Case-control study of lung cancer and truck driving in the Teamsters Union.

We conducted a case-control study of lung cancer deaths in the Teamsters Union to compare the risk of different occupations within the teamsters, after controlling for smoking and other confounders. Occupations with no presumed exposure to diesel fumes were used as the nonexposed group. The study population consisted of 996 cases and 1,085 controls who had died in 1982-83 after applying for pensions. Next of kin provided information on smoking, work history, and other potential confounders. Work history data were also obtained from the Teamsters Union. While no single job category had a significant excess risk compared to the non-exposed group, certain sub-groups were elevated. The odds ratio for those with long-term employment as long-haul truckers after 1959 (an approximate date for the introduction of diesel engines) was 1.55 (95% CI: 0.97, 2.47). Long-term drivers of primarily diesel trucks had an odds ratio of 1.89 (95% CI: 1.04, 3.42). Overall, our results suggest that diesel truck drivers have an excess risk of lung cancer compared to other teamsters in jobs outside the trucking industry. However, our findings were not uniformly consistent and our data have many limitations, the most important of which is the lack of data on exposure to diesel fumes.     

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.     

Diesel exhaust exposure and lung cancer: adjustment for the effect of smoking in a retrospective cohort study

BACKGROUND: The extent that cigarette smoking may confound the relationship between diesel exhaust exposure and lung cancer was assessed in a retrospective cohort study of 55,395 U.S. railroad workers followed from 1959 to 1976. METHODS: The relative risk (RR) of lung cancer due to diesel exhaust was indirectly adjusted using job-specific smoking data from a case-control study of railroad workers who died between 1981-1982 and from a survey of 514 living workers from an active railroad in 1982. Adjustment factors were developed based on the distribution of job-specific smoking rates. RESULTS: The unadjusted RR for lung cancer was 1.58 (95% CI = 1.14-2. 20) for workers aged 40-44 in 1959, who experienced the longest possible duration of exposure, and the smoking adjusted RR was 1.44 (1.01-2.05). CONCLUSIONS: After considering differences in smoking rates between workers exposed and unexposed to diesel exhaust in a relatively large blue-collar cohort, there were still elevated risks of lung cancer in workers in jobs with diesel exhaust exposure.     

Exposure to diesel exhaust enhances total IgE in non-atopic dockers

OBJECTIVES: Diesel exhaust particles (DEPs) containing polycyclic aromatic hydrocarbons stimulate the formation of IgE in humans following single and acute exposure. The aim of the present study was to ascertain whether long-standing occupational exposure to DEPs carries a risk of enhanced serum IgE, and of rhinitis or asthma. METHODS: In this cross-sectional study, findings in 76 dockers were compared with those in 63 reference subjects. Among the dockers, drivers and laborers were exposed to diesel emission from forklifts or trucks in the ship-holds, where benzopyrene levels averaged 4.9 ng/m(3). Serum IgE levels were measured by the UNICAP method. Atopy, an evident source of high IgE levels, was assessed by the Phadiatop test. The subjects' clinical and occupational histories were collected. Interval variables were analyzed with Student's t- and Levene's F-tests. The odds ratio (OR) with the 95% confidence interval (CI) was obtained by the exact method at univariate and multivariate (logistic regression) analysis. RESULTS: In view of the large difference in serum IgE (P=0.00001) and the prevalence of respiratory diseases ( P=0.009) between atopic and non-atopic subjects, we analyzed their data separately. For non-atopic subjects, the risk of presenting high IgE was significantly higher (OR=11.4; CI=1.44-526; P=0.013) and the risk of respiratory disease was significantly lower (OR=0.09; CI=0.00-0.73; P=0.016) in drivers and laborers as a whole than in the reference subjects. None of the ORs was significant among atopic individuals. CONCLUSIONS: In non-atopic dockers, long-standing exposure to DEPs at concentrations similar to those in heavily polluted cities increased serum IgE levels but not the incidence of rhinitis or asthma.     

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).     

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 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.     

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.     

Lung cancer in motor exhaust-related occupations

The association between employment in motor exhaust-related occupations and the risk for lung cancer was examined in 2,291 male cases of lung cancer and 2,570 controls in data pooled from three U.S. case control studies carried out by the National Cancer Institute between 1976 and 1983. Most analyses were limited to subjects providing direct, in-person interviews, including 1,444 cases and 1,893 controls. For those providing direct interviews and employed 10 years or more in motor exhaust-related (MER) occupations, the age, smoking, and study area adjusted odds ratio (OR) for lung cancer was 1.5 (95% CI = 1.2-1.9). Risk was elevated for truck drivers (OR = 1.5; 95% CI = 1.1-1.9) and for other MER occupations (OR = 1.4; 95% CI = 1.1-2.0). The odds ratios associated with MER employment of 10+ years were 1.6 (95% CI = 1.2-2.1) for whites and 1.4 (95% CI = 0.9-2.1) for nonwhites; 1.2 (95% CI = 0.7-2.0) [corrected] for those with possible exposure to other recognized or reported lung carcinogens; and 1.6 (95% CI 1.2-2.1) for those without such exposure. The 50% excess risk for lung cancer associated with employment in motor exhaust-related occupations could not be explained by greater use of cigarettes or by other occupational exposures among these workers.     

