Mortality in a cohort of asbestos cement workers in Bari

The study describes the mortality of 417 workers employed in a asbestos-cement plant, located in Bari, Puglia, Southern Italy. Follow up started on February 1st 1972. The vital status and cause of death were ascertained at 1995. The mortality experience of the Apulian population was used as comparison. Using 90% confidence limits (CLs), a significant increase in mortality was observed in our cohort from: all causes of death (SMR 118, CL 100-139), pneumoconiosis (SMR 14810, CL 10298-20683), all types of cancer (SMR 139, CL 105-181), lung (SMR 191, CL 126-277), pleural (SMR 1560 CL 431-4081) and peritoneum (SMR 1705, CL 303-5367) malignant neoplasms. In our cohort, the discrepancy between observed and expected mortality for lung and pleural cancer occurred 30 years after the first exposure, after 40 years for all neoplasms and peritoneum cancer. Under the Cox regression model, lung cancer SMR showed a curvilinear trend along time since first exposure, the peak being detected at 35 years. Finally, SMRs from our cohort were compared to a previously described cohort including workers from the same plant compensated for asbestosis by INAIL.     

Malignant pleural cancers mortality and compensated cases for asbestos related diseases in Lazio municipalities (1980-2001)

BACKGROUND: Occupational exposure to asbestos has been widely reported in the Region, but a high risk for non-occupational and environmental contaminations have also been documented. OBJECTIVES: To describe the geographical distribution ofpleural cancer deaths and compensated asbestosis cases from 1980 to 2001 in the Lazio Region. METHODS: For each municipality Standardized Mortality Ratios (SMRs) for pleural cancer and Standardized Incidence Ratios (SIRs) for asbestosis were estimated. Expected cases were estimated from age and gender specific rates in Lazio. SatScan software was used to identify clusters and to verf;j their statistical significance. RESULTS: 789 deaths from pleural cancer (495 males and 294 females) occurred in Lazio from 1980 to 2001. The standardized mortality rate per 100.000 inhabitants is 0,74 (0,95 for males and 0,54 for females). The main excess mortality from pleural cancer occurred in the municipalities of Civitavecchia (SMR: 269,9; 95% CI: 164,9 - 416,8), Colleferro (SMR: 304,9; 95% CI: 139,4-578,8) and Rocca Priora (SMR: 379,2; 95% CI: 103,3-970,9). Significant SIRs for compensated asbestosis cases were found in the industrial areas of the Naples-Rome highway and in the shipyard area of Civitavecchia. Nofemale compensated cases were found. The most important clusters were identified in the municipality of Civitavecchia for pleural cancer (p-value = 0,117) and in the Colleferro industrial area for compensated asbestosis cases (p-value = 0,001). CONCLUSIONS: Epidemiological surveillance of incident cases of malignant mesothelioma in the Lazio Region and the investigation of modalities of asbestos exposure are urgently needed for prevention of occupational diseases.     

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.     

Occupational exposure to asbestos and ovarian cancer: a meta-analysis

Objective: A recent Monographs Working Group of the International Agency for Research on Cancer (IARC) concluded that there is sufficient evidence for a causal association between exposure to asbestos and ovarian cancer. We performed a meta-analysis to quantitatively evaluate this association.Data sources: Searches of PubMed and unpublished data yielded a total of 18 cohort studies of women occupationally exposed to asbestos.Data extraction: Two authors independently abstracted data; any disagreement was resolved by consulting a third reviewer.Data synthesis: All but one study reported standardized mortality ratios (SMRs) comparing observed numbers of deaths with expected numbers for the general population; the exception was a study that reported standardized incidence ratios. For simplicity, we refer to all effect estimates as SMRs. The overall pooled SMR estimate for ovarian cancer was 1.77 (95% confidence interval, 1.37–2.28), with a moderate degree of heterogeneity among the studies (I² = 35.3%, p = 0.061). Effect estimates were stronger for cohorts compensated for asbestosis, cohorts with estimated lung cancer SMRs > 2.0, and studies conducted in Europe compared with other geographic regions. Effect estimates were similar for studies with and without pathologic confirmation, and we found no evidence of publication bias (Egger’s test p-value = 0.162).Conclusions: Our study supports the IARC conclusion that exposure to asbestos is associated with increased risk of ovarian cancer.     

