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Asbestos
CASRN 1332-21-4
Contents
0371
Asbestos; CASRN 1332-21-4
Health assessment information on a chemical substance is included in IRIS only
after a comprehensive review of chronic toxicity data by U.S. EPA health
scientists from several Program Offices and the Office of Research and
Development. The summaries presented in Sections I and II represent a
consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Asbestos
File On-Line 09/26/1988
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) no data
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 07/01/1993
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Asbestos
CASRN -- 1332-21-4
Not available at this time.
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Asbestos
CASRN -- 1332-21-4
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Asbestos
CASRN -- 1332-21-4
Last Revised -- 07/01/1993
Section II provides information on three aspects of the carcinogenic
assessment for the substance in question; the weight-of-evidence judgment of
the likelihood that the substance is a human carcinogen, and quantitative
estimates of risk from oral exposure and from inhalation exposure. The
quantitative risk estimates are presented in three ways. The slope factor is
the result of application of a low-dose extrapolation procedure and is
presented as the risk per (mg/kg)/day. The unit risk is the quantitative
estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m
air breathed. The third form in which risk is presented is a drinking water
or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1
in 1,000,000. The rationale and methods used to develop the carcinogenicity
information in IRIS are described in The Risk Assessment Guidelines of 1986
(EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries
developed since the publication of EPA's more recent Proposed Guidelines for
Carcinogen Risk Assessment also utilize those Guidelines where indicated
(Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to
Section I of this IRIS file for information on long-term toxic effects other
than carcinogenicity.
NOTE: The carcinogen assessment summary for asbestos may change in the near
future pending the outcome of a further review now being conducted by the
CRAVE Work Group.
__II.A. EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
___II.A.1. WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification -- A; human carcinogen
Basis -- Observation of increased mortality and incidence of lung cancer,
mesotheliomas and gastrointestinal cancer in occupationally exposed workers
are consistent across investigators and study populations. Animal studies by
inhalation in two strains of rats showed similar findings for lung cancer and
mesotheliomas. Animal evidence for carcinogenicity via ingestion is limited
(male rats fed intermediate-range chrysotile fibers; i.e., >10 um length,
developed benign polyps), and epidemiologic data in this regard are
inadequate.
___II.A.2. HUMAN CARCINOGENICITY DATA
Sufficient. Numerous epidemiologic studies have reported an increased
incidence of deaths due to cancer, primarily lung cancer and mesotheliomas
associated with exposure to inhaled asbestos. Among 170 asbestos insulation
workers in North Ireland followed for up to 26 years, an increased incidence
of death was seen due to all cancers (SMR=390), cancers of the lower
respiratory tract and pleura (SMR=1760) (Elmes and Simpson, 1971) and
mesothelioma (7 cases). Exposure was not quantified.
Selikoff (1976) reported 59 cases of lung cancer and 31 cases of
mesothelioma among 1249 asbestos insulation workers followed prospectively
for 11 years. Exposure was not quantified. A retrospective cohort mortality
study (Selikoff et al., 1979) of 17,800 U.S. and Canadian asbestos insulation
workers for a 10-year period using best available information (autopsy,
surgical, clinical) reported an increased incidence of cancer at all sites
(319.7 expected vs. 995 observed, SMR=311) and cancer of the lung (105.6
expected vs. 486 observed, SMR=460). A modest increase in deaths from
gastrointestinal cancer was reported along with 175 deaths from mesothelioma
(none expected). Years of exposure ranged from less than 10 to greater than
or equal to 45. Levels of exposure were not quantified. In other
epidemiologic studies, the increase for lung and pleural cancers has ranged
from a low of 1.9 times the expected rate, in asbestos factory workers in
England (Peto et al., 1977), to a high of 28 times the expected rate, in
female asbestos textile workers in England (Newhouse et al., 1972). Other
occupational studies have demonstrated asbestos exposure-related increases in
lung cancer and mesothelioma in several industries including textile
manufacturing, friction products manufacture, asbestos cement products, and
in the mining and milling of asbestos. The studies used for the inhalation
quantitative estimate of risk are listed in the table in Section II.C.2.
