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Executive Summary
ORIGIN OF THE STUDY
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Nonoccu tiona1 health risks associated with exposure to airborne
asbestifonm~ fibers have aroused concern because the adverse effects
from occupational exposure to some types of these fibers have been well
documented and because asbestos as well as other mineral and synthetic
particles with similar properties are Widespread in the environment.
Moreover, an excess occurrence of asbestos-related disease has been found
among people who were not themselves occupationally exposed but who lived
either near industrial facilities where asbestos was used or in households
with asbestos workers. In this report, the Committee on Nonoccupational
Health Risks of Asbestiform Fibers considers the health risks posed by
nonoccupational airborne exposures to asbestos and other natural or
synthetic asbestiform fibers. The issue is important because many people
may be exposed to these materials, although at relatively low levels.
To reach a better understanding of the relationship between charac-
teristics of asbestiform fibers and possible adverse health effects from
nonoccupational exposures, the U.S. Environmental Protection Agency asked
the National Academy of Sciences to undertake a Study with two goals:
· to evaluate the human health risks associated with
nonoccupational exposure to asbestifo~" fibers,
with emphasis on inhalation of outdoor arid indoor
air, and
.
to determine the extent to which the physical-
chemical properties of the fibers may be
associated with the development of various human
diseases and the extent to which such information
may be incorporated into assessing health rinks
resulting from exposure to the fibers.
The committee found that much more information is available about
asbestos than about the other materials of concern. Wherever possible,
the committee compared data on the nonasbestos fibers with data on
asbestos. This comparison required assessment of information on asbestos
as well as on other materials.
The term "asbestiform" in this report refers to fibers that share
some specific physical properties with asbestos. These are described
later in this summary and in Chapter 2. The term is a mineralogical one
that has been used for more than a century.
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MAJOR FINDINGS AND RECOMMENDATIONS
Evaluation of Risk
Nonoccupational exposure to asbestiform fibers in air presents a risk
to human health. The extent of this risk i8 highly uncertain, depending
on the nature and amount of exposure and other factors. Evidence for the
existence of the risk includes the following:
· Large excesses of lung cancer, mesothelioma, pulmonary fibrosis,
and other pleural abnormal it lea have been found among workers occupa-
tionally exposed to asbestos. Presumably, nonoccupational exposures would
result in qualitatively similar effects.
· Both a statistically excessive number of cases of mesothelioma and
an excess frequency of pleural abnormalities have been observed among
household contacts of asbestos workers.
· Asbestiform fibers are distributed extensively outside the work-
place, although usually in minute quantities.
· The major pathological effects associated with human exposure to
airborne asbestos have been duplicated experimentally in animals.
· Increases in cell replication and other abnormalities have been
seen in cultures of tracheal lining cells from humans and animals after
the cells were exposed to synthetic or natural asbestiform materials.
Estimating the extent of health risks from nonoccupational exposure to
asbestiform fibers is fraught with uncertainty. Factors contributing to
that uncertainty inc. Jude the fol lowing:
· A great variety of asbestiform fibers has been found in the non-
occupational environment. These fibers occur in a range of sizes and vary
in physicochemical characteristics, such as flexibility and durability.
· It is difficult to standardize methods for measuring amounts and
characteristics of a~bestiform fibers.
· A long time is required for health effects in humans to become
detectable after exposure begins (often 20 to 40 years).
~ There is inadequate knowledge of the mechanisms by which asbestiform
fibers lead to cancer and other health effects.
~ There are uncertainties in determining dose-response relationships
from the occupational environment and then extrapolating them to the
nonoccupational environment, where both exposure and population
characteristics are usually very different and doses are typically much
lower.
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The committee made estimates of comparative risk of adverse health
effects that might result from exposures to various a~bestiform
subetances. It concluded that population risks from exposure to the other
materials considered would generally be lower than the risks from exposure
to chry~otile asbestos because the opportunities for airborne exposure to
particles of respirable size were generally less for the other substances
than for chrysotile. The nonasbestos materials considered were
attapulgite (the trade name for the mineral palygor~kite, which exists in
asbestiform and nonasbestiform varieties); several man-made mineral
fibers, such as fibrous glass, mineral wool, and ceramic fibers; carbon
fibers; and fibrous erionite. These were selected because they seemed
likely to have, or are known to have, at least some of the properties of
asbestiform fibers.
