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.     

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.

     

Effects of work related confounders on the association between silica exposure and lung cancer: a nested case-control study among Chinese miners and pottery workers

Objective The role of silica in the causation of lung cancer is an ongoing debate. In order to explore whether observed association between silica exposure and lung cancer is confounded by exposure to other occupational carcinogens, we updated a previously nested case-control study among a cohort of male workers in 29 Chinese mines and factories on the basis of an extended follow-up. Methods Five hundred and eleven lung cancer cases and 1,879 matched controls were selected. Exposure to respirable silica as well as relevant occupational confounders were quantitatively assessed based on historical industrial hygiene data. The relationship between exposure to silica and lung cancer was analyzed by conditional logistic regression analysis adjusted for exposure to arsenic, polycyclic aromatic hydrocarbons (PAHs), radon, and smoking. Results In a crude analysis adjusted for smoking only, a significant trend of increasing risk of lung cancer with exposure to silica was found for tin, iron/copper miners, and pottery workers. But after adjustment for relevant occupational confounders, no relationship between silica and lung cancer can be observed. Instead, there is a significant association between lung cancer mortality and cumulative exposure to inorganic arsenic (OR = 1.86, 95% CI: 1.14, 3.04 for each mg/m³-year increase) and carcinogenic PAHs (OR = 1.35, 95% CI: 1.08, 1.69 for each 100 μg/m³-year increase). Conclusion This analysis does not provide any evidence to show that exposure to silica causes lung cancer in the absence of confounding factors.     

The effect of asbestosis on lung cancer risk beyond the dose related effect of asbestos alone

Aims: To determine if the presence of asbestosis is a prerequisite for lung cancer in subjects with known exposure to blue asbestos (crocidolite). Methods: Former workers and residents of Wittenoom with known amounts of asbestos exposure (duration, intensity, and time since first exposure), current chest x ray and smoking information, participating in a cancer prevention programme (n = 1988) were studied. The first plain chest radiograph taken at the time of recruitment into the cancer prevention programme was examined for radiographic evidence of asbestosis according to the UICC (ILO) classification. Cox proportional hazards modelling was used to relate asbestosis, asbestos exposure, and lung cancer. Results: Between 1990 and 2002 there were 58 cases of lung cancer. Thirty six per cent of cases had radiographic evidence of asbestosis compared to 12% of study participants. Smoking status was the strongest predictor of lung cancer, with current smokers (OR = 26.5, 95% CI 3.5 to 198) having the greatest risk. Radiographic asbestosis (OR = 1.94, 95% CI 1.09 to 3.46) and asbestos exposure (OR = 1.21 per f/ml-year, 95% CI 1.02 to 1.42) were significantly associated with an increased risk of lung cancer. There was an increased risk of lung cancer with increasing exposure in those without asbestosis. Conclusion: In this cohort of former workers and residents of Wittenoom, asbestosis is not a mandatory precursor for asbestos related lung cancer. These findings support the hypothesis that it is the asbestos fibres per se that cause lung cancer, which can develop with or without the presence of asbestosis.     

Arsenic exposure, smoking, and lung cancer in smelter workers--a case-control study

A cohort of 3,916 Swedish copper smelter workers employed for at least 3 months between 1928 and 1967 was followed up through 1981. Arsenic exposure was estimated for different time periods at each workplace within the smelter. Detailed job records were linked to the exposure matrix, thus forming individual cumulative arsenic exposure measures for each smelter worker. Smoking history was collected for 107 lung cancer cases and 214 controls from the cohort. Lung cancer risks were positively related to cumulative arsenic exposure with smoking standardized relative risks ranging from 0.7 to 8.7 in different exposure groups. A negative confounding by smoking was suggested in the higher exposure categories. The interaction between arsenic and smoking for the risk of developing lung cancer was intermediate between additive and multiplicative and appeared less pronounced among heavy smokers.     

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.     

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).     

