[Federal Register Volume 70, Number 145 (Friday, July 29, 2005)]
[Proposed Rules]
[Pages 43950-43989]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-14510]
[[Page 43949]]
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Part II
Department of Labor
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Mine Safety and Health Administration
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30 CFR Parts 56, 57, and 71
Asbestos Exposure Limit; Proposed Rule
Federal Register / Vol. 70, No. 145 / Friday, July 29, 2005 /
Proposed Rules
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DEPARTMENT OF LABOR
Mine Safety and Health Administration
30 CFR Parts 56, 57, and 71
RIN: 1219-AB24
Asbestos Exposure Limit
AGENCY: Mine Safety and Health Administration (MSHA), Labor.
ACTION: Proposed rule; notice of public hearings.
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SUMMARY: We (MSHA) are proposing to revise our existing health
standards for asbestos exposure at metal and nonmetal mines, surface
coal mines, and surface areas of underground coal mines. The proposed
rule would reduce the full-shift permissible exposure limit and the
excursion limit for airborne asbestos fibers, and make several
nonsubstantive changes to add clarity to the standard. Exposure to
asbestos has been associated with lung and other cancers,
mesotheliomas, and asbestosis. This proposed rule would help assure
that fewer miners who work in an environment where asbestos is present
would suffer material impairment of health or functional capacity over
their working lifetime.
DATES: We must receive your comments on or before September 20, 2005.
We will hold public hearings on October 18 and 20. Details about the
public hearings are in the SUPPLEMENTARY INFORMATION section of this
preamble.
ADDRESSES: (1) To submit comments, please include ``RIN: 1219-AB24'' in
the subject line of the message and send them to us at either of the
following addresses.
Federal e-Rulemaking portal: Go to http://www.regulations.gov and follow the online instructions for submitting
comments.
E-mail: [email protected]. If you are unable to
submit comments electronically, please identify them by ``RIN: 1219-
AB24'' and send them to us by any of the following methods.
Fax: 202-693-9441.
Mail, hand delivery, or courier: MSHA, Office of
Standards, Regulations, and Variances, 1100 Wilson Blvd., Rm. 2350,
Arlington, VA 22209-3939.
(2) We will post all comments on the Internet without change,
including any personal information they may contain. You may access the
rulemaking docket via the Internet at http://www.msha.gov/regsinfo.htm
or in person at MSHA's public reading room at 1100 Wilson Blvd., Rm.
2349, Arlington, VA.
(3) To receive an e-mail notification when we publish rulemaking
documents in the Federal Register, subscribe to our list serve at
http://www.msha.gov/subscriptions/subscribe.aspx.
FOR FURTHER INFORMATION CONTACT: Rebecca J. Smith at 202-693-9440
(Voice), 202-693-9441 (Fax), or mailto:[email protected] (E-mail).
SUPPLEMENTARY INFORMATION:
I. Introduction
A. Outline of Preamble
We are including the following outline to help you find information
in this preamble more quickly.
I. Introduction
A. Outline of Preamble
B. Dates and Locations for Public Hearings
C. Executive Summary
D. Abbreviations and Acronyms
II. Background
A. Scope of Proposed Rule
B. Where Asbestos Is Found at Mining Operations
C. Asbestos Minerals
III. History of Asbestos Regulation
A. MSHA's Asbestos Standards for Mining
B. OSHA's Asbestos Standards for General Industry and
Construction
C. Other Federal Agencies Regulating Asbestos
D. Other Asbestos-Related Activities
E. U.S. Department of Labor, Office of the Inspector General
(OIG)
IV. Health Effects of Asbestos Exposure
A. Summary of Asbestos Health Hazards
B. Factors Affecting the Occurrence and Severity of Disease
C. Specific Human Health Effects
D. Support from Toxicological Studies of Human Health Effects of
Asbestos Exposure
V. Characterization and Assessment of Exposures in Mining
A. Determining Asbestos Exposures in Mining
B. Exposures from Naturally Occurring Asbestos
C. Exposures from Introduced (Commercial) Asbestos
D. Sampling Data and Exposure Calculations
VI. The Application of OSHA's Risk Assessment to Mining
A. Summary of Studies Used by OSHA in Its Risk Assessment
B. Models Selected by OSHA (1986) for Specified Endpoints and
for the Determination of Its PEL and STEL
C. OSHA's Selection of Its PEL (0.1 f/cc)
D. Applicability of OSHA's Risk Assessment to the Mining
Industry
E. Significance of Risk
VII. Section-by-Section Discussion of Proposed Rule
A. Sections 56/57.5001(b)(1) and 71.702(a): Definitions
B. Sections 56/57.5001(b)(2) and 71.702(b): Permissible Exposure
Limits (PELs)
C. Sections 56/57.5001(b)(3) and 71.702(c): Measurement of
Airborne Fiber Concentration
D. Discussion of Asbestos Take-Home Contamination
E. Section 71.701(c) and (d): Sampling; General Requirements
VIII. Regulatory Analyses
A. Executive Order (E.O.) 12866
B. Feasibility
C. Alternatives Considered
D. Regulatory Flexibility Analysis (RFA) and Small Business
Regulatory Enforcement Fairness Act (SBREFA)
E. Other Regulatory Considerations
IX. Copy of the OSHA Reference Method (ORM)
X. References Cited in the Preamble
B. Dates and Locations for Public Hearings
We will hold two public hearings. If you wish to make a statement
for the record, please submit your request to us at least 5 days prior
to the hearing dates by one of the methods listed in the ADDRESSES
section above. The hearings will begin at 9 a.m. with an opening
statement from MSHA, followed by statements or presentations from the
public, and end after the last speaker (in any event not later than 5
p.m.) on the following dates at the locations indicated:
October 18, 2005, Denver Federal Center, Sixth and Kipling, Second
Street, Building 25, Denver, Colorado 80225, Phone: 303-231-5412.
October 20, 2005, Mine Safety and Health Administration, 1100 Wilson
Boulevard, Room 2539, Arlington, Virginia 22209, Phone: 202-693-9457.
We will hear scheduled speakers first, in the order that they sign
in; however, you do not have to make a written request to speak. To the
extent time is available, we will hear from persons making same-day
requests. The presiding official may exercise discretion to ensure the
orderly progress of the hearing by limiting the time allocated to each
speaker for their presentation.
The hearings will be conducted in an informal manner. Although
formal rules of evidence or cross examination will not apply, the
hearing panel may ask questions of speakers and a verbatim transcript
of the proceedings will be prepared and made a part of the rulemaking
record. We also will post the transcript on MSHA's Home Page at http://www.msha.gov, on the Asbestos Single Source Page.
Speakers and other attendees may present information to the MSHA
panel for inclusion in the rulemaking record. We will accept written
comments and data for the record from any interested party, including
those not presenting oral statements. The post-hearing comment period
will close on November 21, 2005, 30 days after the last public hearing.
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C. Executive Summary
In March of 2001, the U.S. Department of Labor, Office of the
Inspector General (OIG) published a report evaluating MSHA's
enforcement actions at the vermiculite mine in Libby, Montana. The
widespread asbestos contamination at this mine and surrounding
community, together with the prevalence of asbestos-related illnesses
and fatalities among persons living in this community, attracted press
and public attention, which prompted the OIG investigation and report.
The OIG found that MSHA had conducted regular inspections and personal
exposure sampling at the mine, as required by the Federal Mine Safety
and Health Act of 1977 (Mine Act). The OIG report stated, ``We do not
believe that more inspections or sampling would have prevented the
current situation in Libby.'' The OIG made five recommendations to
MSHA; two of which we implemented immediately. The remaining
recommendations are listed below:
Lower the existing permissible exposure limit (PEL) for
asbestos to a more protective level.
Use transmission electron microscopy (TEM) instead of
phase contrast microscopy (PCM) in the initial analysis of fiber
samples that may contain asbestos.
Implement special safety requirements to address take-home
contamination.
In response to the OIG's recommendations, MSHA published an advance
notice of proposed rulemaking (ANPRM) on March 29, 2002 (67 FR 15134).
MSHA also held seven public meetings around the country to seek input
and obtain public comment on how best to protect miners from exposure
to asbestos.
Following review of all public comments and testimony taken at the
public meetings, and relying on OSHA's 1986 asbestos risk assessment,
we determined that it is appropriate to propose reducing the PELs for
asbestos and clarify criteria for asbestos sample analysis. To enhance
the health and safety of miners, we are proposing to lower the existing
8-hour, time-weighted average (TWA) PEL of 2.0 f/cc to 0.1 f/cc, and to
lower the short-term limit from 10.0 f/cc over a minimum sampling time
of 15 minutes to an excursion limit PEL of 1.0 f/cc over a minimum
sampling time of 30 minutes. To clarify the criteria for the analytical
method in our existing standards, we are proposing to incorporate a
reference to Appendix A of OSHA's asbestos standard (29 CFR 1910.1001).
Appendix A specifies basic elements of a PCM method for analyzing
airborne asbestos samples. It includes the same analytical elements
specified in our existing standards and allows MSHA's use of other
methods that meet the statistical equivalency criteria in OSHA's
asbestos standard.
The scope of this proposed rule, therefore, is limited to lowering
the permissible exposure limits, an issue raised by the OIG;
incorporating Appendix A of OSHA's asbestos standard for the analysis
of our asbestos samples; and making several nonsubstantive conforming
amendments to our existing rule language. After considering several
regulatory approaches to prevent take-home contamination, we determined
that non-regulatory measures could adequately address this potential
hazard.
D. Abbreviations and Acronyms
As a quick reference, we list below some of the abbreviations used
in the preamble.
29 CFR Title 29, Code of Federal Regulations
30 CFR Title 30, Code of Federal Regulations
AFL-CIO American Federation of Labor and Congress of Industrial
Organizations
ATSDR Agency for Toxic Substances and Disease Registry, Centers for
Disease Control and Prevention, U.S. Department of Health and Human
Services
Bureau former Bureau of Mines, U.S. Department of the Interior
cc cubic centimeter (cm3) = milliliter (mL)
EPA U.S. Environmental Protection Agency
f fiber(s)
FR Federal Register
Lpm liter(s) per minute
MESA former Mining Enforcement and Safety Administration, U.S.
Department of the Interior (predecessor to MSHA)
MSHA Mine Safety and Health Administration, U.S. Department of Labor
mm millimeter = 1 thousandth of a meter (0.001 m)
mL milliliter = 1 thousandth of a liter (0.001 L) = cubic centimeter
NIOSH National Institute for Occupational Safety and Health, Centers
for Disease Control and Prevention, U.S. Department of Health and
Human Services
OIG Office of the Inspector General, U.S. Department of Labor
OSHA Occupational Safety and Health Administration, U.S. Department
of Labor
PCM phase contrast microscopy
PEL permissible exposure limit
PLM polarized light microscopy
STEL short-term exposure limit
SWA shift-weighted average concentration
TEM transmission electron microscopy
TWA time-weighted average concentration
[mu]m micron = micrometer = 1 millionth of a meter (0.000001 m)
USGS U.S. Geological Survey, U.S. Department of the Interior
II. Background
A. Scope of Proposed Rule
This proposed rule would apply to metal and nonmetal mines, surface
coal mines, and the surface areas of underground coal mines. Because
asbestos from any source poses a health hazard to miners if they inhale
it, the proposed rule would cover all miners exposed to asbestos
whether naturally occurring or contained in building materials, in
other manufactured products at the mine, or in mine waste or tailings.
The National Institute for Occupational Safety and Health (NIOSH)
and other research organizations and scientists (see Table VI-5) have
observed the occurrence of cancers and asbestosis among metal and
nonmetal miners involved in the mining and milling of commodities that
contain asbestos. For this reason, our primary focus at metal and
nonmetal mines is on asbestos in pockets or veins of mined commodities.
Historically, there has been no evidence of coal miners encountering
naturally occurring asbestos.\1\ The more likely exposure to asbestos
in coal mining would occur from introduced asbestos-containing
products, such as asbestos-containing building materials (ACBM) in
surface structures.
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\1\ Personal communication with Professor Kot Unrug, Department
of Mining Engineering, University of Kentucky, on November 14, 2003;
and with Syd S. Peng, Chairman, Department of Mining Engineering,
College of Engineering and Mineral Resources, West Virginia
University, the week of October 24, 2003.
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In 2000, the OIG investigated MSHA's activities at the vermiculite
mine in Libby, Montana. The OIG's conclusions and recommendations,
discussed later, are consistent with MSHA's observations and concerns
that--
Miners are exposed to asbestos at mining operations where
the ore body or surrounding rock contains asbestos;
Miners are potentially exposed to airborne asbestos at
mine facilities with installed asbestos-containing material when it is
disturbed during maintenance, construction, renovation, or demolition
activities; and
Family and community are potentially exposed if miners
take asbestos home on their person, clothes, or equipment, or in their
vehicle.
We developed this proposed rule based on our experience with
asbestos, our assessment of the health risks, the OIG's
recommendations, and public comments on MSHA's ANPRM addressing the
OIG's recommendations. We received numerous comments in response to the
ANPRM and at the
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public meetings, some of which suggested or supported additional
requirements beyond those addressed by the OIG. We believe that the
comments to the ANPRM do not justify an expansion of the scope, at this
time, beyond the recommendations specifically raised in the OIG report.
On the contrary, we believe that our data support a narrowed scope
in that we specifically are not proposing two of the OIG's
recommendations, i.e., routine use of TEM for the initial analysis of
exposure samples and promulgation of standards to prevent take-home
contamination. We are proposing, however, to lower our permissible
exposure limits.
We have decided not to propose to change our existing definition of
asbestos in this rulemaking. There are several reasons for this.
First, this rulemaking is limited in scope. We believe that a 20-
fold lowering of the exposure limits, as we have proposed, together
with our enhanced measures to educate the mining community about the
asbestos hazard in mining, would increase protection for miners and
help avoid the future development of situations such as that in Libby,
Montana.
Second, interest in the definition of asbestos extends to numerous
agencies in Federal, state, and local governments. Our existing
definition is consistent with several Federal agencies' regulatory
provisions, including OSHA's. Changing the definition would require
considerable interagency consultation and coordination; additional
scientific evaluation; and an unnecessary delay in providing miners
access to the benefits of this proposed rule.
Third, we believe another Libby-like mining operation would not
exist today because such a business arguably would not be economically
viable. If a mine's ore contained significant amounts of asbestos-like
minerals, there is a strong likelihood of potential liability risks,
both from customers and workers, and the possibility that the mine's
product would be commercially unmarketable. Such market forces are
likely to compel mining companies of all sizes to sample the ore for
the presence of hazardous fibrous minerals before purchasing or
developing a mine site. In our view, these commercial reasons make it
unlikely that a new Libby-like mining condition would arise in the
future.
B. Where Asbestos Is Found at Mining Operations
Asbestos is no longer mined as a commodity in the United States.
Even so, veins, pockets, or intrusions of asbestos have been found in
other ores in specific geographic regions, primarily in metamorphic or
igneous rock.\2\ Although less common, it is not impossible to find
asbestos in sedimentary rock, soil, and air from the weathering or
abrasion of other asbestos-bearing rock.\3\ The areas where asbestos
may be located can be determined from an understanding of the
mineralogy of asbestos and the geology required for its formation. In
some cases, visual inspection can detect the presence of asbestos. MSHA
experience indicates that miners may encounter asbestos during the
mining of a number of mineral commodities,\4\ such as talc, limestone
and dolomite, vermiculite, wollastonite, banded ironstone and taconite,
lizardite, and antigorite. Not all mines of a specific commodity
contain asbestos in the ore, however, and the mines that do have
asbestos in the ore may encounter it rarely.
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\2\ MSHA (Bank), 1980.
\3\ USGS, 1995.
\4\ Roggli et al., 2002; Selden et al., 2001; Amandus et al.,
Part I, 1987; Amandus et al., Part III, 1987; Amandus and Wheeler,
Part II, 1987.
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Asbestos also is contained in building materials and other
manufactured products found at mines. Contrary to the common public
perception, asbestos is not banned in the United States.\5\ The U.S.
Geological Survey (USGS) estimates that about 13,000 metric tons (29
million pounds) of asbestos were used in product manufacturing in the
United States during 2001.\6\ In addition to domestic manufacturing,
the United States continues to import products that contain asbestos.
Asbestos may be used for a number of purposes at a mine including
insulation; reinforcement of cements; reinforcement of floor, wall, and
building tile; and automotive clutch and brake linings.\7\ If asbestos
is present at the mine, miners in the vicinity are potentially at
increased risk from asbestos exposure, regardless of whether or not
they are actually working with asbestos.
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\5\ GETF Report, pp. 12-13, 2003.
\6\ USGS (Virta), p. 28, 2003.
\7\ Lemen, 2003; Paustenbach et al., 2003.
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C. Asbestos Minerals
To understand the scientific literature, information about
asbestos, and the issues raised in the public comments, it is important
to understand the terminology used to describe minerals, asbestos, and
fibers. This section briefly reviews a number of key terms and concepts
associated with asbestos that we use in discussing this proposed rule.
1. Mineralogical Classification and Mineral Names
The terminology used to refer to how minerals form and how they are
named is complex. A mineral's physical properties, composition,
crystalline structure, and morphology determine its classification.
Asbestos minerals belong to either the serpentine (sheet silicate) or
the amphibole (double-chain silicate) family of minerals. Most of the
difficulties in classifying minerals as asbestos have involved the
amphiboles. The formation of a particular mineral (chemical
composition) or habit (morphology, crystalline structure) occurs
gradually and may be incomplete, producing intermediate minerals that
are difficult to classify. In the past, there have been several
different systems used to classify and name minerals that, in some
instances, led to inconsistent terminology and classification.
Currently, there is no single, universally accepted system for naming
minerals.
Asbestos is a commercial term used to describe certain naturally
occurring, hydrated silicate minerals. Several Federal agencies have
regulations that focus on these minerals. The properties of asbestos
that give it commercial value include low electrical and thermal
conductivity, chemical and crystalline stability and durability, high
tensile strength, flexibility, and friability. Much of the existing
health risk data for asbestos uses commercial mineral terminology.
Meeker et al. (2003) recognized the confusion associated with asbestos
nomenclature, stating--
Within much of the existing asbestos literature, mineral names
are not applied in a uniform manner and are not all consistent with
presently accepted mineralogical nomenclature and definitions.
a. Variations in Mineral Morphology.
There are many types of crystal habits, such as fibrous, acicular
(slender and needle-like), massive (irregular form), and columnar
(stout and column-like). The morphology of a mineral may not fit a
precise definition. For example, Meeker et al. (2003) state that the
Libby amphiboles contain ``a complete range of morphologies from
prismatic crystals to asbestiform fibers.'' Some minerals crystallize
in more than one habit. Some minerals, which can form in different
habits, have a different name for each habit; others do not.\8\ For
example, crocidolite is the name for the asbestiform habit and
riebeckite is the name for the same mineral in its nonasbestiform
habit. Tremolite and actinolite do not have different names
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depending on habit; therefore, to distinguish between the different
habits, the descriptive term ``asbestiform'' or ``asbestos'' is added
to the mineral's name. If the identifying, descriptive term is not used
with the mineral name, misunderstandings or mistakes may occur.
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\8\ Reger and Morgan, 1990; ATSDR, p. 138, 2001.
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b. Variations in Mineral Composition.
Atoms similar in size and valence state can replace each other
within a mineral's crystal lattice, resulting in the formation of a
different mineral in the same mineral series. This process is gradual
and can occur to a different extent in the same mineral depending on
the geological conditions during its formation. For example, tremolite
contains magnesium, but no (or little) iron, and holds an end member
position in its mineral series. Iron atoms can replace the magnesium
atoms in tremolite and the resulting mineral may then be called
actinolite. The quantity of iron needed before the mineral is called
actinolite varies depending on the mineral classification scheme used.
Another example is winchite, which is an intermediate member of the
tremolite-glaucophane series, as well as an end member in its own
sodic-calcic series.\9\ Given the chemical similarity within the
series, winchite
[(NaCa)Mg4(Al,Fe3+)Si8O
22(OH)2] often has been reported as tremolite
[Ca2Mg5Si8O22(OH)2
].
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\9\ Leake et al., p. 222, 1997.
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A specific rock formation may contain a continuum of minerals from
one end member of a series to the other end member, creating a solid
solution of intermediate minerals. These intermediate minerals are
sometimes given names, while at other times they are not. Often, when
the exact chemical composition is not determined or determined to be a
number of different intermediate minerals, the mineral is named by one
or more of its end members, such as tremolite-actinolite or
cummingtonite-grunerite. The fibrous amphiboles in the Libby ore body,
for example, contain both end members and several intermediate
minerals. Meeker et al. (2003) state that--
The variability of compositions on the micrometer scale can
produce single fibrous particles that can have different amphibole
names at different points of the particle.
A mineral may also undergo transition to a different mineral
series. Kelse and Thompson (1989), Ross (1978), and USGS (Virta, 2002)
have commented on the chemical transition of anthophyllite to talc.
Stewart and Lee (1992) stated that fibrous talc might contain
intermediate particles not easily differentiated from asbestos. In the
context of systems for naming and classifying fibrous amphiboles,
Meeker et al. (2003) state that the regulatory literature often gives
nominal compositions for a mineral without specifying chemical
boundaries.
2. Differentiating Asbestiform and Nonasbestiform Habit
In the asbestiform habit, mineral crystals grow forming long,
thread-like fibers. When pressure is applied to an asbestos fiber, it
bends much like a wire, rather than breaks. Fibers can separate into
``fibrils'' of a smaller diameter (often less than 0.5 [mu]m). This
effect is referred to as ``polyfilamentous,'' and should be viewed as
one of the most important characteristics of asbestos. Appendix A of
the Environmental Protection Agency's (EPA's) Method for the
Determination of Asbestos in Bulk Building Materials \10\ defines
asbestiform as follows:
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\10\ EPA, 1993.
* * * a mineral that is like asbestos, i.e., crystallized with
the habit [morphology] of asbestos. Some asbestiform minerals may
lack the properties which make asbestos commercially valuable, such
as long fiber length and high tensile strength. With the light
microscope, the asbestiform habit is generally recognized by the
following characteristics:
Mean aspect [length to width] ratios ranging from 20:1 to 100:1
or higher for fibers longer than 5 micrometers. Aspect ratios should
be determined for fibers, not bundles.
Very thin fibrils, usually less than 0.5 micrometers in width,
and two or more of the following:
--Parallel fibers occurring in bundles,
--Fiber bundles displaying splayed ends,
--Matted masses of individual fibers, and/or
--Fibers showing curvature.
In the nonasbestiform habit, mineral crystals do not grow in long
thin fibers. They grow in a more massive habit. For example, a long
thin crystal may not be polyfilamentous nor possess high tensile
strength and flexibility, but may break rather than bend. When pressure
is applied, the nonasbestiform crystals fracture easily into prismatic
particles, which are called cleavage fragments because they result from
the particle's breaking or cleavage, rather than the crystal's
formation or growth. Some particles are acicular (needle shaped), and
stair-step cleavage along the edges of some particles is common.
Cleavage fragments may be formed when nonfibrous amphibole minerals
are crushed, as may occur in mining and milling operations. Cleavage
fragments are not asbestiform and do not fall within our definition of
asbestos. For some minerals, distinguishing between asbestiform fibers
and cleavage fragments in certain size ranges is difficult or
impossible when only a small number of structures are available for
review, as opposed to a representative population. Meeker et al. (2003)
states that it is often difficult or impossible to determine
differences between acicular cleavage fragments and asbestiform mineral
fibers on an individual fiber basis. A determination as to whether a
mineral is asbestiform or not must be made, where possible, by applying
existing analytical methods. Although we have received comments
regarding the hazards associated with cleavage fragments, we do not
intend to modify our existing definition of asbestos with this
rulemaking.
III. History of Asbestos Regulation
When Federal agencies responsible for occupational safety and
health began to regulate occupational exposure to asbestos, studies had
already established that the inhalation of asbestos fibers was a major
cause of disability and death among exposed workers. The intent of
these first asbestos rules was to protect workers from developing
asbestosis.\11\
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\11\ GETF Report, p. 33, 2003.
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A. MSHA's Asbestos Standards for Mining
1967-1969. In 1967, under the former Bureau of Mines, predecessor
to the Mining Enforcement and Safety Administration (MESA) and then
MSHA, the standard for asbestos exposure in mining was an 8-hour, time-
weighted average (TWA) PEL of 5 mppcf (million particles per cubic foot
of air). In 1969, the Bureau promulgated a 2 mppcf and 12 f/mL (fibers
per milliliter) standard.
1974-1976. In 1974, MESA promulgated a 5 f/mL standard for asbestos
exposure in metal and nonmetal mines (39 FR 24316). In 1976, MESA
promulgated a 2 f/cc standard (41 FR 10223) for asbestos exposure in
surface areas of coal mines. We retained these standards under the
authority of the Federal Mine Safety and Health Act of 1977.
1978. In November 1978, we promulgated a 2 f/mL standard for
asbestos exposure in metal and nonmetal mines (43 FR 54064). Since
then, we have made only nonsubstantive changes to our asbestos
standards, e.g., renumbering the section of the standard in 30 CFR.
MSHA's existing standards for asbestos at metal and nonmetal mines
at 30 CFR 56/57.5001 state,
[[Page 43954]]
(b) The 8-hour time-weighted average airborne concentration of
asbestos dust to which employees are exposed shall not exceed 2
fibers per milliliter greater than 5 microns in length, as
determined by the membrane filter method at 400-450 magnification (4
millimeter objective) phase contrast illumination. No employees
shall be exposed at any time to airborne concentrations of asbestos
fibers in excess of 10 fibers longer than 5 micrometers, per
milliliter of air, as determined by the membrane filter method over
a minimum sampling time of 15 minutes. ``Asbestos'' is a generic
term for a number of hydrated silicates that, when crushed or
processed, separate into flexible fibers made up of fibrils.
Although there are many asbestos minerals, the term ``asbestos'' as
used herein is limited to the following minerals: chrysotile,
Amosite, crocidolite, anthophylite asbestos, tremolite asbestos, and
actinolite asbestos.
The existing standard for asbestos at surface coal mines and
surface work areas of underground coal mines at 30 CFR 71.702 states,
(a) The 8-hour average airborne concentration of asbestos dust
to which miners are exposed shall not exceed two fibers per cubic
centimeter of air. Exposure to a concentration greater than two
fibers per cubic centimeter of air, but not to exceed 10 fibers per
cubic centimeter of air, may be permitted for a total of 1 hour each
8-hour day. As used in this subpart, the term asbestos means
chrysotile, amosite, crocidolite, anthophylite asbestos, tremolite
asbestos, and actinolite asbestos but does not include nonfibrous or
nonasbestiform minerals.
(b) The determination of fiber concentration shall be made by
counting all fibers longer than 5 micrometers in length and with a
length-to-width ratio of at least 3 to 1 in at least 20 randomly
selected fields using phase contrast microscopy at 400-450
magnification.
1989. In 1989, as part of our Air Quality rulemaking, we proposed
to lower the full-shift exposure limit for asbestos from 2 f/cc to 0.2
f/cc to address the excessive risk quantified in the Occupational
Safety and Health Administration's (OSHA's) 1986 asbestos rule (54 FR
35760). The Air Quality rulemaking, however, was withdrawn on September
26, 2002 (67 FR 60611). MSHA has not reinstated the Air Quality
rulemaking at this time.
B. OSHA's Asbestos Standards for General Industry and Construction
1971-1972. The initial promulgation of OSHA standards on May 29,
1971 (36 FR 10466) included a 12 f/cc PEL for asbestos. Then, on
December 7, 1971, in response to a petition by the Industrial Union
Department of the AFL-CIO, OSHA issued an emergency temporary standard
(ETS) on asbestos that established an 8-hour, TWA PEL of 5 f/cc and a
peak exposure level (ceiling limit) of 10 f/cc. In June 1972, OSHA
promulgated these limits in a final rule.
1975. In October 1975, OSHA proposed to revise its asbestos
standard by reducing the 8-hour, TWA PEL to 0.5 f/cc with a ceiling
limit of 5 f/cc for 15 minutes (40 FR 47652). OSHA stated that
sufficient medical and scientific evidence had accumulated to warrant
the designation of asbestos as a human carcinogen and that advances in
monitoring and protective technology made re-examination of the
standard appropriate. The final rule, however, reduced OSHA's 8-hour,
TWA asbestos PEL to 2 f/cc due to feasibility concerns. This limit
remained in effect until OSHA revised it in 1986.
1983-1986. On November 4, 1983, OSHA published another emergency
temporary standard (ETS) for asbestos (48 FR 51086), which would have
lowered the 8-hour, TWA PEL from 2 f/cc to 0.5 f/cc. The Asbestos
Information Association challenged the ETS in the U.S. Court of Appeals
for the 5th Circuit. On March 7, 1984, ruling on Asbestos Information
Association/North America v. OSHA (727 F.2d 415, 1984), the Court
invalidated the ETS. Subsequent to this decision, OSHA published a
proposed rule (49 FR 14116) that, together with the ETS, proposed two
alternatives for lowering the 8-hour, TWA PEL: 0.2 f/cc and 0.5 f/cc.
On June 17, 1986, OSHA issued comprehensive asbestos standards (51
FR 22612) governing occupational exposure to asbestos in general
industry workplaces (29 CFR 1910.1001), construction workplaces (29 CFR
1926.1101), and shipyards (29 CFR 1915.1001). The separate standards
shared the same asbestos PEL and most ancillary requirements. These
standards reduced OSHA's 8-hour, TWA PEL to 0.2 f/cc from the previous
2 f/cc limit. OSHA added specific provisions in the construction
standard to cover unique hazards relating to asbestos abatement and
demolition jobs.
Although tremolite, actinolite, and anthophyllite exist in
different forms, OSHA determined that all forms of these minerals would
continue to be regulated. Following promulgation of the rule, several
parties requested an administrative stay of the standard claiming that
OSHA improperly included nonasbestiform minerals. A temporary stay was
granted and OSHA initiated rulemaking to remove the nonasbestiform
types of these minerals from the scope of the asbestos standards.
1988. Several major participants in OSHA's rulemaking challenged
various provisions of the 1986 revised standards. In Building
Construction Trades Division (BCTD), AFL-CIO v. Brock (838 F.2d 1258,
1988), the U.S. Court of Appeals for the District of Columbia upheld
most of the challenged provisions, but remanded certain issues to OSHA
for reconsideration. In partial response, on September 14, 1988, OSHA
promulgated an excursion limit of 1 f/cc for asbestos as measured over
a 30-minute sampling period (53 FR 35610).
