UNITED STATES EPA/eoo/8-91/065
ENVIRONMENTAL PROTECTION JUNE 1988
AGENCY FINAL
RESEARCH AND
DEVELOPMENT
EVALUATION OF THE POTENTIAL CARCIN06ENICITY OF
ASBESTOS
(1332-21-4)
IN SUPPORT OF REPORTABLE QUANTITY ADJUSTMENTS
PURSUANT TO CERCLA SECTION 102
PREPARED FOR
OFFICE OF EMERGENCY AND REMEDIAL RESPONSE
OFFICE OF SOLID WASTE AND EMERGENCY RESPONSE
PREPARED BY
CARCINOGEN ASSESSMENT GROUP
OFFICE OF HEALTH AND
ENVIRONMENTAL ASSESSMENT
WASHINGTON, D.C. 20460
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DISCLAIMER
This document hu been reviewed in accordance with U.S. Environmental
Protection Agency policy and approved for publication. Mention of trade names
or commercial products does not constitute endorsement or recommendation for
use.
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PREFACE
This report surma rises and evaluates information on the potential
carciriogeru.city of a substance designated as hazardous under Section 101 (14)
of the Comprehensive Environmental Response, Compensation and Liability Act of
1980 (CERCLA). Pertinent epidemiologic end toxicologic data were obtained
through on-line searches and fron hard-copy aourcea. On-line searches were
extended as far back as the data bases would allow. Retrieval of historical
data was accomplished through searches of hard-copy sources and bibliographies
of relevant publications. Every attempt has been made to rely upon primary
publications as opposed to data summaries or abstracts contained in secondary
sources such, as monographs, surveys, review articles, criteria documents, etc.
The on-line data bases that were searched included CHEMLXNE {National Library
of Medicine [NLM]), RTECS (NLM) , Toxicology Data Bank (NLM), TOXLINE (NLH),
CANCERLINE (NLM), and Chemical Abstracts (DIALOG Information Services). '•
Unpublished data were not used in this evaluation.
The Agency's Methodology Cor obtaining, evaluating, and ranking CERCLA
potential carcinogens is described in the Technical Background Document to
Support Rulemaking Pursuant to CERCLA Section 102, Volume 3, April 26, 1963
(EPA/600/8-89/053) . This document revises tba previous methodology document
of 1966 according to the public comments received on tba March 16, 1987 Notice
of Proposed Rulena.ki.ng
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effort to produce this document, Environmental Monitoring c Services, Inc.,
under EPA Contract No. 68-03-3182, has been involved in an extensive review of
all the Syracuse documents. In some cases, this review involved updating the
information provided but it was primarily a quality assurance effort. The
present document is a result of this effort.
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ABSTRACT
Asbestos Is a human carcinogen, classified as welght-of-evidence Group A under
the EPA Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1986a). Evidence
on potential carcinogenicIcy from animal studies Is 'Sufficient.' and the
evidence from human studies is 'Sufficient.'
A potency factor (F) estimate for asbestos Is Inappropriate here because the
carcinogenic potential of asbestos Is related to specific fiber shapes, sizes
and atmospheric concentrations. The relationship depends on the type of
environmental sample, the type of asbestos In the air, and the size of the
fibers.
As a deliberate policy choice, asbestos 1m, therefore, assigned a 'HIGH' hazard
ranking, as are most Group A substances.
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T.JHTJ op CONTENTS
Page
1.0 WEIGHT-OF EVIDENCE 1-1
1.1 ANIMAL STUDIES 1-1
1.2 HOHAN STUDIES. 1-4
1.3 BEICST-OF-EVIDERCE ASSESSMENT 1-9
2.0 POTENCY 2-1
3.0 HAZARD BANKING ..... 3-1
4.0 REFEREHCES 4-1
APPENDIX: SUMMARY OF SIGNIFICANT HUMAN AND/OR ANIMAL STUDIES
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1.0 HEIGHT OF EVIDENCE
There are six primary forms of asbestos, all having a unique fibrous structure
and silicate content. The different types of asbestos have not been
distinguished or treated separately in this document. The asbestos forms
are treated separately in IARC (1977). The size and shape of the fibers
of specific asbestos types influence their tumorigenic potential.
