Workplace Exposure to Asbestos:
Review and Recommendations
BIOLOGIC EFFECTS OF
EXPOSURE TO ASBESTOS
IN HUMANS
Memorandum on Asbestos Update and Recommended
Occupational Standard
I. Asbestos Nomenclature/Definitions
II. Asbestos Sampling and Analysis
III. Biologic Effects of Exposure to
Asbestos in Animals
IV. Biologic Effects of Exposure to
Asbestos in Humans
V. Smoking and Asbestos
VI. Exposure to Asbestiform Minerals
other than Commerically Mined Asbestos
VII. Non-Occupational Exposure to Commerical
Sources of Asbestos
VIII. Dose-Response Relationships
References
Amosite
Seidman et al. (1979) have extended their study of amosite asbestos
workers with short-term exposures. The study group consisted of 820 men
first employed between June, 1941 and December, 1945 in the production
of asbestos insulation and who were alive in 1961. Followup was through
1977, with expected deaths adjusted for age and calendar time estimated
using death rates for white males in the general population of New Jersey.
Among the cohort studied by Seidman et al., 83 lung cancers were observed
according to death certificate information, whereas 23.1 were expected.
Among 61 men employed less than 1 month, 3 lung cancers were observed
versus 1.3 expected. Although based on small numbers, excess mortality
from lung cancer showed an increasing trend with employment duration.
Cancer latency periods were progressively shortened with increasing employment
duration. Four mesotheliomas were reported on death certificates in contrast
to 14 which were identified on autopsy and other tissue diagnoses. Three
in the group had less than 1 year of exposure. Although no environmental
data are available for this plant, dust counts were made in another plant
using the same fiber type and production process. Seidman et al. reported
average exposure at this plant to be 23 fibers/cc. Further data available
for this comparison plant were published by NIOSH (1972) showing mean
exposures to range from 14 to 75 fibers/cc. At such concentrations, a
lung cancer relative risk of 2.3 could be calculated with employment less
than 1 month.
Anderson et al. (1979) evaluated the risks of nonmalignant and malignant
disease associated with household exposure to work-derived amosite dust.
Four mesothelioma cases were reported among household contacts of former
workers at a plant manufacturing amosite insulation products in Paterson,
New Jersey. Anderson et al. also reported a 35.9% prevalence of radiographic
abnormalities among household contacts of former employees at this same
amosite plant, compared with a 4.6% prevalence among a control group.
These radiographic abnormalities included pleural thickening, pleural
calcification, pleural plagues, and irregular opacities. These studies
raise the specter of non-occupational hazards associated with casual or
low-level exposures to amosite
Murphy et al. (1978) reported a followup to their first report (1971)
of shipyard pipe coverers exposed predominantly to amosite asbestos. Workers
in the original Murphy report of 1971, with "asbestosis" diagnosed
by multiple criteria, had a poor prognosis as reported in the 1978 longitudinal
survey.
Chrysotile
Robinson et al. (1979) reported an additional 8 years of observation
and 385 deaths to the Wagoner et al. (1973) study of mortality patterns
among workers at one facility manufacturing asbestos textile, friction,
and packing products. Chrysotile constituted over 99% of the total quantity
of asbestos processed per year, except for 3 years during World War II.
During these 3 years, amosite was selectively used to a limited extent
because of U.S. Naval specifications, and accounted for approximately
5% of the total asbestos used per year. Crocidolite and amosite for the
other years accounted for less than 1% of total usage in very selected
areas. Exposures to these other two types may have played some role in
the etiology of disease; however, due to the overwhelming exposure of
the cohort to chrysotile, it is likely that the other exposures played
a minor role in the overall mortality patterns. Robinson et al. confirmed
Wagoner et al.'s observations of statistically significantly excess deaths
due to bronchogenic cancer, suicide, heart disease, and nonmalignant respiratory
disease including asbestosis and a statistically non-significant excess
of digestive cancer and lymphoma. Robinson et al. described 17 mesotheliomas
whereas no mesotheliomas were detected in the Wagoner et al. study where
observation of mortality ceased in 1967. The appearance of 17 mesotheliomas
in the updated study reflects latency periods of 24 to 53 years since
onset of first exposure. Further analysis indicated 14 of 17 mesothelioma
deaths occurred after the original study period. This observation confirms
other findings that mesotheliomas are characterized by very long latency
periods. Chovil and Stewart (1979) also reported latencies of 6 to 44
years, with a mean of 26.9 years.
