA's assessment
and integrated synthesis of the scientific evidence from
epidemiological studies and experimental animal studies evaluating
health effects related to exposures to Pb, with a focus on policy-
relevant considerations as discussed in the PA. The exposure/risk-based
considerations draw from the results of the quantitative analyses
presented in the 2007 REA, augmented as described in the PA, and
summarized in section II.D above, and consideration of those results in
the PA. More specifically, estimates of the magnitude of ambient Pb-
related exposures for young children and associated impacts on IQ
associated with just meeting the current primary Pb NAAQS have been
considered. Together the evidence-based and risk-based considerations
have informed the Administrator's proposed conclusions related to the
adequacy of the current Pb standard in light of the currently available
scientific evidence.
As described in section II.A.2 above, consideration of the evidence
and the exposure/risk information in the PA and by the Administrator is
framed by consideration of a series of key policy-relevant questions.
The following sections describe the consideration of these questions in
the PA, the advice received from CASAC, as well as the comments
received from various parties, and then present the Administrator's
proposed conclusions regarding the adequacy of the current primary
standard.
1. Evidence-Based Considerations in the Policy Assessment
In considering the evidence with regard to the issue of adequacy of
the current standard, the PA addresses several questions that build on
the information summarized in sections II.B and II.C above (and
sections 3.1 through
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3.3 of the PA) to more broadly address the extent to which the current
evidence base supports the adequacy of the public health protection
afforded by the current primary standard. The first question addresses
the integrated consideration of the health effects evidence, in light
of aspects described in sections II.A.1 and II.A.2 above. The second
question focuses on consideration of associated areas of uncertainty.
The third question then integrates consideration of the prior two
questions with a focus on the standard, including each of the four
elements. The PA considerations and conclusions with regard to these
questions are summarized below.
In considering the extent to which information newly available in
this review may have altered scientific support for the occurrence of
health effects associated with Pb in ambient air, the PA concludes that
the current evidence continues to support the EPA's conclusions from
the previous review regarding key aspects of the health effects
evidence for Pb and the health effects of multimedia exposure
associated with levels of Pb occurring in ambient air in the U.S. (PA,
section 4.2.1). The conclusions in this regard are based on
consideration of the assessment of the currently available evidence in
the ISA, particularly with regard to key aspects summarized in Chapter
3 of the PA, in light of the assessment of the evidence in the last
review as described in the 2006 CD and summarized in the notice of
final rulemaking (73 FR 66964, November 12, 2008). Key aspects of these
conclusions are summarized below.
As at the time of the last review, blood Pb continues to be the
predominant biomarker employed to assess exposure and health risk of Pb
(ISA, Chapters 3 and 4), as discussed in section II.C above. This
widely accepted role of blood Pb in assessing exposure and risk is
illustrated by its established use in programs to prevent both
occupational Pb poisoning and childhood Pb poisoning, with the latter
program, implemented by the CDC, recently issuing updated guidance on
blood Pb measurement interpretation (CDC, 2012). As in the past, the
current evidence continues to indicate the close linkage of blood Pb
levels in young children to their body burden; this linkage is
associated with the ongoing bone remodeling during that lifestage (ISA,
section 3.3.5). This tight linkage plays a role in the somewhat rapid
response of children's blood Pb to changes in exposure (particularly to
exposure increases), which contributes to its usefulness as an exposure
biomarker (ISA, sections 3.2.2, 3.3.5, and 3.3.5.1). Additionally, the
weight of evidence documenting relationships between children's blood
Pb and health effects, most particularly those on the nervous and
hematological systems (e.g., ISA, sections 4.3 and 4.7), speaks to its
usefulness in assessing health risk.
As in the last review, the evidence on air-to-blood relationships
available today continues to be composed of studies based on an array
of circumstances and population groups (of different age ranges),
analyzed by a variety of techniques, which together contribute to
appreciable variability in the associated quantitative estimates and
uncertainty with regard to the relationships existing in the U.S.
today. Accordingly, interpretation of this evidence base, as discussed
in section II.C above, also includes consideration of factors that may
be influencing various study estimates. We consider the study estimates
in light of such factors both with regard to the extent to which the
factors affect the usefulness of specific study estimates for the
general purpose here of quantitatively characterizing relationships
between Pb in ambient air and air-related Pb in children's blood and
also with regard to the pertinence of such factors more specifically to
conditions and populations in the U.S. today. As noted in the PA, the
current evidence, while including two additional studies not available
at the time of the last review, is not appreciably changed from that
available in the last review (PA, section 3.1). The range of estimates
that can be derived from the full dataset is broad and not changed by
the inclusion of the newly available estimates. Further, the PA
recognizes significant uncertainties regarding the air Pb to air-
related blood Pb relationship for the current conditions where
concentrations of Pb in both ambient air and children's blood are
substantially lower than they have been in the past. In considering the
strengths, limitations and uncertainties associated with the full
dataset, the currently available evidence appears to continue to
support a range of estimates for the purpose at hand that is generally
consistent with the range given weight in the last review, 1:5 to 1:10
(ISA, section 3.7.4 and Table 3-12; 73 FR 67001-2, 67004, November 12,
2008). The PA additionally notes that the generally central estimate of
1:7 identified for this range in the last review is consistent with the
study involving blood Pb for pre-school children and air Pb conditions
near a large source of Pb to ambient air with concentrations near (and/
or previously above) the level of the current Pb standard (ISA, section
3.5.1; Hilts, 2003).\63\ In so noting, the PA also recognizes the
general overlap of such circumstances with those represented by the
evidence-based, air-related IQ loss framework,\64\ for which air-to-
blood ratio is a key input. In characterizing the range of air-to-blood
ratio estimates, we recognize uncertainty inherent in such estimates as
well as the variation in currently available estimates resulting from a
variety of factors, including differences in the populations examined,
as well as in the Pb sources or exposure pathways addressed in those
study analyses (ISA, section 3.7.4).
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\63\ The older study by Hayes et al. (1994) during time of
leaded gasoline indicated a generally similar ratio of 1:8, although
the blood Pb levels in that study were much higher than those in the
study by Hilts (2003). Among the studies focused on this age group,
the latter study includes blood Pb levels closest to those in U.S.
today.
\64\ Concentrations near air sources are higher than those at
more distant sites (as described in PA, section 2.2.2); it is near-
source locations where there is the potential for concentrations at
or near the current standard.
---------------------------------------------------------------------------
The scientific evidence continues to recognize a broad array of
health effects on multiple organ systems or biological processes
related to blood Pb, including Pb in blood prenatally (ISA, section
1.6). The currently available evidence continues to support
identification of neurocognitive effects in young children as the most
sensitive endpoint associated with blood Pb concentrations (ISA,
section 1.6.1), which as an integrated index of exposure reflects the
aggregate exposure to all sources of Pb through multiple pathways
(inhalation and ingestion). Evidence continues to indicate that some
neurocognitive effects in young children may not be reversible and may
have effects that persist into adulthood (ISA, section 1.9.5). Thus, as
discussed in section II.B. above, the evidence of Pb effects at the low
end of the studied blood Pb levels (closest to those common in the U.S.
today) continues to be strongest and of greatest concern for effects on
the nervous system, most particularly those on cognitive function in
children.
As in the last review, evidence on risk factors continues to
support the identification of young children as an important at-risk
population for Pb health effects (ISA, section 5.4). The current
evidence also continues to indicate important roles as factors that
increase risk of Pb-related health effects for the following:
Nutritional factors, such as iron and calcium intake; elevated blood Pb
levels; and proximity to sources of Pb exposure, such as industrial
releases or buildings with old,
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deteriorating, leaded paint. Further, some races or ethnic groups
continue to demonstrate increased blood Pb levels relative to others,
which may be related to these and other factors (ISA, sections 5.1, 5.2
and 5.4).
With regard to our understanding of the relationship between
exposure or blood Pb levels in young children and neurocognitive
effects, the PA notes that the evidence in this review, as in the last,
does not establish a threshold blood Pb level for neurocognitive
effects in young children (ISA, sections 1.9.4 and 4.3.12). The lowest
blood Pb levels at which associations with neurocognitive impacts have
been observed in pre-school and school age children continue to range
down below 5 [mu]g/dL, with the lowest group levels that have been
associated with such effects ranging down to 2 [mu]g/dL (ISA, sections
1.6.1 and 4.3.15.1). Additionally, as in the last review, there is
evidence that the relationship of young children's blood Pb with
neurocognitive impacts, such as IQ, is nonlinear across a wide range of
blood Pb, with greater incremental impacts at lower versus higher blood
Pb levels (ISA, sections 1.9.4 and 4.3.12). Accordingly, as in the last
review, the PA focuses on C-R relationships from study groups with
blood Pb levels closest to those in children in the U.S. today, which
are generally lower than epidemiological study groups. The currently
available evidence does not identify additional C-R slopes for study
groups of young children (e.g., <=7 years) with mean blood Pb levels
below that of groups identified in the last review, 2.9 - 3.8 [mu]g/dL,
as discussed in section II.B.3 above (ISA, section 4.3.12). Thus, the
blood Pb concentration--IQ response functions or slopes identified in
this review for epidemiological study groups of young children with
mean blood Pb levels closest to that of children in the U.S. today
include the same set recognized at the time of the last review (see
Table 1 above), the median of which is 1.75 IQ points decrement per
[mu]g/dL blood Pb (73 FR 67003, November 12, 2008).
In considering the evidence with regard to the extent to which
important uncertainties identified in the last review have been reduced
or to which new uncertainties have emerged, as summarized in discussing
the previous question and in section II.B above, the PA concludes that
no new uncertainties were identified as emerging since the last review.
However, the PA recognizes important uncertainties identified in the
last review that remain today. Importantly, given our focus in this
review, as in the last review, on neurocognitive impacts associated
with Pb exposure in early childhood, the PA recognizes remaining
uncertainties in our understanding of the C-R relationship of
neurocognitive impacts, such as IQ decrements, with blood Pb level in
young children, particularly across the range of blood Pb levels common
in the U.S. today. With regard to C-R relationships for IQ, the
evidence available in this review does not include studies that
appreciably extend the range of blood Pb levels studied beyond those
available in the last review. As in the last review, the early
childhood (e.g., 2 to 7 years of age) blood Pb levels for which
associations with IQ response have been reported continue to extend at
the low end of the range to study group mean blood Pb levels of 2.9 to
3.8 [mu]g/dL (e.g., 73 FR 67003, November 12, 2008, Table 3). The
studies examining C-R relationships down to these blood Pb levels, as
summarized in section II.B.3 above, continue to indicate higher C-R
slopes in those groups with lower blood Pb levels than in study groups
with higher blood Pb levels (ISA, section 4.3.12). The lack of studies
considering C-R relationships for Pb effects on IQ at still lower blood
Pb levels contributes to uncertainty regarding the quantitative
relationship between blood Pb and IQ response in populations with mean
blood Pb levels closer to the most recently available mean for children
aged 1 to 5 years of age (e.g., 1.17 [mu]g/dL in 2009-2010 [ISA, p. 3-
85]).
Further, the PA recognizes important uncertainties in our
understanding of the relationship between ambient air Pb concentrations
and air-related Pb in children's blood. The evidence newly available in
this review has not reduced such key uncertainties. As in the last
review, air-to-blood ratios based on the available evidence continue to
vary, with our conclusions based on the current evidence generally
consistent with the range of 1:5 to 1:10 given emphasis in the last
review (73 FR 67002, November 12, 2008; ISA, section 3.7.4). There
continues to be uncertainty regarding the extent to which this range
represents the relationship between ambient air Pb and Pb in children's
blood (derived from the full set of air-related exposure pathways) and
with regard to its reflection of exposures associated with ambient air
Pb levels common in the U.S. today and to circumstances reflecting just
meeting the current Pb standard (ISA, section 3.7.4). The PA
additionally notes the significant uncertainty remaining with regard to
the temporal relationships of ambient Pb levels and associated exposure
with occurrence of a health effect (73 FR 67005, November 12, 2008).