Although crocidolice has been reported to be more tunorigenic than
chrysotile or amosito In animals, exposure to all forms of mixed fibers
has resulted In a high Incidence of tumors in animals and humans.
The remainder of this profile is based on, and sometimes quotes from, U.S. EPA
(1966b).
1.1 ANIMAL STUDIES
The inhalation of chrysotile asbestos was tested for carcinogenic activity in
mica (Ac/71 hybrid) by Lynch et al. (19S7). The asbestos dust was administered
for 8-12 hours/day, 5 days/week for 1? months. A higher incidence of pulmonary
adenomas was reported in the exposed group (SB/127) rh*n in the controls
(80/222). These values are not statistically different (P>0.05). Gross et al.
(1967) exposed rats to 86 mg/ir chrysotile dust for 30 hours/week and reported
that 10/41 rats (surviving after 16 motrchs) devatoped lung tumors. No lung
tumors were seen In 39 control rats. :
Reeves et al. (1974) tested the carcinogenicity of various forms of asbestos in
rats, nice., rabbits, guinea pigs, and gerbils. Dusts of chrysotile,
crocidolitiY mod anosite asbestos (47.9-50.2 ng/m3), prepared by ball-milling,
were inhaled Cor up to 24 months by exposed animals. The milling process was
noted to destroy most of the fibrous nature of the asbestos so that actual
fiber counts In the air were 54 fibers/ml (chrysotile), "864 fiber/ml (amosite),
and 1105 fibers/ml (croc idol 1 te). Neoplasms were detected only In rats and
mice.
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Crecidolice, the asbestos with the highest number of fibers/volume, was
associated ulth the induction of 2/18 papillary carcinomas of the bronchus in
mice and 5/46 carcinomas of the lung in treated rats. Rats treated with
chrysotile and anosite developed 3/43 and 3/46 tumors, respectively. No tumors
were seen in--other aniaals (gerbils, guinea pigs, rabbits) treated vith Any of
the three asbestos forms. In a subsequent study. Reeves (1976) exposed rats to
the same three forms of asbestos fiber (chrysotile, amosite, and crocidolite)
at 47.4-50.2 sng/m^ for 2 years. The count of cicroscoplcally visible fibers
was as previously mentioned (54, 864, 1105 million fibers/in^ for chrysotile,
amosite, and crocidolite, respectively). Crocidolite was noted to have che
highest fiber count and tumor incidence (7/50) while chrysotile (3/54) and
anosite (3/61) had fewer tumors in treated aniaals. Tumors were predominantly
of the lung or peritoneal mesotheliua.
Wagner et al. (1974) exposed CD Uistar rats to five forms of asbestos (anosite,
crocidolite, anthophylllte, and Canadian and Rhodesian chrysotiles) and
10.1-14.7 mg/m3 for 1 day, 3, 6, 12, or 24 months for 7 hours/day, 5 days/week.
All forms of asbestos shoved an increased Incidence of lung tumors with
increased exposure. Exposure to the asbestos was demonstrated to Induce
higher incidences of lung carcinomas and mesothellomas (Rhodesian chrysotile
had no mesotheliomas at any exposure). No lung carcinomas oc mesothellomas
were seen la the control group.
Groups of 32 Uiscar SFF rats were fed 100 ing/day Canadian chrysotile on Italian
talc in malted milk powder 5 days/week for a 6-month period (100 days of
treatment) and then observed for cheir lifetime. Mean survival times of
created animals were slightly less than for 16 control rats fed only milk
powder (619 and 614 days, respectively, versus 641 days for controls). One
lelomytvircoma was observed in each exposed group; no similar tumors vere seen
in controls (Vagner et al., 1977).
