Follow up study of workers manufacturing chrysotile asbestos cement products

A cohort study has been carried out of 2167 subjects employed between 1941 and 1983 at an asbestos cement factory in England. The production process incorporated the use of chrysotile asbestos fibre only, except for a small amount of amosite during four months in 1976. Measured airborne fibre concentrations available since 1970 from personal samplers showed mean levels below 1 fibre/ml, although higher levels had probably occurred previously in certain areas of the factory. No excess of lung cancer was observed in the mortality follow up by comparison with either national or local death rates, and analyses of subgroups of the workforce by job, exposure level, duration of employment, duration since entry, or calendar years of employment gave no real suggestion of an asbestos related excess for this cause of death. There was one death from pleural mesothelioma and one with asbestosis mentioned as an associated cause on the death certificate, but neither is thought to be linked to asbestos exposure at this factory. Other suggested asbestos related cancers, such as laryngeal and gastrointestinal, did not show raised risks. Although the durations of exposure were short in this study, the findings are consistent with two other studies of workers exposed to low concentrations of chrysotile fibre in the manufacture of asbestos cement products which reported no excess mortality.     

Lung cancer among asbestos cement workers. A Swedish cohort study and a review.

A cohort study of 1176 Swedish asbestos cement workers did not indicate any asbestos related excess mortality. Possible explanations of the negative outcome are relatively low exposure levels and the predominant use of chrysotile in production. Such a tentative conclusion is supported by a review of five mortality studies of workers exposed to asbestos cement that report considerable differences in relative risks for lung cancer. These differences could be explained by various degrees of cumulative exposure, the amount of amphiboles in the production, and methodological shortcomings. A median exposure of 10-20 fibre-years does not seem to cause an increased risk of lung cancer, particularly when only chrysotile is used.     

Lung cancer among asbestos cement workers. A Swedish cohort study and a review

A cohort study of 1176 Swedish asbestos cement workers did not indicate any asbestos related excess mortality. Possible explanations of the negative outcome are relatively low exposure levels and the predominant use of chrysotile in production. Such a tentative conclusion is supported by a review of five mortality studies of workers exposed to asbestos cement that report considerable differences in relative risks for lung cancer. These differences could be explained by various degrees of cumulative exposure, the amount of amphiboles in the production, and methodological shortcomings. A median exposure of 10-20 fibre-years does not seem to cause an increased risk of lung cancer, particularly when only chrysotile is used.     

Mortality of workers manufacturing friction materials using asbestos

A mortality (1942-80) study was carried out on 13460 workers of a factory producing friction materials. The only type of asbestos used was chrysotile, except during two well-defined periods before 1945 when crocidolite was used, and over 99% of the population was traced. Compared with national death rates there were no detectable excesses of deaths due to lung cancer, gastrointestinal cancer, or other cancers; 11 deaths were due to pleural mesothelioma. A case-control study was carried out on deaths due to mesothelioma; this showed that eight workers had been exposed to crocidolite and another was possibly exposed intermittently to crocidolite. The other two had been employed for most of their working lives outside the factory, and their mesotheliomas could not be definitely attributed to exposure to chrysotile. Limiting the study to cases and controls who had exposure to 5 fibres/ml of chrysotile asbestos it was found that five of the six cases compared with two of the 10 controls had also been exposed to crocidolite. The probability (1:36) of this occurring were there no association with crocidolite is most unlikely. A case-control study was also carried out on deaths due to lung cancer and gastrointestinal cancer to investigate the dose-response relationships between these tumours and exposure to chrysotile. Measured and estimated fibre concentrations were available for the different jobs over the period of the study. No dose-response relationships were observed, but the exposures were low with only 5% of men accumulating 100 fibre-years/ml. The experience at this factory over a 40-year period showed that chrysotile asbestos was processed with no detectable excess mortality.     

Mortality of workers manufacturing friction materials using asbestos.