Risk of lung cancer from exposure to dusts and fibers in Leningrad Province, Russia

BACKGROUND: Exposures to several dusts and fibers (DFs) have been established or suggested as etiologic factors for lung cancer. METHODS: To investigate lung cancer risk in relation to exposure to DFs, we identified 540 pathologically-diagnosed lung cancer cases and 582 controls from the 1993-1998 autopsy records of the 88 hospitals of Leningrad Province, Russia. Lifetime job-specific exposure measurements were available for 15 organic, 15 man-made and 28 natural-inorganic agents. RESULTS: In male workers, increased risks were found for linen dust (OR = 3.68, 95% CI 1.00-13.6, adjusted for age, smoking and residence), and unspecified DFs (OR = 1.44, 95% CI 1.07-1.94). Small non-significant excess risks were observed for quartz dust (OR = 1.27; 95% CI 0.83-1.93) and man-made vitreous fibers (MMVFs) (OR = 1.82, 95% CI 0.88-3.75). In female subjects, risks were non-significantly associated with paper dust (OR = 1.77, 95% CI 0.74-4.20), and unspecified DFs (OR = 1.52, 95% CI 0.77-3.03). CONCLUSIONS: The study showed increased lung cancer risk for selected categories of DFs.     

A case-control study of lung cancer among refinery workers

This case-control study examined the relationship between lung cancer and the work histories of male employees at a large Texas refinery. The study included 112 lung cancer deaths observed between 1946 and 1987 and 490 matched controls. Employment histories were obtained from personnel records, and smoking information was available from medical records. Both stratification methods and conditional logistic regression were used in data analyses. Overall employment in four general job categories (administrative, engineering/laboratory, process, maintenance/mechanical) was not associated with lung cancer mortality. Results by hire period (< 1940, 1940+) showed that workers hired into process jobs before 1940 had a nonsignificantly elevated odds ratio (OR) of 1.71 (95% confidence interval [CI] = 0.85-3.45) compared with nonprocess workers hired before 1940. Among process workers hired before 1940, there was a significant trend toward increasing OR with increasing duration of employment in process jobs, and the association with lung cancer was strongest among smokers in the highest duration category of 30+ years (OR = 2.98, 95% CI = 1.07-8.31). Latency analyses of process workers hired before 1940 indicated that their lung cancer risk had peaked between 30 and 50 years since first employment. Definitive statements about causal factors are limited because results among process workers were based on small numbers of subjects in some exposure categories, and there was no information on specific workplace exposures. The OR for maintenance/mechanical jobs after adjustment for smoking was 1.00 (95% CI = 0.55-1.82). Furthermore, there was no pattern in relation to duration of employment in maintenance/mechanical jobs. The results from this study do not support the hypothesis that work in maintenance/mechanical jobs increases lung cancer risk. On the basis of analyses in this study, it is unlikely that asbestos exposure contributed to excess lung cancer mortality. Additional analyses were conducted for specific maintenance jobs with potential exposure to asbestos and by duration in jobs with occasional or routine asbestos exposure. No significant increase in lung cancer was found in any subgroup. Furthermore, there was no significant trend toward lung cancer risk in relation to duration of employment in jobs with asbestos exposure.     

Diesel exhaust exposure and mortality among males in the American Cancer Society prospective study

In 1982, the American Cancer Society enrolled over 1.2 million American men and women in a prospective mortality study of cancer and other causes in relation to different risk factors. The 2-year mortality of 461,981 males aged 40-79 years with known smoking habit has been analyzed in relation to exposure to diesel exhaust (DE) and to employment in selected occupations related to DE exposure. The relative risk (RR) for all causes of death for those exposed was 1.05 (95% confidence interval [CI]: 0.97-1.13). For lung cancer, the RR was 1.18 (95% CI: 0.97-1.44). A dose-response effect was present. Railroad workers, heavy equipment operators, miners, and truck drivers had a higher mortality both for all causes and for lung cancer when compared with subjects with other occupations and no exposure to DE. Truck drivers exposed to DE were not at excess risk of lung cancer if compared with truck drivers unexposed to DE, but a trend of increasing risk with duration of exposure was suggested. DE exposure was also associated with increase in mortality for accidents, cerebrovascular disease, arteriosclerosis, and cirrhosis of the liver. An association based on small numbers was also present for Hodgkin's disease and lymphoid leukemia. No association with chronic non-neoplastic pulmonary diseases or with bladder cancer was found.     

