Cigarette smoking and male lung cancer risk with special regard to type of tobacco.

BACKGROUND: The mortality rate from lung cancer (LC) increased sharply in Spain between 1957 and 1986. This increase has been related to a previous increase in cigarette smoking. Certain features of cigarette smoking which were frequent among Spanish smokers (use of black tobacco and use of cigarettes without filter) have been related to a higher risk of LC. METHODS: A hospital-based case-control study was conducted between December 1986 and June 1990. The 325 male patients with lung cancer included in the study (cases) were compared with 325 age-matched male controls without LC. Occupation and lifetime tobacco consumption were requested using a structured questionnaire. The LC odds ratios (OR) and 95% CI were estimated with multiple logistic regression. RESULTS: Lung cancer risk increased with cigarette consumption and duration of the habit. After adjusting for lifetime cigarette consumption and for socioeconomic level, LC risk was greater among black tobacco smokers than among exclusive blond tobacco smokers (OR = 5.0, 95% CI: 2.0-12.7); LC risk among long-term (> or =20 years) filter-tipped cigarette users was lower compared to all other smokers (OR = 0.4, 95% CI: 0.2-0.7). CONCLUSIONS: The main results of the study (a higher LC risk among black tobacco users than in exclusive blond tobacco users, and a lower LC risk among long-term filter-tipped cigarette smokers than all other smokers) have been consistent with previous case-control studies and with ecologic studies which took into account past exposure levels.     

CYP1A1和GSTM1基因多态与肺癌发病关系的病例-对照研究

目的 探讨肺癌易感性标记物CYP1A1及GSTM1基因多态以及吸烟等其他环境暴露因素与肺癌发生的关系。方法 采用病例-对照研究的方法，收集原发性肺癌病例91例以及非肺部疾患的住院病例(对照)91例，所有的研究对象均采静脉血进行DNA抽提，并用PCR方法检测CYP1A1以及GSTM1基因多态，同时调查研究对象吸烟等其他环境暴露因素。应用Logistic回归分析方法进行单因素和多因素的分析。结果 无论是单因素分析还是多因素分析均未显示出CYP1A1和GSTM1基因多态与肺癌发病的关联。多因素分析结果表明：化程度的OR为0．63(95％CI：0．45～0．86)，吸烟量的OR为1．56(95％CI：1．14～2．14)，无抽油烟机的OR为3．77(95％CI：1．48～9．56)，食用动物油的OR为1．67(95％CI：1.25～2．24)，常吃胡萝卜的OR为0．47(95％CI：0．22～0．98)，饮酒的OR为6．58(95％CI：1.53～28．30)，家族肺癌史的OR为3．75(95％CI：1．64～8．58)。结论 CYP1A1和GSTM1基因多态与肺癌发病无明显的关联，吸烟、饮酒、食用动物油、家族肺癌吏以及无抽油烟机是肺癌的危险因素，而高化程度和常吃胡萝卜与降低肺癌风险有关。     

Genetic polymorphisms in the base excision repair pathway and cancer risk: a HuGE review

Genetic variations in DNA repair genes are thought to modulate DNA repair capacity and are suggested to be related to cancer risk. However, epidemiologic findings have been inconsistent. The authors conducted meta-analyses of associations between genes in the base excision repair pathway and cancer risk, focusing on three key genes: 8-oxoguanine DNA glycosylase (OGG1), apurinic/apyrimidinic endonuclease (APE1/APEX1), and x-ray repair cross-complementing group 1 (XRCC1). They found increased lung cancer risk among subjects carrying the OGG1 Cys/Cys genotype (odds ratio (OR) = 1.24, 95% confidence interval (CI): 1.01, 1.53), using 3,253 cases and 3,371 controls from seven studies; this is consistent with experimental evidence that this isoform exhibits decreased activity. They found a protective effect of the XRCC1 194Trp allele for tobacco-related cancers (OR = 0.86, 95% CI: 0.77, 0.95), using 4,895 cases and 5,977 controls from 16 studies; this is compatible with evidence of lower mutagen sensitivity for this allele. The XRCC1 399Gln/399Gln genotype was associated with increased risk of tobacco-related cancers among light smokers (OR = 1.38, 95% CI: 0.99, 1.94) but decreased risk among heavy smokers (OR = 0.71, 95% CI: 0.51, 0.99), suggesting effect modification by tobacco smoking. There was no association between cancer risk and the APE1/APEX1 Asp148Glu and XRCC1 Arg280His polymorphisms. Recommendations for future studies include pooling of individual data to facilitate evaluation of multigenic effects and detailed analysis of effect modification by environmental exposure.     