A mortality (1942-80) study was carried out on 13460 workers of a factory producing friction materials. The only type of asbestos used was chrysotile, except during two well-defined periods before 1945 when crocidolite was used, and over 99% of the population was traced. Compared with national death rates there were no detectable excesses of deaths due to lung cancer, gastrointestinal cancer, or other cancers; 11 deaths were due to pleural mesothelioma. A case-control study was carried out on deaths due to mesothelioma; this showed that eight workers had been exposed to crocidolite and another was possibly exposed intermittently to crocidolite. The other two had been employed for most of their working lives outside the factory, and their mesotheliomas could not be definitely attributed to exposure to chrysotile. Limiting the study to cases and controls who had exposure to 5 fibres/ml of chrysotile asbestos it was found that five of the six cases compared with two of the 10 controls had also been exposed to crocidolite. The probability (1:36) of this occurring were there no association with crocidolite is most unlikely. A case-control study was also carried out on deaths due to lung cancer and gastrointestinal cancer to investigate the dose-response relationships between these tumours and exposure to chrysotile. Measured and estimated fibre concentrations were available for the different jobs over the period of the study. No dose-response relationships were observed, but the exposures were low with only 5% of men accumulating 100 fibre-years/ml. The experience at this factory over a 40-year period showed that chrysotile asbestos was processed with no detectable excess mortality.     

Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.     

Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis.

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.     

Further follow-up study of workers from an asbestos cement factory.

A further follow-up traced 1970 workers employed at an asbestos cement factory for at least six months between 1936 and 1977. At the beginning of this period some crocidolite was used in the factory but by the end of 1936 chrysotile had become the only type of asbestos in use. Only 378 women were employed during the period concerned, and of the 30 who had died, none had a cause of death that is generally associated with exposure to asbestos. The mortality experience of the men was examined separately for all workers, all workers alive after 15 or more years after first exposure, and a smaller group of workers who were employed in 1935-6 and may have been exposed to crocidolite. In none of the three groups was there an appreciably raised standardised mortality ratio (SMR) for the causes of death investigated. These were: all causes, all neoplasms, cancers of the lung and pleura, and cancers of the gastrointestinal tract. An excess of lung cancers noted in the first follow-up study in 1964 was not found in this study. Two pleural mesotheliomas were identified but in both cases the men had worked at the factory before 1936 and therefore had been exposed to crocidolite. No cancers of the larynx were found.     

Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos.

OBJECTIVES: To evaluate alternative models and estimate risk of mortality from lung cancer and asbestosis after occupational exposure to chrysotile asbestos. METHODS: Data were used from a recent update of a cohort mortality study of workers in a South Carolina textile factory. Alternative exposure-response models were evaluated with Poisson regression. A model designed to evaluate evidence of a threshold response was also fitted. Lifetime risks of lung cancer and asbestosis were estimated with an actuarial approach that accounts for competing causes of death. RESULTS: A highly significant exposure-response relation was found for both lung cancer and asbestosis. The exposure-response relation for lung cancer seemed to be linear on a multiplicative scale, which is consistent with previous analyses of lung cancer and exposure to asbestos. In contrast, the exposure-response relation for asbestosis seemed to be nonlinear on a multiplicative scale in this analysis. There was no significant evidence for a threshold in models of either the lung cancer or asbestosis. The excess lifetime risk for white men exposed for 45 years at the recently revised OSHA standard of 0.1 fibre/ml was predicted to be about 5/1000 for lung cancer, and 2/1000 for asbestosis. CONCLUSIONS: This study confirms the findings from previous investigations of a strong exposure-response relation between exposure to chrysotile asbestos and mortality from lung cancer, and asbestosis. The risk estimates for lung cancer derived from this analysis are higher than those derived from other populations exposed to chrysotile asbestos. Possible reasons for this discrepancy are discussed.     

