Exposure to asbestos and lung and pleural cancer mortality among pulp and paper industry workers

We studied the mortality from lung and pleural cancers in a cohort of 62,937 male workers employed for at least 1 year in the pulp and paper industry in 13 countries during 1945 to 1996. Mill departments were classified according to probability and level of exposure to asbestos on the basis of available dust measurements and mill-specific information on exposure circumstances. Thirty-six percent of workers were classified as ever exposed to asbestos. Standardized mortality ratios of lung cancer were 0.99 (95% confidence interval [CI], 0.90 to 1.08) among unexposed and 1.00 (95% CI, 0.90 to 1.11) among ever exposed workers. The number of pleural cancer deaths among unexposed workers was 10; that among exposed workers was 14, most of which occurred among maintenance workers. In internal analyses, a trend in mortality from either neoplasm was suggested for estimated cumulative exposure to asbestos, weighted for the individual probability of exposure within the department and for duration of exposure (relative risk for lung cancer for 0.78+ f/cc-years, as compared with < or = 0.01 f/cc-years: 1.44; 95% CI, 0.85 to 2.45; corresponding relative risk for pleural cancer: 2.43; 95% CI, 0.43 to 13.63). Despite a possible nondifferential misclassification of exposure and outcome, this study suggests that the carcinogenic effect of asbestos can be detected among workers employed in industries such as the pulp and paper industry, in which it is not considered to be a major hazard.     

Lung cancer risk and talc not containing asbestiform fibres: a review of the epidemiological evidence

A literature search was done and all epidemiological cancer studies mentioning talc as a risk factor were selected. The talc exposed populations were divided into three groups: (1) populations in which no other occupational carcinogen was mentioned (only talc millers satisfied this criterion); (2) populations of talc miners exposed to talc, quartz, and/or radon; and (3) other industrial populations in which talc is associated with quartz, nitrosamines, and asbestos depending on the study. No excess lung cancer mortality was found for the populations of talc millers exposed to high levels of talc but without any other potential carcinogen (SMR = 0.92, 42 cases) while the summary of mortality of talc miners exposed to quartz and/or radon was in excess (fixed effect SMR = 1.20, random effect RR = 1.85, 40 cases). Six studies in other industrial settings were identified. All reported increased lung cancer mortality among talc exposed workers but the talc exposure was confounded with other carcinogens and only one study was able to adjust on them. In conclusion, no increased lung cancer mortality was observed among talc millers despite their high exposure experience. In populations in which talc was associated with other potential carcinogens, some lung cancer excesses were observed.     

A case-referent study of lung cancer, occupational exposures and smoking. I. Comparison of title-based and exposure-based occupational information

The role of occupational exposures and smoking in the development of lung cancer has been studied among 176 male incident lung cancer cases and 176 referents admitted to two county hospitals in southeast Norway during 1979-1983. After the allocation of all occupational titles in the Nordic Classification of Occupations into three exposure groups according to potential exposure to respiratory carcinogens and other contaminants, each subject was classified according to exposure status of main occupation and number of years in each exposure category. An excess risk of lung cancer was observed both among those in possibly exposed occupations and among those definitely exposed. A more than threefold excess risk was observed among subjects with more than 30 years in exposed occupations. Exposure to 22 agents/processes was further assessed by a separate questionnaire and estimated simultaneously in a logistic regression model. Elevated risks were associated with exposure to asbestos and several other agents/processes, which largely correlated to each other. Smoking was strongly associated with all histological subtypes of lung cancer, while for occupational exposures the risk ratio was highest for small cell carcinoma and lowest for adenocarcinoma. Very high risk ratios for lung cancer were observed among heavy smokers in exposed occupations.     