A significant Increased incidence (F<0.01) of malignant CUmors was seen in
Uistar rats treated with 50 mg/kg bw/day asbestos filter material (52.6%
ehrysctlle) in the dit1: for I1.** Ar»?ng 4? HTiImals, J,?, irellgnsTi
netastases were found ('* kldr.-y c'rcin^sas, 4 liver-cell carcinomas, 3
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reciculum-cell sarcomas, and 1 lung carcinoma) and 7 additional tumors were
noted (2 paplllonas of the forestomach, 2 cholangiomas, 2 mammary
fibroadenomas. and 1 lung adenoma). In a group receiving talc (50 mg/kg/day
for life in the diet), 4 mammary fibroadenomas and 3 liver-cell carcinomas
occurred among 45 rats. In untreated controls, 5 mammary fibroadenomas and 2
liver-cell carcinomas occurred among 49 animals. The mean sunn.al time was
also shorter in asbestos-treated animals (441 days) than in talc-treated (649
days) or control rats (702 days) (Cibel ec al., 1976).
The tntrapleural administration of several types of asbestos has produced
mesotheliomas in rats, rabbits, and Kamacers (IAH.C, 1977). Wagner et al.,
1973) reported evidence of a dose-response to chrysotile and crocidolIce, with
mesotheliomas developing in 8/12 rats treated with 8 mg of 3FA chrysotile and
5/11 rats treated with 8 mg of crocidolite. Stanton and Wrench (1972) also
reported a dose-response for crocidolite. Hesotheliomas developed in 2/2S,
5/23, 11/27, 12/25, and 14/23 female Osborne-Mendel rats exposed to 1, 2, 10,
20. and 40 mg crocidolite in gelatin applied to coarse fibrous glass pledgees
which were placed intrapleurally. The Intact fibrous glass vehicle did not
yield tumors. Both reports (Wagner et al., 1973; SCanton and Wrench, 1972)
indicate that the carcinogenicity of the asbestos fibers is primarily related
to the physical nature of the fibers (size and shape) and that different
asbestos types have different tumorigenlc activities.
Intrapleural injection of asbestos has also resulted in the production of
tumors in mice and rats (1ARC, 1977). Although no control group vas reported.
Shin and Finninger (1973) attributed 9/45 aa& 8/33 tumors (predominantly
epithelioid mesotheliomas) in male Wistar rats to treatment (50 mg) with
crocidolite and chrysotile, respectively. Pott et al. (1976) reported tuaor
incidence data which showed that fibrous dusts (asbestos and others) were Much
more effective «*«i granular dusts in inducing mesotheliomas when injected
intraperitoneally.
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1,2 HDMAK STUDIES
A historical perspective of occupational exposure to asbestos is reviewed in
IARC (1972. 1977). Case reports and epidemiological evidence associating
asbestos with an excess risk of lung cancer began to appear in the literature
in the mid-1930's (IARC, 1972, 1977), Hueper (1965) reviewed early studies on
asbestos-related deaths and carcinogenicity. Since there are many reports on
asbestos exposure in humans (IARC, 1972, 1977), this document will emphasize
the most pertinent data and review published studies (1977 through November,
1987) identified by computer literature searches.
In a study of asbestos factory workers in England, Feto et al. (1977) reported
that 35/143 deaths from lung cancer and pleural znesothelioma were reported in
workers exposed prior to 1933, while only 4.54 were expected (based on national
death rates). Deaths from other respiratory diseases were also higher than
expected In this group (21/143 versus 8.18 expected). More recently, sine* the
implementaion in 1932 of the first Asbestos Industry Regulations, Feto at al.