Lung cancer in a female non-smoker with occupational exposure to asbestos: a case report

BACKGROUND: Until recently, asbestos was widely used in a variety of industrial processes. Workers exposed to asbestos may develop lung and pleural diseases such as asbestosis, lung cancer, benign pleural effusion, pleural plaques and mesothelioma. OBJECTIVE: To describe a clinical case of lung cancer in a female non-smoker with occupational exposure to asbestos. METHODS: The clinical and occupational history was based on the information kindly provided by the Occupational Unit of the National Health Service and on the case history of a hospital admittance in 2001, when the patient underwent surgery for lung cancer. RESULTS: The patient worked for 6 years in an asbestos manufacturing industry where she was exposed to high concentrations of asbestos, and then worked for 14 years in a sugar refinery only during the summer. She had benign pleural effusion, pleural plaques, asbestosis and lung cancer. CONCLUSIONS: We concluded that a six-year exposure to high doses of asbestos may induce lung cancer and asbestosis in a female non-smoker.     

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.     

Cancer risks in a historical UK cohort of benzene exposed workers

Aims: To examine mortality from different causes and cancer incidence among a cohort of benzene workers in England and Wales.

Methods: A cohort of 5514 workers who had been occupationally exposed to benzene in 1966/67 or earlier was assembled by the former Factory Inspectorate and the Medical Research Council from details provided by 233 employers in England and Wales. The cohort was followed up for mortality (1968–2002) and cancer registrations (1971–2001). National mortality rates and cancer registration (incidence) rates were used to calculate standardised mortality ratios and standardised registration ratios.

Results: Mortality was close to expectation for all causes and significantly increased for cancer of the lip, cancer of the lung and bronchus, secondary and unspecified cancers, acute non-lymphocytic leukaemia (ANLL), and all neoplasms. Significant deficits were shown for three non-malignant categories (mental disorders, diseases of the digestive system, accidents). SMRs for other leukaemia, lymphomas, and multiple myeloma were close to or below expectation. There was some evidence of under-ascertainment of cancer registrations, although significantly increased SRRs were shown for lung cancer and cancer of the pleura (mesothelioma).

Conclusions: Many study subjects would have been exposed to carcinogens other than benzene (for example, asbestos, rubber industry fumes, foundry fumes, polycyclic aromatic hydrocarbons), and the excesses of lung cancer and mesothelioma are likely to reflect exposures to these other carcinogens. The carcinogenic effects of benzene exposure on the lymphohaematopoietic system were limited to ANLL.

     

A historical cohort mortality study among shipyard workers in Genoa, Italy

BACKGROUND: A historical cohort mortality study was conducted among 3984 shipyard workers assigned to ship repair, refitting, and construction in the harbor of Genoa, Italy, between 1960 and 1981. These workers were exposed to asbestos fibers, welding fumes and gases, silica dust, polycyclic aromatic hydrocarbons, and solvents. METHODS: Workers were classified in 20 different job-titles depending upon the type of activity. Standardized mortality ratios (SMRs) were computed using male residents of the Province of Genoa as the referent population. RESULTS AND CONCLUSIONS: For the whole cohort significantly increased SMRs were detected for all causes, all cancers, liver, larynx, lung, pleural and bladder cancers, respiratory tract diseases, and cirrhosis of the liver. The analysis by job-title showed increased SMRs not only for pleural cancer, but also for lung, laryngeal cancers and respiratory tract diseases in occupations entailing heavy asbestos exposure. Bladder and liver cancers and liver cirrhosis mortality also appeared to be related to occupational exposure.     