1992. OSHA's 1986 standards had applied to occupational exposure to
nonasbestiform actinolite, tremolite, and anthophylite. On June 8,
1992, OSHA deleted the nonasbestiform types of these minerals from the
scope of its asbestos standards. In evaluating the record, OSHA found
(57 FR 24310-24311) insufficient evidence that nonasbestiform
actinolite, tremolite, and anthophyllite present ``a risk similar in
kind and extent'' to their asbestiform counterparts. Additionally, the
evidence did not show that OSHA's removal of the nonasbestiform types
of these three minerals from its asbestos standard ``will pose a
significant risk to exposed employees.''
1994. On August 10, 1994, OSHA published a final rule (59 FR 40964)
that lowered its 8-hour, TWA PEL for asbestos to 0.1 f/cc and retained
the 1 f/cc excursion limit as measured over 30 minutes.
C. Other Federal Agencies Regulating Asbestos
Because the health hazards of exposure to asbestos are well
recognized, it is highly regulated. OSHA and MSHA have the primary
authority to regulate occupational exposures to asbestos. EPA regulates
asbestos exposure of state and local government workers in those states
that do not have an OSHA State Plan covering them. A number of other
Federal agencies, primarily EPA and the Consumer Product Safety
Commission (CPSC), regulate non-occupational asbestos exposures. For
example, CPSC regulates asbestos in consumer products, such as patching
compounds, under the Federal Hazardous Substances Act.
EPA regulates asbestos in air and materials. EPA's activities have
focused on environmental issues and the public health by reducing
emissions of hazardous gases and dusts from large industrial sources,
such as taconite ore processing,\12\ and the cleanup of contaminated
waste sites. EPA also regulates asbestos in schools. The mining and
processing of vermiculite in Libby, Montana, resulted in the spread
[[Page 43955]]
of asbestos to numerous homes, schools, and businesses throughout the
town. In November 1999, EPA responded to a request to study the
environmental contamination in the town of Libby and widespread
illnesses and death among its residents. In October 2002, EPA
designated the area as a Superfund site.
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\12\ EPA (68 FR 61868), 2003.
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D. Other Asbestos-Related Activities
There have been increasing numbers of studies on asbestos and its
hazards over the past 40 years. These efforts encompass government,
industry, and academia on a local, national, and international scale.
Government agencies and scientific groups in the United States, such as
the National Institute for Occupational Safety and Health (NIOSH), the
Agency for Toxic Substances and Disease Registry (ATSDR), the American
Conference of Governmental Industrial Hygienists (ACGIH), and the
National Toxicology Program (NTP), have addressed issues involving
carcinogens, such as asbestos. Organizations from other countries, such
as the United Kingdom (Health and Safety Executive) and Germany
(Deutche Forschungsgemeinschaft), also have addressed occupational
exposure to asbestos and other carcinogens. Similarly, the
International Agency for Research on Cancer (IARC) has published a
monograph on asbestos that summarizes evidence of its
carcinogenicity.\13\
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\13\ IARC, 1987.
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1. Interagency Asbestos Work Group (IAWG)
OSHA's and EPA's overlapping responsibilities and common interest
in addressing asbestos hazards led to the formation of the IAWG.
Participating Federal agencies include EPA, OSHA, CPSC, MSHA, NIOSH,
ATSDR, USGS, and the National Institute of Standards and Technology
(NIST). This work group of government agencies facilitates the sharing
of information and coordination of activities, including regulatory
activities, environmental assessment, technical assistance, consumer
protection, and developments in environmental analysis of contaminants.
The IAWG also seeks to harmonize the policies, procedures, and
enforcement activities of the participating agencies, thus minimizing
or eliminating potential conflicts for the regulated community. For
example, the IAWG is currently discussing the Federal definition of
asbestos.
2. National Institute for Occupational Safety and Health (NIOSH)
The Workers' Family Protection Act of 1992 (29 U.S.C. 671A)
directed NIOSH to study contamination of workers' homes by hazardous
substances, including asbestos, transported from the workplace. ATSDR,
EPA, OSHA, MSHA, the U.S. Department of Energy (DOE), and the Centers
for Disease Control and Prevention (CDC) assisted NIOSH in conducting
the study. For this proposed rule we focused on the asbestos-related
results of these studies.
NIOSH (1995) published its study results in a Report to Congress on
Workers' Home Contamination Study Conducted under the Workers' Family
Protection Act. This report summarizes incidents of home contamination,
including the health consequences, sources, and levels of
contamination. The study documents cases of asbestos reaching workers'
homes in 36 states in the United States and in 28 other countries.
These cases covered a wide variety of materials, industries, and
occupations. The means by which hazardous substances reached workers'
homes and families included taking the substance home on the worker's
body, clothing, tools, and equipment; cottage industries (i.e., work
performed on home property); and family visits to the workplace. In an
effort to reach employers and workers, NIOSH (1997) published its
recommendations in Protect Your Family: Reduce Contamination at Home.
This pamphlet summarizes the NIOSH study and provides recommendations
to prevent this contamination.
3. Agency for Toxic Substances and Disease Registry (ATSDR)
The Superfund Amendments and Reauthorization Act of 1986 (SARA)
directed ATSDR to prepare toxicological profiles for hazardous
substances most commonly found at specific waste sites. ATSDR and EPA
determined which hazardous substances pose the most significant
potential threat to human health and targeted them for study. Asbestos
is one of these targeted substances. ATSDR published one of the most
current toxicological profiles for asbestos in September 2001, which
was an update of an earlier asbestos profile.
In October 2002, ATSDR sponsored a meeting of expert panelists who
presented their evaluation of state-of-the-art research concerning the
relationship between fiber length and the toxicity of asbestos and
synthetic vitreous fibers. We have reviewed the evidence and arguments
presented in the updated asbestos toxicological profile and the meeting
proceedings and have discussed this information in this preamble, where
appropriate.
E. U.S. Department of Labor, Office of the Inspector General (OIG)
In November 1999, a Seattle newspaper published a series of
articles on the unusually high incidence of asbestos-related illnesses
and fatalities among individuals who had lived in Libby, Montana. There
was extensive national media attention surrounding the widespread
environmental contamination and asbestos-related deaths in Libby. Dust
and construction materials from the nearby vermiculite mine were the
alleged cause. This mine had produced about 90 percent of the world's
supply of vermiculite from 1924 until 1992.
Because MSHA had jurisdiction over the mine for two decades before
it closed, the OIG investigated MSHA's enforcement actions at the mine.
The OIG confirmed that the processing of vermiculite at the mine
exposed miners to asbestos. The miners then, inadvertently, had carried
the asbestos home on their clothes and in their personal vehicles.\14\
In doing this, the miners continued to expose themselves and family
members.
---------------------------------------------------------------------------
\14\ Weis et al., 2001.
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1. OIG Report on MSHA's Handling of Inspections at the W.R. Grace &
Company Mine in Libby, Montana
The OIG published its findings and recommendations in a report
dated March 22, 2001. The OIG found that MSHA had appropriately
conducted regular inspections and personal exposure sampling at the
Libby mine and that there were no samples exceeding the 2.0 f/cc PEL
for the 10 years prior to the mine closing in 1992. The OIG concluded,
``We do not believe that more inspections or sampling would have
prevented the current situation in Libby.'' The OIG stated its belief
that there is a need for MSHA to lower its asbestos PEL.
In its report, the OIG supported the development and implementation
of control measures for asbestos and vermiculite mining and milling.
They also made recommendations for improving our effectiveness in
controlling this hazard. This proposed rule addresses our responses to
several of the OIG's recommendations.
2. MSHA's Libby, Montana Experience
W.R. Grace acquired the vermiculite mine in Libby, Montana, in
1963. At that time, the amphibole in the
[[Page 43956]]
vermiculite was called tremolite, soda tremolite, soda-rich tremolite,
or richterite, and researchers had already linked the mine dust to
respiratory disease.\15\ The suggested exposure limit for asbestos in
mining was much higher than current limits. The federal standard for
asbestos in mining dropped from 5 mppcf (about 30 f/mL) in 1967 to 2 f/
mL in 1978. When MESA (predecessor agency to MSHA) began inspecting the
operation, the exposure limit for asbestos was 5 f/mL.
---------------------------------------------------------------------------
\15\ McDonald et al., 1986; Meeker et al., 2003; Peipins et al.,
2003.
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The mine operator, Federal mine inspectors, and representatives of
the U.S. Public Health Service [part of the Centers for Disease Control
and Prevention (CDC)] routinely sampled for asbestos at the Libby mine,
starting before the mine switched to wet processing in 1974, and
continued sampling periodically until the mine closed in 1992. MSHA
sampling at the Libby mine found no exposures exceeding the 5.0 f/cc
asbestos PEL from 1975 through 1978, and only a few over the 2.0 f/cc
asbestos PEL from 1979 through 1986. Almost all the samples would have
exceeded the 0.1 f/cc proposed limit. Miners' exposures continued to
decrease and more recent sampling since 1986 found few exposures
exceeding the OSHA PEL of 0.1 f/cc.
The results from our personal exposure sampling at the Libby mine
included many of the fibrous amphiboles present. In addition, the
results from TEM analysis of the air samples characterized the
mineralogy of the airborne fibers as tremolite and did not distinguish
between the species of amphiboles. Further characterization of the
amphibole minerals using Scanning Electron Microscopy/Energy Dispersive
X-ray Spectroscopy technology shows proportions of about 84 percent
winchite, 11 percent richterite, and 6 percent tremolite.\16\
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\16\ Meeker et al., 2003
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As early as 1980, MSHA had requested that NIOSH investigate health
problems at all vermiculite operations, including the mine and mill in
Libby, Montana. NIOSH published its study results in a series of three
papers (Amandus et al., Part I, 1987; Amandus and Wheeler, Part II,
1987; Amandus et al., Part III, 1987). The study of Amandus et al.
(Part I, 1987) along with that of McDonald et al. (1986) found that,
historically, the highest exposures to fibers at the Libby operation
had occurred in the mill and that exposures had decreased between the
1960's and 1970's. McDonald et al. (1986) reported--
In 1974, the old dry and wet mills were closed and the ore was
processed in a new mill built nearby which operated on an entirely
wet basis in which separation was made by vibrating screens,
Humphrey separators, and flotation.
McDonald et al. (1986) and Amandus and Wheeler (Part II, 1987) also
showed that, even at reduced exposure levels, there was still increased
risk of lung cancer among the Libby miners and millers.
3. MSHA's Efforts To Minimize Asbestos Take-Home Contamination
``Take-home'' contamination is contamination of workers' homes or
vehicles by hazardous substances transported from the workplace. As
discussed previously in this preamble, the widespread asbestos-related
disease among the residents of Libby, Montana, was attributed, in part,
to take-home contamination from the vermiculite mining and milling
operation in that town. The OIG report on MSHA's activities recommended
that we promulgate special safety standards similar to those in our
1989 proposed Air Quality rule (54 FR 35760) to address take-home
contamination.
In our 1989 Air Quality proposed rule, we had proposed that miners
wear protective clothing and other personal protective equipment before
entering areas containing asbestos. Our Air Quality proposed rule also
would have required miners to remove their protective clothing and
store them in adequate containers to be disposed of or decontaminated
by the mine operator. These proposed requirements were similar to those
in OSHA's asbestos standard and to NIOSH's recommendations.
In March 2000, shortly after the series of articles on asbestos-
related illnesses and deaths in Libby, Montana, we issued a Program
Information Bulletin (PIB No. P00-3) about asbestos. The PIB served to
remind the mining industry of the potential health hazards from
exposure to airborne asbestos fibers and to raise awareness about
potential asbestos exposure for miners, their families, and their
communities. At that time, we also issued a Health Hazard Information
Card (No. 21) about asbestos for distribution to miners to raise their
awareness about the health hazards related to asbestos exposure.
The PIB included information about asbestos, its carcinogenic and
other significant health effects, how miners could be exposed, where
asbestos occurs naturally on mining property, and what types of
commercial products may contain asbestos. It included recommendations
to help mine operators reduce miners' exposures, to prevent or minimize
take-home contamination, and for the selection and use of respiratory
protection. The PIB also urged mine operators to minimize exposures, to
improve controls, and to train miners, listing specific training topics
as essential for miners potentially exposed to asbestos.
During this same period, 2000 to 2003, we conducted an asbestos
awareness campaign and increased asbestos sampling. Section VII.D of
this preamble contains an additional discussion of measures to prevent
asbestos ``take-home'' contamination.
We have decided not to pursue a regulatory approach to minimizing
asbestos ``take-home'' contamination. Based on the existing levels of
asbestos exposures in the mining industry, comments on our 2002 ANPRM,
and testimony at the subsequent public meetings, we have determined
that a non-regulatory approach would be effective in minimizing
asbestos take-home contamination from mining operations.
4. Training Inspectors to Recognize and Sample for Asbestos
The OIG recommended that we increase MSHA inspectors' skills for
providing asbestos compliance assistance to mine operators. In
response, we developed a half-day multimedia training program that
includes the following:
A PowerPoint-based training presentation that examines
MSHA's procedures for air and bulk asbestos sampling.
An updated ``Chapter 8--Asbestos Fibers'' from the Metal
and Nonmetal Health Inspection and Procedures Handbook that serves as a
text for the training sessions.
A ``hands-on'' segment that allows the inspectors to
examine asbestos and asbestiform rock samples and the equipment used
for bulk sampling, and that provides the inspectors instruction and
practice in assembling and calibrating asbestos fiber air sampling
apparatus.
We gave this asbestos training to journeymen inspectors from March
2002 through April 2003, and added it to the training program for
entry-level inspectors.
IV. Health Effects of Asbestos Exposure
The health hazards from exposure to asbestos were discussed
extensively in the preamble to OSHA's 1983 final rule (51 FR 22615).
Subsequently, researchers have confirmed and
[[Page 43957]]
increased our knowledge of these hazards. Exposures in occupational and
environmental settings are generally due to inhalation, although some
asbestos may be absorbed through ingestion. While the part of the body
most likely affected (target organ) is the lung, adverse health effects
may extend to the linings of the chest, abdominal, and pelvic cavities,
and the gastrointestinal tract. The damage following chronic exposure
to asbestos is cumulative and irreversible. Workplace exposures to
asbestos may be chronic, continuing for many years. The symptoms of
asbestos-related adverse health effects may not become evident for 20
or more years after first exposure (latency period).
A. Summary of Asbestos Health Hazards
This section presents an overview of human health effects from
exposure to asbestos. We are proposing to use OSHA's 1986 risk
assessment to estimate the risk from asbestos exposures in mining.
OSHA's risk assessment has withstood legal scrutiny and the more recent
studies discussed later in this preamble support it. MSHA has placed
OSHA's risk assessment in the asbestos rulemaking record. It can also
be found at http://www.osha.gov.
Studies first identified health problems associated with
occupational exposure to asbestos in the early 20th century among
workers involved in the manufacturing or use of asbestos-containing
products.\17\ Early studies identified the inhalation of asbestos as
the cause of asbestosis, a slowly progressive disease that produces
lung scarring and loss of lung elasticity. Studies also found that
asbestos caused lung and several other types of cancer. For example,
mesotheliomas, rare cancers of the lining of the chest or abdominal
cavities, are almost exclusively attributable to asbestos exposure.
Once diagnosed, they are rapidly fatal. Asbestos-related diseases have
long latency periods, commonly not producing symptoms for 20 to 30
years following initial exposure.
---------------------------------------------------------------------------
\17\ GETF Report, p. 38, 2003; OSHA (40 FR 47654), 1975.
---------------------------------------------------------------------------
In the late 1960's, scientists correlated phase contrast microscopy
fiber counting methods with the earlier types of dust measurements.
This procedure provided a means to estimate earlier workers' asbestos
exposures and enabled researchers to develop a dose-response
relationship with the occurrence of disease. The British Occupational
Hygiene Society reported \18\ that a worker exposed to 100 fiber-years
per cubic centimeter (e.g., 50 years at 2 f/cc, 25 years at 4 f/cc, 10
years at 10 f/cc) would have a 1 percent risk of developing early signs
of asbestosis. The correlation of exposure levels with the disease
experience of populations of exposed workers provided a basis for
setting an occupational exposure limit for asbestos measured by the
concentration of the fibers in air.
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\18\ Lane et al., 1968; OSHA (40 FR 47654), 1975.
---------------------------------------------------------------------------
As mentioned previously, the hazardous effects from exposure to
asbestos are now well known. For this reason, our discussion in this
section will focus on the results of the more recent studies and
literature reviews, those published since the publication of OSHA's
risk assessment, and those involving miners. One such review by
Tweedale (2002) stated,
Asbestos has become the leading cause of occupational related
cancer death, and the second most fatal manufactured carcinogen
(after tobacco). In the public's mind, asbestos has been a hazard
since the 1960s and 1970s. However, the knowledge that the material
was a mortal health hazard dates back at least a century, and its
carcinogenic properties have been appreciated for more than 50
years.
Greenberg (2003) also published a recent review of the biological
effects of asbestos and provided a historical perspective similar to
that of Tweedale.
The three most commonly described adverse health effects associated
with asbestos exposure are lung cancer, mesotheliomas, and pulmonary
fibrosis (i.e., asbestosis). OSHA, in its 1986 asbestos rule, reviewed
each of these diseases and provided details on the studies
demonstrating the relationship between asbestos exposure and the
clinical evidence of disease. In 2001, the ATSDR published an updated
Toxicological Profile for Asbestos that also included an extensive
discussion of these three diseases. A search of peer-reviewed
scientific literature using databases, such as Gateway, PubMed, and
ToxLine, accessed through the National Library of Medicine (NLM),
yielded nearly 900 new references on asbestos from January 2000 to
October 2003. Many of these recent articles \19\ continue to
demonstrate and support findings of asbestos-induced lung cancer,
mesotheliomas, and asbestosis, consistent with the conclusions of OSHA
and ATSDR. Thus, in the scientific community, there is compelling
evidence of the adverse health effects of asbestos exposure. This has
led some researchers and stakeholders to recommend a worldwide ban of
asbestos.\20\
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\19\ Baron, 2001; Bolton et al., 2002; Manning et al., 2002;
Nicholson, 2001; Osinubi et al., 2000; Roach et al., 2002.
\20\ Maltoni, 1999.
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B. Factors Affecting the Occurrence and Severity of Disease
The toxicity of asbestos, and the subsequent occurrence of disease,
is related to its concentration (C) in the mine air and to the duration
(T) of the miner's exposure. Other variables, such as the fiber's
characteristics or the effectiveness of the miner's lung clearance
mechanisms, also affect disease severity.
1. Concentration (C)
Currently, the concentration (C) of asbestos is expressed as the
number of fibers per cubic centimeter (f/cc). Some studies have also
reported asbestos concentrations in the number of fibers per milliliter
(f/mL), which is an equivalent concentration to f/cc. MSHA's existing
PELs for asbestos are expressed in f/mL for metal and nonmetal mines
and as f/cc for coal mines. To improve consistency and avoid confusion,
we express the concentration of airborne fibers as f/cc in this
proposed rule, for both coal and metal and nonmetal mines.
Older scientific literature (i.e., 1960's and 1970's) reported
exposure concentrations as million particles per cubic foot (mppcf) and
applied a conversion factor to convert mppcf to f/cc. OSHA (51 FR
22617) used a factor of 1.4 when performing these conversions. More
recently, Hodgson and Darnton (2000) recommended the use of a factor of
3. In our evaluation of the scientific literature, we did not
critically evaluate the impact of these and other conversion factors.
We note this difference here for completeness. Because we are relying
on OSHA's risk assessment, we are using OSHA's conversion factor
2. Time (T)
Epidemiological and toxicological studies generally report time (T)
in years (yr). The product of exposure concentration and exposure
duration (i.e., C x T) is referred to as ``fiber-years''.\21\ When
developing exposure-response relationships for asbestos-induced health
effects, researchers typically use ``fiber-years'' to indicate the
level of workplace exposure. Finkelstein \22\ noted, however, that this
product of exposure concentration times duration of exposure (C x T)
assumes an equal weighting of each variable (C, T).
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\21\ ATSDR, 2001; Fischer et al., 2002; Liddell, 2001; Pohlabeln
et al., 2002.
\22\ Finkelstein, 1995; ATSDR, p. 42, 2001.
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[[Page 43958]]
3. Fiber Characteristics
Baron (2001) reviewed techniques for the measurement of fibers and
stated, ``* * * fiber dose, fiber dimension, and fiber durability are
the three primary factors in determining fiber [asbestos] toxicity * *
*''. Manning et al. (2002) also noted the important roles of bio-
persistence (i.e., durability), physical properties, and chemical
properties in defining the ``toxicity, pathogenicity, and
carcinogenicity'' of asbestos. Roach et al. (2002) stated that--
Physical properties, such as length, diameter, length-to-width
(aspect ratio), and texture, and chemical properties are believed to
be determinants of fiber distribution [in the body] and disease
severity.
Many other investigators \23\ also have concluded that the
dimensions of asbestos fibers are biologically important.
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\23\ ATSDR, 2001; Osinubi et al., 2000; Peacock et al., 2000;
Langer et al., 1979.
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OSHA and MSHA currently specify that analysts count those fibers
that are over 5.0 micrometers ([mu]m) in length with a length to
diameter aspect ratio of at least 3:1. Several recent publications \24\
support this aspect ratio, although larger aspect ratios such as 5:1 or
20:1 have been proposed.\25\ There is some evidence that longer,
thinner asbestos fibers (e.g., greater than 20 [mu]m long and less than
1 [mu]m in diameter) are more potent carcinogens than shorter fibers.
Suzuki and Yuen (2002), however, concluded that ``Short, thin asbestos
fibers should be included in the list of fiber types contributing to
the induction of human malignant mesotheliomas * * * ''. More recently,
Dodson et al. (2003) concluded that all lengths of asbestos fibers
induce pathological responses and that researchers should exercise
caution when excluding a population of inhaled fibers based on their
length.
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\24\ ATSDR, 2001; Osinubi et al., 2000.
\25\ Wylie et al., 1985.
---------------------------------------------------------------------------
We have determined that researchers have found neither a reliable
method for predicting the contribution of fiber length to the
development of disease, nor evidence establishing the exact
relationship between them. There is suggestive evidence that the
dimensions of asbestos fibers may vary with different diseases. A
continuum may exist in which shorter, wider fibers produce one disease,
such as asbestosis, and longer, thinner fibers produce another, such as
mesotheliomas.\26\ The scientific community continues to publish new
data that will enable regulatory agencies, such as MSHA, to better
understand the relationship between fiber dimensions, durability,
inhaled dose, and other important factors that determine the health
risks of exposure not only to asbestos, but also to other fibers.
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\26\ ATSDR, pp. 39-41, 2001; Mossman, pp. 47-50, 2003.
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4. Differences in Fiber Potency
The theory that the differences among fibers have an effect on
their ability to produce adverse effects on human health has received a
great deal of attention. Hodgson and Darnton (2000), Browne (2001), and
Liddell (2001) discuss a fiber gradient hypothesis, which is now termed
the amphibole hypothesis. This hypothesis proposes that the amphiboles
(e.g., crocidolite, amosite) are more hazardous than the serpentine,
chrysotile. ATSDR (p. 39, 2001) recently stated that--
Available evidence indicates that all asbestos fiber types are
fibrogenic, although there may be some differences in relative
potency among fiber types.
In its 1986 asbestos rule, OSHA (51 FR 22628) stated that--
* * * epidemiological and animal evidence, taken together, fail
to establish a definitive risk differential for the various types of
asbestos fiber. Accordingly, OSHA has * * * recognized that all
types of asbestos fiber have the same fibrogenic and carcinogenic
potential * * *
In its comments on MSHA's asbestos ANPRM, NIOSH stated that--
(3) experimental animal carcinogenicity studies with various
minerals have provided strong evidence that the carcinogenic
potential depends on the ``particle'' length and diameter. The
consistency in tumorigenic responses observed for various mineral
particles of the same size provides reasonable evidence that neither
composition nor origin of the particle is a critical factor in
carcinogenic potential; * * *
This issue remains unresolved. Although possible differences in
fiber potency are beyond the scope of this proposed rule, we will
continue to monitor results of research in this area.
5. Lung Clearance Mechanisms
Inhaled asbestos may deposit throughout the respiratory tract,
depending on the aerodynamic behavior of the fibers.\27\ As noted by
Baron (2001), `` * * * fiber aerodynamic behavior indicates that small
diameter fibers are likely to reach into and deposit in the airways of
the lungs.'' Clearing the lungs of deposited asbestos occurs by several
mechanisms. In the mid-airways (i.e., bronchial region), small hair-
like cells sweep the mucus containing asbestos toward the throat, at
which time it is swallowed or expectorated. The swallowing of mucus
through this clearance mechanism can result in inhaled asbestos
reaching the gastrointestinal tract.
---------------------------------------------------------------------------
\27\ ICRP, 1966.
---------------------------------------------------------------------------
In the air sacs deep within the lungs (the alveolar region),
pulmonary macrophages engulf foreign matter, including asbestos fibers.
The macrophages attempt to remove these fibers by transporting them to
the circulatory or lymphatic system. Some studies have shown that
groups of macrophages try to engulf longer fibers.\28\ When asbestos
fibers are not cleared, they may initiate inflammation of the cells
lining the alveoli. This inflammation leads to more serious physical
effects in the lungs. OSHA (1986), ATSDR (2001), and several recent
papers \29\ discuss these mechanisms for the pulmonary clearance of
asbestos.
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\28\ Warheit, p. 308, 1993.
\29\ Baron, 2001; Osinubi et al., 2000.
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C. Specific Human Health Effects
1. Lung Cancer
Lung cancer is a chronic, irreversible, and often fatal disease of
the lungs. Epidemiological studies confirm, and toxicological studies
support, the carcinogenicity of asbestos. (See section IV.D. below.)
The form of lung cancer seen most often in asbestos-exposed individuals
is bronchial carcinoma. Some of the risk factors for lung cancer
include airborne asbestos concentration, duration of exposure, fiber
dimensions, the age of the individual at the time of first exposure,
and the number of years since the first exposure.\30\ Another major
risk factor is the smoking of tobacco products. Numerous studies have
concluded that there are synergistic effects between asbestos and
tobacco smoke in the development of lung cancer.\31\ This is especially
relevant to miners as NIOSH (May 2003) estimates that 33 percent of
miners currently smoke.
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\30\ Yano et al., 2001; ATSDR, 2001.
\31\ Bolton et al., 2002; Manning et al., 2002; OSHA, 1986.
---------------------------------------------------------------------------
The mechanism through which asbestos causes lung cancer is under
study. Recent papers by Manning et al. (2002), Xu et al. (2002), and
Osinubi et al. (2000) describe a scheme of cell signaling and
inflammation with the release of reactive oxygen species and reactive
nitrogen species.
The latency period for asbestos-related lung cancer is generally
20-30 years, although some cases have been reported within 10 years,
and some up to 50 years, after initial asbestos exposure.\32\ Lung
cancer caused by
[[Page 43959]]
asbestos can progress even in the absence of continued exposure. Thus,
in all of its stages, lung cancer constitutes a material impairment of
human health or functional capacity.
---------------------------------------------------------------------------
\32\ Roach et al., 2002.
---------------------------------------------------------------------------
In the preamble to its 1986 asbestos standard (51 FR 22615), OSHA
stated, ``Of all the diseases caused by asbestos, lung cancer
constitutes the greatest health risk for American asbestos workers.''
OSHA (51 FR 22615-22616) also stated, ``* * * Asbestos exposure acts
synergistically with cigarette smoking to multiply the risk of
developing lung cancer.'' MSHA believes that the essential points of
this statement remain true today.
Steenland et al. (2003) estimated that there were about 150,000
lung cancer deaths in 1997 in the United States, and that 6.3 to 13
percent (i.e., 9,700 to 19,900) of these lung cancer deaths were
occupationally-related. Steenland et al. (1996) also had estimated
that, in the mid-1990's, there were about 5,400 asbestos-related lung
cancer deaths per year. NIOSH (May 2003) identified over 10,000 lung
cancer deaths in the United States during 1999 based on only 20 Census
Industry Codes (CIC). This sum was computed from ``selected states,''
not the entire United States. NIOSH (May 2003) also identified 300 lung
cancer deaths among coal miners from 15 selected states.
2. Mesotheliomas
Mesotheliomas are malignant tumors that are rapidly fatal. They
involve thin membranes that line the chest (the pleura) and that
surround internal organs (the peritoneum) following asbestos
exposure.\33\ Mesotheliomas begin with a localized mass and, like other
malignant tumors, they can spread (metastasize) to other parts of the
body.\34\ It does not appear that smoking is a major risk factor in the
development of mesotheliomas.\35\
---------------------------------------------------------------------------
\33\ ATSDR, 2001.
\34\ Roach et al., 2002.
\35\ Bolton et al., 2002.
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As in cases of lung cancer and asbestosis, mesotheliomas also have
a latency period, varying from 15 to over 40 years.\36\ Orenstein et
al. (2000) reported an even wider range for the latency, from a minimum
of 5 years to a maximum of 72 years. In cases involving the pleura,
patients often complain of chest pain, breathing difficulties on
exertion, weakness, and fatigue. Other early symptoms of this disease
may also include weight loss and cough. As the disease progresses,
there is increased restriction of the chest wall and highly abnormal
respiration, often characterized by a rapid and shallow breathing
pattern. Mesotheliomas are rapidly progressive even in the absence of
continued asbestos exposure. Mesotheliomas have a poor prognosis in
most patients; death typically occurs within a year or so of
diagnosis.\37\ Thus, like lung cancer, mesotheliomas materially impair
human health and functional capacity.
---------------------------------------------------------------------------
\36\ Suzuki and Yuen, 2002.
\37\ Bolton et al., 2002; Roach et al., 2002; Osinubi et al.,
2000; West, 2003.
---------------------------------------------------------------------------
As noted by ATSDR (2001), OSHA (1986), and many others,\38\
mesotheliomas are extremely rare tumors, particularly in non-asbestos
exposed individuals. OSHA (1986) has stated, `` * * * In some asbestos-
exposed occupational groups, 10 percent to 18 percent of deaths have
been attributable to malignant mesotheliomas * * * ''. NIOSH (May 2003)
reported that there were about 2,500 deaths due to malignant
mesotheliomas in the United States in 1999. Steenland et al. (2003)
estimated that there were about 2,100 deaths in the United States from
mesotheliomas in 1997, and that, in males, 85-90 percent of these
deaths from mesotheliomas were due to occupational asbestos exposure.