In integrating consideration of the prior two questions with a
focus on the standard, the PA then addresses the question regarding the
extent to which newly available information supports or calls into
question any of the basic elements of the current Pb standard. The PA
addresses this question for each of the elements of the standard in
light of the health effects evidence and other relevant information
available in this review (and summarized in sections II.B and II.C
above). As an initial matter, the PA recognizes the weight of the
scientific evidence available in this review that continues to support
our focus on effects on the nervous system of young children,
specifically neurocognitive decrements, as the most sensitive endpoint.
Consistent with the evidence available in the last review, the
currently available evidence continues to indicate that a standard that
provides requisite public health protection against the occurrence of
such effects in at-risk populations would also provide the requisite
public health protection against the full array of health effects of
Pb. Accordingly, the discussion of the elements below is framed by that
background.
Indicator
The indicator for the current Pb standard is Pb-TSP. Key
considerations in retaining this indicator in the last review are
summarized in section II.A.1. Exposure to Pb in all sizes of particles
passing through ambient air can contribute to Pb in blood and
associated health effects by a wide array of exposure pathways (ISA,
section 3.1). These pathways include the ingestion route, as well as
inhalation (ISA, section 3.1), and a wide array of particle sizes play
a role in these pathways (ISA, section 3.1.1.1). As at the time of the
last review, the PA recognizes the variability of the Pb-TSP FRM in its
capture of airborne Pb particles (as discussed in section 2.2.1.3.1 of
the PA). As in the last review, the PA also notes that an alternative
approach for collection of a conceptually comparable range of particle
sizes, including ultra-coarse particles, is not yet available.
Additionally, the limited available information regarding relationships
between Pb-TSP and Pb in other size fractions indicates appreciable
variation in this relationship, particularly near sources of Pb
emissions where concentrations and potential exposures are greatest.
Thus, the PA concludes that the information available in this review
does not address previously
[[Page 308]]
identified limitations and uncertainties for the current indicator. Nor
does the newly available information identify additional limitations or
uncertainties.
The PA notes that the evidence available in this review continues
to indicate the role of a range of air Pb particle sizes in
contributing to Pb exposure (e.g., ISA, section 3.1.1.1) that
contributes to Pb in blood and associated health effects. For example,
the evidence indicates larger particle sizes for Pb that occurs in soil
and house dust and may be ingested as compared to Pb particles commonly
occurring in the atmosphere and the size fraction of the latter that
may be inhaled (ISA, section 3.1.1.1). Taken together, the PA concludes
that the evidence currently available reinforces the appropriateness of
an indicator for the Pb standard that reflects a wide range of airborne
Pb particles.
Averaging Time and Form
The averaging time and form of the standard were revised in the
last Pb NAAQS review, based on considerations summarized in section
II.A.1 above. The current standard is a not-to-be-exceeded rolling 3-
month average (40 CFR 50.16), derived from three monthly averages
calculated in accordance with the current data handling procedures (40
CFR part 50, Appendix R). The form is a maximum, evaluated within a 3-
year period (40 CFR 50.16). As at the time of the last review, the PA
notes that evidence continues to support the importance of periods on
the order of 3 months and the prominent role of deposition-related
exposure pathways, with uncertainty associated with characterization of
precise time periods associating ambient air Pb with air-related health
effects. The PA concludes that relevant factors continue to be those
pertaining to the human physiological response to changes in Pb
exposures and those pertaining to the response of air-related Pb
exposure pathways to changes in airborne Pb. The PA concludes that the
newly available evidence in this review does not appreciably improve
our understanding of the period of time in which air Pb concentrations
would lead to the health effects most at issue in this review (PA,
section 4.2.1). Newly available evidence accordingly also does not
appreciably improve our understanding of the period of time for which
control of air Pb concentrations would protect against exposures most
pertinent to the health effects most at issue in this review. Thus,
while there continue to be limitations in the evidence to inform our
consideration of these elements of the standard and associated
uncertainty, the available evidence continues to provide support for
the decisions made in the last review regarding these elements of the
current Pb standard.
Level
The level of the current standard is 0.15 [mu]g/m\3\ (40 CFR
50.16). As described in section II.A.1 above, this level was selected
in 2008 with consideration of, among other factors, an evidence-based
air-related IQ loss framework, for which there are two primary inputs:
Air-to-blood ratios and C-R functions for blood Pb-IQ response in young
children. Additionally taken into consideration were the uncertainties
inherent in these inputs.\65\ Application of the framework also
entailed consideration of a magnitude of air-related IQ loss, which as
further described in section II.A.1 above, is used in conjunction with
this specific framework in light of the framework context, limitations
and uncertainties. Additionally, selection of a level for the standard
in 2008 was made in conjunction with decisions on indicator, averaging
time and form.
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\65\ As discussed further below, the Administrator also
considered the exposure/risk-based information, which he found to be
roughly consistent and generally supportive of the framework
estimates (73 FR 67004).
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As an initial matter, the PA considers the extent to which the
evidence-based, air-related IQ loss framework which informed the
Administrator's decision in the last review is supported by the
currently available evidence and information. In so doing, the PA
recognizes the support provided by the currently available evidence for
the key conclusions drawn in the last review with regard to health
effects of greatest concern, at-risk populations, the influence of Pb
in ambient air on Pb in children's blood and the association between
children's blood Pb and decrements in neurocognitive function (e.g.,
IQ). The PA additionally notes the complexity associated with
interpreting the scientific evidence with regard to specific levels of
Pb in ambient air, given the focus of the evidence on blood Pb as the
key biomarker of children's aggregate exposure. The need to make such
interpretations in the face of the associated complexity supported use
of the evidence-based framework in the last review. In considering the
currently available evidence for the same purposes in this review, the
PA concludes that the evidence-based framework continues to provide a
useful tool for consideration of the evidence with regard to the level
of the standard.
The PA next turned to consideration of the primary inputs to the
framework: Air-to-blood ratios and C-R functions for blood Pb-IQ
response in young children. With regard to the former, the PA concludes
the limited newly available information assessed in the ISA, and
discussed in section II.C above, to be generally consistent with the
information in this area that was available at the time of the last
review. The PA additionally recognizes the variability and uncertainty
associated with quantitative air-to-blood ratios based on this
information, as also existed in the last review. As in the last review,
factors contributing to the variability and uncertainty of these
estimates are varied and include aspects of the study populations
(e.g., age and Pb exposure pathways) and the study circumstances (e.g.,
length of study period and variations in sources of Pb exposure during
the study period). The PA notes that the full range of estimates
associated with the available evidence is wide and considers it
appropriate to give emphasis to estimates pertaining to circumstances
closest to those in the U.S. today with regard to ambient air Pb and
children's blood Pb concentrations, while recognizing the limitations
associated with the available information. With that in mind, the PA
considers the currently available evidence to continue to support the
range of estimates for air-to-blood ratios concluded in the last review
to be most appropriate for the current population of young children in
the U.S., in light of the multiple air-related exposure pathways by
which children are exposed and of the levels of air and blood Pb common
today. Identification of this range also included consideration of the
limitations associated with the available information and inherent
uncertainties. This range of air-to-blood ratios included 1:10 at the
upper end and 1:5 at the lower end. The PA further recognizes that the
limited evidence for air Pb and children's blood Pb concentrations
closest to those in U.S. today continues to provide support for the
Administrator's emphasis in the 2008 decision on the relatively central
estimate of 1:7.
With regard to the second input to the evidence-based framework, C-
R functions for the relationship of young children's blood Pb with
neurocognitive impacts (e.g., IQ decrements), the PA considers several
aspects of the evidence. First, as discussed in section II.B.3 above,
the currently available information continues to provide evidence that
this C-R relationship is nonlinear across the range of blood Pb levels
from the higher concentrations
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more prevalent in the past to lower concentrations more common today.
Thus, the PA continues to consider it particularly appropriate to focus
on the evidence from studies with blood Pb levels closest to those of
today's population which, as in the last review, includes studies with
study group mean blood Pb levels ranging roughly from 3 to 4 [mu]g/dL
in children aged 24 months to 7 years (PA, Table 3-3). As discussed in
section II.B.3 above, this is also consistent with the evidence
currently available for this age group of young children, which does
not include additional C-R slopes for incremental neurocognitive
decrement with blood Pb levels at or below this range. In considering
whether this set of functions continues to be well supported by the
evidence, as assessed in the ISA (ISA, section 4.3.2), the PA notes the
somewhat wide range in slopes encompassed by these study groups, while
also noting the stability of the median. For example, omission of any
of the four slopes considered in the last review does not appreciably
change the median (e.g., the median would change from -1.75 IQ points
per [mu]g/dL blood Pb to -1.71 or -1.79). Thus, while differing
judgments might be made with regard to inclusion of each of the four
study groups, these estimates are generally supported by the current
review of the evidence in the ISA. Further, the stability of the median
to modifications to this limited dataset lead the PA to conclude that
the currently available evidence continues to support consideration of
-1.75 IQ points per [mu]g/dL blood Pb as a well-founded and stable
estimate for purposes of describing the neurocognitive impact
quantitatively on this age group of U.S. children.
In summary, in considering the evidence and information available
in this review pertaining to the level of the current Pb standard, the
PA notes that the evidence available in this review, as summarized in
the ISA, continues to support the air-related IQ loss evidence-based
framework, with the inputs that were used in the last review. These
include estimates of air-to-blood ratios ranging from 1:5 to 1:10, with
a generally central estimate of 1:7. Additionally, the C-R functions
most relevant to blood Pb levels in U.S. children today continue to be
provided by the set of four analyses considered in the last review for
which the median estimate is -1.75 IQ points per [mu]g/dL Pb in young
children's blood. Thus, the PA observed that the evidence available in
this review has changed little if at all with regard to the aspects
given weight in the conclusion on level for the new standard in the
last review and would not appear to call into question any of the basic
elements of the standard. In so doing, the PA additionally recognizes
that the overall decision on adequacy of the current standard is a
public health policy judgment by the Administrator.
2. Exposure/Risk-Based Considerations in the Policy Assessment
In consideration of the issue of adequacy of public health
protection provided by the current standard, the PA also considered the
quantitative exposure/risk assessment completed in the last review,
augmented as described in section II.C above. The PA recognizes
substantial uncertainty inherent in the REA estimates of air-related
risk associated with localized conditions just meeting the current
standard, which we have characterized as approximate and falling within
rough bounds.\66\ This approximate estimate of risk for children living
in such areas is generally overlapping with and consistent with the
evidence-based air-related IQ loss estimates described in section
II.A.1 above. The PA discussion with regard to interpretation of the
exposure/risk information for air quality conditions associated with
just meeting the current standard is organized around two questions, as
summarized here (PA, section 4.2.2).
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\66\ We note that the value of the upper bound is influenced by
risk associated with exposure pathways that were not varied with
alternative standard levels, a modeling limitation with the
potential to contribute to overestimation of the upper bound with
air quality scenarios involving air Pb levels below current
conditions for the study area (see sections 3.4.4 and 3.4.7 above).
---------------------------------------------------------------------------
In considering the level of confidence associated with estimates of
air-related risk generated for simulations just meeting the current Pb
standard, the PA recognizes, as an initial matter, the significant
limitations and complexity associated with the risk and exposure
assessments for Pb that are far beyond those associated with similar
assessments typically performed for other criteria pollutants. In
completing the assessment, we were constrained by significant
limitations with regard to data and tools particular to the problem at
hand. Further, the multimedia and persistent nature of Pb and the role
of multiple exposure pathways contribute significant additional
complexity to the assessment as compared to other assessments that
focus only on the inhalation pathway. As a result, the estimates of
air-related exposure and risk are approximate, presented as upper and
lower bounds within which we consider air-related risk likely to fall.
The description of overall confidence in this characterization of air-
related risk is based on consideration of the overall design of the
analysis (summarized in section II.D), the degree to which key sources
of variability are reflected in the design of the analysis (summarized
in section II.D.3), and our characterization of key sources of
uncertainty (summarized in section II.D.3).
With regard to key sources of uncertainty, the PA notes
particularly those affecting the precision of the air-related risk
estimates. Associated sources of uncertainty include the inability to
simulate changes in air-related Pb as a function of changes in ambient
air Pb in exposure pathways other than those involving inhalation of
ambient air and ingestion of indoor dust. This contributes to the
positive bias of the upper bound for the air-related risk estimates.
