Federal Register: February 29, 2008 (Volume 73, Number 41)
DOCID: fr29fe08-26 FR Doc E8-3828
DEPARTMENT OF LABOR
CFR Citation: 30 CFR Parts 56, 57, and 71
RIN ID: RIN 1219-AB24
NOTICE: Part IV
DOCUMENT ACTION: Final rule.
Asbestos Exposure Limit
DATES: This final rule is effective April 29, 2008.
The Mine Safety and Health Administration (MSHA) is revising its existing health standards for asbestos exposure at metal and nonmetal mines, surface coal mines, and surface areas of underground coal mines. This final rule reduces the permissible exposure limits for airborne asbestos fibers and makes clarifying changes to the existing standards. Exposure to asbestos has been associated with lung cancer, mesothelioma, and other cancers, as well as asbestosis and other nonmalignant respiratory diseases. This final rule will help improve health protection for miners who work in an environment where asbestos is present and lower the risk that miners will suffer material impairment of health or functional capacity over their working lifetime.
Labor Department, Mine Safety and Health Administration,
The outline of this preamble is as follows: I. Summary
II. Background to the Final Rule
A. Scope of Final Rule
B. Mineralogy and Analytical Methods for Asbestos
C. Summary of Asbestos Health Hazards
D. Factors Affecting the Occurrence and Severity of Disease
E. MSHA Asbestos Standards
F. OSHA Asbestos Standards
III. Asbestos Exposures in Mines
A. Where Asbestos Is Found at Mines
B. Sampling Data and Exposure Calculations
C. Summary of MSHA's Asbestos Air Sampling and Analysis Results
D. Prevention of Asbestos TakeHome Contamination IV. Application of OSHA'S Risk Assessment to Mining
A. Summary of OSHA's Risk Assessment
B. Risk Assessment for the Mining Industry
C. Characterization of the Risk to Miners
V. SectionbySection Analysis of Final 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. Section 71.701(c) and (d): Sampling; General Requirements VI. Regulatory Analyses
A. Executive Order (E.O.) 12866
C. Alternatives Considered
D. Regulatory Flexibility Analysis (RFA) and Small Business Regulatory Enforcement Fairness Act (SBREFA)
E. Other Regulatory Considerations
VII. Copy of the OSHA Reference Method (ORM)
VIII. References Cited in the Preamble
The final rule lowers MSHA's permissible exposure limits (PELs) for asbestos; incorporates the Occupational Safety and Health
Administration (OSHA) Reference Method (29 CFR 1910.1001, Appendix A) for MSHA's analysis of mine air samples for asbestos; and makes several clarifying changes to MSHA's existing rule. MSHA is issuing this health standard limiting miners' exposure to asbestos under section 101(a)(6)(A) of the Federal Mine Safety and Health Act of 1977 (Mine Act). MSHA based this final rule on its experience, an assessment of the health risks of asbestos, OSHA's rulemaking history and enforcement experience with its asbestos standard and public comments and testimony on MSHA's asbestos proposed rule.
To protect the health of miners, this final rule lowers MSHA's 8 hour, timeweighted average (TWA), fullshift PEL from 2 fibers per cubic centimeter of air (f/cc) to 0.1 f/cc. The existing excursion limit for metal and nonmetal mines is 10 fibers per milliliter (f/mL) for 15 minutes and the existing excursion limit for coal mines is 10 f/ cc for a total of 1 hour in each 8hour day. This final rule lowers these existing excursion limits to 1 f/cc for 30 minutes. Together, these lower PELs significantly reduce the risk of material impairment for exposed miners. These final PELs are the same as proposed and the same as OSHA's asbestos exposure limits. Although OSHA stated in the preamble to its 1994 final rule (59 FR 40967) that there is a remaining significant risk of material impairment of health or functional capacity at the 0.1 f/cc limit, OSHA concluded that this concentration is ``the practical lower limit of feasibility for measuring asbestos levels reliably.'' MSHA agrees with this conclusion.
To clarify the criteria for the analytical method that MSHA will use to analyze mine air samples for asbestos under this final rule, the rule includes a reference to Appendix A of OSHA's asbestos standard (29 CFR 1910.1001). Appendix A specifies basic elements of a phase contrast microscopy (PCM) method for analyzing airborne asbestos samples, which includes the same basic analytical elements as those specified in MSHA's existing standards.
Because the risk assessment used as the basis for MSHA's asbestos PELs relies on PCMbased methodology, MSHA will continue to use PCM as the primary methodology for analyzing air samples to determine compliance with the PELs. PCM provides a relatively quick and cost effective analysis of asbestos samples. In addition, MSHA will continue to followup with its policy of using a transmission electron microscopy (TEM) analysis when PCM results indicate a potential overexposure.
MSHA, however, encourages the development of analytical methods
specifically for asbestos in mine air samples. MSHA will consider using
a method statistically equivalent to Appendix A, if it meets the OSHA
Reference Method (ORM) equivalency criteria in OSHA's asbestos standard
[29 CFR 1910.1001(d)(6)(iii)] and is recognized by a laboratory
accreditation organization. For example, ASTM D720006, ``Standard
Practice for Sampling and Counting Airborne Fibers, Including Asbestos
Fibers, in Mines and Quarries, by Phase Contrast Microscopy and
Transmission Electron Microscopy,'' contains the same procedure as
NIOSH 7400 to identify fibers. ASTM D720006 then has an additional
procedure to discriminate potential asbestos fibers, which NIOSH 7400
does not. NIOSH is supporting an ASTM interlaboratory study to
determine whether this additional procedure can be performed accurately
and consistently. This procedure was developed in part as a result of this rulemaking and has not been validated.