These tumors were generally the underlying (primary) cause of death,
and not just a contributing cause of death. NIOSH found that most
mesothelioma deaths were included with the categories of ``all other
industries'' (56 percent) or ``all other occupations'' (57 percent).
For those death certificates that included a Census Industry Code
(CIC), the most frequently recorded was ``construction.'' The 2003
NIOSH publication, Work-Related Lung Disease Surveillance Report 2002
(WoRLD), did not provide specific data on mesotheliomas among miners.
---------------------------------------------------------------------------
\38\ Bolton et al., 2002; Britton, 2002; Carbone et al., 2002;
Manning et al., 2002; Orenstein et al., 2000; Roach et al., 2002;
Suzuki and Yuen, 2002.
---------------------------------------------------------------------------
One commenter expressed concern that the use of perchlorate in
explosives might be a co-factor for increasing the incidence or
shortening the latency period for mesothelioma among miners. In
investigating this comment, we found that perchlorate can be a
component in explosives \39\ and that perchlorate may cause or
contribute to thyroid disease.\40\ We found no studies linking
perchlorate to mesotheliomas. The California State Department of Toxic
Substances Control states that perchlorate ``* * * has not been linked
to cancer in humans * * *''.\41\
---------------------------------------------------------------------------
\39\ EPA, 2002.
\40\ ATSDR, 1998.
\41\ http://www.dtsc.ca.gov/ToxicQuestions/glossary.html.
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3. Asbestosis
Asbestosis is a chronic and irreversible disease caused by the
deposition and accumulation of asbestos in the lungs. It can lead to
substantial injury and may cause death from the build up of bands of
scar tissue and a loss of lung elasticity (i.e., pulmonary
fibrosis).\42\ It is not a tumor. Following exposure to asbestos,
chronic inflammation may occur that leads to the multiplication of
collagen-producing cells in the lung and the accumulation of thick
collagen bundles in essential lung tissues.\43\ These structural
changes result in a hardening or stiffening of the lungs. Physicians
who specialize in diseases of the lung also classify asbestosis as a
restrictive lung disease due to this loss of elasticity.
---------------------------------------------------------------------------
\42\ ATSDR, 2001.
\43\ Osinubi et al., 2000.
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In asbestosis, the lungs are unable to properly expand and contract
during the breathing cycle and, thus, lung volumes, airflows, and
respiratory frequencies are likely to be abnormal.\44\ Two common
symptoms of this disease are cough and breathing difficulties. Patients
with asbestosis may also complain of a general feeling of discomfort,
weakness, and fatigue. Breathing difficulties, weakness, and fatigue
are often more severe with work or exercise. As the disease progresses,
patients begin to experience symptoms even while resting and are likely
to become permanently disabled.\45\ Patients with severe asbestosis
also may experience heart or circulation problems, such as heart
enlargement. Like lung cancer and mesotheliomas, asbestosis may be
progressive even in the absence of continued asbestos exposure. Thus,
asbestosis, even in its earliest stages, constitutes a material
impairment of human health and functional capacity.
---------------------------------------------------------------------------
\44\ West, 2000; West, 2003.
\45\ OSHA, 1986.
---------------------------------------------------------------------------
NIOSH (May 2003) reported that there were about 1,200 asbestosis-
related deaths in the United States in 1999. Of these, asbestosis was
the underlying cause in about a third of these deaths (400) and a
contributing cause in the others (800). Steenland et al. (2003)
estimated that there were about 400 deaths from asbestosis in 1997, and
that 100 percent of these asbestosis-deaths were due to occupational
exposure. As shown by NIOSH (May 2003), the number of deaths related to
asbestosis increased over ten-fold between 1968 and 1999. NIOSH also
reported that these figures likely reflect improved diagnostic tools
and the long latency period for evidence of disease that follows
asbestos exposure.
[[Page 43960]]
The death certificates for most individuals who died from
asbestosis lacked the Census Industry Code (CIC) and the Census
Occupation Code (COC). Most asbestosis deaths were classified under
``all other industries'' (45 percent) and ``all other occupations'' (57
percent). For those death certificates that included a CIC and a COC,
the most frequently recorded industry and occupation were
``construction'' (CIC = 060) and ``plumbers, pipefitters, and
steamfitters'' (COC = 585), respectively. There were no specific data
on asbestosis-related deaths among miners in the NIOSH WoRLD
publication (May 2003).
4. Other Cancers
OSHA, in its 1986 rule, reviewed epidemiologic studies of asbestos
workers with cancer of the colon, rectum, kidney, larynx (voice box),
throat, or stomach. Of these studies, researchers placed the greatest
emphasis on those involving gastrointestinal cancers. OSHA concluded,
`` * * * the risk of incurring cancers at these [other] sites is not as
great as the increased risk of lung cancer * * *''. Thus, OSHA included
lung and gastrointestinal cancers, and not these other cancer sites, in
its 1986 risk assessment. MSHA believes that the statement remains true
today, based on studies cited by ATSDR (2001) and by recent papers on
kidney cancer,\46\ laryngeal cancer,\47\ lymphomas,\48\ and pancreatic
cancer.\49\ We have not attempted to quantify the risks of these other
cancers, which are small in comparison to lung cancer and
mesotheliomas.
---------------------------------------------------------------------------
\46\ McLaughlin and Lipworth, 2000; Sali and Boffetta, 2000.
\47\ Browne and Gee, 2000.
\48\ Becker et al., 2001.
\49\ Ojajarvi et al., 2000.
---------------------------------------------------------------------------
5. Reversible Airways Obstruction (RAO)
Under normal physiological conditions, oxygen and other inhaled
chemical substances pass through a branching network of airways that
become narrower, shorter, and more numerous as they penetrate deeper
into the lung.\50\ The diameter of each airway has an important effect
on its airflow. A reduction in airway diameter occurs temporarily on
exposure to some chemical substances and permanently in some diseases.
These reductions lead to temporary or permanent airflow limitations. A
temporary reduction of airway diameter and the resulting difficulties
in breathing have also been called broncho-constriction, acute airways
constriction or obstruction, or reversible airways obstruction (RAO).
Such constriction or obstruction typically involves airways in the mid
to lower respiratory tract.
---------------------------------------------------------------------------
\50\ West, 2000.
---------------------------------------------------------------------------
Several recent studies have examined respiratory health and
respiratory symptoms of asbestos-exposed workers.\51\ Wang et al.
(2001) reported permanent changes in airway diameters and, thus,
permanent airflow limitations in diseases such as asbestosis or chronic
obstructive pulmonary disease (COPD). Although patients can recover
from RAO, they do not recover from asbestosis or COPD, which are
typically progressive, leading to increasingly severe illness and
premature death.
---------------------------------------------------------------------------
\51\ Delpierre et al., 2002; Eagen et al., 2002; Selden et al.,
2001.
---------------------------------------------------------------------------
Delpierre et al. (2002) reported that RAO in asbestos workers was
independent of x-ray signs of pulmonary or pleural fibrosis, as well as
a worker's smoking status. The long-term implications of RAO are
unknown at this time. Delpierre et al., however, encouraged physicians
to screen asbestos workers for RAO. Lung function tests may be useful
in the early diagnosis of asbestos-disease, especially if RAO precedes
the development of irreversible pulmonary disease, such as asbestosis.
6. Other Nonmalignant Pleural Disease and Pleural Plaques
The pleura is the membrane lining the chest cavity. Pleural plaques
are discrete, elevated areas of nearly transparent fibrous tissue (scar
tissue) and are composed of thick collagen bundles. Pleural thickening
and pleural plaques are biologic markers reflecting previous asbestos
exposure.\52\ They appear opaque on radiographic images and white to
yellow in microscopic sections.\53\ The American Thoracic Society (ATS,
2004) has described the criteria for diagnosis of non-malignant
asbestos-related pleural disease and pleural plaques.
---------------------------------------------------------------------------
\52\ ATSDR, 2001; Manning et al., 2002.
\53\ Bolton et al., 2002; Manning et al., 2002; Roach et al.,
2002; Peacock et al., 2000; ATSDR, 2001.
---------------------------------------------------------------------------
Pleural plaques are the most common manifestation of asbestos
exposure.\54\ Only rarely do they occur in persons who have no history
or evidence of asbestos exposure. Pleural thickening and pleural
plaques may occur in individuals exposed to asbestos in both
occupational settings, such as miners, and non-occupational settings,
such as family members. For example, the prevalence of pleural plaques
ranges from 0.53 percent to 8 percent in environmentally exposed
populations, such as the residents of Libby, Montana; 3 percent to 14
percent in dockyard workers; and up to 58 percent among insulation
workers.
---------------------------------------------------------------------------
\54\ Cotran et al., p. 732-734, 1999; Peacock et al., 2000.
---------------------------------------------------------------------------
Pleural plaques may develop within 10-20 years after an initial
asbestos exposure \55\ and slowly progress in size and amount of
calcification, independent of any further exposure. There is no
evidence that pleural plaques undergo malignant degeneration into
mesothelioma.\56\ Pleural thickening and pleural plaques, however, may
impair lung function and may precede chronic lung disease that develops
in some individuals.\57\ Rudd (1996), for example, reported that the
incidence of lung cancer in patients with pleural plaques is higher
than that of other patients. These plaques are also part of the
clinical picture of asbestosis.
---------------------------------------------------------------------------
\55\ Bolton et al., 2002; OSHA, 1986.
\56\ Peacock et al., 2000; West, 2003.
\57\ Schwartz et al., 1994.
---------------------------------------------------------------------------
7. Asbestos Bodies
Some asbestos-exposed individuals may expel asbestos fibers from
the lungs with a coating of iron and protein. These collections of
coated fibers, found in sputum or broncho-alveolar lavage (BAL) fluid,
are called asbestos bodies or ferruginous bodies.\58\ Like pleural
thickening and pleural plaques, these bodies indicate prior asbestos
exposure.
---------------------------------------------------------------------------
\58\ ATSDR, 2001; Peacock et al., 2000.
---------------------------------------------------------------------------
D. Support From Toxicological Studies of Human Health Effects of
Asbestos Exposure
Many studies are available that clearly demonstrate the toxicity of
asbestos (e.g., carcinogenicity, genotoxicity, pneumotoxicity) and
confirm observed human responses.\59\ Studies conducted in baboons,
mice, monkeys, and rats have all demonstrated that asbestos fibers are
carcinogenic.\60\ OSHA's risk assessment, however, did not rely on data
from in vivo or in vitro toxicological studies to determine the human
health effects from exposure to asbestos. In the preamble to its 1986
asbestos rule (51 FR 22632), OSHA stated--
\59\ OSHA, 1986; ATSDR, 2001.
\60\ Davis et al., 1986; Davis and Jones, 1988; Davis et al.,
(in IARC) 1980; Davis et al., 1980; Donaldson et al., 1988;
Goldstein and Coetzee, 1990; McGavran et al., 1989; Reeves, et al.,
1974; Wagner et al., 1974, 1980; Webster et al., 1993.
---------------------------------------------------------------------------
OSHA chose not [emphasis added] to use animal studies to predict
quantitative estimates of risk from asbestos exposure because of the
many high quality human studies available that were conducted in
actual workplace situations * * * OSHA has supplemented the human
data with results from the animal studies when evaluating the
[[Page 43961]]
---------------------------------------------------------------------------
health information and determining the significance of risk.
Because we are relying on OSHA's 1986 asbestos risk assessment for this
proposed rule, we do not use the toxicological studies for a
quantitative assessment of risk, but as supportive of the causative
relationship between asbestos exposure and observed human health
effects.
Toxicological studies are providing important information on
possible mechanism(s) through which asbestos causes disease. The ATSDR
Toxicological Profile for Asbestos (updated 2001) contains a more
detailed discussion on this topic and describes several mechanisms of
action for asbestos. These include--
Its direct interaction with cellular macromolecules,
Its recruitment of pulmonary macrophages that produce
reactive oxygen and nitrogen species, and
Its initiation of other cellular responses (e.g.,
inflammation).
V. Characterization and Assessment of Exposures in Mining
Asbestos minerals are widespread in the environment.\61\ The use of
asbestos-contaminated crushed rocks in roads, asbestos in insulation
and other building materials, and the release of asbestos from brakes
on vehicles contributes to its presence in the environment.
Occupational asbestos exposures can be much higher than the asbestos
levels the public typically encounters.
---------------------------------------------------------------------------
\61\ ATSDR, 2001.
---------------------------------------------------------------------------
Miners may be exposed to asbestos in nature, as well as in
commercial products. Mining, milling, maintenance, or other activities
at the mine may result in the release or re-suspension of asbestos into
the air.\62\ In some geologic formations, asbestos may be in isolated
pockets or distributed throughout the ore. Mining operations, such as
blasting, cutting, crushing, grinding, or simply disturbing the ore or
surrounding earth may cause the asbestos to become airborne. Milling
operations may transform bulk ore containing asbestiform minerals into
respirable fibers. Similarly, other activities conducted at mine sites,
such as removing asbestos-containing materials during renovation or
demolition of buildings and equipment repair work,\63\ may contribute
to a miner's asbestos exposure.
---------------------------------------------------------------------------
\62\ MSHA (Bank), 1980; Amandus et al., Part I, 1987.
\63\ EPA, 1986, 1993, April 2003.
---------------------------------------------------------------------------
A. Determining Asbestos Exposures in Mining
To evaluate asbestos exposures in mines, MSHA collects personal
exposure air samples using a personal sampling pump and a filter-
cassette assembly, composed of a 50-mm electrically conductive
extension cowl and a 25-mm diameter mixed cellulose ester (MCE) filter.
Following standard sampling procedures, we also submit blank filters
for analysis. Analysts use the blanks to correct the sampling results
for background fiber counts due to variations in the manufacturing and
analysis of the filter.
Since 2001, we have used contract laboratories to analyze our
asbestos samples by PCM. The contract laboratories report analytical
results as the fiber concentration (f/cc) for each filter analyzed.
Then, to evaluate a miner's full-shift exposure, MSHA calculates an 8-
hour time-weighted average concentration from a consecutive series of
individual filters.
Several factors complicate the evaluation of personal exposure
levels in mining. Non-asbestos particles collected on the filter can
hide the asbestos fibers (overloading) and, as discussed earlier (see
section II.C.2), mining samples may also contain intermediate fibers
that are difficult to classify. (See section II.B in this preamble.)
B. Exposures From Naturally Occurring Asbestos
Mining and milling of asbestos-contaminated ore can release fibers
into the ambient air. Beginning in January 2000, we initiated a focused
effort to determine the extent of asbestos exposure among miners. We
chose 124 metal and nonmetal mines for sampling based on the following:
Geological information linking a higher probability for
asbestos contamination with certain types of ores or commodities.
Historical records identifying locations of potential
problem mines.
Complaints from miners reporting asbestos on mine
property.
Asbestos tends to accumulate during the milling process, which is
often in enclosed buildings. The use of equipment and machinery or
other activities in these locations may re-suspend the asbestos-
containing dust from workplace surfaces into the air. For this reason,
we generally find higher airborne concentrations in mills than among
mobile equipment operators or in ambient environments, such as pits.
The following example supports this finding.
1. Asbestos-Contaminated Ore Case Study: Wollastonite
Wollastonite is a monocalcium silicate found in the United States,
Mexico, and Finland. It occurs as prismatic crystals that can split
into massive-to-acicular (needle-like) fragments when processed, and is
used mainly in ceramics.\64\
---------------------------------------------------------------------------
\64\ Warheit, p. 18, 1993.
---------------------------------------------------------------------------
A consumer recently sent a sample of the final bulk product from a
wollastonite mine to a commercial laboratory for analysis. When the
analysis indicated the presence of asbestos contamination, the consumer
informed the mine operator. The mine operator contacted MSHA and
informed us of this finding after their contract laboratory confirmed
the presence of tremolite in product samples. MSHA then conducted
industrial hygiene sampling in the mill and the pit to verify and track
the source of the tremolite. We found that concentrations in the mill
exceeded 2.0 f/cc as measured by PCM. Although asbestos averaged only
about 1.3 percent of the total fibers, over half of the exposures in
the mill exceeded 0.1 f/cc of asbestos (the OSHA 8-hour, TWA PEL).
Miners' exposures in the pit were much lower and further analyses
indicated that few of these samples contained asbestos.
The mine instituted an aggressive cleanup and control policy in the
interest of the company and their miners' health. This wollastonite
facility provides and launders uniforms for the millers, provides
physical examinations to miners and their families, and uses other
administrative controls to limit take-home contamination. In addition
to conducting personal asbestos sampling, MSHA assisted mine management
through the following compliance assistance activities:
Assistance in developing cleanup and monitoring
procedures.
Discussion of hazards of asbestos exposure with miners and
the operator.
Identification of accredited laboratories familiar with
mining samples to perform asbestos analyses.
Assistance in implementation of a respiratory protection
program.
Instruction in recognition and avoidance of asbestos. MSHA
and the mine operator worked together in recognizing the problem,
evaluating the hazard, and determining ways to control exposures. This
case study demonstrates successful cooperation to protect the health of
miners.
[[Page 43962]]
2. Methods of Reducing or Avoiding Miners' Exposures to Naturally
Occurring Asbestos
Some mine operators mining other commodities that are likely to
contain asbestos, such as vermiculite, have stated that they are making
an effort to avoid deposits and seams likely to contain substantial
quantities of asbestos. They use knowledge of the geology of the area,
visual inspections of the working face, and sample analysis to avoid
encountering asbestos deposits, thus preventing asbestos contamination
of their product.\65\ In addition, some mine operators have voluntarily
adopted the OSHA 8-hour, TWA PEL (0.1 f/cc), thus reducing the
potential for asbestos-related illness among miners.
---------------------------------------------------------------------------
\65\ GETF Report, pp. 17-18, 2003.
---------------------------------------------------------------------------
C. Exposures From Introduced (Commercial) Asbestos
Asbestos is an important component in some commercial products and
may be found as a contaminant in others. Due to improved technology and
increased awareness, however, substitutes for asbestos in products are
available for almost all uses, and manufacturers have removed the
asbestos from many new products.\66\ Nevertheless, there are mines,
including coal mines, that have introduced commercial asbestos-
containing products on their property. Some of these introduced
products may include asbestos-containing building materials, such as
Transite[supreg] board, used during construction, rehabilitation, or
demolition projects. Other examples of introduced commercial products
that may contain asbestos are brake linings for mining equipment,
insulation, joint and packing compounds, and asbestos welding blankets.
---------------------------------------------------------------------------
\66\ GETF Report, pp. 12 and 15, 2003.
---------------------------------------------------------------------------
Occasionally, miners report incidents of possible asbestos release
through MSHA's Hazard Complaint Program. Inspectors also report mines
with noticeably deteriorated asbestos-containing building materials
(ACBM). We investigate these reported situations and take appropriate
action. The following example describes an incident in which miners
unsafely removed asbestos at a mining operation.
1. Introduced Asbestos Case Study: Potash
In June 2003, eight miners removed siding on three transfer
conveyors originally installed in 1962 at a potash mine in Utah. The
siding was weathered and deteriorated to the point of being friable
(crumbling). The type of siding was a commercial product named
Galbestos[supreg], which contains 7 percent chrysotile asbestos, as
indicated on the Material Safety Data Sheet (MSDS). Analysis of bulk
samples of the debris left behind by the removal of the siding
confirmed that it contained chrysotile asbestos. When the miners
removed it without using special precautions, they released asbestos
into the air. It is possible that these miners contaminated themselves
with asbestos and carried it to their families and communities (i.e.,
take-home contamination).
MSHA became aware of this asbestos-removal work when one of the
miners made a hazard complaint to the MSHA District Office. We
conducted an investigation and determined that the company officials
had known of the potential asbestos hazard for at least 2 years. We
found no asbestos in the personal air samples collected after the
siding had been removed. Although we did not issue citations for
overexposure to asbestos, we issued citations to the company for
failure to implement special work procedures, failure to issue
appropriate personal protective equipment, and failure to train the
affected miners for the task. The mine operator took corrective action
and we terminated these citations.
2. Methods of Reducing or Avoiding Miners' Exposures to Introduced
(Commercial) Asbestos
Existing Federal and state standards already address the removal of
asbestos-containing building materials (ACBM). If the asbestos-
containing material is intact, it is preferable to leave it where it
is. If the asbestos-containing material is worn or deteriorating, these
standards require the use of special precautions (e.g., personal
protective equipment, training, decontamination) to prevent or minimize
exposure of workers and the public and contamination of the
environment. We train our inspectors to encourage mine operators to
have worn or deteriorating asbestos-containing products removed by
persons specially trained to remove the asbestos-containing material
safely.
D. Sampling Data and Exposure Calculations
After the national publicity surrounding asbestos-related diseases
and death among the population of Libby, Montana, MSHA closely reviewed
and updated its asbestos-related health procedures and policies for
metal and nonmetal mines. We then made sure these procedures and
policies were applied consistently across the country. For example, we
switched from a 37-mm to a 25-mm filter cassette and recommended
appropriate flow rates and sampling times. We also allocated additional
resources to asbestos sampling and analysis to verify and evaluate the
extent of asbestos exposures in mining.
1. Explanation of Sampling Data and Related Calculations
The time-weighted average (TWA) concentration (f/cc) for individual
filters (n = 1, 2 * * *) is calculated by dividing the number of fibers
(f) collected on the filter by the volume of air (cc) drawn through the
filter. TWAsum is the total time-weighted average
concentration for all filters in the series over the total sampling
time. The exposure limits in MSHA standards are based on an 8-hour
workday, regardless of the actual length of the shift. MSHA measures
the miner's exposure for the entire time the miner works. We then
calculate a full-shift airborne exposure concentration as if the fibers
had been collected over an 8-hour shift. This allows us to compare the
miner's exposure to the 8-hour TWA, full-shift exposure limit. MSHA
calls this calculated 8-hour TWA a ``shift-weighted average (SWA).''
We calculate the TWAsum and SWA exposure levels for each
miner sampled according to the following formulas, respectively.
TWAsum = (TWA1t1 +
TWA2t2 + * * * + TWAntn)/
(t1 + t2 + * * * + tn)
SWA = (TWA1t1 + TWA2t2 + *
* * + TWAntn)/480 minutes
Where:
TWAn is the time-weighted average concentration for filter
``n''.
tn is the duration sampled in minutes for filter ``n''.
TWAntn is the time-weighted average concentration
for filter ``n'' multiplied by the duration sampled for filter ``n''.
(t1 + t2 + * * * + tn) is the total
time sampled in minutes.
MSHA defines a ``sample'' as the average 8-hour full-shift airborne
concentration that represents an individual miner's full-shift
exposure.
The following information from our database illustrates the
sampling results from these calculations. For one mechanic at the
potash mine in our previous example, MSHA used a series of three
filter-cassettes to determine the miner's full-shift exposure. We
sampled a total of 577 minutes. The highest TWA concentration for one
filter-cassette in this series was 4.100 f/cc as analyzed by PCM. MSHA
calculated the mechanic's full-shift exposure to report the fiber
concentration as if the mechanic had received the full exposure in 8
hours
[[Page 43963]]
(480 minutes). The mechanic's shift-weighted average (SWA) was 1.982 f/
cc.
Table V-1.--Example of Personal Sampling Results
------------------------------------------------------------------------
PCM TWA fiber
Mechanic sampled 6/17/2003 at 1.7 Lpm Sampling time concentration
(minutes) (f/cc)
------------------------------------------------------------------------
Filter-cassette 1....................... 230 4.100
Filter-cassette 2....................... 252 0.016
Filter-cassette 3....................... 95 0.045
TWAsum result........................... 577 1.649
Sample (SWA) result..................... 480 1.982
------------------------------------------------------------------------
2. Summary of MSHA's Asbestos Sampling and Analysis Results
To assess exposures and present our asbestos sampling results to
the public, we compiled our asbestos sampling data for the period
January 1, 2000 through December 31, 2003. We formatted these data into
four Excel[supreg] workbooks, one for each year, and placed them,
together with additional explanatory information, on our Asbestos
Single Source Page at http://www.msha.gov/asbestos/asbestos.htm.
We calculated an 8-hour full-shift exposure for each miner sampled
from the TWA of individual filters, typically three filters per shift.
These data include the results of 703 full-shift personal exposure
samples, comprised of 2,184 filter-cassettes, and cover 163 industrial
hygiene sampling visits at 125 mines (124 metal and nonmetal mines and
one coal mine), including some mines and mills that are now closed.
Because the last remaining asbestos mine in the United States (Joe 5
Pit in California) closed in December 2002 and its associated mill
(King City) closed in June 2003, we excluded those data in our
analysis.
Of the remaining 123 mines that MSHA sampled during this 4-year
period, 18 mines could be potentially impacted by the lowering of the
full-shift permissible exposure limit to 0.1 f/cc as measured by PCM.
These 18 mines have had at least one miner exposed to airborne fiber
concentrations exceeding 0.1 f/cc during this period. Two of the 18
mines (iron ore and wollastonite) had personal asbestos exposures
confirmed by TEM exceeding 0.1 f/cc. Excluding the 42 samples from the
asbestos mine and mill, 8 percent of the remaining 661 personal samples
had 8-hour TWA, full-shift fiber concentrations greater than the
proposed 0.1 f/cc PEL, as measured by PCM. Table V-2 below summarizes
these sampling results.
Table V-2.--Personal Exposure Samples, Analyzed by PCM, at Currently Active Mines \1\ by Commodity (1/2000-12/
2003)
----------------------------------------------------------------------------------------------------------------
Number (%) of Number (%) of
Commodity Number of mines >0.1 f/cc Number of samples >0.1 f/
mines sampled SWA samples cc SWA \2\
----------------------------------------------------------------------------------------------------------------
Rock & quarry products \3\.................. 61 4 (7%) 215 7 (3%)
Vermiculite................................. 4 3 (75%) 127 5 (4%)
Wollastonite................................ 1 1 (100%) 18 18 (100%)
Iron (taconite)............................. 14 5 (36%) 178 17 (10%)
Talc........................................ 12 1 (8%) 38 2 (5%)
Boron....................................... 2 1 (50%) 9 4 (44%)
Other \4\................................... 29 \5\ 3 (10%) 76 3 (4%)
-----------------
Total................................... 123 \6\ 18 (15%) 661 56 (8%)
----------------------------------------------------------------------------------------------------------------
\1\ Excludes data from a closed asbestos mine and mill.
\2\ MSHA uses TEM to confirm the presence of asbestos on samples showing exposures exceeding 0.1 f/cc.
\3\ Including stone, sand and gravel mines.
\4\ Coal, potash, gypsum, salt, cement, clay, lime, mica, metal ore NOS, olivine, shale, pumice, trona, perlite,
and gold.
\5\ Coal, potash, and gypsum (Coal and potash personal exposures are due to commercially introduced fiber
release episodes, i.e., not from a mineral found at the mine).
\6\ TEM confirmed asbestos exposures exceeding 0.1 f/cc in two of the 18 mines.
MSHA is proposing to lower its 8-hour TWA, full-shift PEL from 2.0
f/cc to 0.1 f/cc to provide increased protection for miners. As noted
in OSHA's risk assessment for its 1986 asbestos rule, there is
significant risk of material impairment of health or functional
capacity even at this lower PEL. MSHA compliance data indicate that
some miners' asbestos exposures have exceeded 0.1 f/cc. Available data
from death certificates in 24 states confirm that there is asbestos-
related mortality among miners.\67\
---------------------------------------------------------------------------
\67\ NIOSH World, p. E-1, 2003.
---------------------------------------------------------------------------
VI. The Application of OSHA's Risk Assessment to Mining
We are applying OSHA's risk assessment to our exposure sampling
data on miners to estimate the risk from asbestos exposure in mining.
In response to the ANPRM, the National Mining Association (NMA)
expressed their belief that health risk is related to fiber type and
that OSHA's risk assessment is no longer adequate or appropriate for us
to use for the mining industry. In developing this proposed rule, we
evaluated studies published over the last 20 years since OSHA completed
its risk assessment, and studies that specifically focused on asbestos
exposures of miners. We have found that these additional studies
confirm OSHA's conclusions.
Section VIII of this preamble contains a summary of our findings
from applying OSHA's quantitative assessment of risk to the mining
industry. The Preliminary Regulatory Economic Analysis (PREA) contains
a more in-depth discussion of our methodology and conclusions. We
placed our PREA in the rulemaking docket and posted it on our Asbestos
Single Source Page at http://www.msha.gov/asbestos/asbestos.htm. We
also placed OSHA's risk assessment in the rulemaking docket.
[[Page 43964]]
A. Summary of Studies Used by OSHA in Its Risk Assessment
OSHA relied on eight non-mining and milling studies to estimate the
risk of lung cancer due to asbestos exposure. They used four studies to
estimate the risk of mesotheliomas, and two studies, involving three
occupational cohorts, for asbestosis. We briefly review these studies
below, since they also serve as the basis of our risk assessment. For
completeness, we are including Table VI-1 of some mining and milling
studies that have been conducted.
EPA, in its Integrated Risk Information System (IRIS), presents a
useful table summarizing data from lung cancer and mesothelioma
studies. We extracted that portion of their table dealing with the
studies included in OSHA's risk assessment. This is the basis for Table
VI-1 below.
Table VI-1.--Summary of Lung Cancer and Mesothelioma Studies
--------------------------------------------------------------------------------------------------------------------------------------------------------
Reported Percent (%)
average increase in
Human data occupational group Fiber type exposure (f-yr/ cancer per f- Reference
mL) yr/mL
--------------------------------------------------------------------------------------------------------------------------------------------------------
Lung Cancer
--------------------------------------------------------------------------------------------------------------------------------------------------------
Friction Products................... Chrysotile............. 32 0.058 Berry and Newhouse, 1983.
Textile Products..................... Mostly Chrysotile...... 44 2.8 Dement et al., 1982.
Cement Products...................... Mixed (Amosite, 112 6.7 Finkelstein, 1983.
Chrysotile,
Crocidolite).
--------------------------------------
Asbestos Products.................... Mixed (Amosite, 374 0.49 Henderson and Enterline, 1979.
Chrysotile,
Crocidolite).
Textile Products..................... Chrysotile............. 200 1.1 Peto, 1980.
Insulation Products.................. Amosite................ 67 4.3 Seidman et al., 1979; Seidman, 1984.
Insulation Workers................... Mixed (Amosite, 300 0.75 Selikoff et al., 1979.
Chrysotile,
Crocidolite).
Cement Products...................... Mixed (Amosite, 89 0.53 Weill et al., 1979.
Chrysotile,
Crocidolite).
