United States
Environmental Protection
Agency
Office of Health and
Environmental Assessment
Washington DC 20460
Research and Development
EPA/600/S8-84/003F Apr. 1991
EPA Project Summary
Airborne Asbestos Health
Assessment Update
W.J. Nicholson
Data developed since the early 1970s,
from large population studies with long
follow-up, have added to our knowl-
edge of asbestos-related diseases and
strengthened the evidence for associa-
tions between asbestos and specific
types of health effects. Lung cancer
and mesothelioma are the most Impor-
tant asbestos-related causes of death
among exposed individuals. Cancer
other than lung has also been associ-
ated with asbestos exposure. The accu-
mulated data suggest that the excess
risk of lung cancer from asbestos expo-
sure is proportional to the cumulative
exposure (the duration times the inten-
sity) and the underlying risk in the ab-
sence of exposure. The risk of death
from mesothelioma Is approximately
proportional to the cumulative expo-
sure to asbestos and increases sharply
with time since onset of exposure.
Animal studies confirm the human
epidemiologies! results and indicate that
all major asbestos varieties produce
lung cancer and mesothelioma, with
only limited differences in carcinogenic
potency. Some measurements demon-
strate that asbestos exposures exceed-
ing 100 times background occur in
non-occupational environments. Cur-
rently, the most important of these non-
occupational exposures is the release
of fibers from asbestos-containing sur-
facing building materials or from
sprayed asbestos fireproofing in high-
rise buildings.
Extrapolations of risks of asbestos
cancers from occupational circum-
stances can be made, although numeri-
cal estimates in a specific exposure
circumstance have a large (approxi-
mately tenfold) uncertainty. Because of
this uncertainty, calculations of unit risk
values for asbestos at low concentra-
tions must be viewed with caution and
are subject to the following limitations:
1) variability in the exposure-response
relationship at high exposures; 2) un-
certainty 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.
This Project Summary was devel-
oped by EPA's Environmental Criteria
and Assessment Office, Research Tri-
angle Park, NC, to announce key find-
Ings of the research project published
In 1986 that Is fully documented In a
separate report of the same title (see
Project Report ordering Information at
back).
Introduction
The principal objective of this docu-
ment is to provide the U.S. Environmental
Protection Agency (EPA) with a sound sci-
entific basis for review and revision, as
appropriate, of the national emission stan-
dard for asbestos, 40 CFR 61, subpart B,
as required by the 1977 Clean Air Act
Amendments, Sections 111 and 112. The
health effects basis for designating asbes-
tos as a hazardous pollutant and minimiz-
ing emissions via the original 1973 National
Emissions Standard for Hazardous Air
Pollutants was scrutinized, at that time,
during two public hearings and a public
comment period. Once a pollutant has been
Printed on Recycled Paper
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designated as a "hazardous" air pollutant,
the burden of proof is placed on proving
that designation wrong.
The original health effects basis for
designating asbestos as a hazardous air
pollutant was qualitative evidence estab-
lishing asbestos-associated carcinogenic
effects. However, insufficient bases then
existed by which to define pertinent quanti-
tative dose-response relationships; i.e., unit
risk values could not be credibly estimated.
The main focus of the update document is
to describe asbestos-related health effects
developments since 1972 and to deter-
mine if new data warrant the specification
of unit risk values for asbestos. The docu-
ment forms part of the basis to perform a
risk assessment.
The National Academy of Sciences
(NAS) in 1983 suggested a definition of
risk assessment as the use of the factual
data base to define the health effects of
exposure of individuals or populations to
hazardous materials, such as asbestos.
Therefore, the update document is mainly
concerned with the excess risk of cancer
from inhalation of asbestos fibers, with
emphasis placed on the literature pub-
lished after 1972, and on those reports
that provide information on the risk from
low-level exposures, such as those en-
countered in the non-occupational envi-
ronment.
Occupational Exposure
The International Agency for Research
on Cancer (IARC) lists asbestos as a group
1 carcinogen, meaning that exposure to
asbestos is carcinogenic to humans. EPA's
proposed guidelines would categorize as-
bestos as Group A, human carcinogen.