The committee made a quantitative estimate of the risk of excess lung
cancer and mesothelioma that might occur in persons breathing low levels
of asbestos in the air. A concentration of 0.0004 fibera/cm was deemed
reasonable to use in such calculations because a variety of measurements
of indoor and outdoor air indicated that 0.0004 fibere/cm3 is the
approximate average level that may be encountered. If a person inhaled
air containing asbestos at that level throughout a 73-year lifetime, the
committee's best judgment in that the lifetime risk of mesothelioma would
be approximately nine in a million (range O to 350 per million, depending
on assumptions regarding the relationship of dose to risk). Others have
produced different estimates that are discussed in this report. Risks for
continuous lifetime exposures to higher or lower levels would be
proportionately higher or lower. Epidemiological data and the estimates
derived from them indicate that the corresponding lifetime risk for lung
cancer would be about 64 in a million for male smokers (range 0 to 290),
23 in a million for female smokers (0 to 110), and 6 and 3 in a million,
respectively, for male and female nonsmokers. The risk to nonsmokers
appears greater for mesothelioma than for lung cancer.
Because of the great reliance on assumptions and on clearly deficient
exposure and effects data, the committee views these risk estimates as
guides to the qualitative assessment of nonoccupational health risks from
asbestos and asbestiform fibers--not as definitive estimates of the amount
of disease to be anticipated. These estimates and other considerations
lead to the following five conclusions about risk:
0 Some deaths from mesothelioma and lung cancer will probably result
from current and past levels of exposure to asbestos in ambient air.
· Excess deaths from other diseases, such as asbestosis, and from
exposures to other asbestifo.= fibers are also possible but are not likely
to be as numerous as those from asbestos-induced mesotheliomas or lung
cancer.
0 The numbers of annual or cumulative deaths expected to result from
such exposures are very uncertain, but they are virtually certain to be
lower, and probably much lower, than those resulting from past, heavier
occupational exposures to asbestos.
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o Deaths from past occupational exposures to asbestos can reasonably
be estimated to total several thousand per year in the United States during
the next few years. Among these, more deaths from lung cancer than from
mesothelioma can be expected.
O The greatest risks of continuous lifetime exposure to asbestos
would be to smokers, who would be most at risk of lung cancer. However,
the risks to nonsmokers might well be greater for mesothelioma than for
lung cancer, because of the strong dependence of mesothelioma rates on
time from first exposure. The time dependence factor also implies that
restricting exposures of children to asbestos would be even more effective
than a corresponding restriction for adults in reducing the lifetime risk
of mesothelioma.
Physicochemical Properties and Health Effects
Some of the physical properties of asbestiform fibers appear to be
important in causing adverse health effects, but the specific properties
that are necessary and sufficient are not known. One clearly important
characteristic is respirability. In addition, longer, thinner fibers
appear to be more pathogenic than shorter, thicker fibers, but there is
not a minimum size below which no effects would be expected. However,
nonfibrous particles generally do not induce mesotheliomas in animals.
Number, rather than mars, and durability of fibers also seem to be
significant factors in pathogenicity of asbestiform fibers.
All major commercial types of asbestos fibers used in the United
States have been associated with lung cancer, mesothelioma, and asbestosis
in humane. It is not known whether the physicochemical fiber properties
responsible for fibrosis are similar to those involved in carcinogenesis.
Recommenda t ions
The committee's findings ant analysis let to the following
recommends t ions:
1. Systematic monitoring and characterization of asbentiform fibers
with standardized methods should be undertaken in nonoccupational
environments, including urban, rural, indoor' and outdoor locations where
exposure may be of special concern.
2. A program of systematic surveillance should be undertaken to
determine the extent to which the occurrence of mesothelioma and lung
cancer is associated with exposure to asbe~tifos~m fibers.
