Lung cancer and exposure to man-made vitreous fibers: results from a pooled case-control study in Germany

BACKGROUND: To investigate the association between lung cancer and occupational exposure to man-made vitreous fibers (MMVF), a pooled analysis of two case-control studies was conducted in the years 1988-1994. METHODS: The case series consisted of 3498 males who were histologically or cytologically verified primary lung cancer cases. 3541 male population controls were drawn at random from the general population and matched to cases by sex, age, and place of residence. To examine the relationship between MMVF and lung cancer we asked all study subjects who worked for at least 6 months as construction and installation workers whether they ever installed or removed insulations and what kind of insulation material they used. RESULTS: Some 304 (8.7%) cases and 170 (4.8%) controls reported to have insulated with glass wool or mineral wool mats. Coded as ever/never exposed, the odds ratio was 1.48 (95% CI: 1.17-1.88), adjusted for smoking and asbestos. To be sure to exclude any confounding effect of asbestos, we tried to identify those cases and controls who insulated with glass wool or mineral wool mats only and never reported any asbestos exposure. For this group we calculated an odds ratio of 1.56 (95% CI: 0.92-2.65), after adjustment for smoking. An elevated risk was also estimated on the basis of an expert rating which was done for a subgroup of cases and controls. Ever exposure to MMVF (but not to asbestos) in this subgroup yielded an odds ratio of 1.30 (95% CI: 0.82-2.07). CONCLUSIONS: Our study provides some indication for an excess risk of man-made vitreous fibers. This result also persists after adjustment for smoking and asbestos.     

Occupational risk factors for lung cancer among young men

OBJECTIVES: This study evaluated whether occupational exposure plays a role for lung cancer at a very young age. METHODS: In a pooled analysis of 2 German case-referent studies including 3498 incident cases among men and 3541 male population referents, a group of men (187 cases and 202 referents) aged > or =45 years was compared with a group of 2186 cases and 2146 referents aged 55-69 years. Occupational exposure to known (A list) or suspected (B list) lung carcinogens was assessed using job and industry codes, and exposure to asbestos was assessed using job-specific supplementary questionnaires. A conditional logistic regression was used to calculate the odds ratios (OR) and to control for smoking. RESULTS: Asbestos exposure showed an odds ratio (OR) of 2.39 [95% confidence interval (95% CI) 1.41-4.04] for the younger group and 1.46 (95% CI 1.24-1.72) for the older group. Having ever worked in a job belonging to the A list as compared with never working in an A- or B-list job was associated with a significantly increased risk for the younger (OR 2.06, 95% CI 1.03-4.12) and older (OR 1.35, 95% CI 1.10-1.65) groups, adjusted for asbestos. Lung cancer risk for those working in A-list jobs at a very young age (under 16 years) was increased in the younger group (OR 6.14, 95% CI 1.41-28.01) in contrast to the older group (OR 1.19, 95% CI 0.91-1.63). CONCLUSION: Occupational risk factors play an important role for lung cancer among young men. Early age at first exposure may favor an early age of the onset of 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.     

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.     

Epidemiological investigation on the health status of employees in two factories manufacturing and repairing railway rolling stock: a historical perspective study of mortality