Mesothelioma and lung tumors attributable to asbestos among petroleum workers

BACKGROUND: Asbestos exposure has been definitively found to be associated with both mesothelioma and lung cancer. Nevertheless, in the overall population of oil refinery workers potentially exposed to asbestos, many studies clearly show a definitely increased risk of mesothelioma, but no proven excess of lung cancer after comparison to the general population. Through the presentation of new data and the re-appraisal of two recent and independent epidemiological studies conducted in Liguria, Italy, and Ontario, Canada, we attempt to shed light on this apparently paradoxical finding. METHODS: Lung cancer mortality was studied among maintenance workers exposed to asbestos, and among two other subgroups of refinery employees: blue collar and white collar workers. The comparison with blue collar workers was performed in order to take into account the role of healthy worker effect, smoking habit, and the socioeconomic level. The comparison with white collar workers was performed to control for other occupational lung carcinogens. RESULTS AND CONCLUSIONS: Results reveal a consistency between the two studies and show that 96-100% of the mesotheliomas and 42-49% of the lung tumors arising among maintenance workers were attributable to asbestos exposure. Our new analysis, estimating two cases of asbestos-related lung cancer for each case of mesothelioma, confirms published findings on the magnitude of asbestos-related tumors in oil refineries.     

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.     

Association between asbestos exposure,cigarette smoking,myeloperoxidase (MPO) genotypes,and lung cancer risk

BACKGROUND: As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. METHODS: RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. RESULTS: Asbestos exposure was associated with a significantly elevated risk estimate (OR = 1.45; 95% CI 1.04-2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09-2.66), while A-allele carriers (G/A + A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56-1.44). The OR was further reduced to 0.73 (0.49-1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR = 2.19; 95% CI 1.16-4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR = 1.18; 95% CI 0.58-2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. CONCLUSIONS: For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer.     

Asbestos as a systemic carcinogen: The evidence from eleven cohorts

Most known occupational carcinogens are site-specific, which implies that they are “complete” carcinogens with both “initiating” and “promoting” properties (Berenblum's terminology). Excess cancer at gastrointestinal sites among cohorts occupationally exposed to asbestos has been interpreted as reflecting additional site-specific effects, although excess at other sites has also been observed in some studies. The hypothesis that excess cancer at gastrointestinal sites cannot be distinguished from excess cancer at all nonpulmonary sites is tested by data from New York-New Jersey insulation workers working in 1943; similar workers employed after 1943; U.S.-Canadian insulation workers; London factory workers, male and female; Quebec miners and millers; retired U.S. factory workers; U.S. shipyard insulators; Italian shipyard workers in Genoa; Amosite factory workers; and U.S. factory workers. Excluding lung cancer and mesothelioma, observed-expected ratios for nonpulmonary cancer mortality range from 0.97 to 2.78, and do not differ significantly from gastrointestinal ratios. A dose-response gradient is observed for both ratios, when dose is estimated from lung cancer ratios, or in some studies, measured exposures. Site-specificity is unlikely for nonpulmonary cancer associated with asbestos exposure more than 20 years previously. Systemic carcinogenesis may be an example of promotion or impairment by asbestos of some cancer defense mechanism; immunological mechanisms have been suggested by Turner-Warwick and Parkes. Prospective studies are indicated.     

The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure

Mortality reports on asbestos exposed cohorts which gave information on exposure levels from which (as a minimum) a cohort average cumulative exposure could be estimated were reviewed. At exposure levels seen in occupational cohorts it is concluded that the exposure specific risk of mesothelioma from the three principal commercial asbestos types is broadly in the ratio 1:100:500 for chrysotile, amosite and crocidolite respectively. For lung cancer the conclusions are less clear cut. Cohorts exposed only to crocidolite or amosite record similar exposure specific risk levels (around 5% excess lung cancer per f/ml.yr); but chrysotile exposed cohorts show a less consistent picture, with a clear discrepancy between the mortality experience of a cohort of xhrysotile textile workers in Carolina and the Quebec miners cohort. Taking account of the excess risk recorded by cohorts with mixed fibre exposures (generally<1%), the Carolina experience looks uptypically high. It is suggested that a best estimate lung cancer risk for chrysotile alone would be 0.1%, with a highest reasonable estimate of 0.5%. The risk differential between chrysotile and the two amphibole fibres for lunc cancer is thus between 1:10 and 1:50.Examination of the inter-study dose response relationship for the amphibole fibres suggests a non-linear relationship for all three cancer endpoints (pleural and peritoneal mesotheliomas, and lung cancer). The peritoneal mesothelioma risk is proportional to the square of cumulative exposure, lung cancer risk lies between a linear and square relationship and pleural mesothelioma seems to rise less than linearly with cumulative dose. Although these non-linear relationships provide a best fit ot the data, statistical and other uncertainties mean that a linear relationship remains arguable for pleural and lung tumours (but not or peritoneal tumours).Based on these considerations, and a discussion fo the associated uncertainties, a series of quantified risk summary statements for different elvels of cumulative exposure are presented.     