Asbestos-related lung cancer and mesothelioma in Japan

In Japan, crocidolite had been used for asbestos cement pipe and spraying, and amosite had been used for building board and spraying. These two types of asbestos had stopped to use in Japan in the late 1970s. An extreme increase in imported asbestos (all 3 commercial types) was observed between 1960 and 1974. In 1960, 77,000 tons of asbestos were imported, and reached the peak as 352,316 tons in 1974. This extreme rise of asbestos imports corresponds with the recent rapid increase in mortality of malignant pleural mesothelioma. Between 1995 and 1999, an estimated mean annual death from pleural mesothelioma was about 500. The annual number of compensated occupational respiratory cancers due to asbestos exposure has also been increasing. Up to the end of March 2000, 162 cases with malignant mesothelioma and 197 cases with lung cancer were compensated. As for lung cancer, epidemiological studies are scanty in Japan. Limited environmental data of the working places in asbestos textile factories suggests that heavy asbestos exposure in the past made deaths from respiratory diseases. Less asbestos exposure will enable exposed workers to survive enough to reach cancer age. Even now smoking rate among males in Japan are over 50%. So lung cancer deaths caused by the interaction between smoking and asbestos exposure will be continuing.     

Lung cancer risk in past asbestos workers a few decades after exposure cessation and prospects for screening

To ascertain whether the current risk of lung cancer in former asbestos workers was higher than in the general population, 1,557 past asbestos workers were recruited during statutory health examinations (from 2000 onward) and followed up for mortality. Standardized mortality ratios (SMRs) were calculated. Poisson regression was used to adjust the rate ratios (RRs) for confounders. SMR was about 1.00 in workers with or without pleural plaques and 4.62 (95% confidence interval: 0.61–18.1) in those with asbestosis. Adjusted RRs for lung cancer were 4.70 (0.99–22.5) for asbestosis, 4.35 (0.97–19.5) for former smokers, 6.82 (1.38–34.4) for current smokers. Currently, lung cancer mortality in past asbestos workers is similar to the general population, probably because workers more exposed /more susceptible could have died from lung cancer before the beginning of follow-up.     

Mortality study in an asbestos cement factory in Naples, Italy

The objective of this paper is to investigate mortality among 1247 male asbestos-cement workers employed in an asbestos-cement plant located in Naples. The cohort included 1247 men hired between 1950 and 1986. The follow-up began on January 1st 1965. The vital status and causes of death were ascertained up to December 31 2005. Cause-specific mortality rates of the Campania Region population were used as reference. Relative risks were estimated using Standardized Mortality Ratios (SMRs), and the confidence intervals were calculated at a 95% level (95% CI). A significant increase in mortality was observed for respiratory disease (81 deaths; SMR = 187; 95% CI = 149- 233), particularly for pneumoconiosis (42 deaths; SMR = 13 313; 95% CI = 9595-17 996) of which 41 deaths for asbestosis (SMR = 43 385; 95% CI = 31 134-58 857), for pleural cancer (24 deaths; SMR = 2617; 95% CI = 1677-3893), for lung cancer (84 deaths; SMR=153; 95% CI = 122-189) and for peritoneal cancer (9 deaths; SMR = 1985; 95% CI = 908-3769). Non-significant increases were also observed for rectum cancer (6 deaths; SMR = 157; 95% CI = 58-342). In conclusion, consistently with other mortality studies on asbestos-cement workers performed in different countries, an increased mortality from asbestosis, lung cancer, pleural and peritoneal mesothelioma was detected in the present cohort.     