Cigarette smoking and breast cancer.

An epidemiological case-control study was conducted in New York State, with 1617 primary breast cancer patients and an equal number of controls, to examine the relationship between cigarette smoking and breast cancer. Results showed no overall association between ever smokers versus never smokers and breast cancer risk (odds ratio [OR] = 1.03, 95% confidence interval [CI]: 0.90-1.19), nor was there any dose response trend observed with increased levels of smoking. In addition, no association was found with risk and age started smoking, age stopped smoking, amount smoked or total years smoked. Controlling for previously identified risk factors for breast cancer in the analysis did not significantly alter these relationships. Previous studies have found a difference in menopausal age among smokers compared to nonsmokers. The mean menopausal age was only slightly lower in smokers than in never smokers for both cases and controls. Breast cancer risk was observed to be close to unity for premenopausal women (OR = 0.97, 95% CI: 0.74-1.34) and postmenopausal women (OR = 1.06, 95% CI: 0.91-1.26). A recent study suggested breast cancer risk was more strongly related to starting smoking at a young age among women who smoked at least 25 or more cigarettes per day in the most recent year of smoking. This hypothesis was not supported by these data.     

Glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) null polymorphisms, smoking, and their interaction in oral cancer: a HuGE review and meta-analysis

The association between glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) null polymorphisms and oral cancer is not consistent across studies, and data on their interaction with smoking in oral cancer are lacking. The authors systematically searched PubMed and SciVerse Scopus for case-control studies examining the association between null genotypes of the GSTM1 and GSTT1 genes and oral cancer. Twenty-eight case-control studies published in English were identified. Summary odds ratios were derived via random-effects models. The summary odds ratio for the GSTM1 null genotype was 1.43 in Asians (95% confidence interval (CI): 1.14, 1.78; P < 0.01, I (2) = 73%) and 0.98 in Caucasians (95% CI: 0.76, 1.28; P = 0.91, I (2) = 0%). Case-only analysis of 6 studies (552 cases) showed an inverse multiplicative interaction between GSTM1 null polymorphisms and smoking (ever/high levels of smoking vs. never/low levels) (odds ratio (OR) = 0.51, 95% CI: 0.32, 0.82; P = 0.01, I (2) = 34%). The GSTT1 null genotype was not significantly associated with oral cancer in Asians (OR = 1.07, 95% CI: 0.82, 1.38; P = 0.63, I (2) = 65%) or Caucasians (OR = 1.04, 95% CI: 0.41, 2.65; P = 0.93, I (2) = 55%). In conclusion, the GSTM1 null genotype may be associated with a higher risk of oral cancer in Asians but not in Caucasians, and this effect may be modified by smoking status. The GSTT1 null genotype may not be associated with oral cancer.     

