A dose-response analysis and quantitative assessment of lung cancer risk and occupational cadmium exposure.

We performed a quantitative assessment of the risk of lung cancer from exposure to cadmium based on a retrospective cohort mortality study of cadmium-exposed workers. The study population consisted of white male workers who were employed for at least 6 months at a cadmium smelter between January 1, 1940, and December 31, 1969, and who were first employed at the facility on or after January 1, 1926. The study findings were analyzed using a modified life-table analysis to estimate standardized mortality ratios (SMRs), and various functional forms (i.e., exponential, power, additive relative rate, and linear) of Poisson and Cox proportional hazards models to examine the dose-response relationship. Estimates of working lifetime risk (45 years) were developed using an approach that corrects for competing causes of death. An excess in mortality from lung cancer was observed for the entire cohort (SMR = 149, 95% confidence interval (CI) = 95, 222). Mortality from lung cancer was greatest among non-Hispanic workers (SMR = 211, 95% CI = 131, 323), among workers in the highest cadmium exposure group (SMR = 272, 95% CI = 123, 513), and among workers with 20 or more years since the first exposure (SMR = 161, 95% CI = 100, 248). A statistically significant dose-response relationship was evident in nearly all of the regression models evaluated. Based on our analyses, the lifetime excess lung cancer risk at the current Occupational Safety and Health Administration standard for cadmium fumes of 100 micrograms/m3 is approximately 50 to 111 lung cancer deaths per 1000 workers exposed to cadmium for 45 years.     

Cancer mortality among European asphalt workers: an international epidemiological study. I. Results of the analysis based on job titles

BACKGROUND: Inhalation of bitumen fumes is potentially carcinogenic to humans. METHODS: We conducted a study of 29,820 male workers exposed to bitumen in road paving, asphalt mixing and roofing, 32,245 ground and building construction workers unexposed to bitumen, and 17,757 workers not classifiable as bitumen workers, from Denmark, Finland, France, Germany, Israel, the Netherlands, Norway, and Sweden, with mortality follow-up during 1953-2000. We calculated standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) based on national mortality rates. Poisson regression analyses compared mortality of bitumen workers to that of building or ground construction workers. RESULTS: The overall mortality was below expectation in the total cohort (SMR 0.92, 95% CI 0.90-0.94) and in each group of workers. The SMR of lung cancer was higher among bitumen workers (1.17, 95% CI 1.04-1.30) than among workers in ground and building construction (SMR 1.01, 95% CI 0.89-1.15). In the internal comparison, the relative risk (RR) of lung cancer mortality among bitumen workers was 1.09 (95% CI 0.89-1.34). The results of cancer of the head and neck were similar to those of lung cancer, based on a smaller number of deaths. There was no suggestion of an association between employment in bitumen jobs and other cancers. CONCLUSIONS: European workers employed in road paving, asphalt mixing and other jobs entailing exposure to bitumen fume might have experienced a small increase in lung cancer mortality risk, compared to workers in ground and building construction. However, exposure assessment was limited and confounding from exposure to carcinogens in other industries, tobacco smoking, and other lifestyle factors cannot be ruled out.     

Mortality among chemical plant workers exposed to acrylonitrile and other substances.

OBJECTIVES: To examine the association between exposure to acrylonitrile (AN) and cancer mortality by performing an independent and extended historical cohort study of workers from a chemical plant in Lima, Ohio included in a recent NCI-NIOSH study. METHODS: Subjects were 992 white males who were employed for three or more months between 1960 and 1996. We identified 110 deaths and cause of death for 108. Worker exposures were estimated quantitatively for AN and qualitatively for nitrogen products. Statistical analyses included U.S. and local county-based SMRs and internal relative risk regression of internal cohort rates. RESULTS: No statistically significant excess mortality risks were observed among the total cohort for the cancer sites implicated in previous studies: stomach, lung, breast, prostate, brain, and hematopoietic system. We observed a statistically significant bladder cancer excess based on four deaths (SMR=7.01, 95% CI=1.91-17.96) among workers not exposed to AN. Among 518 AN-exposed workers, we observed a not statistically significant excess of lung cancer based on external (SMR=1.32, 95% CI=.60-2.51) and internal (RR=1.98, 95% CI=.60-6.90) comparisons. Although the trends were not statistically significant, exposure-response analyses of internal cohort rates showed monotonically increasing lung cancer rate ratios with increasing AN exposure, with RRs exceeding 2.0 in the highest exposure categories. CONCLUSIONS: With the possible exception of lung cancer, this study provides little evidence that exposure to AN at levels experienced by Lima plant workers is associated with an increased risk of death from any cause including the implicated cancer sites.     