The PA additionally recognizes the significant uncertainty associated
with estimating upper percentiles of the distribution of air-related
blood Pb concentration estimates (and associated IQ loss estimates) due
to limitations in available information. Lastly, the PA recognizes the
uncertainty associated with application of the C-R function at the
lower blood Pb levels in the distribution; this relates to the limited
representation of blood Pb levels of this magnitude in the dataset from
which the C-R function is derived (PA, section 4.2.2).
In the quantitative risk information available in this review, we
have air-related risk estimates for simulations just meeting the
current standard from one of the location-specific urban case studies
(Chicago) and from the generalized (local) urban case study. With
regard to the latter, the PA notes its simplified design that does not
include multiple exposure zones; thus reducing the dimensions
simulated. The PA concludes a reasonable degree of confidence in
aspects of the generalized (local) urban case study for the specific
situation we consider it to represent (i.e., a temporal pattern of air
Pb concentrations that just meets the level of the standard), and when
the associated estimates are characterized as approximate, within upper
and lower bounds (as described above), while also recognizing
considerable associated uncertainty.
In considering the extent to which the estimated air-related risks
remaining upon just meeting the current Pb standard are important from
a public health perspective, the PA considers the nature and magnitude
of such estimated risks (and attendant uncertainties), including such
impacts on the affected
[[Page 310]]
population, and additionally considers the size of the affected
population. In considering the quantitative risk estimates for
decrements in IQ, we recognize that although some neurocognitive
effects may be transient, some effects may persist into adulthood,
affecting success later in life (ISA, sections 1.9.5 and 4.3.14). The
PA additionally recognizes the potential population impacts of small
changes in population mean values of metrics such as IQ, presuming a
uniform manifestation of Pb-related decrement across the range of
population IQ (ISA, section 1.9.1; PA, section 3.3).
As summarized in sections II.D above, limitations in modeling tools
and data affected our ability to develop precise risk estimates for
air-related Pb exposure pathways and contributed uncertainties to the
risk estimates. The results are approximate estimates which we describe
through the use of rough upper and lower bounds within which we
estimate air-related risk to fall. We have recognized a number of
uncertainties in the underlying risk estimates from the 2007 REA and in
the interpolation approach employed in the new analyses for this
review. We have characterized the magnitude of air-related risk
associated with the current standard with a focus on median estimates,
for which we have appreciably greater confidence than estimates for
outer ends of risk distribution (see section 3.4.7 of the PA) and on
risks derived using the C-R function in which we have greatest
confidence (see sections 3.4.3.3.1 and 3.4.7 of the PA). These risk
estimates include estimates from the last review for one of the
location-specific urban study area populations as well as estimates
newly derived in this review based on interpolation from 2007 REA
results for the generalized (local) urban case study, which is
recognized to reflect a generalized high end of air-related exposure
for localized populations. Taken together, these results for just
meeting the current standard include a high-end localized risk estimate
for air-related Pb of a magnitude falling within general rough bounds
of 1 and 3 points IQ loss, with attendant uncertainties, and with
appreciably lower risks with increasing distance from the highest
exposure locations.
In considering the importance of such risk from a public health
perspective, the PA also considers the size of at-risk populations
represented by the REA case studies. As summarized in section II.D.1
above (and described more fully in the PA, section 3.4), the
generalized (local) urban case study is considered to represent a
localized urban population exposed near the level of the standard, such
as a very small, compact neighborhood near a source contributing to air
Pb concentrations just meeting the standard. This case study provides
representation in the risk assessment for such small populations at the
upper end of the gradient in ambient air concentrations expected to
occur near sources; thus estimates for this case study reflect
exposures nearest the standard being evaluated. While we do not have
precise estimates of the number of young children living in such areas
of the U.S. today, we have information that informs our understanding
of their magnitude. For example, as summarized in section II.B.5 above,
the PA estimates some 2,700 children, aged 5 years and younger, to be
living in localized areas with elevated air Pb concentrations that are
above or near the current standard. Based on the 2010 census estimates
of approximately 24.3 million children in the U.S. aged 5 years or
younger, this indicates the size of the population of young children of
this age living in areas in close proximity to areas where air Pb
concentrations may be above or near the current standard to be
generally on the order of a hundredth of a percent of the full
population of correspondingly aged children.67 68 While
these estimates pertain to the age group of children aged 5 years and
younger, the PA additionally notes that a focus on an alternative age
range (e.g., through age 7), while increasing the number for children
living in such locations, would not be expected to appreciably change
the percentage of the full U.S. age group that the subset represents.
---------------------------------------------------------------------------
\67\ The areas included in this estimate where the standard is
currently exceeded are treated, for present purposes, as areas with
air Pb concentrations just meeting the current standard and are
included for purposes of this analysis (PA, pp. 3-36 to 3-38). This
is in light of the requirement for areas not in attainment with the
standard to attain the standard as expeditiously as practicable, but
no later than 5 years after designation.
\68\ A second PA analysis, performed in recognition of the
potential for the first analysis to under-represent sites with
elevated Pb concentrations, but with its own attendant
uncertainties, indicates the potential for the population group in
such areas to be only slightly larger, in terms of hundredths of a
percent of the full population of children in this age group (PA,
pp. 3-36 to 3-38, 4-25, 4-32).
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3. CASAC Advice
In the current review of the primary standard for Pb, the CASAC has
provided advice and recommendations in their review of drafts of the
ISA, of the REA Planning Document, and of the draft PA. We have
additionally received comments from the public on drafts of these
documents.\69\
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\69\ As noted in section II.E.3 above, written comments
submitted to the agency, as well as transcripts and minutes of the
public meetings held in conjunction with CASAC's reviews of
documents for the review will be available in the docket for this
rulemaking.
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In their comments on the draft PA, the CASAC concurred with staff's
overall preliminary conclusions that it is appropriate to consider
retaining the current primary standard without revision, stating that
``the current scientific literature does not support a revision to the
Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS)''
(Frey, 2013b). They further noted that ``[a]lthough the current review
incorporates a substantial body of new scientific literature, the new
literature does not justify a revision to the standards because it does
not significantly reduce substantial data gaps and uncertainties (e.g.,
air-blood Pb relationship at low levels; sources contributing to
current population blood Pb levels, especially in children; the
relationship between Pb and childhood neurocognitive function at
current population exposure levels; the relationship between ambient
air Pb and outdoor dust and surface soil Pb concentrations).'' In
recognition of these limitations in the available information, the
CASAC provided recommendations on research to address these data gaps
and uncertainties so as to inform future Pb NAAQS reviews (Frey,
2013b).
The CASAC comments indicated agreements with key aspects of staff's
consideration of the exposure/risk information and currently available
evidence in this review (Frey, 2013b, Consensus Response to Charge
Questions, p. 7).
The use of exposure/risk information from the previous Pb NAAQS
review appears appropriate given the absence of significant new
information that could fundamentally change the interpretation of
the exposure/risk information. This interpretation is reasonable
given that information supporting the current standard is largely
unchanged since the current standard was issued.
The CASAC agrees that the adverse impact of low levels of Pb
exposure on neurocognitive function and development in children
remains the most sensitive health endpoint, and that a primary Pb
NAAQS designed to protect against that effect will offer
satisfactory protection against the many other health impacts
associated with Pb exposure.
The CASAC concurs with the draft PA that the scientific findings
pertaining to air-to-blood Pb ratios and the C-R relationships
between blood Pb and childhood IQ decrements that formed the basis
of the current Pb NAAQS remain valid and are consistent with current
data.
[[Page 311]]
The CASAC concurred with the appropriateness of the application of
the evidence-based framework from the last Pb NAAQS review. With regard
to the key inputs to that framework, CASAC concluded that ``[t]he new
literature published since the previous review provides further support
for the health effect conclusions presented in that review'' and that
the studies newly available in this review ``do not fundamentally alter
the uncertainties for air-to-blood ratios or C-R functions for IQ
decrements in young children'' (Frey, 2013b, Consensus Response to
Charge Questions, p. 6).
The comments from CASAC also took note of the uncertainties that
remain in this review, which contribute to the uncertainties associated
with drawing conclusions regarding air-related exposures and associated
health risk at or below the level of the current standard, stating
their agreement with ``the EPA conclusion that `there is appreciable
uncertainty associated with drawing conclusions regarding whether there
would be reductions in blood Pb levels from alternative lower levels as
compared to the level of the current standard' '' (Frey, 2013b,
Consensus Response to Charge Questions, p. 6).
Of the limited public comments received on this review to date that
have addressed adequacy of the current primary Pb standard, all but one
state support for retaining the current standard without revision,
citing uncertainties in the available evidence and risk information.
The other commenter expressed the view that the standard should be
revised to be more restrictive given the evidence of Pb effects in
populations with mean blood Pb levels below 10 [micro]g/dL.
4. Administrator's Proposed Conclusions on the Adequacy of the Current
Primary Standard
Based on the large body of evidence concerning the health effects
and potential public health impacts of exposure to Pb emitted into
ambient air, and taking into consideration the attendant uncertainties
and limitations of the evidence, the Administrator proposes to conclude
that the current primary standard provides the requisite protection of
public health, with an adequate margin of safety and should be
retained.
In considering the adequacy of the current standard, the
Administrator has carefully considered the assessment of the available
evidence and conclusions contained in the ISA; the technical
information, including exposure/risk information, staff conclusions,
and associated rationale, presented in the PA; the advice and
recommendations from CASAC; and public comments to date in this review.
In the discussion below, the Administrator gives weight to the PA
conclusions, with which CASAC has concurred, and takes note of key
aspects of the rationale presented for those conclusions which
contribute to her proposed decision.
As an initial matter, the Administrator takes note of the PA
discussion with regard to the complexity involved in considering the
adequacy of protection in the case of the primary Pb standard, which
differs substantially from that involved in consideration of the
primary NAAQS for other pollutants, for which the limited focus on the
inhalation pathway is a relatively simpler context. Additionally, while
an important component of the evidence base for most other NAAQS
pollutants is the availability of studies that have investigated an
association between current concentrations of the pollutant in ambient
air and the occurrence of health effects plausibly related to ambient
air exposure to that pollutant, the evidence base that supports
conclusions in this review of the Pb NAAQS includes most prominently
epidemiological studies focused on associations of blood Pb levels in
U.S. populations with health effects plausibly related to Pb exposures.
Support for conclusions regarding the plausibility for ambient air Pb
to play a role in such findings derives, in part, from studies linking
Pb in ambient air with the occurrence of health effects. However, such
studies (dating from the past or from other countries) involve ambient
air Pb concentrations many times greater than those that would meet the
current standard. Thus, in considering the adequacy of the current Pb
standard, rather than considering studies that have directly
investigated current concentrations of Pb in ambient air (including in
locations where the current standard is met) and the occurrence of
health effects, we primarily consider the evidence for, and risk
estimated from, models, based upon key relationships, such as those
among ambient air Pb, Pb exposure, blood Pb and health effects. This
evidence, with its associated limitations and uncertainties,
contributes to the EPA's conclusions regarding a relationship between
ambient air Pb conditions under the current standard and health
effects.
With regard to the current evidence, the Administrator first takes
note of the well-established body of evidence on the health effects of
Pb, augmented in some aspects since the last review, which continues to
support identification of neurocognitive effects in young children as
the most sensitive endpoint associated with Pb exposure. The evidence,
as summarized in the PA and discussed in detail in the ISA, continues
to indicate that a standard that provides protection from
neurocognitive effects in young children additionally provides
protection for other health effects of Pb, such as those reported in
adult populations. The Administrator takes note of the PA finding that
application of the evidence-based, air-related IQ loss framework,
developed in the last review, continues to provide a useful approach
for considering and integrating the evidence on relationships between
Pb in ambient air and Pb in children's blood and risks of
neurocognitive effects (for which IQ loss is used as an indicator). She
additionally takes note of the PA finding (described in section II.E.1
above) that the currently available evidence base, while somewhat
expanded since the last review, is not appreciably expanded or
supportive of appreciably different conclusions with regard to air-to-
blood ratios or C-R functions for neurocognitive decrements in young
children. She concurs with the PA findings, summarized in section
II.E.1 above, that application of this framework, in light of the
current evidence and exposure/risk information, continues to support a
standard as protective as the current standard.