(1977) reported a decrease in lung cancer, pleural mesotheliomas, and
respiratory disease related deaths froa the previous levels, but an excess
mortality from these causes still exists. In workers exposed after 1933,
36/963 (19.3 expected; P<0.001) lung cancer and mesothelioma deaths were
reported. Deaths due to respiratory disease numbered 35/963 while 25 were
expected (P-0.03).
Selikoff (1976) reviewed data froa a previous study (Selikoff et al., 1964) and
presented additional data on asbestos Insulation workers of the New York
metropolitan area. T""g cancer among these workers vas very prevalent (89/1002
observed versus 12.2 expected) and an increase in the incidence of stomach,
colon, and rectal cancer was reported (43/1002 observed versus 13.63/1002
expected).
*
The mortality (from all causes) of insulation workers exposed to chronic
asbestos dust vas 2.6 tines thac expected (98/165 observed deaths v^tsuj 37
expected) (Elmes and Simpson, 1971). The number of deaths doe to cancers of
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the respiratory tract and pleura was 17.6 times the expected number, (28/165
observed versus 1.64 expected). The expected incidence of mesothelicmas for a
group of 165 men is negligible but seven confirmed cases were reported for the
asbestos-exposed workers. This incidence also seems highly significant.
Newhouse et al. (1972) reported on the mortality of female workers exposed to
asbestos. A higher incidence of deaths due to lung and pleural cancer was
reported for workers exposed for >2 years than In workers exposed for <2 years
(14/239 versus 6/557) In "severe" exposure jobs. The incidence of lung and
pleura! cancer deaths far low to moderately exposed workers was 2/126. All
three groups of asbestos-exposed workers had higher observed lung and pleural
cancers than expected (14/239 in severely exposed workers for >2 years versus
0.5 expected, P<0.001; 6/557 in severely exposed for <2 years versus 1.0
expected, P<0.001; 2/126 in low to moderately exposed for any period of time
versus 0.3 expected, P<0.05). The incidence of mesothelioma deaths was also
shown to increase with both the length of exposure and severity of exposure in
men and women asbestos workers (Newhouse and Berry, 1976).
Gillam et al. (1976) reported a significant increase in mortality from
malignant respiratory diseases in mine workers exposed to anosite asbestos at
average concentrations of 4.82 fibers/cm^. Tha exposure Co other carcinogens
within the mine were almost negligible. The observed number of deaths due to
respiratory cancers was 10/440, while only 2.7 deaths were expected (P<0.01).
In addition to the increase in lung cancers, mesotheliomas, and occasionally
gastrointestinal cancers, recent studies (Kagan et al., 1979; Haidak ec al.,
1979; Rouhier et al., 1982) have reported cases of leukemia and myeloma in
patients who had extensive exposure to asbestos. Two patients, one with
multiple myeloma, the other with chronic lymphocytic leukemia, had subsequent
pulmonary asbestosis. A tbird patient, with multiple myeloma, developed a
massive pleural mesothelioma (Kagan et al., 1979; Haidak et al., 1979).
Another patient, who had been occupationally exposed to asbestos for 30 years,
developed malignant alpha-chain disease and was found to have malignant
lymphooas (Rouhier et £.1., 1982). All these cases showed pathological
evidence of asbestos exposure In. addition to the diagnosed malignancies.
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In a case control study of shipyard workers exposed Co asbestos insulation,
Morris et al. (1979) studied a group of 1976 deaths. Cases of respiratory
cancer and chronic pulmonary disease (n-454) were compared with a matched set
of controls"based on age. sex, and residency. Data on the subject's residence,
occupation, tobacco consumption, and general health history was recorded. A
preliminary analysis of this study shows an elevated risk of lung cancer in
workers exposed to asbestos.
A study of the incidence of mesothelioma. calcified pleural plaques and chronic
pleural fibrosis was conducted by Baris et al. (1979) in a region of Turkey
which has environmentally high levels of asbestos minerals. The 148 cases of
malignant pleural aesothelioma, occurring in 92 males and 56 females, was
believed to be linked to exposure to environmental asbestos and other fibers.