BACKGROUND: Epidemiological studies of cancer risk due to occupational exposure to asbestos in production and repair of railway rolling stock has so far given consistent results for mesothelioma, but conflicting evidence for lung cancer. OBJECTIVES: The main purpose of this study was to investigate risk for mesothelioma and lung cancer in relation to estimated patterns of exposure in the occupational environment of railway rolling stock manufacture and repair. METHODS: A historical prospective study approach was adopted. The mortality experience of the study population was compared to that of the population of the Veneto Region. Two historical cohorts of workers employed in two plants manufacturing and repairing railway coaches were followed up for mortality. A total of 1,621 workers were enrolled in the study from the first factory, and 1,190 from the second. RESULTS: An elevation of both pleural mesothelioma and lung cancer was reported in the two factories with SMRs of 21.52 (CI 95%=1.64-32.29) and 6.46 (CI 95%=1.33-18.88), and 1.26 (CI 95%=1.01-1.54) and 1.18 (CI 95%=0.81-1.66) respectively. The two excesses however showed different patterns in relation to historical exposure estimates, which appear to correlate with mesotheliomas but not with lung cancer. An elevation of mortality for non-neoplastic respiratory diseases was associated with employment during periods when it was estimated that exposure was at higher levels in one of the two firms. CONCLUSIONS: The results confirm the high carcinogenic risk deriving from asbestos exposure, although inconsistencies were found between target organs in relation to exposure estimates, and the existence of time periods in production in which cancer risk was different.     

Lung cancer risk and welding: Results from a case-control study in Germany

In a case-control study, 839 male hospital-based cases of primary lung cancer and the same number of population-based controls—matched by sex, age, and region of residence—were personally interviewed for their job and smoking histories. The study allows to quantify occupational asbestos exposure that was thought to be a welding-associated risk: 6% of cases and 2% of controls were classified into the occupational category “welders or burners” (odds ratio [OR] = 2.65). This OR was reduced to 1.93 (95% confidence limit [CL]: 1.03–3.61) after adjustment for smoking and asbestos. In contrast, a history of welding in general for at least a half-year is 28% among cases and 23% among controls, yielding an OR of 1.25 (95% CL: 0.94–1.65) after adjustment for both confounders. The OR of welding for more than 6,000 hr is 1.45 (95% CL = 1.04–2.02), reduced to 1.10 after adjustment for smoking and asbestos. Oxyacetylene welding for more than 6,000 hr lifelong is associated with an OR of 1.86 (95% CL = 1.01–3.43) reduced to 1.46 (n.s.) after adjustment for smoking and asbestos. The risk of oxyacetylene welding seems to be highest for oat cell carcinoma with an adjusted OR for ever-exposure of 1.46 (95% CL = 0.69–3.10). Therefore, the present study supports the hypothesis that some, but not all, of the excess risk of welders observed in the literature may be due to a history of cigarette smoking and occupanional asbestos exposure. The elevated risk for the subgroup of employees in the aircraft industry reported for the midterm evaluation of the study still prevails, though no longer statistically significant. However, employees in this industry who ever welded show an OR of 2.29 (95% CL = 1.19–4.42) after adjustment for smoking and asbestos. Am. J. Ind. Med. 33:313–320, 1998. © 1998 Wiley-Liss, Inc.     

Laryngeal and hypopharyngeal cancer and occupational exposure to asbestos and man-made vitreous fibers: results of a case-control study

BACKGROUND: The data from a case-control study performed in France between 1989 and 1991 were used to test whether exposure to either asbestos or to man-made vitreous fibers (MMVF) is a risk factor for cancer of the larynx or the hypopharynx. METHODS: This study involved 315 incident cases of laryngeal cancer, 206 cases of hypopharyngeal cancer, and 305 hospital-based controls with other types of cancer, all recruited in 15 hospitals in six French cities. The subjects' past occupational exposure to asbestos and to four types of MMVF (mineral wool, refractory ceramic fibers, glass filaments, and microfibers) was evaluated based on their job history, with the aid of a job-exposure matrix. Odds ratios were calculated with unconditional logistic regression, with adjustment for smoking and drinking levels. RESULTS: Exposure to asbestos resulted in a significant increase in the risk of hypopharyngeal cancer (OR = 1.80, 95% CI: 1.08-2.99) and a nonsignificant increase in the risk of laryngeal cancer (OR = 1.24, 95% CI: 0.83-1.90). Risk was highest for the epilarynx (highest cumulative level of exposure: OR = 2.22, 95% CI: 1.05-4.71). Exposure to mineral wools was of borderline significance for the risk of hypopharyngeal cancer (OR = 1.55, 95% CI: 0.99-2.41), and nonsignificantly associated with the risk of laryngeal cancer (OR-1.33, 95% CI: 0.91-1.95). The risk was again highest for the epilarynx (OR = 1.85, 95% CI: 1.08-3.17). No significant results were observed for the other MMVF. CONCLUSIONS: These results suggest that asbestos exposure increases the risk of epilaryngeal and hypopharyngeal cancers. It is difficult to reach a conclusion about the effects of mineral wools, because nearly all the exposed subjects were also exposed to asbestos. The possible effects of other MMVF were difficult to assess in this study, because of the paucity of exposed subjects.     