In considering the nature and magnitude of the array of
uncertainties that are inherent in the scientific evidence and
analyses, the Administrator recognizes that our understanding of the
relationships between the presence of a pollutant in ambient air and
associated health effects is based on a broad body of information
encompassing not only more established aspects of the evidence, but
also aspects in which there may be substantial uncertainty. In the case
of the Pb NAAQS review, she takes note of the recognition in the PA of
increased uncertainty in characterizing the relationship of effects on
IQ with blood Pb levels below those represented in the evidence base
and in projecting the magnitude of blood Pb response to ambient air Pb
concentrations at and below the level of the current standard. The PA
recognizes this increased uncertainty, particularly in light of the
multiple factors that play a role in such a projection (e.g.,
meteorology, atmospheric dispersion and deposition, human physiology
and behavior), each of which carry attendant uncertainties. The
Administrator recognizes that collectively, these aspects of the
[[Page 312]]
evidence and associated uncertainties contribute to a recognition that
for Pb, as for other pollutants, the available health effects evidence
generally reflects a continuum, consisting of levels at which
scientists generally agree that health effects are likely to occur,
through lower levels at which the likelihood and magnitude of the
response become increasingly uncertain.
In making a judgment on the point at which health effects
associated with Pb become important from a public health perspective,
the Administrator has considered the public health significance of a
decrement of a very small number of IQ points in the at-risk population
of young children, in light of associated uncertainties. She notes that
her judgment on this matter relates to her consideration of the IQ loss
estimates yielded by the air-related IQ loss evidence-based framework
for specific combinations of standard level, air-to-blood ratio and C-R
function. In considering the public health significance of IQ loss
estimates in young children, the Administrator gives weight to the
comments of CASAC and some public commenters in the last review which
recognized a population mean IQ loss of 1 to 2 points to be of public
health significance and recommended that a very high percentage of the
population be protected from such a magnitude of IQ loss (73 FR 67000,
November 12, 2008). In so doing, the Administrator additionally notes
that the EPA is aware of no new information or new commonly accepted
guidelines or criteria within the public health community for
interpreting public health significance of neurocognitive effects in
the context of a decision on adequacy of the current Pb standard (PA,
pp. 4-33 to 4-34).
With the objective identified by CASAC in the 2008 review in mind,
the Administrator considers the role of the air-related IQ loss
evidence-based framework in informing consideration of standards that
might be concluded to provide such a level of protection. In so doing,
she first recognizes, like the Administrator at the time of the last
review, that the IQ loss estimates produced with the evidence-based
framework do not correspond to a specific quantitative public health
policy goal for air-related IQ loss that would be acceptable or
unacceptable for the entire population of children in the U.S. Rather,
the conceptual context for the evidence-based framework is that it
provides estimates for the mean air-related IQ loss of a subset of the
population of U.S. children (i.e., the subset living in close proximity
to air Pb sources that contributed to elevated air Pb concentrations
that equal the current level of the standard). This is the subset
expected to experience air-related Pb exposures at the high end of the
national distribution of such exposures. The associated mean IQ loss
estimate is the average for this highly exposed subset and is not the
average air-related IQ loss projected for the entire U.S. population of
children. Further, the Administrator recognizes uncertainties
associated with those estimates, and notes the PA conclusion that the
uncertainties increase with estimates associated with successively
lower standard levels. The Administrator additionally takes note of the
PA estimates for the size of such a population, drawn from information
on numbers of young children (aged 5 years or younger) living near
monitors registering ambient Pb concentrations above or within 10
percent of the NAAQS, which indicate it to be on the order of one
hundredth of one percent of the U.S. population of children of this
age, with an upper bound of approximately four hundredths of one
percent, drawn from similar demographic information based on proximity
to large Pb sources, as identified using the NEI (PA, pp. 3-36 to 3-
38). In summary, the current evidence, as considered within the
conceptual and quantitative context of the evidence-based framework,
and current air monitoring information indicates that the current
standard would be expected to satisfy the public health policy goal
recommended by CASAC in the last Pb NAAQS review, and CASAC did not
provide a different goal in the present review. Thus, the evidence
indicates that the current standard provides protection for young
children from neurocognitive impacts, including IQ loss, consistent
with advice from CASAC regarding IQ loss of public health significance.
In drawing conclusions from application of the evidence-based
framework with regard to adequacy of the current standard, the
Administrator further recognizes the degree to which IQ loss estimates
drawn from the air-related IQ loss evidence-based framework reflect
mean blood Pb levels that are below those represented in the currently
available evidence for young children. For example, in the case of the
current standard level of 0.15 [micro]g/m\3\, multiplication by the
air-to-blood ratio of 1:7, the value that was the focus of the last
review and which the evidence continues to support in this review,
yields a mean air-related blood Pb level of 1.05 [micro]g/dL. This
blood Pb level is half the level of the lowest blood Pb subgroup of
pre-school children in which neurocognitive effects have been observed
(PA, Table 3-2; Miranda et al., 2009) and well below the means of
subgroups for which continuous C-R functions have been estimated (Table
1 above). The Administrator views such an extension below the lowest
studied levels to be reasonable given the lack of identified blood Pb
level threshold in the current evidence base for neurocognitive effects
and the need for the NAAQS to provide a margin of safety. She takes
note, however, of the PA finding that the framework IQ loss estimates
for standard levels lower than the current standard level represent
still greater extrapolations from the current evidence base with
corresponding increased uncertainty (PA, section 3.2, pp. 4-32 to 4-
33).
In considering application of the evidence-based framework in this
review with regard to the extent there is support within the evidence
for a standard with greater protection, the Administrator additionally
takes note of the uncertainties that remain in our understanding of
important aspects of ambient air Pb exposure and associated health
effects, as discussed in the PA (PA, Chapter 3) and summarized in
sections II.B and II.C above. With regard to the air-to-blood ratios
that reflect the relationship between concentrations of Pb in ambient
air and air-related Pb in children's blood, she particularly notes the
limitations and uncertainties identified in the ISA and PA with regard
to the available studies and the gaps and uncertainties in the evidence
base. These include gaps and uncertainties with regard to studies that
have investigated such quantitative relationships under conditions
pertaining to the current standard (e.g., in localized areas near air
Pb sources where the standard is just met in the U.S. today), as well
as with regard to evidence to inform our understanding of the
quantitative aspects of relationships between ambient air Pb and
outdoor soil/dust Pb and indoor dust Pb. These critical exposure
pathways are also represented in the evidence-based air-related IQ loss
framework within the estimates of air-to-blood ratios. In light of
these uncertainties and limitations in the evidence base, the
Administrator gives weight to the PA conclusion of greater uncertainty
with regard to relationships between concentrations of Pb in ambient
air and air-related Pb in children's blood, and with regard to
estimates of the slope of the C-R function of neurocognitive impacts
(IQ loss) for application of the framework to
[[Page 313]]
levels below the current standard, given the weaker linkage with
existing evidence as discussed in the PA (PA, sections 3.1, 3.2 and
4.2.1).
With respect to exposure/risk-based considerations, as in the last
review, the Administrator notes the complexity of the REA modeling
analyses and the associated limitations and uncertainties. Based on
consideration of the risk-related information for conditions just
meeting the current standard, the Administrator takes note of the
attendant uncertainties, discussed in detail in the PA (PA, sections
3.4 and 4.2.2), while finding that the quantitative risk estimates,
with a focus on those for the generalized (local) urban case study, are
``roughly consistent with and generally supportive'' of estimates from
the evidence-based air-related IQ loss framework. She further takes
note of the PA finding of increasing uncertainty for air quality
scenarios involving air Pb concentrations increasingly below the
current conditions for each case study, due in part to modeling
limitations that derive from uncertainty regarding relationships
between ambient air Pb and outdoor soil/dust Pb and indoor dust Pb (PA,
sections 3.4.3.1 and 3.4.7).
Based on the above considerations and with consideration of advice
from CASAC, the Administrator reaches the conclusion that the current
body of evidence, in combination with the exposure/risk information,
supports a primary standard as protective as the current standard.
Based on consideration of the evidence and exposure/risk information
available in this review with its attendant uncertainties and
limitations and information that might inform public health policy
judgments, as well as advice from CASAC, including their concurrence
with the PA conclusions that revision of the primary Pb standard is not
warranted at this time, the Administrator further concludes that it is
appropriate to consider retaining the current standard without
revision.
The Administrator bases these proposed conclusions on consideration
of the health effects evidence, including consideration of this
evidence in the context of the evidence-based, air-related IQ loss
framework, and with support from the exposure/risk information,
recognizing the uncertainties attendant with both. In so doing, she
takes note of the PA description of the complexities and limitations in
the evidence base associated with reaching conclusions regarding the
magnitude of risk associated with the current standard, as well as the
increasing uncertainty of risk estimates for lower air Pb
concentrations. Inherent in the Administrator's conclusions are public
health policy judgments on the public health implications of the blood
Pb levels and risk estimated for air-related Pb under the current
standard, including the public health significance of the Pb effects
being considered, as well as aspects of the use of the evidence-based
framework that may be considered to contribute to the margin of safety.
These public health policy judgments include judgments related to the
appropriate degree of public health protection that should be afforded
to protect against risk of neurocognitive effects in at-risk
populations, such as IQ loss in young children, as well as with regard
to the appropriate weight to be given to differing aspects of the
evidence and exposure/risk information, and how to consider their
associated uncertainties. Based on these considerations and the
judgments identified here, the Administrator concludes that the current
standard provides the requisite protection of public health with an
adequate margin of safety, including protection of at-risk populations,
such as young children living near Pb emissions sources where ambient
concentrations just meet the standard.
In reaching this conclusion with regard to the adequacy of public
health protection afforded by the existing primary standard, the
Administrator recognizes that in establishing primary standards under
the Act that are requisite to protect public health with an adequate
margin of safety, she is seeking to establish standards that are
neither more nor less stringent than necessary for this purpose. The
Act does not require that primary standards be set at a zero-risk
level, but rather at a level that avoids unacceptable risks to public
health, even if the risk is not precisely identified as to nature or
degree. The CAA 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, as described in section I.A above. This
requirement was also intended to provide a reasonable degree of
protection from hazards that research has not yet identified.
In this context, the Administrator's proposed conclusion that the
current standard provides the requisite protection and that a more
restrictive standard would not be requisite additionally recognizes
that the uncertainties and limitations associated with the many aspects
of the estimated relationships between air Pb concentrations and blood
Pb levels and associated health effects are amplified with
consideration of increasingly lower air concentrations. In so doing,
she takes note of the PA conclusion, with which CASAC has agreed, that
based on the current evidence, there is appreciable uncertainty
associated with drawing conclusions regarding whether there would be
reductions in blood Pb levels and risk to public health from
alternative lower levels of the standard as compared to the level of
the current standard (PA, pp. 4-35 to 4-36; Frey, 2013b, p. 6). The
Administrator judges this uncertainty to be too great for the current
evidence and exposure/risk information to provide a basis for revising
the current standard. Thus, based on the public health policy judgments
described above, including the weight given to uncertainties in the
evidence, the Administrator proposes to conclude that the current
standard should be retained, without revision. The Administrator
solicits comment on this conclusion.
III. Rationale for Proposed Decision on the Secondary Standard
This section presents information relevant to the rationale for the
Administrator's proposed decision to retain the existing secondary Pb
standard, which as discussed more fully below, is based on a thorough
review in the ISA of the latest scientific information, generally
published through September 2011,\70\ on ecological or welfare effects
associated with Pb and pertaining to the presence of Pb in the ambient
air. This proposal also takes into account: (1) The PA's staff
assessments of the most policy-relevant information in the ISA and
staff analyses of potential ecological exposures and risk, upon which
staff conclusions regarding appropriate considerations in this review
are based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the ISA and PA at public meetings, in separate
written comments, and in CASAC's letters to the Administrator; and (3)
public comments received during the development of these documents,
either in connection with CASAC meetings or separately.
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\70\ In addition to the review's opening ``call for
information'' (75 FR 8934), ``literature searches were conducted
routinely to identify studies published since the last review,
focusing on studies published from 2006 (close of the previous
scientific assessment) through September 2011'' and references
``that were considered for inclusion or actually cited in this ISA
can be found at http://hero.epa.gov/lead'' (ISA, p. 1-2).