Weiss (1977) reported no unusual mortality experience over a 30-year
period for a cohort of workers employed in a paper and millboard plant
stated to be using only chrysotile The author concluded that the study
results were suggestive of a minimal hazard from chrysotile This conclusion
must be viewed in light of the limitations inherent in the study. The
study population was small (n= 264) and only 66 workers had died at the
time of analyses. Two of these workers died of asbestosis. Moreover, the
unusually low Standard Mortality Ratio (SMR) for many causes of death
in the Weiss et al. paper suggests the possibility of a selection bias
greater than that usually seen when contrasting industrial populations
with the general population.
McDonald et al. (1973, 1974) reported an increased risk of lung cancer
among men employed in Quebec chrysotile mines and mills. The risk of lung
cancer among those workers most heavily exposed was 5 times greater than
those least exposed. Liddell et al. (1977) further analyzed the mortality
experience of the cohort of chrysotile asbestos miners and millers previously
studied by McDonald et al. and found excesses of respiratory cancer, asbestosis,
and mesothelioma. These same chrysotile miners and millers of Quebec,
as of 1977, had experienced nine confirmed and two suspected mesotheliomas
(McDonald, 1978). The author concluded for the seven cases observed at
Thetford mines that "There is therefore no good reason to doubt chrysotile
exposures as the cause."
A recent study by Nicholson et al. (1979) examined the mortality of
544 Quebec chrysotile mine and mill employees which corresponded closely
in terms of duration of exposure and periods of observation to cohorts
of mixed fiber asbestos factory workers and insulation workers established
in other studies. Among this cohort of 544 men with at least 20 years
of employment in chrysotile mining and milling at Thetford Mines, Canada,
16% of the deaths were from lung cancer and 15% from asbestosis. The risk
of death for asbestosis, at equal times from onset of exposure, was very
similar in the miners and millers to that found in the factory workers
and insulators. Lung cancer was similar among the miners and millers and
in the factory workers but higher in the insulators. One death from mesothelioma
was reported in this study.
Selikoff (1977b) surveyed 485 current employees of a chrysotile mine
in Baire-Verte, Newfoundland, which had been in operation since 1963.
Fifty employees (10%) had one or more radiographic abnormalities of the
type commonly associated with asbestos exposure. Parenchymal abnormalities
were most common, and pleural changes were detected in only 3% of the
individuals surveyed. For those individuals employed less than 5 years
the prevalence of abnormalities was 5%, and this increased with duration
of employment. Changes occurred most commonly in those with the most intense
exposures. This study was designed only to assess asbestos-related disease
under more modern conditions than have previous studies (Kogan et al.,
1972; Rossiter et al., 1972); thus, assessments of the effects of short
duration of exposure and long latency could not be made. The interpretation
of these data is further complicated by the lack of a control population
and environmental measurements. The study does demonstrate the prevalence
of chest X-ray changes in an appreciable proportion of employed workers,
despite a short period since initial exposure.
Rubino et al. (1979) reported nine asbestosis deaths among chrysotile
asbestos miners in northern Italy. Excess lung cancer (7 vs. 3.4) was
seen only during the last quinquennium of observation, 1971-1975, that
period of time after greatest latency. Also, one mesothelioma was reported
in this latest period.
Studies examining lung tissue of mesothelioma cases and comparison groups
have shown equivocal results as to the possible relationship of chrysotile
in lung tissue and mesothelioma. Jones et al. (1979) found no evidence
to indict chrysotile, while Acheson and Gardner (1979) estimated a 6-fold
relative risk of mesothelioma for persons with only chrysotile in lung
tissue as compared with controls with no asbestos fiber in their lungs.