Epidemiologic study of cancer mortality among Israeli asphalt workers

BACKGROUND: We describe the results of a cancer mortality study among asphalt workers in Israel. METHODS: Personal identifiers and employment histories of 2,176 workers were extracted from company records. RESULTS: Mortality from all malignant neoplasms was significantly reduced in the whole cohort (SMR 0.68, 95% confidence interval (CI) 0.56-0.83). SMR for lung cancer was elevated in workers exposed to bitumen (SMR 1.05, 95% CI 0.62-1.66). No significant elevation or reduction in mortality was observed in relation to a specific site. SMRs for lung cancer was higher among ever exposed to bitumen than among unexposed. There was no association between lung cancer risk and estimated exposure to bitumen fume, and no dose-response was apparent. CONCLUSIONS: While the results of this cohort study indicate a slightly increased SMR for lung cancer, it did not produce evidence of a causal link between lung cancer and exposure to bitumen fume.     

Dust exposure and mortality in an American factory using chrysotile, amosite, and crocidolite in mainly textile manufacture.

This report describes the second in a series of three parallel cohort studies of asbestos factories in South Carolina, Pennsylvania, and Connecticut to assess the effects of mineral fibre type and industrial process on mortality from malignant mesothelioma, respiratory cancer, and asbestosis. In the present plant (in Pennsylvania) mainly chrysotile, with some amosite and a small amount of crocidolite, were used primarily in textile manufacture. Of a cohort of 4137 men comprising all those employed 1938-59 for at least a month, 97% were traced. By the end of 1974, 1400 (35%) had died, 74 from asbestosis and 70 from lung cancer. Mesothelioma was mentioned on the certificate in 14 deaths mostly coded to other causes. All these deaths occurred after 1959, and there were indications that additional cases of mesothelioma may have gone unrecognised, especially before that date. The exposure for each man was estimated in terms of duration and dust concentration in millions of dust particles per cubic foot (mpcf) from available measurements. Analyses were made both by life table and case referent methods. The standardised mortality ratio for respiratory cancer for the whole cohort was 105.0, but the risk rose linearly from 66.9 for men with less than 10 mpcf.y to 416.1 for those with 80 mpcf.y or more. Lines fitted to relative risks derived from SMRs in this and the textile plant studied in South Carolina were almost identical in slope. This was confirmed by case referent analysis. These findings support the conclusion from the South Carolina study that the risk of lung cancer in textile processing is very much greater than in chrysotile production and probably than in the friction products industry. The much greater risk of mesothelioma from exposure to processes in which even quite small quantities of amphiboles were used was also confirmed.     

Dust exposure and mortality in an American chrysotile asbestos friction products plant.

Cohort studies in three American asbestos factories were undertaken to investigate the effect of fibre type and manufacturing process on lung cancer, mesothelioma, and asbestosis. Reports have been published on a chrysotile textile plant in South Carolina and a mainly textile plant in Pennsylvania, which also used amphiboles. In the third plant in Connecticut friction products and packings were made from chrysotile only. In a cohort of 3641 men employed for one month or more, 1938-58, 3513 (96.5%) were traced, 1267 (36%) had died, and death certificates were obtained for 1228 (96.9%). Individual exposures were estimated (in mcpf . years) from impinger measurements. Life table analyses using Connecticut mortality rates gave an SMR for all causes of 108.5 (USA 107.9). The SMR (all causes) for men who had worked for less than a year was 129.9 and for those who had worked for a year or more, 101.2. The equivalent SMRs for respiratory cancer were 167.4 and 136.7 respectively. Excluding men who had worked for less than a year, there was possible evidence of some increase in risk of lung cancer with increasing exposure, supported also by a "log-rank" (case-control) analysis, of the same order as that observed in chrysotile mining and milling. These findings may be compared with chrysotile textile manufacture where the risk of lung cancer was some 50-fold greater. It is suggested that the differences in risk are perhaps related to the higher proportion of submicroscopic fibres in textile manufacture that may result from the traumatic carding , spinning, and weaving processes. No case of mesothelioma was found, consistent with a much lower risk of this tumour with chrysotile than with amphiboles. Twelve deaths (nine in men with very short and low asbestos exposure) were given ICD code 523 (pneumoconiosis); all but two were ascribed to anthracosilicosis or silicosis and none to asbestosis.     