--------------------------------------
Mesotheliomas
--------------------------------------------------------------------------------------------------------------------------------------------------------
Cement Products...................... Mixed (Amosite, 108 1.2 \E\ \5\ Finkelstein, 1983.
Chrysotile,
Crocidolite).
Textile Products..................... Chrysotile............. 67 3.2 \E\ \6\ Peto et al., 1982.
Insulation Products.................. Amosite................ 400 1.0 \E\ \6\ Seidman et al., 1979; Seidman, 1984.
Insulation Workers................... Mixed (Amosite, 375 1.5 \E\ \6\ Selikoff et al., 1979.
Chrysotile,
Crocidolite).
--------------------------------------------------------------------------------------------------------------------------------------------------------
1. Lung Cancer
a. Berry and Newhouse, 1983
Berry and Newhouse (1983) conducted a retrospective mortality study
(1942-1980) using data from an English factory that manufactured
asbestos-containing friction materials (e.g., brake blocks, stair
treads). There were 13,460 workers included in this study, of which
two-thirds were men. Most had worked in this factory for 2-10 years.
The asbestos exposures generally involved chrysotile, although this
site also had used crocidolite for two brief periods, one from 1922-
1933 and a second from 1939-1944.
Personal air sampling for the assessment of asbestos concentrations
in this factory began in 1968. Fiber levels for time periods prior to
1968 were ``estimated by reproducing earlier work conditions using
detailed knowledge of when processes were changed and exhaust
ventilation introduced.'' Asbestos fiber concentrations were determined
over four time periods: Pre-1931, 1932-1950, 1951-1969, and 1970-1979.
Before 1931, asbestos levels typically exceeded 20 f/mL throughout the
factory. From 1932-1969, asbestos levels decreased and most exposures
ranged from 2-5 f/mL. After 1970, levels decreased to below 1 f/mL.
Berry and Newhouse (1983) did not detect excessive mortality at
this factory over the period 1942 to 1980. OSHA noted, however, the
relatively short duration of employee exposures and the short follow-up
period (e.g., less than 20 years for 33 percent of the men). In the
preamble to their 1986 asbestos rule, OSHA stated,
* * * Because of the short follow-up period used, OSHA does not
believe that the non-significant increases in lung cancer mortality
found by these investigators [Berry and Newhouse] contradict the
findings from other studies which show that low-level exposure to
asbestos has resulted in excessive mortality from lung cancer * * *
b. Dement et al., 1982
Dement et al. (1982) conducted a retrospective cohort mortality
(1930-1975) study of 768 men. These men had worked in an asbestos
textile factory located in South Carolina where ``only an insignificant
quantity of asbestos fiber other than chrysotile was ever processed.''
The men in this study had at least 1 month of employment between
January 1, 1940 and December 31, 1965. Dement et al. then followed the
cohort for another 10 years.
Air samples were collected in this factory between 1930 and 1975 to
determine asbestos levels. Impinger samples were collected prior to
1965; then membrane filter sampling was introduced. Membrane filter
sampling fully replaced the impinger method in 1971. There were 193 air
samples collected in 1930-1945, 183 in 1945-1960, and 5,576 in 1960-
1975. The estimated mean asbestos exposure levels by job and calendar
time periods, using linear regression models, were as high as 78 f/cc
before 1940 and generally ranged from 5-10 f/cc after 1940.
Dement et al. (1982) demonstrated a linear dose-response
relationship for lung cancer mortality that did not appear to have a
threshold. They also found a linear dose-response relationship for non-
malignant respiratory disease, other than upper respiratory infection,
influenza,
[[Page 43965]]
pneumonia, or bronchitis. Like the lung cancer data, the dose-response
relationship for non-malignant respiratory disease did not appear to
have a threshold.
OSHA's 1986 rulemaking considered that Dement et al.'s report of
excess risk at low cumulative [asbestos] exposures was well supported
because of their ``* * * careful estimation of exposure histories for
members of the cohort * * *''.
c. Finkelstein, 1983
Finkelstein (1983) studied a group of 328 men who worked in an
Ontario, Canada, factory that manufactured asbestos-cement pipe and
rock-wool insulation. Men selected to participate in this study began
working at the factory prior to 1961 and worked for the company for at
least 9 years. Finkelstein divided the men into three groups based on
estimated levels of asbestos exposure: 186 in production (consistent
exposure), 55 in maintenance (intermittent exposure), and 87 controls
(minimal exposure). The asbestos exposures involved chrysotile and
crocidolite, both of which the factory mixed with cement and silica.
This study report did not indicate the proportions of asbestos and
silica used in the cement.
Air samples were collected to assess asbestos levels at this cement
factory. Impinger sampling was conducted between 1943 and 1968. In
1969-1970, the factory began to use the personal membrane filter
sampling method and used this sampling data to classify the men who
worked in cement production according to their probable cumulative
asbestos exposure. They used three sub-groups (A, B, C) of estimated
exposure ranges and means as follows:
Cumulative Exposure
[Fiber-years/mL]
------------------------------------------------------------------------
Range Mean
------------------------------------------------------------------------
Subgroup A........................................ 8-69 44
Subgroup B........................................ 69-121 92
Subgroup C........................................ 122-420 180
------------------------------------------------------------------------
Finkelstein also relied on detailed employment histories and
medical records for each man in the study. Finkelstein (1983) found
that the asbestos-exposed workers had all-cause mortality rates that
were twice that of the general Ontario population. He also reported
that the mortality rates due to malignancies and the deaths
attributable to lung cancer were five and eight times those of the
general population, respectively.
d. Henderson and Enterline, 1979
In 1979, Henderson and Enterline published an update of their 1941-
1967 mortality study. The extended study provided data through 1973 and
included 1,075 men who had worked for an asbestos company in the United
States for an average of 25 years. Most of the workplace exposures
involved chrysotile, although some involved amosite or crocidolite.
Henderson and Enterline conducted impinger sampling to determine
asbestos levels for this study and reported asbestos concentrations in
millions of particles per cubic foot (mppcf). They also identified five
cumulative exposure categories (87, 255, 493, 848, and 1,366 fiber-
years/cc) by converting their original data, reported in mppcf, to f/cc
using a factor of 1:1.4 as discussed in the 1986 OSHA asbestos rule (51
FR 22617).
For the period 1941-1973, Henderson and Enterline (1979) found that
this cohort had an overall mortality rate that was about 20 percent
higher than that of males in the general population. This increase in
mortality rate was mainly due to lung cancer and other respiratory
diseases.
OSHA (1986) noted that the excess mortality risk found by Henderson
and Enterline (1979) was less than that found by Dement et al. (1982).
Henderson and Enterline, however, studied retired asbestos workers,
which ``constitute a select group of survivors'' (51 FR 22617), and
which might explain the difference in results of these two mortality
studies.
e. Peto, 1980
Peto (1980) continued the study of workers in an asbestos textile
factory in England. His paper, published in 1980, was an extension of
two earlier reports, one by Doll (1955) and a second by Peto et al.
(1977). In this updated study (1980), Peto included 679 men who were
hired in 1933 or later, and who had been employed by the company for at
least 10 years by 1972. Peto divided the workers into two cohorts:
those first exposed before 1951 (Cohort 1, n = 424 men) and those first
exposed during or after 1951 (Cohort 2, n = 255 men). The National
Health Central Register and factory personnel followed the workers
until 1978. The exposures in this textile factory involved chrysotile.
Although routine measurements of asbestos levels were not made
prior to 1951, Peto et al. (1977) had estimated the workers' exposures
in an earlier study. Between 1951 and 1961, a thermal precipitator was
used to sample for asbestos, then was gradually replaced by membrane
filters. In this study, Peto revised earlier estimates of asbestos
exposure concentrations and reported mean levels in fibers/mL for six
selected years as follows: 32.4 (1951), 23.9 (1956), 12.2 (1961), 12.7
(1966), 6.7 (1971), and 1.1 (1974). Peto et al. then used these values
to calculate cumulative exposures. The average cumulative exposure for
men first exposed to asbestos during or after 1951 (i.e., Cohort 2) was
200-300 fiber-years/mL.
Peto (1980) confirmed earlier conclusions by Doll (1955) and Peto
et al. (1977) that there was excess lung cancer mortality in this
asbestos textile factory. Although Peto et al. (1977) suggested a dose-
response relationship for lung cancer using measurements from a static
dust sampler, Peto did not demonstrate such a dose-response
relationship in this later study (1980).
f. Seidman et al., 1979 (With Update to OSHA in 1984)
Seidman et al. (1979) conducted a mortality study (1946-1977) of
820 men who worked in an amosite factory in New Jersey. This factory
supplied the U.S. Navy with insulation for pipes, boilers, and
turbines. The men in this study were first employed between 1941 and
1945 and were followed for 35 years. Due to wartime conditions,
however, there was a changing composition of the workforce. Seidman et
al. (1979) stated that--
This resulted in a unique experience; men with a very limited
duration of intense exposure to Amosite asbestos, followed by long
observation * * *
The men were classified according to the time in which they came into
direct contact with the amosite: Less than 1 month, 1 month, 2 months,
3-5 months, 6-11 months, 1 year, or 2 or more years. Thus, this cohort
is unlike those of other studies where workers were exposed to asbestos
for long periods, often 20 or more years.
In this amosite factory, there were no direct measurements of
asbestos levels. The determination of asbestos concentrations was made
solely by analogy with another factory in which air sampling was done
in the late 1960's and in the 1970's. Seidman et al. reported that, in
samples taken in this latter factory in October of 1971, asbestos
counts averaged as high as 23 f/mL.
Seidman et al. (1979) demonstrated that the amosite workers were at
risk of developing lung cancer and dying from this disease. Seidman et
al. (1979) concluded that--
Prolonged follow-up is necessary to evaluate the effects
of asbestos on
[[Page 43966]]
health, especially with lower concentration or shorter duration
exposures.
Asbestos retained in tissues may continue to produce
adverse effects long after the exposure may have stopped.
The length of the latency period for asbestos-related
diseases depends directly on the dosage and the age at which exposure
takes place. For example, older workers will show a more pronounced and
quicker effect than younger workers with the same level of exposure.
The longer the time after first exposure to asbestos, the
more pronounced the excesses in mortality.
Reducing the asbestos exposure (lowering the dosage) can
both delay the occurrence of adverse effects (e.g., time to death) and
lower the frequency of their occurrence (e.g., fewer deaths).
In 1984, Seidman updated his earlier work by adding 593 cases
involving deaths that occurred 5-40 years beyond each man's first
amosite exposure. Seidman again developed a classification scheme, but
now he based it on cumulative exposure to amosite and not on time
alone. The exposure categories were less than 6, 6-11.9, 12-24.9, 25-
49.9, 50-99.9, 100-149.9, 150-249.9, and 250 or more fiber-years/cc.
Using this new information, he was able to demonstrate an exposure-
response relationship for lung cancer mortality.
g. Selikoff et al., 1979.
Selikoff et al. (1979) conducted a mortality study (1943-1976) of
17,800 men who belonged to the insulation workers' union. Members of
this insulation union worked mainly in construction in the United
States and Canada, but some worked in refineries, industrial plants,
shipyards, and power plants. Selikoff et al. (1979) described the
content of the asbestos insulation as follows.
Until approximately the early 1940s, chrysotile alone was
utilized in the manufacture of the asbestos insulation products used
by these men. Amosite began to be used in the mid-1930s in small
quantities but became more widely utilized during World War II and
subsequently.
The ages of men in this study ranged from 15 to over 85 years and
Selikoff et al. (1979) established a series of ``age categories,'' each
including a 5-year age span (e.g., 15-19 years, 20-24 years, etc.)
Those men age 85 or older were grouped together. The investigators
identified the time at which each man was first exposed to asbestos and
then separated the data into a series of categories based on how long
it had been since their first exposure (e.g., less than 20, 20-34, and
35 or more years ago).
Selikoff et al. (1979) reported that few measurements were made to
assess asbestos levels in insulation work until the mid-1960's. For
this reason, they estimated exposure levels using reconstructions of
past work conditions and extrapolations of more current measurements to
past conditions. They concluded that insulation workers would have been
exposed to TWA concentrations of 4-12 f/mL.
Selikoff et al. (1979) concluded that the asbestos insulation
workers were at ``extraordinary increased risk of death of cancer and
asbestosis.'' The study had found an excessive number of lung cancers
(486) in this cohort, particularly at 15-35 years after the first
exposure to asbestos. This figure was even more striking when compared
to the expected number of lung cancer cases (106) for this same group
of men.
h. Weill et al., 1979.
Weill et al. (1979) conducted a mortality study of 5,645 men who
had at least 1 month of continuous employment before January 1, 1970 in
one of two asbestos cement building materials plants in New Orleans,
Louisiana. The men in this study had worked at some time during the
1940's to the mid-1970's. The investigators followed this cohort for at
least 20 years and found that--
For both plants, 7 percent [of the men] were initially employed
before 1940, 76 percent during the 1940s, and 17 percent during 1950
to 1954. Sixty percent were employed for less than one year, 24
percent for one to 10 years, and 16 percent for more than 10 years.
The asbestos exposures mainly involved chrysotile, although the two
plants also processed crocidolite and amosite. The cement products were
comprised of about 15-28 percent asbestos and some silica. Weill et al.
(1979), however, did not provide the proportion of silica in the
asbestos cement mixture.
Impinger sampling was conducted in this factory to determine
asbestos levels. The sampling results were reported in millions of
particles per cubic foot (mppcf). Based on sampling data, Weill et al.
(1979) defined five categories of exposure in mppcf/year as follows:
Less than 10, 11-50, 51-100, 101-200, and more than 200. OSHA (51 FR
22618) converted the original data of Weill et al. (1979) from mppcf/
year to fiber-years/cc using a factor of 1:1.4, as given in the 1986
OSHA rule (51 FR 22617). This yielded the following exposure categories
in fiber-years/cc: Less than 14, 15-70, 71-140, 141-280, more than 280.
Weill et al. (1979) found excess mortality due to cancers, mainly
lung cancer, in men whose cumulative exposures were moderate (141-280
fiber-years/cc) to high (greater than 280 fiber-years/cc). About 25
percent of their cohort, however, was lost in the follow-up period. For
the purpose of the study, Weill et al. assumed they were alive. This
assumption may have led to an underestimation of lung cancer risk. For
this reason, OSHA (51 FR 22618) stated its opinion as follows:
* * * the presence of an excess risk of mortality from lung cancer
could not be ruled out for the cohorts in these exposure categories.
[The other three, lower exposure categories defined by Weill et al.,
1979.]
2. Mesotheliomas
a. Finkelstein, 1983.
We reviewed the most important aspects of this study above. (See
section VI.A.1.) Based on death records, Finkelstein (1983) found 11
mesotheliomas among the total of 58 deaths in his study. The mean age
at which these men were first exposed to asbestos was 25 years, and
their mean latency period for mesotheliomas was 25 years. The mean age
at death was 51 years, and none was over 60 years. This demonstrates
that death follows quickly after this disease becomes evident.
Finkelstein noted that the rates of death from mesotheliomas were
proportional to the magnitude of cumulative asbestos exposure, as shown
in Table VI-2 below.
Table VI-2.--Mesotheliomas Mortality Rates Compared to Exposure
------------------------------------------------------------------------
Estimated Estimated mean
Mesotheliomas mortality rates (per exposure exposure
1,000 man-years) range (fiber- fiber-years/
years/mL) mL)
------------------------------------------------------------------------
1.9..................................... 8-69 44
[[Page 43967]]
4.9..................................... 70-121 92
11.9.................................... 122-420 180
------------------------------------------------------------------------
Based on the exposure-response data, Finkelstein concluded, ``* * *
the relation is compatible with a linear function through the origin *
* *.'' Accordingly, Finkelstein's data suggest the lack of a threshold
for mesotheliomas.
b. Peto et al., 1982.
Peto et al. (1982) evaluated mesothelioma mortality (1967-1979) in
the same group of 17,800 insulation workers previously described by
Selikoff et al. (1979). We reviewed the salient features of Selikoff et
al. (1979) above. (See section VI.A.1.) Members of this insulation
workers' union worked in the United States and Canada and were exposed
to chrysotile and amosite.
Peto et al. (1982) reported ``a high incidence'' of mesotheliomas
in this cohort. There were 236 deaths from mesotheliomas, of which 87
were pleural and 149 were peritoneal. They closely examined each man's
age at the first asbestos exposure and the number of years since his
first exposure. Peto et al. (1982) concluded that mesothelioma
mortality was strongly dependent on the number of years since the first
asbestos exposure, but was independent of the age at the first
exposure. They stated--
Mesothelioma death rates in asbestos workers appear to be
proportional to the third or fourth power of time * * * Age at first
exposure has little or no influence, however, which supports the
multi-stage model of carcinogenesis * * * mesotheliomas may
constitute a high proportion of cancer deaths resulting from early
exposure to asbestos.
Peto et al. (1982) also reviewed mesothelioma mortality data from
several other studies in addition to those from Selikoff et al. (1979).
They were interested in determining if they could establish a
relationship between deaths from mesotheliomas and fiber type. Although
there were some data to suggest that deaths from mesotheliomas were
more common in men who worked with amphiboles (e.g., crocidolite), Peto
et al. (1982) were cautious when drawing conclusions. They stated
that--
Chemical [and physical] differences between different fibre
types may also be important, but until carcinogenic effects of such
differences have been demonstrated, it would seem sensible to
concentrate on fibre dimension rather than mineral type in
developing dose-response relationships. * * * It may therefore be
dangerously optimistic to attribute the substantial incidence of
pleural mesothelioma among chrysotile factory workers to occasional
crocidolite exposure * * *
c. Seidman et al. 1979 (With Update to OSHA in 1984).
We reviewed the salient features of this study and its update
above. (See section VI.A.1.) Based on death records, Seidman et al.
(1979) found 14 mesotheliomas among the total 528 deaths in their
study. They reported an additional three mesotheliomas in their update.
OSHA commented that this was ``a finding of great significance given
the rarity of the disease'' (51 FR 22617).
d. Selikoff et al. (1979).
The salient features of this study were reviewed above. (See
section IV.A.1.) Based on death records, Selikoff et al. (1979) found
38 mesotheliomas (pleural and peritoneal) in their initial cohort of
632 asbestos insulation workers. There were 223 deaths in this part of
their study (1943-1976). Some of these deaths from mesotheliomas
occurred 20-34 years after the first exposure to asbestos, described by
the authors as ``duration from onset.'' For most men who died from
mesotheliomas, however, it was 35 or more years after their first
exposure.
In the second and much larger cohort (n = 17,800) of Selikoff et
al. (1979), there were 175 deaths due to mesotheliomas of the total
2,271 deaths in this group. Some (14) of these deaths caused by
mesotheliomas occurred 15-24 years after the first asbestos exposure,
while most (161) were recorded 25 or more years after the first
exposure. Selikoff et al. (1979) had been unable to provide expected
death rates for mesotheliomas due to their rarity in the general
population. This study demonstrated an unequivocal association between
mesotheliomas and prior asbestos exposure. In the 25 years since this
paper was published, there has been no evidence to the contrary.
3. Asbestosis
a. Berry and Lewinsohn, 1979.
Berry and Lewinsohn (1979) studied the same group of textile
workers that was originally described by Berry et al. (1979) and, thus,
a short summary of the original paper is presented here.
Berry et al. (1979) studied a group of 379 men who worked in an
asbestos textile factory located in northern England. Most of the
worker exposures involved chrysotile, although this site also used
crocidolite. Asbestos fiber levels were measured in this factory since
1951 and had been estimated since 1936. Berry et al. defined two
cohorts. One included men who were first employed between 1933 and
1950, and were still working in this textile factory in 1966. The other
included men who were employed after 1966, and had worked for at least
10 years in this textile factory. Berry et al. (1979) found
relationships between cumulative asbestos exposure and crepitations
(abnormal lung sounds), possible asbestosis, and certified asbestosis.
As noted above, Berry and Lewinsohn (1979) used data from the same
textile factory as that described by Berry et al. (1979); but Berry and
Lewinsohn (1979) defined two different cohorts. One included men who
were first employed before 1951. The other included men first employed
after 1950. Berry and Lewinsohn (1979) plotted the incidence of cases
of possible asbestosis against the cumulative asbestos exposure up to
1966. They stated--
The data are compatible with a linear relationship through the
origin [indicating no threshold], with no statistically significant
difference between the two groups [cohorts].
b. Finkelstein, 1982.
Finkelstein (1982) studied a group of 201 men who worked in a
factory in Ontario, Canada, that manufactured asbestos-cement pipe and
rock-wool insulation. Finkelstein defined two subsets in his study
population: A group of 157 production workers and a group of 44
maintenance workers. The men selected to participate in this study
worked in the pipe or board shop for at least one year prior to 1961
and had been employed at least 15 years. Most of the asbestos exposures
involved
[[Page 43968]]
chrysotile and crocidolite, both of which were mixed with cement and
silica.
Between the 1940's and 1968, impinger sampling was conducted to
assess total dust levels. In 1969/1970, the company began to conduct
quarterly personal sampling for asbestos using the membrane filter
method. Finkelstein used the results of such sampling as baseline
values for various jobs.
Of the workers in this study, 39 percent of those in production and
20 percent of those in maintenance had certified asbestosis.
Finkelstein demonstrated that there was a relationship between
cumulative asbestos exposure and certified asbestosis. He describes the
exposure-response curve as sigmoidal, a shape commonly observed in
toxicology. The curve also appears to intersect the origin, which
suggests a lack of threshold.
B. Models Selected by OSHA (1986) for Specified Endpoints and for the
Determination of Its PEL and STEL
Based on their critical review of the studies described above (see
section VI.A), OSHA (51 FR 22631) concluded--
* * * asbestos exposure causes lung disease, respiratory cancer,
mesothelioma, and gastrointestinal cancer. * * * excess disease risk
has been observed at cumulative exposures at or below those
permitted by the existing OSHA 8-hour permissible exposure limit
[PEL] of 2 f/cc. In addition, OSHA has made risk estimates of the
excess mortality from lung cancer, mesothelioma, gastrointestinal
cancer, and the incidence of asbestosis using mathematical models *
* *
The following is a summary of the mathematical models that OSHA
used in its asbestos risk assessment.
1. Lung Cancer
For lung cancer, OSHA (1986) relied on a relative risk model that
was linear in dose, as described by the following equation:
RL = RE[1 + (KL)(f)(dt-10)]
Where:
RL = Predicted lung cancer mortality.
RE = Expected lung cancer mortality in the absence of
asbestos exposure.
KL = Slope of the dose-response relationship for lung
cancer.
f = Asbestos fiber concentration (f/cc).
d = Duration of the exposure (minus 10 years to account for latency).
The following list gives the KL values for the eight
studies used by OSHA. OSHA (51 FR 22637) used KL = 0.01, the
geometric mean of these eight studies, in their risk assessment.
------------------------------------------------------------------------
Study KL
------------------------------------------------------------------------
Berry and Newhouse, 1983.................................. 0.0006
Dement et al., 1982....................................... 0.042
Finkelstein, 1983......................................... 0.048
Henderson and Enterline, 1979............................. 0.0047
Peto, 1980................................................ 0.0076
Seidman et al., 1979; Seidman, 1984....................... 0.045
Selikoff et al., 1979..................................... 0.020
Weill et al., 1979........................................ 0.0033
------------------------------------------------------------------------
2. Mesotheliomas
For mesotheliomas, OSHA (1986) relied on an absolute risk model
that is linear in dose, but exponentially related to the time after the
first exposure to asbestos. The following three equations describe the
risk.
ARM = (f)(KM)[(t-10)\3\ - (t-10-d)\3\], for t >
10 + d
ARM = (f)(KM)[(t-10)\3\], for 10 + d > t > 10
ARM = 0, for 10 > t
Where:
RM = Excess risk of mesotheliomas.
f = Asbestos fiber concentration.
KM = Slope of the dose-response relationship for
mesotheliomas.
d = Duration of the exposure.
t = Time after the first exposure to asbestos.
The following list gives the KM values for the four
studies used by OSHA. OSHA (51 FR 22640 and 22642) used KM =
1 x 10-8, the ratio of KM/KL, rather
than KM = 2.91 x 10-8, the geometric mean of
these four studies, to account for the bias in its analysis and avoid
overestimation of mesotheliomas in their risk assessment.
------------------------------------------------------------------------
Study KM(10-8)
------------------------------------------------------------------------
Finkelstein, 1983......................................... 12
Peto et al., 1982......................................... 0.7
Seidman et al., 1979; Seidman, 1984....................... 5.7
Selikoff et al., 1979..................................... 1.0
------------------------------------------------------------------------
3. Asbestosis
For asbestosis, OSHA (1986) relied on an absolute risk model that
was linear in cumulative dose. The following equation describes the
lifetime incidence of asbestosis:
RA = m(f)(d)
Where:
RA = Predicted lifetime incidence of asbestosis.
f = Asbestos fiber concentration.
d = Duration of the exposure.
m = Slope of the linear regression.
OSHA stated (48 FR 51132), ``the best estimates of asbestosis
incidence are derived from the Finkelstein data `` and OSHA did not
rely on the values for the slope as determined by Berry and Lewinsohn
(1979). Thus, based on Finkelstein's data (1982) alone, the slope (m)
is 0.055 and the equation becomes RA = 0.055(f)(d).
Using this linear model, OSHA also calculated estimates of lifetime
asbestosis incidence at five exposure levels of asbestos (i.e., 0.5, 1,
2, 5, 10 f/cc) and published Table VI-3 (48 FR 51132), which we have
reproduced below. OSHA concluded that for lifetime exposures to
asbestos at concentrations of 2 or 0.5 f/cc, there would be a 5 percent
or a 1.24 percent incidence of asbestosis, respectively (48 FR 51132).
Based on Finkelstein's linear relationship for lifetime asbestosis
incidence, OSHA later stated (51 FR 22646) that, ``Reducing the
exposure to 0.2 f/cc [a concentration not included in Table VI-3] would
result in a lifetime incidence of asbestosis of 0.5%.''
Table VI-3.--Estimates of Lifetime Asbestosis Incidence
----------------------------------------------------------------------------------------------------------------
Percent (%) Incidence
-----------------------------------------------
Exposure level, fiber/cc Berry Berry (first
Finkelstein (employed employed after
before 1951) 1950)
----------------------------------------------------------------------------------------------------------------
0.5............................................................. 1.24 0.45 0.35
1............................................................... 2.49 0.89 0.69
2............................................................... 4.97 1.79 1.38
5............................................................... 12.43 4.46 *3.45
10.............................................................. 24.86 8.93 6.93
Slope........................................................... 0.055 0.020 0.015
[[Page 43969]]
R\2\............................................................ 0.975 0.901 0.994
----------------------------------------------------------------------------------------------------------------
* Note: 1.38 in original table was a typographical error. The text (48 FR 51132) and the regression formula
indicate that 3.45 is the correct percent.
C. OSHA's Selection of Its PEL (0.1 f/cc)
Using the models described above in section VI.B., OSHA estimated
cancer mortality for workers exposed to asbestos at various cumulative
exposures (i.e., combining exposure concentration and duration of
exposure). These data were published in its 1986 risk assessment (51 FR
22644), which we have reproduced in the following Table VI-4.
It is clear from Table VI-4 that the estimated mortality from
asbestos-related cancer decreases significantly by lowering exposure.
This is true regardless of the type of cancer: lung, pleural,
peritoneal, or gastrointestinal. Although excess relative risk is
linear in dose, the excess mortality rates in Table VI-4 are not
strictly linear in dose.\68\
---------------------------------------------------------------------------
\68\ Nicholson, p. 53, 1983.
Table VI-4.--Estimated Asbestos-Related Cancer Mortality per 100,000 by Number of Years Exposed and Exposure
Level
----------------------------------------------------------------------------------------------------------------
Cancer Mortality per 100,000 Exposed
Asbestos fiber concentration (fiber/cc) -----------------------------------------------------------------
Lung Mesothelioma Gastrointestinal Total
----------------------------------------------------------------------------------------------------------------
1-year exposure
----------------------------------------------------------------------------------------------------------------
0.1........................................... 7.2 6.9 0.7 14.8
0.2........................................... 14.4 13.8 1.4 29.6
0.5........................................... 36.1 34.6 3.6 74.3
2.0........................................... 144 138 14.4 296.4
4.0........................................... 288 275 28.8 591.8
5.0........................................... 360 344 36.0 740.0
10.0.......................................... 715 684 71.5 1,470.5
-----------------------------------------------
20-year exposure
----------------------------------------------------------------------------------------------------------------
0.1........................................... 139 73 13.9 225.9
0.2........................................... 278 146 27.8 451.8
0.5........................................... 692 362 69.2 1,123.2
2.0........................................... 2,713 1,408 271.3 4,392.3
4.0........................................... 5,278 2,706 527.8 8,511.8
5.0........................................... 6,509 3,317 650.9 10,476.9
10.0.......................................... 12,177 6,024 1,217.7 13,996.7
-----------------------------------------------
45-year exposure
----------------------------------------------------------------------------------------------------------------
0.1........................................... 231 82 23.1 336.1
0.2........................................... 460 164 46.0 670.0
0.5........................................... 1,143 407 114.3 1,664.3
2.0........................................... 4,416 1,554 441.6 6,411.6
4.0........................................... 8,441 2,924 844.1 12,209.1
5.0........................................... 10,318 3,547 1,031.8 14,896.8
10.0.......................................... 18,515 6,141 1,851.5 26,507.5
----------------------------------------------------------------------------------------------------------------
OSHA's PEL for asbestos was 2 f/cc in 1983. Table VI-4 shows that
after 45 years of exposure to asbestos at this concentration, there
would be an estimated 6,411.6 deaths (per 100,000 workers). This is the
sum of deaths from 4,416 lung cancers, 1,554 mesotheliomas, and 441.6
gastrointestinal cancers. By lowering its PEL to 0.1 f/cc, OSHA
decreased the risk of cancer mortality to an estimated 336.1 deaths
(per 100,000 workers), which is the sum of deaths from 231 lung
cancers, 82 mesotheliomas, and 23.1 gastrointestinal cancers.
As shown above in Table VI-3, there is also a significant reduction
in the incidence of asbestosis by lowering exposures. For example, the
lifetime incidence of asbestosis would be reduced from 4.97 percent
(4,970 cases per 100,000 workers) at 2 f/cc to 1.24 percent (1,240
cases per 100,000 workers) at 0.5 f/cc. Using the linear model
described above [RA = 0.055(f)(d)], the incidence of
asbestosis can also be calculated at a concentration of 0.1 f/cc (not
included by OSHA in Table VI-4) following 45 years of exposure to
asbestos. This yields 0.25 percent, or 250 cases per 100,000 workers.