A case-control study (Newhouse and Thompson, 1965) of 83 patients with
mesothelioma reported 52.6% had occupational exposure to asbestos or lived
with asbestos workers compared with 11.8% of the controls. Of the remaining
subjects, 30.6% of the mesothelioma cases lived within one-half mile of an
asbestos factory compared with 7.6% of the controls.
The occurrence of pleural mesothelioma has been associated with the
presence of asbestos fibers in water, fields and streets in a region of
Turkey with very high environmental levels of naturally-occurring asbestos
(Baris et al., 1979).
Kanarek et al. (1980) conducted an ecologic study of cancer deaths in 722
census tracts in the San Francisco Bay area, using cancer incidence data from
the period of 1969-1971. Chrysotile asbestos concentrations in drinking
water ranged from nondetectable to 3.6E+7 fibers/L. Statistically significant
dose-related trends were reported for lung and peritoneal cancer in white
males and for gall bladder, pancreatic and peritoneal cancer in white
females. Weaker correlations were reported between asbestos levels and
female esophageal, pleural and kidney cancer, and stomach cancer in both
sexes. In an extension of this study, Conforti et al. (1981) included cancer
incidence data from the period of 1969-1974. Statistically significant
positive associations were found between asbestos concentration and cancer of
the digestive organs in white females, cancers of the digestive tract in
white males and esophageal, pancreatic and stomach cancer in both sexes.
These associations appeared to be independent of socioeconomic status and
occupational exposure to asbestos.
Marsh (1983) reviewed eight independent ecologic studies of asbestos in
drinking water carried out in five geographic areas. It was concluded that
even though one or more studies found an association between asbestos in
water and cancer mortality (or incidence) due to neoplasms of various organs,
no individual study or aggregation of studies exists that would establish
risk levels from ingested asbestos. Factors confounding the results of these
studies include the possible underestimates of occupational exposure to
asbestos and the possible misclassification of peritioneal mesothelioma as GI
cancer.
Polissar et al. (1984) carried out a case-control study which included
better control for confounding variables at the individual level. The authors
concluded that there was no convincing evidence for increased cancer risk from
asbestos ingestion. At the present time, an important limitation of both the
case-control and the ecologic studies is the short follow-up time relative to
the long latent period for the appearance of tumors from asbestos exposure.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. There have been about 20 animal bioassays of asbestos.
Gross et al. (1967) exposed 61 white male rats (strain not reported) to 86 mg
chrysotile asbestos dust/cu.m for 30 hours/week for 16 months. Of the 41
animals that survived the exposure period, 10 had lung cancer. No lung cancer
was observed in 25 controls.
Reeves (1976) exposed 60-77 rats/group for 4 hours/day, 4 days/week for 2
years to doses of 48.7-50.2 mg/cu.m crocidolite, 48.2-48.6 mg/cu.m amosite
and 47.4-47.9 mg/cu.m chrysotile. A 5-14% incidence of lung cancer was
observed among concentration groups and was concentration-dependent.
Wagner et al. (1974) exposed CD Wistar rats (19-52/group) to 9.7-14.7
mg/cu.m of several types of asbestos for 1 day to 24 months for 7 hours/day,
5 days/week. A duration-dependent increased incidence of lung carcinomas and
mesotheliomas was seen for all types of asbestos after 3 months of exposure
compared with controls.
F344 rats (88-250/group) were exposed to intermediate range chrysotile
asbestos (1291E+8 f/g) in drinking water by gavage to dams during lactation
and then in diet throughout their lifetime (NTP, 1985). A statistically
significant increase in incidence of benign epithelial neoplasms (adenomatous
polyps in the large intestine) was observed in male rats compared with pooled
controls of all NTP oral lifetime studies (3/524). In the same study, rats
exposed to short range chrysotile asbestos (6081E+9 f/g) showed no
significant increase in tumor incidence.
Ward et al. (1980) administered 10 mg UICC amosite asbestos 3 times/week
for 10 weeks by gavage to 50 male F344 rats. The animals were observed for
an additional 78-79 weeks post-treatment. A total of 17 colon carcinomas
were observed. This result was statistically significant compared with
historical controls; no concurrent controls were maintained.