Follow-up study of chrysotile textile workers: cohort mortality and exposure-response

Objectives

This report provides an update of the mortality experience of a cohort of South Carolina asbestos textile workers.

Methods

A cohort of 3072 workers exposed to chrysotile in a South Carolina asbestos textile plant (1916–77) was followed up for mortality through 2001. Standardised mortality ratios (SMRs) were computed using US and South Carolina mortality rates. A job exposure matrix provided calendar time dependent estimates of chrysotile exposure concentrations. Poisson regression models were fitted for lung cancer and asbestosis. Covariates considered included sex, race, age, calendar time, birth cohort and time since first exposure. Cumulative exposure lags of 5 and 10 years were considered by disregarding exposure in the most recent 5 and 10 years, respectively.

Results

A majority of the cohort was deceased (64%) and 702 of the 1961 deaths occurred since the previous update. Mortality was elevated based on US referent rates for a priori causes of interest including all causes combined (SMR 1.33, 95% CI 1.28 to 1.39); all cancers (SMR 1.27, 95% CI 1.16 to 1.39); oesophageal cancer (SMR 1.87, 95% CI 1.09 to 2.99); lung cancer (SMR 1.95, 95% CI 1.68 to 2.24); ischaemic heart disease (SMR 1.20, 95% CI 1.10 to 1.32); and pneumoconiosis and other respiratory diseases (SMR 4.81, 95% CI 3.84 to 5.94). Mortality remained elevated for these causes when South Carolina referent rates were used. Three cases of mesothelioma were observed among cohort members. Exposure‐response modelling for lung cancer, using a linear relative risk model, produced a slope coefficient of 0.0198 (fibre‐years/ml) (standard error 0.00496), when cumulative exposure was lagged 10 years. Poisson regression modelling confirmed significant positive relations between estimated chrysotile exposure and lung cancer and asbestosis mortality observed in previous updates of this cohort.

Conclusions

This study confirms the findings from previous investigations of excess mortality from lung cancer and asbestosis and a strong exposure‐response relation between estimated exposure to chrysotile and mortality from lung cancer and asbestosis.Asbestos is well recognised to be a cause of malignant and non‐malignant respiratory diseases. However, a continuing debate exists over whether or not, and if so to what extent, the chrysotile form of asbestos is a cause of these diseases. Some have suggested that “pure” chrysotile may not in fact be carcinogenic and that respiratory cancer excesses that have been observed in studies of chrysotile exposed workers may be explained by trace tremolite contamination in commercially used chrysotile.¹ This speculation has been referred by some as the “amphibole hypothesis”. Others have argued against this hypothesis.^2,3A recent study, which provides evidence against the amphibole hypothesis, is a 25‐year longitudinal study of male workers (n = 515) at an asbestos plant in China, where exposure was to chrysotile with little tremolite contamination (<0.001%).⁴ An age‐ and smoking‐adjusted relative risk of 8.1 (95% CI 1.8 to 36.1) was observed for lung cancer among highly exposed workers (workers in poorly ventilated raw material and textile sections) relative to workers with low exposure to asbestos (office workers and workers in the well‐ventilated asbestos cement section) and two cases of malignant mesothelioma were observed.⁴Another line of evidence against the amphibole hypothesis is the strong relation between lung cancer and chrysotile observed in a cohort of textile workers in South Carolina.⁵ The strong exposure‐response relations between chrysotile and lung cancer, in addition to pneumoconiosis and other respiratory diseases (including asbestosis), have persisted in updates of this cohort.^6,7,8 In addition, a case‐control analysis of this cohort indicated that the relation between chrysotile exposure and lung cancer was not confounded by exposures to mineral oil.⁷ Predicted lifetime excess risks of lung cancer and asbestosis from exposure to chrysotile, based on extensive exposure‐response modelling of this cohort, were estimated by Stayner et al.⁸ Vital status follow‐up was recently extended through 2001 for the cohort of South Carolina textile workers. The primary objectives of this study were to update mortality and exposure‐response relations between chrysotile and lung cancer and asbestosis mortality. This study was approved by the National Institute for Occupational Safety and Health Human Subjects Review Board.     