3. Cessation of cigarette smoking should be encouraged in view of the
multiplicative effect of smoking and asbestos exposure in increasing the
risk for lung cancer.
4. Steps should be taken to educate both the medical profession and
the general public concerning possible exposures to asbestiform fibers and
the resulting health effects.
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The committee also made several recommendations concerning future
research to resolve the many questions about the health risks of
nonoccupational exposure to asbestifo~m f ibers.
1. A standardized terminology for asbestiform fibers should be
adopted. The terminology should be based on mineralogical analysis and
should distinguish these fibers from other types of particles.
2. The various characteristics of asbestiform fibers or ocher
particles used in experiments should be described as completely as
possible.
3. Standardized methods for measuring and characterizing asbestiform
fibers should be improved.
4. In viva and in vitro laboratory ~ tud ie s wi th a she s t i f arm f ibe r s
and non fib rous substances should be conducted to investigate the physico-
chemical properties that are responsible for the biological effects.
5. Clinical studies of lung cancer, mesothelioma, and fibrosis should
be continued with emphasis on the possible role of asbestiform fibers.
6. Epidemiological studies are needed to clarify further the rela-
tionships between exposure to fibers and adverse health effects. These
studies should include case-control studies for mesothelioma and lung
cancer and prospective cohort studies among persons occupationally exposed
to materials such as asbestos, attapulgite, and man-made mineral fibers.
7. To improve risk assessments, studies should be conducted to
elucidate the relationships between amount of exposure and time factors
and the development of adverse health effects.
SUMMARY OF THE STUDY
l
Background
Asbestos has been detected in both outdoor and indoor air, although
almost always at concentrations far below the standard established by the
Occupational Safety and Health Administration (OSHA) for the workplace.
Since 1976 the workplace standard has been 2 fibere/cm3 for fibers
longer than 5 Am seen in a phase contrast light microscope under specified
conditions. The general population is also exposed to other fibrous
materials with some of the same physical properties as asbestos but whose
effects on health are not well known. These materials include man-made
mineral fibers such as fibrous glans and mineral wool, which are sometimes
used as substitutes for asbestos, as well as certain natural asbestiform
varieties of minerals not marketed as asbestos.
Sources of exposure to asbestiform fibers may be roughly divides into
three broad categories:
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· naturally occurring asbestiform fibers used commercially, such as
asbe stop;
· commercially used synthetic fibers with some properties similar to !
those of asbestos; and
· naturally occurring types of asbestiform fibers that are not used
commercially.
There is a substantial amount of data on exposures in the workplace,
but very little information on nonoccupational exposures. In the
occupational setting, four diseases have been clearly associated with
exposures to asbestos. These are (1) lung cancer; (2) mesothelioma, a
rare but almost invariably fatal cancer of the tissues that line the chest
cavity (pleural mesothelioma) or the abdominal cavity (peritoneal
mesothelioma); (3) asbestosis, a nonmalignant, progressive fibrosis of the
lung that may result in severe disability and death; and (4) nonmalignant
pleural disease, including diffuse pleural thickening and effusions and
the formation of fibrous and calcified plaques. The occurrence of these
four diseases in various occupational settings and the presence of
asbestiform fibers in the general environment led to current concern about
potential health effects from nonoccupational exposures.
During the course of its study, the committee was confronted with
several difficulties:
· Fibers in the general outdoor environment seem to differ in size
and other physicochemical properties from those in the workplace; however,
it is not easy to characterize these materials. Dif ferent types and
samples of fibrous materials vary greatly in their physical properties,
even when they are composed of the same mineral. Therefore, it is
difficult to develop a consistent methodology for determining and
expressing the characteristics and concentrations of fibers found in
different environments or used in laboratory studies.
· Because most health effects data are based on workplace exposures,
it is necessary to extrapolate results from relatively high occupational
concentrations to the much lower concentrations of fibers typically found
outside the workplace. Although the health consequences are presumably
similar among workers and nonworkers, incidence rates would be expected to
be lower and the nonmalignant changes less severe among persons
nonoccupationally exposed to lower levels of asbestos. Thus, the effects
would be more difficult to detect.