Syrian golden hamsters (126-253/group) were exposed to short and
intermediate range chrysotile asbestos at a concentration of 1% in the diet
for the lifetime of the animals (NTP, 1983). An increased incidence of
neoplasia of the adrenal cortex was observed in both males and females
exposed to intermediate range fibers and in males exposed to short range
fibers. This increase was statistically significant by comparison to pooled
controls but not by comparison to concurrent controls. NTP suggested that
the biologic importance of adrenal tumors in the absence of target organ (GI
tract) neoplasia was questionable.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Sincock (1977) reported an increased number of chromosomes and chromosome
breaks after passive inclusion of asbestos with CHO-K1 cells. Chamberlain
and Tarmy (1977) reported asbestos not to be mutagenic for E. coli or S.
typhimurium. A positive response was unlikely, however, since prokaryotic
cells do not phagocytize particles as do eukaryotic cells.
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
Not available.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
___II.C.1. SUMMARY OF RISK ESTIMATES
Inhalation Unit Risk -- 2.3E-1 per (f/mL)
Extrapolation Method -- Additive risk of lung cancer and mesothelioma, using
relative risk model for lung cancer and absolute risk model for mesothelioma
Air Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 4E-4 f/mL
E-5 (1 in 100,000) 4E-5 f/mL
E-6 (1 in 1,000,000) 4E-6 f/mL
___II.C.2. DOSE-RESPONSE DATA FOR CARCINOGENICITY, INHALATION EXPOSURE
Reported
Average
Human Data Fiber Exposure % Increase Reference
Occupational Type (fiber- in Cancer per
Group yr/mL) fiber-yr/mL
------------------- ------------- -------- -------------- ---------------
Lung Cancer:
Textile Products Predominantly 44 2.8 Dement et al.,
Chrysotile 1983b
Textile Products Chrysotile 31 2.5 McDonald et
al., 1983a
Textile Products Chrysotile 200 1.1 Peto, 1980
Textile Products Chrysotile 51 1.4 McDonald et
al., 1983b
Friction Products Chrysotile 32 0.058 Berry and
Newhouse, 1983
Friction Products Chrysotile 31 0.010 McDonald et
al., 1984
Insulation Products Amosite 67 4.3 Seidman, 1984
Insulation Workers Mixed 300 0.75 Selikoff et
(Chrysotile, al., 1979
Crocidolite
and Amosite)
Asbestos Products 374 0.49 Henderson and
Enterline, 1979
Cement Products 89 0.53 Weill et al.,
1979
112 6.7 Finkelstein,
1983
Mesothelioma:
Insulation workers Mixed 375 1.5E-6 Selikoff et
al., 1979;
Peto et al.,
1982
Insulation Products Amosite 400 1.0E-6 Seidman et al.,
1979
Textile Products Chrysotile 67 3.2E-6 Peto, 1980;
Manufacturer Peto et al.,
1982
Cement Products Mixed 108 1.2E-5 Finkelstein,
1983
___II.C.3. ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
Risks have been calculated for males and females according to smoking
habits for a variety of exposure scenarios (U.S. EPA, 1986). The unit risk
value is calculated for the additive combined risk of lung cancer and
mesothelioma, and is calculated as a composite value for males and females.
The epidemiological data show that cigarette smoking and asbestos exposure
interact synergistically for production of lung cancer and do not interact
with regard to mesothelioma. The unit risk value is based on risks
calculated using U.S. general population cancer rates and mortality patterns
without consideration of smoking habits. The risks associated with
occupational exposure were adjusted to continuous exposure by applying a
factor of 140 cu.m/50 cu.m based on the assumption of 20 cu.m/day for total
ventilation and 10 cu.m/8-hour workday in the occupational setting.
The unit risk is based on fiber counts made by phase contrast microscopy
(PCM) and should not be applied directly to measurements made by other
analytical techniques. The unit risk uses PCM fibers because the
measurements made in the occupational environment use this method. Many
environmental monitoring measurements are reported in terms of fiber counts
or mass as determined by transmission electron microscopy (TEM). PCM detects
only fibers longer than 5 um and >0.4 um in diameter, while TEM can detect
much smaller fibers. TEM mass units are derived from TEM fiber counts. The
correlation between PCM fiber counts and TEM mass measurements is very poor.
