Occupational lung cancer risk for men in Germany: results from a pooled case-control study

Occupational exposures such as crystalline silica, diesel engine exhaust, polycyclic aromatic hydrocarbons, and man-made mineral fibers are strongly suspected to increase lung cancer risk. Two case-control studies in Germany conducted between 1988 and 1996 were pooled for a joint analysis. A total of 3,498 male cases and 3,541 male population controls, frequency matched for age and region, were included in the study. The lifelong history of all jobs and industries was coded and occupational exposures were evaluated by expert rating. Odds ratios, crude and adjusted for smoking and asbestos exposure, were calculated by conditional logistic regression. Job-related evaluation showed a statistically significant increased odds ratio adjusted for smoking among farmers; forestry workers, fishermen, and livestock workers; miners and quarrymen; chemical processors; cabinet makers and related wood workers; metal producers and processors; bricklayers and carpenters; road construction workers, pipelayers and well diggers; plasterers, insulators, and upholsterers; painters and lacquerers; stationary engine and heavy equipment operators; transport workers and freight handlers; and service workers. With regard to specific occupational exposures, elevated odds ratios (OR) (95% confidence intervals (CI)) for lung cancer risk adjusted for smoking and asbestos exposure were observed for man-made mineral fibers (OR = 1.48, 95% CI 1.17, 1.88); crystalline silica (OR = 1.41, 95% CI 1.22, 1.62); diesel engine exhaust (OR = 1.43, 95% CI 1.23, 1.67); and polycyclic aromatic hydrocarbons (OR = 1.53, 95% CI 1.14, 2.04). The risk of asbestos exposure, adjusted for smoking was also increased (OR = 1.41, 95% CI 1.24, 1.60).     

Occupational exposure to diesel motor exhaust and risk of lung cancer by histological subtype: a population-based case–control study in Swedish men

We investigated occupational exposure to diesel motor exhaust (DME) and the risk of lung cancer by histological subtype among men, using elemental carbon (EC) as a marker of DME exposure. 993 cases and 2359 controls frequency-matched on age and year of study inclusion were analyzed by unconditional logistic regression in this Swedish case–control study. Work and smoking histories were collected by a questionnaire and telephone interviews. DME was assessed by a job-exposure matrix. We adjusted for age, year of study inclusion, smoking, occupational exposure to asbestos and combustion products (other than motor exhaust), residential exposure to radon and exposure to air pollution from road traffic. The OR for lung cancer for ever vs. never exposure to DME was 1.15 (95% CI 0.94–1.41). The risk was higher for squamous and large cell, anaplastic or mixed cell carcinoma than for alveolar cell cancer, adenocarcinoma and small cell carcinoma. The OR in the highest quartile of exposure duration (≥34 years) vs. never exposed was 1.66 (95% CI 1.08–2.56; p for trend over all quartiles: 0.027) for lung cancer overall, 1.73 (95% CI 1.00–3.00; p: 0.040) for squamous cell carcinoma and 2.89 (95% CI 1.37–6.11; p: 0.005) for the group of undifferentiated, large cell, anaplastic and mixed cell carcinomas. We found no convincing association between exposure intensity and lung cancer risk. Long-term DME exposure was associated with an increased risk of lung cancer, particularly to squamous cell carcinoma and the group of undifferentiated, large cell, anaplastic or mixed carcinomas.     

Urban air pollution and lung cancer in Stockholm

We conducted a population-based case-control study among men 40-75 years of age encompassing all cases of lung cancer 1985-1990 among stable residents of Stockholm County 1950-1990. Questionnaires to subjects or next-of-kin (primarily wives or children) elicited information regarding smoking and other risk factors, including occupational and residential histories. A high response rate (>85%) resulted in 1,042 cases and 2,364 controls. We created retrospective emission databases for NOx/NO2 and SO2 as indicators of air pollution from road traffic and heating, respectively. We estimated local annual source-specific air pollution levels using validated dispersion models and we linked these levels to residential addresses using Geographical Information System (GIS) techniques. Average traffic-related NO2 exposure over 30 years was associated with a relative risk (RR) of 1.2 (95% confidence interval 0.8-1.6) for the top decile of exposure, adjusted for tobacco smoking, socioeconomic status, residential radon, and occupational exposures. The data suggested a considerable latency period; the RR for the top decile of average traffic-related NO2 exposure 20 years previously was 1.4 (1.0-2.0). Little association was observed for SO2. Occupational exposure to asbestos, diesel exhaust, and other combustion products also increased the risk of lung cancer. Our results indicate that urban air pollution increases lung cancer risk and that vehicle emissions may be particularly important.     