Thus, by lowering the 8-hour TWA PEL from 2 f/cc to 0.1 f/cc, we
[[Page 43970]]
would reduce the lifetime asbestosis risk from 4,970 cases to 250 cases
per 100,000 exposed miners.
Based on these reductions in cancer deaths and asbestosis cases,
OSHA demonstrated that a lowering of the PEL below 2 f/cc would
``substantially reduce that risk'' (51 FR 22612). OSHA also noted--
Evidence in the record `` has shown that employees exposed at the
revised standards'' PEL of 0.2 fiber/cc [OSHA's 1986 standard]
remain at significant risk of incurring a chronic exposure-related
disease, but considerations of feasibility have constrained OSHA to
set the revised PEL at the 0.2 fiber/cc level.
When OSHA further reduced its PEL from 0.2 to 0.1 f/cc in 1994,
this statement was still true and the PEL continued to reflect
technical feasibility issues. OSHA stated (59 FR 40967)--
The 0.1 f/cc level leaves a remaining significant risk. However as
discussed below [in OSHA's 1994 Final Rule] and in earlier
documents, OSHA believes that this is the practical lower limit of
feasibility for measuring asbestos levels reliably.
D. Applicability of OSHA's Risk Assessment to the Mining Industry
In its asbestos emergency temporary standard, and in its proposed,
amended, and final asbestos rules (1983, 1984, 1986, 1992, 1994), OSHA
discussed few mining and milling studies and excluded these data in
their risk assessment. OSHA (51 FR 22637) stated,
The distinct nature of mining-milling data (and hence the estimate
of KL from these data) has been considered earlier. There is some
evidence that risks in the asbestos mining-milling operations are
lower than other industrial operations due to differences in fiber
size. `` Thus, in determining the KL for the final rule, the data
from mining and milling processes were not considered.
OSHA suggested that the proportionality constants (i.e.,
KL, KM), also known as the slopes of the
respective dose response curves, from mining and milling studies are
lower than the slopes for the studies included in its risk assessment
(51 FR 22632 and 22637). This difference in slopes may suggest that the
risk of asbestos-related cancers is lower in miners and millers.
Because there is remaining significant risk of asbestos-related cancer
at the OSHA PEL of 0.1 f/cc, we may be accepting a higher estimate of
risk by relying on OSHA's quantitative risk assessment that excluded
mining and milling studies.
Although we are relying on OSHA's risk assessment, we also reviewed
the scientific literature to identify studies that involved the
exposure of miners and millers to asbestos. Most of these studies were
conducted in Canada, although some have been conducted in Australia,
India, Italy, South Africa, and the United States. Table VI-5 lists
some of these mining and milling studies, in chronological order, and
gives the salient features of each study. These studies are in the
rulemaking docket.
Table VI-5.--Selected Studies Involving Miners Exposed to Asbestos
------------------------------------------------------------------------
Author(s), year of Study group, type of Major finding(s) or
publication asbestos conclusion(s)
------------------------------------------------------------------------
Rossiter et al., 1972....... Canadian miners and Radiographic changes
millers, Chrysotile. (opacities) related
to age and
exposure.
Becklake, 1979.............. Canadian miners and Weak relationship
millers, Chrysotile. between exposure
and disease.
Gibbs and du Toit, 1979..... Canadian and South Need for workplace
African miners, epidemiologic
Chrysotile. surveillance and
environmental
programs.
Irwig et al., 1979.......... South African Parenchymal
miners, Amosite and radiographic
crocidolite. abnormalities
preventable by
reduced exposure.
McDonald and Liddell, 1979.. Canadian miners and Lower risk of
millers, Chrysotile. mesotheliomas and
lung cancer from
chrysotile than
crocidolite.
Nicholson et al., 1979...... Canadian miners and Miners and millers:
millers, Chrysotile. At lower risk of
mesotheliomas, at
risk of asbestosis
(as factory workers
and insulators), at
risk of lung cancer
(as factory
workers).
Rubino et al., Ann NY Ac Sci Italian miners, Role of individual
1979. Chrysotile. susceptibility in
appearance and
progression of
asbestosis.
Rubino et al., Br J Ind Med Italian miners, Elevated risk of
1979. Chrysotile. lung cancer.
Solomon et al., 1979........ South African Sign of exposure to
miners, Amosite and asbestos: Thickened
Crocidolite. interlobar
fissures.
McDonald et al., 1980....... Canadian miners and No statistically
millers, Chrysotile. significant
increases in SMRs.
McDonald et al., 1986....... U.S. miners, A. Increased risk of
Tremolite. mortality from
respiratory cancer.
McDonald et al., 1980....... U.S. miners, B. Increased
Tremolite. prevalence of small
opacities by
retirement age.
Cookson et al., 1986........ Australian miners No threshold dose
and millers, for development of
Crocidolite. radiographic
abnormality.
Amandus et al., 1987........ U.S. miners, and Part I: Increased
millers, Tremolite- prevalence of
Actinolite. radiographic
abnormalities
associated with
past exposure.
Amandus and Wheeler, 1987... U.S. miners, and Part II: Increased
millers, Tremolite- mortality from
Actinolite. nonmalignant
respiratory disease
and lung cancer.
Amandus et al., 1987........ U.S. miners, and Part III: Exposures
millers, Tremolite- below 1 f/cc after
Actinolite. 1977, up to 100-
200X higher in
1960's and 1970's.
Armstrong et al., 1988...... Australian miners Increased mortality
and millers, from mesotheliomas
Crocidolite. and lung cancer.
Enarson et al., 1988........ Canadian miners, Increased cough,
Chrysotile. breathlessness,
abnormal lung
volume and
capacity.
McDonald et al., 1988....... U.S. miners, and Low exposure and no
millers, Tremolite. statistically
significant SMRs.
McDonald et al., 1993....... Canadian miners and Increased SMRs for
millers, Chrysotile. lung cancer and
mesotheliomas as
cohort aged.
[[Page 43971]]
Dave et al., 1996........... Indian miners and Higher exposures in
millers, Chrysotile. surface than
underground mines;
higher exposures in
mills than mines;
restrictive lung
impairment and
radiologic
parenchymal changes
more common in
millers.
McDonald et al., 1997....... Canadian miners and Risk of
millers, Chrysotile. mesotheliomas
related to
geography and
mineralogy of
region;
mesotheliomas
caused by
amphiboles.
Nayebzadeh et al., 2001..... Canadian miners and Respiratory disease
millers, Chrysotile. related to regional
differences in
fiber concentration
and not dimension.
Ramanathan and Subramanian, Indian miners and Increased risk of
2001. millers, Chrysotile cancer, restrictive
and tremolite. lung disease,
radiologic changes,
and breathing
difficulties; more
common in milling.
------------------------------------------------------------------------
These studies of miners and millers provide further evidence of
potential adverse health effects from asbestos exposure. MSHA found
that many of the observations presented in these studies (e.g., age of
first exposure, latency, radiologic changes) are consistent with those
from studies of factory and insulation workers. The exposure to
asbestos, a known human carcinogen, results in similar disease
endpoints regardless of the occupation that has been studied.
E. Significance of Risk
1. Defining ``Significant'' Risk: The Benzene Case
We (MSHA) believe that this proposed rule for asbestos meets the
requirements set forth by the OSHA Benzene Case described below. We
have relied on OSHA's risk assessment, the studies used by OSHA in its
development, and our review of more recent studies and mining studies,
which further support OSHA's findings.
In the Benzene Case, Industrial Union Department, AFL-CIO v.
American Petroleum Institute et al. (448 U.S. 607, 1980), the U.S.
Supreme Court ruled that, prior to the issuance of a new or revised
standard regulating occupational exposures to toxic materials, such as
asbestos, OSHA is required to make two findings:
They must determine that a ``significant'' health risk
exists, and
They must demonstrate that the new standard will reduce or
eliminate that risk.
In the preamble to its 1994 final asbestos rule (59 FR 40966,
1994), OSHA provided an interpretation of a ``significant health
risk''. They stated,
OSHA has always considered that a working lifetime risk of death
of over 1 per 1000 from occupational causes is significant. This has
been consistently upheld by the courts.
When OSHA lowered its PEL for asbestos from 2 to 0.2 f/cc (1986),
and then to 0.1 f/cc (1994), they used this definition of a
``significant health risk'' and made the two findings as outlined in
the Benzene Case. With respect to the first finding, OSHA estimated the
excess lifetime cancer risk to be 3.4 deaths per 1,000 workers exposed
to asbestos at 0.1 f/cc for a working lifetime. OSHA stated (51 FR
22646),
The finding that a significant risk exists is supported by
OSHA's quantitative risk assessment, which is based upon studies of
asbestos-exposed worker populations.
With respect to the second finding, OSHA went on to say (51 FR
22647),
In accordance with the second element [finding, sic] of the
Supreme Court's Benzene decision on the determination of significant
risk, OSHA has determined that reducing the permissible exposure
limit for asbestos [from 2 f/cc, sic] to 0.2 f/cc is reasonably
necessary to reduce the cancer mortality risk from exposure to
asbestos. * * * significant risks of asbestos-related cancer
mortality and asbestosis are not eliminated at the exposure level
that is permitted under the new standard [0.2 f/cc, sic]; however,
the reduction in the risk of asbestos-related death and disease
brought about by promulgation of the new standard is both
significant and dramatic.
OSHA concluded that the lowering of their PEL from 0.2 to 0.1 f/cc
would ``further reduce a significant health risk'' (59 FR 40966-40967).
2. Demonstrating Significant Health Risk for the Miner
The Federal Mine Safety and Health Act of 1977 (Mine Act), Title I,
section 101(a), requires MSHA
* * * to develop, promulgate, and revise as may be appropriate,
improved mandatory health or safety standards for the protection of
life and prevention of injuries in coal or other mines.
Furthermore, section 101(a)(6)(A) of the Mine Act requires MSHA to
set health or safety standards--
* * * on the basis of the best available evidence that no miner
shall suffer material impairment of health or functional capacity
even if such miner has regular exposure to the hazards * * * for the
period of his working lifetime.
A significant health risk exists for miners exposed to asbestos at
our existing 8-hour full-shift exposure limit of 2 f/cc. Miners, like
the insulation workers in the studies cited by OSHA, are at risk of
developing lung cancer, mesotheliomas, and asbestosis. These effects
are significant and clearly constitute a material impairment of health
and functional capacity. They also emphasize the need for us to lower
our PEL. By lowering the 8-hour full-shift exposure limit to 0.1 f/cc,
we would significantly reduce the risk of asbestos-related lung
cancers, mesotheliomas, and asbestosis.
3. Using the Experience of OSHA and Current Studies to Demonstrate
Significant Risk
Under the Mine Act, section 101(a)(6)(A), MSHA must base its health
and safety standards on--
* * * the latest available scientific data in the field, the
feasibility of the standards, and experience gained under this and
other health and safety laws.
In our proposed rule for asbestos, we have relied heavily on the
experience of OSHA, which demonstrates the feasibility of a 0.1 f/cc
exposure limit for asbestos. We believe that this limit is technically
and economically feasible for the mining industry. (See section VIII.B.
Feasibility.) We also have obtained and reviewed the latest available
scientific data on the health effects of asbestos exposure. MSHA
concludes that these studies provide further support of the significant
risk of
[[Page 43972]]
adverse health effects following exposure to asbestos.
Using OSHA's risk assessment, we have demonstrated that a lowering
of our 8-hour full-shift exposure limit from 2 to 0.1 f/cc would
significantly reduce the risk of asbestos-related disease in miners.
MSHA believes that other existing standards help reduce the remaining
significant risk at this new 0.1 f/cc PEL. For example, MSHA requires
the use of engineering and work practice controls to reduce a miner's
exposure to the PEL and, until this concentration is reached, the use
of an approved respirator. MSHA also requires the use of personal
protective clothing and equipment, as necessary, for equipment repair
and for construction or demolition activities \69\ and hazard
communication and task training.\70\ As long as miners are likely to
encounter asbestos, miners and mine operators will need to follow
adequate safety procedures to ensure a reduction of exposures. We
anticipate risk reduction to occur by the use of engineering controls
and accepted industrial hygiene administrative controls that
effectively avoid disturbing asbestos on mine property.
---------------------------------------------------------------------------
\69\ 30 CFR 56/57.5005, 56/57.15006, and 71.701
\70\ 30 CFR parts 46, 47, and 48.
---------------------------------------------------------------------------
VII. Section-by-Section Discussion of Proposed Rule
In the ANPRM, we asked commenters for supporting information to
help us evaluate whether or not to--
Lower our asbestos PEL,
Revise our analytical methods and criteria to make them
more appropriate for the mining industry, and
Implement safeguards to limit take-home exposures.
We received almost 100 comments, considered the commenters'
concerns, and discussed them in the following sections.
To make the standard easier to read, we have divided the
requirements in the proposed standards into three paragraphs:
Definitions, Permissible Exposure Limits (PELs), and Measurement of
Airborne Fiber Concentration. For Sec. Sec. 56/57.5001(b), the metal
and nonmetal asbestos standards, we numbered the paragraphs (b)(1),
(b)(2), and (b)(3). For Sec. 71.702, the coal asbestos standard, we
assigned the paragraphs letters (a), (b), and (c).
A. Sections 56/57.5001(b)(1) and 71.702(a): Definitions
Our existing definition of asbestos is consistent with several
Federal agencies' regulatory provisions, including OSHA's. As discussed
in section II.B of this preamble and in the existing regulatory
language, asbestos is not a definitive mineral name, but rather a
commercial name for a group of minerals with specific characteristics.
Our existing standards clearly state that, ``when crushed or processed,
[asbestos] separate[s] into flexible fibers made up of fibrils''
[Sec. Sec. 56/57.5001(b)]; and ``does not include nonfibrous or
nonasbestiform minerals'' (Sec. 71.702). Although there are many
asbestiform minerals, the term ``asbestos'' in our existing standards
is limited to the following six (Federal Six): \71\
---------------------------------------------------------------------------
\71\ ATSDR, p.136, 2001; NIOSH Pocket Guide, 2003.
---------------------------------------------------------------------------
Chrysotile (serpentine asbestos, white asbestos);
Amosite (cummingtonite-grunerite asbestos, brown
asbestos);
Crocidolite (riebeckite asbestos, blue asbestos);
Anthophylite asbestos (asbestiform anthophyllite);
Tremolite asbestos (asbestiform tremolite); and
Actinolite asbestos (asbestiform actinolite).
Substantive changes to the definition of asbestos are beyond the
scope of this proposed rule. We recognize that there are limitations in
the general analytical methods, such as PCM and TEM, used to identify
and quantify the Federal Six. Without the use of more complicated and
costly analyses, it may not always be possible to differentiate other
chemically similar amphiboles from the Federal Six. Also, the
International Minerals Association has proposed more specific
nomenclature in the literature to classify some of the amphiboles.\72\
We decline to adopt such classifications here, because they are beyond
the scope of this proposed rule, and propose to continue to use the
existing regulatory designations. However, we are proposing a few
nonsubstantive changes to the existing regulatory language to clarify
the standard. These wording changes would have no impact on the
minerals that we regulate as asbestos from that contained in the
existing standards. This proposed rule would--
---------------------------------------------------------------------------
\72\ Leake et al., 1997.
---------------------------------------------------------------------------
Clarify the term ``amosite,'' a name tied to asbestos from
a specific geographical region, by adding the mineralogical term
``cummingtonite-grunerite asbestos'' parenthetically.
Add a definition for fiber to be more consistent with
OSHA. This change would clarify that the dimensional criteria in our
existing standards refer to the asbestiform habit of the listed
minerals.
Conform the asbestos standards for metal and nonmetal
mines, surface coal mines, and the surface work areas of underground
coal mines by using the same structure and wording in the rule text.
For example, we retain the descriptive language ``Asbestos is a generic
term for a number of hydrated silicates that, when crushed or
processed, separate into flexible fibers made up of fibrils'' from the
metal and nonmetal standards rather than the comparable language from
the coal standards. We believe that this descriptive language assists
mine operators in understanding the scope of the standard.
MSHA's ANPRM did not specifically solicit information about which
asbestiform minerals we should regulate. Even so, some commenters
suggested that MSHA should expand its definition of asbestos to include
other asbestiform minerals, so long as our analytical method excluded
the counting of cleavage fragments. One commenter recommended that the
PEL be reduced not only for the six currently regulated asbestos
minerals, but also for other amphibole minerals in their asbestiform
habit. NIOSH commented that cleavage fragments of the serpentine
minerals antigorite and lizardite and amphibole minerals contained in
the series cummingtonite-grunerite, tremolite-ferro-actinolite, and
glaucophane-riebeckite should be counted as asbestos if they meet the
counting requirements for a fiber (3:1 aspect ratio and greater than 5
[mu]m in length). Another commenter asked that MSHA not include
nonasbestiform fibrous minerals and mineral cleavage fragments when we
perform microscopic analysis of samples.
Most commenters did not want MSHA to make changes to the fibers
regulated as asbestos in the existing standards. Specifically, they do
not want us to address other asbestiform amphiboles found in mineral
deposits because they may not pose the same health problems that
asbestos does. Some said that it would be unreasonable and expensive to
try to meet exposure limits for all these minerals. Other commenters at
MSHA's public hearing in New York (2002) stated that, whatever they are
called, these minerals cause illness.
At this time, we decline to propose substantive changes to the
definition of asbestos as suggested by some commenters. These changes
are beyond the scope of this rulemaking. We will continue to monitor
the toxicological, epidemiological, and mineralogical research studies
and other new
[[Page 43973]]
information relevant to protecting the health of miners.
B. Sections 56/57.5001(b)(2) and 71.702(b): Permissible Exposure Limits
(PELs)
MSHA currently limits a miner's 8-hour TWA, full-shift exposure to
2.0 f/cc over a full shift; and limits a miner's short-term exposure to
10 f/cc over a 15-minute sampling period for metal and nonmetal miners
and 10 f/cc for a total of one hour in an 8-hour day for miners at
surface work areas of coal mines. We are proposing to adopt OSHA's 8-
hour TWA, full-shift exposure limit of 0.1 f/cc and their 30-minute
excursion limit of 1.0 f/cc for the mining industry. These actions
would reduce by almost 20-fold the risk of asbestos-related deaths from
a lifetime exposure at MSHA's existing permissible exposure limits. The
proposed exposure limits, however, were based on feasibility and would
not completely eliminate the risk. We believe that the proposed
excursion limit would help reduce the residual risk from long-term
exposure at the 0.1 f/cc 8-hour TWA, full-shift exposure limit.
As noted by the OIG, the continued occurrence of asbestos-related
diseases and deaths among miners emphasizes the need to reduce asbestos
exposures. MSHA's recent field sampling data (2000 through 2003) show
that 2 percent of the total number of MSHA's samples exceed OSHA's PEL
of 0.1 f/cc based on TEM analysis. This same data indicate that 10
percent of the samples exceed OSHA's PEL of 0.1 f/cc based on PCM.
MSHA's asbestos ANPRM requested information to help us determine
appropriate exposure limits for the mining industry, considering the
health risk and technological and economic feasibility. We specifically
asked what would be an appropriate agency action considering these
levels, and if OSHA's asbestos exposure limits would afford sufficient
protection to miners. Most commenters supported our adoption of OSHA's
exposure limits.
As discussed below in section VII.C of this preamble, we are
proposing to incorporate the generic elements of PCM analytical methods
for asbestos exposure monitoring by referencing Appendix A of OSHA's
asbestos standard (29 CFR 1910.1001). Appendix A lists both NIOSH 7400
and OSHA ID 160 as examples of analytical methods that meet the
equivalency criteria in OSHA's asbestos standard. The evaluation or
inclusion of other protocols that deviate from the criteria for
counting fibers in our existing standards is beyond the scope of this
rulemaking.
1. Sections 56/57.5001(b)(2)(i) and 71.702(b)(1): 8-Hour Time-Weighted
Average (TWA), Full-Shift Exposure Limit
Our sampling results indicate that there is not widespread
overexposure to asbestos in the mining industry. Recognizing this low
exposure, many industry commenters generally supported reducing the PEL
for asbestos to the OSHA level of 0.1 f/cc, if MSHA also ensured that
the analytical method only counted asbestos fibers. Labor
representatives supported reducing the PEL for asbestos to the OSHA
level of 0.1 f/cc and recommended that MSHA propose additional
requirements from the OSHA asbestos standard.
Even though there was general agreement among the commenters to the
ANPRM that MSHA should adopt OSHA's asbestos exposure limits, some
commenters from a community association expressed concern about
asbestos originating at a local mine. They seemed concerned not only
with the health of miners, but also with exposures of people in
relative proximity to the mining operations. They believe that any
level of airborne asbestos is unacceptable.
While we are concerned about the spread of asbestos from mine sites
into the atmosphere, asbestos occurs naturally in many types of soils
and ore bodies. Although comments concerning the asbestos exposure of
those living close to a mining operation fall outside the scope of this
rule, the proposed reduction in the permissible exposure limits may
reduce environmental levels as well.
We are proposing an 8-hour TWA, full-shift exposure limit of 0.1 f/
cc. This limit would significantly reduce the risk of material
impairment of health or functional capacity for miners exposed to
asbestos.
2. Sections 56/57.5001(b)(2)(ii) and 71.702(b)(2): Excursion Limit
As previously discussed, asbestos poses a long-term health risk to
exposed workers. There are no toxicological data identifying a ``dose-
rate'' \73\ health effect from exposure to airborne concentrations of
asbestos. ``Dose-rate'' effect means that a specific dose can cause
different health problems depending on the length of exposure. For
example, asbestos does not seem to have a ``dose-rate'' effect because
exposure to a high concentration over a short time period poses no
greater risk of an adverse health effect than if the worker received
the same dose at a lower concentration over a longer time period. An
excursion limit sets boundaries for peak episodes of exposure that are
not based on toxicological data. We are proposing an excursion limit
for asbestos to help maintain the average airborne concentration below
the full-shift exposure limit. For example, the 8-hour, TWA airborne
asbestos concentration would be 0.06 f/cc for miners exposed to one 30-
minute excursion per day at 1.0 f/cc and 0.13 f/cc for miners exposed
to two 30-minute excursions per day at 1.0 f/cc.
---------------------------------------------------------------------------
\73\ OSHA (51 FR 22709), 1986.
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In the ANPRM, we requested comments on an appropriate level for a
short-term exposure limit (67 FR 15134). We specifically asked whether
adopting the OSHA limit of 1 f/cc over 30 minutes would afford
sufficient protection to miners in light of the health risk and the
technical and economic feasibility of such a limit. Commenters offered
no objections to adopting OSHA's excursion limit for airborne asbestos,
and some agreed that this level is appropriate.
a. OSHA's Short-Term Exposure Limit.
When OSHA issued its 1986 asbestos standard, it decided not to
issue an explicit short-term exposure limit (STEL). OSHA stated the
basis for its decision (51 FR 22709) as follows.
To summarize, OSHA is not promulgating a short-term exposure
limit for asbestos because toxicological and dose-response evidence
fail to show that short-term exposure to asbestos is associated with
an independent or greater adverse health effect than is exposure to
the corresponding 8-hour TWA level; that is, there is no evidence
that exposure to asbestos results in a ``dose-rate'' effect. This is
reflected in OSHA's risk models for lung cancer and mesothelioma,
which associate health risk with cumulative dose. The decision not
to promulgate a short-term exposure limit for asbestos is consistent
with OSHA's recent policy decision described in the Supplemental
Statement of Reasons for the Final Rule for Ethylene Oxide (50 FR
64) in which OSHA established that short-term exposure limits for
toxic substances are not warranted in the absence of health evidence
demonstrating a dose-rate effect.
OSHA's decision not to issue a STEL was challenged in Public
Citizen Health Research Group v. OSHA (796 F.2d 1505), 1986. The U.S.
Court of Appeals for the District of Columbia held that the
Occupational Safety and Health Act compels OSHA to adopt a short-term
limit, if the rulemaking record shows that it would further reduce a
significant health risk and is feasible to implement, regardless of
whether the record supports a ``dose-rate'' effect. Subsequently, OSHA
found that
[[Page 43974]]
compliance with a short-term limit would further reduce a significant
health risk remaining after complying with the 8-hour TWA, full-shift
exposure limit. OSHA also found that the lowest excursion level which
is feasible both to measure and to achieve primarily through
engineering and work practice controls is 1 f/cc measured over 30
minutes. For these reasons, in 1988, OSHA promulgated an asbestos
excursion limit of 1 f/cc over a sampling period of 30 minutes (53 FR
35610).
b. Minimum Detectable Level and Feasibility of Measuring Short-Term
Excursions.
As discussed in OSHA's 1986 asbestos final rule (51 FR 22686), the
key factor in sampling precision is fiber loading. To determine whether
the analytical method described in Appendix A of its asbestos standard
could be used to analyze short-term samples, OSHA calculated the lowest
reliable limit of quantification using the following formula:
C = [(f/[(n)(Af)])(Ac)]/[(V)(1,000)]
where:
C is fiber concentration (in f/cc of air);
f is the total fiber count;
n is the number of microscope fields examined;
Af is the field area (0.00785 mm2) for a properly
calibrated Walton-Beckett graticule;
Ac is the effective area of the filter (in mm2); and
V is the sample volume (liters).
Table VII-1 was generated from the above equation. The table shows
that 1.0 f/cc measured over 30 minutes can be reliably measured when
pumps are used at the higher flow rates of 1.6 Lpm or more, using the
25-mm filters.
Table VII-1.--Relationship of Sampling Method to Measurement of Asbestos
------------------------------------------------------------------------
Lowest level
reliably
Flow rate (Lpm) Sampling time measured (f/
cc) using 25-
mm filters
------------------------------------------------------------------------
2.5............................... 15 minutes.......... 1.05
2.0............................... .................... 1.31
1.6............................... .................... 1.63
1.0............................... .................... 2.61
0.5............................... .................... 5.23
2.5............................... 30 minutes.......... 0.51
2.0............................... .................... 0.65
1.6............................... .................... 0.82
1.0............................... .................... 1.31
0.5............................... .................... 2.61
------------------------------------------------------------------------
We recognize that in some situations, such as low background dust
levels, ower exposures could be measured; however, the risk of
overloading the filter with debris increases when using the higher flow
rates. We can be confident that we are measuring the actual airborne
concentrations of asbestos, within a standard sampling and analytical
error (25 percent), when we use the minimum loading
suggested by the OSHA Reference Method (29 CFR 1910.1001, Appendix A).
The excursion limit of 1.0 f/cc for 30 minutes is the lowest
concentration that we can measure reliably for determining compliance
with the excursion limit.
Some commenters supported MSHA's adoption of OSHA's asbestos
excursion limit of 1.0 f/cc for 30-minutes. Many other commenters
offered no objections, choosing to remain silent on this issue. We have
considered the comments and are proposing an asbestos excursion limit
of 1.0 f/cc over a minimum sampling time of 30 minutes.
C. Sec. Sec. 56/57.5001(b)(3) and 71.702(c): Measurement of Airborne
Fiber Concentrations
We currently require asbestos samples to be analyzed by PCM for the
initial determination of exposure and compliance with the PELs. We are
proposing to retain this requirement for PCM analysis. The proposed
rule would require fiber concentration to be determined by PCM using a
method statistically equivalent to the OSHA Reference Method in OSHA's
asbestos standard (29 CFR 1910.1001, Appendix A).
The OIG recommended that we use TEM for the initial analysis of
samples collected to evaluate a miner's personal exposure to asbestos.
In our 2002 asbestos ANPRM, we requested information to help us
determine the benefits and feasibility of changing our asbestos
analytical method from PCM to TEM for evaluating a miner's exposure to
asbestos. For the reasons discussed in this preamble, we cannot justify
using a TEM analytical method for the initial determination of
compliance with our asbestos PELs.
1. Brief Description and Comparison of Three Analytical Techniques
To ease understanding of the discussion that follows, this section
briefly describes the three analytical techniques that MSHA has used
for analyzing asbestos samples. All three techniques involve counting
fibers. MSHA has used--
Phase contrast microscopy (PCM) on air samples to
determine a miner's exposure for comparison with our permissible
exposure limits (PELs) for asbestos.
Transmission electron microscopy (TEM) on the same air
samples analyzed by PCM when we need to confirm the presence of
asbestos and distinguish asbestos from other fibers in the sample.
Polarized light microscopy (PLM) to analyze bulk samples
collected from an area suspected of having asbestos in the ore or dust,
not for air samples collected to determine a miner's exposure.
Table VII-2 below presents a brief summary of various features of
these three analytical techniques. The values listed are approximate.
Table VII-2.--MSHA's Comparison of Three Analytical Techniques \74\ Used to Analyze Asbestos Samples
----------------------------------------------------------------------------------------------------------------
Criteria PCM TEM PLM
----------------------------------------------------------------------------------------------------------------
Magnification........................ Up to 1,000X; typically Up to 1,000,000X; Up to 1,000X; typically
400-450X. typically 10,000X. 10-45X.
Resolution........................... 0.2 [mu]m.............. 0.001 [mu]m \75\....... 0.2 [mu]m.
Sample Area Examined................. Minimum: 100 fibers & 100 fibers or 4.4 mm2 Scan entire prepared
20 fields; or 100 minimum (0.06-0.4 sample (1 cm2).
fields (0.157-0.785 mm2)*.
mm2).
Additional information............... None................... Crystal structure & Refractive index.
elemental composition.
Microscope cost...................... $1,500-$2,000.......... $200,000-$300,000...... $1,500-$2,000.
Analysis cost/filter................. $10-$15................ $100-$400.............. $10-$15.
Analysis time/filter................. 0.25-0.5 hour.......... 3-4 hours or more...... 0.25-0.5 hour.
[[Page 43975]]
Degree of expertise of analysts...... Requires a moderate Requires a high level Requires a moderate
level of expertise; 40 of expertise and level of expertise; 40
hours training minimum. experience. hours training
minimum.
----------------------------------------------------------------------------------------------------------------
* NIOSH 7402 depends on loading: light-40 fields; medium-40 fields or 100 fibers; heavy-6 fields and 100 fibers.
2. Fiber Identification Using Transmission Electron Microscopy (TEM)
a. Advantages and Disadvantages of TEM Analysis
The transmission electron microscope (TEM), equipped with an energy
dispersive x-ray spectrometer (EDS) and using selected area electron
diffraction (SAED) is generally capable of identifying the mineralogy
of individual asbestos fibers. Even so, TEM does not always have
sufficient precision to make definitive distinctions between closely
related minerals, such as between winchite
[(NaCa)Mg4(Al,Fe3+)Si8O22(OH
)2] and tremolite
[Ca2Mg5Si8O22(OH)2
].\76\ Because electron microscopes provide greater magnification and
greater image clarity, including sharper three-dimensional images than
light microscopes, TEM can detect fibers that are undetectable using
PCM. Routine use of TEM analysis, however, would have some significant
disadvantages.