Diseases considered to be associated
with asbestos exposure include asbestosis,
mesothelioma, bronchogenic carcinoma,
and cancers of the gastrointestinal (Gl)
tract, including the esophagus, stomach,
colon, and rectum. Lung cancer is associ-
ated with exposure to four principal com-
mercial varieties of asbestos fiber: amosite,
anthophyllite, crocidolite, and chrysolite.
Excess risks of bronchogenic carcinoma
are documented in mining and milling,
manufacturing, and end product use (ap-
plication of insulation materials). Mesothe-
lioma is a cause of death among factory
employees, insulation applicators, and
workmen employed in the mining and mill-
ing of crocidolite. A much lower risk of
death from mesothelioma is observed
among chrysolite or amosite mine and mill
employees, and no cases are associated
with anthophyllite exposure. The IARC Ad-
visory Committee suggests that the risk of
death from mesothelioma is greatest with
crocidolite, less with amosite, and still less
with chrysotile. This suggestion was based
on the association of disease with expo-
sures. No unit exposure risk information
existed prior to 1972.
Information on exposure-response re-
lationships for lung cancer risk among vari-
ous exposed groups was scanty. Data from
Canadian mine and mill employees clearly
indicated an increasing risk with increasing
exposure, measured in terms of millions of
particles per cubic foot-years (mppcf-y),
but data on the risk at minimal exposure
were uncertain because the number of
expected deaths calculated using adjacent
county rates suggested that all exposure
categories were at elevated risk. A study
of retirees of the largest U.S. asbestos
manufacturer showed lung cancer risks
ranging from 1.7 times that expected in the
lowest exposure category to 5.6 times that
expected in the highest. Exposures were
expressed in mppcf-y, and information on
conversion of mppcf to fibers per milliliter
was available only for textile production.
Despite the paucity of data, the 1973 re-
port of the Advisory Committee on Asbes-
tos Cancers to the IARC stated, "The
evidence ... suggests that an excess lung
carcinoma risk is not detectable when the
occupational exposure has been bw. These
low occupational exposures have almost
certainly been much greater than that to
the public from general air pollution." Lim-
ited data existed on the association of Gl
cancer with asbestos exposure, but the
"excess is relatively small compared with
that for bronchial cancer."
The prevalence of asbestosis, particu-
larly as manifested by X-ray abnormalities
of the pleura or parenchyma! tissue, had
been documented more extensively than
the risk of the asbestos-related malignan-
cies. In part, this documentation resulted
from knowledge of this disease extending
back to the turn of the century, whereas
the malignant potential of asbestos was
not suggested until 1935 and not widely
appreciated until the 1940s. Asbestosis
had been documented in a wide variety of
work circumstances and associated with
all commercial types of asbestos fibers.
Among some heavily exposed groups, 50
to 80 percent of individuals employed for
20 or more years were found to have
abnormal X-rays characteristic of asbestos
exposure. A lower percentage of abnormal
X-rays was present in lesser exposed
groups.
Company data supplied to the British
Occupational Hygiene Society (BOHS) on
X-ray and clinical abnormalities among 290
employees of a large textile production
facility in Great Britain were analyzed in
terms of a fiber exposure-response rela-
tionship. The results were utilized in estab-
lishing the 1969 British regulation on
asbestos. These data suggested that the
risk of developing the earliest signs of
asbestosis was less than 1 percent for
accumulated fiber exposure of 100 fiber-
years/ml (f-y/ml), e.g., 2 fibers/millili-
ter (f/ml) for 50 years. However, shortly
after the establishment of the British stan-
dard, additional data from the same fac-
tory population suggested a much greater
prevalence of X-ray abnormalities than was
believed to exist at the time the British
standard was set in 1972. These data
resulted from use of the new International
Labour Office (ILO) standard classification
of X-rays and the longer time from onset of
employment. Of the 290 employees whose
clinical data were reviewed by the BOHS,
only 13 tiad been employed for 30 or more
years; 172 had less than 20 years of em-
ployment. The progression of asbestosis
depends on both cumulative exposure and
time from exposure; therefore, analysis in
terms of only one variable can be mislead-
ing.