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[[Page 314]]
Section III.A provides background on the general approach for
review of the secondary NAAQS for Pb, including a summary of the
approach used in the last review (section III.A.1) and the general
approach for the current review (section III.A.2). Section III.B
summarizes the body of evidence on ecological or welfare effects
associated with Pb exposures, focusing on consideration of key policy-
relevant questions, and section III.C summarizes the exposure/risk
information in this review. Section III.D presents the Administrator's
proposed conclusions on adequacy of the current standard, drawing on
both evidence-based and exposure/risk-based considerations (sections
III.D.1), and advice from CASAC (section III.D.2).
A. General Approach
The past and current approaches described below are all based most
fundamentally on using the EPA's assessment of the current scientific
evidence and previous quantitative analyses to inform the
Administrator's judgment with regard to the secondary standard for Pb.
In drawing conclusions for the Administrator's consideration with
regard to the secondary standard, we note that the final decision on
the adequacy of the current secondary Pb standard is largely a public
welfare policy judgment to be made by the Administrator. The
Administrator's final decision must draw upon scientific information
and analyses about welfare effects, exposure and risks, as well as
judgments about the appropriate response to the range of uncertainties
that are inherent in the scientific evidence and analyses. This
approach is consistent with the requirements of the NAAQS provisions of
the Act. These provisions require the Administrator to establish a
secondary standard that, in the judgment of the Administrator, 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.'' In so doing, the Administrator seeks to establish
standards that are neither more nor less stringent than necessary for
this purpose.
1. Approach in the Last Review
In the last review, completed in 2008, the current secondary
standard for Pb was set equal to the primary standard (73 FR 66964,
November 12, 2008). As summarized in sections I.C and II.A.1 above, the
primary standard was substantially revised in the last review. The 2008
decision considered the body of evidence as assessed in the 2006 CD
(USEPA, 2006a) as well as the 2007 Staff Paper assessment of the
policy-relevant information contained in the 2006 CD and the screening-
level ecological risk assessment (2006 REA; USEPA, 2007b), the advice
and recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b),
and public comment.
In the previous review, the Staff Paper concluded, based on
laboratory studies and current media concentrations in a wide range of
locations, that it seemed likely that adverse effects were occurring
from ambient air-related Pb, particularly near point sources, under the
then-current standard (73 FR 67010, November 12, 2008). Given the
limited data on Pb effects in ecosystems, and associated uncertainties,
such as those with regard to factors such as the presence of multiple
metals and historic environmental burdens, it was at the time, as it is
now, necessary to look at evidence of Pb effects on organisms and
extrapolate to ecosystem effects. Taking into account the available
evidence and current media concentrations in a wide range of locations,
the Administrator concluded that there was potential for adverse
effects occurring under the then-current standard; however there were
insufficient data to provide a quantitative basis for setting a
secondary standard different from the primary (73 FR 67011, November
12, 2008). Therefore, citing a general lack of data that would indicate
the appropriate level of Pb in environmental media that may be
associated with adverse effects, as well as the comments of the CASAC
Pb panel that a significant change to current air concentrations (e.g.,
via a significant change to the standard) was likely to have
significant beneficial effects on the magnitude of Pb exposures in the
environment, the secondary standard was revised to be consistent with
the revised primary standard (73 FR 67011, November 12, 2008).
2. Approach for the Current Review
Our approach for reviewing the current secondary standard takes
into consideration the approaches used in the last Pb NAAQS review and
involves addressing key policy-relevant questions in light of currently
available scientific and technical information. In evaluating whether
it is appropriate to consider retaining the current secondary Pb
standard, or whether consideration of revision is appropriate, we have
adopted an approach in this review that builds on the general approach
from the last review and reflects the body of evidence and information
now available. As summarized above, the Administrator's decisions in
the previous review were based on the conclusion that there was the
potential for adverse ecological effects under the previous standard.
In our approach here, we focus on consideration of the extent to
which a broader body of scientific evidence is now available that would
inform decisions on either the potential for adverse effects to
ecosystems under the current standard or the ability to set a more
ecologically relevant secondary standard than was feasible in the
previous review. In considering the scientific and technical
information in sections II.B and II.C below, as in the PA, we draw on
the ecological effects evidence presented in detail in the ISA and
aspects summarized in the PA, along with the information associated
with the screening-level risk assessment also in the PA. In section
III.D below, we have taken into account both evidence-based and risk-
based considerations framed by a series of policy-relevant questions
presented in the PA. These questions generally discuss the extent to
which we are able to better characterize effects and the likelihood of
adverse effects in the environment under the current standard. Our
approach to considering these issues recognizes that the available
welfare effects evidence generally reflects laboratory-based evidence
of toxicological effects on specific organisms exposed to
concentrations of Pb. It is widely recognized, however, that
environmental exposures from atmospherically derived Pb are likely to
be lower than those commonly assessed in laboratory studies and that
studies of exposures similar to those in the environment are often
accompanied by significant confounding and modifying factors (e.g.,
other metals, acidification), increasing our uncertainty about the
likelihood and magnitude of organism and ecosystem responses.
B. Welfare Effects Information
Welfare effects addressed by the secondary NAAQS include, but are
not limited to, effects on soils, water, crops, vegetation, manmade
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
wellbeing. This discussion presents key aspects of the current evidence
of Pb-related welfare effects that are assessed in the ISA and the 2006
CD, drawing from the summary of policy-relevant aspects in the PA (PA,
section 5.1).
Lead has been demonstrated to have harmful effects on reproduction
and development, growth, and survival in
[[Page 315]]
many species as described in the assessment of the evidence available
in this review and consistent with the conclusions drawn in the last
review (ISA, section 1.7; 2006 CD, sections 7.1.5 and 7.2.5). A number
of studies on ecological effects of Pb are newly available in this
review and are critically assessed in the ISA as part of the full body
of evidence. The full body of currently available evidence reaffirms
conclusions on the array of effects recognized for Pb in the last
review (ISA, section 1.7). In so doing, in the context of pollutant
exposures considered relevant the ISA determines \71\ that causal \72\
or likely causal \73\ relationships exist in both freshwater and
terrestrial ecosystems for Pb with effects on reproduction and
development in vertebrates and invertebrates; growth in plants and
invertebrates; and survival in vertebrates and invertebrates (ISA,
Table 1-3). In drawing judgments regarding causality for the criteria
air pollutants, the ISA places emphasis on ``evidence of effects at
doses (e.g., blood Pb concentration) or exposures (e.g., air
concentrations) that are relevant to, or somewhat above, those
currently experienced by the population.'' The ISA notes that the
``extent to which studies of higher concentrations are considered
varies . . . but generally includes those with doses or exposures in
the range of one to two orders of magnitude above current or ambient
conditions.'' Studies ``that use higher doses or exposures may also be
considered . . . [t]hus, a causality determination is based on weight
of evidence evaluation for health, ecological or welfare effects,
focusing on the evidence from exposures or doses generally ranging from
current levels to one or two orders of magnitude above current levels''
(ISA, pp. lx to lxi).
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\71\ Since the last Pb NAAQS review, the ISAs, which have
replaced CDs in documenting each review of the scientific evidence
(or air quality criteria), employ a systematic framework for
weighing the evidence and describing associated conclusions with
regard to causality, using established descriptors: ``causal''
relationship with relevant exposure, ``likely'' to be a causal
relationship, evidence is ``suggestive'' of a causal relationship,
``inadequate'' evidence to infer a causal relationship, and ``not
likely'' to be a causal relationship (ISA, Preamble).
\72\ In determining that a causal relationship exists for Pb
with specific ecological or welfare effects, the EPA has concluded
that ``[e]vidence is sufficient to conclude that there is a causal
relationship with relevant pollutant exposures (i.e., doses or
exposures generally within one to two orders of magnitude of current
levels)'' (ISA, p. lxii).
\73\ In determining a likely causal relationship exists for Pb
with specific ecological or welfare effects, the EPA has concluded
that ``[e]vidence is sufficient to conclude that there is a likely
causal association with relevant pollutant exposures . . . but
uncertainties remain'' (ISA, p. lxii).
---------------------------------------------------------------------------
Although considerable uncertainties are recognized in generalizing
effects observed under particular, small-scale conditions, up to the
ecosystem level of biological organization, the ISA determines that the
cumulative evidence reported for Pb effects at such higher levels of
biological organization and for endpoints in single species with direct
relevance to population and ecosystem level effects (i.e., development
and reproduction, growth, survival) is sufficient to conclude that a
causal relationship is likely to exist between Pb exposures and
community and ecosystem-level effects in freshwater and terrestrial
systems (ISA, section 1.7.3.7).
The ISA also presents evidence for saltwater ecosystems, concluding
that current evidence is inadequate to make causality determinations
for most population-level responses, as well as community and ecosystem
effects, while finding the evidence to be suggestive linking Pb and
effects on reproduction and development in marine invertebrates (ISA,
Table 1-3, sections 6.3.12 and 6.4.21).
As in prior reviews of the Pb NAAQS, this review is focused on
those effects most pertinent to ambient air Pb exposures. Given the
reductions in ambient air Pb concentrations over the past decades,
these effects are generally those associated with the lowest levels of
Pb exposure that have been evaluated. Additionally, we recognize the
limitations on our ability to draw conclusions about environmental
exposures from ecological studies of organism-level effects, as most
studies were conducted in laboratory settings which may not accurately
represent field conditions or the multiple variables that govern
exposure.
The relationship between ambient air Pb and ecosystem response is
important in making the connection between current emissions of Pb and
the potential for adverse ecological effects. The limitations in the
data available on this subject for the last review were significant.
There is no new evidence since the last review that substantially
improves our understanding of the relationship between ambient air Pb
and measurable ecological effects. As stated in the last review, the
role of ambient air Pb in contributing to ecosystem Pb has been
declining over the past several decades. It remains difficult to
apportion exposure between air and other sources to inform our
understanding of the potential for ecosystem effects that might be
associated with air emissions. As noted in the ISA, ``[t]he amount of
Pb in ecosystems is a result of a number of inputs and it is not
currently possible to determine the contribution of atmospherically-
derived Pb from total Pb in terrestrial, freshwater or saltwater
systems'' (ISA, section 6.5). Further, considerable uncertainties also
remain in drawing conclusions from effects evidence observed under
laboratory conditions with regard to effects expected at the ecosystem
level in the environment. In many cases it is difficult to characterize
the nature and magnitude of effects and to quantify relationships
between ambient concentrations of Pb and ecosystem response due to the
existence of multiple stressors, variability in field conditions, and
differences in Pb bioavailability at that level of organization (ISA,
section 6.5). In summary, the ISA concludes that ``[r]ecent information
available since the 2006 Pb AQCD, includes additional field studies in
both terrestrial and aquatic ecosystems, but the connection between air
concentration and ecosystem exposure continues to be poorly
characterized for Pb and the contribution of atmospheric Pb to specific
sites is not clear'' (ISA, section 6.5).
It is also important to consider the fate and transport of both
current Pb and Pb emitted in the past. It is this past legacy of Pb
that was cited as a significant source of uncertainty in the last
review. The extensive history of Pb uses in developed countries coupled
with atmospheric transport processes has left a legacy of Pb in
ecosystems globally (e.g., 2006 CD, sections 2.3.1 and 7.1; 1977 CD,
section 6.3.1). Records of U.S. atmospheric emissions of Pb in the
twentieth and late nineteenth centuries have been documented in
sediment cores (PA, section 2.3; ISA, section 2.6.2; Landers et al.,
2010). Once deposited, Pb can be transported by stormwater runoff or
resuspension to catchments and nearby water bodies or stored in soil
layers in forested areas, its further movement influenced by soil or
sediment composition and chemistry and physical processes. Some new
studies are available that provide additional information, briefly
summarized below, on Pb cycling, flux and retention within terrestrial
and aquatic systems. This new information does not fundamentally change
our understanding from the last review of Pb movement through or
accumulation in ecosystems over time but rather improves our
understanding of some of the underlying processes and
[[Page 316]]
mechanisms in soil, water and sediment. There is little new
information, however, on fate and transport in ecosystems specifically
related to air-derived Pb (ISA, section 2.3). There is limited newly
available information with regard to the timing of ecosystem recovery
from historic atmospheric deposition of Pb (ISA, sections 2.3.2.4 and
2.3.3.3).
