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OCR for page 97
Effects of Asbestiform Fibers
on Human Health
This chapter begins with a discussion of the types of evidence that
researchers generally use in determining causes of disease. It then
pro~ldes information on biodispositlon of fibers and on diseases
associated with exposure to asbestos. A discussion of health
consequences that have been associated with nonoccupational exposure of
humane to asbestos and other asbestiform fibers is followed by a
description of occupational epidemiological studies.
NATURE OF EVIDENCE
Three lines of evidence--clinical, epidemiological, and
laboratory- are considered when determining whether a particular
environmental agent may cause adverse effects on human health. For
asbestos, as for most hazardous environmental agents, the first evidence
of health effects was provided by clinical observations. Physicians
observed that individual or clusters of cases of pneumoconiosis,} lung
cancer, and finally mesothelioma were associated with exposure to
asbestos.
Paeumoconiosis was the first health effect to be associated with
asbestos. In 1907 Dr. Montague Murray reported his observations of such
disease in a man who had worked in a carding room at an asbestos plant in
England (Murray, 1907~. In 1924, Cooke wrote that "medical men in areas
where asbestos is manufactured have long suspected the dust to be the
cause of chronic bronchitis and fibrosis....- (Cooke, 19241. Numerous
other reports followed. Other types of paeumoconioses, such as
silicosis, were also known at that time, so asbestosis, the fibrotic
disease caused by asbestos, was not an entirely new type of disease.
However, mesothelioma was sufficiently rare that its connection with
asbestos was not accepted until 1960 (Wagner, 1960~.
Clinical observations led to the hypothesis that asbestos caused the
observed disease. Epidemlologists then conducted studies to ascertain
whether the hypothesis was true. The association was eventually
Pneumoconiosis is the pathological reaction of tissue to the
inhalation and accumulation of dust in the lunge.
97
.
..
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98
established primarily through cohort studies, in which the rate of
disease occurrence in an exposed group is compared with the rate in a
group not exposed to the material of concern (Do1l, 1955; McDonald and
McDor - ~d, 1981; Selikoff and Hammond, 1979~.
In laboratory studies, asbestos was administered to avowals to
determine whether pathological effects similar to those found in humans
could be induced. These experiments followed the methodology established
in the Scientific study of infectious agents as causes of disease--a
methodology later extended to the investigation of noninfectious agenda.
However, performing the experiments and interpreting the results are more
complicated for diseases with long latency periods. The laboratory
studies demonstrated that asbestos could cause rung cancer and
mesotheliomas in animals. Fibrotic reactions, however, usually differed
somewhat from the lesions observed in humans with asbestosis. This
difference could be attributed to variation among species and in the
nature and amount of fibers (Wagner, 1960~.
Each of the three kinds of data have strengths and weaknesses. The
clinician distinguishes the observed disease from similar conditions and
considers the possible links to environmental and other factors. Thus
the clinical contribution to understanding lies primarily in the
definition of clinical entities and in suggesting possible etiological
factors. Erroneous conclusions may be drawn--or new insights gained--if
an atypical group of cases comes to a particular clinician's attention.
Difficulties may also arise if the observed effects are confused with
other syndromes with similar signs and symptoms. Misinterpretation may
also occur because of the usual reliance at this stage on nonquantitative
methods of assessing the relationship to environmental circumstances.
The epidemiological approach results in the quantification of risk
for a defined health effect associated with exposure to particular
environmental circumstances. During the application of this method, two
types of errors are commonly made: (~) the findings are generalized too
far beyond the population and circumstances studied and (2) there is a
failure to adequately take into account the presence of other factors
that may be involved in addition to, or instead of, the major factor
being examined.
In laboratory experiments in animals, the investigator has the great
advantage of being able to exercise control over the conditions of
observation, rather than having to rely on observations of natural
phenomena as in most nonintervention clinical and epidemiological
studies. Also, the laboratory investigator can make more detailed
observations over time, thereby increasing the potential for ascertaining
the mechanism or steps by which the agent exerts its effect. On the
other hand, inference from one species to another carries some
uncertainty. There is also uncertainty in extrapolating from laboratory
observations to the exposures and resulting effects experienced by
humans. Furthermore, laboratory animals are usually exposed to one
agent, whereas humans are exposed to many.