Mortality from lung cancer and population risk attributable to asbestos in an asbestos cement manufacturing town in Italy

OBJECTIVE: To estimate mortality from lung cancer and the risk attributable to asbestos separately for asbestos cement workers and for the general (non-occupationally exposed) population in the town of Casale Monferrato, where the largest Italian asbestos cement factory had been in operation in 1907-86. According to cancer registry data, in the same town the incidence of malignant mesothelioma in the general population is about 10 times higher than in comparable Italian provinces. METHOD: Decedents from lung cancer in 1989-95 were nominally identified in the list of decedents kept at the Local Health Authority of Casale Monferrato. Workers in the asbestos cement factory have been identified with a search in the nominal list of workers and the same was done for the wives of asbestos cement workers. These lists have already been used in cohort studies. Sensitivity and specificity of the linkage procedure with occupational activity in asbestos cement production have been evaluated in a previous study. Population at risk was estimated on the basis of official figures and on the results of the cohort study of asbestos cement workers. RESULTS: 227 deaths from lung cancer were included (184 men and 43 women). Among the asbestos cement workers mortalities were 234.0 x 100,000 person-years among men and 35.5 among women. Corresponding figures in the general (non- occupationally exposed) population in Casale Monferrato were 80.6 and 18.7. The rates in the general population were not higher than in the rest of the region. Attributable risk (AR) among the asbestos cement workers (and wives) is 67.5% (95% confidence interval (95% CI) 56.8 to 78.2) for men and 51.3% (95% CI 14.9 to 87.8) among women. Population AR to occupational or paraoccupational exposure in the asbestos cement production is 18.3% (95% CI 11.1 to 25.6) among men and 10.1% (95% CI 0 to 24.6) among women. CONCLUSION: This work did not show an increase in mortality from lung cancer for the population not exposed occupationally, but a large excess was found among men and women occupationally exposed in asbestos cement production. The total burden of lung cancer due to occupational exposure to asbestos may be underestimated, as only occupational exposure in asbestos cement production was taken into consideration. Nevertheless even a single factory can be responsible for a considerable proportion of deaths from lung cancer in a population.

 

     

Occupational asbestos exposure among respiratory cancer patients in Lithuania

BACKGROUND: Despite intensive use of asbestos, no cancer case has ever been diagnosed as asbestos related in Lithuania. This paper attempts to estimate the proportion of those occupationally exposed to asbestos among respiratory cancer patients. MATERIAL AND METHODS: Occupational exposure to asbestos was assessed retrospectively for 298 lung cancer and four mesothelioma patients, admitted to the Institute of Oncology, Vilnius. The evaluation was based on personal interview data using an internationally established questionnaire covering most likely activities of asbestos exposure at the workplace. Cumulative exposure to asbestos at work was estimated in fiber years. Lung tissue asbestos fiber burden analysis was conducted by scanning transmission electron microscopy on 23 samples. RESULTS: A cumulative asbestos exposure of > or =25 fiber years was found for 10 lung cancer patients (3.4%). They worked in foundries, construction, installation, shipyard, power plant, railway, asbestos cement, glass and chemical industry. In a further 56 lung cancer patients (18.8%) and for one (25%) mesothelioma patient, a cumulative exposure from 5 to 24.9 fiber years was assessed. Asbestos fibers were detected in 18 cases, the burden ranged from 0.1 to 4.1 million fibers/g dry lung tissue; concentrations exceeding 1 million f/g dry lung tissue were found in four cases. All fibers were chrysotile. CONCLUSIONS: Findings indicate that a fraction (3.4%) of the lung cancer cases could be attributed to heavy occupational exposure to asbestos using the Helsinki criterion of > or =25 fiber years. Therefore, approximately 50 lung cancer cases per year in Lithuania could be asbestos-related compensable occupational diseases.     