Dust exposure and mortality in an American chrysotile textile plant

Three parallel cohort studies of asbestos factory workers were undertaken to investigate the effects of mineral fibre type and industrial process on malignant mesothelioma, respiratory cancer, and asbestosis. This report describes the mortality of a cohort of 2543 men, defined as all those employed for at least a month from 1938 to 1958 in a textile plant in South Carolina in which chrysotile was the only type of asbestos used. Of these, 863 men (34%) had died before 31 December 1977, one from malignant mesothelioma. Twenty one deaths were ascribed to asbestosis and 66 to cancer of the lung. Compared with the number expected from South Carolina, there was an excess of 30 deaths from respiratory cancer (ICD 160-164) in men 20 or more years after first employment (SMR 199.5). In men employed five years or more, no SMRs for this category rose above 300. Individual exposures were estimated (in mpcf X years) from recorded environmental measurements. Life table analyses and "log-rank" (case-control) analyses both showed a steep linear exposure-response that was some 50-fold greater at similar accumulated dust exposures than in Canadian chrysotile mining and milling. These findings agree closely with those from another study in this plant and confirm that mesothelioma is rarely associated with chrysotile exposure. Cigarette smoking habits did not greatly differ between the textile workers and the Canadian miners and millers. The far greater risk of lung cancer in the textile industry, if not attributable to other identified cocarcinogens, may be related to major differences in the size distribution of fibres in the submicroscopic range which are not detected by the usual fibre or particle counting procedures.     

Dust exposure and mortality in an American chrysotile textile plant.

Three parallel cohort studies of asbestos factory workers were undertaken to investigate the effects of mineral fibre type and industrial process on malignant mesothelioma, respiratory cancer, and asbestosis. This report describes the mortality of a cohort of 2543 men, defined as all those employed for at least a month from 1938 to 1958 in a textile plant in South Carolina in which chrysotile was the only type of asbestos used. Of these, 863 men (34%) had died before 31 December 1977, one from malignant mesothelioma. Twenty one deaths were ascribed to asbestosis and 66 to cancer of the lung. Compared with the number expected from South Carolina, there was an excess of 30 deaths from respiratory cancer (ICD 160-164) in men 20 or more years after first employment (SMR 199.5). In men employed five years or more, no SMRs for this category rose above 300. Individual exposures were estimated (in mpcf X years) from recorded environmental measurements. Life table analyses and "log-rank" (case-control) analyses both showed a steep linear exposure-response that was some 50-fold greater at similar accumulated dust exposures than in Canadian chrysotile mining and milling. These findings agree closely with those from another study in this plant and confirm that mesothelioma is rarely associated with chrysotile exposure. Cigarette smoking habits did not greatly differ between the textile workers and the Canadian miners and millers. The far greater risk of lung cancer in the textile industry, if not attributable to other identified cocarcinogens, may be related to major differences in the size distribution of fibres in the submicroscopic range which are not detected by the usual fibre or particle counting procedures.     

Fibre type and concentration in the lungs of workers in an asbestos cement factory

The predominant asbestos fibre type used in the production of asbestos cement is chrysotile. The use of asbestos in relation to fibre type in a Norwegian asbestos cement plant during 1942-80 was 91.7% chrysotile, 3.1% amosite, 4.1% crocidolite, and 1.1% anthophyllite respectively. Electron microscopy and x ray microanalysis of lung tissue samples of asbestos cement workers who had died of malignant pleural mesothelioma or bronchogenic carcinoma showed a completely inverse ratio with regard to fibre type. The percentage of chrysotile asbestos in lung tissue varied between 0% and 9% whereas the corresponding numbers for the amphiboles were 76% and 99%. These differences are discussed with respect to the behaviour of different fibre types in the human body and to the occurrence of malignant mesothelioma in this asbestos cement factory.     

Alterations in the laryngeal mucosa after exposure to asbestos

The laryngeal mucosa of 195 workers in an asbestos cement factory (Salonit Anhovo, Yugoslavia) and in a control group was examined. The factory manufactures asbestos cement products containing about 13% of asbestos (8% amosite, 12% crocidolite, and 80% chrysotile) of different provenance. Alterations in the laryngeal mucosa were more frequent in the factory workers than in the control group. The changes, mostly consistent with chronic laryngitis, were closely related to the degree of workplace pollution and less so to the duration of employment Ten workers exhibiting the most severe clinical changes underwent biopsy, the results of which showed histomorphological changes characteristic of hyperplastic chronic laryngitis. Four tissue specimens were examined also by scanning electron microscopy and in three of them asbestos fibres were found on the epithelial surface. No case of laryngeal carcinoma was identified. On the basis of our results it is thought that asbestos related changes of the larynx should receive more attention and that the use of the term "laryngeal asbestosis" is justified. The clinical picture is non-specific but in view of their frequency such changes should be considered a consequence of exposure to asbestos.     