OCR for page 99
99
Ultimately, the determination of a causal relationship between
exposure to an environmental agent and a health effect is a Judgment
based on careful evaluation of evidence. Guidelines for making such
causal inferences have been suggested and generally adopted. For
example, Koch's postulates for infectious agents constituted a powerful
and widely accepted framework for Judging laboratory evidence to
determine whether a particular microbiological agent is responsible for a
certain disease. No such guidelines have been generally established for
noninfectious agents. Perhaps the closest approximation is provided by
the frequently cited criteria adopted by the Surgeon General's Advisory
Committee on Smoking and Health (1964~:
-
The causal significance of an association is a matter of judgment
which goes beyond any statement of statistical probability. To judge
or evaluate the causal significance of the association between the
attribute or agent and the disease, or effect upon health, a renumber
of criteria must be utilized, no one of which is an all-sufficient
basis for judgment. These criteria include:
(a) The consistency of the association [with
diverse methods and among multiple studies]
(b) The strength of the association [ratio of
rates among those exposed to rates among those
not exposed ~
(c) The specificity of the association [precision
with which one component of the associated pair can be used
to predict the other ~
(d) The temporal relationship of the association
[i.e., which comes first, the agent or the disease]
(e) The coherence of the association [with the
natural history and biology of the disease]
The more of these criteria tat are met and the stronger the evidence
related to them, the more likely it is that a causal relationship
exists. As another example, Hackney and Lit (1979) have updated Koch's
postulates and applied them to environmental toxicology.
ID evaluating relationships between exposure to hazardous
environmental agents and adverse health effects, it is useful to proceed
beyond identifying and confirming the hazard to quantifying the risks
under various conditions. In a recent publication of the National
Research Council (1983b), the authors noted that the steps of risk
assessment involve (~) identification of a toxic agent and its effects,
(2) determine Lion of dose-response relationships, (3) determiD.ation of
the extent of exposure, and finally (4) determination of risk.
.
-
..
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100
In some situations, it is difficult to identify the effects of an
agent because a given disease, such as lung cancer, may be caused by a
variety of agents. mus, exposure to cigarette smoke, asbestos, certain
chromates, ionizing radiation, some chemicals, and possibly other agents
may all increase the chance that a person will develop lung cancer. By
contrast, for infectious diseases such as typhoid fever or tuberculosis,
the microorganism is the specific and only cause, although not everyone
infected by the organism gets the disease.
For most cancers, there is some chance that an individual will get
the disease even with no known exposure to an identified cause. In
comparing the risk of developing the disease in an exposed person to the
risk for an unexposed person, it is often crucial and difficult to
determine the existence and value of a 'background" rate for the
disease. A background rate is the rate of occurrence of a disease with
no association, or no known association, with the agents being
considered. Exposure to an agent such as asbestos may then increase this
background rate. For example, some lung cancer occurs in the absence of
cigarette smoking or exposure to asbestos. In the absence of exposure to
asbestos, cigarette smoking increases the chance of getting lung cancer
(compared with nonsmokers) up to a factor of about 10, varying with the
number of c igarettes smoked (U. S. Department of Health, Education, and
Welfare, 1979~. Asbestos exposure among insulation workers who do not
smoke cigarettes increases the risk for lung cancer up to about 5 times
(Harmond et al., 1979~. Together, the cigarette smoking and asbestos
exposure appear to produce a multiplicative effect, i.e., the lung cancer
rate is inc reased up to 50-fold above background .
Expressing the relationship as an absolute risk, rather than as a
re let ive risk, may provide informal ion about the magnitude of the pub 1 ic
health problem. If a relatively small risk is increased 10-fold, the
resulting public health problem may still be much smaller than would
result from doubling a larger risk. For example, the risk for coronary
heart disease among smokers is about 1.6 times greater than the risk for
nonsmokers, as contracted with a lO-fold increase in risk for lung cancer
among smokers compared with nonsmokers. However, cigarette smoking
causes more deaths from coronary heart disease than it toes from lung
cancer, because the base line "background" risk for heart disease is much
higher than for lung cancer.