Dust exposure and mortality in an American chrysotile asbestos friction products plant

Cohort studies in three American asbestos factories were undertaken to investigate the effect of fibre type and manufacturing process on lung cancer, mesothelioma, and asbestosis. Reports have been published on a chrysotile textile plant in South Carolina and a mainly textile plant in Pennsylvania, which also used amphiboles. In the third plant in Connecticut friction products and packings were made from chrysotile only. In a cohort of 3641 men employed for one month or more, 1938-58, 3513 (96.5%) were traced, 1267 (36%) had died, and death certificates were obtained for 1228 (96.9%). Individual exposures were estimated (in mcpf . years) from impinger measurements. Life table analyses using Connecticut mortality rates gave an SMR for all causes of 108.5 (USA 107.9). The SMR (all causes) for men who had worked for less than a year was 129.9 and for those who had worked for a year or more, 101.2. The equivalent SMRs for respiratory cancer were 167.4 and 136.7 respectively. Excluding men who had worked for less than a year, there was possible evidence of some increase in risk of lung cancer with increasing exposure, supported also by a "log-rank" (case-control) analysis, of the same order as that observed in chrysotile mining and milling. These findings may be compared with chrysotile textile manufacture where the risk of lung cancer was some 50-fold greater. It is suggested that the differences in risk are perhaps related to the higher proportion of submicroscopic fibres in textile manufacture that may result from the traumatic carding , spinning, and weaving processes. No case of mesothelioma was found, consistent with a much lower risk of this tumour with chrysotile than with amphiboles. Twelve deaths (nine in men with very short and low asbestos exposure) were given ICD code 523 (pneumoconiosis); all but two were ascribed to anthracosilicosis or silicosis and none to asbestosis.     

Health hazards from fine asbestos dusts

Summary For the period from 1973 to the end of 1986, 70656 data sets on occupational preventive medical examinations in employees exposed occupationally to asbestos dust (G 1.2) were made available to us by the Central Registry for Employees Exposed to Asbestos Dust (ZAS). On the basis of this data, an analysis of asbestosis risk was to be made in relation to specific areas of work, taking into consideration the beginning and duration of exposure. Proceedings for declaratory appraisal in accordance with occupational disease no. 4103 were instituted in 1760 cases in the report period. In accordance with the character of the available data, the X-ray findings in the lungs were available from the persons investigated as parameters of possible asbestosis risk on the basis of coding consistent with the International Pneumoconiosis Classification (ILO U/C 1971 and/or ILO 1980 West Germany). The major result of the statistical analyses on the mainframe macrocomputer of the University of Erlangen-Nuremberg was that the relatively highest risk of asbestosis was present in persons whose exposure began before 1955. On the other hand, with increasing duration of exposure, an unequivocal rise of the asbestosis risk could not be detected on the basis of the overall population. In relation to the individual fields of work, the relatively highest risk of asbestosis was shown to be in the asbestos textile and paper industry, as well as in the asbestos cement industry. No detectable risk of asbestosis was present in the fields of mining, traffic and health service and for women in the industrial sectors of building material, gas and water, catering trade, building, commerce as well as banking and insurance. Accordingly, it can be assumed that certain fields of work are or were exposed to such a small extent or not at all that a risk of asbestosis which is relevant in terms of occupational medicine is no longer to be assumed or was not to be assumed. This applies above all to certain work in the frictional coating (brake lining) and asbestos paper industry. Furthermore, the analysis of the data material did not provide any unequivocal indications that inhalative smoking habits have a negative effect on the risk of asbestosis. In prinicple, it can be stated that the occupational preventive medical investigations according to G 1.2 are effective. However, irrespective of this, the analysis has shown that a regular exchange of experience on the part of authorized physicians should be institutionalized and the second X-ray appraisal should be retained in order to ensure a high measure of reliability and diagnostic relevance of the available investigation data. Besides this, all expert appraisal results from patients with recognized occupational diseases according to subparagraphs, 4103, 4104 and 4105 BeKV (no. 4103: asbestosis, no. 4104: asbestosis in connection with lung cancer, no. 4105: mesothelioma of the pleura or peritoneum) should be centrally registered both in persons exposed to asbestos dust and in persons with asbestosis and accompanying malignant diseases, would then be possible.     