Occupational exposure to carcinogens and risk of lung cancer: results from The Netherlands cohort study.

OBJECTIVES: To investigate risk of lung cancers associated with common established carcinogenic occupational exposures (asbestos, paint dust, polycyclic aromatic hydrocarbons, and welding fumes) in a prospective cohort study among the general population, and to estimate the proportion of lung cancer cases attributable to these occupational exposures. METHODS: A prospective cohort study on diet, other lifestyle factors, job history, and cancer risk that started in 1986 in The Netherlands on 58,279 men, aged 55-69 years. Based on information about job history obtained from a self-administered questionnaire, case by case expert assessment was carried out to assign to each study subject a cumulative probability of occupational exposure for each carcinogenic exposure. For analysis, a case-cohort approach was used, in which the person-years at risk were estimated from a randomly selected subcohort (n = 1688). After 4.3 years of follow up, 524 lung cancer cases with complete job history were available. RESULTS: After adjustment for age, each of the other occupational exposures, and for smoking habits and intake of vitamin C, beta-carotene, and retinol, significant associations were found between risk of lung cancer and cumulative probability of occupational exposure to asbestos (relative risk (RR) highest/no exposure = 3.49, 95% confidence interval (95% CI) 1.69 to 7.18, trend P < 0.01 or paint dust (RR highest/no exposure = 2.48, 95% CI 0.88 to 6.97, trend P < 0.01). The population attributable risks (PARs) for the four exposures based on the multivariately adjusted RRs for ever exposed versus never exposed workers were calculated. The PAR of lifetime occupational exposure to asbestos was calculated to be 11.6%. CONCLUSIONS: This prospective cohort study among the general population showed that occupational exposure to asbestos or paint dust is associated with higher RRs for lung cancer. This study shows that after adjustment for smoking and diet about 11.6% of the cases of lung cancer in men is attributable to lifetime occupational exposure to asbestos.     

Socioeconomic status and lung cancer incidence in men in The Netherlands: is there a role for occupational exposure?

STUDY OBJECTIVE: To evaluate the influence of occupational exposure to carcinogens in explaining the association between socioeconomic status and lung cancer. DESIGN: A prospective cohort study. Data on diet, other lifestyle factors, sociodemographic characteristics and job history were collected by means of a self administered questionnaire. Follow up for incident cancer was established by record linkage with a national pathology register and with regional cancer registries. SETTING: Population originating from 204 municipalities in The Netherlands. PARTICIPANTS: These comprised 58 279 men aged 55-69 years in September 1986. After 4.3 years of follow up there were 470 microscopically confirmed incident lung cancer cases with complete data on dietary habits and job history. MEASUREMENTS AND MAIN RESULTS: Estimation of occupational exposure to asbestos, paint dust, polycyclic aromatic hydrocarbons, and welding fumes was carried out by two experts, using information on job history from the baseline questionnaire. Socioeconomic status was measured by means of highest attained level of education and two indicators based on occupation. In the initial multivariate analyses of socioeconomic status and lung cancer, adjustment was made for age, smoking habits, intake of vitamin C, beta-carotene and retinol, and history of chronic obstructive pulmonary disease or asthma. Additional adjustment for occupational exposure to the four carcinogens mentioned above did not change the inverse association between the level of education and lung cancer risk (initial model: RR highest/lowest level of education = 0.53; 95% CI 0.34, 0.82; additional model: RR highest/lowest level of education = 0.53; 95% CI 0.34, 0.84). Nor was the association between the two occupation based indicators of socioeconomic status and lung cancer risk influenced by occupational exposure to carcinogens. The effect of occupational exposure on the association between the level of education and lung cancer risk did not differ between ex-smokers and current smokers. CONCLUSIONS: Occupational exposure to asbestos, paint dust, polycyclic aromatic hydrocarbons, and welding fumes could not explain the inverse association between socioeconomic status and lung cancer risk. More research which explicitly addresses possible explanations for the association between socioeconomic status and lung cancer risk is needed.     