· Other factors associated with the diseases must be considered. For
example, cigarette smoking multiplies the effect of asbestos in causing
lung cancer.
· The mechanisms by which the fibers produce disease are not well
understood, nor is it clear how the fibers reach various parts of the
body.
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~ The length of time from initial exposure to the expression of
certain health consequences is often several decades. Thus, current
disease is the result of past exposures, whereas present exposures will
produce disease only many years in the future. Exposure in childhood may
increase the possibility of ultimate damage to health, because disease can
occur long after external exposure has ceased and more years of life
remain for children.
Thus, great uncertainty is likely to attend any conclusions drawn
about the relevant fiber characteristics and the health risks that may
accompany exposure.
The committee agreed that the major potential for future fiber-
associated health problems is probably presented by inhalation exposures
to airborne fibers rather than by the ingestion of there materials, for
example, in water. Mont of the committee's attention was therefore
devoted to airborne fibers of respirable size, that is, to fibers less
than approximately 3 Em in diameter.
The committee made quantitative risk assessments for lung cancer and
mesothelioma from inhaled asbestos, but it did not attempt quantitative
risk assessments for other cancers, from inhalation of other asbestiform
fibers, or from ingestion of asbestifo~m fibers in water or food.
Materials of Concern
For purposes of this report, the term "asbestiform fibers" is used
broadly to include both naturally occurring and certain synthetic
inorganic and carbon fibers that share some specific physical properties
with asbestos.
Asbestos, the prime example of an asbestiform material, consists of
the commercially marketed asbestiform varieties of several silicate
minerals. They are primarily chrysotile, crocidolite, and the asbestiform
variety of some amphibole minerals marketed as "amosite." Chrysotile
accounts for approximately 95: of the asbestos currently sold in the
United States. Because of its great strength, flexibility, and heat
resistance, asbestos came into extensive use during the 20th century for
textiles, thermal and electrical insulation, and high strength reinforce-
ment in such products as vinyl-asbestos flooring and asbestos-cement sheet
and pipe. In 1982, the United States used approximately 6: of the world
production of asbestos.
Five basic physical properties distinguish asbestifonm fibers from
other materials. The presence of these properties generally depends on
the physical and chemical conditions under which the fibers grow. Compared
with a nonasbestiform variety of the same mineral, the properties are:
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· microscopic, fiberlike dimensions and morphology, i.e., the fibers
are much longer than wide;
· enhanced strength and flexibility;
· inverse relationship between diameter and strength, i.e., the
smaller the diameter, the greater the strength per unit cross-sectional
area;
· enhanced physical and chemical durability; and
· high quality, relatively defect-free surface structure.
"High quality" fibers have all these properties to a great extent;
"low quality" fibers possess them to a lesser extent. The presence of
these properties does not necessarily indicate that a material is either
carcinogenic or fibrogenic. Because these properties are interdependent
and variable, naturally occurring asbestifo~m fibers, even those composed
of the same mineral, have a range of physical characteristics. In contrast
to fibers in the workplace, it is not currently possible to determine the
sources of most fibers in the ambient environment or the extent to which
these fibers have the above properties.
Mineralogical terms pertaining to asbestiform fibers have sometimes
been used inaccurately in scientific reports, including the literature on
biological effects. As a result, it may be impossible to discern the
composition of materials studied and extremely difficult to draw
conclusions about their physical properties and biological effects.
Relationship of Fiber Characteristics to Health Effects
Various physical properties of asbestiform fibers appear to play a
role in causing adverse health effects; however, the specific properties
that are necessary and sufficient to produce such effects have not been
postively identified. Furthermore, it is not known whether the properties
associated with a given effect, for example, lung cancer, are the same or
different from those associated with other effects, such as fibrosis or
mesothelioma. Some characteristics that appear to be important are
discussed below, in approximately descending order of the strength of the
positive evidence.