BIODISPOSITION OF FIBERS
-
In this section the co~nmittee briefly describes how asbestiform
fibers enter the body, the properties of fibers that are important in
cellular injury, and factors affecting durability of fibers after
deposition and interaction with cells. Figure 5-l shows the anatomy of
the respiratory tract ant the individual cell types ins olved in
asbestos-associated diseased. The pathological effects of asbestos begin
OCR for page 101
Epiglottis Ail
Visceral _
Pleura
Parietal _
Pleura
Alveol i-
~ Figure 5
101
~ Esophagus
Trachea- /~\\ \
Peritoneal Cavity ~ Diaphragm
I Cavity
Pharynx
Main Bronchus
See Figure 5-1B
Pleural Cavity (the pleura consists of the
membrane enveloping the lungs and
lining e chest cavity)
FIGURE 5-1A. Routes of inhalation and ingestion of asbeseifonm fibers
are shown by small arrows. Mesothelial cells line the
outside of the lungs ant the pleural and peritoneal
cavities. Interaction of asbestos with these cells can
result in either pleural or peritoneal me~othelioma.
Adapted from Wagner, 1980.
OCR for page 102
102
niacin Granule
Epi~elium
Connemive Tissue
so Tr;chea ~ #! ~ ~
.
~ ~' at
,
Macrophap~]'il~l'
Ciiia~e~ Cell it} ., ~ ~ 4~/ I
'~/)j?.2
torus ,~
,,,.,~";'1.~}'
~ "..,
FIGURE 5-1B. Cells of the bronchus, or large airways, leading from the
trachea. The epithelial cell layer conalats of ciliated
cells, mucin-secreting goblet cells, and basal cells. the
interaction of asbestos with the epithelium and with
macrophages is be' ieved to be related to the onset of
asbestos-related diseases. Epithelial cells are the target
for most lung cancer, whereas the macrophages serve as
intermediary cells.
In'.rss't.~t Soace
Alveo'at
Ep''bel~um
FlUed Layer ~ \
my,
Surtactent I\
Layer ~\
ALVEOLUS
D'ffuslon
~-
~ Cao~ll.rV Basement
/ l~kmDrane
/ ~CapellarY Entlot~l,um
l.\ {~:
of
CAPILLARY} ~
FIGURE 5-1C.
. _ . . i.
Dittus~on'/ot ~ |Carbon Dioxide /f,
L ~/~
Cells of the alveoli, where gas exchange occurs. Interac-
tion of asbestos with fibroblasts within the interstitial
space can result in fibrosis, whereas interaction of
asbestos with alveolar epithelial cells can give rise to
lung cancer. (Drawing from Guyton, 1971.)
r
..
OCR for page 103
103
when fibers are inhaled and ingested. Subsequently, they are deposited
either in the respiratory tract or in the gastrointestinal tract. Fibers
can then interact with resident cells and eventually move to the pleura
and various organs. The mechanisms by which fibers reach the peritoneum
are not known.
Fiber Deposition
Various factors influence the deposition of inhaled particles in the
respiratory tract. When nonfibrous compact dust particles are inhaled,
the ones greater than about 5 Am in diameter are generally trapped in the
nasal passages before reaching the respiratory system (Walton, 1982~.
However, inhaled fibers align parallel to the airways and act as spheres
of approximately "equivalent" diameter (Gross, 1931; Timbrell et al.,
1970), where the equivalent or aerodynamic diameter of a particle is
defined as the diameter of a sphere with a density of 1 g/cm3 that has
the same falling speed as the particle. There is no sharp cutoff of
particle sizes determining their deposition site (Brain and Valberg,
1974).
The aerodynamic diameter of fibers depends primarily on the
diameter. For fibers with aspect ratios greater than about 10:1, it is
only slightly affected by length (Timbrell, 1965~. From his experiments
in rats, Timbrell (1965) found that the aerodynamic diameter of fibers
was about 3 times the actual diameter of the fibers. Fibers with
diameters greater than about 3 Am would be very unlikely to reach the
alveoli.
The sizes of inhaled and deposited fibers have been compared. Morgan
et al. (1979) showed the relationship between median aerodynamic diameter
and alveolar deposition in rats using a variety of fibers. Hammad et al.
(1982) experimented with retention of sized glass fibers in lungs of rats
and found that fibers less than 1 Am in diameter accounted for most of
the fibers retained (Figure 5-2~. Although the count median length of
fibers in the aerosol inhaled by the rats was 13 ~m, the count median
length fo''nd in lungs was 7 Am; for actual (as opposed to aerodynamic)
diameters, the respective values were 1.2 Am and 0.5 ~m. They also found
that length played some role. Timbrell (1982) compared the sizes of
fibers found in the air of an anthophyllite mine and mill with the sizes
of fibers found in the lungs of three adult workers.