Review of occupational lung carcinogens

Lung cancer is the most common malignancy in the United States and is ranked second only to bladder cancer in the proportion of cases thought to be due to occupational exposures. We review the epidemiology of occupational lung cancer, focusing on agents identified as pulmonary carcinogens by the International Agency for Research on Cancer. We derive estimates of overall relative risks from the major studies of these lung carcinogens, and we also provide estimates of the number of exposed workers. Using our data as well as estimates from other authors, we estimate that approximately 9,000–10,000 men and 900–1,900 women develop lung cancer annually in the United States due to past exposure to occupational carcinogens. More than half of these lung cancers are due to asbestos. This estimate is likely conservative, in that we have restricted our analysis to confirmed lung carcinogens and have ignored occupations with documented excess risk but for which the specific agents are unknown. Also, our estimate of the proportion of workers exposed in the past is probably too low. Our estimate should be viewed only as a broad approximation. Nevertheless, it is in line with other estimates by authors using different methods. The current number of cases estimated to be due to occupational exposures reflects past high exposures and is likely to drop in the future, unless other occupational lung carcinogens are confirmed or new carcinogens are introduced into the workplace. (This article is a US Government work and, as such, is in the public domain in the United States of America.) © 1996 Wiley-Liss, Inc.     

Occupational exposure and lung cancer risk in a coastal area of Northeastern Italy

Summary A case-control study of lung cancer and occupational exposure was conducted in a coastal area of Northeastern Italy where metallurgical and mechanical industries, docks and shipyards are located. Cases comprised 756 men who died of primary lung cancer in a 5-year period. Controls comprised 756 male subjects dying from other causes during the same period. Occupational exposures to lung carcinogens were assessed according to a job title-based approach, using two separate lists of industries/occupations recognized as being causally associated (list A) or suspected of being causally associated (list B) with lung cancer in humans. Exposure to asbestos was classified as absent, possible, or definite. After adjustment for cigarette smoking and place of residence, a significant association was found between lung cancer and occupations in both list A [relative risk (RR) = 2.25, 95% confidence interval (CI) = 1.68–3.03] and list B (RR = 1.33, 95% CI = 1.03–1.71). A significant excess risk was found for workers with definite exposure to asbestos as compared to those with no exposure to lung carcinogens (RR = 1.98, 95% CI = 1.42–2.75). Among occupations with recognized exposure to lung carcinogens other than asbestos, a significant excess risk for lung cancer was observed in iron and metalware workers. In occupational groups with definite exposure to asbestos, elevated risk estimates were found for shipyard workers, dockworkers, carpenters, and electricians. The combined effect of smoking and asbestos was found to be compatible with that expected under a multiplicative model. The overall population-attributable risk (ARp) for cigarette smoking was found to be 87.5%. The ARp estimate for occupations in list A was 16.0%. The estimate increased to 25.3% (95% CI = 16.2–34.4) when occupations in list B were included. The ARp estimate for possible or definite exposure to asbestos was 20.0% (95% CI = 11.5–28.5). With regard to the histologic types of lung cancer, significant associations were found between definite exposure to asbestos and squamous cell carcinoma (RR = 2.00, 95% CI = 1.28-–3.11), small cell carcinoma (RR = 2.11, 95% CI = 1.31–3.39), and adenocarcinoma (RR = 2.16, 95% CI = 1.32–3.53).     