1.
Respirability. For significant health effects to result from
inhalation of asbestiform fibers, the fibers must reach the lower portions
of the respiratory tract where they cause the most damage. Although the ,
limiting upper diameter appears to be about 3 ~m, fibers that are much i
longer than wide can penetrate deeply in the respiratory tract.
l
Length, Diameter, and Aspect Ratio (i.e., Ratio of Length to Diameter). ;
Experiments inducing mesothelioma in rodents by injections of test
material have indicated that long, thin fibers yield more tumors than do
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short, thick fibers. Samples with an overwhelming majority of fibers
shorter than 5Pm yielded mesotheliomas in rata when injected
intraperitoneally, but the pathogenic role of abort fibers, especially
those shorter than 3 Am, is unclear. Fibers longer than approximately
10 Pm cannot be completely engulfed and inactivated by macrophages, and
they have tended to produce more disease in animal tests than have the
shorter fibers.
Other Properties. The number of fibers, which is also correlated with
surface area, generally appears to be a more relevant measure than mass in
determining pathogenicity. Durability also appears to be a factor. The
more durable fibers appear to be more pathogenic in some studies than
fibers that are less durable. The relevance of fiber surface charge to
effects on human health remains to be demonstrated. Some experimental
studies have indicated that surface charge appears to be involved in
cytotoxicity. Although chemical composition is related to physical
properties of asbestiform fibers, a direct role for chemical composition
Per se in biological activity has not been demonstrated.
Measurement and Extent of Exposure
Measurement. Information about asbestiform fibers in the ambient
environment, although scanty, indicates that they differ from those in the
workplace. Different techniques for measuring the concentrations in the
two environments have been used. The phase contrast light microscope has
been adequate for counting fibers in the workplace. However, that
technique has been less useful for the ambient environment, where fiber
identity and character are usually unknown; almost all fibers are too
small to be seen by light microscopy; and concentrations, expressed as
mass, are usually hundreds or thousands of times lower than those in the
workplace.
Data on workplace fiber concentrations are generally given as numbers
of fibers longer than 5 pm, whereas data on ambient concentrations
obtained with transmission electron microscope techniques have usually
been espresseed as mass per unit volume. Substantial uncertainty may be
introduced in calculations that assume that ambient and workplace
exposures differ only in fiber concentration. Furthermore, it is not
usually possible to convert mass measurements to fiber concentrations
accurately because the various conversion factors that are used assume
particular fiber dimensions, and these vary greatly with different
environments and sampling techniques. During the early 1970s, mass
measurements of asbestos made in various U.S. cities ranged from 1 to 100
ng/m3. If we assume that 30 pg/m3 is equivalent to 1 fiber/cm3
(counting fibers longer than 5 pm through a light microscope), the mass
measurements in those cities would feat to an expected concentration of
0.00003 to 0.003 asbestos fibers per cubic centimeter.
Extent of Exposure. In assessing the likelihood that individuals
would be exposed to various asbestiform fibers, the committee considered
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patterns of use; production or consumption levels; fiber dimensions, i.e.,
whether the fibers are of respirable size; and potential for population
exposure. In many situations, the fibers are tightly bound in a matrix
during product manufacture and, therefore, might be expected to produce
little subsequent exposure.
Irk the United States, the annual use of asbestos peaked in 1973 at
almost 800,000 metric tons, but decreased to approximately 250,000 metric
tone, or about 6% of world production, in 1982. However, much of the more
than 30 million metric tons of asbestos used in the United States since
1900 is still present in its original application and provides a potential
for exposure.
Attapulgite (palygorskite) is the only natural asbestiform material
used in the United States in amounts greater than those of asbestos. Of
the more than 700,000 metric tons used annually, most appears to be
classifiable as anbestiform. Most attapulgite fibers are less than 5 Am
long and have diameters of approximately 0.03 pm. Some uses of this
material could result in the release of fibers, but the committee found no
reported measurements of attapulgite in ambient air.