Both the configuration and dimension of asbestiform fibers determine
where they impact after inhalation. Because the curlier chrysotile fiber
has a relatively large cross-sectional area, its chance for interception
in the airways is greater. Hence, these fibers are more likely to
deposit in larger bronchioles (Morgan et al., 1973), whereas thin,
rodlike fibers are carried peripherally to the terminal airways and
alveoli (Timbrell, 1965; Timbrell et al., 1970; Wagner et al., 1974~.
OCR for page 104
104
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OCR for page 105
105
In addition to diameter and shape, factors such as changes in
breathing rate, individual anatomic variat ions , smoking, and the presence
of bronchitis or lung disease also influence both the extent and site of
fiber deposition in humans (Brain and Valberg, 1979; Sanchis en al.,
1971).
Studies in animals have demonstrated that most deposited fibers are
removed from the respiratory tract within a few days. However, at least
a quarter of the initial burden remains 1 month later (Evans et al.,
1973; Muggenburg et al., 1981~. Since much of the inhaled asbestos is
not readily cleared, pulmonary tissue burden in humans may be a useful
index of exposure. Attempts have been made to quantify the amount of
fibers and ferruginous bodies in human and animal lungs in order to reach
a better understanding of the mechanism of action of the fibers. In
addition to pulmonary or other tissues, sputum and ravage samples have
been stud fed ~ Di Menza, 1980 ~ .
Analyses of lung tissue samples from humans indicate that heavily
exposed workers can be distinguished from those lightly exposed or from
controls. Sebase fen et al. (1977) reported that the number of
fibers/cm3 of lung sample, as seen by the light microscope, was
approximately 106 for a heavily exposed group, 103 for lightly
exposed workers, and 102 for controls.
Early researchers discovered the presence of asbestos bodies as well
as asbestos fibers in pulmonary tissues of exposed workers, especially in
those with asbestosis ~ Cooke, 1927, 1929; Cooke and Hill, 1930; Gloyne,
1929; Sebastien et al., 1979~. Asbestos bodies are asbestos fibers coated
with an iron-protein material that is readily visible with a light micro-
scope. The coating, which is produced by macrophages (Suzuki and Churg,
1969), seems to prevent the fiber from interacting with cells as
effectively as uncoated fibers. Because the coating may also be found on
other types of fibers, the term ferruginous body is now often used
instead of asbestos body. There are many reports of ferruginous bodies
counted under various circumstances (Sebastian et al., 1979), but the
pathological significance of these bodies is unclear. Asbestos bodies
form with greater efficiency on varieties of amphibole asbestos than on
chrysotile (Pooley, 1972~. Because the vast majority of deposited fibers
are not converted to ferruginous bodies, the presence of these bodies
reflects past exposure in only a very limited way.
Electron microscope observations have provided detailed information
on the deposition of fibers in animal and human tissues (Lange r et al.,
1973; Pooley, 1972~. Chrysotile seems to degrade or be removed In Vito
more readily than the amphiboles (Lange r et al., 1972a, b; Wagner et al. ,
1974, 1982 ; Rowlands, 1983) . Fibers found in tissue samples obtained
from the general population tend to be shorter in length and diameter
than those found in workers (Larger et al., 1971; Pooley en al., 1970~.
Fibers have also been detected in extrapulmonary tissues from both humans
and animals. (For reviews, see Sebastien et al ., 1979 and Cook, 1983) .
-
OCR for page 106
106
Fiber burden in the lung parenchyma ( the body of the lung) may be
different from that in the parietal pleura (the pleura lining the chest
cavity) as shown in a study of 29 persons, most of whom had pleural
asbestosis (Sebastian et al., 1979~. The parenchymal samples had both
amphibole and chrysotile fibers. Their average length was 4.9 ~m; 15% of
them were longer than ~ Am. The pleural samples were predominantly
chrysotile fiber, with an average length of 2.3 Am; 2X of these fibers
were longer than 8 Am. Thus, short chrysotile fibers tended to
predominate in the parietal pleura.