Occupational exposures and head and neck cancers among Swedish construction workers

OBJECTIVES: Occupational exposures in the construction industry may increase the risk of head and neck cancers, although the epidemiologic evidence is limited by problems of low study power and inadequate adjustment for tobacco use. In an attempt to address this issue, the relationship between selected occupational exposures and head and neck cancer risk was investigated using data from a large cohort of Swedish construction workers. METHODS: Altogether 510 squamous cell carcinomas of the head and neck (171 in the oral cavity, 112 in the pharynx, 227 in the larynx) were identified during 1971-2001 among 307 799 male workers in the Swedish construction industry. Exposure to diesel exhaust, asbestos, organic solvents, metal dust, asphalt, wood dust, stone dust, mineral wool, and cement dust was assessed using a semi-quantitative job-exposure matrix. Rate ratios (RR) and 95% confidence intervals (95% CI) were calculated for head and neck cancers in relation to occupational exposure, using Poisson regression with adjustment for age and smoking status. RESULTS: Asbestos exposure was related to an increased laryngeal cancer incidence (RR 1.9, 95% CI 1.2-3.1). Excesses of pharyngeal cancer were observed among workers exposed to cement dust (RR 1.9, 95% CI 1.2-3.1). No occupational exposures were associated with oral cavity cancer. These findings did not materially change upon additional adjustment for cigarette pack-years. CONCLUSIONS: These findings offer further evidence that asbestos increases the risk of laryngeal cancer. The observation of a positive association between cement dust exposure and pharyngeal cancer warrants further investigation.     

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.     

Low-dose exposure to asbestos and lung cancer: dose-response relations and interaction with smoking in a population-based case-referent study in Stockholm,Sweden

This population-based case-referent study investigated the lung cancer risk associated with occupational exposure to asbestos, focusing on dose-response relations and the interaction with tobacco smoking. Incident cases of lung cancer among males aged 40-75 years in Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected randomly within strata (age, inclusion year) of the study base. Questionnaires administered to subjects or their next of kin gave information on occupations, tobacco smoking habits, and residences. Response rates of 87% and 85% resulted in 1,038 cases and 2,359 referents, respectively. Occupational exposures were assessed by an industrial hygienist. Lung cancer risk increased almost linearly with cumulative dose of asbestos. The risk at a cumulative dose of 4 fiber-years was 1.90 (95% confidence interval (CI): 1.32, 2.74), higher than that predicted by downward linear extrapolation from highly exposed occupational cohorts. The relative risk (exp(beta)) for a transformed dose variable ln(fiber-years + 1) was 1.494 (95% CI: 1.193, 1.871) per unit of exposure. The joint effect of asbestos and smoking was estimated to be 1.15 (95% CI: 0.77, 1.72) times that predicted from the sum of their individual effects and 0.31 (95% CI: 0.11, 0.86) times that predicted from their product, indicating a joint effect between additivity and multiplicativity.     

Welding and lung cancer in Central and Eastern Europe and the United Kingdom

Occupation as a welder has been associated with a 25%-40% increase in lung cancer risk. This study aims to elucidate to what extent confounding by smoking and asbestos drives this association and to evaluate the role of welding-related exposures such as chromium. The study included 2,197 male incident lung cancer cases and 2,295 controls from Romania, Hungary, Poland, Russia, Slovakia, the Czech Republic, and the United Kingdom from 1998 to 2001. Information on risk factors was collected through face-to-face interviews. Experts assessed exposure to 70 agents, and risk estimates were adjusted for smoking and occupational exposures. Occupation as a welder/flame cutter (prevalence controls: 3.7%) was associated with an odds ratio of 1.36 (95% confidence interval (CI): 1.00, 1.86) after adjustment for smoking and occupational exposures including asbestos. An odds ratio of 1.18 (95% CI: 1.01, 1.38) was found for welding fumes (prevalence controls: 22.8%), increasing to 1.38 for more than 25 exposure years (95% CI: 1.09, 1.75). A duration-response association was also observed for mild steel welding without chromium exposure. In this population, occupational exposure to welding fumes accounted for approximately 4% of lung cancer cases, to which both stainless and mild steel welding contributed equally. Given that welding remains a common task for many workers, exposure to welding fumes represents an important risk factor for lung cancer.     