Synthetic fibers with some physical properties similar to those of
asbestos include man-made mineral fibers, of which more than 1 million
metric tons are produced annually I the United States. Typical diameters
of most of these fibers exceed the respirable size range, although
diameters of fine grades of fibrous glass and some rock wool and slag wool
are mostly below 3 ~m.
Some fibrous erionite found in deposits in the western United States
falls into the respirable size range. Mining and natural weathering of
this material could lead to significant local air concentrations, but the
committee did not find any measurements of such concentrations. Moreover,
the population exposed is probably small.
(;urrent U.S. consumption figures and use patterns indicate that future
exposure of the general population to attapulgite and fibrous glass is
likely to be somewhat greater than exposure to chrysotile, whereas
exposure to mineral wool, ceramic fibers, other asbestos fibers, and
carbon fibers would be less. However, material already in place would
also contribute to total exposure.
Health Effects Methodology
To develop an understanding of the health risks associated with
exposure to environmental agents such as asbestiform fibers, investigators
usually evaluate data from clinical, epidemiological, and laboratory
studies. Clinical observations often provide the first suggestion that
exposure to a particular substance may cause an adverse health effect.
Epidemiological studies are then undertaken to attempt to confirm the
hypothesized association and to quantify it. Laboratory studies of the
l
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1
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response in animals (in viva) and in cells growing outside the body (in
vitro) can provide further information. If a substance administered to
animals produces pathological effects similar to those found in humans,
the case for its being a causative agent in humans is strengthened. For
asbestos, the major diseases observed in humans have been produced in
animals by exposure to asbestos.
In vitro and in viva studies do not necessarily adequately reflect the
amounts or routes of exposures experienced by humans, nor do they take
into account individual susceptibilities or other substances to which
people might be exposed. Thus, such studies should be extrapolated to
humans only with great caution. Except for smoking, however, no environ-
mental or genetic factors have been unequivocally shown to influence the
chance that a person will develop an asbestos-induced disease.
Health Effects of Asbestos
Appendix A of this report contains a chronological list of the major
findings associating adverse health effects with exposure to asbestos.
The first disease to be associated with asbestos exposure was asbestos~s,
which was first noted in the early l900s. From 1938 to 1949, numerous
autopsy reports indicated that a high proportion of persons dying of
asbestosis also had lung cancer. In the 1950s, when the sharp increase in
lung cancer attributable to smoking was occurring in the United States and
other industrial nations, epidemiologists found that occupational exposure
to asbestos also increased the risk of lung cancer, especially among
cigarette smokers. In the early 1960s, the association with mesothelioma
was established among asbestos miners in South Africa.
Lung Cancer. Exposure to asbestos appears to increase a worker's
underlying risk of getting lung cancer as much as fivefold. Since a
smoker's risk of getting lung cancer is approximately 10 times greater
than that of a nonsmoker, an asbestos worker who smokes has up to a
50-fold greater chance of dying from lung cancer than does a nonsmoker who
does not work with asbestos. An increase in exposure, expressed as con-
centration of asbestos and duration of exposure, appears to increase the
lung cancer risk. Epidemiological data suggest that this relationship is
linear; the data do not indicate the presence of an exposure threshold
below which there is no increased risk.
Mesotheliom~. Approximately 1,600 cases of mesothelioma occurred in
the United states during 1980, according to projections from cases
reported in the lOX of the U.S. population monitored by the National
Cancer Institute's Surveil lance , Epidemiology , and End Results (SEER)
program. Although exposure to asbestos has been strongly associated with
most mesothelioma cases studied, some cases may occur without apparent
asbestos exposure. The evidence does not exclude the possibility that
ambient exposure to asbestiform fibers was associated with mesotheliomas
for which exposure court not be documented. The percentage of workers
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with mesothelioma has ranged from O to 2Z among chrysotile miners and
chrysotile textile workers, but has been as high as 10: among workers who
manufactured crocidolite-containing gsa masks. The disease seems to be
independent of smoking but related to dose and to time from first exposure.