Exposures to silica mixed dust and cohort mortality study in tin mines: exposure-response analysis and risk assessment of lung cancer

BACKGROUND: Mineral dusts that contain crystalline silica have been associated directly or indirectly with the development of pneumoconiosis or silicosis, non-malignant respiratory diseases, lung cancer, and other diseases. The health impacts on workers with silica mixed dust exposure in tin mines and dose-response relationships between cumulative dust exposure and the mortality from lung cancer are investigated. METHODS: A cohort of 7,837 workers registered in the employment records in 4 Chinese tin mines between 1972 and 1974 was identified for this study and the mortality follow-up was traced through 1994. Of the cohort, the cause of death was ascertained for 1,061 (97%) of the 1,094 deceased workers. Standardized mortality ratios (SMRs) were calculated for all workers, non-exposed workers, and dust-exposed workers with different exposure levels, silicotics, and non-silicotics based on Chinese national rates. RESULTS: The mortality from all causes in four tin mines was nearly the same as the national mortality. Malignant neoplasm, cerebrovascular disease, and cardiovascular disease accounted for 68.6% of all deaths. Mortality excess from lung cancer, liver cancer, all malignant diseases, and non-malignant respiratory diseases was observed among dust-exposed workers; a 50-fold excess of pneumoconiosis was observed. There was an upward trend for SMRs of lung cancer was noted from no exposure to low, medium, and high exposure levels (SMRs=1.29, 2.65, 2.66, 3.33). The shape of the exposure-response curve for risk of lung cancer at high exposure levels was inconsistent in these four mines. CONCLUSIONS: The findings indicated a positive dose-response relation between exposure to cumulative dust and the mortality of lung cancer. High arsenic content in dust particles, together with crystalline silica, may play an important role in causing increased mortality from lung cancer.     

Mortality due to asbestos-related causes among railway carriage construction and repair workers

The objective of this study was to further clarify the cancer risk associated with asbestos exposure in railway carriage construction and repair. The cohort included 734 subjects employed between 1 January 1945 and 31 December 1969. Vital status was ascertained at 31 December 1997. Mortality was investigated in the time span 1970-97. Forty-two subjects (6%) were lost to follow-up and eight causes of death (4%) could not be ascertained. The overall mortality was not above the expected value. Among neoplastic diseases, excesses were observed for lung ?tandardized mortality ratio (SMR) = 124; 90% confidence interval (CI) = 87-172; 26 obs), pleura (SMR = 1,327; CI = 523-2,790; 5 obs), larynx (SMR = 240; CI = 95-505; 5 obs), liver (SMR = 241; CI = 126-420; 9 obs), pancreas (SMR = 224; CI = 98-443; 6 obs) and multiple myeloma (SMR = 429; CI = 117-1,109; 3 obs). The observed excess of lung and pleural neoplasms can be causally related to asbestos exposure in the manufacture of railway carriages. A causal role of asbestos exposure in the raised SMRs from laryngeal and pancreatic neoplasms and multiple myeloma cannot be conclusively proven.