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.     

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.     

Occupational exposure and lung cancer risk: a population-based case-referent study in Sweden

This case-referent study investigated the lung cancer risk from occupational exposure to diesel exhaust, mixed motor exhaust, other combustion products, asbestos, metals, oil mist, and welding fumes. All cases of lung cancer in males aged 40-75 years among stable residents of Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected as a stratified (age, inclusion year) random sample. Information on lifetime occupational history, residency, and tobacco smoking was obtained from the study subjects or from next of kin. Response rates of 87% and 85% resulted in 1,042 cases and 2,364 referents, respectively. Occupational exposures were assessed by an occupational hygienist who coded the intensity and probability of each exposure. Risk estimates were adjusted for tobacco smoking, other occupational exposures, residential radon, and environmental exposure to traffic-related air pollution. For the highest quartile of cumulative exposure versus no exposure, the relative risk was 1.63 (95% confidence interval (CI): 1.14, 2.33) for diesel exhaust, 1.60 (95% CI: 1.09, 2.34) for combustion products, and 1.68 (95% CI: 1.15, 2.46) for asbestos. Dose-response analyses indicated an increase in lung cancer risk of 14% per fiber-year/ml for asbestos exposure. No increased risk was found for the other exposure factors. An overall attributable proportion of 9.5% (95% CI: 5.5, 13.9) was estimated for lung cancer related to diesel exhaust, other combustion products, and asbestos.     

A case-control study of lung cancer at a dye and resin manufacturing plant.

This case-control study evaluated the relationship between lung cancer and occupational factors among employees at a dye and resin manufacturing plant. The study included 51 lung cancer cases and 102 controls who were members of a cohort of workers investigated in a previous retrospective follow-up study. Information on area of employment and on potential exposure to certain chemicals was obtained from plant personnel and medical records and from interviews with long-term employees. Information on potential confounders, including cigarette smoking, was obtained by interviewing study subjects or their next-of-kin. The odds ratio (OR) for heavy smokers compared with light or nonsmokers was 5.9 (95% confidence interval (CI) = 2.4-15). An elevated OR for lung cancer was observed for subjects who worked in the anthraquinone dye and epichlorohydrin manufacturing area of the plant (OR = 2.4; 95% CI = 1.1-5.2) and for employees who were seen at the plant infirmary for acute exposure to chlorine (OR, adjusted for smoking = 27; 95% CI = 3.5-205). Pipefitters employed at the plant for five or more years also had an elevated OR (3.3; 95% CI = 0.8-14).     

Lung cancer and occupation: results of a multicentre case-control study.