Alterations in the laryngeal mucosa after exposure to asbestos.

The laryngeal mucosa of 195 workers in an asbestos cement factory (Salonit Anhovo, Yugoslavia) and in a control group was examined. The factory manufactures asbestos cement products containing about 13% of asbestos (8% amosite, 12% crocidolite, and 80% chrysotile) of different provenance. Alterations in the laryngeal mucosa were more frequent in the factory workers than in the control group. The changes, mostly consistent with chronic laryngitis, were closely related to the degree of workplace pollution and less so to the duration of employment Ten workers exhibiting the most severe clinical changes underwent biopsy, the results of which showed histomorphological changes characteristic of hyperplastic chronic laryngitis. Four tissue specimens were examined also by scanning electron microscopy and in three of them asbestos fibres were found on the epithelial surface. No case of laryngeal carcinoma was identified. On the basis of our results it is thought that asbestos related changes of the larynx should receive more attention and that the use of the term "laryngeal asbestosis" is justified. The clinical picture is non-specific but in view of their frequency such changes should be considered a consequence of exposure to asbestos.     

Fibre type and concentration in the lungs of workers in an asbestos cement factory.

The predominant asbestos fibre type used in the production of asbestos cement is chrysotile. The use of asbestos in relation to fibre type in a Norwegian asbestos cement plant during 1942-80 was 91.7% chrysotile, 3.1% amosite, 4.1% crocidolite, and 1.1% anthophyllite respectively. Electron microscopy and x ray microanalysis of lung tissue samples of asbestos cement workers who had died of malignant pleural mesothelioma or bronchogenic carcinoma showed a completely inverse ratio with regard to fibre type. The percentage of chrysotile asbestos in lung tissue varied between 0% and 9% whereas the corresponding numbers for the amphiboles were 76% and 99%. These differences are discussed with respect to the behaviour of different fibre types in the human body and to the occurrence of malignant mesothelioma in this asbestos cement factory.     

A mortality study of workers manufacturing friction materials: 1941-86

The mortality of workers employed at a factory producing friction materials has been studied from 1941 to 1986, extending a previous study by seven years. Apart from two periods before 1944, when crocidolite asbestos was used on one particular contract, only chrysotile asbestos has been used. Thirteen deaths were attributed to mesothelioma and of these, 11 were of subjects who had known contact with crocidolite asbestos. Of the remaining two, in one instance the diagnosis is uncertain and in the other the occupational history of the subject is not well established. There was no excess of deaths from lung cancer or other asbestos related tumours, or from chronic respiratory disease. After 1950 hygienic control was progressively improved and from 1970 levels of asbestos in air have not exceeded 0.5-1.0 f/ml. It is concluded that with good environmental control chrysotile asbestos may be used in manufacture without causing excess mortality.     

A mortality study of workers manufacturing friction materials: 1941-86.

The mortality of workers employed at a factory producing friction materials has been studied from 1941 to 1986, extending a previous study by seven years. Apart from two periods before 1944, when crocidolite asbestos was used on one particular contract, only chrysotile asbestos has been used. Thirteen deaths were attributed to mesothelioma and of these, 11 were of subjects who had known contact with crocidolite asbestos. Of the remaining two, in one instance the diagnosis is uncertain and in the other the occupational history of the subject is not well established. There was no excess of deaths from lung cancer or other asbestos related tumours, or from chronic respiratory disease. After 1950 hygienic control was progressively improved and from 1970 levels of asbestos in air have not exceeded 0.5-1.0 f/ml. It is concluded that with good environmental control chrysotile asbestos may be used in manufacture without causing excess mortality.     

Mortality of workers employed in two asbestos cement manufacturing plants.