Arsenic methylation and skin cancer risk in southwestern Taiwan

Arsenic is a known carcinogen, but data are especially lacking on the health effects of low-level exposure, and on the health significance of methylation ability. We conducted a case-control study (76 cases and 224 controls from 1996 to 1999) in southwestern Taiwan to explore the association among primary and secondary arsenic methylation index (PMI and SMI, respectively), cumulative arsenic exposure (CAE), and the risk of skin cancer. As compared with the controls, the skin cancer group reported more sun exposure (P = 0.02) and had a lower BMI (P = 0.03), as well as lower education level (P = 0.01). Skin cancer patients and controls were similar with regard to age, gender, smoking and alcohol consumption. Given a low SMI (< or = 5), CAE > 15 mg/L-year was associated with an increased risk of skin cancer (OR, 7.48; 95% CI, 1.65-33.99) compared to a CAE < or = 2 mg/L-year. Given the same level of PMI, SMI, and CAE, men had a higher risk of skin cancer (OR, 4.04; 95% CI, 1.46-11.22) when compared to women. Subjects with low SMI and high CAE have a substantially increased risk of skin cancer. Males in all strata of arsenic exposure and methylation ability had a higher risk of skin cancer than women.     

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).     

毒物代谢酶基因多态性与职业性慢性苯中毒危险性的单纯病例研究

目的研究环境暴露因素与毒物代谢酶基因多态性对发生慢性苯中毒危险性的影响.方法以152例慢性苯中毒工人为研究对象,应用单纯病例方法进行分析.结果中等强度接触组慢性苯中毒工人GSTT1基因缺失突变的发生率明显高于低接触组,差异有显著性(68.63%vs38.00%,ORadj=4.32,95%CI1.75～10.66,p=0.002);NQO1 C.609T/T基因在饮酒组的比例明显高于不饮酒组,差异有显著性(61.11%vs20.00%,ORadi=8.03,95%CI 2.28～28.25,P=0.001),在吸烟又同时饮酒组的比例明显高于其他组,差异有显著性(85.71%vs22.76%,ORadj=18.62,95%CI2.01～172.72,P=0.01),在饮酒×接触等级组的比例明显高于非饮酒×接触等级组,差异有显著性(61.11%vs 20.00%,ORadj=3.18,95%CI 1.55～6.52,P=0.002);GSTM1基因缺失突变在饮酒×接触等级组的比例明显高于非饮酒×接触等级组,差异有显著性(66.67%vs47.06%,0Radj=1.99,95%CI 1.05～3.76,P=0.036).结论 GSTT1的基因多态与中等强度苯接触存在交互作用;不同强度的苯接触同饮酒一起与GSTM1基因缺失突变增加了个体发生慢性苯中毒的风险性;NQ01基因C.609位点的多态与饮酒存在交互作用,而吸烟*饮酒与NQO1基因多态的交互作用更是增加了苯中毒的风险性.     

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.     

Protective effect of selenium on lung cancer in smelter workers.

A possible protective effect of selenium against lung cancer has been indicated in recent studies. Workers in copper smelters are exposed to a combination of airborne selenium and carcinogens. In this study lung tissue concentrations of selenium, antimony, arsenic, cadmium, chromium, cobalt, lanthanum, and lead from 76 dead copper smelter workers were compared with those of 15 controls from a rural area and 10 controls from an urban area. The mean exposure time for the dead workers was 31.2 years, and the mean retirement time after the end of exposure 7.2 years. Lung cancer appeared in the workers with the lowest selenium lung tissue levels (selenium median value 71 micrograms/kg wet weight), as compared with both the controls (rural group, median value 110; urban group, median value 136) and other causes of death among the workers (median value 158). The quotient between the metals and selenium was used for comparison: a high quotient indicating a low protective effect of selenium and vice versa. The median values of the quotients between antimony, arsenic, cadmium, lanthanum, lead, chromium, and cobalt versus selenium were all numerically higher among the cases of lung cancer, the first five significantly higher (p less than 0.05) in 28 of the 35 comparisons between the lung cancer group and all other groups of smelter workers and controls. The different lung metal concentrations for each person were weighted according to their carcinogenic potency (Crx4 + Asx3 + Cdx2 + Sbx1 + Cox1 + Lax1 + Pbx1) against their corresponding selenium concentrations. From these calculations the protective effect of selenium was even more pronounced.     