The objective of the current study was to estimate the risk of lung cancer attributable to occupational factors and not due to tobacco. At 24 hospitals in nine metropolitan areas in the United States, 1793 male lung cancer cases were matched for race, age, hospital, year of interview, and cigarette smoking (never smoker, ex-smoker, smoker (1-19 and > or = 20 cigarettes per day)) to two types of controls (cancer and non-cancer hospital patients). Information on usual occupation, exposure to specific potential carcinogens, and cigarette smoking was obtained by interview. Risk of lung cancer was increased significantly for electricians; sheetmetal workers and tinsmiths; bookbinders and related printing trade workers; cranemen, derrickmen, and hoistmen; moulders, heat treaters, annealers and other heated metal workers; and construction labourers. All of these occupations are potentially exposed to known carcinogens. Odds ratios (ORs) were increased for exposure to coal dust (adjusted OR = 1.5; 95% confidence interval (95% CI) 1.1-2.1). After stratification, this association was statistically significant only after 10 or more years of exposure. Lung cancer was also related to exposure to asbestos (adjusted OR = 1.8; 95% CI 1.5-2.2). The ORs increased with increasing duration of exposure to asbestos for all smoking categories except for current smokers of 1-19 cigarettes per day. The statistical power to detect ORs among occupations that were previously reported to be at increased risk of lung cancer but that failed to show an OR of at least 1.5 in the current study was small. The cumulative population attributable risk (PAR) of lung cancer due to occupation was 9.2%. It is concluded that occupational factors play an important part in the development of lung cancer independently of cigarette smoking. Because occupations at high risk of lung cancer were under-represented, the cumulative PAR of the present study is likely to be an underestimate of the true contribution of occupation to risk of lung cancer.     

Mesothelioma and lung cancer among motor vehicle mechanics: a meta-analysis

We conducted a systematic review and analysis of the epidemiological literature that examines the risk of lung cancer and mesothelioma among motor vehicle mechanics who may have been engaged in brake repair and, thus, were potentially exposed to asbestos. All relevant studies were classified into three tiers according to their quality. Tier III (lowest quality) studies were cited for completeness, but were not included in the meta-analysis. Meta relative risks (meta-RRs) were calculated for mesothelioma and lung cancer using both fixed and random effects models for Tiers I and II, separately, followed by stratified analyses based on study design or exposure characterization (garage workers versus brake workers) and, for lung cancer studies, based on adequate adjustment for smoking. The meta-analysis for Tier I (higher quality) and Tier II (lower quality) studies of mesothelioma yielded RR estimates of 0.92 (95% CI 0.55-1.56) and 0.81 (95% CI 0.52-1.28), respectively. Further stratification according to exposure characterization did not affect the results. The meta-analysis for lung cancer produced RR estimates of 1.07 (95% CI 0.88-1.31) for Tier I and 1.17 (95% CI 1.01-1.36) for Tier II. When the lung cancer analysis was limited to studies that used adequate control for smoking, the resulting RR estimate was 1.09 (95% CI 0.92-1.28). Based on these findings, we conclude that employment as a motor vehicle mechanic does not increase the risk of developing mesothelioma. Although some studies showed a small increase in risk of lung cancer among motor vehicle mechanics, the data on balance do not support a conclusion that lung cancer risk in this occupational group is related to asbestos exposure.     

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 case-control study of malignant and non-malignant respiratory disease among employees of a fiberglass manufacturing facility. II. Exposure assessment.