In 1974, in a town of only 604 inhabitants. 11 of 18 deaths were due to
malignant pleural mesothelioma. Asbestiform fibers and fibers of volcanic
glass have been detected in the water, streets, and field soils of this region,
A comprehensive research program into the health effects of exposure to
asbestos in the chrysotile mines and mills of Quebec (McDonald et al.. 1974)
included cross-sectional observations on 1,015 current mala workers; it
demonstrated associations between exposure and breathlessness on axartion and
declines in certain lung functions. A follow-up study (Becklaka et al., 1982)
was undertaken to add serial measurements on thesa 1,015 man. The primary
objective was to assasa the relationship of changa over tint* to occupational
exposure; age, smoking, and health status at the first survey wera taken into
account. It was found that there was a higher proportion of man eligible for
attack in the lower than in the higher exposure groups; this finding was
consistent'for almost all the features of the men with and without
radiographs. There were substantial proportions of men showing change between
surveys assessed as attack and progression, with rates somewhat higher for men
without than for men with radiographs. The former wera Jn.so, on the average,
older and had had longer and heavier exposure than the latter. In addition.
for substantial proportion of the cen, regression vas reeordsd for br-»2th-
Icssness arid MMEF (zeasurrment= of oeximcn mid-expiratory flow), but ir vas
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assessed as definite for relatively few men. Little radiographie regression
was read.
Mortality data from a chrysotile textile plant studied by Dement et al., (1982,
1983a, 1983b) allow a direct estimate of lung cancer risk per fiber exposure.
The study cohort consisted of all 1261 white males employed one or more months
between January 1, 1940 and December 31. 1965. Dement et al. <1983b) uses U.S.
rates for calculating expected deaths and presents arguments for using national
rates. Local rates are probably influenced by nearby shipyard employment (and
perhaps by the study plant) and the smoking habits of the study population
reflect those of the U.S. general population.
Exposure-related mortality data at the same plant used by Dement et al., (1982,
1983a, 1983b) have recently been published by McDonald at al. (1983a). Their
cohort consisted of all individuals employed for one or more months prior to
January 1, 1959. and for vhcm a Social Security Administration (SSA) record
existed. This eliminated from consideration individuals who began and ended
their employment prior to mid-1937, when SSA numbers were first assigned. The
same data used by Dement on past exposures were utilized to assign cumulative
dust exposures, in mppcf-y, to each study participant. Mala deaths, by cause,
20 years after first employment, are related to dusc exposure accumulated to 10
years prior to death.
British Occupational Hygiene Society (1983) reported information on the
differences between personal and static sampling. Data were presented for
thirty-one simultaneous samples comparing the two techniques, the personal
samplers indicating a greater fiber concentration in 22 cases. Using these
data, the BOHS conanitt.ee evaluated the cumulative fiber exposure (as of
approximately 1976) for 284 individuals employed for 10 or more years
subsequent to 1951. The overall avarage of the entire group was 182 f-y/ml.
This is slightly less than the estimate of Peto (1980), who suggested that the
exposure of 1C* year employees -«« 2CG-300 f-y/mi. However, Peto-s estimate
was based on preliminary daca on only 126 men first employed between 1951 and
1955. The BOHS data are directly contradicted by published data from the
factory on other comparisons of scitic and personal sampling results bv job
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(Smlther and Lewinsohn, 1973). Dr. Lewinsohn (1983) confirmed these results.
He stated that the static sampler concentrations were generally higher than
those of the personal samplers of men working at the monitored job.
Doll and Peto (1985) recently reviewed the new information on the health
effects of asbestos for the British Health and Safety Commission. Many of the
above uncertainties, particularly that of the ratio of personal to static
sampling counts, are discussed. A regression analysis of the ratio of personal
to static counts against mean concentration indicated that the ratio is greater
than one for concentrations less than 2 f/rnl, but less than one for higher
concentrations. Doll and Peto (1985) estimate values of KL from the mortality
in an expanded and updated study of the Rochdale cohort.