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\74\ MSHA's summary of its literature reviews and experience.
\75\ Clark, p. 5, 1977.
\76\ Leake et al., 1997.
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Epidemiological data correlating TEM asbestos exposure
levels with asbestos-related diseases is not available for conducting a
new risk assessment.
TEM analysis is time consuming and expensive, requiring
highly skilled personnel for instrument operation and data
interpretation, especially when applied as the primary analytical
method.
Few facilities offer TEM analysis for asbestos air samples
collected in a mining environment.
Another disadvantage of TEM is that it uses an even smaller amount
of sample than is used in PLM or PCM analysis. Asbestos fibers may not
be present in the small portion of sample examined under the electron
microscope, even when it is present in the larger sample examined by
PLM or PCM. Despite its disadvantages, TEM allows us to better identify
asbestos minerals in air samples collected in a mine.
b. Use of TEM to Determine Compliance with MSHA's PELs.
The OIG recommended that MSHA use TEM for its initial analysis to
determine if an asbestos sample is over the PEL. MSHA believes that
analyzing an airborne dust sample from a mine, which might contain
asbestos, requires additional expertise not readily developed through
experience analyzing samples known to contain asbestos. We recognize
that EPA routinely uses TEM for the analysis of air samples collected
for asbestos abatement under the Asbestos Hazard Emergency Response Act
(AHERA) and requires the use of TEM to characterize workers' asbestos
exposures (40 CFR part 763). MSHA currently uses TEM on a limited
basis, when necessary, to verify the presence of asbestos in samples.
These samples often contain few fibers among much dust and a variety of
other interferences.
In the ANPRM, we requested comments on the use of TEM including
cost, availability, comparisons of PCM to TEM, and a possible
relationship of TEM to a PEL. In response to the ANPRM, some commenters
suggested that MSHA use TEM to augment PCM measurements. Overall,
industry commenters did not recommend the use of TEM for the initial
analysis of fiber samples for comparison to the PELs. Commenters did
not dispute additional, confirmatory analysis of samples that show
possible exposure to asbestos in excess of the PELs. NIOSH also did not
believe that TEM should be used for routine monitoring even though they
consider TEM a valuable tool in mineral identification. NIOSH comments
stated the reasons for not using TEM as the primary method for
determining compliance with the PELs as (i) the lack of health risk
data associated with TEM, (ii) the level of expertise required, and
(iii) the high cost.
(i) Lack of Health Risk Data Based on TEM.
OSHA did not use analytical results based on TEM in its original
risk assessment for asbestos. Although attempts have been made,\77\
researchers have not reported a strong, consistent correlation between
PCM and TEM analyses. The relationships that are reported are specific
to the fiber type and environment sampled.\78\ To set a meaningful
permissible exposure limit based on TEM analysis, we must have either--
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\77\ Snyder et al., 1987.
\78\ Verma and Clark, 1995.
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Peer-reviewed epidemiology or toxicology studies relating
TEM analysis and adverse health effects, or
A predictive relationship correlating TEM and PCM for
samples collected in a mining environment.
(ii) Level of Expertise.
One commenter representing an industry association at MSHA's public
hearing in Charlottesville, Virginia (2002) testified that TEM was not
a method for routine monitoring. This commenter also pointed out--
* * *that very few commercial TEM labs are competent to perform
valid analyses of the complicated mineralogical mixtures that you
find in mining and quarrying operations.
Another commenter at the Charlottesville public hearing testified
that TEM is fallible. This commenter said that electron diffraction
patterns for structurally similar minerals can be difficult to
distinguish from one another. Each particle in the sample may be of a
different composition and the analyst cannot assume that every particle
with the same shape is the same mineral.
(iii) High Cost of TEM Analysis.
Several commenters representing an industry association each
commented on the high cost of TEM analysis. One commenter stated that,
because the variability of the measurement increases at the lower
concentrations, when the PEL is lowered it is important to increase the
frequency of monitoring and, therefore, the cost of sample analysis
becomes an issue.
3. Phase Contrast Microscopy (PCM) for the Analysis of Personal
Exposure Samples
The use of PCM for quantitative analysis of samples does not
differentiate between mineral species. There is industry concern that
misidentification of fibers as asbestos can lead to incorrect
conclusions, resulting in unnecessary expenses for mining companies.
PCM counting schemes address the key problem of
[[Page 43976]]
needing to make a relatively fast, cost-effective evaluation of a
situation in a mine so as to protect miners from danger to their
health. PCM maintains the integrity, meaning, and usefulness of the
analytical method for evaluating samples relative to the historic
health data.\79\
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\79\ Wylie et al., 1985.
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a. Discussion of Microscope Properties.
One issue commenters mentioned repeatedly concerning PCM is the
limited resolution and magnification of light microscopes compared to
electron microscopes.
(i) Resolution.
The resolution of the microscope is the smallest separation between
two objects that will allow them to be distinctly visible. The higher
the resolving power of a microscope, the smaller the distance can be
between two particles and have them still appear as two distinct
particles. Resolution is about 0.22 [mu]m using PCM and 0.00025 [mu]m
using TEM. This means that where the analyst sees a single fiber using
PCM, that same analyst might see a number of thinner fibers using TEM.
(ii) Magnification.
The level of magnification is another PCM microscopy issue.
Magnification is the ratio of the size that the object appears under
the microscope to its actual size. PCM analytical methods specify a
magnification of 400 to 450 times (x) the object's actual size. The
magnification using TEM can be 10,000X to 1,000,000X. This means that
the analyst sees a smaller amount of the sample using TEM than when
using PCM.
b. Health Risk Data Based on PCM.
Historically, asbestos samples have been analyzed by mass
(weighing), counting (microscopy), or a qualitative property
(spectroscopy). When recommending an exposure standard for chrysotile
asbestos, the British Occupational Hygiene Society contended \80\ that
the microscopic counting of particles greater than 5 [mu]m in length
would show a relationship with the prevalence of asbestosis similar to
those based on the mass of respirable asbestos. Many scientific papers
have suggested that counting only fibers longer than 5 [mu]m would
minimize variations between microscopic techniques \81\ and improve the
precision of the results.\82\ Nonetheless, this criterion was accepted
as an index of exposure, even though some believed that, due to their
possible health effects, the smaller fibers should not be excluded.\83\
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\80\ Lane et al., 1968.
\81\ ACGIH-AIHA, 1975.
\82\ Wylie, 2000.
\83\ ACGIH-AIHA, 1975; NIOSH, 1972.
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In recommending an asbestos standard in 1972, NIOSH suggested using
the same size criteria that the British adopted. They also recommended
reevaluating these criteria when more definitive information on the
biologic response and precise epidemiologic data were developed. When
exposure data were not obtained using PCM, NIOSH applied a conversion
factor to the non-PCM data to estimate PCM concentrations for use as
the basis of a recommended permissible occupational exposure level.
A number of commenters testified (Charlottesville, 2002) that PCM
methodology includes more than asbestos when determining fiber
concentration in air. The commenters suggested that the lower risk seen
in epidemiological studies relating PCM to adverse health outcomes in
miners was possibly due to the background material inherent in air
samples taken in a mining environment. They speculated that the
background material had been counted and included in the estimated
asbestos concentrations. This may have overestimated exposures and
resulted in a dilution of the dose-response relationship presented in
scientific publications.
c. Subjectivity and Consistency of Counting Asbestos Fibers
The fiber count obtained using the PCM method is dependent on
several factors. These factors include the analyst's interpretation of
the counting rules, the analyst's visual acuity, the optical
performance of the microscope, and the optical properties of the
prepared sample.\84\ Much of the variability is attributed to the
ability of the analyst to observe and size fibers.
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\84\ Rooker et al., 1982.
---------------------------------------------------------------------------
The American Industrial Hygiene Association (AIHA) Proficiency
Analytical Testing Program (PAT), operated in cooperation with NIOSH,
maintains a database for historical data relating to asbestos fiber
counting using PCM. This program, begun in 1972, provides statistical
evaluation of laboratory performance on test samples. At its inception
in 1968, the method used by laboratories participating in this program
was the U.S. Public Health Service method (USPHS 68).\85\ The counting
rules for this method were vague and required little microscope
standardization.
---------------------------------------------------------------------------
\85\ Schlecht and Shulman, 1995.
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Work has been done to modify the PCM method to address these
consistency issues.\86\ Commenters to our asbestos ANPRM suggested that
we consider thoracic sampling to minimize interference from large
particles. Testimony at MSHA's public hearing in Charlottesville (2002)
presented a counting technique based on the typical characteristics of
asbestos in air. Another commenter stated that several approaches have
been tried to remove non-asbestos minerals from samples, such as low
temperature ashing or dissolution, but they would not be useful for
mining samples. Another commenter suggested using a higher aspect ratio
to increase the probability that the structures counted are fibers.
Several commenters suggested the development of a new analytical
method.
---------------------------------------------------------------------------
\86\ Pang, 2000; Harper and Bartolucci, 2003.
---------------------------------------------------------------------------
Overall, commenters recognized that it takes far less time to
develop expertise in counting fibers using PCM than in developing
expertise using TEM. NIOSH has developed a 40-hour training course for
teaching analysts to count asbestos fibers.
The availability of analyst training courses, and the formation of
accreditation bodies requiring laboratory quality assurance programs,
helps minimize the variations in measurements between and within
laboratories. Accreditation bodies require laboratories to use
standardized analytical methods. AIHA also has the Asbestos Analyst
Registry that specifies criteria for competence, education, and
performance for analysts. In addition to these programs, our
incorporation of OSHA's Appendix A would help minimize the subjectivity
and increase consistency of measuring airborne asbestos concentrations
by specifying core elements of acceptable analytical PCM methods.
4. MSHA's Incorporation of OSHA's Appendix A
Commenters generally supported the use of PCM for the initial
analysis of fiber samples for determining compliance with the PELs.
Commenters' major concerns focused on fiber counting procedures.
Commenters suggested that differential counting techniques be developed
to analyze air samples for asbestos using PCM and taking into
consideration the fiber morphology and the distributions or populations
of distinct fiber groups with characteristic dimensions. Other
commenters stated that particle characteristics could not reliably be
used to differentiate fibers from cleavage fragments when examining
relatively small numbers of fibers.
[[Page 43977]]
In this rulemaking, we propose to continue to use PCM to determine
asbestos concentrations. PCM was used in the development of past
exposure assessments and risk estimates and is relatively quick and
cost-effective. Thus, with respect to analytical methods, this proposed
rule is not substantively different than our existing standards. We
also have added language to allow for our acceptance of other asbestos
analytical methods that are at least as effective in identifying
potential overexposures.
The OSHA Reference Method, mandatory Appendix A to the OSHA
asbestos standard (29 CFR 1910.1001), specifies the elements of an
acceptable analytical method for asbestos and the quality control
procedures that laboratories performing the analysis must implement.
Paragraph (d)(6)(iii) of OSHA's asbestos standard (29 CFR 1910.1001)
requires employers, who must monitor for asbestos exposure, to use a
method for collecting and analyzing samples that is equivalent to the
OSHA Reference Method (ORM), and also describes the criteria for
equivalency. For the purpose of this proposed rule, MSHA would consider
a method equivalent if it meets the following criteria:
[from 29 CFR 1910.1001(d)(6)(iii)]
(A) Replicate exposure data used to establish equivalency are
collected in side-by-side field and laboratory comparisons; and
(B) The comparison indicates that 90% of the samples collected
in the range 0.5 to 2.0 times the permissible limit have an accuracy
range of plus or minus 25 percent of the ORM results at a 95%
confidence level as demonstrated by a statistically valid protocol;
and
(C) The equivalent method is documented and the results of the
comparison testing are maintained.
Appendix A of OSHA's asbestos standard lists NIOSH 7400 and OSHA
ID-160 as examples of analytical methods that meet these criteria. In
addition, there are other PCM analytical methods for asbestos:
The Asbestos International Association (AIA), AIA RTM1,
``Airborne Asbestos Fiber Concentrations at Workplaces by Light
Microscopy (Membrane Filter Method).''
The International Organization for Standardization (ISO),
ISO 8672:1993(E), ``Air quality--Determination of the number
concentration of airborne inorganic fibres by phase contrast
microscopy--Membrane filter method.''
MSHA recognizes that there are advantages and disadvantages of
various PCM analytical methods, especially as they relate to the
processing of samples collected in a mining environment. For example,
the ASTM dilution method (D 5755-95) for overloaded samples has allowed
laboratories to recover useable results from airborne exposure samples
that, in the past, had been invalidated. We note that both ASTM and the
National Stone Sand and Gravel Association are pursuing the development
of an analytical method for asbestos in mining samples. We would
consider analytical methods that afford a better measurement
alternative as they become available. We believe that allowing
statistically equivalent analytical methods would remove barriers to
innovation and technological advancement.
We specifically request information on additional criteria for
equivalency for use in evaluating alternative analytical methods for
the determination of asbestos in air samples collected in a mining
environment. We also request information about analytical methods for
which equivalency has already been demonstrated.
5. MSHA Asbestos Control Program
In the ANPRM, we asked whether or not our current sampling methods
met the needs of the mining community and how mineral dust
interferences could be removed from mining samples. The ANPRM also
asked for comments on other ways to reduce miners' exposures, such as
increased awareness of potential asbestos hazards at the mine site and
the provision of adequate protection. We also asked for suggestions on
what educational and technical assistance MSHA could provide and what
other factors, circumstances, or measures we should consider when
engineering controls are unable to reduce asbestos exposure below the
PEL.
We received some criticism concerning our sampling and analysis
procedures from a few commenters who believed that we should develop
specific test procedures for the sampling and analysis of bulk samples
for the mining environment, as well as specific air sampling procedures
(including pump flow rates, cassette types, and filter matrix). They
also believed that we should improve our reports by including
inspection field notes, location, purpose, and procedure followed, as
well as descriptions of the accuracy, meaning, and limitations of the
results. In its comments to the ANPRM, one trade association
recommended that we maintain our current, established asbestos
monitoring protocols with emphasis on full-shift monitoring for
comparison to the PEL. Another trade association stated that our
current field sampling methods are adequate for most mines and
quarries, particularly when no significant amount of asbestos is found.
They also suggested that respirable dust sampling using a cyclone might
be a means to remove interfering dust from the sample. NIOSH suggested
that we could use thoracic samplers, but that studies performed on
their use did not include mines and further positive test results would
be needed before they could promote their use in mining.
We believe that our current sampling procedures are adequate and we
are proposing to continue using them. Our current procedures, which we
updated in 2000, specify using several, typically three, 25-mm filter-
cassettes in series to collect a full-shift sample. Depending on the
amount of visible dust in the air, these procedures allow the setting
of pump flow rates to optimize fiber loading and minimize or eliminate
mixed dust overload. We are not considering the use of a cyclone to
capture respirable dust because research indicates that larger durable
fibers also could cause adverse health effects.
6. Bulk Sample Analysis Using Polarized Light Microscopy (PLM)
In the ANPRM, we asked what method was most appropriate for MSHA to
use to analyze bulk samples for asbestos in the mining industry. The
presence of asbestos in a bulk sample does not mean that it poses a
hazard. The asbestos must become airborne and be respirable, or
contaminate food or water, to pose a health hazard to miners. The
detection of asbestos in a bulk sample serves to alert mine operators,
miners, and MSHA to the possible presence of asbestos. One mining
association stated that air monitoring is not the preferred scheme to
screen for possible asbestos exposure. They believe, and we agree, that
knowledge of the geology of asbestos and identification of asbestos in
bulk samples may be a useful step in determining whether asbestos is
present in the ore or host rock.
We are not proposing to use bulk samples to determine asbestos
exposures in mining. We are requesting comments on whether MSHA's use
of routine, periodic bulk sampling would be useful in determining
whether or not we should take personal exposure air samples to evaluate
miners' exposures to asbestos at mines suspected of having naturally
occurring asbestos.
MSHA also uses the detection of asbestos in bulk samples as a
trigger for its compliance assistance activities. We have trained MSHA
inspectors on ways to identify asbestos in the ore and
[[Page 43978]]
surrounding rock formations at mines and to pass this information on to
mine operators. Analysis of samples of accumulated settled dust from a
mill or construction debris can identify areas or activities that would
require special precautions. After considering the results of the bulk
sample analysis, together with its strengths and weaknesses, the mine
operator, miners, and MSHA can take appropriate action to reduce the
risk of exposure, which would help reduce the risk of asbestos-related
diseases among miners.
Analysis of bulk samples is usually performed using PLM. Commenters
to the ANPRM expressed concern that the PLM analysis may not detect
asbestos when it is present. A particle must be at least 0.5 [mu]m in
diameter to refract light and many asbestos fibers are too thin to
refract light. Asbestos may be a small percentage of the parent
material or not uniformly dispersed in the sample and, therefore, may
not be seen in the small portion of sample that is examined under the
microscope. In addition, the method could detect asbestos erroneously
because a nonasbestiform mineral could have a refractive index similar
to one of the asbestos minerals. Another problem with identifying
asbestos using PLM is that all varieties of a mineral show the same
refractive index. For example, even an experienced analyst might not
differentiate between the asbestiform and nonasbestiform varieties of a
mineral based on their refractive indices.
Although a trained individual may be able to identify bulk asbestos
by its appearance and physical properties, the identification can be
more difficult when the asbestos is dispersed in a dust sample or is
present in low concentration in a rock. A commenter at MSHA's hearing
in Charlottesville (2002) testified that none of the existing methods
for bulk sample analysis (EPA, NIOSH, ASTM) were designed for complex
mine environments.
D. Discussion of Asbestos Take-Home Contamination
This proposed rule does not include standards to address asbestos
take-home contamination. We recognize the important role of take-home
exposures in contributing to asbestos disease of workers and their
family members. We believe that a combination of enforcement and
compliance assistance activities, together with increased education and
training of mine inspectors, mine operators, and miners, coupled with
the lowering of the PELs, would be effective in preventing asbestos
take-home contamination. Mine operators are encouraged to measure the
potential for take-home contamination and provide protective measures
where necessary to minimize secondary take-home exposures.
1. MSHA's Request for Information
MSHA's ANPRM for measuring and controlling asbestos exposures at
mines included requests for information and data to help us evaluate
what we could do to eliminate or minimize take-home contamination. We
asked how and/or should MSHA be addressing take-home contamination. We
also asked about provisions for the special needs of small mine
operators and what assistance (e.g., step-by-step instructions, model
programs, certification of private programs) we could provide. We also
requested information on the types of protective clothing miners
currently use when working in areas where asbestos may be present, and
the types of preventive measures currently in use when miners leave the
area, to prevent the spread of asbestos exposure.
2. Commenters' Responses to the Take-Home Contamination Issue in MSHA's
Asbestos ANPRM
Commenters expressed concern that we would apply the requirements
in OSHA's and EPA's standards to trace levels of fibrous mineral
exposures at mines, pits, and quarries. Many industry commenters urged
MSHA to limit protective measures for take-home contamination to those
activities involving known asbestos and asbestos-containing products,
such as those regulated by OSHA and EPA. For example, commenters
suggested that MSHA adopt appropriate provisions from the OSHA asbestos
standard for construction workers, for asbestos abatement workers, and
for those miners whose exposures exceed MSHA's PEL.
Commenters cautioned MSHA to be mindful of the definitions of
asbestos when analyzing samples to determine compliance. They also
urged MSHA to acknowledge the presence of interferences in mining
samples, as well as the differences between nonasbestiform amphiboles
and their asbestos analogues. Some commenters cautioned that, unless
MSHA constructed the provisions for reducing take-home contamination
carefully, the consequences for the mining industry might be costly
with little or no benefit to miners.
NIOSH encouraged MSHA to adopt measures included in its 1995 Report
to Congress on their Workers' Home Contamination Study Conducted under
the Workers' Family Protection Act. Labor participants also supported
protective measures, such as personal protective equipment and showers
before leaving work, to prevent take-home contamination.
3. MSHA's Considerations in Making Its Decision To Use Non-Regulatory
Methods To Address the Hazard From Take-Home Contamination
In determining an appropriate proposed action for preventing take-
home contamination, we considered the comments to the ANPRM, OSHA's and
EPA's requirements, and the recommendations of NIOSH and the OIG. We
based our determination to propose to address asbestos take-home
contamination through non-regulatory measures on the following factors:
Existing standards requiring engineering controls for
airborne contaminants, respiratory protection, personal protective
clothing, hazard communication, and housekeeping, together with a lower
PEL, would provide sufficient enforcement authority to assure that mine
operators take adequate measures when necessary to prevent asbestos
take-home contamination.
There are no asbestos mines or mills currently operating
in this country and different ore bodies of the same commodity, such as
vermiculite mining, are not consistent in the presence, amount, or
dispersion of asbestiform minerals. Currently, asbestos exposures in
mining are low. As discussed in section V.D.2 of this preamble, only
two of the 123 mines sampled for asbestos in the ore show personal
asbestos exposures exceeding 0.1 f/cc. This is less than 2 percent of
the sampled mines.
Some mines with asbestos minerals in the ore or host rock
have implemented protective measures voluntarily. MSHA experience in
the recent past indicates that mine operators and mining companies are
increasingly aware of asbestos hazards and have been willing to
cooperate with MSHA to eliminate this hazard.
The measures taken to prevent take-home contamination are
varied, and mine operators would have the freedom to eliminate this
hazard in a manner based on site-specific exposure measurements and the
nature of the asbestos exposures at the mine. For example, mine
operators could minimize or prevent asbestos take-home contamination by
providing disposable coveralls or on-site shower facilities coupled
with clothing changes.
[[Page 43979]]
4. MSHA's Activities for Eliminating the Risk of Asbestos Take-Home
Contamination
We believe that mine operators and miners would take action to
eliminate any possible recurrence of a disaster, such as that in Libby,
Montana, if they understand the hazards and ways to minimize the risk.
To that end, we are placing special emphasis on the potential hazard
from asbestos take-home contamination in our enforcement, compliance
assistance, and educational activities as follows.
a. Enforcement Activities.
Enforce the new, lower PELs when they become effective.
Continue enforcement of standards applicable to providing
special protective equipment and clothing whenever environmental
hazards are encountered in a manner capable of causing injury or
impairment, e.g., Sec. 56.15006.
Ensure that mine operators provide miners, who are at risk
of being exposed, with information about the signs, symptoms, and risk
for developing asbestos-related illness as required by the hazard
communication standard.
b. Compliance Assistance.
Continue to monitor targeted mines for the presence of
asbestos.
Encourage mine operators to comply with OSHA's asbestos
standard, or hire professionals skilled and certified in working with
asbestos, when they engage in construction, demolition, or renovation
activities at the mine.
Issue an updated Program Information Bulletin (PIB) on
asbestos to include a greater emphasis on protective measures to reduce
take-home contamination. We expect distribution this year.
c. Educational Activities.
Continue outreach to mine operators through training
courses, informational materials, and topical local meetings.
Issue an updated Health Hazard Information Card for miners
this year to increase miners' awareness of the hazards of take-home
contamination from asbestos or other asbestiform minerals and to
suggest measures that the miners can take to prevent it.
Continue specialized asbestos hazard and sampling training
for mine inspectors.
E. Section 71.701(c) and (d): Sampling; General Requirements
[Controlling Asbestos Exposures in Coal Mines]
For surface coal mines and surface worksites at underground coal
mines, we are proposing to add a reference to Sec. 71.702 (the
asbestos standard for coal mines) in paragraphs (c) and (d) of Sec.
71.701, which contain the requirements for controls and sampling. The
existing language in Sec. 71.701(c) and (d) references the Threshold
Limit Values (TLVs[supreg]) and excursion limits in Sec. 71.700, but
not the asbestos exposure limits in Sec. 71.702. MSHA regulations
currently require mine operators to control miners' exposures to
airborne contaminants and to sample for airborne contaminants, as
necessary, to determine when and where such controls may be needed. In
developing this proposed rule, we determined that Sec. 71.701 was
unclear as to its applicability to asbestos exposures. This proposed
rule would clarify our intent that coal mine operators control miners'
exposures to asbestos.
VIII. Regulatory Analyses
A. Executive Order (E.O.) 12866
In our ANPRM on asbestos exposure, we specifically requested
information, data, and comments on the costs and benefits of an
asbestos rule, including what engineering controls and personal
protective equipment are being used to protect miners from exposure to
asbestos and to prevent take-home contamination. Considering the public
comments, and MSHA data and experience, we assessed both the costs and
benefits of this proposed rule in accordance with Executive Order
12866. The following sections summarize the analysis of benefits and
costs presented in the Preliminary Regulatory Economic Analysis (PREA)
for this proposed rule. The PREA contains a full disclosure of our
methodology and the basis for our estimates.
1. Discussion of Benefits
The benefits of a rulemaking addressing measurement and control of
asbestos would be the reduction or elimination of diseases arising from
exposure to asbestos. Exposure to airborne asbestos can cause the
development of lung cancer, mesothelioma, gastrointestinal cancer, and
asbestosis. Other associated adverse health effects include cancers of
the larynx, pharynx, and kidneys. A person with an asbestos-related
disease suffers material impairment of health or functional capacity.
a. Summary of Benefits.
We estimate that between 1 and 19 deaths could be avoided during
the next 65 years by lowering the 8-hour TWA, full-shift exposure limit
from 2.0 f/cc to 0.1 f/cc. This equates to a reduction of between 9 and
84 percent of occupationally related deaths caused by asbestos
exposures. Additional deaths would be avoided by decreasing miners'
exposures to short-term bursts of airborne asbestos undetectable by the
proposed 8-hour TWA, full-shift exposure limit. We estimate that
lowering the excursion limit from 10 f/cc over 15 minutes to 1 f/cc
over 30 minutes would reduce the risk of death from lung cancer,
mesothelioma, or gastrointestinal cancer by 1 additional avoidable
death for every 1,000 miners exposed to asbestos at the proposed PELs.
We are aware that lowering our PELs would not completely eliminate
the risk of asbestos-related material impairment of health or
functional capacity. We expect some additional risk reduction from mine
operators' management directives to avoid disturbing asbestos on mine
property.
b. Calculation of Deaths Avoided.
The benefits resulting from the lowered PELs depend on several
factors including--
Existing and projected exposure levels,
Age of the miner at first exposure,
Number of workers exposed, and
Risk associated with each exposure level.
We estimate the number of miners currently exposed and their level
of exposure from personal exposure information gathered during our
inspections between January 2000 and December 2003. These data are
available on our Web site at http://www.msha.gov. Section V of this
preamble contains the characterization and assessment of exposures in
mining.
Laboratory results indicate that exposure concentrations are
unevenly distributed across mines and miners. We use four fiber
concentration levels to estimate the risk to miners. The break points
for these exposure levels are the proposed and existing exposure
limits. Observations show that 90 percent of the sampling results are
below 0.1 f/cc.
To estimate the expected number of asbestos-related deaths, we
applied OSHA's linear, no-threshold, dose-response risk assessment
model to our existing and proposed PELs. The upper exposure limit is 10
f/cc because the range of information derived from the epidemiological
studies used to determine the dose-response relationship in OSHA's
quantitative risk assessment does not include higher levels. The
expected reduction of deaths resulting from lowering the PELs would
[[Page 43980]]
be the differences between the expected deaths at each exposure
level.\87\
---------------------------------------------------------------------------
\87\ Nicholson, 1983; JRB Associates, 1983; OSHA (51 FR 22612),
1986; OSHA (53 FR 35609), 1988; OSHA (59 FR 40964), 1994.
---------------------------------------------------------------------------
OSHA estimated cancer mortality for workers exposed to asbestos and
published these data in their 1986 final rule (51 FR 22644). We discuss
OSHA's asbestos risk assessment in section VI of this preamble and have
reproduced OSHA's mortality data in Table VI-4.
c. Benefit of the Proposed 0.1 f/cc 8-hour TWA, Full-Shift Exposure
Limit.
The current deaths from lung cancer, mesotheliomas,
gastrointestinal cancer, and asbestosis are the result of past
exposures to much higher air concentrations of asbestos than those
found in mines today. The risks of these diseases still exist, however,
and these risks are significant for miners exposed to lower air
concentrations of asbestos. Most diseases resulting from a current
asbestos exposure may not become evident for another 20 to 30 years.
Most likely, the full benefits will occur over a 65-year period
following implementation of the lower PELs. The rate at which the
incidence of the cancers decreases depends on several factors
including--
Latency of onset of cancer,
Attrition of the mining workforce,
Changing rates of competing causes of death,
Dynamics of other risk factors,
Changes in life expectancy, and
Advances in cancer treatments.
It is not possible to quantify accurately the complete dynamics of this
process.
Supplemental examination of MSHA's personal exposure samples using
TEM analysis indicates that not all fibers counted by PCM are the
currently regulated asbestos minerals. This is especially true for
operations mining and processing wollastonite. We distinguish between
different mineralogical fibers using TEM and combine this supplemental
information with PCM information to calculate our lower estimate of
benefits.
We estimate that there would be from 0.5 to 13.1 lung cancer deaths
avoided, 0.2 to 4.4 mesothelioma deaths avoided, and 0.1 to 1.3
gastrointestinal cancer deaths avoided. The total number of cancer
deaths avoided by this rule would be the sum of cancer deaths avoided
at all the mines included in the exposure data, that is, the mines we
have sampled. Based on the best available information, we expect a
reduction of between 1 and 19 deaths avoided due to lowering the 8-hour
TWA PEL to 0.1 f/cc.
d. Benefits of the Proposed 1.0 f/cc Excursion Limit.
We are proposing an asbestos excursion limit of 1.0 f/cc as
measured over a 30-minute period for metal and nonmetal miners and coal
miners working at surface work areas. We intend that the excursion
limit protect miners from the adverse health risks associated with
brief fiber-releasing episodes. We anticipate that some mining
operations will be subject to brief fiber-releasing episodes even after
lowering airborne asbestos concentrations to the 8-hour TWA, full-shift
exposure limit. We have insufficient data, however, to obtain a
meaningful estimate of the frequency of these episodes, the actual
exposure concentrations, or the numbers of miners exposed. Miners may
encounter brief fiber-releasing episodes from exposure to commercial
asbestos in asbestos-containing building materials (ACBM) or as settled
dust containing asbestos; while working on equipment that may have
asbestos-containing parts; and while drilling, dozing, blasting, or
roof bolting in areas of naturally occurring asbestos.