谷胱甘肽转硫酶M1、T1基因型及烟酒嗜好与胃癌易感性的关系

[目的]探讨谷胱甘肽转硫酶基因多态性M1（GSTM1）、T1（GSTT1）及烟酒嗜好与胃癌易感性的关系，并对GST基因多态性GSTT1、GSTM1与烟酒暴露在胃癌发生中的交互作用进行分析。[方法]采用1：1配对病例-对照研究方法和PCR技术，检测121例原发性胃癌患者和相应对照的GSTM1和GSTT1基因型，结合研究对象的烟酒嗜好，应用SAS统计分析系统，分析GSTM1和GSTT1基因型及烟酒暴露与胃癌发病的关系，并对基因-基因，基因-烟酒暴露在胃癌发生中的交互作用进行分析。[结果]GSTM1（-）基因型频率在病例组和对照组中分别占44．63％和33．88%，分布无显著性差异（χ^2=2．6436，P〉0．05），GSTT1（-）基因型频率在病例组和对照组中分别为52．89％和44．63名，分布也无显著性差异（χ^2=1．1650，P〉0．05）。吸烟者比非吸烟者发生胃癌的危险高（OR=2．538，95％CI：1．336～4．823）；饮酒者比非饮酒者发生胃癌的危险高（OR=2．097，95％CI：1．025～4．291）。同时携带GSTM1（-）和GSTT1（-）基因型者发生胃癌的危险性高于GSTM1（＋）和GSTT1（＋）基因型携带者（OR=2．097，95％CI：1．025～4．291）；同时有烟酒嗜好的个体发生胃癌的危险性高于无烟酒嗜好者（OR=2．330，95％CI：1．211～4．482）。携带GSTM1（-）和GSTT1（-）且有烟酒嗜好者，发生胃癌的危险显著高于携带GSTM1（＋）和GSTT1（＋）的无烟酒嗜好者（OR=3．600，95％CI：1．025～12．650）。[结论]吸烟、饮酒与胃癌易感性增加有关，GSTM1和GSTT1基因型及烟酒嗜好在胃癌发生中存在一定的交互作用。     

Cigarette smoking, genetic variants in carcinogen-metabolizing enzymes, and colorectal cancer risk

The risk of colorectal cancer associated with smoking is unclear and may be influenced by genetic variation in enzymes that metabolize cigarette carcinogens. The authors examined the colorectal cancer risk associated with smoking and 26 variants in carcinogen metabolism genes in 1,174 colorectal cancer cases and 1,293 population-based controls recruited in Canada by the Ontario Familial Colorectal Cancer Registry from 1997 to 2001. Adjusted odds ratios were calculated by multivariable logistic regression. Smoking for >27 years was associated with a statistically significant increased colorectal cancer risk (adjusted odds ratio (AOR) = 1.25, 95% confidence interval (CI): 1.02, 1.53) in all subjects. Colorectal cancer risk associated with smoking was higher in males for smoking status, duration, and intensity. The CYP1A1-3801-CC (AOR = 0.47, 95% CI: 0.23, 0.94) and CYP2C9-430-CT (AOR = 0.82, 95% CI: 0.68, 0.99) genotypes were associated with decreased risk, and the GSTM1-K173N-CG (AOR = 1.99, 95% CI: 1.21, 3.25) genotype was associated with an increased risk of colorectal cancer. Statistical interactions between smoking and genetic variants were assessed by comparing logistic regression models with and without a multiplicative interaction term. Significant interactions were observed between smoking status and SULT1A1-638 (P = 0.02), NAT2-857 (P = 0.01), and CYP1B1-4390 (P = 0.04) variants and between smoking duration and NAT1-1088 (P = 0.02), SULT1A1-638 (P = 0.04), and NAT1-acetylator (P = 0.03) status. These findings support the hypothesis that prolonged cigarette smoking is associated with increased risk of colorectal cancer and that this risk may be modified by variation in carcinogen metabolism genes.     

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).     

谷胱甘肽硫转移酶Mul—1（GSTM1）基因多态性与肺癌易感性关系的研究

目的　探讨中国汉族广东人群中谷胱甘肽硫转移酶 Mul- 1(GSTM1)基因缺失及吸烟与肺癌易感性的关系。　方法　采用病例 -对照研究方法 ,应用 PCR技术检测 91例肺癌患者、138例对照的 GSTM1基因多态性。　结果　GSTM1基因缺失在肺癌组和对照组中的频率分别为 6 1.5 %和 5 2 .9% ,OR=1.38(0 .80～ 2 .38)差异无统计学意义 (P>0 .0 5 ) ,与吸烟联合分析时发现 GSTM1基因缺失的 OR值为 3.0 7,比单纯吸烟对肺癌的 OR值 (1.87)大 (P<0 .0 1)。　结论　 GSTM1基因缺失与吸烟可能协同增加患肺癌的危险性     

Attributed risk to smoking for lung cancer,laryngeal cancer and esophageal cancer