II. Background to the Final Rule
A. Scope of Final Rule
This final rule applies to all metal and nonmetal mines, surface
coal mines, and surface areas of underground coal mines. It is
substantively unchanged from the proposed rule and contains the same
PELs and analytical method as in OSHA's asbestos standard. Some
commenters supported additional changes to MSHA's definition of
asbestos and its analytical method. Others recommended that MSHA
propose additional requirements from the OSHA asbestos standard to
prevent takehome contamination. Such changes were not contemplated in the proposed
rule and, therefore, are beyond the scope of this final rule. B. Mineralogy and Analytical Methods for Asbestos
Asbestos is a generic term used to describe the fibrous habits of
specific naturally occurring, hydrated silicate minerals. Several
federal agencies \1\ have regulations that address six asbestos
minerals: chrysotile, crocidolite, cummingtonitegrunerite asbestos
(amosite), actinolite asbestos, anthophyllite asbestos, and tremolite
asbestos. Other agencies address asbestos more generally.\2\
\1\ In addition to MSHA's and OSHA's existing worker protection
standards, other federal statutory and regulatory requirements that
apply only to the six commercial varieties of asbestos include the
Asbestos Hazard Emergency Response Act (AHERA) [15 U.S.C. 2642(3)]
and the Clean Air Act's National Emission Standards for Hazardous Air Pollutants (NESHAP) [40 CFR 61.141].
\2\ Asbestos is listed as a hazardous air pollutant under the Clean Air Act [42 U.S.C. 7412(b)(1)]; as a hazardous substance under the Comprehensive Environmental Response, Compensation and Liability Act [40 CFR 302.4]; and in EPA's Integrated Risk Information System (IRIS), a collection of health assessment information regarding the toxicity of asbestos, http://www.epa.gov/IRIS/susbst/0371.htm.
The terminology used to refer to how minerals form and how they are
named is complex. Much of the existing health risk data for asbestos
uses the commercial mineral terminology.\3\ In the asbestiform habit,
mineral crystals grow forming long, threadlike fibers. The U.S. Bureau
of Mines defined asbestiform minerals to be ``a certain type of mineral
fibrosity in which the fibers and fibrils possess high tensile strength
and flexibility.'' \4\ When light pressure is applied to an asbestiform
fiber, it bends much like a wire, rather than breaks. In the
nonasbestiform habit, mineral crystals do not grow in long thin fibers;
they grow in a more massive habit. When pressure is applied, the
nonasbestiform crystals fracture into prismatic particles, which are
called cleavage fragments because they result from the particle's
breaking or cleavage. Cleavage fragments may be formed when nonfibrous
minerals are crushed, as may occur in mining and milling operations.
Distinguishing between asbestiform fibers and cleavage fragments in
certain size ranges can be difficult or impossible for some minerals.\5\
\3\ Asbestos mineralogy was discussed more fully in the proposed rule (70 FR 4395243953).
\4\ U.S. Bureau of Mines (Campbell et al.), 1977.
\5\ Meeker et al., 2003.
C. Summary of Asbestos Health Hazards
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 asbestoscontaining
products.\6\ These 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.\7\ 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. The damage following many years
of workplace exposure to asbestos is generally cumulative and
irreversible. Most asbestosrelated diseases have long latency periods,
typically not producing symptoms for 20 to 30 years following initial
exposure. Studies also indicate adverse health effects in workers who have had relatively brief exposures to asbestos.\8\
\6\ GETF Report, p. 38, 2003; OSHA (40 FR 47654), 1975. \7\ Doll, 1955; Reeves et al., 1974; Becker et al., 2001; Browne and Gee, 2000; Sali and Boffetta, 2000; IARC, 1987.
\8\ Sullivan, 2007.
Several studies have examined respiratory health and respiratory
symptoms of asbestosexposed workers.\9\ Asbestosinduced pleurisy is
the most common asbestosrelated condition to occur during the 20year
period immediately following a worker's first exposure to asbestos.\10\
Pleural plaques may develop within 1020 years after an initial
asbestos exposure \11\ and slowly progress in size and amount of
calcification, independent of any further exposure. Diffuse pleural
thickening and pleural plaques are biologic markers reflecting previous
asbestos exposure.\12\ In addition, presence in lung tissue of asbestos
fibers with a coating of iron and protein, called asbestos bodies, is
one of the criteria that serve to support a pathologic diagnosis of
asbestosis.\13\ These nonmalignant respiratory conditions can be used
to identify atrisk miners prior to their developing a more serious asbestos disease.
\9\ Wang et al., 2001; Delpierre et al., 2002; Eagen et al., 2002; Selden et al., 2001.
\10\ Rudd, 2002.
\11\ Bolton et al., 2002; OSHA, 1986.
\12\ ATSDR, 2001; Manning et al., 2002.
\13\ ATSDR, 2001; Peacock et al., 2000; Craighead et al, 1982.
Because the hazardous effects from exposure to asbestos are well known, MSHA's discussion in this section will focus on the results of studies and literature reviews 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.\14\ In 2001, the Agency for Toxic
Substances and Disease Registry (ATSDR) published an updated
Toxicological Profile for Asbestos that also included an extensive
discussion of these three diseases. A search of peerreviewed
scientific literature yielded many new articles \15\ that continue to
demonstrate and support findings of asbestosinduced 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.
\14\ Berry and Newhouse, 1983; Dement et al., 1982; Finkelstein,
1983; Henderson and Enterline, 1979; Peto, 1980; Peto et al., 1982;
Seidman et al., 1979; Seidman, 1984; Selikoff et al., 1979; Weill et al., 1979.
\15\ Baron, 2001; Bolton et al., 2002; Manning et al., 2002; Nicholson, 2001; Osinubi et al., 2000; Roach et al., 2002.
D. Factors Affecting the Occurrence and Severity of Disease
The toxicity of asbestos, and the subsequent occurrence of disease, is related to its concentration in the air and the duration of exposure. Other variables, such as the fiber's characteristics or the effectiveness of a person's lung clearance mechanisms, lung fiber burden, residencetimeweighted cumulative exposures, and susceptible populations are also relevant factors affecting disease severity.\16\ \16\ ICRP, 1966; EPA, 1986; West, 2000 and 2003; Manning et al., 2002.