Overall, recent studies in terrestrial ecosystems provide
deposition data consistent with deposition fluxes reported in the 2006
CD and demonstrate consistently that atmospheric deposition of Pb has
decreased since the phase-out of leaded on-road gasoline (PA, section
2.3.2.2; ISA, section 2.3.3). Follow-up studies in several locations at
high elevation sites indicate little change in soil Pb concentrations
since the phase-out of leaded onroad gasoline in surface soils,
consistent with the high retention reportedly associated with reduced
microbial activity at lower temperatures associated with high elevation
sites. However, amounts of Pb in the surface soils at some lower
altitude sites were reduced over the same time period in the same study
(ISA, section 2.3.3). New studies in the ISA also enhance our
understanding of Pb sequestration in forest soils by providing
additional information on the role of leaf litter as a Pb reservoir in
some situations and the effect of litter decomposition on Pb
distribution (ISA, section 2.3.3).
Recent research on Pb transport in aquatic systems has provided a
large body of observations confirming that such transport is dominated
by colloids rich in iron and organic material (ISA, section 2.3.2).
Recent research on Pb flux in sediments provides greater detail on
resuspension processes than was available in the 2006 CD, including
research on resuspended Pb largely associated with organic material or
iron and manganese particles and research on the important role played
by anoxic or depleted oxygen environments in Pb cycling in aquatic
systems. This newer research is consistent with prior evidence in
indicating that appreciable resuspension and release from sediments
largely occurs during discrete events related to storms. It has also
confirmed that resuspension is an important process that strongly
influences the lifetime of Pb in bodies of water. Finally, there have
been advances in understanding and modeling of Pb partitioning between
organic material and sediment in aquatic environments (ISA, section
2.7.2).
The bioavailability of Pb is also an important component of
understanding the effects Pb is likely to have on organisms and
ecosystems (ISA, section 6.3.3). It is the amount of Pb that can
interact within the organism that leads to toxicity, and there are many
factors which govern this interaction (ISA, sections 6.2.1 and 6.3.3).
The bioavailability of metals varies widely depending on the physical,
chemical, and biological conditions under which an organism is exposed
(ISA, section 6.3.3). Studies newly available since the last Pb NAAQS
review provide additional insight into factors that influence the
bioavailability of Pb to specific organisms (ISA, section 6.3.3). In
general, this evidence is supportive of previous conclusions and does
not identify significant new variables from those identified
previously. Section 6.3.3 of the ISA provides a detailed discussion of
bioavailability in terrestrial systems. With regard to aquatic systems,
a detailed discussion of bioavailability in freshwater systems is
provided in sections 6.4.3 and 6.4.4 of the ISA, and section 6.4.14 of
the ISA discusses bioavailability in saltwater systems.
In terrestrial systems, the amount of bioavailable Pb present
determines the impact of soil Pb to a much greater extent than does the
total amount present (ISA, section 6.3.11). In such ecosystems, Pb is
deposited either directly onto plant surfaces or onto soil where it can
bind with organic matter or dissolve in pore water. The Pb dissolved in
pore water is particularly bioavailable to organisms in the soil and,
therefore, the impact of this Pb on the ecosystem is potentially
greater than soil Pb that is not in pore water (ISA, section 6.3.11).
In aquatic systems as in terrestrial systems, the amount of Pb
bioavailable to organisms is a better predictor of effect on organisms
than the overall amount of Pb in the system. Once atmospherically
derived Pb enters surface water bodies through deposition or runoff,
its fate and bioavailability are influenced by many water quality
characteristics, such as pH, suspended solids levels and organic
content (ISA, section 6.4.2). In sediments, bioavailability of Pb to
sediment-dwelling organisms may be influenced by the presence of other
metals, sulfides, iron oxides and manganese oxides and also by physical
disturbance (ISA, section 2.6.2). For many aquatic organisms, Pb
dissolved in the water column can be the primary exposure route, while
for others sediment ingestion is significant (ISA, section 2.6.2). As
recognized in the 2006 CD and further supported in the ISA, there is a
body of evidence showing that uptake and elimination of Pb vary widely
among aquatic species.
There is a substantial amount of new evidence in this review
regarding the ecological effects of Pb on individual terrestrial and
aquatic species with less new information available on marine species
and ecosystems. On the whole, this evidence supports previous
conclusions that Pb has effects on growth, reproduction and survival,
and that under some conditions these effects can be adverse to
organisms and ecosystems. The ISA provides evidence of effects in
additional species and in a few cases at lower exposures than reported
in the previous review, but does not substantially alter our
understanding of the ecological endpoints affected by Pb from the
previous review. Looking beyond organism-level evidence, the evidence
of adversity in natural systems remains sparse due to the difficulty in
determining the effects of confounding factors such as co-occurring
metals or system characteristics that influence bioavailability of Pb
in field studies. The following paragraphs summarize the information
presented in this review for terrestrial, aquatic and marine systems.
With regard to terrestrial ecosystems, recent studies cited in this
review support previous conclusions about the effects of Pb, namely
that increasing soil Pb concentrations in areas of Pb contamination
(e.g., mining sites and industrial sites) can cause decreases in
microorganism abundance, diversity, and function. Previous reviews have
also reported on effects on bird and plant communities (2006 CD,
section AX7.1.3). The shifts in bacterial species and fungal diversity
have been observed near long-established sources of Pb contamination
(ISA, section 6.3.12.7). Most recent evidence for Pb toxicity to
terrestrial plants, invertebrates and vertebrates is from single-
species assays in laboratory studies which do not capture the
complexity of bioavailability and other modifiers of effect in natural
systems (ISA, section 6.3.12.7). Further, models that might account for
modifiers of bioavailability have proven difficult to develop (ISA, p.
6-16).
Evidence presented in the ISA and prior CDs demonstrates the
toxicity of Pb in aquatic ecosystems and the role of many factors,
including Pb speciation and various water chemistry properties, in
modifying toxicity (ISA, section 1.7.2). Since the 2006 CD, additional
evidence for community and ecosystem level effects of Pb is available,
primarily in microcosm studies or field studies with other metals
present (ISA, section 6.4.11). Such evidence described in
[[Page 317]]
previous CDs includes alteration of predator-prey dynamics, species
richness, species composition, and biodiversity. New studies available
in this review provide evidence in additional habitats for these
community and ecological-scale effects, specifically in aquatic plant
communities and sediment-associated communities at both acute and
chronic exposures involving concentrations similar to those previously
reported (ISA, section 6.4.7). In many cases, it is difficult to
characterize the nature and magnitude of effects and to quantify
relationships between ambient concentrations of Pb and ecosystem
response due to existence of multiple ecosystem-level stressors,
variability in field conditions, and differences in Pb bioavailability
(ISA, sections 1.7.3.7 and 6.4.7). Additionally, the degree to which
air concentrations have contributed to such effects in freshwater
ecosystems is largely unknown.
With regard to evidence in marine ecosystems, recently available
evidence on the toxicity of Pb to marine algae augments the 2006 CD
findings of variation in sensitivity across marine species. Recent
studies on Pb exposure include reports of growth inhibition and
oxidative stress in a few additional species of marine algae (ISA,
section 6.4.15). Recent literature provides little new evidence of
endpoints or effects in marine invertebrates beyond those reported in
the 2006 CD. For example, some recent studies strengthen the evidence
presented in the 2006 CD regarding negative effects of Pb exposure on
marine invertebrates (ISA, section 6.4.15.2). Recent studies also
identify several species exhibiting particularly low sensitivity to
high acute exposures (ISA, section 6.4.15.2). Little new evidence is
available of Pb effects on marine fish and mammals for reproductive,
growth and survival endpoints that are particularly relevant to the
population level of biological organization and higher (ISA, section
6.4.15). New studies on organism-level effects from Pb in saltwater
ecosystems (ISA, section 6.4.15) provide little evidence to inform our
understanding of linkages among atmospheric concentrations, ambient
exposures in saltwater systems and such effects or to inform our
conclusions regarding the likelihood of adverse effects under
conditions associated with the current NAAQS for Pb. Nor does the
currently available evidence indicate significantly different exposure
levels from the previous review at which ecological systems or
receptors are expected to experience effects.
During the last review, the 2006 CD assessed the available
information on critical loads for Pb (2006 CD, section 7.3). This
information included publications on methods and example applications,
primarily in Europe, specific to the bedrock geology, soil types,
vegetation, and historical deposition trends in each European country
(2006 CD, p. E-24), with no analyses available for U.S. locations (2006
CD, sections 7.3.4-7.3.6). As a result, the 2006 CD concluded that
``[c]onsiderable research is necessary before critical load estimates
can be formulated for ecosystems extant in the United States'' (2006
CD, p. E-24).
For this current review, newly available evidence pertaining to
critical loads analysis includes limited recent research on
consideration of bioavailability in characterizing Pb effect
concentrations or indices and on modeling approaches to incorporate
chemistry effects on Pb speciation and bioavailability (ISA, sections
6.3.7 and 6.4.8). With consideration of this information and the four
critical load analysis studies newly available in this review (none of
which are for U.S. ecosystems), the ISA does not modify the conclusions
noted above from the 2006 CD (ISA, sections 6.1.3, 6.3.7 and 6.4.8). In
summary, the new information in this review does not appreciably change
our evidence base or further inform our understanding of critical loads
of Pb, including critical loads in sensitive U.S. ecosystems.
There is no new evidence since the last review that substantially
improves our understanding of the relationship between ambient air Pb
and measurable ecological effects. As stated in the last review, the
role of ambient air Pb in contributing to ecosystem Pb has been
declining over the past several decades. It remains difficult to
apportion exposure between air and other sources to better inform our
understanding of the potential for ecosystem effects that might be
associated with air emissions. As noted in the ISA, ``[t]he amount of
Pb in ecosystems is a result of a number of inputs and it is not
currently possible to determine the contribution of atmospherically-
derived Pb from total Pb in terrestrial, freshwater or saltwater
systems'' (ISA, section 6.5). Further, considerable uncertainties also
remain in drawing conclusions from evidence of effects observed under
laboratory conditions with regard to effects expected at the ecosystem
level in the environment. In many cases it is difficult to characterize
the nature and magnitude of effects and to quantify relationships
between ambient concentrations of Pb and ecosystem response due to the
existence of multiple stressors, variability in field conditions, and
differences in Pb bioavailability at that level of organization (ISA,
section 6.5). In summary, the ISA concludes that ``[r]ecent information
available since the 2006 Pb AQCD, includes additional field studies in
both terrestrial and aquatic ecosystems, but the connection between air
concentration and ecosystem exposure continues to be poorly
characterized for Pb and the contribution of atmospheric Pb to specific
sites is not clear'' (ISA, section 6.5).
C. Summary of Risk Assessment Information
The risk assessment information available in this review and
summarized here is based on the screening-level risk assessment
performed for the last review, described in the 2006 REA, 2007 Staff
Paper and 2008 notice of final decision (73 FR 66964, November 12,
2008), as considered in the context of the evidence newly available in
this review (PA, section 5.2). As described in the REA Planning
Document, careful consideration of the information newly available in
this review, with regard to designing and implementing a full REA for
this review, led us to conclude that performance of a new REA for this
review was not warranted (REA Planning Document, section 3.3). Based on
their consideration of the REA Planning Document analysis, the CASAC Pb
Review Panel generally concurred with the conclusion that a new REA was
not warranted in this review (Frey, 2011b). Accordingly, the risk/
exposure information considered in this review is drawn primarily from
the 2006 REA as summarized below (PA, section 5.2 and Appendix 5A; REA
Planning Document, section 3.1).
The 2006 screening-level assessment focused on estimating the
potential for ecological risks associated with ecosystem exposures to
Pb emitted into ambient air (PA, section 5.2; 2006 REA, section 7). A
national-scale screen was used to evaluate surface water and sediment
monitoring locations across the U.S. for the potential for ecological
impacts that might be associated with atmospheric deposition of Pb
(2006 REA, section 7.1.2). In addition to the national-scale screen
(2006 REA, section 3.6), the assessment involved a case study approach,
with case studies for areas surrounding a primary Pb smelter (2006 REA,
section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as
well as a location near a non-urban roadway (2006 REA, section 3.4). An
additional case study, focused on
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consideration of atmospherically derived Pb effects on an ecologically
vulnerable ecosystem (Hubbard Brook Experimental Forest), was
identified (2006 REA, section 3.5). The Hubbard Brook Experimental
Forest (HBEF), in the White Mountain National Forest, near North
Woodstock, New Hampshire, was selected as a fourth case study because
of its location and its long record of available data on concentration
trends of Pb in three media (air or deposition from air, soil, and
surface water). The HBEF case study was a qualitative analysis focusing
on a summary review of the literature, without new quantitative
analyses (2006 REA, Appendix E). For the other three case studies,
exposure concentrations of Pb in soil, surface water, and/or sediment
concentrations were estimated from available monitoring data or
modeling analysis and then compared to ecological screening benchmarks
(2006 REA, section 7.1).