A mortality study of workers at seven beryllium processing plants.

The International Agency for Research on Cancer (IARC) has found that the evidence for the carcinogenicity of beryllium is sufficient based on animal data but "limited" based on human data. This analysis reports on a retrospective cohort mortality study among 9,225 male workers employed at seven beryllium processing facilities for at least 2 days between January 1, 1940, and December 31, 1969. Vital status was ascertained through December 31, 1988. The standardized mortality ratio (SMR) for lung cancer in the total cohort was 1.26 (95% confidence interval [CI] = 1.12-1.42); significant SMRs for lung cancer were observed for two of the oldest plants located in Lorain, Ohio (SMR = 1.69; 95% CI = 1.28-2.19) and Reading, Pennsylvania (SMR = 1.24; 95% CI = 1.03-1.48). For the overall cohort, significantly elevated SMRs were found for "all deaths" (SMR = 1.05; 95% CI = 1.01-1.08), "ischemic heart disease" (SMR = 1.08; 95% CI = 1.01-1.14), "pneumoconiosis and other respiratory diseases" (SMR = 1.48; 95% CI = 1.21-1.80), and "chronic and unspecified nephritis, renal failure, and other renal sclerosis" (SMR = 1.49; 95% CI = 1.00-2.12). Lung cancer SMRs did not increase with longer duration of employment, but did increase with longer latency (time since first exposure). Lung cancer was particularly elevated (SMR = 3.33; 95% CI = 1.66-5.95) among workers at the Lorain plant with a history of (primarily) acute beryllium disease, which is associated with very high beryllium exposure. The lung cancer excess was not restricted to plants operating in the 1940s, when beryllium exposures were known to be extraordinarily high. Elevated lung cancer SMRs were also observed for four of the five plants operating in the 1950s for workers hired during that decade. Neither smoking nor geographic location fully explains the increased lung cancer risk. Occupational exposure to beryllium compounds is the most plausible explanation for the increased risk of lung cancer observed in this study. Continued mortality follow-up of this cohort will provide a more definitive assessment of lung cancer risk at the newer plants and among cohort members hired in the 1950s or later at the older plants. Further clarification of the potential for specific beryllium compounds to induce lung cancer in humans, and the possible contribution of other exposures in specific processes at these plants, would require a nested case-control study. We are currently assessing whether available industrial hygiene data would support such an analysis.     

The Drake Health Registry Study: cause-specific mortality experience of workers potentially exposed to beta-naphthylamine

OBJECTIVE: To examine the cause-specific mortality experience of an occupational cohort with probable past exposure to beta-naphythylamine (BNA). METHODS: Subjects were 374 male and 26 female workers employed at a Pennsylvania chemical plant that produced or used beta-naphthylamine (BNA) between 1940 and 1981. Vital status through 1998 was determined for 97.5% of the cohort and cause of death for 100% of 79 deaths. Limited industrial hygiene data and reports from former employees were used to categorize workers as high, medium, or low risk for BNA exposure. Statistical analyses included US and local county-based standardized mortality ratios (SMRs). RESULTS: We observed statistically significantly elevated county rate-based SMRs for all causes combined (SMR = 1.98, 95% confidence interval (CI) = 1.56-2.49), all malignant neoplasms combined (28 deaths, SMR = 3.08, 95% CI = 2.05-4.46), respiratory system cancer (12 deaths, SMR = 3.91, 95% CI = 2.02-6.83), and bladder cancer (four deaths, SMR = 16.83, 95% CI = 4.59-43.1). Three bladder cancer cases were classified as high risk (SMR = 26.79, 95% CI = 5.53-78.29). Mortality risks were also elevated for most other malignant and non-malignant cause of death categories examined. CONCLUSIONS: Bladder cancer risk remains highly elevated among Drake/Kilsdonk workers and appears to be causally related to past BNA exposure. While lifestyle and behavioral risk factors may explain some of the mortality excesses for non-urological cancers, the possibility remains that BNA exposure may have also played a role in these and other observed cancer excesses.     

