[Federal Register: July 29, 2005 (Volume 70, Number 145)]
[Proposed Rules]
[Page 43949-43989]
-----------------------------------------------------------------------
Part II
Department of Labor
-----------------------------------------------------------------------
Mine Safety and Health Administration
-----------------------------------------------------------------------
30 CFR Parts 56, 57, and 71
Asbestos Exposure Limit; Proposed Rule
[[Page 43950]]
-----------------------------------------------------------------------
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.
-----------------------------------------------------------------------
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: zzMSHA-comments@dol.gov. 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:smith.rebecca@dol.gov (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.
[[Page 43951]]
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.
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
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
[[Page 43952]]
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.
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\5\ GETF Report, pp. 12-13, 2003.
\6\ USGS (Virta), p. 28, 2003.
\7\ Lemen, 2003; Paustenbach et al., 2003.
---------------------------------------------------------------------------
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
[[Page 43953]]
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.
---------------------------------------------------------------------------
\8\ Reger and Morgan, 1990; ATSDR, p. 138, 2001.
---------------------------------------------------------------------------
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
].
---------------------------------------------------------------------------
\9\ Leake et al., p. 222, 1997.
---------------------------------------------------------------------------
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:
---------------------------------------------------------------------------
\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\
---------------------------------------------------------------------------
\11\ GETF Report, p. 33, 2003.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\12\ EPA (68 FR 61868), 2003.
---------------------------------------------------------------------------
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\
---------------------------------------------------------------------------
\13\ IARC, 1987.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
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\
---------------------------------------------------------------------------
\16\ Meeker et al., 2003
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\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\
---------------------------------------------------------------------------
\19\ Baron, 2001; Bolton et al., 2002; Manning et al., 2002;
Nicholson, 2001; Osinubi et al., 2000; Roach et al., 2002.
\20\ Maltoni, 1999.
---------------------------------------------------------------------------
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).
---------------------------------------------------------------------------
\21\ ATSDR, 2001; Fischer et al., 2002; Liddell, 2001; Pohlabeln
et al., 2002.
\22\ Finkelstein, 1995; ATSDR, p. 42, 2001.
---------------------------------------------------------------------------
[[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.
---------------------------------------------------------------------------
\23\ ATSDR, 2001; Osinubi et al., 2000; Peacock et al., 2000;
Langer et al., 1979.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
\26\ ATSDR, pp. 39-41, 2001; Mossman, pp. 47-50, 2003.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\28\ Warheit, p. 308, 1993.
\29\ Baron, 2001; Osinubi et al., 2000.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
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. H |