A job-exposure matrix for use in population based studies in England and Wales

The job-exposure matrix described has been developed for use in population based studies of occupational morbidity and mortality in England and Wales. The job axis of the matrix is based on the Registrar General's 1966 classification of occupations and 1968 classification of industries, and comprises 669 job categories. The exposure axis is made up of 49 chemical, physical, and biological agents, most of which are known or suspected causes of occupational disease. In the body of the matrix associations between jobs and exposures are graded to four levels. The matrix has been applied to data from a case-control study of lung cancer in which occupational histories were elicited by means of a postal questionnaire. Estimates of exposure to five known or suspected carcinogens (asbestos, chromates, cutting oils, formaldehyde, and inhaled polycyclic aromatic hydrocarbons were compared with those obtained by detailed review of individual occupational histories. When the matrix was used exposures were attributed to jobs more frequently than on the basis of individual histories. Lung cancer was significantly more common among subjects classed by the matrix as having potential exposure to chromates, but neither method of assigning exposures produced statistically significant associations with asbestos or polycyclic aromatic hydrocarbons. Possible explanations for the failure to show a clear effect of these known carcinogens are discussed. The greater accuracy of exposures inferred directly from individual histories was reflected in steeper dose response curves for asbestos, chromates, and polycyclic aromatic hydrocarbons. The improvement over results obtained with the matrix, however, was not great. For occupational data of the type examined in this study, direct exposure estimates offer little advantage over those provided at lower cost by a matrix.     

A job-exposure matrix for use in population based studies in England and Wales.

The job-exposure matrix described has been developed for use in population based studies of occupational morbidity and mortality in England and Wales. The job axis of the matrix is based on the Registrar General's 1966 classification of occupations and 1968 classification of industries, and comprises 669 job categories. The exposure axis is made up of 49 chemical, physical, and biological agents, most of which are known or suspected causes of occupational disease. In the body of the matrix associations between jobs and exposures are graded to four levels. The matrix has been applied to data from a case-control study of lung cancer in which occupational histories were elicited by means of a postal questionnaire. Estimates of exposure to five known or suspected carcinogens (asbestos, chromates, cutting oils, formaldehyde, and inhaled polycyclic aromatic hydrocarbons were compared with those obtained by detailed review of individual occupational histories. When the matrix was used exposures were attributed to jobs more frequently than on the basis of individual histories. Lung cancer was significantly more common among subjects classed by the matrix as having potential exposure to chromates, but neither method of assigning exposures produced statistically significant associations with asbestos or polycyclic aromatic hydrocarbons. Possible explanations for the failure to show a clear effect of these known carcinogens are discussed. The greater accuracy of exposures inferred directly from individual histories was reflected in steeper dose response curves for asbestos, chromates, and polycyclic aromatic hydrocarbons. The improvement over results obtained with the matrix, however, was not great. For occupational data of the type examined in this study, direct exposure estimates offer little advantage over those provided at lower cost by a matrix.     

A case-referent study of lung cancer, occupational exposures and smoking. III. Etiologic fraction of occupational exposures

The proportion of lung cancer related to occupational exposure to respiratory carcinogens and other workplace contaminants has been studied in a hospital-based case-referent study of 176 incident cases and 176 referents, recruited from the medical ward of two county hospitals in southern Norway. On the basis of job title and exposure information, three different approaches for the estimation of etiologic fraction were used, all based upon a trichotomous categorization of the exposure variable. Among the definitely exposed subjects, the etiologic fraction for lung cancer related to occupational exposure factors was from 22 to 35%, increasing to 37-47% when the "possibly exposed" categories were included. When asbestos was the only factor to be eliminated, the etiologic fraction estimate suggested a 23% reduction in the lung cancer incidence in the study population. More than 90% of the lung cancer cases would theoretically have been prevented if smoking had been completely removed. The relative merits of preventing one or several of the study factors simultaneously is discussed.     