Most studies of fibers in human tissues have been conducted in
workers known to have been exposed to asbestos (Churg, 1983a). However,
there have been some studies of the amounts and types of fibers in the
general population (Churg, 1983b; Churg and Warnock, 1980~. Churg
(1983b) examined mineral fibers2 in the pulmonary tissues of 20
patients with no known occupational exposure to asbestos. He reported 13
types or groups of minerals, other than asbestos, including silica, talc,
and attapulgite . More than 85: of the part ic les counted, and al 1 of the
a~ctapulgite particles, were less than 5 Am long.
Clearance and Transport
Several mechanisms are involved in clearing fibrous materials from
the lung. These include removal by the beating of ciliated cells and
secretion of mucin (i.e., mucociliary clearance), transport by alveolar
macrophages to regional lymph nodes and distal sites (Lippmann en al.,
1980; Morgan et al., 1978, 1982), uptake by epithelial cells that line
the airways and alveoli (Mossman et al., 1977; Suzuki, 1974), and direct
translocation of fibers between ep~thelial cells to the interstitium and
the pleura.
The physical properties (i.e., length and cross-sectional dimensions)
of fibers appear to determine the mechanisms of cellular interaction and
transport. For example, short fibers with fine diameters can be
translocated within cells, whereas longer fibers (approximately 20 Am
long) are not completely engulfed by macrophages and are cleared
ineffectively (Morgan et al., 1978~. Incomplete mucociliary clearance
might result from discont~nuities in the mucus layer or hypersecretion, a
situation observed in people who smoke or have infections.
Alternatively, toxic irritants such as cigarette smoke cause dysfunction
and loss of ciliated ant secretory cells that line the airways (Sanchis
_ al., 1971~.
Clearance of asbestos from the gastrointestinal tract is less well
understood, although it has been reported that fibers cross the mucosa of
2The materials detected did not necessarily have the characteristics of
asbestiform fibers. -
OCR for page 107
107
the stomach and intestines (Cook, 1983; Westiake et al., 1965~. Fibers
have been detected in urine and feces (Muggenburg et al., 1981~. When
injected into the femoral vein of pregnant rats, chrysotile crosses the
placenta and has been observed in fetal liver and lung (Cunningham and
Pontefract, 19743.
CLINICAL ASPECTS OF "BESTOS-"SOCIATED DISHES
l
m e four major asbestos-related diseases or changes are: (1) lung
cancer; (2) mesothelioma; (3) pulmonary asbestosis; and (4) pleural
plaques or diffuse thickening, calcifications, and effusion. Some other
cancers may also be related to asbestos exposure (Selikoff et al..
1979~. Lung cancer and mesothelioma are typically fatal cancers.
Therefore, the degrees of severity are generally not relevant. Pulmonary
asbestosis and the pleural changes noted above are nonmalignant
pathological conditions that may range from mild to severe. They are
usually related to the amount (intensity and duration) of exposure that
the individual has experienced.
Although lung cancer can usually be diagnosed with reasonable
certainty, menothelioma and asbestonis are often more difficult to
identify. For example, by the time a tumor is observed in a patient with
mesothelioma, it may be difficult to ascertain both cell type and tissue
of origin. For asbestosis, there is no complete agreement as to what
constitutes a definitive diagnosis, especially for milder cases. These
diagnostic uncertainties present difficulties to those analyzing results
of epidemiological studies and determining incidence rates.
Inhalation is the major route by which asbestiform fibers enter the
body. They may also enter the digestive tract via ingested material such
as water or drugs or via asbestos-containing secretions from the lung
airways that are brought up into the mouth and then swallowed (Bouhuys,
1974; Langer et al., 1979; Selikoff and Lee, 1978~.
_ ~
Necessary AsSumptioD8 Used in Determining Health Effects
In the absence of adequate data on the health effects of low-level
and nonoccupational exposure, certain assumptions must be made in order
to predict and identify possible health effects. One assumption is that
clinical manifestations in nonoccupational and occupational illness will
be similar in kind but not necessarily in extent or degree. In cases of
lung carcinoma and mesothelioma, malignancy is usually the cause of
death. Both the time from exposure to onset of symptoms and the rate of
progression from time of diagnosis are assumed to be similar in
nonoccupational and occupational disease.
..
OCR for page 154
154
Hilt, J. W., C. E. Rossiter, and D. W. Fode. 1982. A pilot respiratory
study of cancers in a MUFF plant in the United Kingdom. Presented at
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Hobbs, M. S. T., S . D. Woodward , B. Murphy , A. W. Musk, and J. E. Elder.
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r
Representative terms from entire chapter:
asbestos exposure