Aabeatosis. All types of asbestos appear to be implicated in the
development of asbesto~is. Data indicate that the incidence rate
increases and the disease becomes more severe with increasing dust
exposure, which is expressed as concentration of dust and duration of
exposure. It is not clear whether an exposure threshold exists. Persons
in the early stages of this condition may be free of symptoms, but beyond
a certain stage the disease seems able to progress even in the absence of
further exposure.
Pleural Thickening. Another nonmalignant pathological effect of
asbestos exposure is the formation of fibrous and sometimes calcified
plaques and diffuse thickening of the pleural lining of the chest cavity.
Effusion of fluid into the pleural cavity may also occur. Such pleural
thickening is suggestive of asbestos exposure but is rarely a cause of
significant, direct respiratory impairment.
Gastrointestinal Cancer. Excess gastrointestinal (GI) cancers have
been fount among some cohorts of asbestos workers, but the excesses were
usually substantially less than for lung cancer. Dose-response data are
not available. Recent animal feeding studies have failed to demonstrate
asbestos induction of GI cancers. Moreover, because of inherent
limitations in the epidemiological studies, including the limited sizes of
the exposed populations and the lack of individual exposure data, it has
not been possible to determine from these studies the extent to which
there may be an association between GI cancers in humans and the presence
of asbestiform fibers in drinking water.
Wealth Effects of Nonasbestos Asbestiform Fibers
. .
Some natural asbestiform subatances other than asbestos seem to have
biological effects similar to those of asbestos. For example, erionite, a
fibrous zeolite, readily induces mesothelioma in animal tests, and
populations living in central Turkey, where it is present in volcanic
Luff, are reported to have an excess incidence of lung cancer,
mesothelioma, and pulmonary fibrosis. As another example, epidemiological
studisa are being conducted on workers exposes to attapulgite, but as yet
there are essentially no data on humans indicating whether it is toxic
when inhaled.
- Exposure to man-mate mineral fibers is relatively recent, ant the
occupational exposure levels apparently have not been as high as those for
asbestos. Some epitemiological data do suggest, however, that diseases of
the respiratory tract, such as pulmonary fibrosis and lung cancer, may
result from long-term occupational exposure to these fibers.
it,
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Evidence Associatin Fiber Pro erties with Adverse Health Effects
Asbestos and other asbestiform fibers appear to react with Celia in a
variety of ways. They may alter normal cell function, they may cause cell
death, or they may directly or indirectly alter the genetic Information
and the way cells replicate. Studies of cells lining the respiratory
passages suggest that asbestos may act as a promoter (in the
initiator/promoter model of carcinogenesis). The In vitro evidence that
asbestos can damage DNA directly or be mutagenic to gene n or chromosomes
is weak and inconclusive.
Laboratory studies have not identified one type of asbestos as being
more potent than others. In animal inhalation experiments, however,
asbestos generally appears to be more pathogenic than most other
asbestiform fiber e that have been tested. At present, none of the
available in vitro motels can be uset to quantify the relative fibrogenic
or carcinogenic potential of asbestiform fibers either in animals or in
humans. Interpretation of results is hindered by the failure of most
reported studies to define the test materials precisely, by the paucity of
experiments showing dose-response information, and by the differences in
response among species and cell types.
Results of studies of various groups of workers indicate that it is
extremely difficult to assess the role of fiber type (e.g., chrysotile or
crocidolite) in determining the risk for developing either lung cancer or
mesothelioma. Analysis of the epidemiological studies is complicated
because of variations in type of industry, the diverse fiber
characteristics within an industry, and the usual inadequacy of exposure
data. Some of the apparent discrepancies may be explained by differences
in physical properties of the fibers, their concentrations, and their
characteristics in the different environments. These possibilities need
further testing.
Risk Assessments
In general, three steps are necessary before one can assess health
risk from environmental exposures: determination that a material is toxic
and identification of adverse effects; determination of dose-response
relationships; and determination of the extent of exposure. At least Rome
types of asbestifonm fibers are toxic and have identifiable adverse health
effects. However, few occupational studies have demonstrated tose-
response relationships, ant there is great variability among those few
studies. Entimates of exposure outside the workplace are particularly
difficult to obtain, ant it is the risk from such exposure that is the
focus of this report.