Environmental Exposure
Several research groups had shown
that asbestos disease risk could develop
from other than direct occupational expo-
sures. Various researchers in 1960 have
shown that a mesothelioma risk in environ-
mental circumstances existed in the mining
areas of the Northwest Cape Province of
South Africa. Of 33 mesotheliomas reported
over a 5-year period, roughly half were
from occupational exposure. However, all
but one of the remainder resulted from
exposure occasioned by living or working
in the area of the mining activity. Another
study in 1965 that showed an extra-occu-
pational risk investigated the occupational
and residential background of 76 individu-
als deceased of mesothelioma in a Lon-
don hospital. Forty-five of the decedents
had been employed in an asbestos indus-
try; of the remaining 31, 9 lived with
someone employed in asbestos work and
11 were individuals who resided within half
a mile of an asbestos factory. In 1973,
investigators identified environmental as-
bestos exposure in 38 mesothelioma cases
without occupational exposure who resided
near an asbestos factory, further defining
residential risk. A final study, which is par-
ticularly important because of the size of
the population implied to be at risk of as-
bestos disease from indirect occupational
exposure in the shipbuilding industry, was
conducted in 1968. It described the pres-
ence of asbestosis in 13 individuals and
mesothelioma in 5 others who were em-
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ployed in a shipyard but were not mem-
bers of trades that regularly used asbes-
tos. Rather, they were exposed to the dust
created by other employees placing or re-
moving insulation.
Evidence of ubiquitous general popula-
tion exposure and environmental contami-
nation from the spraying of asbestos on
the steel-work of high-rise buildings was
established by 1972. Asbestos was com-
monly found at concentrations of nano-
grams per cubic meter (ng/m3) in virtually
all United States cities, and at concentra-
tions of micrograms per liter (u.g/1) in river
systems of the United States. Concentra-
tions of hundreds of nanograms per cubic
meter were documented at distances up to
one-quarter of a mile from fireproofing sites.
Mesothelioma was acknowledged by the
Advisory Committee to be associated with
environmental exposures, but it suggested
that "the evidence relates to conditions
many years ago .... There is no evidence
of a risk to the general public at present."
Analytical Methodology
During the late 1960s and early 1970s,
significantly improved methods were de-
veloped for assessing asbestos disease
and quantifying asbestos in the environ-
ment. In 1971, a standardized methodol-
ogy was established. It provided a uniform
criterion for assessing the prevalence of
asbestos-related X-ray abnormalities.
Significant advances were also
achieved in the quantification of asbestos
aerosols. In the late 1960s, the membrane
filter technique was developed for the
measurement of asbestos fibers in work-
place aerosols. While this procedure has
some limitations, it did establish a stan-
dardized method, using simple instrumen-
tation, that was far superior to any that
existed previously. This method subse-
quently allowed epidemiological studies to
be done that based exposure estimates on
a standardized criterion. Experimental
techniques in the quantification of asbes-
tos at concentrations of tenths of ng/m3 of
air and tenths of u.g/1 of water were also
developed, extending the sensitivity of ex-
posure estimates approximately three or-
ders of magnitude below those of
occupational aerosols and allowing as-
sessment of general population exposures.
Finally, techniques for the analysis of as-
bestos in lung and other body tissues were
developed. Tissue digestion techniques and
the use of electron microscopy to analyze
fibers contained in the digest and in thin
sections of lung tissue showed that asbes-
tos fibers were commonly present in the
lung tissue of general population residents
as well as individuals exposed in occupa-
tional circumstances.
Experimental Studies
Experimental animal studies using as-
bestos fibers confirmed the risks of lung
cancer and mesothelioma from amosite,
crockJolite, and chrysotile. In each case,
the establishment of a risk in animals fol-
lowed the association of the malignancy
with human exposure. For example, a
causal relationship between lung cancer
and asbestos exposure in humans was
suggested in 1935 and confirmed in the
late 1940s but was not described in the
open literature in animals until 1967. Me-
sothelioma, reported in an asbestos worker
in 1953, was produced in animal experi-
mentation in 1965. Other animal experi-
mentation showed that combinations of
asbestos and other carcinogenic materials
produced an enhanced risk of asbestos
cancer. Asbestos exposure combined with
exposure to benz(a)pyrene was demon-
strably more carcinogenic than exposure
to either agent alone. Additionally, organic
and metal compounds associated with as-
bestos fibers were ruled out as important
factors in the carcinogenicity of fibers.