Mortality among aircraft manufacturing workers

OBJECTIVES: To evaluate the risk of cancer and other diseases among workers engaged in aircraft manufacturing and potentially exposed to compounds containing chromate, trichloroethylene (TCE), perchloroethylene (PCE), and mixed solvents. METHODS: A retrospective cohort mortality study was conducted of workers employed for at least 1 year at a large aircraft manufacturing facility in California on or after 1 January 1960. The mortality experience of these workers was determined by examination of national, state, and company records to the end of 1996. Standardised mortality ratios (SMRs) were evaluated comparing the observed numbers of deaths among workers with those expected in the general population adjusting for age, sex, race, and calendar year. The SMRs for 40 cause of death categories were computed for the total cohort and for subgroups defined by sex, race, position in the factory, work duration, year of first employment, latency, and broad occupational groups. Factory job titles were classified as to likely use of chemicals, and internal Poisson regression analyses were used to compute mortality risk ratios for categories of years of exposure to chromate, TCE, PCE, and mixed solvents, with unexposed factory workers serving as referents. RESULTS: The study cohort comprised 77,965 workers who accrued nearly 1.9 million person-years of follow up (mean 24.2 years). Mortality follow up, estimated as 99% complete, showed that 20,236 workers had died by 31 December 1996, with cause of death obtained for 98%. Workers experienced low overall mortality (all causes of death SMR 0.83) and low cancer mortality (SMR 0.90). No significant increases in risk were found for any of the 40 specific cause of death categories, whereas for several causes the numbers of deaths were significantly below expectation. Analyses by occupational group and specific job titles showed no remarkable mortality patterns. Factory workers estimated to have been routinely exposed to chromate were not at increased risk of total cancer (SMR 0.93) or of lung cancer (SMR 1.02). Workers routinely exposed to TCE, PCE, or a mixture of solvents also were not at increased risk of total cancer (SMRs 0.86, 1.07, and 0.89, respectively), and the numbers of deaths for specific cancer sites were close to expected values. Slight to moderately increased rates of non-Hodgkin''s lymphoma were found among workers exposed to TCE or PCE, but none was significant. A significant increase in testicular cancer was found among those with exposure to mixed solvents, but the excess was based on only six deaths and could not be linked to any particular solvent or job activity. Internal cohort analyses showed no significant trends of increased risk for any cancer with increasing years of exposure to chromate or solvents. CONCLUSIONS: The results from this large scale cohort study of workers followed up for over 3 decades provide no clear evidence that occupational exposures at the aircraft manufacturing factory resulted in increases in the risk of death from cancer or other diseases. Our findings support previous studies of aircraft workers in which cancer risks were generally at or below expected levels.       

Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility

Aim: To evaluate the mortality experience of a cohort of employees of a perfluorooctanesulphonyl fluoride (POSF) based fluorochemical production facility.

Methods: A retrospective cohort mortality study followed all workers with at least one year of cumulative employment at the facility. The jobs held by cohort members were assigned to one of three exposure subgroups; high exposed, low exposed, and non-exposed, based on biological monitoring data for perfluorooctane sulphonate (PFOS).

Results: A total of 145 deaths were identified in the 2083 cohort members. Sixty five deaths occurred among workers ever employed in high exposed jobs. The overall mortality rates for the cohort and the exposure subcohorts were lower than expected in the general population. Two deaths from liver cancer were observed in the workers with at least one year of high or low exposure (standardised mortality ratio (SMR) 3.08, 95% CI 0.37 to 11.10). The risk of death from bladder cancer was increased for the entire cohort (three observed, SMR 4.81, 95% CI 0.99 to 14.06). All three bladder cancers occurred among workers who held a high exposure job (SMR 12.77, 95% CI 2.63 to 37.35). The bladder cancer cases primarily worked in non-production jobs, including maintenance and incinerator and wastewater treatment plant operations.