A plant located near Lancaster, Pennsylvania, which produced mainly textiles
but also friction products and packings, was studied by Robinson et al. (1979),
McDonald et al. (1983b), and earlier by Mancuso and Coulter (1963) and Mancuao
and El-attar (1967). Robinson et al. (1979), Hancuso and Coulter (1963), and
Mancuso and El-attar (1967) provide no information on the exposure of the
cohort members to asbestos; so they cannot be used in establishing exposure-
response relationships. In the study of McDonald et al. (1983b), dust
concentrations, measured in mppcf. available from che 1930s through 1970 v«r«
used. However, no attempt was mada to relate particle exposures to fiber
exposures. The study cohort of McDonald et al. (1983b) comprised all
individuals employed for one or more months prior to January 1. 1959, with
their Social Security file identifiable in the Social Security Administration
offices. These individuals were traced through December 31, 1977, and
cause-specific mortality ratios, based on state rates, were related to
cumulative dust exposure.
Berry and Newhouse analyzed the mortality of a large workforce manufacturing
friction products. All individuals employed in 1941 or later were included la
the study, and the mortality experience through 1979 was ^determined. Exposure
estimates vere made by reconstructing the work and ventilation condition* of
earlier ycorr. Fiber meas
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seldom exceeded 5 f/ml. From 1970. exposures were less than 1 f/tnl. These
relatively low intensities of exposure kept the £ arage cumulative exposure for
the group to less than 40 f-y/ml. The overall mortality of all scudy
participants. 10 years and more after onset of exposure, was no greater than
expected for all causes. Cancer of the lung and pleura vas slightly elevated
in men (151 observed versus 139.5), but the excess was largely accounted for by
eight mesothelloma deaths. No unusual mortality was found in those employed 10
or more years.
McDonald et al. (1984) analyzed the mortality of Che workforce employed in
friction products production in the United States and attempted to relate ic
to cumulative dust exposure. However, a highly unusual mortality experience is
observed. The overall mortality shows an elevated risk of death in the
complete cohort for virtually all causes, largely confined to individuals
employed for less than one year. The correlation of respiratory cancer SMR
with cumulative dust exposure of those employed for more th^" one year shows
little, if any, trend with increasing dust exposure, even though the overall
SMR for lung cancer is 137 for these individuals.
The study by Seidman et al. (1979) also can be used for quantitative risk
estimates. The study was recently updated and the new mortality results were
submitted for the OSHA. hearings record on a revised standard for asbestos
(Seidman, 1984). In this update, dose-response data, based upon estimates of
individual exposures for each cohort number, are available. The study covered:
the cumulative observed and expected deaths from lung cancer 5 to 40 elapsed
years since onset of work in an aaoslte asbestos factory, 1941-1945, by
estimated fiber exposure (Seidman, 1984).
1.3 WEIGHT-OF-EVIDENCE ASSESSMENT
Animal studies indicate that asbestos, when there is sufficient fibrous
content, is carcinogenic if inhaled, consumed in the di^t, or administered by
non-nacural routes. Predominantly, cancer of the respiratory tract develops in
animals (alee, rars. hamsters) imposed to asbestos by inhalation. Vhea.
consumed in the diet, asbestos Ir.ducad gastrointestinal, rencl, and hepatic
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malignancies, although these findings have been questioned. Intrapleural or
iotraperitoneal administration leads to a high incidence of mesenterie
mesothelimoas.