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.     

Smoking imputation and lung cancer in railroad workers exposed to diesel exhaust

BACKGROUND: An association between diesel exhaust exposure and lung cancer mortality in a large retrospective cohort study of US railroad workers has previously been reported. However, specific information regarding cigarette smoking was unavailable. METHODS: Birth cohort, age, job, and cause of death specific smoking histories from a companion case-control study were used to impute smoking behavior for 39,388 railroad workers who died 1959-1996. Mortality analyses incorporated the effect of smoking on lung cancer risk. RESULTS: The smoking adjusted relative risk of lung cancer in railroad workers exposed to diesel exhaust compared to unexposed workers was 1.22 (95% CI = 1.12-1.32), and unadjusted for smoking the relative risk was 1.35 (95% CI = 1.24-1.46). CONCLUSIONS: These analyses illustrate the use of imputation in record-based occupational health studies to assess potential confounding due to smoking. In this cohort, small differences in smoking behavior between diesel exposed and unexposed workers did not explain the elevated lung cancer risk.     

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).     

Quantifying the mediating effects of smoking and occupational exposures in the relation between education and lung cancer: the ICARE study

Smoking only partly explains the higher lung cancer incidence observed among socially deprived people. Occupational exposures may account for part of these inequalities, but this issue has been little investigated. We investigated the extent to which smoking and occupational exposures to asbestos, silica and diesel motor exhaust mediated the association between education and lung cancer incidence in men. We analyzed data from a large French population-based case–control study (1976 lung cancers, 2648 controls). Detailed information on lifelong tobacco consumption and occupational exposures to various carcinogens was collected. We conducted inverse probability-weighted marginal structural models. A strong association was observed between education and lung cancer. The indirect effect through smoking varied by educational level, with the strongest indirect effect observed for those with the lowest education (OR = 1.34 (1.14–1.57)). The indirect effect through occupational exposures was substantial among men with primary (OR = 1.22 (1.15–1.30) for asbestos and silica) or vocational secondary education (OR = 1.18 (1.12–1.25)). The contribution of smoking to educational differences in lung cancer incidence ranged from 22 % (10–34) for men with primary education to 31 % (?3 to 84) for men with a high school degree. The contribution of occupational exposures to asbestos and silica ranged from 15 % (10–20) for men with a high school degree to 20 % (13–28) for men with vocational secondary education. Our results highlight the urgent need for public health policies that aim at decreasing exposure to carcinogens at work, in addition to tobacco control policies, if we want to reduce socioeconomic inequalities in the cancer field.     

Occupation and lung cancer risk in the province of Trieste: a case-control study]

To investigate the relationship between occupation and lung cancer, a case-control study was performed in the province of Trieste, Italy, where metallurgical and mechanical industries, dock activities and shipbuilding and ship repairing are predominant. Through the local Cancer Registry, pathology records of 938 men who died of primary lung cancer (ICD 162) in a five-year period were examined. Residential, smoking and occupational histories were obtained from interviews of next of kin of 756 cases and 756 age-matched male controls (+/- 2 years). Occupational exposures to lung carcinogens were assessed according to a job-title based approach, identifying industries/occupations with well-recognized lung carcinogen exposures (list A) and industries/occupations with suspected lung carcinogen exposures (list B). Exposure to asbestos was classified as absent, possible or definite. After adjustment for cigarette smoking (four levels) and residence (three levels), a significant association was found between lung cancer and occupations in list A (RR = 2.28, 95% CI = 1.70-3.07) and in list B (RR = 1.33, 95% CI = 1.04-1.71). A significant excess risk was found for workers with definite exposure to asbestos when compared to those with no exposure to lung carcinogens (RR = 1.99, 95% CI = 1.43-2.76). A very high relative risk was observed among heavy smokers with definite exposure to asbestos (RR = 42.8). A stratified analysis showed that the combined effect of asbestos and smoking was compatible with that expected under a multiplicative model. The overall attributable risk in the population (ARp) for cigarette smoking was found to be 87.6%. The ARp fraction for occupations with well-established exposures to lung carcinogens (list A) was 16.2%. The ARp fraction increased to 25.5% (85% CI = 1.4-34.6) when occupations with suspected exposure to lung carcinogens (list B) were included. The ARp fraction for possible or definite exposure to asbestos was 20.1% (95% CI = 11.6-28.6).     