Conclusion: Workers employed in high exposure jobs had an increased number of deaths from bladder cancer; however it is not clear whether these three cases can be attributed to fluorochemical exposure, an unknown bladder carcinogen encountered during the course of maintenance work, and/or non-occupational exposures. With only three observed cases the possibility of a chance finding cannot be ruled out.

     

Cause-specific mortality in the unionized U.S. trucking industry

BACKGROUND: Occupational and population-based studies have related exposure to fine particulate air pollution, and specifically particulate matter from vehicle exhausts, to cardiovascular diseases and lung cancer. OBJECTIVES: We have established a large retrospective cohort to assess mortality in the unionized U.S. trucking industry. To provide insight into mortality patterns associated with job-specific exposures, we examined rates of cause-specific mortality compared with the general U.S. population. METHODS: We used records from four national trucking companies to identify 54,319 male employees employed in 1985. Cause-specific mortality was assessed through 2000 using the National Death Index. Expected numbers of all and cause-specific deaths were calculated stratifying by race, 10-year age group, and calendar period using U.S. national reference rates. Standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) were calculated for the entire cohort and by job title. RESULTS: As expected in a working population, we found a deficit in overall and all-cancer mortality, likely due to the healthy worker effect. In contrast, compared with the general U.S. population, we observed elevated rates for lung cancer, ischemic heart disease, and transport-related accidents. Lung cancer rates were elevated among all drivers (SMR = 1.10; 95% CI, 1.02-1.19) and dockworkers (SMR = 1.10; 95% CI, 0.94-1.30); ischemic heart disease was also elevated among these groups of workers [drivers, SMR = 1.49 (95% CI, 1.40-1.59); dockworkers, SMR = 1.32 (95% CI, 1.15-1.52)], as well as among shop workers (SMR = 1.34; 95% CI, 1.05-1.72). CONCLUSIONS: In this detailed assessment of specific job categories in the U.S. trucking industry, we found an excess of mortality due to lung cancer and ischemic heart disease, particularly among drivers.     

Cancer mortality in German carbon black workers 1976-98

Background

Few studies have investigated cancer risks in carbon black workers and the findings were inconclusive.

Methods

The current study explores the mortality of a cohort of 1535 male German blue‐collar workers employed at a carbon black manufacturing plant for at least one year between 1960 and 1998. Vital status and causes of death were assessed for the period 1976–98. Occupational histories and information on smoking were abstracted from company records. Standardised mortality ratios (SMR) and Poisson regression models were calculated.

Results

The SMRs for all cause mortality (observed deaths (obs) 332, SMR 120, 95% CI 108 to 134), and mortality from lung cancer (obs 50, SMR 218, 95% CI 161 to 287) were increased using national rates as reference. Comparisons to regional rates from the federal state gave SMRs of 120 (95% CI 107 to 133) and 183 (95% CI 136 to 241), respectively. However, there was no apparent dose response relationship between lung cancer mortality and several indicators of occupational exposure, including years of employment and carbon black exposure.

Conclusions

The mortality from lung cancer among German carbon black workers was increased. The high lung cancer SMR can not fully be explained by selection, smoking, or other occupational risk factors, but the results also provide little evidence for an effect of carbon black exposure.     

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.     

A mortality study of cobalt production workers: An extension of the follow-up

The follow-up of a cohort of workers employed in an electrochemical plant producing cobalt and sodium, previously studied from 1950–1980, has been extended from 1981–1988. The standardized mortality ratio (SMR) for all causes of death was 0.85 (95% confidence interval [CI] + 0.76–0.95, 309 observed) for the whole cohort, and 0.95 (95% CI + 0.83–1.08, 247 observed) for the subcohort of workers born in France. With regard to lung cancer mortality among cobalt production workers, which is the main objective of the study, the SMRs were, respectively, 0.85 (95% CI + 0.18–2.50, 3 observed) and 1.16 (95% CI + 0.24–3.40, 3 observed). Neither did any excess of mortality from diseases of the circulatory and of the respiratory systems appear among cobalt production workers. Maintenance workers, however, exhibited high SMRs for lung cancer, reaching statistical significance for duration of exposure and time since first exposure ≥ 30 years. This study does not support the hypothesis of a relationship between lung cancer and cobaltexposure. © 1993 Wiley-Liss. Inc.     