Six data sets which include both measurements show a conversion between TEM
mass and PCM fiber count that range from 5-150 (ug/cu.m)/(f/mL). The
geometric mean of these results, 30 (ug/cu.m)/(f/mL), was adopted as a
conversion factor (U.S. EPA, 1986), but it should be realized that this value
is highly uncertain. Likewise, the correlation between PCM fiber counts and
TEM fiber counts is very uncertain and no generally applicable conversion
factor exists for these two measurements.
In some cases TEM results are reported as numbers of fibers <5 um long
and of fibers longer than 5 um. Comparison of PCM fiber counts and TEM
counts of fibers >5 um show that the fraction of fibers detected by TEM that
are also >0.4 um in diameter (and detectable by PCM) varies from 22-53% (U.S.
EPA, 1986).
It should be understood that while TEM can be specific for asbestos, PCM
is a nonspecific technique and will measure any fibrous material.
Measurements by PCM which are made in conditions where other types of fibers
may be present may not be reliable.
In addition to the studies cited above, there were three studies of
asbestos workers in mining and milling which showed an increase in lung
cancer (McDonald et al., 1980, Nicholson et al., 1979; Rubino et al., 1979).
The slope factor calculated from these studies was lower than the other
studies, possibly because of a SUBSTantially different fiber size
distribution, and they were not included in the calculation. The slope
factor was calculated by life table methods for lung cancer using a relative
risk model, and for mesothelioma using a absolute risk model. The final
slope factor for lung cancer was calculated as the weighted geometric mean of
estimates from the 11 studies cited in section II.C.2. The final slope
factor for mesothelioma is based on the calculated values from the studies of
Selikoff et al. (1979), Peto et al. (1982), Seidman et al. (1979), Peto
(1980) and Finkelstein (1983) adjusted for the mesothelioma incidence from
several additional studies cited previously.
There is some evidence which suggests that the different types of
asbestos fibers vary in carcinogenic potency relative to one another and site
specificity. It appears, for example, that the risk of mesothelioma is
greater with exposure to crocidolite than with amosite or chrysotile exposure
alone. This evidence is limited by the lack of information on fiber exposure
by mineral type. Other data indicates that differences in fiber size
distribution and other process differences may contribute at least as much to
the observed variation in risk as does the fiber type itself.
The unit risk should not be used if the air concentration exceeds 4E-2
fibers/ml, since above this concentration the slope factor may differ from
that stated.
___II.C.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE)
A large number of studies of occupationally-exposed workers have
conclusively demonstrated the relationship between asbestos exposure and lung
cancer or mesothelioma. These results have been corroborated by animal
studies using adequate numbers of animals. The quantitative estimate is
limited by uncertainty in the exposure estimates, which results from a lack
of data on early exposure in the occupational studies and the uncertainty of
conversions between various analytical measurements for asbestos.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1985
The 1985 Drinking Water Criteria Document for Asbestos and the 1986 Airborne
Asbestos Health Assessment Update have received Agency review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 09/15/1987, 12/02/1987
Verification Date -- 12/02/1987
___II.D.3. U.S. EPA CONTACTS (CARCINOGENICITY ASSESSMENT)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_VI. BIBLIOGRAPHY
Substance Name -- Asbestos
CASRN -- 1332-21-4
Last Revised -- 07/01/1993
__VI.A. ORAL RfD REFERENCES
None
__VI.B. INHALATION RfD REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Baris, Y.I., M. Artivinli and A.A. Sahin. 1979. Environmental mesothelioma
in Turkey. Ann. N.Y. Acad. Sci. 330: 423-432.
Berry, G. and M.L. Newhouse. 1983. Mortality of workers manufacturing
friction materials using asbestos. Br. J. Ind. Med. 40: 1-7.
Chamberlain, M. and E.M. Tarmy. 1977. Asbestos and glass fibers in bacterial
mutation tests. Mutat. Res. 43: 159-164.
Conforti, P.M., M.S. Kanarek, L.A. Jackson, R.C. Cooper and J.C. Murchio.
1981. Asbestos in drinking water and cancer in the San Francisco Bay Area:
1969-1974 incidence. J. Chr. Dis. 34: 211-224.