Lung cancer risk of workers in shoe manufacture and repair

BACKGROUND: The occupational lung cancer risk in manufacturing and repair of shoes was studied by pooling of two major case-control studies from Germany. METHODS: Some 4184 incident hospital-based cases of primary lung cancer and 4253 population controls, matched for sex, age, and region of residence were intensively interviewed with respect to their occupational and smoking history. Based on the occupational coding and a free text search, all individuals who had ever worked in shoe manufacturing or repair for at least half a year were identified. Shoemaker-years were calculated as the cumulated duration of working in shoe manufacturing or repair. Odds ratios (OR) and 95% confidence intervals (CI) were calculated via conditional logistic regression. Additional adjustment for smoking and occupational asbestos exposure was used. RESULTS: Seventy-six cases and 42 controls who had ever worked in shoe manufacture or repair (OR = 1.89, 95% CI: 1.29-2.78). After adjustment for smoking, this risk was lowered to 1.69 (95% CI: 1.09-2.62). Further adjustment for asbestos exposure only slightly changed the risk estimates upwards. The smoking adjusted OR in males was 1.50 (95% CI: 0.93-2.41) and 2.91 (95% CI: 0.90-9.44) in females. Logistic regression modeling showed a positive dose-effect relationship between duration of exposure in shoe manufacture and repair and lung cancer risk. The odds ratio for 30 years of exposure varied between 1.98 and 2.24 depending on the model specified. CONCLUSIONS: The study demonstrates an increased lung cancer risk for shoemakers and workers in shoe manufacturing. The risk seems to double after being 30 years in these occupations.     

Case-control study on occupational exposure to diesel exhaust and lung cancer risk.

The association between lung cancer and occupations with probable exposure to diesel exhaust (DE) was studied among 2,584 cases and 5,099 hospital controls. The crude odds ratio (OR) for probable exposure was 1.31 (95% confidence interval [CI] 1.09-1.57), but adjustment for smoking and other confounders reduced the estimate to 0.95 (95% CI = 0.78-1.16). Similar results were observed for truck drivers, the only occupational category large enough for separate analysis. Data on self-reported exposure for 477 cases and 946 controls revealed a crude OR of 1.45 (95% CI = 0.93-2.27), which was reduced to 1.21 (95% CI = 0.78-2.02) after controlling for smoking and other confounders. The present results and a review of the literature do not definitively support an etiologic association between DE exposure and elevated lung cancer risk.     

Occupational exposure to diesel and gasoline engine exhausts and risk of lung cancer among Finnish workers

BACKGROUND: Studies on engine exhausts and lung cancer have given inconsistent results. METHODS: Economically active Finns were followed-up for lung cancer during 1971-95 (33,664 cases). Their Census occupations in 1970 were converted to exposures to diesel and gasoline engine exhausts with a job-exposure matrix. The relative risks (RRs) for cumulative exposure (CE) were defined by Poisson regression, adjusted for smoking, asbestos, and quartz dust exposure, and socioeconomic status. RESULTS: RR for engine exhausts among men did not increase with increasing CE. In women, RR for gasoline engine exhaust was 1.58 (95% CI 1.10-2.26) in the CE-category of 1-99 mg/m(3)-y and 1.66 (1.11-2.50) among those with > or =100 mg/m(3)-y (lag 20 years). With a lag of 10 years RR for the middle/highest diesel exhaust category in women was 1.42 (0.94-2.13). CONCLUSIONS: Occupational exposure to engine exhausts was not consistently associated with lung cancer in this study, possibly due to low exposure levels.     

