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.     

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.     

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.     

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.     

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.     

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.     

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。     

Study of lung cancer histologic types, occupation, and smoking in Missouri

A case-control study of lung cancer was conducted to evaluate the relationship between lung cancer histologic types and occupation, adjusted for smoking. A total of 4,431 white male cases and 11,326 cancer controls, diagnosed between 1980 and 1985, were identified through the Missouri Cancer Registry. For all histologic types combined, excess risk was observed among many a priori suspected high-risk occupations. Lung cancer was elevated among men employed as insulators (odds ratio [OR] = 6.0; 95% confidence interval [CI] = 0.7, 137.8), carpenters (OR = 1.3; 95% CI = 1.0, 1.7), painters, plasterers, and wallpaper hangers (OR = 2.0; 95% CI = 1.2,3.3), structural metal workers (OR = 1.9; 95% CI = 0.6,6.0), mechanics and repairers (OR = 1.3; 95% CI = 1.0,1.7), motor vehicle drivers (OR = 1.5; 95% CI = 1.2,1.8), police and firefighters (OR = 1.6; 95% CI = 1.1,2.3), and food service personnel (OR = 1.8; 95% CI = 1.0,3.5). A deficit of lung cancer was observed among farmers (OR = 0.9; 95% CI = 0.7,1.0). Adenocarcinoma of the lung was elevated among carpenters (OR = 1.6; 95% CI = 1.0,2.5) and cabinet and furniture makers (OR = 2.0; 95% CI = 0.4,8.1), which is interesting because of the previous reports of excess adenocarcinoma of the nasal cavity associated with wood dust exposure. Adenocarcinomas were also elevated among plumbers (OR = 2.0; 95% CI = 1.0,3.8) and printers (OR = 1.8; 95% CI = 0.7,4.2). Electricians were at slightly increased risk for adenocarcinoma (OR = 1.5; 95% CI = 0.7,2.8) and "other" or mixed cell types of lung cancer (OR = 1.5; 95% CI = 0.8,2.9) but at decreased risk for small cell (OR = 0.8; 95% CI = 0.3,2.0) and squamous cell (OR = 0.8; 95% CI = 0.4,1.6) tumors. Among welders, adenocarcinoma (OR = 1.7; 95% CI = 0.7,3.8) and squamous cell (OR = 1.7; 95% CI = 0.9,3.3) cancers were elevated, but small cell and "other" lung cancers were not. Despite the limitations of the Cancer Registry data, some interesting associations were observed that merit further study, particularly the association between lung adenocarcinoma and occupational exposure to wood and wood dust.     

Reevaluation of the confounding effect of cigarette smoking on the relationship between alcohol use and lung cancer risk, with larynx cancer used as a positive control

BACKGROUND: The effect of smoking on lung cancer risk has been well documented, while the effect of alcohol remains controversial. We examined the hypothesis that the apparent association between alcohol intake and lung cancer risk is fully due to the confounding effect of cigarette smoke. METHODS: Our sample of hospitalized patients included 2,953 male and 1,622 female lung cancer cases; 521 male and 159 female larynx cancers cases; and 8,169 male and 4,154 female controls, admitted to participating hospitals between 1981 and 1994. All controls had been diagnosed with non-smoking-related diseases. Larynx cancer was used as a positive control for lung cancer. Relative risks were estimated through odds ratios, adjusted through multiple logistic regression. RESULTS: Although the odds ratios for alcohol had been significantly elevated prior to adjustment for smoking (OR = 2.4, 95% CI = 2.0-2.8), alcohol had no effect on lung cancer following this adjustment (OR = 1.2, 95% CI = 1.0-1.4). By contrast, the effect of alcohol on larynx cancer remained high even after adjustment for smoking (OR = 5.6, 95% CI = 3.7-8.6). CONCLUSION: The often-reported association between alcohol and lung cancer risk can be fully explained by the confounding effect of cigarette use.     

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.     