1. Fiber Concentration
Early airborne asbestos dust measurements had counted particles [[Page 11286]]
and reported the results as millions of particles per cubic foot of air (mppcf). Most recent studies express the concentration of asbestos 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, MSHA expresses the concentration of asbestos fibers as f/cc in this final rule, for both coal and metal and nonmetal mines.
In the late 1960s, scientists correlated PCMbased fiber counting methods with the earlier types of dust measurements, which provided a means to estimate earlier workers' asbestos exposures and enabled researchers to develop a doseresponse relationship with the occurrence of disease. The British Occupational Hygiene Society reported \17\ that a worker exposed to 100 fiberyears 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. \17\ Lane et al., 1968; OSHA (40 FR 47654), 1975; NIOSH, 1980.
OSHA (51 FR 22617) applied a conversion factor of 1.4 to convert mppcf, which includes all particles of respirable size, to f/cc, which includes only those particles greater than 5 [mu]m in length with at least a 3:1 aspect ratio. More recently, Hodgson and Darnton (2000) recommended the use of a factor of 3. In reviewing the scientific literature, MSHA did not critically evaluate the impact of these and other conversion factors. MSHA notes this difference here for completeness. MSHA is relying on OSHA's risk assessment and, thus, is using OSHA's conversion factor.
2. Duration of Exposure
The duration of exposure (T) is reported in both epidemiological and toxicological studies, and is generally much shorter in animal studies (e.g., months versus years). In epidemiological studies involving toxic substances that do not have acute health effects, such as asbestos, duration of exposure is typically expressed in years. 3. Cumulative Exposure
When developing doseresponse relationships for asbestosinduced
health effects, researchers typically use the product of exposure
concentration (C in f/cc) and exposure duration (T in years), expressed
as fiberyears,\18\ to indicate the level of exposure or dose. When
summed over all periods of exposure, this measure is called cumulative
exposure. Because of the difficulties in obtaining good quantitative
exposure assessments, cumulative exposure expressed in fiberyears is
often selected as the common metric for the levels of exposures reported in epidemiological studies.
\18\ ATSDR, 2001; Fischer et al., 2002; Liddell, 2001; Pohlabeln et al., 2002.
Finkelstein\19\ noted that this product of exposure concentration
times duration of exposure (C x T) assumes an equal weighting of each
variable (C, T). Finkelstein stated further that exposure at a low
concentration for a long period of time may be numerically equivalent
to exposure at a high concentration for short periods of time; but,
they may not be biologically equivalent. What this means is that, in
some studies, either concentration or duration of exposure may be more
important in predicting disease. For example, in the case of
mesothelioma risk following asbestos exposure, Finkelstein \20\
concluded that ``* * * duration of exposure may dominate the exposure term * * *''.
\19\ Finkelstein, 1995; ATSDR, p. 42, 2001.
\20\ Finkelstein, 1995
4. 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 toxicity * * *''. Manning et al. (2002) also noted the important roles of biopersistence (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, lengthtowidth
(aspect ratio), and texture, and chemical properties are believed to
be determinants of fiber distribution [in the body] and disease severity.
Many other investigators \21\ also have concluded that the dimensions of asbestos fibers are biologically important.
\21\ ATSDR, 2001; ATSDR, 2003; Osinubi et al., 2000; Peacock et al., 2000; Langer et al., 1979.
The NIOSH 7400 analytical method used by MSHA's contract
laboratories specifies that analysts count those fibers that are
greater than 5 micrometers (microns, [mu]m) in length with a length to
diameter aspect ratio of at least 3:1. Several recent publications \22\
support this aspect ratio, although larger aspect ratios such as 5:1 or
20:1 have been proposed.\23\ 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 asbestos fibers based on their length.
\22\ ATSDR, 2001; Osinubi et al., 2000.
\23\ Wylie et al., 1985.
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.\24\
\24\ ATSDR, pp. 3941, 2001; ATSDR, 2003; Mossman, pp. 4750, 2003; Kuempel et al., 2006.
Some commenters suggested that MSHA consider additional fiber
characteristics, such as durability, in evaluating risk. Some
emphasized that not all fibers with the same dimensions will lead to
the same disease endpoint. The science is inconclusive on the
relationship between the various fiber characteristics and the disease endpoints.\25\
\25\ Hodgson and Darnton, 2000; Browne, 2001; Liddell, 2001; ATSDR, 2001.
E. MSHA Asbestos Standards
The early PELs for asbestos in mining dropped dramatically as more
information on the health effects of asbestos exposure became evident
20 to 30 years (latency period) following its widespread use during the 1940s.
Year 8hour TWA, Asbestos PEL 1967.............................. 5 mppcf (30 f/mL)
1969.............................. 2 mppcf (12 f/mL)
1974.............................. 5 f/mL for metal and nonmetal mines 1976.............................. 2 f/cc for surface areas of coal mines (41 FR 10223)
1978.............................. 2 f/mL for metal and nonmetal mines (43 FR 54064)
On March 29, 2002 (67 FR 15134), MSHA published an advance notice of proposed rulemaking to obtain public comment on how best to protect miners from exposure to asbestos. MSHA published the proposed rule on July 29, 2005 (70 FR 43950) and held two public hearings in October 2005.
F. OSHA's Asbestos Standards
Like MSHA's, OSHA's 8hour TWA PEL for occupational exposure to
asbestos dropped dramatically over the past several decades.
Year 8hour TWA Asbestos PEL 1971.............................. 12 f/cc
1971.............................. 5 f/cc
1972.............................. 2 f/cc
1983.............................. 0.5 f/cc \26\
1986.............................. 0.2 f/cc \27\
1994.............................. 0.1 f/cc
In addition, on September 14, 1988, OSHA promulgated an asbestos excursion limit of 1 f/cc over a sampling period of 30 minutes (53 FR 35610).
\26\ U.S. Court of Appeals for the 5th Circuit invalidated this rule on March 7, 1984, in Asbestos Information Association/North America v. OSHA (727 F.2d 415, 1984).
\27\ OSHA added specific provisions in the construction standard to cover unique hazards relating to asbestos abatement and demolition jobs.