Dement, J.M., R.L. Harris Jr., M.J. Symons and C.M. Shy. 1983. Exposures and
mortailty among chrysotile asbestos workers. Part II: Mortality. Am. J. Ind.
Med. 4: 421-433.
Elmes, P.C. and M.J. Simpson. 1971. Insulation workers in Belfast. III.
Mortality 1940-1966. Br. J. Ind. Med. 28: 226-236.
Finkelstein, M.M. 1983. Mortality among long-term employees of an Ontario
asbestos-cement factory. Br. J. Ind. Med. 40: 138-144.
Gross, P., R.T.P. deTreville, E.B. Tolker, M. Kaschak and M.A. Babyak. 1967.
Experimental asbestosis: The development of lung cancer in rats with pulmonary
deposits of chrysotile asbestos dust. Arch. Environ. Health. 15: 343-355.
Henderson, V.L. and P.E. Enterline. 1979. Asbestos exposure: Factors
associated with excess cancer and respiratory disease mortality. Ann. N.Y.
Acad. Sci. 330: 117-126.
Kanarek, M.S., P.M. Conforti, L.A. Jackson, R.C. Cooper and J.C. Murchio.
1980. Asbestos in drinking water and cancer incidence in the San Francisco
bay area. Am. J. Epidemiol. 12-1: 54-72.
Marsh, G.M. 1983. Critical review of epidemiologic studies related to
ingested asbestos. Environ. Health. Perspect. 53: 49-56.
McDonald, J.C., F.D.K. Liddell, G.W. Gibbs, G.E. Eyssen and A.D. McDonald.
1980. Dust exposure and mortality in chrysotile mining, 1910-1975. Br. J.
Ind. Med. 37: 11-24.
McDonald, A.D., J.S. Fry, A.J. Wooley and J.C. McDonald. 1983a. Dust
exposure and mortality in an American chrysotile textile plant. Br. J. Ind.
Med. 40: 361-367.
McDonald, A.D., J.S. Fry, A.J. Wooley and J.C. McDonald. 1983b. Dust
exposure and mortality in an American factory using chrysotile, amosite and
crocidolite in mainly textile manufacturing. Br. J. Ind. Med. 40: 368-374.
McDonald, A.D., J.S. Fry, A.J. Wooley and J.C. McDonald. 1984. Dust exposure
and mortality in an American chrysotile asbestos friction products plant. Br.
J. Ind. Med. 41: 151-157.
Newhouse, M.L. and H. Thompson. 1965. Mesothelioma of the pleura and
peritoneum following exposure to asbestos in the London area. Br. J. Ind.
Med. 22: 261-269.
Newhouse, M.L., G. Berry, J.C. Wagner and M.E. Turok. 1972. A study of the
mortility of female asbestos workers. Br. J. Ind. Med. 29: 134-141.
Nicholson, W.J., I.J. Selikoff, H. Seidman, R. Lilis and P. Formby. 1979.
Long-term mortality experience of chrysotile miners and millers in Thetford
Mines, Quebec. Ann. N.Y. Acad. Sci. 330: 11-21.
NTP (National Toxicology Program). 1983. Carcinogenesis lifetime studies of
chrysotile asbestos (CAS No. 12001-29-5) in Syrian golden hamsters (feed
studies). Technical report series No. 246. Department of Health and Human
Services, Research Triangle Park, NC.
NTP (National Toxicology Program). 1985. Toxicology and carcinogenesis
studies of chrysotile asbestos (CAS No. 12001-29-5) in F344/N rats (feed
studies). Technical report series No. 295. Department of Health and Human
Services, Research Triangle Park, NC.
Peto, J. 1980. Lung cancer mortality in relation to measured dust levels in
an asbestos textile factory. In: Biological effects of mineral fibers: Effets
biologiques des fibers minerals, Vol. 2, J.C. Wagner and W. Davis, Ed.
Proceedings of a symposium, September 1979, Lyon, France. World Health
Organization, International Agency for Research on Cancer Lyon, France. p.
829-836. (IARC scientific publ. no. 30; INSERM symposia series: Vol. 92.)