A mortality study among workers in a French aluminium reduction plant

Objective: A mortality study on the association between lung cancer and occupational exposure to polycyclic aromatic hydrocarbons (PAHs) was carried out in a French aluminium reduction plant. This study updated a previous mortality study. Method: The historical cohort included every male worker who had been employed in the plant for at least 1 year between 1950 and 1994. Workers were followed-up for mortality from 1968 to 1994. Causes of death were obtained from death certificates. Standardised mortality ratios (SMRs) and 95% confidence intervals (CI) were computed using regional mortality rates as external reference to compare observed and expected numbers of deaths, adjusted for gender, age and calendar time. Results: The cohort comprised 2,133 men, of whom 335 died during the follow-up period. The observed mortality was lower than expected for all causes of death (SMR=0.81, CI 0.72–0.90) and for lung cancer (observed=19, SMR=0.63, CI 0.38–0.98). No lung cancer excess was observed in workshops where PAH exposure was likely to have occurred, and no trend was observed according to duration of exposure and time since first exposure. This low lung cancer mortality could be partly explained by a marked healthy worker effect and a possible negative confounding by smoking. An excess was observed for bladder cancer (observed=7, SMR=1.77, CI 0.71–3.64) in the whole cohort, that was higher among workers employed in workshops where PAH exposure was likely to have occurred (observed=6, SMR=2.15, CI 0.79–4.68). In addition, an SMR higher than unity was observed for “psychoses and neuro-degenerative diseases” (observed=6, SMR=2.39, CI 0.88–5.21), that could not be related to occupational aluminium exposure. Conclusion: No lung cancer risk was detected. Non-significant excesses were observed for bladder cancer and for psychoses and neuro-degenerative diseases. Received: 11 June 1999 / Accepted: 22 January 2000     

A cohort mortality study of employees in the U.S. carbon black industry

OBJECTIVES: The objectives of this study are to evaluate historical mortality patterns, especially due to cancers, among employees of the U.S. carbon black industry and to address the methodological shortcomings of previous U.S. mortality studies. METHODS: We followed mortality of 5011 workers employed 1 year or more since the 1930s at 18 carbon black facilities through December 31, 2003. Age-, race-, sex-, and calendar year-adjusted standardized mortality ratios (SMRs) were calculated using state-specific mortality rates. RESULTS: Follow up was 96% complete. All-cause (SMR = 0.74, 95% confidence interval [CI] = 0.70-0.78) and all-cancer mortality (SMR = 0.83, 95% CI = 0.74-0.92) showed significant deficits. No excess was observed from lung (SMR = 0.97, 95% CI = 0.82-1.15) or bladder (SMR = 0.93, 95% CI = 0.47-1.87) cancers or from nonmalignant respiratory diseases (SMR = 0.99, 95% CI = 0.83-1.18). No trends were seen with duration of employment or time since hire for any cause of death. CONCLUSION: Employment in carbon black production in the United States seems not to be associated with increased mortality overall, cancer overall and, in particular, lung cancer. Further research, however, incorporating a detailed exposure assessment is needed to determine whether exposure to carbon black at high levels may be associated with an increased risk of cancer.     

Mortality from lung cancer in workers exposed to sulfur dioxide in the pulp and paper industry

Our objective in this study was to evaluate the mortality of workers exposed to sulfur dioxide in the pulp and paper industry. The cohort included 57,613 workers employed for at least 1 year in the pulp and paper industry in 12 countries. We assessed exposure to SO(2) at the level of mill and department, using industrial hygiene measurement data and information from company questionnaires; 40,704 workers were classified as exposed to SO(2). We conducted a standardized mortality ratio (SMR) analysis based on age-specific and calendar period-specific national mortality rates. We also conducted a Poisson regression analysis to determine the dose-response relations between SO(2) exposure and cancer mortality risks and to explore the effect of potential confounding factors. The SMR analysis showed a moderate deficit of all causes of death [SMR = 0.89; 95% confidence interval (CI), 0.87-0.96] among exposed workers. Lung cancer mortality was marginally increased among exposed workers (SMR = 1.08; 95% CI, 0.98-1.18). After adjustment for occupational coexposures, the lung cancer risk was increased compared with unexposed workers (rate ratio = 1.49; 95% CI, 1.14-1.96). There was a suggestion of a positive relationship between weighted cumulative SO(2) exposure and lung cancer mortality (p-value of test for linear trend = 0.009 among all exposed workers; p = 0.3 among workers with high exposure). Neither duration of exposure nor time since first exposure was associated with lung cancer mortality. Mortality from non-Hodgkin lymphoma and from leukemia was increased among workers with high SO(2) exposure; a dose-response relationship with cumulative SO(2) exposure was suggested for non-Hodgkin lymphoma. For the other causes of death, there was no evidence of increased mortality associated with exposure to SO(2). Although residual confounding may have occurred, our results suggest that occupational exposure to SO(2) in the pulp and paper industry may be associated with an increased risk of lung cancer.     