Because we have little information from short-term exposure
measurements, we estimate the benefit of an excursion limit from the
difference in concentration between the 8-hour TWA, full-shift exposure
limit (0.1 f/cc) and the excursion limit averaged over the full shift
[(1 f/cc)/(16 30-minute periods) = 0.063 f/cc]. The lifetime risk
associated with an exposure to 0.1 f/cc from either of the three types
of cancer is 0.00336, if first exposed at age 25 and exposure continues
every work day at that level for a duration of 45 years. The risk
associated with exposure to 0.063 f/cc using the same age and duration
of exposure is 0.00212. The difference in lifetime risk is 0.00124.
This risk equates to 1.24 additional deaths avoided for every 1,000
miners exposed to asbestos at a concentration afforded by the proposed
excursion limit.
e. Further Consideration of Benefits.
We believe that the pressure of public scrutiny and government
intervention has prompted mine operators to take precautionary measures
to limit miners' exposures to asbestos. If public pressures were to
subside, and we did not have a regulation limiting exposures to 0.1 f/
cc over an 8-hour shift, we would not have a means to enforce the same
level of protection provided in other industries.
Enforcement of the lower PELs together with the direct support from
the federal government in education, identification, and elimination of
the asbestos hazard would increase awareness and attention to the
presence of asbestos on mine property. These activities also would help
focus efforts on preventing exposures, thus providing miners with added
health benefits. As seen in Chart VIII-1, mining operations with ore
containing naturally occurring asbestos seem to have reduced miners'
exposures, perhaps due to their awareness of the lower exposure limits
OSHA promulgated in 1986.\88\
---------------------------------------------------------------------------
\88\ NIOSH WoRLD pp. 16-17 and 19-23, 2003.
\89\ NIOSH WoRLD, 2003.
---------------------------------------------------------------------------
[[Page 43981]]
[GRAPHIC] [TIFF OMITTED] TP29JY05.005
The estimates of the cancer deaths avoided by reducing the PELs
understate the total amount of benefit gained from this rule. These
benefits do not include the reduced incidence of asbestosis-related
disabilities. Asbestosis cases often lead to tremendous societal costs
in terms of health care utilization, loss of worker productivity, and a
decrease in the quality of life of the affected individual. Similarly,
MSHA's analysis does not quantify benefits among groups incidentally
exposed, such as miners' family members. We note that several published
articles document and discuss the health effects resulting from
exposure to asbestos incident to living with a miner.\90\
---------------------------------------------------------------------------
\90\ NIOSH Publication No. 2002-113, May 2002.
---------------------------------------------------------------------------
This analysis overstates health benefits to the extent that we do
not account for differential risks posed by different types of fibers
as identified by PCM, and differences in the cancer mortality risk for
asbestos-exposed workers who smoke and those who do not.
2. Discussion of Costs
The proposed rule would result in total yearly costs of about
$136,100. The cost would be about $91,500 per year for metal and
nonmetal mines and about $44,600 per year for coal mines. These costs
represent less than 0.001 percent of the yearly revenues of $38.0
billion for the metal and nonmetal mining industry and $10.1 billion
for the surface coal mining industry.
Table VIII-1 presents our estimate of the total yearly compliance
costs by compliance strategy and mine size. The total costs reported
are projected costs, in 2002 dollars, based on our knowledge,
experience, and available information.
Table VIII-1.--Summary of Yearly Compliance Costs
----------------------------------------------------------------------------------------------------------------
Compliance strategy
---------------------------------------------------------------- Total for
Metal and nonmetal mine size Removal of metal and
Selective Wet methods Mill introduced nonmetal mines
mining ventilation asbetos
----------------------------------------------------------------------------------------------------------------
Small (<20)..................... $1,058 $1,235 $747 $1,750 $4,790
Large (20-500).................. 4,922 8,614 12,916 21,000 47,452
Large (>500).................... 1,641 2,871 19,001 15,750 39,264
-----------------
Total....................... 7,622 12,721 32,664 38,500 91,506
----------------------------------------------------------------------------------------------------------------
Compliance strategy
----------------------------------------------------------------
Coal mine size Removal of Total for coal
Selective Wet methods Mill introduced mines
mining ventilation asbetos
----------------------------------------------------------------------------------------------------------------
Small (<20)..................... .............. .............. .............. $875 $875
Large (20-500).................. .............. .............. .............. 12,250 12,250
Large (>500).................... .............. .............. .............. 31,500 31,500
-----------------
[[Page 43982]]
Total....................... .............. .............. .............. 44,625 44,625
----------------------------------------------------------------------------------------------------------------
B. Feasibility
MSHA has concluded that the requirements of this proposed rule
would be both technologically and economically feasible. This proposed
rule is not a technology-forcing standard and does not involve
activities on the frontiers of scientific knowledge. All devices that
would be required by the proposed rule are already available in the
marketplace and have been used in either the United States or the
international mining community. We have concluded, therefore, that this
proposed rule is technologically feasible.
As previously estimated, the mining industry would incur costs of
about $136,100 yearly to comply with this proposed rule. These
compliance costs represent well less than 0.001 percent of the yearly
revenues of the mines covered by this rule, thus providing convincing
evidence that the proposed rule is economically feasible.
C. Alternatives Considered
In our discussion of PELs in section VII.B of this preamble, we
recognize that there is a remaining residual risk of adverse health
effects for miners exposed at the proposed asbestos 8-hour TWA PEL. We
considered proposing a lower PEL as a regulatory alternative to further
reduce the risk of adverse health effects from a working lifetime of
exposure. Assuming 0.05 f/cc, for example, and interpolating the data
from OSHA's risk assessment summarized in Table VI-4 of this preamble,
there would be about 1.68 cancer deaths per 1,000 miners exposed to
asbestos at 0.05 f/cc for 45 years. The 1.68 cancer mortality rate is
50 percent less than the rate of 3.36 cancer deaths per 1,000 exposed
miners calculated for the proposed 0.1 f/cc PEL; and about 97 percent
less than we estimate for our existing standard (64.12 cancer deaths
per 1,000 exposed miners). We also project that reducing miner's
exposure to an 8-hour TWA of 0.05 f/cc would reduce the expected cases
of asbestosis to about 50 percent less than at the proposed 8-hour TWA
PEL.
About 85 percent of the 123 sampled mines are already well in
compliance with the 0.1 f/cc proposed PEL. We believe that,
theoretically, almost all of the mining industry could be in compliance
with a lower alternative PEL (0.05 f/cc 8-hour TWA). However, we cannot
enforce an 8-hour TWA limit below 0.1 f/cc. The diversity of airborne
particles prevalent in mining environments can interfere with sample
analysis. Our existing standardized sampling techniques minimize
interferences, but also impose limitations of accuracy below
concentrations of 0.1 f/cc. We address these limitations in more detail
in Chapter III of the PREA that accompanies this proposed rule. These
accuracy issues make it infeasible for us to enforce a concentration
lower than 0.1 f/cc airborne asbestos.
Although TEM provides greater characterization of asbestos fibers
than PCM methodology, there is no predictable relationship between PCM
and TEM measures of exposure using either method alone. We do not know
of a risk assessment correlating TEM measures of exposure with adverse
health effects. TEM measurements, therefore, cannot be used as the
basis for an occupational exposure limit at this time. Additionally,
TEM is much more expensive and time consuming than PCM. If we were to
analyze each of the 2,184 personal exposure filters (collected by us to
determine full-shift asbestos exposures from 2000 through 2003) using
TEM, rather than PCM, it would cost us about $186,000 to $852,000 more.
The mine operator's costs would increase in so far as the operator
would do comparable sampling. We expect the operator to sample to
determine whether control measures are needed, what controls might be
needed, and the effectiveness of controls when implemented. A number of
commenters supported our continued use of PCM for the initial analysis
of asbestos samples.
We conclude that it is not feasible to regulate the mining industry
below the proposed limit at this time. We welcome comments on the
exposure limit proposed and the rationale used for choosing it over the
alternative discussed above.
D. Regulatory Flexibility Analysis (RFA) and Small Business Regulatory
Enforcement Fairness Act (SBREFA)
Based on our data, our experience, and information submitted to the
record, we determined, and here certify, that this proposed rule would
not have a significant economic impact on a substantial number of small
entities. The PREA for this proposed rule (RIN: 1219-AB24), Measuring
and Controlling Asbestos Exposure, contains the factual basis for this
certification as well as complete details about data, equations, and
methods used to calculate the costs and quantified benefits. We have
placed the PREA in the rulemaking docket and posted it on MSHA's Web
site at http://www.msha.gov.
E. Other Regulatory Considerations
1. The National Environmental Policy Act of 1969 (NEPA)
We have reviewed this proposed rule in accordance with the
requirements of NEPA (42 U.S.C. 4321 et seq.), the regulations of the
Council on Environmental Quality (40 CFR 1500), and the Department of
Labor's NEPA procedures (29 CFR 11) and have assessed its environmental
impacts. We found that this proposed rule would have no significant
impact on air, water, or soil quality; plant or animal life; the use of
land; or other aspects of the human environment.
2. Paperwork Reduction Act of 1995
This proposed rule contains no information collection or
recordkeeping requirements. Thus, there are no additional paperwork
burden hours and related costs associated with the proposed rule.
Accordingly, the Paperwork Reduction Act requires no further agency
action or analysis.
3. The Unfunded Mandates Reform Act of 1995
This proposed rule does not include any Federal mandate that may
result in increased expenditures by State, local, or tribal
governments; nor would it significantly or uniquely affect small
governments. It would not increase private sector expenditures by more
than $100 million annually. Accordingly, the Unfunded Mandates Reform
Act requires no further agency action or analysis.
[[Page 43983]]
4. Treasury and General Government Appropriations Act of 1999, (Section
654: Assessment of Impact of Federal Regulations and Policies on
Families)
This proposed rule would have no affect on family well-being or
stability, marital commitment, parental rights or authority, or income
or poverty of families and children. Accordingly, the Treasury and
General Government Appropriations Act requires no further agency
action, analysis, or assessment.
5. Executive Order 12630: Government Actions and Interference With
Constitutionally Protected Property Rights
This proposed rule would not implement a policy with takings
implications. Accordingly, Executive Order 12630 requires no further
agency action or analysis.
6. Executive Order 12988: Civil Justice Reform
We have drafted and reviewed this proposed rule in accordance with
Executive Order 12988. We wrote this proposed rule to provide a clear
legal standard for affected conduct and carefully reviewed it to
eliminate drafting errors and ambiguities, thus minimizing litigation
and undue burden on the Federal court system. MSHA has determined that
this proposed rule would meet the applicable standards in section 3 of
Executive Order 12988.
7. Executive Order 13045: Protection of Children From Environmental
Health Risks and Safety Risks
This proposed rule would have no adverse impact on children. This
proposed asbestos standard might benefit children by reducing
occupational exposure limits, thus reducing their risk of disease from
take-home contamination. Accordingly, Executive Order 13045 requires no
further agency action or analysis.
8. Executive Order 13132: Federalism
This proposed rule would not have ``federalism implications,''
because it would 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.'' Accordingly, Executive Order 13132 requires no
further agency action or analysis.
9. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
This proposed rule would not have ``tribal implications,'' because
it would not ``have substantial direct effects on one or more Indian
tribes, on the relationship between the Federal government and Indian
tribes, or on the distribution of power and responsibilities between
the Federal government and Indian tribes.'' Accordingly, Executive
Order 13175 requires no further agency action or analysis.
10. Executive Order 13211: Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use
In accordance with Executive Order 13211, we have reviewed this
proposed rule for its impact on the supply, distribution, and use of
energy. This proposed rule would regulate both the coal and metal and
nonmetal mining sectors. Because this proposed rule would result in
negligible yearly costs of less than 0.001 percent of revenues to the
coal mining industry, the proposed rule would neither significantly
reduce the supply of coal nor significantly increase its price.
Regulation of the metal and nonmetal sector of the mining industry has
no significant impact on the supply, distribution, or use of energy.
This proposed rule is not a ``significant energy action,'' because
it would not be ``likely to have a significant adverse effect on the
supply, distribution, or use of energy'' ``(including a shortfall in
supply, price increases, and increased use of foreign supplies).''
Accordingly, Executive Order 13211 requires no further agency action or
analysis.
11. Executive Order 13272: Proper Consideration of Small Entities in
Agency Rulemaking
In accordance with Executive Order 13272, we have thoroughly
reviewed this proposed rule to assess and take appropriate account of
its potential impact on small businesses, small governmental
jurisdictions, and small organizations. As discussed in section VIII.C.
above and in chapter V of the PREA, MSHA has determined and certified
that this proposed rule would not have a significant economic impact on
a substantial number of small entities.
IX. Copy of the OSHA Reference Method (ORM)
MSHA's existing asbestos standards require that the analyst
determine fiber concentrations using a phase contrast microscopy
analytical method with 400-450X magnification and count fibers 5 [mu]m
or longer having a length to diameter aspect ratio of at least 3:1. The
OSHA Reference Method contains these requirements.
29 CFR 1910.1001 Appendix A: OSHA Reference Method--Mandatory
This mandatory appendix specifies the procedure for analyzing
air samples for asbestos and specifies quality control procedures
that must be implemented by laboratories performing the analysis.
The sampling and analytical methods described below represent the
elements of the available monitoring methods (such as Appendix B of
their regulation, the most current version of the OSHA method ID-
160, or the most current version of the NIOSH Method 7400). All
employers who are required to conduct air monitoring under paragraph
(d) of the [OSHA] standard are required to utilize analytical
laboratories that use this procedure, or an equivalent method, for
collecting and analyzing samples.
Sampling and Analytical Procedure
1. The sampling medium for air samples shall be mixed cellulose
ester filter membranes. These shall be designated by the
manufacturer as suitable for asbestos counting. See below for
rejection of blanks.
2. The preferred collection device shall be the 25-mm diameter
cassette with an open-faced 50-mm electrically conductive extension
cowl. The 37-mm cassette may be used if necessary but only if
written justification for the need to use the 37-mm filter cassette
accompanies the sample results in the employee's exposure monitoring
record. Do not reuse or reload cassettes for asbestos sample
collection.
3. An air flow rate between 0.5 liter/min and 2.5 liters/min
shall be selected for the 25-mm cassette. If the 37-mm cassette is
used, an air flow rate between 1 liter/min and 2.5 liters/min shall
be selected.
4. Where possible, a sufficient air volume for each air sample
shall be collected to yield between 100 and 1,300 fibers per square
millimeter on the membrane filter. If a filter darkens in appearance
or if loose dust is seen on the filter, a second sample shall be
started.
5. Ship the samples in a rigid container with sufficient packing
material to prevent dislodging the collected fibers. Packing
material that has a high electrostatic charge on its surface (e.g.,
expanded polystyrene) cannot be used because such material can cause
loss of fibers to the sides of the cassette.
6. Calibrate each personal sampling pump before and after use
with a representative filter cassette installed between the pump and
the calibration devices.
7. Personal samples shall be taken in the ``breathing zone'' of
the employee (i.e., attached to or near the collar or lapel near the
worker's face).
8. Fiber counts shall be made by positive phase contrast using a
microscope with an 8 to 10 X eyepiece and a 40 to 45 X objective for
a total magnification of approximately 400 X and a numerical
aperture of 0.65 to 0.75. The microscope shall also be fitted with a
green or blue filter.
9. The microscope shall be fitted with a Walton-Beckett eyepiece
graticule calibrated
[[Page 43984]]
for a field diameter of 100 micrometers (+/-2 micrometers).
10. The phase-shift detection limit of the microscope shall be
about 3 degrees measured using the HSE phase shift test slide as
outlined below.
a. Place the test slide on the microscope stage and center it
under the phase objective.
b. Bring the blocks of grooved lines into focus.
Note: The slide consists of seven sets of grooved lines (ca. 20
grooves to each block) in descending order of visibility from sets 1
to 7, seven being the least visible. The requirements for asbestos
counting are that the microscope optics must resolve the grooved
lines in set 3 completely, although they may appear somewhat faint,
and that the grooved lines in sets 6 and 7 must be invisible. Sets 4
and 5 must be at least partially visible but may vary slightly in
visibility between microscopes. A microscope that fails to meet
these requirements has either too low or too high a resolution to be
used for asbestos counting.
c. If the image deteriorates, clean and adjust the microscope
optics. If the problem persists, consult the microscope
manufacturer.
11. Each set of samples taken will include 10 percent blanks or
a minimum of 2 field blanks. These blanks must come from the same
lot as the filters used for sample collection. The field blank
results shall be averaged and subtracted from the analytical results
before reporting. A set consists of any sample or group of samples
for which an evaluation for this standard must be made. Any samples
represented by a field blank having a fiber count in excess of the
detection limit of the method being used shall be rejected.
12. The samples shall be mounted by the acetone/triacetin method
or a method with an equivalent index of refraction and similar
clarity.
13. Observe the following counting rules.
a. Count only fibers equal to or longer than 5 micrometers.
Measure the length of curved fibers along the curve.
b. In the absence of other information, count all particles as
asbestos that have a length-to-width ratio (aspect ratio) of 3:1 or
greater.
c. Fibers lying entirely within the boundary of the Walton-
Beckett graticule field shall receive a count of 1. Fibers crossing
the boundary once, having one end within the circle, shall receive
the count of one half (\1/2\). Do not count any fiber that crosses
the graticule boundary more than once. Reject and do not count any
other fibers even though they may be visible outside the graticule
area.
d. Count bundles of fibers as one fiber unless individual fibers
can be identified by observing both ends of an individual fiber.
e. Count enough graticule fields to yield 100 fibers. Count a
minimum of 20 fields; stop counting at 100 fields regardless of
fiber count.
14. Blind recounts shall be conducted at the rate of 10 percent.
Quality Control Procedures
1. Intralaboratory program. Each laboratory and/or each company
with more than one microscopist counting slides shall establish a
statistically designed quality assurance program involving blind
recounts and comparisons between microscopists to monitor the
variability of counting by each microscopist and between
microscopists. In a company with more than one laboratory, the
program shall include all laboratories and shall also evaluate the
laboratory-to-laboratory variability.
2.a. Interlaboratory program. Each laboratory analyzing asbestos
samples for compliance determination shall implement an
interlaboratory quality assurance program that as a minimum includes
participation of at least two other independent laboratories. Each
laboratory shall participate in round robin testing at least once
every 6 months with at least all the other laboratories in its
interlaboratory quality assurance group. Each laboratory shall
submit slides typical of its own work load for use in this program.
The round robin shall be designed and results analyzed using
appropriate statistical methodology.
2.b. All laboratories should also participate in a national
sample testing scheme such as the Proficiency Analytical Testing
Program (PAT), or the Asbestos Registry sponsored by the American
Industrial Hygiene Association (AIHA).
3. All individuals performing asbestos analysis must have taken
the NIOSH course for sampling and evaluating airborne asbestos dust
or an equivalent course.
4. When the use of different microscopes contributes to
differences between counters and laboratories, the effect of the
different microscope shall be evaluated and the microscope shall be
replaced, as necessary.
5. Current results of these quality assurance programs shall be
posted in each laboratory to keep the microscopists informed.
[57 FR 24330, June 8, 1992; 59 FR 40964, Aug. 10, 1994]
X. References Cited in the Preamble
Agency for Toxic Substances and Disease Registry (ATSDR).
Perchlorate Contamination in the Citizens Utilities' Suburban and
Security Park Water Service Areas, Prepared by California Department
of Health Services under CERCLIS No. CAD980358832, March 18, 1998.
Agency for Toxic Substances and Disease Registry (ATSDR).
Toxicological Profile for Asbestos (Update), Prepared by Syracuse
Research Corp. under Contract No. 205-1999-00024, U.S. Department of
Health and Human Services, Public Health Service, September 2001.
Agency for Toxic Substances and Disease Registry (ATSDR). Report on
the Expert Panel on Health Effects of Asbestos and Synthetic
Vitreous Fibers: The Influence of Fiber Length (Proceedings of panel
discussion, October 29-30, 2002, New York City), Prepared by Eastern
Research Group, Inc., March 17, 2003.
Amandus, H.E., R. Wheeler, J. Jankovic, and J. Tucker. ``The
Morbidity and Mortality of Vermiculite Miners and Millers Exposed to
Tremolite-Actinolite: Part I. Exposure Estimates,'' American Journal
of Industrial Medicine, 11(1):1-14, 1987.
Amandus, H.E., and R. Wheeler. ``The Morbidity and Mortality of
Vermiculite Miners and Millers Exposed to Tremolite-Actinolite: Part
II. Mortality,'' American Journal of Industrial Medicine, 11(1):15-
26, 1987.
Amandus, H.E., R. Althouse, W.K.C. Morgan, E.N. Sargent, and R.
Jones. ``The Morbidity and Mortality of Vermiculite Miners and
Millers Exposed to Tremolite-Actinolite: Part III. Radiographic
Findings,'' American Journal of Industrial Medicine, 11(1):27-37,
1987.
American Conference of Governmental Industrial Hygienists-American
Industrial Hygiene Association, Joint ACGIH-AIHA Aerosol Hazards
Evaluation Committee. ``Background Documentation on Evaluation of
Occupational Exposure to Airborne Asbestos,'' American Industrial
Hygiene Association Journal, February 1975, pp. 91-103.
American Thoracic Society. ``Diagnosis and Initial Management of
Nonmalignant Diseases Related to Asbestos,'' American Journal of
Respiratory and Critical Care Medicine, 170:691-715, 2004.
Armstrong, B.K., N.H. de Klerk, A.W. Musk, and M.S.T. Hobbs.
``Mortality in Miners and Millers of Crocidolite in Western
Australia, British Journal of Industrial Medicine, 45:5-13, 1988.
Asbestos International Association (AIA). ``Airborne Asbestos Fiber
Concentrations at Workplaces by Light Microscopy (Membrane Filter
Method),'' AIA Health and Safety Recommended Technical Method No. 1
(RTM1), London, September 7, 1979.
Baron, Paul A. ``Measurement of Airborne Fibers: A Review,''
Industrial Health, 39:39-50, 2001.
Becker, Nikolaus, Jurgen Berger, and Ulrich Bolm-Audorff. ``Asbestos
Exposure and Malignant Lymphomas-- a Review of the Epidemiological
Literature,'' International Archives of Occupational and
Environmental Health, 74:459-469, 2001.
Becklake, Margaret R. ``Clinical Measurements in Quebec Chrysotile
Miners: Use for Future Protection of Workers,'' Annals New York
Academy of Sciences, pp. 23-29, 1979.
Berry, G., and H.C. Lewinsohn. ``Dose-Response Relationships for
Asbestos-Related Disease: Implications for Hygiene Standards, Part
I. Morbidity,'' Annals New York Academy of Sciences, pp. 185-194,
1979.
Berry, G., and M.L. Newhouse. ``Mortality of Workers Manufacturing
Friction Materials Using Asbestos,'' British Journal of Industrial
Medicine, 40:1-7, 1983.
Bolton, C., A. Richards, and P. Ebden. ``Asbestos-Related Disease,''
Hospital Medicine, 63(3):148-151, March 2002.
Britton, Mark. ``The Epidemiology of Mesothelioma,'' Seminars in
Oncology, 29(1):18-25, February 2002.
Browne, Kevin. ``The Quantitative Risks of Mesothelioma and Lung
Cancer in Relation to Asbestos Exposure,'' Annals of Occupational
Hygiene (Letters to the Editor), 45(4):327-329, 2001.
Browne, Kevin, and J. Bernard L. Gee. ``Asbestos and Laryngeal
Cancer,'' Annals
[[Page 43985]]
of Occupational Hygiene, 44:239-250, 2000.
Carbone, Michele, Robert A. Kratzke, and Joseph R. Testa. ``The
Pathogenesis of Mesothelioma,'' Seminars in Oncology, 29(1):2-17,
February 2002.
Clark, R.L. ``Metallic Substrates as an Internal Standard for
Transmission Electron Microscope,'' Annals of the Institute for the
Certification of Engineering Technicians, 1977.
Cookson, W.O.C.M., N.H. de Klerk, A.W. Musk, B.K. Armstrong, J.J.
Glancy, and M.S.T. Hobbs. ``Prevalence of Radiographic Asbestosis in
Crocidolite Miners and Millers at Wittenoom, Western Australia,''
British Journal of Industrial Medicine, 43:450-457, 1986.
Cotran, Ramzi S., Vinay Kumar, and Tucker Collins. Robbins
Pathological Basis of Disease, Sixth Edition (W.B. Saunders Company,
Philadelphia), pp. 732-734, 1999.
Crane, Dan. Letter to Kelly Bailey dated May 16, 1989. (1219-AB24-
COMM-28-10).
Dave, S.K., L.J. Bhagia, P.K. Mazumdar, G.C. Patel, P.K. Kulkarni,
and S.K. Kashyap. ``The Correlation of Chest Radiograph and
Pulmonary Function Tests in Asbestos Miners and Millers,'' Indian
Journal of Chest Disease and Allied Sciences, 38:81-89, 1996.
Davis, J.M.G., S.T. Beckett, R.E. Bolton, and K. Donaldson. ``The
Effects of Intermittent High Asbestos Exposure (Peak Dose Levels) on
the Lungs of Rats,'' British Journal of Experimental Pathology,
61:272-280, 1980.
Davis, J.M.G., S.T. Beckett, R.E. Bolton, and K. Donaldson. ``A
Comparison of the Pathological Effects in Rat of the UICC Reference
Samples of Amosite and Chrysotile with Those of Amosite and
Chrysotile Collected from the Factory Environment,'' In: Biological
Effects of Mineral Fibres, J.C. Wagner (Editor-in-Chief), IARC
Scientific Publications No. 30 (2 volumes), pp. 285-292, 1980.
Davis, J.M.G., J. Addison, R.E. Bolton, K. Donaldson, A.D. Jones and
T. Smith. ``The Pathogenicity of Long versus Short Fibre Samples of
Amosite Administered to Rats by Inhalation and Intraperitoneal
Injection,'' British Journal of Experimental Pathology, 67:415-430,
1986.
Davis, J.M.G., and A.D. Jones. ``Comparison of the Pathogenicity of
Long and Short Fibres of Chrysotile Asbestos in Rats,'' British
Journal of Experimental Pathology, 69:717-737, 1988.
Delpierre, Stephane, Yves Jammes, Marie Jose Delvogo-Gori, and
Marion Faucher. ``High Prevalence of Reversible Airway Obstruction
in Asbestos-Exposed Workers,'' Archives of Environmental Health,
57(5):441-445, September/October, 2002.
Dement, J.M., R.L. Harris, M.J. Symons, and C. Shy. ``Estimates of
Dose-Response for Respiratory Cancer among Chrysotile Asbestos
Textile Workers,'' Annals of Occupational Hygiene, 26(14):869-887,
1982.
Dodson, Ronald F., Mark A.L. Atkinson, and Jeffrey L. Levin.
``Asbestos Fiber Length as Related to Potential Pathogenicity: A
Critical Review,'' American Journal of Industrial Medicine, 44:291-
297, 2003.
Doll, Richard. ``Mortality from Lung Cancer in Asbestos Workers,''
British Journal of Industrial Medicine, 12:81-86, 1955.
Donaldson, K., R.E. Bolton, A. Jones, G.M. Brown, M.D. Robertson, J.
Slight, H. Cowie, and J.M.G. Davis. ``Kinetics of the
Bronchoalveolar Leucocyte Response in Rats during Exposure to Equal
Airborne Mass Concentrations of Quartz, Chrysotile Asbestos, or
Titanium Dioxide,'' Thorax, 43:525-533, 1988.
Eagen, Tomas M.L., Amund Gulsvik, Geir E. Eide, and Per S. Bakke.
``Occupational Airborne Exposure and the Incidence of Respiratory
Symptoms and Asthma,'' American Journal of Respiratory Critical Care
Medicine, 166:933-938, 2002.
Enarson, D.A., Valerie Embree, Lonia Maclean, and S. Grzybowski.
``Respiratory Health in Chrysotile Asbestos Miners in British
Columbia: A Longitudinal Study,'' British Journal of Industrial
Medicine, 45:459-463, 1988.
Finkelstein, Murray M. ``Asbestosis in Long-Term Employees of an
Ontario Asbestos-Cement Factory,'' American Review of Respiratory
Disease, 125:496-501, 1982.
Finkelstein, M.M. ``Mortality among Long-Term Employees of an
Ontario Asbestos-Cement Factory,'' British Journal of Industrial
Medicine, 40:138-144, 1983.
Finkelstein, Murray M. ``Potential Pitfall in Using Cumulative
Exposure in Exposure-Response Relationships: Demonstration and
Discussion,'' American Journal of Industrial Medicine, 28:41-47,
1995.
Fischer, M., S. Gunther, and K.-M. Muller. ``Fibre-Years, Pulmonary
Asbestos Burden and Asbestosis,'' International Journal of Hygiene
and Environmental Health, 205:245-248, 2002.
Gibbs, Graham W., and R.S.J. du Toit. ``Environmental Considerations
in Surveillance of Asbestos Miners and Millers,'' Annals New York
Academy of Sciences, pp. 163-178, 1979.
Global Environmental & Technology Foundation (GETF). ``Report of
Findings and Recommendations on the Use and Management of
Asbestos,'' Asbestos Strategies, 2003.
Goldstein, B., and F.S.J. Coetzee. ``Experimental Malignant
Mesotheliomas in Baboons,'' South African Journal of Science, 86:89-
93, February 1990.
Greenberg, Morris. ``Biological Effects of Asbestos: New York
Academy of Sciences 1964,'' American Journal of Industrial Medicine
(Historical Perspective), 43:543-552, 2003.
Harper, Martin, and Al Bartolucci. ``Preparation and Examination of
Proposed Consensus Reference Standards for Fiber-Counting,''
American Industrial Hygiene Association Journal, 64:283-287, 2003.
Henderson, Vivian L., and Philip E. Enterline. ``Asbestos Exposure
Factors Associated with Excess Cancer and Respiratory Disease
Mortality,'' Annals New York Academy of Sciences (prepublication
copy), 1979.
Hodgson, John T., and Andrew Darnton. ``The Quantitative Risks of
Mesothelioma and Lung Cancer in Relation to Asbestos Exposure,''
Annals of Occupational Hygiene, 44(8):565-601, 2000.
International Agency for Research on Cancer (IARC). ``Asbestos,''
Monographs (Volume 14), Supplement 7, p. 106, 1987.
International Commission on Radiation Protection (ICRP), Prepared by
the Task Group on Lung Dynamics for Committee II of the ICRP.