Lung cancer and exposure to diesel exhaust among bus garage workers.

Mortality and cancer incidence was investigated among the 695 bus garage workers employed as mechanics, servicemen, or hostlers for at least six months in five bus garages in Stockholm between 1945 and 1970. The exposure to diesel exhaust and asbestos was estimated by industrial hygienists. A small excess of lung cancer mortality was found in the cohort when occupationally active men in Stockholm were used as the reference group. A case-referent study was performed within the cohort, six referents being selected for each of the 20 lung cancer cases. The lung cancer risk increased with increasing cumulative exposure to diesel exhaust, but not with cumulative asbestos exposure. The relative risk for lung cancer among the highly exposed men was 2.4 (95% CI 1.3-4.5) as compared with those with low exposure. The study indicates that exposure to diesel exhaust increases the risk for lung cancer.     

Occupational exposure to diesel and gasoline emissions and lung cancer in Canadian men

The International Agency for Research on Cancer classifies diesel exhaust as a probable human carcinogen; this decision is based largely from lung cancer evidence. Gasoline exhaust is classified as a possible carcinogen. Epidemiological studies are needed that improve upon some of the limitations of previous research with respect to the characterization of exposure, and the control for the potential confounding influence of smoking and other occupational exposures. Our objective was to investigate associations between occupational exposure to diesel and gasoline engine emissions and lung cancer. We used a case-control study design that involved men 40 years of age and older at the time of interview. Analyses are based on 1681 incident cases of lung cancer and 2053 population controls. A self-reported questionnaire elicited a lifetime occupational history, including general tasks, and information on other potential risk factors. Occupational exposures to diesel and gasoline emissions, crystalline silica, and asbestos were assigned to each job held by study subjects by industrial hygienists who were blind to case-control status. Exposure metrics for diesel and gasoline emissions that were modeled included: ever exposure, cumulative exposure, and concentration of exposure. We found a dose–response relationship between cumulative occupational exposure to diesel engine emissions and lung cancer. This association was more pronounced for the squamous and large cell subtypes with adjusted odds ratios across the three increasing tertiles of cumulative lifetime exposure relative to those with no exposure of 0.99, 1.25, and 1.32 (p=0.04) for squamous cell carcinoma, and 1.06, 1.19, 1.68 (p=0.02) for large cell carcinoma. While the association with cumulative exposure to gasoline was weakly positive, it was not statistically significant. Our findings suggest that exposure to diesel engine emissions increases the risk of lung cancer particularly for squamous and large cell carcinoma subtypes.     

Lung cancer risk in male workers occupationally exposed to diesel motor emissions in Germany.

BACKGROUND: Although in several epidemiological studies exposure to diesel motor emissions (DME) shows an elevated lung cancer risk, it is still controversial whether DME is a human carcinogen. METHODS: In a pooled analysis of two case-control studies on lung cancer in Germany a total of 3498 male cases with histologically or cytologically ascertained lung cancer and 3541 male population controls were included. Information about lifelong occupational and smoking history was obtained by questionnaire. Drivers of lorries, buses, taxies, diesel locomotives and forklift trucks, bulldozers, graders, excavators, and tractors, were considered as exposed to DME and their cumulative exposure was estimated. All odds ratios were adjusted for smoking and asbestos exposure. RESULTS: The evaluation of lung cancer risk for all jobs with DME-exposure combined showed an odds ratio of OR=1.43 (95%-CI: 1.23-1.67). Most pronounced was the increase in lung cancer risk in heavy equipment operators (OR=2. 31 95%-CI: 1.44-3.70). The risk of tractor drivers increased with length of employment and reached statistical significance for exposures longer than 30 years (OR=6.81, 95%-CI: 1.17-39.51). The group of professional drivers (e.g., trucks, buses, and taxies), showed an increased risk only in West Germany (OR=1.44, 95%-CI: 1. 18-1.76), but not in East Germany (OR=0.83, 95%-CI: 0.60-1.14). DME-exposure in other traffic related jobs (e.g., diesel engine locomotive drivers, switchmen, forklift operators) was associated with an odds ratio of OR=1.53 (95%-CI: 1.04-2.24). CONCLUSIONS: The study provides further evidence that occupational exposure to diesel motor emissions is associated with an increased lung cancer risk.     