Boutin et al. (1979) reported on a study of chest film abnormalities
among chrysotile miners and millers in Corsica. They studied 166 ex-workers
of the mines and mill closed in 1965, and compared them with 156 controls
without asbestos exposure and with similar demographic variables. Chest
films were read according to the ILO U/C Classification system. Compared
with controls, chrysotile workers had a prevalence of all parenchymal
abnormalities 2.4 times that of controls. For those with a profusion of
1/2 or more, the prevalence ratio was approximately twice the controls.
Pleural changes were twice as prevalent in chrysotile workers as in controls.
Exposures among this cohort were reported to have been very high, with
exposure levels ranging from 85 to 267 million parts per cubic foot (mppcf).
Crocidolite
Jones et al. (1976) reported a high incidence of mesothelioma among
women who worked predominantly with crocidolite in a factory producing
gas mask canisters during World War II, and have recently extended observations
on this population (Jones et al., 1979). Among this group of 1,088 workers
exposed only between 1940 and 1945, 22 pleural and 7 peritoneal mesotheliomas
were observed. This is likely an underestimate since 373 women were lost
to observation. A linear dose-response relationship with length of employment
was observed for mesothelioma, with three mesotheliomas observed among
those exposed 5-10 months.
McDonald and McDonald (1978) have also studied mortality of 199 workers
exposed to crocidolite during gas mask manufacture in Canada during 1939
to 1942. This cohort was followed through 1975, and 56 deaths occurred.
Out of these 56 deaths, 4 (7%) were from mesothelioma and 8 from lung
cancer. It should be pointed out that an additional five mesotheliomas
not reported on death certificates were diagnosed on review of pathology
or autopsy material.
Mixed Fiber Types
Weill et al. (1979) and Hughes and Weill (1979) reported on the mortality
experience of a cohort of 5,645 men employed in production of asbestos
cement products and who had at least 20 years since first exposure. These
workers were exposed largely to chrysotile, with some crocidolite and
amosite Among this group, 601 persons were identified as deceased by the
Social Security Administration. Those with unknown vital status (25%)
by this source were assumed to be alive, thus likely resulting in underestimation
of the true risk. Death certificates were obtained for 91% of the known
deaths. Dust exposures were estimated using each worker's employment history
in conjunction with historical industrial hygiene data.
Weill et al. (1979) observed increased respiratory cancer mortality
only among those with exposure in excess of 100 mppcf/year, where 23 cases
were observed versus the 9.3 expected. The unusually low SMR for all causes
in the low exposure groups suggests the possibility of a selection bias,
and any interpretation of risks at low exposures should be done with caution.
Two pleural mesotheliomas were reported. Separating the cohort by type
of fiber exposure, the authors concluded that the addition of crocidolite
to chrysotile enhanced the risk for respiratory malignancy; however, an
excess risk (8 observed vs. 4.4 expected) was observed among those not
exposed to crocidolite, with cumulative exposures in excess of 200 mppcf-months
(16.6 mppcf-years). Both average concentration of exposure and duration
of exposure were found to be related to cancer risk.
Jones et al. (1979) studied the progression of radiographic abnormalities
and lung function among asbestos cement workers. Chest films taken in
1970 and 1976 on 204 workers were read independently by two readers according
to the ILO U/C 1971 Classification scheme. These films were read side-by-side
in known order and ranked according to progression. Spirometric measurements
were made in 1973 and 1976. The major findings of the Jones et al. study
were: (1) the progression of small opacities was dependent upon both average
and cumulative exposure; (2) significant declines in lung function were
shown to result from both smoking and cumulative exposure; and (3) pleural
abnormalities progressed as a function of time with little association
to additional exposure. No estimates were made of the incidence of various
respiratory abnormalities in relation to exposure.