In interpreting the results from the 2006 REA, the PA considers
newly available evidence that may inform interpretation of risk under
the now current standard (PA, section 5.2). Factors that could alter
our interpretation of risk would include new evidence of harm at lower
concentrations of Pb, new linkages that enable us to draw more explicit
conclusions as to the air contribution of environmental exposures, and
new methods of interpreting confounding factors that were largely
uncontrolled in the previous risk assessment. In general, however, the
key uncertainties identified in the last review remain today.
The results for the ecological screening assessment for the three
case studies and the national-scale screen for surface water and for
sediment in the last review indicated a potential for adverse effects
from ambient Pb to multiple ecological receptor groups in terrestrial
and aquatic locations. Detailed descriptions of the location-specific
case studies and the national screening assessment, key findings of the
risk assessment for each, and an interpretation of the results with
regard to past air conditions can be found in the 2006 REA. In
considering the potential for adverse welfare effects to result from
levels of air-related Pb that would meet the current standard, the
findings of the 2006 REA, as summarized in the PA, are discussed below.
While the contribution to Pb concentrations from air as compared to
nonair sources is not quantified, air emissions from the primary Pb
smelter case study facility were substantial (2006 REA, Appendix B). In
addition, this facility, which closed in 2013, had been emitting Pb for
many decades, including some seven decades prior to establishment of
any Pb NAAQS, such that it is likely air concentrations associated with
the facility were substantial relative to the 1978 NAAQS, which it
exceeded at the time of the last review. At the time of the last review
and also since the adoption of the current standard, concentrations
monitored near this facility have exceeded the level of the applicable
NAAQS (2007 Staff Paper, Appendix 2B-1; PA, Appendices 2D and 5A).
Accordingly, this case study is not informative for considering the
likelihood of adverse welfare effects related to Pb from air sources
under air quality conditions associated with meeting the current Pb
standard.
The secondary Pb smelter case study location continues to emit Pb,
and the county where this facility is located does not meet the current
Pb standard (PA, Appendices 2D and 5A). Given the exceedances of the
current standard, which likely extend back over 4 to 5 decades, this
case study also is not informative for considering the likelihood of
adverse welfare effects related to Pb from air sources under air
quality conditions associated with meeting the current Pb standard.
The locations for the near-roadway non-urban case study are highly
impacted by past deposition of gasoline Pb. It is unknown whether
current conditions at these sites exceed the current Pb standard, but,
given evidence from the past of Pb concentrations near highways that
ranged above the previous (1978) Pb standard (1986 CD, section 7.2.1),
conditions at these locations during the time of leaded gasoline very
likely exceeded the current standard. Similarly, those conditions
likely resulted in Pb deposition associated with leaded gasoline that
exceeds that being deposited under air quality conditions that would
meet the current Pb standard. Given this legacy, consideration of the
potential for environmental risks from levels of air-related Pb
associated with meeting the current Pb standard in these locations is
highly uncertain.
The extent to which past air emissions of Pb have contributed to
surface water or sediment Pb concentrations at the locations identified
in the national scale surface water and sediment screen is unclear. For
some of the surface water locations, nonair sources likely contributed
significantly to the surface water Pb concentrations. For other
locations, a lack of nearby nonair sources indicated a potential role
for air sources to contribute to observed surface water Pb
concentrations. Additionally, these concentrations may have been
influenced by Pb in resuspended sediments and may reflect contribution
of Pb from erosion of soils with Pb derived from historic as well as
current air emissions.
The most useful case study to the current review is that of the
Vulnerable Ecosystem Case Study located in the HBEF. This case study
was focused on consideration of information which included a long
record (from 1976 through 2000) of available data on concentration
trends of Pb in three media (air or deposition from air, soil, and
surface water). While no quantitative analyses were performed, a
summary review of literature published on HBEF was developed. This
review indicated: (1) Atmospheric Pb inputs do not directly affect
stream Pb levels at HBEF because deposited Pb is almost entirely
retained in the soil profile; and (2) soil horizon analysis results
showed Pb to have become more concentrated at lower soil depths over
time, with the soil serving as a Pb sink, appreciably reducing Pb in
pore water as it moves through the soil layers to streams (dissolved Pb
concentrations were reduced from 5 [mu]g/L to about 5 ng/L from surface
soil to streams). As a result, the HBEF studies concluded that the
contribution of dissolved Pb from soils to streams was insignificant
(2006 REA, Appendix E). Further, atmospheric input of Pb, based on bulk
precipitation data, was estimated to decline substantially from the
mid-1970s to 1989; forest floor soil Pb concentrations between 1976 and
2000 were also estimated to decline appreciably (2006 REA, sections E.1
and E.2). In considering HBEF and other terrestrial sites with Pb
burdens derived primarily from long-range atmospheric transport, the
2006 CD found that ``[d]espite years of elevated atmospheric Pb inputs
and elevated concentrations in soils, there is little evidence that
sites affected primarily by long-range Pb transport have experienced
significant effects on ecosystem structure or function'' (2006 CD, p.
AX7-98). The explanation suggested by the 2006 CD for this finding is
``[l]ow concentrations of Pb in soil solutions, the result of strong
complexation of Pb by soil organic matter'' (2006 CD, p. AZX7-98).
While more recent soil or stream data on Pb concentrations are not
available, we find it unlikely, given the general evidence for air Pb
emissions and concentration
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declines over the past several decades (e.g., PA, Figures 2-1, 2-7 and
2-8), that conditions would have worsened from those on which these
conclusions were drawn (e.g., soil data through 2000). Therefore, this
information suggests that the now-lower ambient air concentrations
associated with meeting the current standard would not be expected to
directly impact stream Pb levels.
With regard to new evidence of Pb effects at lower concentrations,
it is necessary to consider that the evidence of adversity due
specifically to Pb in natural systems is limited, in no small part
because of the difficulty in determining the effects of confounding
factors such as multiple metals and modifying factors influencing
bioavailability in field studies. Modeling of Pb-related exposure and
risk to ecological receptors is subject to a wide array of sources of
both variability and uncertainty. Variability is associated with
geographic location, habitat types, physical and chemical
characteristics of soils and water that influence Pb bioavailability
and terrestrial and aquatic community composition. Lead uptake rates by
invertebrates, fish, and plants may vary by species and season. For
wildlife, variability also is associated with food ingestion rates by
species and season, prey selection, and locations of home ranges for
foraging relative to the Pb contamination levels (USEPA, 2005b).
There are significant difficulties in quantifying the role of air
emissions under the current standard, which is significantly lower than
the previous standard. As recognized in the PA, Pb deposited before the
standard was enacted remains in soils and sediments, complicating
interpretations regarding the impact of the current standard; historic
Pb emitted from leaded gasoline usage continues to move slowly through
systems along with more recently deposited Pb and Pb derived from
nonair sources (PA, section 1.3.2). The results from the location-
specific case studies and the surface and sediment screen performed in
the last review are difficult to interpret in light of the current
standard and are largely not useful in informing judgments of the
potential for adverse effects at levels of deposition meeting the
current standard.
D. Conclusions on Adequacy of the Current Secondary Standard
1. Evidence- and Risk-Based Considerations in the Policy Assessment
The current evidence, as discussed more fully in the PA, continues
to support the conclusions from the previous review regarding key
aspects of the ecological effects evidence for Pb and the effects of
exposure associated with levels of Pb occurring in ecological media in
the U.S. The EPA's conclusions in this regard are based on
consideration of the assessment of the currently available evidence in
the ISA, particularly with regard to key aspects summarized in the PA.
In considering the welfare effects evidence with respect to the
adequacy of the current standard, the PA considers the array of
evidence newly assessed in the ISA with regard to the degree to which
this evidence supports conclusions about the effects of Pb in the
environment that were drawn in the last review and the extent to which
it reduces previously recognized areas of uncertainty. Further, the PA
considers the current evidence and associated conclusions about the
potential for effects to occur as a result of the much lower ambient Pb
concentrations allowed by the current secondary standard (set in 2008)
than those allowed by the prior standard, which was the focus of the
last review. These considerations, as discussed below, inform the
Administrator's conclusions regarding the extent to which the evidence
supports or calls into question the adequacy of protection afforded by
the current standard.
The range of effects that Pb can exert on terrestrial and aquatic
organisms indicated by information available in the current review is
summarized in the ISA (ISA, sections 1.7, 6.3 and 6.4) and largely
mirrors the findings of the previous review (PA, section 5.1). The
integrated synthesis contained in the ISA conveys how effects of Pb can
vary with species and life stage, duration of exposure, form of Pb, and
media characteristics such as soil and water chemistry. A wide range of
organism effects are recognized, including effects on growth,
development (particularly of the nervous system) and reproductive
success (ISA, sections 6.3 and 6.4). Lead is recognized to distribute
from the air into multiple environmental media, as summarized in
section I.D above, contributing to multiple exposure pathways for
ecological receptors. As discussed in section 5.1 of the PA, many
factors affect the bioavailability of Pb to receptors in terrestrial
and aquatic ecosystems, contributing to differences between laboratory-
assessed toxicity and Pb toxicity in these ecosystems, and challenging
our consideration of environmental impacts of Pb emitted to ambient
air.
In studies in a variety of ecosystems, adverse ecosystem-level
effects (including decreases in species diversity, loss of vegetation,
changes to community composition, primarily in soil microbes and
plants, decreased growth of vegetation, and increased number of
invasive species) have been demonstrated near smelters, mines and other
industries that have released substantial amounts of Pb, among other
materials, to the environment (ISA, sections 6.3.12 and 6.4.12). As
noted in the PA, however, our ability to characterize the role of air
emissions of Pb in contributing to these effects is complicated because
of coincident releases to other media and of other pollutants. Co-
released pollutants include a variety of other heavy metals, in
addition to sulfur dioxide, which may cause toxic effects in themselves
and may interact with Pb in the environment, contributing uncertainty
to characterization of the role of Pb from ambient air with regard to
the reported effects (PA, section 5.1). These uncertainties limit our
ability to draw conclusions regarding the extent to which Pb-related
effects may be associated with ambient air conditions that would meet
the current standard.
The role of historically emitted Pb poses additional complications
in addressing this question, as discussed in the PA (PA, section
1.3.2). The vast majority of Pb in the U.S. environment today,
particularly in terrestrial ecosystems, was deposited in the past
during the use of Pb additives in gasoline (2006 CD, pp. 2-82, AX7-36
to AX7-38, AX7-98; Johnson et al., 2004), although contributions from
industrial activities, including metals industries, have also been
documented (ISA, section 2.2.2.3, Jackson et al., 2004). The gasoline-
derived Pb was emitted in very large quantities (2006 CD, p. AX7-98 and
ISA, Figure 2-8) and predominantly in small sized particles which were
widely dispersed and transported across large distances, within and
beyond the U.S. (ISA, section 2.2). As recognized in the PA, historical
records provided by sediment cores in various environments document the
substantially reduced Pb deposition (associated with reduced Pb
emissions) in many locations (PA, sections 2.3.1 and 2.3.3.2; ISA,
section 2.2.1). As Pb is persistent in the environment, these
substantial past environmental releases are expected to generally
dominate current nonair media concentrations.