Reevaluation of lung cancer risk in the acrylonitrile cohort study of the National Cancer Institute and the National Institute for Occupational Safety and Health

OBJECTIVES: The present study provides additional analyses of data obtained earlier on lung cancer risk among workers with acrylonitrile exposure. METHODS: The original authors provided the data. For total mortality and the cancer sites of a priori interest (lung, stomach, brain, breast, prostate, and the lymphatic and hematopoietic systems), standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were computed, the total United States and surrounding counties being used as standard populations. Regional rate-based SMR values were also computed between lung cancer and cumulative acrylonitrile exposure. RESULTS: Except for lung cancer, the external comparisons corroborated the earlier internal comparisons (no increased cancer mortality risk). For lung cancer, the external comparisons revealed death deficits for the unexposed workers (SMR 0.68, 95% CI 0.5-0.9) and all categories of acrylonitrile-exposed workers. The SMR obtained using external rates and the most exposed group (SMR 0.92. 95% CI 0.6-1.4) differed from the corresponding relative risk (RR) of the internal rates (RR 1.5, 95% CI 0.9-2.4). CONCLUSIONS: The analysis of the present study provides little evidence that acrylonitrile exposure increases the mortality risk of cancers of a priori interest, including lung cancer. The lung cancer findings of the external comparison differed from the earlier findings of the internal comparisons. Selection bias (as the healthy worker effect) was probably not responsible. Additional follow-up and analyses, especially of the unexposed workers with low lung cancer rates, may help elucidate the internal and external comparison differences. Results from both comparisons should be presented when the relative risks differ markedly, as both have advantages and disadvantages.     

Respiratory cancer and other chronic disease mortality among silicotics in california

Silicotics have increased mortality from tuberculosis (TB) and from nonmalignant respiratory diseases (NMRD), including silicosis and silicotuberculosis. Since the publication of the International Agency for Research on Cancer monograph in 1987 indicating that silica was a probable human carcinogen, there has been an extensive debate about the cancer risks among silicotics. The authors identified 590 claims for silicosis among a registry of lung diseases compiled from California Workers' Compensation cases from 1945 to 1975. Using state vital records, we determined the mortality risks from 1946 to 1991. Our findings confirmed that these claimants had a significantly elevated risk for all causes of death with a standardized mortality ratio (SMR) of 1.30 (95% confidence interval [CI] = 1.18, 1.43); TB had a SMR of 56.35 (95% CI = 41.10, 75.40) and NMRD a SMR of 3.80 (95% CI = 3.11, 4.60). Cancers of the trachea, bronchus, and lung had a SMR of 1.90 (95% CI = 1.35, 2.60). For malignancies of the large intestine, there was a previously unreported SMR of 2.08 (95% CI = 1.14, 3.50). Mortality from all diseases of the heart was significantly less than expected with a SMR of 0.68 (95% CI = 0.55, 0.83); cancers of the prostate and lymphatic system were also significantly low with SMRs of 0.26 (95% CI = 0.03, 0.94) and 0.17 (95% CI = 0.04, 0.97), respectively. Workers with silicosis should be warned about these chronic disease risks, and prevention efforts to control occupational silica dust exposure should become a higher priority.     

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.     