Lastly, in 1973 experimentation involving
the application of fibers onto the pleura of
animals indicated that the important factor
in the carcinogenicity was the length and
width of the fibers rather than their chemi-
cal properties. The greatest carcinogenic-
ity was related to fibers that were less than
2.5 u.m in diameter and longer than 10 u.m.
Current Asbestos Standards
The current Occupational Safety and
Health Administration (OSHA) standards
for an 8-hour time-weighted average (TWA)
occupational exposure to asbestos is 2
fibers longer than 5 urn in length per millili-
ter of air (2 f/ml or 2,000,000 f/m3). Peak
exposures of up to 10 f/ml are permitted
for no more than 10 min. This standard
has been in effect since July 1, 1976,
when it replaced an earlier one of 5 f/ml
TWA. In Great Britain, a value of 0.5 f/ml is
now the accepted level for chrysotile. This
standard has evolved from recommenda-
tions made in 1979 by the Advisory Com-
mittee on Asbestos, which also
recommended a TWA of 0.5 f/ml for amosite
and 0.2 f/ml for crocidolite. From 1969 to
1983, 2 f/ml TWA was the standard for
chrysotile. This earlier British standard
served as a guide for the 1972 OSHA
standard.
The 1969 British standard was devel-
oped specifically to prevent asbestosis
among working populations; data that would
allow a determination of a standard for
cancer were felt to be lacking. Among
occupational groups, cancer is the primary
cause of excess death among workers.
Three-fourths or more of asbestos-related
deaths are from malignancy. This fact led
OSHA to propose a lowered TWA stan-
dard to 0.5 f/ml (500,000 f/m3) in October
1975. The National Institute for Occupa-
tional Safety and Health (NIOSH) antici-
pated hearings on a new standard and
proposed a value of 0.1 f/ml in 1976 in an
update of their 1972 criteria document. In
the discussion of the NIOSH proposal, it
was stated that the value was selected on
the basis of the practical limitations of ana-
lytical techniques using optical microscopy,
and that 0.1 f/ml may not necessarily pro-
tect against cancer. The preamble to the
OSHA proposal acknowledges that no in-
formation exists by which to define a
threshold for asbestos carcinogenesis. The
OSHA proposal has been withdrawn, and
a new proposal was submitted on April 10,
1984. In it, OSHA proposed a TWA stan-
dard of either 0.2 or 0.5 f/ml depending
upon information to be obtained in hear-
ings (held during the summer of 1984).
NIOSH reaffirmed its position on a 0.1 f/ml
TWA standard.
The existing federal national emission
standards for asbestos are published in
Part 61, Title 40, Code of Federal Regula-
tions. In summary, these apply to milling,
manufacturing, and fabrication sources, and
to demolition, renovation, and waste dis-
posal, and include other limitations. In
general, the standards allow compliance
alternatives, either (1) no visible emissions,
or (2) employment of specified control
techniques. The standards do not include
any mass or fiber count emission limita-
tions. However, some local governmental
agencies have numerical standards (e.g.,
New York: 27 ng/m3), but these have little
regulatory relevance.
Other Reviews of Asbestos
Health Effects
Recently, several government agen-
cies in different countries reviewed asbes-
tos health effects. The most important of
the reviews outside the United States are
those of the Advisory Committee on As-
bestos of the British Health and Safety
Commission and the report of the Ontario
Royal Commission. Each of these major
reports was the result of lengthy testimony
by many scientists and deliberations by
selected committees over a long period of
time. In the United States, the NAS has
reviewed the non-occupational health risk
of asbestiform fibers, and a Chronic Haz-
ard Advisory Panel convened by the U.S.
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Consumer Product Safety Commission re-
ported on the hazards of asbestos.
There are large areas of agreement
and some of disagreement between these
reviews and those of the full document
with regard to the spectrum of asbestos-
related disease, the models describing as-
bestos-related lung cancer and
mesothelioma, unit exposure risks in occu-
pational circumstances, possible differ-
ences in carcinogenic potency of different
asbestos minerals, and risk estimates at
low, non-occupational exposures.
Summary
Lung cancer and mesothelioma are the
most important asbestos-related causes of
death among exposed individuals. Gas-
trointestinal cancers are also increased in
most studies of occupationally exposed
workers. Cancer at other sites (larynx, kid-
ney, ovary) has also been shown to be
associated with asbestos exposure in some
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 IARC
lists asbestos as a group 1 carcinogen,
meaning that exposure to asbestos is car-
cinogenic to humans. EPA's proposed
guidelines categorize asbestos as Group
A, human carcinogen.