There is very limited evidence to relate specific ecosystem effects
with current ambient air concentrations of Pb through deposition to
terrestrial and aquatic ecosystems and subsequent movement of deposited
Pb through the environment (e.g., soil, sediment, water,
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organisms). The potential for ecosystem effects of Pb from atmospheric
sources under conditions meeting the current standard is difficult to
assess due to limitations on the availability of information to fully
characterize the distribution of Pb from the atmosphere into ecosystems
over the long term, as well as limitations on information on the
bioavailability of atmospherically deposited Pb (as affected by the
specific characteristics of the receiving ecosystem). Therefore, while
information available since the 2006 CD includes additional terrestrial
and aquatic field studies, ``the connection between air concentration
and ecosystem exposure and associated potential for welfare effects
continues to be poorly characterized for Pb'' (ISA, section 6.5). Such
a connection is even harder to characterize with respect to the current
standard than it was in the last review with respect to the previous,
much higher, standard.
The current evidence also continues to support conclusions from the
last review with regard to interpreting the risk and exposure results.
These conclusions are based on consideration of the screening-level
ecological risk assessment results from the last review as described in
the 2006 REA and summarized in the notice of final rulemaking (73 FR
67009, November 12, 2008) and in light of the currently available
evidence in the ISA (PA, section 5.2). As noted in section III.C above,
the results from three of the four case studies and from the national
screens are largely not useful in informing judgments of the potential
for adverse effects at levels of deposition associated with conditions
that meet the current standard. The Vulnerable Ecosystem Case Study at
the HBEF is more illustrative with regard to the current review and,
accordingly, is given primary consideration. The EPA concluded that
atmospheric Pb inputs of the past did not directly affect stream Pb
levels at HBEF because deposited Pb is almost entirely retained in the
soil profile and that there was ``little evidence that sites affected
primarily by long-range Pb transport [such as this one] have
experienced significant effects on ecosystem structure or function''
(2006 CD, p. AX-98). We further note here that, as conditions are
unlikely to have worsened since those on which those conclusions were
based, we find it likely that current ambient air concentrations do not
directly impact stream Pb levels under air quality conditions
associated with meeting the now-current standard.
The available risk and exposure information continues to be
sufficient to conclude that the 1978 standard was not providing
adequate protection to ecosystems and, when considered with regard to
air-related ecosystem exposures likely to occur with air Pb levels that
just meet the now-current standard, additionally does not provide
evidence of adverse effects under the current standard.
2. CASAC Advice
In the current review of the secondary standard for Pb, the CASAC
has provided advice and recommendations in their review of drafts of
the ISA, of the REA Planning Document, and of the draft PA. We have
additionally received comments from the public on drafts of these
documents.\74\
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\74\ All written comments submitted to the agency will be
available in the docket for this rulemaking, as will be transcripts
and minutes of the public meetings held in conjunction with CASAC's
review of drafts of the PA, the REA Planning Document and the ISA.
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In their advice and comments conveyed in the context of their
review of the draft PA, the CASAC agreed with staff's preliminary
conclusions that the available information since the last review is not
sufficient to warrant revision to the secondary standard (Frey, 2013b).
On this subject, the CASAC letter said that ``[o]verall, the CASAC
concurs with the EPA that the current scientific literature does not
support a revision to the Primary Lead (Pb) National Ambient Air
quality Standard (NAAQS) nor the Secondary Pb NAAQS'' (Frey, 2013b, p.
1). The CASAC also recognized the many uncertainties and data gaps in
the new scientific literature and recommended that research be
performed in the future to address these limitations (Frey, 2013b, p.
2).
Given the existing scientific data, the CASAC concurs with
retaining the current secondary standard without revision. However,
the CASAC also notes that important research gaps remain. For
example questions remain regarding the relevance of the primary
standard's indicator, level, averaging time, and form for the
secondary standard. Other areas for additional research to address
data gaps and uncertainty include developing a critical loads
approach for U.S. conditions and a multi-media approach to account
for legacy Pb and contributions from different sources. Addressing
these gaps may require reconsideration of the secondary standard in
future assessments.
The very few public comments received on this review to date that
have addressed adequacy of the current secondary Pb standard indicate
support for retaining the current standard without revision, generally
grouping the secondary standard with their similar view on the primary
standard.
3. Administrator's Proposed Conclusions on the Adequacy of the Current
Standard
Based on the evidence and risk assessment information that is
available in this review concerning the ecological effects and
potential public welfare impacts of Pb emitted into ambient air, the
Administrator proposes to conclude that the current secondary standard
provides the requisite protection of public welfare from adverse
effects and should be retained.
In considering the adequacy of the current standard, the
Administrator has considered the assessment of the available evidence
and conclusions contained in the ISA; the staff assessment of and
conclusions regarding the policy-relevant technical information,
including screening-level risk information, presented in the PA; the
advice and recommendations from CASAC; and public comments to date in
this review. In the discussion below, the Administrator gives weight to
the PA conclusions, with which CASAC has concurred, and takes note of
key aspects of the rationale presented for those conclusions which
contribute to her proposed decision.
The Administrator notes the conclusion in the PA that the body of
evidence on the ecological effects of Pb, expanded in some aspects
since the last review, continues to support identification of
ecological effects in organisms relating to growth, reproduction, and
survival as the most relevant endpoints associated with Pb exposure. In
consideration of the appreciable influence of site-specific
environmental characteristics on the bioavailability and toxicity of
environmental Pb in our assessment here, the PA noted the lack of
studies conducted under conditions closely reflecting the natural
environment. The currently available evidence, while somewhat expanded
since the last review, does not include evidence of significant effects
at lower concentrations or evidence of higher level ecosystem effects
beyond those reported in the last review. There continue to be
significant difficulties in interpreting effects evidence from
laboratory studies to the natural environment and linking those effects
to ambient air Pb concentrations. Further, the PA notes that the EPA is
aware of no new critical loads information that would inform our
interpretation of the public welfare significance of the effects of Pb
in various U.S. ecosystems (PA, section 5.1). In summary, while new
research has added to the understanding of Pb biogeochemistry and
expanded the
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list of organisms for which Pb effects have been described, the PA
notes there remains a significant lack of knowledge about the potential
for adverse effects on public welfare from ambient air Pb in the
environment and the exposures that occur from such air-derived Pb,
particularly under conditions meeting the current standard (PA, section
6.2.1). Thus, the scientific evidence presented in detail in the ISA,
inclusive of that newly available in this review, is not substantively
changed, most particularly with regard to the adequacy of the now
current standard, from the information that was available in and
supported the decision for revision in the last review (PA, section
6.2.1).
With respect to exposure/risk-based considerations, the PA
recognizes the complexity of interpreting the previous risk assessment
with regard to the ecological risk of ambient air Pb associated with
conditions meeting the current standard and the associated limitations
and uncertainties of such assessments. For example, the location-
specific case studies as well as the national screen conducted in the
last review reflect both current air Pb deposition as well as past air
and nonair source contributions (PA, section 6.3). The Administrator
takes note of the PA conclusion that the previous assessment is
consistent with and generally supportive of the evidence-based
conclusions about Pb in the environment, yet the limitations on our
ability to apportion Pb between past and present air contributions and
between air and nonair sources remain significant.
In the Administrator's consideration of the information available
in this review of the Pb secondary standard, she gives weight to the PA
conclusion that the currently available evidence and exposure/risk
information do not call into question the adequacy of the current
standard to provide the requisite protection for public welfare (PA,
section 6.3). In so doing, she also notes the advice from CASAC in this
review, including that ``[g]iven the existing scientific data, the
CASAC concurs with retaining the current secondary standard without
revision.'' In light of these and the above considerations, the
Administrator finds that the currently available information does not
call into question the adequacy of the current standard to provide the
requisite protection for public welfare and, accordingly, reaches the
conclusion that it is appropriate to retain the current secondary
standard without revision. The Administrator solicits comment on this
conclusion.
IV. Statutory and Executive Order Reviews
Additional information about these statutes and Executive Orders
can be found at http://www2.epa.gov/laws-regulations/laws-and-executive-orders.
A. Executive Order 12866: Regulatory Planning and Review and Executive
Order 13563: Improving Regulation and Regulatory Review
This action is not a significant regulatory action and was,
therefore, not submitted to the Office of Management and Budget for
review.
B. Paperwork Reduction Act
This action does not impose an information collection burden under
the Paperwork Reduction Act. There are no information collection
requirements directly associated with revisions to a NAAQS under
section 109 of the CAA and this action does not propose any revisions
to the NAAQS.
C. Regulatory Flexibility Act
I certify that this action will not have a significant economic
impact on a substantial number of small entities under the Regulatory
Flexibility Act. This action will not impose any requirements on small
entities. Rather, this action proposes to retain, without revision,
existing national standards for allowable concentrations of lead in
ambient air as required by section 109 of the CAA. See also American
Trucking Associations v. EPA. 175 F.3d at 1044-45 (NAAQS do not have
significant impacts upon small entities because NAAQS themselves impose
no regulations upon small entities).
D. Unfunded Mandates Reform Act
This action does not contain any unfunded mandate as described in
the Unfunded Mandates Reform Act, 2 U.S.C. 1531-1538 and does not
significantly or uniquely affect small governments. This action imposes
no enforceable duty on any state, local or tribal governments or the
private sector.
E. Executive Order 13132: Federalism
This action does not have federalism implications. It will not have
substantial direct effects on the states, on the relationship between
the national government and the states, or on the distribution of power
and responsibilities among the various levels of government.
F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
This action does not have tribal implications, as specified in
Executive Order 13175. This action does not change existing
regulations. It does not have a substantial direct effect on one or
more Indian Tribes, since Tribes are not obligated to adopt or
implement any NAAQS. The Tribal Authority Rule gives Tribes the
opportunity to develop and implement CAA programs such as the Pb NAAQS,
but it leaves to the discretion of the Tribe whether to develop these
programs and which programs, or appropriate elements of a program, they
will adopt. Thus, Executive Order 13175 does not apply to this action.
G. Executive Order 13045: Protection of Children From Environmental
Health and Safety Risks
This action is not subject to Executive Order 13045 because it is
not economically significant as defined in Executive Order 12866. The
health effects evidence and risk assessment information for this
action, which focuses on children in addressing the at-risk population,
is summarized in sections II.B, II.C and II.D, and described in the ISA
and PA, copies of which are in the public docket for this action.
H. Executive Order 13211: Actions That Significantly Affect Energy
Supply, Distribution or Use
This action is not subject to Executive Order 13211, because it is
not a significant regulatory action under Executive Order 12866.
I. National Technology Transfer and Advancement Act
This rulemaking does not involve technical standards.
J. Executive Order 12898: Federal Actions To Address Environmental
Justice in Minority Populations and Low-Income Populations
The EPA believes that this action will not have disproportionately
high and adverse human health or environmental effects on minority,
low-income or indigenous populations. The action proposed in this
notice is to retain without revision the existing NAAQS for Pb based on
the Administrator's conclusion that the existing standards protect
public health, including the health of sensitive groups, with an
adequate margin of safety. As discussed earlier in this preamble (see
section II), the EPA expressly considered the available information
regarding health effects among at-risk populations in reaching the
proposed decision that the existing standards are requisite.
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K. Determination Under Section 307(d)
Section 307(d)(1)(V) of the CAA provides that the provisions of
section 307(d) apply to ``such other actions as the Administrator may
determine.'' Pursuant to section 307(d)(1)(V), the Administrator
determines that this action is subject to the provisions of section
307(d).
References
Advisory Committee on Childhood Lead Poisoning Prevention (ACCLPP).
(2012). Low Level Lead Exposure Harms Children: A Renewed Call for
Primary Prevention. Report of the Advisory Committee on Childhood
Lead Poisoning Prevention of the Centers for Disease Control and
Prevention. January 4, 2012. Available at: http://www.cdc.gov/nceh/lead/ACCLPP/blood_lead_levels.htm.
Alliance to End Childhood Lead Poisoning. (1991). The First
Comprehensive National Conference: Final Report. October 6,7,8,
1991.
Bellinger, D.C. and Needleman, H.L. (2003). Intellectual impairment
and blood lead levels [letter]. N. Engl. J. Med. 349: 500.
Bellinger, D. (2008). Email message to Jee-Young Kim, U.S. EPA.
February 13, 2008. Docket document number EPA-HQ-OAR-2006-0735-5156.
Billick, I.H.; Curran, A.S.; Shier, D.R. (1979). Analysis of
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List of Subjects in 40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
Dated: December 19, 2014.
Gina McCarthy,
Administrator.
[FR Doc. 2014-30681 Filed 1-2-15; 8:45 am]
BILLING CODE 6560-50-P