In a study of the mortality experience of 6931 employees of two New Orleans asbestos cement products manufacturing plants over 95% were traced. Chrysotile was the primary fibre used in both plants. Plant 1 also used small amounts of amosite and, later, crocidolite irregularly whereas plant 2 used crocidolite steadily in pipe production. Previously reported exposure concentration estimates were revised, based on additional air sampling data and re-evaluation of these data. Workers in the two plants had similar duration of employment (overall, a mean of 3.8 years) and estimated exposure concentration (a mean of 7.6 million particles per cubic foot (mppcf)). Mortality was similar for these plants and comparable with Louisiana rates for all causes combined, nonmalignant causes, and primary cancers of specified sites other than lung. Short term workers from both plants showed raised and similar risk of lung cancer, but risk among longer term workers differed--for example, for workers employed over one year there was no excess in plant 1 (16 observed, 17.2 expected) but a significant excess in plant 2 (52 observed, 28.9 expected, p less than 0.001). After excluding short term workers, risk of lung cancer in plant 2 showed a significant trend with estimated cumulative asbestos exposure; using a conversion of 1.4 fibres/ml = 1 mppcf, the slope of the line was 0.0076. The slope for plant 1 was 0.0003. Among all workers (the 6931, plus 167 early employees) ten mesotheliomas had occurred up to 1984: two from plant 1, eight from plant 2. In plant 2 a case-control analysis found a relation between risk of mesothelioma and duration of employment (p less than 0.01) and proportion of time spent in the pipe area (p less than 0.01), thus adding to the evidence of a greater risk of mesothelioma from crocidolite than chrysotile asbestos. A review of the mortality findings of eight cohorts of asbestos cement workers is presented.     

Urinary fibres in occupational exposure to asbestos

Urine samples from 10 workers from an asbestos cement factory and from a control group of 10 workers from a foundry, were obtained; drastic precautions were taken to avoid contamination. Each urinary mineral fibre was sized and identified by transmission electron microscopy. Results show that contamination problems encountered by other authors have been overcome and that the workers exposed to chrysotile appear to excrete more chrysotile fibres, but that this difference is not statistically significant. Possibly only a few of the exposed workers are significantly exposed to asbestos, the overall exposure level being very low. The degradability of chrysotile fibres in biological fluids or the retention of fibres in some organ could explain the lack of apparent correlation between exposure and urinary concentration. Unexpectedly high concentrations of crocidolite fibres of unknown origin were detected in both groups of workers.     

Mortality of workers employed in two asbestos cement manufacturing plants

In a study of the mortality experience of 6931 employees of two New Orleans asbestos cement products manufacturing plants over 95% were traced. Chrysotile was the primary fibre used in both plants. Plant 1 also used small amounts of amosite and, later, crocidolite irregularly whereas plant 2 used crocidolite steadily in pipe production. Previously reported exposure concentration estimates were revised, based on additional air sampling data and re-evaluation of these data. Workers in the two plants had similar duration of employment (overall, a mean of 3.8 years) and estimated exposure concentration (a mean of 7.6 million particles per cubic foot (mppcf)). Mortality was similar for these plants and comparable with Louisiana rates for all causes combined, nonmalignant causes, and primary cancers of specified sites other than lung. Short term workers from both plants showed raised and similar risk of lung cancer, but risk among longer term workers differed--for example, for workers employed over one year there was no excess in plant 1 (16 observed, 17.2 expected) but a significant excess in plant 2 (52 observed, 28.9 expected, p less than 0.001). After excluding short term workers, risk of lung cancer in plant 2 showed a significant trend with estimated cumulative asbestos exposure; using a conversion of 1.4 fibres/ml = 1 mppcf, the slope of the line was 0.0076. The slope for plant 1 was 0.0003. Among all workers (the 6931, plus 167 early employees) ten mesotheliomas had occurred up to 1984: two from plant 1, eight from plant 2. In plant 2 a case-control analysis found a relation between risk of mesothelioma and duration of employment (p less than 0.01) and proportion of time spent in the pipe area (p less than 0.01), thus adding to the evidence of a greater risk of mesothelioma from crocidolite than chrysotile asbestos. A review of the mortality findings of eight cohorts of asbestos cement workers is presented.