Data from a study of U.S. insulation
workers allow models to be developed for
the time and age dependence of lung can-
cer and mesothelioma risk. Thirteen other
studies provide exposure-response infor-
mation. 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. How-
ever, 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 to be proportional to the
cumulative exposure to asbestos in a given
period. The dose and time relationships for
other asbestos cancers are uncertain.
Values characterizing lung cancer risk
obtained from different studies vary widely.
Some of the variability can be attributed to
specific processes. Chrysotile mining and
milling, and perhaps friction product manu-
facture, appear to have lower unit expo-
sure risks than chrysotile textile production
and other uses of asbestos. Other variability
can be associated with the uncertainties of
small numbers in epidemiological studies
and improper estimates of exposures in
earlier years. Some differences between
studies may be related to differences in
fiber type, but these are much less than
those associated with specific processes.
Four studies provide similar quantita-
tive data on the unit exposure risk for
mesothelioma and six additional studies
provide corroborative, but less accurate,
quantitative data. The same factors that
affect the lung cancer unit exposure risk
appear to affect that of mesothelioma, as
the ratio of a measure of mesothelioma
risk to excess lung cancer risk is roughly
constant across the ten studies. However,
in other studies the ratio of number of
mesothelioma deaths to lung cancer deaths
among groups exposed to substantial
quantities of crocidolite is two to four times
higher than among groups exposed pre-
dominantly to other fibers. Further, the risk
of peritoneal mesothelioma appears to be
less from exposure to chrysotile than to
either crocidolite or amosite, but this sug-
gestion is tempered by uncertainties asso-
ciated with the greater possibility of
misdiagnosis of the disease.
Animal studies confirm the human epi-
demiological results. All major asbestos
varieties produce lung cancer and meso-
thelioma with only limited differences in
carcinogenic potency. Implantation and
injection studies show that fiber dimen-
sionality, not chemistry, is the most impor-
tant factor in fiber-induced carcinogenicity.
Long (>4 urn) and thin (<1 urn) fibers are
the most carcinogenic at a cancer-induc-
ible site. However, the size dependence of
the deposition and migration of fibers also
affects their carcinogenic action in humans.
Measurements demonstrate that as-
bestos 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 build-
ing materials, or from sprayed asbestos-
containing fireproof ing in high-rise buildings.
A high potential exists for future exposure
from maintenance, repair, and removal of
these materials.
Extrapolations of risks of asbestos can-
cers 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 environ-
ment must be viewed with caution. The
best estimate of risk to the United States
general population for a lifetime continu-
ous exposure to 0.0001 f/ml is 2.8 meso-
thelioma deaths and 0.5 excess lung cancer
deaths per 100,000 females. Correspond-
ing numbers for males are 1.9 mesothe-
lioma deaths and 1.7 excess lung cancer
deaths per 100,000 individuals. Excess Gl
cancer mortality is approximately 10-30
percent that of excess lung cancer mortality.
These risks are subjective, to some extent,
and are also subject to variability in the
exposure-response relationship at high
exposures, uncertainty in extrapolating to
exposures 1/100 as much, and uncertain-
ties in conversion of optical fiber counts to
electron microscopic fiber counts or mass
determinations.
Recently, several government agencies
in different countries reviewed asbestos
health effects. Areas of agreement and
disagreement between various reviews are
presented in the full document. A compari-
son of the different risk estimates is also
provided.
&U. S. GOVERNMENT PRINTING OFFICE: 199 1/548-028/20206
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W.J. Nicholson is with Mt. Sinai School of Medicine, New York, NY 10029.
D. Kotchmar is the EPA Project Officer, (see below).
The complete report, entitled "Airborne Asbestos Health Assessment Update," (Order
No. PB86-242864/AS; Cost: $31.00, subject to change) will be available only from:
National Technical Information Service
5285 Port Royal Road
Springfield, VA 22161
Telephone: 703-487-4650
The EPA Project Officer can be contacted at:
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
United States
Environmental Protection
Agency
Center for Environmental Research
Information
Cincinnati. OH 45268
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