Lung cancer development in primary smelter workers: a nested case-referent study

OBJECTIVE: The objective of this study was to study the impact of work-related exposure to mainly arsenic and lead versus smoking in primary smelter workers developing lung cancer. METHODS: In a cohort of 3979 primary smelter workers, 46 subjects had contracted respiratory malignancies. They were compared with 141 age-matched male referents by conditional logistic regression analysis. RESULTS: Cases showed a significantly higher smoking rate as compared with referents: odds ratio (OR) = 4.0; 95% confidence interval (CI) = 1.6-10.1; P = 0.003. When restricted to smokers (33 cases, 63 referents), the cumulative air arsenic exposure index, but not the lead exposure indices, was significantly higher among the cases: OR = 1.07; 95% CI = 1.02-1.11; P = 0.005. CONCLUSIONS: Cumulative arsenic exposure and smoking were identified as risk factors for the development of lung cancer; lead exposure, however, was not.     

Lung cancer and indoor air pollution arising from Chinese-style cooking among nonsmoking women living in Shanghai, China.

Associations between indoor air pollution from Chinese-style cooking and lung cancer have been found in several investigations. To provide more detailed estimates of the associations while accounting for key confounding factors, we conducted a population-based, case-control study of lung cancer among nonsmoking women living in Shanghai, the People's Republic of China. Five hundred four incident, primary lung cancer cases diagnosed from February 1992 through January 1994 were identified through the population-based Shanghai Cancer Registry. A control group of 601 nonsmoking women was selected randomly from the Shanghai-Residential Registry, and they were frequency-matched to the expected age distribution of the cases. Exposure to indoor air pollutants from Chinese-style cooking was ascertained through in-person interviews. We estimated adjusted odds ratios (OR) and 95% confidence intervals (CI) by unconditional logistic regression. There were similar patterns of excess risk for exposure to indoor air pollutants from Chinese-style cooking across different histological types of lung cancer. Women who did not have a separate kitchen experienced a 28% increased risk of lung cancer (OR = 1.28; 95% CI = 0.98-1.68). We found little association with area of the windows of the apartment where subjects had lived for the longest period of time. Heating cooking oils to high temperatures was associated with a 1.64-fold increased risk of lung cancer (95% CI = 1.24-2.17). An 84% excess risk was found among women who most often cooked with rapeseed oil (OR = 1.84; 95% CI = 1.12-3.02). Lung cancer risks were also related to "considerable" smokiness of the kitchen during cooking (OR = 2.38; 95% CI = 1.58-3.57), frequent eye irritation during cooking (OR = 1.68; 95% CI = 1.02-2.78), to a more than weekly use of frying (OR = 2.09; 95% CI = 1.14-3.84) and deep-frying (OR = 1.88; 95% CI = 1.06-3.32). This population-based case-control study confirmed that exposure to indoor air pollution from Chinese-style cooking, especially cooking unrefined rapeseed oil at high temperatures in woks, may increase the risk of lung cancer.     

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.     

Sugarcane farming,occupational solvent exposures,and the risk of oral cancer in Puerto Rico

The work history information from a population-based case-control study conducted in Puerto Rico was analyzed using a job exposure matrix to investigate the relationship between occupational exposures and cancers of the oral cavity or pharynx. After adjustment for age, alcohol, smoking, and residence in a logistic model, the risk for cancer of the oral cavity, but not the pharynx, was significantly elevated among farm workers in the sugarcane industry (OR = 4.4, 95% CI = 1.4-13.6). An exposure-response trend was seen for cumulative exposure to solvents, with an OR = 3.2 (95% CI = 0.8-12.6) in the highest exposure category. The overall contribution to the risk of cancer of the oral cavity or pharynx associated with occupational exposures in Puerto Rico appears to be small, however, the elevated risks were seen among sugarcane farmers and subjects with high cumulative exposure to solvents.     

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).     