``Deposition and Retention Models for Internal Dosimetry of the
Human Respiratory Tract,'' Health Physics, 12:173-207, 1966.
[``Errata and Revisions to Health Physics 12, 173 (1966),'' Health
Physics, 13:1251, 1967.]
International Organization for Standardization (ISO). ``Air
quality--Determination of the number concentration of airborne
inorganic fibres by phase contrast microscopy--Membrane filter
method,'' ISO 8672:1993(E).
Irwig, L.M., R.S.J. du Toit, G.K. Sluis-Cremer, A. Solomon, R. Glyn
Thomas, P.P.H. Hamel, I. Webster, and T. Hastie. ``Risk of
Asbestosis in Crocidolite and Amosite Mines in South Africa,''
Annals New York Academy of Sciences, pp. 35-52, 1979.
JRB Associates. ``Benefits Assessment of Emergency Temporary and
Proposed Asbestos Standards, Final Report,'' Prepared by Marthe B.
Kent, William G. Perry, and Christine B. New for OSHA Office of
Regulatory Analysis, November 3, 1983.
Kelse, John W., and C. Sheldon Thompson. ``The Regulatory and
Mineralogical Definitions of Asbestos and their Impact on Amphibole
Dust Analysis,'' American Industrial Hygiene Association Journal,
50:613-622, 1989.
Lane, R.E. (Chairman) et al., Subcommittee on Asbestos, Committee on
Hygiene, British Occupational Hygiene Society. ``Hygiene Standards
for Chrysotile Asbestos Dust,'' Annals of Occupational Hygiene,
11:47-69, 1968. (1219-AB24-COMM-29-2)
Langer, Arthur M., Arthur N. Rohl, Mary Snow Wolf, and Irving J.
Selikoff. ``Asbestos, Fibrous Minerals and Acicular Cleavage
Fragments: Nomenclature and Biological Properties,'' Dusts and
Disease, 1979. (1219-AB24-COMM-29-11)
Leake, Bernard E. (Chairman), et al. ``Nomenclature of Amphiboles:
Report of the Subcommittee on Amphiboles of the International
Mineralogical Association, Commission on New Minerals and Mineral
Names,'' Canadian Mineralogist, 35:219-246, 1997.
Lemen, Richard A. ``Asbestos in Brakes,'' October 16, 2003. [Paper
received from Ralph D. Zumwalde (NIOSH) via Tom Simons (EPA),
December 5, 2003.]
Liddell, Douglas. Letter to the Editor, ``Asbestos and Cancer,''
Annals of Occupational Hygiene, 45(4):329-335, 2001.
Maltoni, Cesare. ``Call for an International Ban on Asbestos,''
Toxicology and Industrial Health, 15:529-531, 1999.
Manning, Christopher B., Val Vallyathan, and Brooke Mossman.
``Diseases Caused by Asbestos: Mechanisms of Injury and Disease
Development, International Immunopharmacology, 2:191-200, 2002.
McDonald, J. Corbett, and F. Douglas K. Liddell. ``Mortality in
Canadian Miners and Millers Exposed to Chrysotile, Annals
[[Page 43986]]
New York Academy of Sciences, pp. 1-9, 1979.
McDonald, J.C., F.D.K. Liddell, G.W. Gibbs, G.E. Eyssen, and A.D.
McDonald. ``Dust Exposure and Mortality in Chrysotile Mining, 1910-
75,'' British Journal of Industrial Medicine, 37:11-24, 1980.
(A) McDonald, J.C., A.D. McDonald, B. Armstrong, and P. Sebastien.
``Cohort study of mortality of vermiculite miners exposed to
tremolite,'' British Journal of Industrial Medicine, 43:436-444,
1986.
(B) McDonald, J.C., P. Sebastien, and B. Armstrong. ``Radiological
Survey of Past and Present Vermiculite Miners Exposed to
Tremolite,'' British Journal of Industrial Medicine, 43:445-449,
1986.
McDonald, J.C., A.D. McDonald, P. Sebastien, and K. Moy. ``Health of
Vermiculite Miners Exposed to Trace Amounts of Fibrous Tremolite,''
British Journal of Industrial Medicine, 45:630-634, 1988.
McDonald, J.C., F.D.K. Liddell, A. Dufresne, and A.D. McDonald.
``The 1891-1920 Birth Cohort of Quebec Chrysotile Miners and
Millers: Mortality 1976-1988,'' British Journal of Industrial
Medicine, 50:1073-1081, 1993.
McDonald, A.D., B.W. Case, A. Churg, A. Dufresne, G.W. Gibbs, P.
Sebastien, and J.C. McDonald. ``Mesothelioma in Quebec Chrysotile
Miners and Millers: Epidemiology and Aetiology,'' Annals of
Occupational Hygiene, 41(6):707-719, 1997.
McGavran, Patricia D., Charles J. Butterick, and Arnold R. Brody.
``Tritiated Thymidine Incorporation and the Development of an
Interstitial Lesion in the Bronchiolar-Alveolar Regions of the Lungs
of Normal and Complement Deficient Mice after Inhalation of
Chrysotile Asbestos,'' Journal of Environmental Pathology,
Toxicology and Oncology (JEPTO), 9(5)/9(6):377-392, 1989.
McLaughlin, Joseph K., and Loren Lipworth. ``Epidemiologic Aspects
of Renal Cell Cancer,'' Seminars in Oncology, 27(2):115-123, April
2000.
Meeker, G.P., A.M. Bern, I.K. Brownfield, H.A. Lowers, S.J. Sutley,
T.M. Hoefen, and J.S. Vance. ``The Composition and Morphology of
Amphiboles from the Rainy Creek Complex, Near Libby, Montana,''
American Mineralogist, 88:1955-1969, 2003.
Mine Safety and Health Administration (MSHA). Walter Bank,
``Asbestiform and/or Fibrous Minerals in Mines, Mills, and
Quarries,'' Informational Report IR 1111, 1980.
Mine Safety and Health Administration (MSHA). ``Asbestos Hazards in
the Mining Industry,'' Health Hazard Information Card No. 21, March
2000.
Mine Safety and Health Administration (MSHA). ``Chapter 8 Asbestos
Fibers,'' Metal/Nonmetal Health Inspection Procedures Handbook
(PH04-IV-5), November 2003; and ``Chapter 8 Asbestos,'' MSHA
Handbook Series: Coal Mine Health Inspection Procedures (Handbook
No. 89-V-1), February 1989.
Mine Safety and Health Administration (MSHA). Program Information
Bulletin No. P00-3 from J. Davitt McAteer, re: Potential Exposure to
Airborne Asbestos on Mining Properties, dated March 2, 2000.
Mossman, Brooke. In Report of the Expert Panel on Health Effects of
Asbestos and Synthetic Vitreous Fibers: The Influence of Fiber
Length, (Proceedings of Panel, October 29-30, 2002, New York City),
Prepared by Eastern Research Group for the Agency for Toxic
Substances and Disease Registry (ATSDR), March 17, 2003.
National Institute for Occupational Safety and Health (NIOSH).
Criteria for a Recommended Standard Occupational Exposure to
Asbestos, U.S. Department of Health, Education, and Welfare, 1972.
National Institute for Occupational Safety and Health (NIOSH).
Report to Congress on Workers' Home Contamination Study Conducted
Under the Workers' Family Protection Act, DHHS (NIOSH) Publication
No. 95-123 (September 1995).
National Institute for Occupational Safety and Health (NIOSH).
Protect Your Family: Reduce Contamination at Home, DHHS (NIOSH)
Publication No. 97-125 (1997).
National Institute for Occupational Safety and Health (NIOSH).
Protecting Workers' Families: A Research Agenda: Report of the
Workers' Family Protection Task Force, DHHS (NIOSH) Publication No.
2002-113 (2002).
National Institute for Occupational Safety and Health (NIOSH).
Division of Respiratory Disease Studies, Work Related Lung Disease
Surveillance Report 2002 [World 2003], DHHS (NIOSH) Publication No.
2003-111, May 2003.
National Institute for Occupational Safety and Health (NIOSH).
Pocket Guide to Chemical Hazards, DHHS (NIOSH) Publication No. 2004-
103, October 2003.
Nayebzadeh, Ataollah, Andre Dufresne, Bruce Case, Hojatolah Vali,
A.E. Williams-Jones, Robert Martin, Charles Normand, and James
Clark. ``Lung Mineral Fibers of Former Miners and Millers from
Thetford-Mines and Asbestos Regions: A Comparative Study of Fiber
Concentration and Dimension, Archives of Environmental Health,
56(1):65-76, January/February 2001.
Nicholson, William J., Irving J. Selikoff, Herbert Seidman, Ruth
Lillis, and Paul Formby. ``Long-Term Mortality Experience of
Chrysotile Miners and Millers in Thetford Mines, Quebec,'' Annals
New York Academy of Sciences, pp. 11-21, 1979.
Nicholson, William J. ``Quantitative Risk Assessment for Asbestos
Related Cancers,'' Prepared in conjunction with U.S. Department of
Labor, Occupational Safety and Health Administration (OSHA), Office
of Carcinogen Standards, under OSHA Contract No. J-9-F-2-0074,
October 1983.
Nicholson, William J. ``The Carcinogenicity of Chrysotile Asbestos--
A Review,'' Industrial Health, 39:57-64,2001.
Nolan, R.P., A.M. Langer, and Richard Wilson. ``A Risk Assessment
for Exposure to Grunerite Asbestos (Amosite) in an Iron Ore Mine,''
Paper presented at the National Academy of Sciences Colloquium
``Geology, Mineralogy, and Human Welfare,'' Irvine, CA, November 8-
9, 1998. In: Proceedings of the National Academy of Science,
96(7):3412-3419, March 1999.
Ojajarvi, I. Anneli, Timo J. Partanen, Anders Ahlbom, Paolo
Boffetta, Timo Hakulinen, Nadia Jourenkova, Timo P. Kauppinen,
Manolis Kogevinas, Miquel Porta, Harri U. Vainio, Elisabete
Weiderpass, and Catharina H. Wesseling. ``Occupational Exposures and
Pancreatic Cancer: A Meta-Analysis,'' Occupational and Environmental
Medicine, 57:316-324, 2000.
Orenstein, Marla R., and Marc B. Schenker. ``Environmental Asbestos
Exposure and Mesothelioma,'' Pulmonary Medicine (Current Opinion),
6:371-377, 2000.
Osinubi, Omowunmi Y.O., Michael Gochfeld, and Howard M. Kipen.
``Health Effects of Asbestos and Nonasbestos Fibers,'' Environmental
Health Perspectives, 108 (Supplement 4): 665-674, 2000.
Pang, Thomas W.S. ``Precision and Accuracy of Asbestos Fiber
Counting by Phase Contrast Microscopy,'' American Industrial Hygiene
Association Journal, 61:529-538, 2000.
Paustenbach, Dennis J., Richard O. Richter, Brent L. Finley, and
Patrick J. Sheehan. ``An Evaluation of the Historical Exposures of
Mechanics to Asbestos in Brake Dust,'' Applied Occupational and
Environmental Hygiene, 18:786-804, 2003.
Peacock, C., S.J. Copley, and D.M. Hansell. ``Asbestos-Related
Benign Pleural Disease,'' Clinical Radiology (Review), 55:422-432,
2000.
Peipins, Lucy A., Michael Lewin, Sharon Campolucci, Jeffrey A.
Lybarger, Aubrey Miller, Dan Middleton, Christopher Weis, Michael
Spence, Brad Black, and Vikas Kapil. ``Radiographic Abnormalities
and Exposure to Asbestos-Contaminated Vermiculite in the Community
of Libby, Montana, USA,'' Environmental Health Perspectives,
111(14):1753-1759, November 2003.
Peto, J., R. Doll, S.V. Howard, L.J. Kinlen, and H.C. Lewinsohn. ``A
Mortality Study among Workers in an English Asbestos Factory,''
British Journal of Industrial Medicine, 34:169-173, 1977.
Peto, Julian. ``Lung Cancer Mortality in Relation to Measured Dust
Levels in an Asbestos Textile Factory,'' In: Biological Effects of
Mineral Fibres, J.C. Wagner (Editor-in-Chief), IARC Scientific
Publications No. 30 (2 volumes), pp. 829-836, 1980.
Peto, J., H. Seidman, and I.J. Selikoff. ``Mesothelioma Mortality in
Asbestos Workers: Implications for Models of Carcinogenesis and Risk
Assessment,'' British Journal of Cancer, 45:124-135 (prepublication
copy), 1982.
Pohlabeln, H., P. Wild, W. Schill, W. Ahrens, I. Jahn, U. Bolm-
Audorff, and K-H Jockel. ``Asbestos Fibre Years and Lung Cancer: A
Two Phase Case-Control Study with Expert Exposure Assessment,''
Occupational and Environmental Medicine, 59:410-414, 2002.
Ramanathan, A.L., and V. Subramanian. ``Present Status of Asbestos
Mining and Related Health Problems in India--A Survey,'' Industrial
Health, 39:309-315, 2001.
Reeves, Andrew L., Henry E. Puro, and Ralph G. Smith. ``Inhalation
Carcinogenesis from
[[Page 43987]]
Various Forms of Asbestos,'' Environmental Research, 8:178-202,
1974.
Reger, Robert, and W.K. Morgan. ``On talc, tremolite, and
tergiversation,'' British Journal of Industrial Medicine, 47:505-
507, 1990.
Roach, Huw D., Gareth J. Davies, Richard Attanoos, Michael Crane,
Haydn Adams, and Sian Phillips. ``Asbestos: When the Dust Settles--
An Imaging Review of Asbestos-Related Disease,'' RadioGraphics,
22:S167-S184, 2002.
Roggli, Victor L., Robin T. Vollmer, Kelly J. Butnor, and Thomas A.
Sporn. ``Tremolite and Mesothelioma,'' Annals of Occupational
Hygiene, 46(5):447-453, 2002.
Rooker, Stephen J., Nicholas P. Vaughan, and Jean M. Le Guen. ``On
the Visibility of Fibers by Phase Contrast Microscopy,'' American
Industrial Hygiene Association Journal, 43:505-515, July 1982.
(1219-AB24-COMM-29-19)
Ross, Malcom. ``The `Asbestos' Minerals: Definitions, Description,
Modes of Formation, Physical and Chemical Properties, and Health
Risk to the Mining Community,'' Proceedings of the Workshop on
Asbestos: Definitions and Measurement Methods, November 1978.
Rossiter, Charles E., Leonard J. Bristol, Paul H. Cartier, John G.
Gilson, T. Roger Grainger, Gerald K. Sluis-Cremer, and J. Corbett
McDonald. ``Radiographic Changes in Chrysotile Asbestos Mine and
Mill Workers of Quebec,'' Archives of Environmental Health, 24:388-
400, June 1972.
Rubino, G.F., M. Newhouse, R. Murray, G. Scansetti, G. Piolatto, and
G. Aresini. ``Radiologic Changes after Cessation of Exposure among
Chrysotile Asbestos Miners in Italy,'' Annals New York Academy of
Sciences, pp. 157-161, 1979.
Rubino, G.F., G. Piolatto, M.L. Newhouse, G. Scansetti, G.A.
Aresini, and R. Murray. ``Mortality of Chrysotile Asbestos Workers
at the Balangero Mine, Northern Italy,'' British Journal of
Industrial Medicine, 36:187-194, 1979.
Rudd, Robin M. ``New Developments in Asbestos-Related Pleural
Disease,'' Thorax, 51:210-216, 1996.
Sali, Davide, and Paolo Boffetta. ``Kidney Cancer and Occupational
Exposure to Asbestos: A Meta-Analysis of Occupational Cohort
Studies,'' Cancer Causes and Control, 11:37-47, 2000.
Schlecht, Paul C., and Stanley A. Shulman. ``Phase Contrast
Microscopy Asbestos Fiber Counting Performance in the Proficiency
Analytical Testing Program,'' American Industrial Hygiene
Association Journal, 56:480-489, 1995.
Schneider, Andrew. ``A P-I Special Report: Uncivil Action,'' Seattle
Post-Intelligencer, November 18-19, 1999.
Schwartz, David A., Charles S. Davis, James A. Merchant, W. Bruce
Bunn, Jeffrey R. Galvin, D. Scott Van Fossen, Charles S. Dayton, and
Gary W. Hunninghake. ``Longitudinal Changes in Lung Function among
Asbestos-Exposed Workers,'' American Journal of Respiratory Critical
Care Medicine, 150:1243-1249, 1994.
Seidman, Herbert, Irving J. Selikoff, and E. Cuyler Hammond.
``Short-Term Asbestos Work Exposure and Long-Term Observation,''
Annals New York Academy of Sciences, pp. 61-89, 1979.
Seidman, Herbert. ``Short-Term Asbestos Work Exposure and Long-Term
Observation,'' from OSHA Asbestos Docket (Exh-261-A), July 1984
Updating.
Selden, A.I., N.P. Berg, E.A.L. Lundgren, G. Hillerdal, N.-G. Wik,
C.-G. Ohlson, and L.S. Bodin. ``Exposure to Tremolite Asbestos and
Respiratory Health in Swedish Dolomite Workers,'' Occupational and
Environmental Medicine, 58:670-677, 2001.
Selikoff, Irving J., E. Cuyler Hammond, and Herbert Seidman.
``Mortality Experience of Insulation Workers in the United States
and Canada, 1943-1976,'' Annals New York Academy of Sciences, pp.
91-116, 1979.
Snyder, J.G., R.L. Virta, and J.M. Segreti. ``Evaluation of the
Phase Contrast Microscopy Method for the Detection of Fibrous and
Other Elongated Mineral Particulates by Comparison with a STEM
Technique,'' American Industrial Hygiene Association Journal,
48(5):471-477, 1987.
Solomon, A., L.M. Irwig, G.K. Sluis-Cremer, R. Glyn Thomas, and
R.S.J. du Toit. ``Thickening of Pulmonary Interlobar Fissures:
Exposure-Response Relationship in Crocidolite and Amosite Miners,''
British Journal of Industrial Medicine, 36:195-198, 1979.
Steenland, Kyle, Dana Loomis, Carl Shy, and Neal Simonsen. ``Review
of Occupational Carcinogens,'' American Journal of Industrial
Medicine, 29:474-490, 1996.
Steenland, Kyle, Carol Burnett, Nina Lalich, Elizabeth Ward, and
Joseph Hurrell. ``Dying for Work: The Magnitude of U.S. Mortality
from Selected Causes of Death Associated with Occupation,'' American
Journal of Industrial Medicine, 43:461-482, 2003.
Stewart, I.M., and R.J. Lee. Considerations in the Regulation of
Actinolite, Tremolite and Anthophyllite, Society for Mining,
Metallurgy and Exploration, Inc., 1992.
Suzuki, Yasunosuke, and Steven R. Yuen. ``Asbestos Fibers
Contributing to the Induction of Human Malignant Mesothelioma,''
Annals New York Academy of Sciences, 982:160-176, 2002.
Tweedale, Geoffrey. ``Asbestos and Its Lethal Legacy,'' Nature
Reviews/Cancer (Perspectives), 2:1-5, April 2002.
U.S. Department of Labor, Office of the Inspector General.
Evaluation of MSHA's Handling of Inspections at the W.R. Grace &
Company Mine in Libby, Montana, Report No. 2E-06-620-0002, March 22,
2001.
U.S. Environmental Protection Agency (EPA). Guidance for Preventing
Asbestos Disease Among Auto Mechanics, EPA-560-OPTS-86-002, June
1986.
U.S. Environmental Protection Agency (EPA). Method for the
Determination of Asbestos in Bulk Building Materials, EPA Report No.
EPA/600/R-93/116 (NTIS/PB93-218576), July 1993. [Updates and
replaces Interim version in 40 CFR 763, Subpart F, App A].
U.S. Environmental Protection Agency (EPA, Region 8).
``Environmental News `` Asbestos in Libby, EPA Proposes Libby as a
National Priority,'' EPA Action Update 12, February 26,
2002.
U.S. Environmental Protection Agency (EPA, Region 2). World Trade
Center Background Study Report, Prepared for U.S. Federal Emergency
Management Agency, IAG No.: EMW-2002-IA-0127, April 2003.
U.S. Environmental Protection Agency (EPA). ``40 CFR Part 63,
National Emission Standards for Hazardous Air Pollutants: Taconite
Iron Ore Processing; Final Rule,'' Federal Register (68 FR 61868),
October 30, 2003.
U.S. Geological Survey (USGS). ``Preliminary Compilation of
Descriptive Geoenvironmental Mineral Deposit Models,'' Open-file
Report 95-831, 1995.
U.S. Geological Survey (USGS). Robert L. Virta, ``Talc and
Pyrophyllite,'' U.S. Geological Survey Minerals Yearbook, 2002.
U.S. Geological Survey (USGS). Robert L. Virta, ``Asbestos,'' U.S.
Geological Survey 2003 Mineral Commodity Summary, online at http://minerals.er.usgs.gov/minerals/pubs/commodity/asbestos/070303.pdf.
Verma, Dave K., and Nancy E. Clark. ``Relationships between Phase
Contrast Microscopy and Transmission Electron Microscopy Results of
Samples from Occupational Exposure to Airborne Chrysotile
Asbestos,'' American Industrial Hygiene Association Journal, 56:866-
873, 1995.
Wang, Xiao-Rong, Eiji Yano, Mianzheng Wang, Zhiming Wang, and David
C. Christiani. ``Pulmonary Function in Long-Term Asbestos Workers in
China,'' Journal of Occupational and Environmental Health, 43(7)623-
629, July 2001.
Wagner, J.C., G. Berry, J.W. Skidmore, and V. Timbrell. ``The
Effects of the Inhalation of Asbestos in Rats,'' British Journal of
Cancer, 29:252-269, 1974.
Wagner, J.C., G. Berry, J.W. Skidmore, and F.D. Pooley. ``The
Comparative Effects of Three Chrysotiles by Injection and Inhalation
in Rats,'' In: Biological Effects of Mineral Fibres, J.C. Wagner
(Editor-in-Chief), IARC Scientific Publications No. 30 (2 volumes),
pp. 363-372, 1980.
Warheit, David B. (Editor). Fiber Toxicology, Academic Press, Inc.,
1993.
Webster, Ian, Bertie Goldstein, Frans Coetzee, and Gerhardus C.H.
van Sittert. ``Malignant Mesothelioma Induced in Baboons by
Inhalation of Amosite Asbestos,'' American Journal of Industrial
Medicine, 24:659-666, 1993.
Weill, Hans, Janet Hughes, and Carmel Waggenspack. ``Influence of
Dose and Fiber Type on Respiratory Malignancy Risk in Asbestos
Cement Manufacturing,'' American Review of Respiratory Disease,
120:345-354, 1979.
Weis, Christopher P., Aubrey K. Miller, and Paul Peronard. ``Task-
based exposure monitoring for residential exposure to amphibole
asbestos in Libby, Montana,'' U.S. Environmental Protection Agency,
Paper presented at 129th Annual APHA Meeting, October 21-25, 2001.
West, John B. Respiratory Physiology, The Essentials (Sixth
Edition), Lippincott Williams & Wilkins: Baltimore, MD, pp. 4-6 and
131-133, 2000.
[[Page 43988]]
West, John B. Pulmonary Pathophysiology, The Essentials (Sixth
Edition), Lippincott Williams & Wilkins: Baltimore, MD, pp. 82-91
and 126-137, 2003.
Wylie, Ann G., Robert L. Virta, and Estelle Russek. ``Characterizing
and Discriminating Airborne Amphibole Cleavage Fragments and Amosite
Fibers: Implications for the NIOSH Method'', American Industrial
Hygiene Association Journal, 46(4):197-201, 1985.
Wylie, Ann G. ``The Habit of Asbestiform Amphiboles: Implications
for the Analysis of Bulk Samples,'' Advances in Environmental
Measurement Methods for Asbestos, ASTM STP 1342, M.E. Beard and H.L.
Rooks (editors), American Society for Testing and Materials (ASTM),
West Conshohocken, PA, 2000.
Xu, An, Hongning Zhou, Dennis Zengliang Yu, and Tom K. Hei.
``Mechanisms of the Genotoxicity of Crocidolite Asbestos in
Mammalian Cells: Implication from Mutation Patterns Induced by
Reactive Oxygen Species,'' Environmental Health Perspectives,
110:1003-1008, 2002.
Yano, Eiji, Zhi-Ming Wang, Xiao-Rong Wang, Mian-Zheng Wang, and Ya-
Jia Lan. ``Cancer Mortality among Workers Exposed to Amphibole-Free
Chrysotile Asbestos, American Journal of Epidemiology, 154(6):538-
542, 2001.
List of Subjects
30 CFR Parts 56 and 57
Air quality, Asbestos, Chemicals, Hazardous substances, Metals,
Mine safety and health.
30 CFR Part 71
Air quality, Asbestos, Chemicals, Coal mining, Hazardous
substances, Mine safety and health.
Dated: July 14, 2005.
David G. Dye,
Deputy Assistant Secretary of Labor for Mine Safety and Health.
For the reasons set out in the preamble, and under the authority of
the Federal Mine Safety and Health Act of 1977, we are proposing to
amend chapter I of title 30 of the Code of Federal Regulations as
follows.
PART 56--[AMENDED]
1. The authority citation for part 56 would continue to read as
follows:
Authority: 30 U.S.C. 811.
2. Section 56.5001 would be amended by revising paragraph (b) to
read as follows:
Sec. 56.5001 Exposure limits for airborne contaminants.
* * * * *
(b) Asbestos standard. (1) Definitions. Asbestos is a generic term
for a number of hydrated silicates that, when crushed or processed,
separate into flexible fibers made up of fibrils. As used in this
part--
Asbestos means chrysotile, amosite (cummingtonite-grunerite
asbestos), crocidolite, anthophylite asbestos, tremolite asbestos, and
actinolite asbestos.
Fiber means a particulate form of asbestos 5 micrometers ([mu]m) or
longer with a length-to-diameter ratio of at least 3-to-1.
(2) Permissible Exposure Limits (PELs).
(i) Full-shift exposure limit. A miner's personal exposure to
asbestos shall not exceed an 8-hour time-weighted average, full-shift
airborne concentration of 0.1 fibers per cubic centimeter of air (f/
cc).
(ii) Excursion limit. No miner shall be exposed at any time to
airborne concentrations of asbestos in excess of 1.0 fiber per cubic
centimeter of air (f/cc) as averaged over a sampling period of 30
minutes.
(3) Measurement of airborne fiber concentration. Fiber
concentration shall be determined by phase contrast microscopy using a
method statistically equivalent to the OSHA Reference Method in OSHA's
asbestos standard found in 29 CFR 1910.1001, appendix A.
* * * * *
PART 57--[AMENDED]
3. The authority citation for part 57 would continue to read as
follows:
Authority: 30 U.S.C. 811.
4. Section 57.5001 would be amended by revising paragraph (b) to
read as follows:
Sec. 57.5001 Exposure limits for airborne contaminants.
* * * * *
(b) Asbestos standard. (1) Definitions. Asbestos is a generic term
for a number of hydrated silicates that, when crushed or processed,
separate into flexible fibers made up of fibrils. As used in this
part--
Asbestos means chrysotile, amosite (cummingtonite-grunerite
asbestos), crocidolite, anthophylite asbestos, tremolite asbestos, and
actinolite asbestos.
Fiber means a particulate form of asbestos 5 micrometers ([mu]m) or
longer with a length-to-diameter ratio of at least 3-to-1.
(2) Permissible Exposure Limits (PELs).
(i) Full-shift exposure limit. A miner's personal exposure to
asbestos shall not exceed an 8-hour time-weighted average, full-shift
airborne concentration of 0.1 fibers per cubic centimeter of air (f/
cc).
(ii) Excursion limit. No miner shall be exposed at any time to
airborne concentrations of asbestos in excess of 1.0 fiber per cubic
centimeter of air (f/cc) as averaged over a sampling period of 30
minutes.
(3) Measurement of airborne fiber concentration. Fiber
concentration shall be determined by phase contrast microscopy using a
method statistically equivalent to the OSHA Reference Method in OSHA's
asbestos standard found in 29 CFR 1910.1001, appendix A.
* * * * *
PART 71--[AMENDED]
5. The authority citation for part 71 would be revised to read as
follows:
Authority: 30 U.S.C. 811, 951, 957.
6. Section 71.701 would be amended by revising paragraphs (c) and
(d) to read as follows:
Sec. 71.701 Sampling; general requirements.
* * * * *
(c) Where concentrations of airborne contaminants in excess of the
applicable threshold limit values, permissible exposure limits, or
permissible excursions are known by the operator to exist in a surface
installation or at a surface worksite, the operator shall immediately
provide necessary control measures to assure compliance with Sec.
71.700 or Sec. 71.702, as applicable.
(d) Where the operator has reasonable grounds to believe that
concentrations of airborne contaminants in excess of the applicable
threshold limit values, permissible exposure limits, or permissible
excursions exist, or are likely to exist, the operator shall promptly
conduct appropriate air sampling tests to determine the concentration
of any airborne contaminant which may be present and immediately
provide the necessary control measures to assure compliance with Sec.
71.700 or Sec. 71.702, as applicable.
7. Section 71.702 would be revised to read as follows:
Sec. 71.702 Asbestos standard.
(a) Definitions. Asbestos is a generic term for a number of
hydrated silicates that, when crushed or processed, separate into
flexible fibers made up of fibrils. As used in this part--
Asbestos means chrysotile, amosite (cummingtonite-grunerite
asbestos), crocidolite, anthophylite asbestos, tremolite asbestos, and
actinolite asbestos.
Fiber means a particulate form of asbestos 5 micrometers ([mu]m) or
longer with a length-to-diameter ratio of at least 3-to-1.
[[Page 43989]]
(b) Permissible Exposure Limits (PELs). (1) Full-shift exposure
limit. A miner's personal exposure to asbestos shall not exceed an 8-
hour time-weighted average, full-shift airborne concentration of 0.1
fibers per cubic centimeter of air (f/cc).
(2) Excursion limit. No miner shall be exposed at any time to
airborne concentrations of asbestos in excess of 1.0 fiber per cubic
centimeter of air (f/cc) as averaged over a sampling period of 30
minutes.
(c) Measurement of airborne fiber concentration. Fiber
concentration shall be determined by phase contrast microscopy using a
method statistically equivalent to the OSHA Reference Method in OSHA's
asbestos standard found in 29 CFR 1910.1001, appendix A.
[FR Doc. 05-14510 Filed 7-28-05; 8:45 am]
BILLING CODE 4510-43-P