OSHA's 1986 standards had applied to occupational exposure to both asbestiform and nonasbestiform actinolite, tremolite, and anthophylite. On June 8, 1992, OSHA removed the nonasbestiform types of these minerals from the scope of its asbestos standards (57 FR 24310). III. Asbestos Exposures in Mines
A. Where Asbestos Is Found at Mines
Asbestos exposure of miners can come from either naturally occurring asbestos in the ore or host rock or from asbestos contained in manufactured products.
1. Metal and Nonmetal Mines
The National Institute for Occupational Safety and Health (NIOSH)
and other research organizations and scientists have noted the
occurrence of cancers and asbestosis among miners involved in the
mining and milling of commodities that contain asbestos.\28\ (See Table
IV3.) Although asbestos is no longer mined as a commodity in the
United States, veins, pockets, or intrusions of asbestoscontaining
minerals have been found in other ores in specific geographic regions,
primarily in metamorphic or igneous rock.\29\ It is possible to find
asbestos in sedimentary rock. The U.S. Geological Survey (USGS) has
reported weathering or abrasion of asbestosbearing rock and soil, or
air transportation, to carry asbestos to sedimentary deposits.\30\
MSHA's experience is that miners may encounter asbestos during the
mining of a number of mineral commodities,\31\ such as talc, limestone
and dolomite, vermiculite, wollastonite, banded ironstone and taconite,
lizardite, and antigorite. Even if asbestos contamination is found in a
specific mineral commodity, not all mines of that commodity will
encounter asbestos and those that do may encounter it rarely. (See Table III1.)
\28\ NIOSH WoRLD, 2003.
\29\ MSHA (Bank), 1980; Ross, 1978.
\30\ USGS, 1995.
\31\ 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; Meeker et al., 2003.
Mining activities, such as blasting, cutting, crushing, grinding, or simply disturbing the ore or surrounding earth may cause asbestos fibers to become airborne.\32\ Milling may transform bulk ore containing asbestos into respirable fibers. Asbestos tends to deposit on workplace surfaces and accumulate during the milling process, which is often in enclosed buildings. The use of equipment and machinery or other activities in these locations may resuspend the asbestos containing dust from these surfaces into the air. For this reason, MSHA generally finds higher asbestos concentrations in mills than among mobile equipment operators or in ambient environments, such as pits. \32\ MSHA (Bank), 1980; Amandus et al., Part I, 1987.
Some mine operators are making an effort to avoid deposits that are likely to contain asbestos minerals. They use knowledge of the geology of the area, core or bulk sample analysis, and workplace examinations (of the pit) to avoid encountering asbestos deposits, thus preventing asbestos contamination of their process stream and final product.\33\ \33\ GETF Report, pp. 1718, 2003; Nolan et al., 1999.
2. Coal Mines
MSHA is aware of only one coal formation in the United States that
contains naturally occurring asbestos; however, there is no coal mining
in this formation.\34\ The more likely exposure to asbestos in coal
mining occurs at surface operations from introduced asbestoscontaining materials (ACM).
\34\ Brownfield et al., 1995.
3. AsbestosContaining Materials (ACM)
Asbestos is a component in some commercial products and may be found as a contaminant in others. The USGS estimates that, during 2006, manufacturers in the United States used about 2,340 metric tons (5.2 million pounds) of asbestos, primarily in roofing products and coatings and compounds. In addition to domestic manufacturing, the United States continues to import products that contain asbestos, primarily cement products, such as flat cement panels, sheets, and tiles.\35\
Although manufacturers have removed the asbestos from many new products,\36\ asbestos may still be found at mines. Asbestoscontaining building materials (ACBM), such as Transite[reg] board and reinforced cements, could present a hazard during maintenance, construction, remodeling, rehabilitation, or demolition projects. Asbestos in manufactured products, such as electrical insulation, joint and packing compounds, automotive clutch and brake linings,\37\ and fireproof protective clothing and welding blankets, could present a hazard during activities at the mine site that may cause a release of fibers.\38\ MSHA expects mine operators to determine whether ACM or ACBM are present on mine property by reading the labels or Material Safety Data Sheets (MSDS) required by the OSHA Hazard Communication Standard (29 CFR 1910.1200). The presence of asbestos at a mine indicates that there is a potential for exposure.
B. Sampling Data and Exposure Calculations
To evaluate asbestos exposures in mines, MSHA collects personal exposure samples. MSHA samples a miner's entire work shift using a personal airsampling pump and a filtercassette assembly. This assembly is composed of a 50mm staticreducing, electrically conductive, extension cowl and a 0.8 [mu]m pore size, 25mm diameter, mixed cellulose ester (MCE) filter. Following standard sampling procedures, MSHA also submits blank filters for analysis.
MSHA collects a sample over the entire time the miner works; 10 to
12hour shifts are common. The timeweighted average (TWA) PELs in
MSHA's standards, however, are based on an 8hour workday. Regardless
of the actual shift length, MSHA calculates a fullshift concentration
as if the fibers had been collected over an 8hour shift. For work
schedules less than or greater than 8 hours, this technique allows MSHA to compare a miner's exposure
directly to the 8hour TWA PEL. MSHA calls this calculated equivalent, 8hour TWA a ``shiftweighted average'' (SWA).
MSHA's existing sampling procedures specify using several, typically three, filtercassette assemblies in a consecutive series to collect a fullshift sample. For results from both PCM and TEM analyses, MSHA calculates the SWA exposure levels for each miner sampled from the individual filters according to the following formulas.
SWA = (TWA1t1 + TWA2t2 + * * * + TWAntn)/480 minutes Where:
TWAn is the timeweighted average concentration for filter ``n'' calculated by dividing the number of fibers (f) collected on the filter by the volume of air (cc) drawn through the filter.
tn is the duration sampled in minutes for filter ``n''.