Lung and bladder cancer in a Norwegian municipality with iron and steel producing industry: population based case-control studies

OBJECTIVES: To investigate the influence of occupation on the rising incidence of lung and bladder cancer among men in a Norwegian municipality where an iron and steel plant constituted the key industry between 1955 and 1989. METHODS: Based on the lung cancer cases reported to the Cancer Registry of Norway from 1980 to 1992 a population based case-control study was performed, including 86 cases and 196 controls. Information on occupations and smoking habits was collected through interviews and from the personnel files from the industrial plants. A case-control study on bladder cancer with 52 cases and 156 controls was carried out to cast light on the role of polycyclic aromatic hydrocarbons (PAHs). RESULTS: An odds ratio (OR) for lung cancer of 2.9 (95% confidence interval (95% CI) 1.2 to 6.7) was associated with exposure to PAHs. Based on data from personnel files, increased risk of lung cancer (OR 2.8 95% CI 1.1 to 7.0) was associated with work experience in the pig iron department at the ironworks. A non- significant OR of 1.8 was associated with exposure to asbestos. Bladder cancer was not associated with exposure to PAHs at the iron, steel, and coke plant, or with experience from any of the production departments at the plant. CONCLUSIONS: One fifth of the lung cancer cases were attributed to exposure to PAHs or asbestos. More than 80% of the cases of lung cancer were attributed to tobacco smoking. The cancer risk in the pig iron department may be due to a combination of exposures to PAH, asbestos, or dust of mixed composition.

 

     

鞍钢工人的肿瘤危险度——肺癌病例-对照研究

对鞍钢男工中６１０例肺癌新发病例及９５９例对照进行了访问调查。经吸烟、其他肺疾患、家族肿瘤史、食用水果等非职业因素调整后，岗位工龄等于或超过１５年的下列工人的肺癌危险度显著增高：冶炼工和轧钢工（ＱＲ＝１．５，９５％ＣＩ＝１．１～２．２），耐火砖厂工（ＯＲ＝２．９，９５％ＣＩ＝１．４～５．９），装卸工（ＯＲ＝２．５，９５％ＣＩ＝１．０～６．１），焦炉工（ＯＲ＝３．４，９５％ＣＩ＝１．４～８．５）。各种粉尘和Ｂ［ａ］Ｐ暴露与肺癌危险性呈显著的剂量－反应关系，但与粉尘的特殊成分未见此种关联。长期暴露于污染物的钢铁工人的肺癌的危险度增加４０％。     

Nested case-control study of lung cancer in four Chinese tin mines

Objectives: To evaluate the relation between occupational dust exposure and lung cancer in tin mines. This is an update of a previous study of miners with high exposure to dust at four tin mines in southern China.

Methods: A nested case-control study of 130 male lung cancer cases and 627 controls was initiated from a cohort study of 7855 subjects employed at least 1 year between 1972 and 1974 in four tin mines in China. Three of the tin mines were in Dachang and one was in Limu. Cumulative total exposure to dust and cumulative exposure to arsenic were calculated for each person based on industrial hygiene records. Measurements of arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon in the work sites were also evaluated. Odds ratios (ORs), standard statistic analysis and logistic regression were used for analyses.

Results: Increased risk of lung cancer was related to cumulative exposure to dust, duration of exposure, cumulative exposure to arsenic, and tobacco smoking. The risk ratios for low, medium, and high cumulative exposure to dust were 2.1 (95% confidence interval (95% CI) 1.1 to 3.8), 1.7 (95% CI 0.9 to 3.1), and 2.8 (95% CI 1.6 to 5.0) respectively after adjustment for smoking. The risk for lung cancer among workers with short, medium, and long exposure to dust were 1.9 (95% CI 1.0 to 3.5), 2.3 (95% CI 1.3 to 4.1), and 2.3 (95% CI 1.2 to 4.2) respectively after adjusting for smoking. Several sets of risk factors for lung cancer were compared, and the best predictive model included tobacco smoking (OR=1.6, 95% CI 1.1 to 2.4) and cumulative exposure to arsenic (ORs for different groups from low to high exposure were 2.1 (95% CI 1.1 to 3.9); 2.1 (95% CI 1.1 to 3.9); 1.8 (95% CI 1.0 to 3.6); and 3.6 (95% CI 1.8 5 to 7.3)). No excess of lung cancer was found among silicotic subjects in the Limu tin mine although there was a high prevelance of silicosis. Exposures to radon were low in the four tin mines and no carcinogenic PAHs were detected.

Conclusions: These findings provide little support for the hypothesis that respirable crystalline silica induces lung cancer. Ore dust in work sites acts as a carrier, the exposure to arsenic and tobacco smoking play a more important part in carcinogenesis of lung cancer in tin miners. Silicosis seems not to be related to the increased 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.