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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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