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.     

Increased risk of lung cancer among different types of professional drivers in Denmark

OBJECTIVES: To study risk of lung cancer among groups of professional drivers probably exposed to different levels of traffic exhaust fumes. METHODS: A nationwide case-control study (1970-89) based on employees comprising 28,744 men with primary lung cancer and incidence density sampled matched controls (1:1). Employment histories were reconstructed back to 1964 for each study subject from the records of a nationwide pension scheme with compulsory membership. Socioeconomic status was derived from the individual job title taken from the national population registry. Information on tobacco smoking habits was available from historical surveys. Relative risks were estimated by odds ratios (ORs) based on conditional logistic regression analyses. RESULTS: In total 2251 of the male lung cancer cases had been employed as bus, lorry, taxi, or unspecified drivers. No significant difference in tobacco smoking habits was found among professional male Danish drivers and the total employed population. The OR for lung cancer adjusted for socioeconomic status was 1.6 (95% confidence interval (95% CI) 1.2 to 2.2) among taxi drivers, who were considered to be exposed to the highest concentrations of vehicle exhaust fumes, and 1.3 (1.2 to 1.5) for bus and lorry drivers. The OR was 1.4 (1.3 to 1.5) for unspecified drivers. The adjusted risk of lung cancer increased significantly with increasing duration of employment as a driver, and the risk was highest for long term taxi drivers with 10 years of lag time (OR 3.0; 1.2 to 6.8). CONCLUSION: Occupational factors, probably exposure to vehicle exhaust, seems to play an important part in the development of lung cancer among drivers.     

Occupational risks for laryngeal cancer: a case-control study

The most solidly established risk factors for laryngeal cancer are tobacco and alcohol. As for occupational factors, the only established carcinogen is exposure to strong inorganic acid mists. However, asbestos, pesticides, paints, gasoline, diesel engine emissions, dusts, and other factors have been reported in the literature as occupational agents that increase the risk of laryngeal cancer. A hospital-based case-control study was conducted to investigate occupational risk factors for laryngeal cancer. Detailed data on smoking, alcohol consumption, and occupational history were collected for 122 laryngeal cancers and 187 controls matched by frequency (according to sex and age). Laryngeal cancer was associated with exposure to respirable free crystalline silica (OR = 1.83; 95%CI: 1.00-3.36), soot (from coal, coke, fuel oil, or wood) (odds ratio - OR = 1.78; 95% confidence interval - 95%CI: 1.03-3.03), fumes (OR = 2.55; 95%CI: 1.14-5.67), and live animals (OR = 1.80; 95%CI: 1.02-3.19).     

A case-control study of occupational risk factors for laryngeal cancer.

To determine whether specific jobs and occupational exposures are associated with laryngeal cancer lifetime occupational histories from a population-based case-control study in western Washington were examined. The study included 235 cases diagnosed between September 1983 and February 1987, and 547 controls identified by random digit dialing. After controlling for alcohol use, cigarette smoking, age and education, significantly increased risks were found for painters in construction (odds ratio (OR)) = 2.8, (95% confidence interval (95% CI) 1.1-6.9), supervisors and miscellaneous mechanics (OR = 2.3, 95% CI 1.1-4.8), construction workers (OR = 3.4, 95% CI 1.4-8.1), metalworking and plastic working machine operators (OR = 2.6, 95% CI 1.3-4.9) and handlers, and equipment cleaners and labourers (OR = 1.5, 95% CI 1.0-2.2). Allowing for a 10 year induction and latent period did not have a consistent effect on the associations. Potential exposures to asbestos, chromium, nickel, formaldehyde, diesel fumes, and cutting oils were assessed by using a job exposure matrix developed for this study. Three measures of exposure were examined--namely, peak, duration, and an intensity weighted exposure score. No significantly raised risks were seen, although increased risk was suggested among those exposed long term to formaldehyde in jobs with the highest exposures.     

A case-control study of occupational risk factors for laryngeal cancer.