Some commenters criticized MSHA's sampling and analytical procedures. A few commenters believed that MSHA should develop specific test procedures for the sampling and analysis of bulk samples for the mining environment, as well as specific air sampling procedures. Some commenters suggested that respirable dust sampling using a cyclone might be a means to remove interfering dust from the sample. NIOSH recommended that thoracic samplers be evaluated in a mining environment. Cyclones and thoracic samplers are not included in MSHA's existing sampling and analytical protocols for asbestos and are not included in existing approved methods. Exposures determined using these devices have not been correlated with the risk assessment that forms the basis of the PELs in the final rule.
Some commenters supported MSHA's existing asbestos monitoring protocols with emphasis on fullshift monitoring for comparison to the PEL. Other commenters stated that MSHA's existing field sampling and analysis methods are adequate for most mines and quarries, particularly when no significant amount of asbestos is found.
Some commenters stated that MSHA should improve its inspection
reports by including inspection field notes; sampling location,
purpose, and procedure; as well as descriptions of the accuracy,
meaning, and limitations of the analytical results. MSHA routinely
provides the sampling and analytical results and, when requested, will provide the additional information.
C. Summary of MSHA's Asbestos Air Sampling and Analysis Results
To assess personal exposures and present the Agency's sampling data
for January 1, 2000 through May 31, 2007, MSHA calculated an SWA
exposure for each miner from the TWA results of individual filters.
MSHA has compiled these data into a PowerPoint[reg] slide, and has
posted it, together with additional explanatory information, on MSHA's
Asbestos Single Source Page at http://www.msha.gov/asbestos/ asbestos.htm.
\35\ USGS (Virta), 2007.
\36\ GETF Report, pp. 12 and 15, 2003.
\37\ Lemen, 2003; Paustenbach et al., 2003.
\38\ EPA, 1986; EPA, 1993; EPA, October 2003.
MSHA conducted asbestos sampling at 207 mines (206 nonasbestos metal and nonmetal mines and one coal mine) during the period January 1, 2000 through May 31, 2007. Some were sampled multiple times over the seven and one quarter years. MSHA found 29 mines with at least one miner exposed to an equivalent 8hour TWA (SWA) fiber concentration exceeding 0.1 f/cc. Out of a total of 917 SWA personal fullshift fiber exposure sample results, 113 (12 percent) exceeded 0.1 f/cc using the existing PCMbased analytical screening method.
Further analysis of the 113 samples with TEM confirmed asbestos
fiber exposures exceeding 0.1 f/cc in 23 of them. Using the existing
TEMbased analytical method, 3 percent of the total number of SWA
samples taken exceeded 0.1 asbestos f/cc. Five mines (two taconite, one
wollastonite, one sand and gravel, and one olivine), out of the 29
mines potentially impacted by lowering the PEL, had at least one miner
with an SWA asbestos fiber exposure exceeding 0.1 f/cc. Although MSHA
has no evidence of asbestos exposure above the new PEL in coal mines,
the Agency anticipates that some coal mines will encounter asbestos
from asbestos containing materials (ACM) brought onto mine property.
These operators may have to take corrective action. Table III1 below
summarizes MSHA's asbestos sampling results for the period January 2000 through May 2007.
Table III1.Personal Exposure Samples at Mines \1\ by Commodity [1/20005/2007] Number (%) of Number (%) Number of mines with SWA Number of Number (%) of of SWA Commodity mines samples >0.1 f/ SWA SWA samples >0.1 samples >0.1 sampled cc by PCM samples f/cc by PCM \2\ f/cc by TEM Rock & quarry products \3\.......... 127 11 (9%) 326 20 (6%) 2 (1%) Vermiculite......................... 4 3 (75%) 149 13 (9%) 0 Wollastonite........................ 1 1 (100%) 18 18 (100%) 9 (50%) Iron (taconite)..................... 15 5 (33%) 254 43 (17%) 11 (4%) Talc................................ 12 1 (8%) 38 2 (5%) 0 Alumina \4\......................... 1 0 1 0 0 Feldspar............................ 7 0 \5\ 6 0 0 Boron............................... 2 1 (50%) 12 7 (58%) 0 Olivine............................. 2 2 (100%) 9 3 (33%) 1 (11%) Other \6\........................... 36 \7\ 5 (14%) 104 7 (6%) 0
TOTAL........................... 207 \8\ 29 (14%) 917 113 (12%) 23 (3%)
\1\ Excludes data from an asbestos mine and mill closed in 2003.
\2\ MSHA uses TEM to identify asbestos on samples with results exceeding 0.1 f/cc. \3\ Including stone, and sand and gravel mines.
\4\ 15minute sample.
\5\ Incomplete SWA at one mine.
\6\ Coal, potash, gypsum, cement, perlite, clay, lime, mica, metal ore NOS, shale, pumice, trona, salt, gold, and copper.
\7\ Coal, potash, gypsum, cement, and perlite. (Coal and potash exposures were due to fiber release episodes from commercially introduced asbestos).
\8\ TEM confirmed airborne asbestos exposures exceeding 0.1 f/cc at five (2%) mines. [[Page 11289]]
The USGS has published a series of maps showing historic asbestos prospects and natural asbestos occurrences in the United States. The USGS published a map covering the eastern states in 2005; the central states in 2006; and the Rocky Mountain states in 2007. These maps served as a guide for the investigation of possible naturally occurring asbestos within the vicinity of mining operations. MSHA found that stone mines and quarries are the predominate types of mining operations in the vicinity of naturally occurring asbestos locations identified on the maps. MSHA conducted fiber sampling at these mines to screen for potential asbestos exposures. The results of the sampling indicated a small degree of asbestos at some of these mining operations, but no widespread asbestos contamination. Although not included on the USGS maps, MSHA also surveyed two mines in El Dorado County, California. Sampling at one of the mines resulted in two personal asbestos exposures greater than 0.1 f/cc, confirmed by TEM analysis, and 2 to 5 percent naturally occurring asbestos in an associated bulk sample. Air sampling at the other mine had low PCM fiber results.
D. Asbestos TakeHome Contamination
The final rule, like the proposal, does not address takehome
contamination. In making this decision, MSHA considered its enforcement
experience; comments and testimony on the proposal; as well as OSHA,
NIOSH, and EPA publications and experience.\39\ MSHA based its
determination to address asbestos takehome contamination, without
promulgating new regulatory provisions, on the following factors: \39\ NIOSH (Report to Congress) September 1995.