Peto (1979) reported on the mortality experience of a cohort of asbestos
textile workers previously studied by Doll (1955), Knox et al. (1968),
and Peto et al. (1977). Data from this factory had previously been used
by the British Occupational Hygiene Society (BOHS, 1968) in establishing
occupational exposure standards and was subsequently studied by Lewinsohn
(1972). Routine dust measurements in this factory were first made in 1951.
Among the 255 males first employed after 1951, 12 lung cancers were observed,
whereas only 4.65 were expected, based on national death rates. Among
those with 20 or more years since initial employment, 8 lung cancers were
observed versus 1.62 expected. Fiber exposures were estimated to be 32.4
fibers/cc in 1951, decreasing to 1.1 fibers/cc in 1974. These estimates
are 2.4 times previously estimated values for this plant (Peto et al.,
1977). Peto estimated the relative risk for cumulative exposures of 200-300
fibers/cc-year to be between 2 and 3. The cohort is too small and followup
too short to estimate cancer risks at lower exposures. No mesotheliomas
were observed in the cohort first employed after 1951; however, the followup
period is insufficient to address this question.
Berry et al. (1979) extended their 1968 observations concerning asbestosis
by including persons completing 10 or more years employment by 1972. Persons
who left after June 30, 1966, were also contacted and encouraged to participate,
with 68 of 113 persons eventually participating. Outcome measures studied
included chest radiographs, medical examination including assessment of
basal crepitations, and pulmonary function (FEV, FVC, FRC, TLC, RF, TL,
PaCO2 ). Chest films were read by four readers by the ILO/UC
1971 Classification system with readings being averaged. Dust exposures
were estimated for each person using available hygiene data and estimates
of control effectiveness.
In this study, "possible asbestosis" was diagnosed based on
one or more combinations of basal rales or crepitations, radiological
changes, a falling transfer factor, and restrictive lung function changes.
Among these 379 men, 60 cases of possible asbestosis were diagnosed by
the factory medical officer, where as 85 cases were diagnosed by an independent
clinician. Collaboration by these investigators subsequently resulted
in 82 men with crepitations, 58 with "possible asbestosis,"
and 34 with certified asbestosis. Using the exposure data, these authors
estimated the cumulative dose necessary for a 1% incidence for crepitations,
possible asbestosis, and certified asbestosis to be 43, 55, and 72 fibers/cc-year,
respectively. These authors pointed out limitations of the cumulative
dose concept and acknowledged the imprecision of their exposure estimates.
Two cases of certified asbestosis were observed among nonsmokers and nine
among ex-smokers. There were, in general, fewer respiratory symptoms and
signs in nonsmokers and light smokers than in heavy and ex-smokers.
Elmes and Simpson (1977) have extended their earlier (1971) report
to include deaths occurring since 1965 through 1975. The mortality trend
has shifted from a preponderance of asbestosis and gastrointestinal cancer
deaths to malignancies of the lung and mesothelioma, diseases associated
with longer latent periods. These authors stated that their findings would
suggest any standard based "on the prevention of asbestosis may not
provide adequate protection against neoplasia."
Morbidity and mortality analysis by Lacquet et al. (1979) of workers
in a Belgian asbestos cement factory revealed a strong dose-response relationship
for asbestosis, and pleural and parenchymal lung changes. Pleural thickening
and adhesions began occurring in the lowest dose category (0-49 fibers/cc-year).
Parenchymal lung changes occurred less frequently. No cases of asbestosis
were recognized in workers with less than 100 fiber-years of exposure.
Asbestosis occurs more frequently and with shorter latency periods (as
the exposure levels increase) and adverse mortality tends to occur at
longer latency periods (as the dose decreases) (Seidman et al., 1979).
Because the observation period of the Lacquet et al. study was only 15
years, it cannot be assumed that the absence of asbestosis in the low
dose categories currently observed will not occur in these low dose categories
after a longer latent period, or that pleural and parenchymal lung changes
are not indicators of early lung change that can or will progress to asbestosis.