An updated mortality study of workers at a petroleum refinery in Beaumont, Texas, 1945 to 1996

The present investigation represents an update of a previous cohort mortality study of 7543 workers who were employed at a petroleum refinery in Beaumont, Texas, for at least 1 year between 1945 and 1996. The updated study covered an observation period of 51 years, from 1946 to 1996, with a total of 208,627 person-years of observation. A total of 3020 (40.0%) cohort members were known to have died. The mortality data were analyzed in terms of cause-specific standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs). The overall mortality of the cohort was significantly lower than expected when compared with that of the general US population (SMR, 95.7; 95% CI, 92.3 to 99.2). Overall cancer mortality was also lower than expected (SMR, 85.8; 95% CI, 79.4 to 92.5). For specific cancer sites, significant mortality deficits were observed for the following: buccal cavity and pharynx, esophagus, large intestine, rectum, larynx, lung, and bladder and other urinary organs. No significant increase was reported for any site-specific cancer. A non-significant increase in acute myeloid leukemia was observed among male employees (SMR, 147.2; 95% CI, 76.1 to 257.2). Detailed analyses indicated that the excess was restricted to workers hired before 1950. No increase was detected for other leukemia cell-types, non-Hodgkin's lymphoma, or multiple myeloma. For non-malignant diseases, the majority of SMRs were below 100, and no significant increase was observed for any cause. In particular, significant mortality deficits were reported for ischemic heart disease (SMR, 91.0; 95% CI, 85.4 to 96.9), non-malignant respiratory disease (SMR, 61.5; 95% CI, 52.2 to 72.0), pulmonary fibrosis (SMR, 51.0; 95% CI, 22.0 to 100.4), cirrhosis of the liver (SMR, 47.2; 95% CI, 30.6 to 69.7), and accidents (SMR, 81.7; 95% CI, 66.3 to 99.6). Separate analyses of male workers by job classification (process and maintenance) were conducted. Mortality from acute myeloid leukemia was elevated among employees in maintenance jobs (8 observed deaths vs 4.31 expected; SMR, 185.5; 95% CI, 80.1 to 365.6). However, no upward trend by length of service was found. A detailed analysis indicated that the acute myeloid leukemia mortality excess was limited to maintenance workers who were hired before 1950. No other significant excess was detected for any cause among maintenance or process workers. These findings from the present study were discussed in conjunction with results from previous investigations of employees at the Beaumont refinery and with results from other refinery studies. Potential limitations of the study were also discussed.     

Workplace risk factors for cancer in the German rubber industry: Part 1. Mortality from respiratory cancers

OBJECTIVES: To determine the cancer specific mortality by work area among active and retired male workers in the German rubber industry. METHODS: A cohort of 11,663 male German workers was followed up for mortality from 1 January 1981 to 31 December 1991. Cohort members were classified as active (n = 7536) or retired (n = 4127) as of 1 January 1981 and had been employed for at least one year in one of five study plants producing tyres or technical rubber goods. Work histories were reconstructed with routinely documented "cost centre codes" which were classified into six categories: I preparation of materials; II production of technical rubber goods; III production of tyres; IV storage and dispatch; V maintenance; and VI others. Standardised mortality ratios (SMRs) adjusted for age and calendar year and 95% confidence intervals (95% CIs), stratified by work area (employment in respective work area for at least one year) and time related variables (year of hire, lagged years of employment in work area), were calculated from national reference rates. RESULTS: SMRs for laryngeal cancer were highest in work area I (SMR 253; 95% CI 93 to 551) and were significant among workers who were employed for > 10 years in this work area (SMR 330; 95% CI 107 to 779). Increased mortality rates from lung cancer were identified in work areas I (SMR 162; 95% CI 129 to 202), II (SMR 134; 95% CI 109 to 163), and V (SMR 131; 95% CI 102 to 167). Mortality from pleural cancer was increased in all six work areas, and significant excesses were found in work areas I (SMR 448; 95% CI 122 to 1146), II (SMR 505; 95% CI 202 to 1040), and V (SMR 554; 95% CI 179 to 1290). CONCLUSION: A causal relation between the excess of pleural cancer and exposure to asbestos among rubber workers is plausible and likely. In this study, the pattern of excess of lung cancer parallels the pattern of excess of pleural cancer. This points to asbestos as one risk factor for the excess deaths from lung cancer among rubber workers. The study provides further evidence for an increased mortality from laryngeal cancer among workers in the rubber industry, particularly in work area I.