Commenters urged MSHA to expand the rulemaking to include specific requirements to prevent takehome contamination. NIOSH also encouraged MSHA to adopt measures included in its 1995 Report to Congress on their Workers' Home Contamination Study Conducted under the Workers' Family Protection Act. Other commenters, however, supported MSHA's decision and stated that takehome contamination requirements could not be justified at this time.
IV. Application of OSHA's Risk Assessment to Mining
MSHA has determined that OSHA's 1986 asbestos risk assessment (51
FR 22644) is applicable to asbestos exposures in mining. In developing
this final rule, MSHA also evaluated studies published since OSHA
completed its 1986 risk assessment, and studies that specifically
focused on asbestos exposures of miners. These additional studies corroborate OSHA's conclusions in its risk assessment.
A. Summary of OSHA's Risk Assessment
1. Cancer Mortality
In its 1986 risk assessment, OSHA estimated cancer mortality for
workers exposed to asbestos at various cumulative exposures (i.e.,
combining exposure concentration and duration of exposure). MSHA has
reproduced this data in Table IV1. Table IV1 shows that the estimated
mortality from asbestosrelated cancer decreases significantly by
lowering exposure. This is true regardless of the type of cancer, e.g.,
lung, pleural or peritoneal mesotheliomas, or gastrointestinal.
Although excess relative risk is linear in dose, the excess mortality rates in Table IV1 are not.\40\
\40\ Nicholson, p. 53, 1983.
Table IV1.Estimated AsbestosRelated Cancer Mortality per 100,000 by Number of Years Exposed and Exposure Level Cancer mortality per 100,000 exposed Asbestos fiber concentration (f/cc)
Lung Mesothelioma Gastrointestinal Total 1year exposure 0.1........................................... 7.2 6.9 0.7 14.8 0.2........................................... 14.4 13.8 1.4 29.6 0.5........................................... 36.1 34.6 3.6 74.3 2.0........................................... 144 138 14.4 296.4 4.0........................................... 288 275 28.8 591.8 5.0........................................... 360 344 36.0 740.0 10.0.......................................... 715 684 71.5 1,470.5 20year exposure 0.1........................................... 139 73 13.9 225.9 0.2........................................... 278 146 27.8 451.8 0.5........................................... 692 362 69.2 1,123.2 2.0........................................... 2,713 1,408 271.3 4,392.3 4.0........................................... 5,278 2,706 527.8 8,511.8 [[Page 11290]]
5.0........................................... 6,509 3,317 650.9 10,476.9 10.0.......................................... 12,177 6,024 1,217.7 13,996.7 45year exposure 0.1........................................... 231 82 23.1 336.1 0.2........................................... 460 164 46.0 670.0 0.5........................................... 1,143 407 114.3 1,664.3 2.0........................................... 4,416 1,554 441.6 6,411.6 4.0........................................... 8,441 2,924 844.1 12,209.1 5.0........................................... 10,318 3,547 1,031.8 14,896.8 10.0.......................................... 18,515 6,141 1,851.5 26,507.5
Table IV1 shows that, by lowering the PEL from 2 f/cc to 0.1 f/cc, the risk of cancer mortality drops 95 percent from an estimated 6,411 to 336 deaths (per 100,000 workers).
Finkelstein (1982) studied a group of 201 men who worked in a factory in Ontario, Canada, that manufactured asbestoscement pipe and rockwool insulation. Finkelstein demonstrated that there was a relationship between cumulative asbestos exposure and confirmed asbestosis.
Berry and Lewinsohn (1979) studied a group of 379 men who worked in an asbestos textile factory in northern England. Berry and Lewinsohn (1979) defined two different cohorts: Men who were first employed before 1951, when asbestos fiber levels were estimated; and men first employed after 1950, when asbestos fiber levels were measured. They plotted cases of possible asbestosis to determine a dose response curve.
OSHA stated that ``* * * the best estimates of asbestosis incidence
are derived from the Finkelstein data * * *'' (48 FR 51132). OSHA did
not rely on the values for the slope as determined by Berry and
Lewinsohn (1979). Based on Finkelstein's (1982) linear relationship for
lifetime asbestosis incidence, OSHA calculated estimates of lifetime
asbestosis incidence at five exposure levels of asbestos (i.e., 0.5, 1,
2, 5, and 10 f/cc) and published its estimate in tabular form (48 FR
51132). MSHA has reproduced OSHA's estimates in Table IV2 below. OSHA
stated (51 FR 22646) that ``Reducing the exposure to 0.2 f/cc, a
concentration not included in Table IV2, would result in a lifetime incidence of asbestosis of 0.5%.''
\41\ Finkelstein, 1982; Berry and Lewinsohn, 1979.
Table IV2.Estimates of Lifetime Asbestosis Incidence \41\ Percent (%) Incidence
Exposure level, f/cc Berry and Lewinsohn Finkelstein Berry and Lewinsohn (first employed after (employed before 1951) 1950) 0.5.................................. 1.24 0.45 0.35 1.................................... 2.49 0.89 0.69 2.................................... 4.97 1.79 1.38 5.................................... 12.43 4.46 * 3.45 10................................... 24.86 8.93 6.93 Slope................................ 0.055 0.020 0.015 R \2\................................ 0.975 0.901 0.994 * Note: 1.38 in original table was a typographical error. The text (48 FR 51132) and the regression formula indicate that 3.45 is the correct percent.
Similar to the cancer risk, Table IV2 shows a significant reduction in the incidence of asbestosis by lowering asbestos exposures. MSHA calculated the incidence of asbestosis following 45 years of exposure to asbestos at a concentration of 0.1 f/cc, which OSHA had not included in Table IV1, to be 0.25 percent or 250 cases per 100,000 workers. Thus, by lowering the 8hour TWA PEL from 2 f/cc to 0.1 f/cc, MSHA will reduce the lifetime asbestosis risk by 95 percent from an estimated 4,970 cases to 250 cases (per 100,000 workers).