The mortality portion of the study revealed asbestosis and an excess of
digestive cancer, but not excesses for lung cancer or mesothelioma. This,
again, is not surprising since lung cancer and mesothelioma tend to develop
after latent periods greater than 15 years.
Baselga-Monte and Segarra's (1978) examination of 1,262 workers employed
in four factories in the Barcelona area demonstrated a dose-response relationship
based upon radiologic images. The authors demonstrated a quick response
for pleural radiological changes at individual cumulative doses as low
as 5 fibers/cc-years, while the pulmonary and pleuropulmonary responses
tend to appear later, but not at statistically different doses. The authors
were reluctant to draw conclusions because of the design of the epidemiologic
evaluation, which considered only active employees. Other epidemiologic
studies of worker populations would indicate that evaluation of only active
employees tends to underestimate the health risk since diseased workers
oftentimes tend to self-select out of the active workforce (Fox and Collier,
1976; Enterline et al., 1972; Borow et al., 1973). Baselga-Monte and Segarra
concluded that "the present worldwide trend to establish more exigent
hygienic criteria for exposure to asbestos is confirmed." Based on
their working model, this level for a 50-year working life should be 0.07-0.10
fiber/cc, "taking into account protection levels of 89 and 95%."
Malignant Neoplasms other than Mesothelioma and Cancer of the Lung.
A number of epidemiological studies indicate less striking associations
of excess risks of other types of cancers (in addition to bronchial and
mesothelial) and occupational asbestos exposure. Selikoff (1977a) reported
increased rates for cancer of the stomach and esophagus (20 observed vs.
6.46 expected) and cancer of colon (23 observed vs. 7.64 expected) among
632 asbestos insulation workers in the New York and New Jersey area. Selikoff
et al. (1979) made similar observations among 17,800 asbestos insulation
workers in the United States and Canada. They reported increased mortality
from cancer of the esophagus (18 observed vs. 7.1 expected), stomach (18
observed vs. 14.2 expected), and colon and rectum (58 observed vs. 38.1
expected) among this study cohort. Similar observations have been reported
by others (Elmes and Simpson, 1971; Kogan et al., 1972).
Cook and Olson (1979) have recently shown that sediment in human
urine contains amphibole fibers, thus providing the first evidence that
mineral fibers pass through the human gastrointestinal mucosa under normal
conditions of the alimentary canal.
Stell and McGill (1973) found that of 100 men with squamous-cell
carcinomas of the larynx, 31 had known exposure to asbestos, compared
with only 3 in matched controls. Similar associations have been reported
by Morgan and Shettigara (1976); Shettigara and Morgan (1975); Rubino
et al. (1979); and Selikoff et al. (1979a). Newhouse et al. (1979), however,
utilizing an interview of patients at the Royal National Throat, Nose,
and Ear Hospital in London, found that asbestos exposure was not more
common among cases as compared to controls.
Significant increases in cancer of the buccal cavity and of the
pharynx have been reported by Selikoff et al. (1979a). Among 17,800 asbestos
insulation workers they observed 16 deaths due to cancer of these sites
whereas 10.1 deaths would have been expected based on U.S. white male
rates.
Robinson et al. (1979) reported an excess of deaths due to lymphosarcoma
and malignant lymphoma among white males employed in an asbestos textile,
friction, and packing products manufacturing facility. There were 7 deaths
due to cancer of these sites, while 3.28 cases were expected.
Memorandum on Asbestos Update and Recommended
Occupational Standard
I. Asbestos Nomenclature/Definitions
II. Asbestos Sampling and Analysis
III. Biologic Effects of Exposure to
Asbestos in Animals
IV. Biologic Effects of Exposure to
Asbestos in Humans
V. Smoking and Asbestos
VI. Exposure to Asbestiform Minerals
other than Commerically Mined Asbestos
VII. Non-Occupational Exposure to Commerical
Sources of Asbestos
VIII. Dose-Response Relationships
References
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