To determine whether specific jobs and occupational exposures are associated with laryngeal cancer lifetime occupational histories from a population-based case-control study in western Washington were examined. The study included 235 cases diagnosed between September 1983 and February 1987, and 547 controls identified by random digit dialing. After controlling for alcohol use, cigarette smoking, age and education, significantly increased risks were found for painters in construction (odds ratio (OR)) = 2.8, (95% confidence interval (95% CI) 1.1-6.9), supervisors and miscellaneous mechanics (OR = 2.3, 95% CI 1.1-4.8), construction workers (OR = 3.4, 95% CI 1.4-8.1), metalworking and plastic working machine operators (OR = 2.6, 95% CI 1.3-4.9) and handlers, and equipment cleaners and labourers (OR = 1.5, 95% CI 1.0-2.2). Allowing for a 10 year induction and latent period did not have a consistent effect on the associations. Potential exposures to asbestos, chromium, nickel, formaldehyde, diesel fumes, and cutting oils were assessed by using a job exposure matrix developed for this study. Three measures of exposure were examined--namely, peak, duration, and an intensity weighted exposure score. No significantly raised risks were seen, although increased risk was suggested among those exposed long term to formaldehyde in jobs with the highest exposures.     

Risk of lung cancer and exposure to industrial acids, solvents, and metals in leningrad province, Russia

OBJECTIVE: We sought to investigate the association of occupational exposure to industrial acids, solvents, and metals with lung cancer in Leningrad Province, Russia, where an excess of occupationally related lung cancer was reported recently. METHODS: We identified 540 pathologically diagnosed lung cancer cases and 582 controls from the 1993-1998 autopsy records of the 88 Leningrad Province hospitals. Lifetime job-specific exposure measurements were available for 12 industrial acids, 15 solvents, and 17 metals. RESULTS: Exposures were frequent in the study group and mostly occurred after World War II. However, lung cancer risks for industrial acids (odds ratio [OR] = 1.2; 95% confidence interval [CI] = 0.8-1.7), solvents (OR = 0.8; 95% CI = 0.6-1.2), and metals (OR = 0.8; 95% CI = 0.5-1.0) were not increased. Also, no significant excess risk was found for any of the specific agents investigated. CONCLUSIONS: The excess of occupationally related lung cancer in the Province is not explained by exposure to the agents investigated.     

Aggregation of lung cancer in families: results from a population-based case-control study in Germany

The authors investigated familial aggregation of lung cancer by means of a population-based case-control study, conducted in Germany between 1988 and 1993. They compared lung cancer prevalence in first degree relatives of 945 patients and 983 controls, accounting for various potential risk factors using logistic regression and generalized estimating equations. Some 83% of the study participants were male, and about 14% were below age 51 (young age group). Overall, lung cancer in parents or siblings was associated with a 1.67-fold (95% confidence interval (CI): 1.11, 2.52) increase in lung cancer risk. For the young participants, this risk was 4.75 (95% CI: 1.20, 18.77). Having multiple affected relatives (two or more) was related to a threefold risk elevation (odds ratio (OR) = 2.99, 95% CI: 0.32, 27.55). Paternal (OR = 1.64, 95% CI: 0.91, 2.96) but not maternal (OR = 0.91, 95% CI: 0.32, 2.61) lung cancer was associated with an increased risk of the disease. Lung cancer risk from smoking was particularly pronounced in the parents of cases (OR = 12.20, 95% CI: 3.34, 44.62 vs. OR = 7.93, 95% CI: 2.43, 25.91 in parents of controls). No risk elevation was detected for other smoking-related and other cancers in general. Results confirm previous findings and support the etiologic role of a genetic predisposition to lung cancer.     

Environmental tobacco smoke and lung cancer: a case-control study in Germany

To assess the association between exposure to environmental tobacco smoke (ETS) and lung cancer, the authors personally interviewed 292 lifelong nonsmoking lung cancer cases (recruited from 15 hospitals in the study area) and 1,338 nonsmoking controls (randomly selected by population registries) between 1990 and 1996 in Germany. Subjects were asked by a standardized questionnaire about exposure to ETS in childhood, by spouse, at work, and in transportation and social settings. Several indicators of these different sources of exposure were investigated, using not or low exposed subjects as the reference category. The most informative quantification index was weighted duration of exposure (hours x level of smokiness). No effect of ETS exposure during childhood and no clear effect of spousal ETS were observed. However, for the highest category of exposure, clear effects of ETS at the workplace (odds ratio (OR) = 1.93; 95% confidence interval (CI): 1.04, 3.58), in vehicles (OR = 2.64; 95% CI: 1.30, 5.36), and from all sources combined (OR = 1.39; 95% CI: 0.96, 2.01) were found. Adjustment for occupational carcinogens, radon, and diet did not appreciably change the results. These findings suggest that exposures to high levels of ETS at the workplace and in other public indoor settings appear to be important risk factors for lung cancer risk in nonsmokers.