B. Risk Assessment for the Mining Industry
OSHA stated in the preamble to its 1986 asbestos rule that it
excluded mining studies in its risk assessment because it believed that
risks in the asbestos miningmilling operations are lower than other
industrial operations due to differences in fiber size (51 FR 22637).
MSHA reviewed the studies OSHA used to develop its risk assessment.\42\
In addition, MSHA obtained and reviewed the latest available scientific studies on the health
effects of asbestos exposure. MSHA recognizes that there are uncertainties in any risk assessment. MSHA concluded, however, that these studies provide further support of the significant risk of adverse health effects following exposure to asbestos.
\42\ Berry and Newhouse, 1983; Dement et al., 1982; Finkelstein, 1983; Henderson and Enterline, 1979; Peto, 1980; Peto et al., 1982; Seidman et al., 1979; Seidman, 1984; Selikoff et al., 1979; Weill et al., 1979.
MSHA reviewed the mining studies described in OSHA's asbestos risk assessment, as well as other studies that involved the exposure of miners to asbestos. Most of these studies were conducted in Canada, although some have been conducted in Australia, India, Italy, South Africa, and the United States. Table IV3 lists some of these mining studies, in chronological order, and gives the salient features of each study. These studies are in MSHA's rulemaking docket.
Table IV.3Selected Studies Involving Miners Exposed to Asbestos
Study group, type Major finding(s) or
Author(s), year of publication of asbestos conclusion(s)
Rossiter et al., 1972......... Canadian miners Radiographic changes
and millers, (opacities) related
Chrysotile. to age and exposure.
Becklake, 1979................ Canadian miners Weak relationship
and millers, between exposure and
Gibbs and du Toit, 1979....... Canadian and Need for workplace
South African epidemiologic
miners, surveillance and
Irwig et al., 1979............ South African Parenchymal
miners, Amosite radiographic
and Crocidolite. abnormalities
McDonald and Liddell, 1979.... Canadian miners Lower risk of
and millers, mesotheliomas and
Chrysotile. lung cancer from
Nicholson et al., 1979........ Canadian miners Miners and millers:
and millers, at lower risk of
Chrysotile. mesotheliomas, at
risk of asbestosis
(as factory workers
and insulators), at
risk of lung cancer
Rubino et al., Ann NY Ac Sci Italian miners, Role of individual
1979. Chrysotile. susceptibility in
Rubino et al., Br J Ind Med Italian miners, Elevated risk of lung
1979. Chrysotile. cancer.
Solomon et al., 1979.......... South African Sign of exposure to
miners, Amosite asbestos: thickened
and Crocidolite. interlobar fissures.
McDonald et al., 1980......... Canadian miners No statistically
and millers, significant
Chrysotile. increases in SMRs.
McDonald et al., 1986......... U.S. miners, A. Increased risk of
Tremolite.. mortality from
McDonald et al., 1986......... U.S. miners, B. Increased
Tremolite. prevalence of small
Cookson et al., 1986.......... Australian miners No threshold dose for
and millers, development of
Amandus et al., 1987.......... U.S. miners and Part I: Exposures
millers, below 1 f/cc after
Tremolite 1977, up to 100200
Actinolite. x higher in 1960's
Amandus and Wheeler, 1987..... U.S. miners and Part II: Increased
millers, mortality from
Actinolite. respiratory disease
and lung cancer.
Amandus et al., 1987.......... U.S. miners and Part III: Increased
millers, prevalence of
associated with past
Armstrong et al., 1988........ Australian miners Increased mortality
and millers, from mesotheliomas
Crocidolite. and lung cancer.
Enarson et al., 1988.......... Canadian miners, Increased cough,
abnormal lung volume
McDonald et al., 1988......... U.S. miners and Low exposure and no
Tremolite. significant SMRs.
McDonald et al., 1993......... Canadian miners Increased SMRs for
and millers, lung cancer and
Chrysotile. mesotheliomas as
Dave et al., 1996............. Indian miners and Higher exposures in
millers, surface than
Chrysotile. underground mines;
higher exposures in
mills than mines;
more common in
McDonald et al., 1997......... Canadian miners Risk of mesotheliomas
and millers, related to geography
Chrysotile. and mineralogy of
Nayebzadeh et al., 2001....... Canadian miners Respiratory disease
and millers, related to regional
Chrysotile. differences in fiber
Ramanathan and Subramanian, Indian miners and Increased risk of
2001. millers, cancer, restrictive
Chrysotile and lung disease,
tremolite. radiologic changes,
common in milling.
Bagatin et al., 2005.......... Brazilian miners Decreased risk of non
and millers, malignant
Chrysotile. abnormalities with
Nayebzadeh et al., 2006....... Canadian miners Possible use of lung
and millers, fiber concentration,
Chrysotile, especially short
Tremolite, tremolite fibers, to
Amosite. predict fibrosis grade.
Sullivan, 2007................ U.S. miners, Increased mortality millers, and from asbestosis, processors, cancer of the Tremolite. pleura, and lung cancer that were doserelated.
MSHA found that many of the observations presented in these mining studies (e.g., age of first exposure, latency, radiologic changes) are consistent with those from the studies OSHA relied on in its risk assessment, as well as studies of other asbestosexposed factory and insulation workers. MSHA concludes that exposure to asbestos, a known human carcinogen, results in similar disease endpoints regardless of the occupation that has been studied. Because there is evidence of asbestosrelated disease among miners, MSHA is applying the OSHA risk assessment to the mining industry.
Some commenters stated that there is a differential health risk
related to fiber type and that OSHA's risk assessment is not adequate
or appropriate for the mining industry. The OSHA risk assessment
addresses adverse health effects from exposure to six asbestos minerals. MSHA applies TEM analysis
to its PCM results to determine exposure to these same six asbestos minerals. Exposure of miners to these asbestos minerals, at the same concentrations and length of exposures as workers in other industries, can be expected to result in the same disease endpoints as quantified in OSHA's risk assessment. (See section II.C and II.D of this preamble and chapter III of the REA.)