Assessing the component associations of the healthy worker survivor bias: occupational asbestos exposure and lung cancer mortality

BackgroundThe healthy worker survivor bias is well-recognized in occupational epidemiology. Three component associations are necessary for this bias to occur: i) prior exposure and employment status; ii) employment status and subsequent exposure; and iii) employment status and mortality. Together, these associations result in time-varying confounding affected by prior exposure. We illustrate how these associations can be assessed using standard regression methods.MethodsWe use data from 2975 asbestos textile factory workers hired between January 1940 and December 1965 and followed for lung cancer mortality through December 2001.ResultsAt entry, median age was 24 years, with 42% female and 19% non-Caucasian. Over follow-up, 21% and 17% of person-years were classified as at work and exposed to any asbestos, respectively. For a 100 fiber-year/mL increase in cumulative asbestos, the covariate-adjusted hazard of leaving work decreased by 52% (95% confidence interval [CI], 46–58). The association between employment status and subsequent asbestos exposure was strong due to nonpositivity: 88.3% of person-years at work (95% CI, 87.0–89.5) were classified as exposed to any asbestos; no person-years were classified as exposed to asbestos after leaving work. Finally, leaving active employment was associated with a 48% (95% CI, 9–71) decrease in the covariate-adjusted hazard of lung cancer mortality.ConclusionsWe found strong associations for the components of the healthy worker survivor bias in these data. Standard methods, which fail to properly account for time-varying confounding affected by prior exposure, may provide biased estimates of the effect of asbestos on lung cancer mortality under these conditions.     

Mortality experience of male workers at a UK tin smelter

BACKGROUND: Between 1937 and 1991, Capper Pass and Sons Limited operated a tin smelter complex in North Humberside, UK, at which employees were potentially exposed to a number of substances, including lead, arsenic, cadmium and natural series radionuclides. Decommissioning and site clearance continued until 1995. Between 1967 and 1995 the company was a subsidiary of Rio Tinto plc. AIMS: The aim was to identify any significant excess, or deficits, in mortality among former employees that might be attributable to factors associated with occupation. METHODS: We defined a cohort of 1462 males who had been employed for at least 12 months between 1/11/1967 and 28/7/1995, followed-up through to 31/12/2001. The mortality of the cohort was compared against that expected for both national and regional populations. RESULTS: Mortality from all causes and all cancers did not differ from that expected. Mortality from ischaemic heart disease showed a deficit and mortality from lung cancer showed a statistically significant excess. Mortality from smoking related diseases other than lung cancer showed a non-significant deficit. CONCLUSIONS: The pattern of lung cancer mortality is consistent with the hypothesis that the risk of lung cancer has been enhanced by occupational exposure to one or more carcinogens, the effect of which diminishes with time since exposure. The deficit in ischaemic heart disease may be attributed to a protective effect from manual labour. The results provide no evidence for attribution of other excess or deficits in mortality to factors associated with employment.     

Cohort mortality study of women compensated for asbestosis in Italy.

BACKGROUND: The carcinogenic effect of asbestos is accepted for lung cancer and mesothelioma, while conflicting opinions exist for other cancer sites. The aim of the present investigation is to study cause-specific mortality of women compensated for asbestosis who had certainly been exposed to high levels of asbestos fibers. METHODS: The cause-specific mortality of all Italian women compensated for asbestosis and alive December 31, 1979, was investigated through October 30, 1997. In the total cohort, which included 631 subjects, 277 deaths occurred. Cause-specific SMRs (Standardized Mortality Ratio) were computed using the national rates for comparison. RESULTS: A significantly increased mortality for all diseases related to asbestos exposure was observed. Mortality for all causes, all neoplasms, lung cancer, uterine cancer, ovarian cancer, and non-neoplastic respiratory diseases was significantly increased. Separate analyses for textile (n = 276) and asbestos-cement (n = 278) workers were performed. Women employed in the textile industry, mainly exposed to chrysotile, who are compensated at a younger age, showed higher SMRs for lung cancer and asbestosis. Women in the asbestos-cement industry, mainly exposed to crocidolite containing asbestos mixtures, experienced higher mortality for pleural malignancies. CONCLUSIONS: The role of asbestos exposure in the development of gastrointestinal and genital neoplasms is discussed.