Protective effect of selenium on lung cancer in smelter workers

A possible protective effect of selenium against lung cancer has been indicated in recent studies. Workers in copper smelters are exposed to a combination of airborne selenium and carcinogens. In this study lung tissue concentrations of selenium, antimony, arsenic, cadmium, chromium, cobalt, lanthanum, and lead from 76 dead copper smelter workers were compared with those of 15 controls from a rural area and 10 controls from an urban area. The mean exposure time for the dead workers was 31.2 years, and the mean retirement time after the end of exposure 7.2 years. Lung cancer appeared in the workers with the lowest selenium lung tissue levels (selenium median value 71 micrograms/kg wet weight), as compared with both the controls (rural group, median value 110; urban group, median value 136) and other causes of death among the workers (median value 158). The quotient between the metals and selenium was used for comparison: a high quotient indicating a low protective effect of selenium and vice versa. The median values of the quotients between antimony, arsenic, cadmium, lanthanum, lead, chromium, and cobalt versus selenium were all numerically higher among the cases of lung cancer, the first five significantly higher (p less than 0.05) in 28 of the 35 comparisons between the lung cancer group and all other groups of smelter workers and controls. The different lung metal concentrations for each person were weighted according to their carcinogenic potency (Crx4 + Asx3 + Cdx2 + Sbx1 + Cox1 + Lax1 + Pbx1) against their corresponding selenium concentrations. From these calculations the protective effect of selenium was even more pronounced.     

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.     

The Occupational Cancer Incidence Surveillance Study (OCISS): risk of lung cancer by usual occupation and industry in the Detroit metropolitan area

This case-referent study assesses occupational risk factors associated with lung cancer, utilizing colon and rectum cancer referents. Complete occupational and tobacco use histories were obtained by telephone interview for 5,935 incident lung cancer cases and 3,956 incident colon and rectum cancer referents. The analysis included 43 usual occupational groups and 48 usual industry groups comprised of at least 10 cases. Among all cases, there were significant elevated risks for excavating and mining workers (OR = 4.01), furnace workers (OR = 3.11), armed services personnel (OR = 3.10), agricultural workers (OR = 2.05), driver sales (OR = 2.21), mechanics (OR = 1.72), painters (OR = 1.96), and drivers (OR = 1.88). Industries with significant elevated lung cancer risk included farming (OR = 2.21), mining (OR = 2.98), and primary ferrous metals manufacturing (OR = 2.43). Analyses of white and black men separately revealed that the excess of lung cancer among mechanics is restricted to black males (OR = 4.16). The risk of lung cancer among armed services personnel is higher among black men (OR = 10.54) than among white men (OR = 3.06). Five of the occupations observed more often among lung cancer cases have probable exposure to diesel exhaust.     

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。     

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 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.     

Nested case-control study of lung cancer among pulp and paper workers in relation to exposure to dusts

BACKGROUND: Numerous studies have indicated an increased risk of lung cancer in pulp and paper industry workers. In a 1990 survey, standardized mortality ratio (SMR) was found to be 122 (95% CI:96-153) for lung cancer in Polish male workers in the pulp and paper industry, and 166 (95% CI:95-270) among workers engaged in paper production. METHODS: A nested case-control design within a cohort of pulp and paper workers was applied. Seventy-nine lung cancer cases and 237 "healthy" controls were selected from the cohort of 10,460 workers employed during the years 1968-1990, and observed until the end of 1995. Based on personnel files, occupational exposure was reconstructed by experts. Using a questionnaire, data on smoking habits were collected. ORs unadjusted and adjusted for smoking were calculated applying the model of conditional logistic regression. RESULTS: Occupational exposure to inorganic dusts (kaolin, lime, cement, brick, grindstone) adjusted for smoking was a significant lung cancer risk factor, with a 4.0-fold risk (95% CI:1.3-12.6), and a dose-response by cumulative dose index. Among organic dusts only wood dust increased albeit insignificantly the risk for those exposed (adjusted for smoking OR = 2.1, 95% CI:0.9-4.9), but without dose-response relationship. CONCLUSIONS: Exposure to occupational dust with relatively low content of silica, but at high concentrations may be considered as a factor increasing lung cancer risk. However, the observation made in this study should be viewed with caution as it was based on a small number of cases, and further evidence is needed to confirm or refute the authors' hypothesis.