Peto, J., R. Doll, S.V. Howard, L.J. Kinlen and H.C. Lewinsohn. 1977. A
mortility study among workers in an English asbestos factory. Br. J. Ind.
Med. 34: 169-172.
Peto, J., H. Siedman and I.J. Selikoff. 1982. Mesothelioma mortality in
asbestos workers: Implications for models of carcinogenesis and risk
assessment. Br. J. Cancer. 45: 124-135.
Polissar, L., R.K. Severson and E.S. Boatman. 1984. A case-control
study of asbestos in drinking water and cancer risk. Am. J. Epidemiol.
119(3): 456-471.
Reeves, A.L. 1976. The carcinogenic effect of inhaled asbestos fibers.
Ann. Clin. Lab. Sci. 6: 459-466.
Rubino, G.F., G. Piolatto, M.L. Newhouse, G. Scansetti, G.A. Aresini and R.
Murrary. 1979. Mortality of chrysotile asbestos workers at the Balangero
mine, Northern Italy. Br. J. Ind. Med. 36: 187-194.
Seidman, H. 1984. Short-term asbestos work exposure and long-term
observation. In: [Docket of current rulemaking for revision of the asbestos
(dust) standard]. U.S. Department of Labor, Occupational Safety and Health
Administration, Washington, DC Available for inspection at U.S. Department
of Labor, OSHA Technical Data Center, Francis Perkins Building; docket no.
H033C, exhibit nos. 261-A and 261-B.
Seidman, H., I.J. Selikoff and E.C. Hammond. 1979. Short-term asbestos work
exposure and long-term observation. Ann. N.Y. Acad. Sci. 330: 61-89.
Selikoff, I.J. 1976. Lung cancer and mesothelioma during prospective
surveillance of 1249 asbestos insulation workers, 1963-1974. Ann. N.Y. Acad.
Sci. 271: 448-456.
Selikoff, I.J., E.C. Hammond and H. Siedman. 1979. Mortality experience of
insulation workers in the United States and Canada, 1943-1976. Ann. N.Y.
Acad. Sci. 330: 91-116.
Sincock, A.M. 1977. Preliminary studies of the in vitro cellular effects of
asbestos and fine glass dusts. In: Origins of Human Cancer: Book B,
Mechanisms of Carcinogenesis, H.H. Hiatt, J.D. Watson and J.A. Winsten, Ed.
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. p. 941-954. (Cold
Spring Harbor conference on cell proliferation: Vol. 4.)
U.S. EPA. 1985. Drinking Water Criteria Document for Asbestos. Prepared by
the Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Drinking Water,
Washington, DC.
U.S. EPA. 1986. Airborne Asbestos Health Assessment Update. Prepared by
the Environmental Criteria and Assessment Office, Research Triangle Park,
NC. EPA 600/8-84/003F.
Wagner, J.C., G. Berry, J.W. Skidmore and V. Timbrell. 1974. The effects of
the inhalation of asbestos in rats. Br. J. Cancer. 29: 252-269.
Ward, J.M., A.L. Frank, M. Wenk, D. Devor and R.E. Tarone. 1980. Ingested
asbestos and intestinal carcinogenesis in F344 rats. J. Environ. Pathol.
Toxicol. 3: 301-312.
Weill, H., J. Hughes and C. Waggenspack. 1979. Influence of dose and fiber
type on respiratory malignancy risk in asbestos cement manufacturing. Am.
Rev. Respir. Dis. 120: 345-354.
_VII. REVISION HISTORY
Substance Name -- Asbestos
CASRN -- 1332-21-4
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
09/26/1988 II. Carcinogen summary on-line
05/01/1989 II. Carcinogen summary noted as pending change
12/01/1989 VI. Bibliography on-line
03/01/1991 II.A.1. Text revised
07/01/1991 II.C.3. Last paragraph units changed from ug/cu.m to fibers/ml
01/01/1992 IV. Regulatory Action section on-line
07/01/1993 II.D.1. EPA Documentation clarified
07/01/1993 VI.C. References alphabetized correctly
VIII. SYNONYMS
Substance Name -- Asbestos
CASRN -- 1332-21-4
Last Revised -- 09/26/1988
1332-21-4
Asbestos
calidria-asbestos
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0371.HTM
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