Other factors that introduce uncertainty into risk assesaments for
nonoccupational exposures include assumptions about the magnitude of
effects at low doses; differences in the characteristics of fibers in the
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occupational and nonoccupational environments, especially regarding size
and composition; and differences in the populations exposed, age at onset
of exposure, and duration of exposure.
In this report, risk assessments are limited primarily to mesothelioma
ant lung cancer as end points and to inhalation as the route of exposure.
For asbestos, sufficient information was available for the committee to
make quantitative estimates--albeit with great uncertainty--of the risk
for lung cancer or mesothelioma after inhalation exposure. These risk
assessments were conducted for a "generalized" asbestos exposure, rather
than for exposure to a specific type of asbestos. However, the committee
assumed that the rink estimates would also apply if chrysotile were the
primary agent of exposure. For the other types of fibers considered, the
committee made comparative, i.e., qualitative, risk assessments that were
subject to yet greater uncertainty.
For the quantitative risk assessment, the committee concluded that the
epidemiological data supported the use of a linear, no-threshold model.
Dose-response data from workplace studies were used in developing the
equations. To estimate nonoccupational exposures, measurements of the
mass of asbestos in the ambient environment were converted to the number
of fibers longer than 5 Am that would have been found in the workplace at
a similar mass concentration.
These measured concentrations indicated to the committee that
0.0004 fibere/cm3 was a reasonable level to use in the risk assessment.
However, there could be specific circumstances, such as schoolrooms with
flaking asbestos, where persons are exposed to higher levels for limited
periods. If a person were to inhale air containing asbestos at an average
of 0.0004 fibere/cm3 throughout a 73-year lifetime, the committeets best
estimate is that the lifetime risk of mesothelioma would be approximately
nine in a million (range 0 to 350 per million, depending on assumptions
regarding the relationship of dose to risk). The corresponding lifetime
risk for lung cancer would be about 64 in a million for male smokers
(range 0 to 290), 23 in a million for female smokers (range 0 to 110), and
6 and 3 in a million for male and female nonsmokers, respectively.
The risk for mesothelioma is greater than that for lung cancer among
nonsmokers because of the strong dependence of mesothelioma risk on time
since first exposure. Occupational studies indicate the t me sothe 1 ioma
usually fires appears about 20 years after onset of workplace exposures
and that the incidence increases rapidly thereafter. The calculations
suggest that a given exposure to asbestos in childhood markedly increases
the lifetime risk of mesothelioma compared with an equivalent dose later.
The risk estimates remain uncertain, especially because they are based
on the assumption that the data on occupational exposures are transferable
to the nonoccupational ~ ituation. Smal ler f iber s ize in the ambient
environment would probably tend to lead to lower risk.
The comparative or qualitative risk assessments for the other
asbestiform fibers were based on chrysotile and lung cancer an the
baseline case. Population risk for particular f ibers was compared with
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the population rink for lung cancer from chrysotile. In making
comparative risk assessments, the committee considered such factors as
respirsbility, biodisposition, and intrinsic toxicity as they are related
to population exposures and to individual risk. The materials considered
were crocidolite, other asbestos fibers as a group, attapulgite, fibrous
glass, mineral wool, ceramic fibers, and carbon fibers. (Appendix H of
this report presents the qualitative assessments for each substance.)
The risks for developing lung cancer or mesothelioma as a result of
exposure to the other materials considered by the committee were usually
much lower than those for chrysotile, principally because of a lower
potential for airborne exposure or because the fibers are less
respirable--not because their intrinsic toxicity is necessarily less. For
example, both ceramic and carbon fibers can be found in respirable size
ranges and may have some biological properties similar to those of
asbestos, but production and opportunities for exposure are low, although
increasing. The materials with potentially greatest impact are fibrous
glass and attapulgite because of their current large production volume and
extensive use.
.
Representative terms from entire chapter:
asbestiform fibers