Epidemiologlcal studies and case reports nave provided a direct relationship
between exposure to asbestos and lung cancer and mesothelioma. Several studies
ha-ve ascertained smoking-habit data, in cases of lung cancer, but were unable to
attibute the malignancies to tobacco intake. Shettigara and Morgan (1975)
concluded that both asbestos and cigarette smoking were potent factors in the
development of respiratory cancer. Cancers, other than lung cancer, that have
been attributed to the inhalation of asbestos fibers, include cancers of the
gastrointestinal tract, lymphosarcona, malignant lymphoma, and squamous
carcinoma of the larynx (Lemen et al.. 1980).
An evaluation of the epidemlological studies done on human risk from ingested
asbestos concludes that such studies have not provided quantitative data
useable for estimating levels associated with a defined risk. Due to the
shortness of the exposure and limited power in such studies, clearly safe and
clearly unsafe ranges could not: be definitely identified (Erdreich, 1983).
This inability to identify safe or unsafe ranges for oral intake of asbestos
contrasts sharply with the definitive evidence established in humans when
asbestos gain entrance to the body via inhalation.
EPA has recently reviewed the latest studies on asbestos (See U.S. EPA, 1986b).
Their conclusions are repeated below:
Data developed since the early 1970s, from large population studies with
long follow-up, have added to our knowledge of asbestos disease. These
data strengthen and quantitatively define the association of asbestos
exposure with disease. Lung cancer and mesothelioma are the most
important asbestos-related causes of death among exposed individuals.
Gastrointestinal cancers are also increased in most studies of
occupatlonally exposed workers. Cancer at other sites (larynx, kidney,
every) his also been shown to b3 oasociatad with asbestos exposure. Iw sout
studies, but the degree of excess risk and the strength of the association
are less for these and the gastrointestinal cancers than for lung cancer
or mesothelioma. The International Agency for Research on Cancer (1982)
lists asbeseos as a group I carcinogen, meaning that exposure to asbestos
1-10
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la carcinogenic to humans. EPA's proposed guidelines would categorize
asbestos as Group A, human carcinogen (Federal Register, 1984b).
Data from a scudy of U.S. insulation workers allow models to be developed
for the time and age dependence of lung cancer and mesothelioma risk.
Thirteen other studies provide exposure-response information. The
accumulated data suggest that the excess risk of death from lung cancer
from asbestos exposure is proportional to the cumulative exposure (the
duration times the intensity) and the underlying risk in the absence of
exposure. The time course of lung cancer is determined primarily by the
time course of the underlying risk. However, the risk of death from
mesothelioma Increases very rapidly after the onset of exposure and is
Independent of age and cigarette smoking. As with lung cancer, the risk
appears Co be proportional to the cumulative exposure to asbestos in a
given period. The dose and time relationships for other asbestos cancers
are uncertain.
Animal studies confirm the human epidemiological results. All major
asbestos varieties produce lung cancer and mesothelioma with only limited
differences in carcinogenic potency. Implantation and injection studies
show that fiber dimensionality, not chemistry, is the most important
factor In fiber-induced carclnogenicity. Long (>4 urn) and thin (<1 um)
fibers are the most carcinogenic at a. cancer-inducible site. However, the
size dependence of the deposition and migration of fibers also affects
their carcinogenic action in humans.
Measurements demonstrate that asbestos exposures exceeding 100 times the
background occur to individuals in some non-occupational settings.
Currently, the most important of these non-occupational exposures is from
the release of fibers from asbestos-containing surfacing materials in
schools, auditoriums, and other public buildings, or from sprayed
asbestos-contain ing fireproof ing in high-rise office buildings. A high
potential exists for future exposure from the maintenance, repair, and
removal of these materials.
Extrapolations of risks of asbestos cancers from occupational
circumstances can be made, although numerical estimates in a specific
exposure circumstance have a large (approximately tenfold) uncertainty,
Because of this uncertainty. calculations of unit risk values for asbestos
at the low concentrations measured in the environment must be viewed with
caution. The best estimate of risk to the United States general
population for a lifetime continuous exposure Co 0.0001 f/ml Is 2.8
mesothelioma deaths and 0.5 excess lung cancer deaths per 100,000 females.