A case-control study of malignant and non-malignant respiratory disease among employees of the Owens-Corning Fiberglas Corporation's Newark, Ohio plant was undertaken. The aim was to determine the extent to which exposures to substances in the Newark plant environment, to non-workplace factors, or to a combination may play a part in the risk of mortality from respiratory disease among workers in this plant. A historical environmental reconstruction of the plant was undertaken to characterise the exposure profile for workers in this plant from its beginnings in 1934 to the end of 1987. The exposure profile provided estimates of cumulative exposure to respirable fibres, fine fibres, asbestos, talc, formaldehyde, silica, and asphalt fumes. Employment histories from Owens-Corning Fiberglas provided information on employment characteristics (duration of employment, year of hire, age at first hire) and an interview survey obtained information on demographic characteristics (birthdate, race, education, marital state, parent's ethnic background, and place of birth), lifetime residence, occupational and smoking histories, hobbies, and personal and family medical history. Matched, unadjusted odds ratios (ORs) were used to assess the association between lung cancer or non-malignant respiratory disease and the cumulative exposure history, demographic characteristics, and employment variables. Only the smoking variables and employment characteristics (year of hire and age at first hire) were statistically significant for lung cancer. For non-malignant respiratory disease, only the smoking variables were statistically significant in the univariate analysis. Of the variables entered into a conditional logistic regression model for lung cancer, only smoking (smoked for six months or more v never smoked: OR = 26.17, 95% confidence interval (95% CI) 3.316-206.5) and age at first hire (35 and over v less than 35: OR = 0.244, 95% CI 0.083-0.717) were statistically significant. There were, however, increased ORs for year of employment (first hired before 1945 v first hire after 1945: OR = 1.944, 95% CI 0.850-4.445), talc (cumulative exposure >1000 fibres/ml days v never exposed: OR = 1.355, 95% CI 0.407-5.515), and asphalt fumes (cumulative exposure >0.01 mg/m(3) days v never exposed: OR 1.131, 95% CI 0.468-2.730). For non-malignant respiratory disease, only the smoking variable was significant in the conditional logistic regression analysis (OR = 2.637, 95% CI 1.146-6.069). There were raised ORs for the higher cumulative exposure categories for respirable fibres, asbestos, silica, and asphalt fumes. For both silica and asphalt fumes, ORs were more than double the reference groups for all exposure categories. A limited number of subjects were exposed to fine fibres. The scarcity of cases and controls limits the extent to which analyses for fine fibre may be carried out. Within those limitations, among those who had worked with fine fibre, the unadjusted, unmatched OR for lung cancer was (1.0 (95% CI 0.229-4.373) and for non-malignant respiratory disease, the OR was 1.5 (95% CI 0.336-6.702). The unadjusted OR for lung cancer for exposure to fine fibre was consistent with that for all respirable fibre and does not suggest an association. For non-malignant respiratory disease, the unadjusted OR for fine fibre was opposite in direction from that for all respirable fibres. Within the limitations of the available data on fibre, there is o suggestion that exposure to fine fibre has resulted in an increase in risk of lung cancer. The increased OR for non-malignant respiratory disease is inconclusive. The results of this population, in this place and time, neither respirable fibres nor any of the substances investigated as part of the plant environment are statistically significant factors for lung cancer risk although there are increased ORs for exposure to talc and asphalt fumes. Smoking is the most important factors in risk for lung cancer in this population. The situation is less clear for non-malignant respiratory disease. Unlike lung cancer, non-malignant respiratory represents a constellation of outcomes and not a single well defined end point. Although smoking was the only statistically significant factor for non-malignant respiratory disease in this analysis, the ORs for respirable fibres, asbestos, silica, and asphalt fumes were greater than unity for the highest exposure categories. Although the raised ORs for these substances may represent the results of a random process, they may be suggestive of an increased risk and require further investigation.     

Lung cancer risk associated to exposure to radon and smoking in a case-control study of French uranium miners

A case-control study nested in the cohort of French uranium miners took smoking information into account in investigating the effect of radon exposure on lung cancer risk. This study included 100 miners who died of lung cancer and 500 controls matched for birth period and attained age. Data about radon exposure came from the cohort study, and smoking information was retrospectively determined from a questionnaire and occupational medical records. Smoking status (never vs. ever) was reconstructed for 62 cases and 320 controls. Statistical analyses used conditional logistic regression. The effect of radon exposure on lung cancer risk was assessed with a linear excess relative risk model, and smoking was considered as a multiplicative factor. Mean cumulative radon exposures were 114.75 and 70.84 Working Level Months (WLM) among exposed cases and controls, respectively. The crude excess risk of lung cancer per 100 WLM was 0.98 (95% CI: 0.18-3.08%). When adjusted for smoking, the excess risk was 0.85 per 100 WLM (95% CI: 0.12-2.79%), which is still statistically significant. The relative risk related to smoking was equal to 3.04 (95% CI: 1.20-7.70). This analysis shows a relative risk of lung cancer related to smoking similar to that estimated from previous miners' cohorts. After adjustment for smoking, the effect of radon exposure on lung cancer risk persists, and its estimated risk coefficient is close to that found in the French cohort without smoking information.     