The influence of occupational exposure to pesticides, polycyclic aromatic hydrocarbons, diesel exhaust, metal dust, metal fumes, and mineral oil on prostate cancer: a prospective cohort study

Aims: To investigate the relation between exposure to pesticides, polycyclic aromatic hydrocarbons (PAHs), diesel exhaust, metal dust, metal fumes, and mineral oil in relation to prostate cancer incidence in a large prospective study. Methods: This cohort study was conducted among 58 279 men in the Netherlands. In September 1986, cohort members (55–69 years) completed a self-administered questionnaire on potential cancer risk factors, including job history. Follow up for prostate cancer incidence was established by linkage to cancer registries until December 1995 (9.3 years of follow up). The analyses included 1386 cases of prostate cancer and 2335 subcohort members. A blinded case-by-case expert exposure assessment was carried out to assign cases and subcohort members a cumulative probability of exposure for each potential carcinogenic exposure. Results: In multivariate analyses there was a significant negative association for pesticides (RR 0.60; 95% CI 0.37 to 0.95) when comparing the highest tertile of exposure to pesticides with no exposure. No association was found for occupational exposure to PAHs (RR 0.75; 95% CI 0.42 to 1.31), diesel exhaust (RR 0.81; 95% CI 0.62 to 1.06), metal dust (RR 1.01; 95% CI 0.72 to 1.40), metal fumes (RR 1.11; 95% CI 0.80 to 1.54), or mineral oil (RR 0.99; 95% CI 0.66 to 1.48) when comparing the highest tertile of exposure with no exposure. In subgroup analysis, with respect to tumour invasiveness and morphology, null results were found for occupational exposure to pesticides, PAH, diesel exhaust, metal dust, metal fumes, and mineral oil. Conclusions: These results suggest a negative association between occupational exposure to pesticides and prostate cancer. For other carcinogenic exposures results suggest no association between occupational exposure to PAHs, diesel exhaust, metal dust, metal fumes, or mineral oil and prostate cancer.     

A Case–Control Study of Lung Cancer Nested in a Cohort of European Asphalt Workers

Background

We conducted a nested case–control study in a cohort of European asphalt workers in which an increase in lung cancer risk has been reported among workers exposed to airborne bitumen fume, although potential bias and confounding were not fully addressed.

Objective

We investigated the contribution of exposure to bitumen, other occupational agents, and tobacco smoking to the risk of lung cancer among asphalt workers.

Methods

Cases were cohort members in Denmark, Finland, France, Germany, the Netherlands, Norway, and Israel who had died of lung cancer between 1980 and the end of follow-up (2002–2005). Controls were individually matched in a 3:1 ratio to cases on year of birth and country. We derived exposure estimates for bitumen fume and condensate, organic vapor, and polycyclic aromatic hydrocarbons, as well as for asbestos, crystalline silica, diesel motor exhaust, and coal tar. Odds ratios (ORs) were calculated for ever-exposure, duration, average exposure, and cumulative exposure after adjusting for tobacco smoking and exposure to coal tar.

Results

A total of 433 cases and 1,253 controls were included in the analysis. The OR was 1.12 [95% confidence interval (CI), 0.84–1.49] for inhalation exposure to bitumen fume and 1.17 (95% CI, 0.88–1.56) for dermal exposure to bitumen condensate. No significant trend was observed between lung cancer risk and duration, average exposure, or cumulative exposure to bitumen fume or condensate.

Conclusions

We found no consistent evidence of an association between indicators of either inhalation or dermal exposure to bitumen and lung cancer risk. A sizable proportion of the excess mortality from lung cancer relative to the general population observed in the earlier cohort phase is likely attributable to high tobacco consumption and possibly to coal tar exposure, whereas other occupational agents do not appear to play an important role.