Corresponding numbers for males are 1.9 mesothelioma deaths and 1.7 excess
lung cancer deaths per 100,000 individuals. Excess CI cancer mortality is
approximately 10-30 percent that of excess lung cancer mortality. These
risks are subjective, tc soac encent, and ore also subjecr ra the
following limitations in data: 1) variability In the exposure-response
relationship ac high exposures; 2) uncertainty in extrapolating to
exposures 1/100 as much; and 3) uncertainties in conversion of optical
fiber counts to electron microscopic fiber counts or mass determinations.
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1C Is significant that the cancer types seen in humans that are attributed to
asbestos exposure have been repeatedly reproduced in animal models. Aninals,
which are not exposed to tobacco smoke, also develop respiratory cancers as a
result of asbestos Inhalation. Based on the available evidence, and using the
EFA Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1986a) for evaluating
the overall veight- of -evidence to humans, asbestos is classified as a Group A
chemical. The appendix contains summaries of the significant human and/or
animal studies cited in this review.
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2.0 POTENCY
A potency factor (F) estimate for asbestos is inappropriate here because the
carcinogenic potential of asbestos is related co specific fiber shapes, sizes
and atmospheric concentrations. The relationship depends on the type of
environmental sample, the type of asbestos in the air, and the size of the
fibers.
2-i
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, TECHNICAL REPORT DATA
fPitese res', Jniinieiiems on the reverse bcfarr comrjien-
NO,
EPA/600/8-91/065
TITLE ANQ SUBTITLE
f the Potential Carcinogen;city of
valuation o
Asbestos
s. REPORT DATE
June 1988
6. PERFORMING ORGANIZATION CODE
. AUTHORCSI
Syracuse Research Corporation;
Environmental Monitoring & Services, Inc.
8. PERFORMING ORGANIZATION R6PO«T NO.
OHEA-C-073-023
PERFORMING ORGANIZATION NAME AND
yracuse Research Corporation, Syracuse, NY;
nvironmental Monitoring & Services, Inc. (now ABB
nvironmental Se-vices, Inc.), Washington, DC
10. PROGRAM 6l_£M6N7 NO.
11. CONTRACT/GRANT NO.
68-03-3112
68-03-3182
2, SPONSORING AGENCY NAME ANO ADDRESS
ffice of Health and Environmental Assessment
arcinogen Assessment Group (RD-689)
.5. Environmental Protection Agency
ashington, DC 20460
13. TYPE OF FtEPOHT AND PERIOD COVERED
Report
14. SPONSORING AGENCY CODE
EPA/600/021
, SUPPLEMENTARY NOTES
6, ABSTRACT
Asbestos is a human carcinogen, classified as weight-of-evidence Group A under the EPA
Guidelines lor Carcinogen Risk Assessment Evidence on potential carcinogenicity from animal
studies is "Sufficient." and the evidence from human studies is •Sufficient"
The potency factor (F) estimate for asbestos is inappropriate here because the carcinogenic
potential of asbestos is related to specific fiber shapes, sizes and atmospheric concentrations. The
relationship depends on_the type of environmental sample, the type of asbestos in the air, and the
size of the fibers.
As a deliberate policy choice, asbestos is, therefore, assigned a "HIGH" hazard ranking, as
are most Group A substances.
7.
KEY WJRDS AND DOCUMENT ANALYSIS
DeSCHIPTOflS
b.lOENTIFIERS/OPEN ENDED TERMS
c. COSATi Field, Group
18. DISTRIBUTION STATEMENT
Release to Public
19. SECURITY CLASS iTIus Repnrri
line! asslfied
j 2" NO. Or
45
2Q.S1CUH1TY CLASS
Unclassified
EP4 Farm 1230-! (H«y. 4-771 PREVIOUS EDITION 11 OBSOLETE
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