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.     

Lung cancer and occupation: results of a multicentre case-control study.

The objective of the current study was to estimate the risk of lung cancer attributable to occupational factors and not due to tobacco. At 24 hospitals in nine metropolitan areas in the United States, 1793 male lung cancer cases were matched for race, age, hospital, year of interview, and cigarette smoking (never smoker, ex-smoker, smoker (1-19 and > or = 20 cigarettes per day)) to two types of controls (cancer and non-cancer hospital patients). Information on usual occupation, exposure to specific potential carcinogens, and cigarette smoking was obtained by interview. Risk of lung cancer was increased significantly for electricians; sheetmetal workers and tinsmiths; bookbinders and related printing trade workers; cranemen, derrickmen, and hoistmen; moulders, heat treaters, annealers and other heated metal workers; and construction labourers. All of these occupations are potentially exposed to known carcinogens. Odds ratios (ORs) were increased for exposure to coal dust (adjusted OR = 1.5; 95% confidence interval (95% CI) 1.1-2.1). After stratification, this association was statistically significant only after 10 or more years of exposure. Lung cancer was also related to exposure to asbestos (adjusted OR = 1.8; 95% CI 1.5-2.2). The ORs increased with increasing duration of exposure to asbestos for all smoking categories except for current smokers of 1-19 cigarettes per day. The statistical power to detect ORs among occupations that were previously reported to be at increased risk of lung cancer but that failed to show an OR of at least 1.5 in the current study was small. The cumulative population attributable risk (PAR) of lung cancer due to occupation was 9.2%. It is concluded that occupational factors play an important part in the development of lung cancer independently of cigarette smoking. Because occupations at high risk of lung cancer were under-represented, the cumulative PAR of the present study is likely to be an underestimate of the true contribution of occupation to risk of lung cancer.     

中国非吸烟女性肺癌危险因素的病例-对照研究

目的探讨中国非吸烟女性患肺癌的危险因素。方法应用1∶2配对的病例对照方法,收集2001年9月~2004年2月在北京、上海和成都指定医院经病理诊断确诊的非吸烟女性新发肺癌住院病例157例,按照性别、年龄(±2岁)、不吸烟等配对因素选取医院对照和人群对照。利用统一调查表对调查对象进行面对面问卷调查,收集病例和对照有关危险因素的暴露史等情况。通过单因素分析和多因素条件Logistic回归分析筛选肺癌的主要危险因素。结果单因素分析发现28个暴露因素与非吸烟女性肺癌发生有关。多因素分析发现,被动吸烟指数≥50人年(OR=1·77,95%CI为1·07~2·92)、经常吃动物内脏(OR=1·85,95%CI为1·06~3·22)、职业接触粉尘(OR=2·47,95%CI为1·21~5·03)和工作场所通风不良(OR=4·02,95%CI为1·74~9·29)为非吸烟女性肺癌发生的危险因素;常吃蔬菜(OR=0·26,95%CI为0·12~0·59)、经常服用维生素(OR=0·53,95%CI为0·30~0·93)、结婚后家庭人均月收入≥500元(OR=0·50,95%CI为0·28~0·91)和初次生育年龄在24~30岁之间(OR=0·53,95%CI为0·32~0·90)为非吸烟女性肺癌发生的保护因素。趋势性检验发现,被动吸烟与非吸烟女性发生肺癌的相对危险度之间存在一定剂量反应关系。结论被动吸烟、职业接触粉尘、经常吃动物内脏和工作场所通风不良会增加非吸烟女性患肺癌的危险性。常吃蔬菜和经常服用维生素等因素可以降低非吸烟女性发生肺癌的危险性。