Some commenters also expressed concern regarding the health risks of fibrous minerals that are not currently regulated under MSHA's existing standards and suggested that MSHA conduct a new risk assessment to include them. MSHA considered these comments and determined that a new risk assessment is not necessary for this final rule, since fibrous minerals that are not currently regulated under MSHA's existing standards are beyond the scope of this rulemaking.
Some commenters stressed the lack of asbestosrelated disease among
miners in studies conducted at gold, taconite, and talc operations
where there was asbestos contamination in the ore. In developing this final rule, MSHA considered a number of environmental and
epidemiological studies conducted at mining operations. These studies demonstrated adverse health effects among miners consistent with exposure to asbestos in other workers. Researchers have found excessive incidence of asbestosrelated disease in miners at a vermiculite mining operation.\43\ Studies of talc miners have shown excess lung cancer and nonmalignant respiratory disease.\44\ Researchers are now studying excessive mesotheliomas among iron miners in northeastern Minnesota to determine the source of the asbestos exposure.
\43\ Sullivan, 2007.
\44\ NIOSH (HETA/MHETA), 1990; NIOSH (Technical Report), 1980.
Section VI of this preamble contains a summary of MSHA's findings from applying OSHA's quantitative assessment of risk to the mining industry. MSHA's Regulatory Economic Analysis (REA) contains a more in depth discussion of the Agency's methodology and conclusions. MSHA placed the REA in the rulemaking docket and posted it on the Asbestos Single Source Page at http://www.msha.gov/asbestos/asbestos.htm. MSHA also placed OSHA's risk assessment in its rulemaking docket. C. Characterization of the Risk to Miners
After reviewing the evidence of adverse health effects associated
with exposure to asbestos, MSHA evaluated that evidence to ascertain
whether exposure levels currently existing in mines warrant regulatory
action. The criteria for this evaluation are established by the Federal
Mine Safety and Health Act of 1977 (Mine Act) and related court decisions.\45\
\45\ Industrial Union Department, AFLCIO v. American Petroleum Institute, 448 U.S. 607, 100 S.Ct. 2844 (1980) (``Benzene case'')
Section 101(a) of the Mine Act requires MSHA `` * * * to develop, promulgate, and revise * * * improved mandatory health or safety standards for the protection of life and prevention of injuries in coal or other mines.'' Further, section 101(a)(6)(A) provides that
The Secretary, in promulgating mandatory standards dealing with toxic materials or harmful physical agents under this subsection, shall set standards which most adequately assure on the basis of the best available evidence that no miner will suffer material impairment of health or functional capacity even if such miner has regular exposure to the hazards dealt with by such standard for the period of his working life.
Section 101(a)(6)(A) also requires that MSHA base its health and safety standards on ``* * * the latest available scientific data in the field, the feasibility of the standards, and experience gained under this and other health and safety laws.'' As discussed in section VI.B, a 0.1 f/cc TWA PEL for asbestos is technologically and economically feasible.
Based on court interpretations of similar language under the
Occupational Safety and Health Act, MSHA has addressed the following three questions:
(1) Do the health effects associated with asbestos exposure constitute a ``material impairment'' to miner health or functional capacity? Miners exposed to asbestos are at risk of developing lung cancer, mesotheliomas, and other cancers, as well as asbestosis and other nonmalignant respiratory diseases.\46\ These health effects constitute a ``material impairment of health or functional capacity.'' \46\ American Thoracic Society, 2004; Delpierre et al., 2002. (2) Are exposed miners at significant risk of incurring any of these material impairments? Based on OSHA's risk assessment, MSHA has determined that a significant health risk exists for miners exposed to asbestos at MSHA's existing 8hour TWA PEL of 2 f/cc. Over a 45year working life, exposure at this level can be expected to result in a 6.4 percent incidence of cancer (lung cancer, mesotheliomas, and gastrointestinal cancer) and a 5.0 percent incidence of asbestosis. (3) Will this final rule substantially reduce such risks? By lowering the 8hour TWA PEL to 0.1 f/cc, MSHA will reduce the risk of asbestosrelated cancers from 6.4 percent to 0.34 percent and the risk of asbestosis from 5.0 percent to 0.25 percent. MSHA considers this reduction to be substantial.
V. SectionbySection Analysis of Final Rule
The final rule is substantively the same as the proposed rule. To make the standard easier to read, however, MSHA has divided the requirements in the final standards into three paragraphs: Definitions, Permissible Exposure Limits (PELs), and Measurement of Airborne Fiber Concentration. For Sec. Sec. 56/57.5001(b), the metal and nonmetal asbestos standards, MSHA designated the paragraphs (b)(1), (b)(2), and (b)(3). For Sec. 71.702, the coal asbestos standard, MSHA designated the paragraphs (a), (b), and (c).
A. Sec. Sec. 56/57.5001(b)(1) and 71.702(a): Definitions
The final rule, like the proposal, makes no substantive changes to
the definition of asbestos in MSHA's existing standards. MSHA's
existing definition of asbestos is consistent with the regulatory
provisions of several Federal agencies including EPA, OSHA, and CPSC,
among others. Asbestos is not a definitive mineral, but rather a
generic name for a group of minerals with specific characteristics.
MSHA's existing standards state that, ``when crushed or processed,
[asbestos] separates into flexible fibers made up of fibrils''
[Sec. Sec. 56/57.5001(b)]; and ``does not include nonfibrous or
nonasbestiform minerals'' (Sec. 71.702). Although there are many
asbestiform minerals,\47\ the term asbestos in MSHA's existing
standards and this final rule is limited to the following six: \48\ \47\ Leake et al., 1997; Meeker et al., 2003.
\48\ ATSDR, p.136, 2001; NIOSH Pocket Guide, 2003.
FOR FURTHER INFORMATION CONTACT
Patricia W. Silvey at firstname.lastname@example.org (Email), 2026939440 (Voice), or 2026939441 (Fax).