OBJECTIVE: Lung, laryngeal and esophageal cancers have smoking as one of their main risk factors. The objective of this study was to evaluate the population attributed risk (PAR) of smoking for these forms of cancer. METHODS: The study was based in three case-control studies conducted in medium size cities in Brazil. Incident cases of lung cancer, laryngeal cancer and esophageal cancer seen at a hospital setting and diagnosed through biopsy were analyzed; controls were hospitalized patients with another diagnoses. Smoking was the exposure factor measured at three levels: non-smokers, former smokers and smokers, which were defined using a questionnaire applied by trained interviewers. For effect measure, odds ratio was used and the populational attributed risk for smoking was then calculated for a 95% CI. RESULTS: A total of 122 lung cancer cases and 244 controls, 50 cases of laryngeal cancer and 48 cases of esophageal cancer, and 96 controls for both of them were studied. The prevalence of smoking exposure was 34%, which is the overall prevalence of smoking in this city's adult population. Odds ratios (OR) for the PAR analysis were the adjusted OR for confounding variables from each study. Lung cancer PAR was 63% (95% IC, 0.58-0.68) for former smokers and 71% (95%IC, 0.65-0.77) for smokers. Larynx cancer PAR was 74% (95% IC, 0.70-0.78) and 86% (95%IC, 0.81-0.85) for former smokers and smokers, respectively. Esophageal cancer PAR was 54% (95%IC, 0.46-0.62) for smokers. CONCLUSION: Smoking is an avoidable risk factor and smoking cessation could be responsible for significant reductions in the incidence of these three forms of cancer.     

谷胱甘肽-S-转移酶M1基因多态与食管癌的Meta分析

目的 对谷胱甘肽-S-转移酶M1(GSTM1)基因多态与食管癌的关联性进行Meta分析。方法 以食管癌组与对照组人群基因型分布的OR值为效应指标,各资料间进行一致性检验,以确定采用固定或随机效应模型进行合并分析。发表偏倚评估用漏斗图法进行。结果 共收集国内外相关资料11篇,积累病例1190例,对照1964名,合并OR值为1.197(95％CI:0.846～1.692)。对其中5篇资料按吸烟与否分层,吸烟组合并OR值为1.523(95％CI:1.099～2.109);不吸烟组合并OR值为0.933(95％CI:0.469～1.692)。结论 GSTM1基因多态与食管癌的易感性无关,但携带GSTM1空白基因型的吸烟者患食管癌的危险性可能会增加。     

Glutathione S-transferase M1 (GSTM1) polymorphisms and lung cancer: a literature-based systematic HuGE review and meta-analysis

Multiple genes have been studied for potential associations with lung cancer. The gene most frequently associated with increased risk has been glutathione S-transferase M1 (GSTM1). The glutathione S-transferase enzyme family is known to catalyze detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins, and products of oxidative stress. In this review, the authors summarize the available evidence associating lung cancer with the GSTM1 gene. They describe results from an updated meta-analysis of 98 published genetic association studies investigating the relation between the GSTM1 null variant and lung cancer risk including 19,638 lung cancer cases and 25,266 controls (counting cases and controls in each study only once). All studies considered, the GSTM1 null variant was associated with an increased risk of lung cancer (odds ratio (OR) = 1.22, 95% confidence interval (CI): 1.14, 1.30), but no increase in risk was seen (OR = 1.01, 95% CI: 0.91, 1.12) when only the five largest studies (>500 cases each) were considered. Furthermore, while GSTM1 null status conferred a significantly increased risk of lung cancer to East Asians (OR = 1.38, 95% CI: 1.24, 1.55), such a genotype did not confer increased risk to Caucasians. More data regarding the predictive value of GSTM1 genetic testing are needed before population-based testing may be reasonably considered.     

Smoking and lung cancer in China: combined analysis of eight case-control studies.

Smoking is well established as a principal risk factor for lung cancer. The risk of lung cancer is about ten times higher in smokers in Western countries. In China, a number of epidemiological studies have investigated the association between lung cancer and smoking and in the present paper, a combined analysis of eight such case-control studies is described. The summary odds ratio (OR), calculated by the Mantel-Haenszel method, and attributable risk (AR) of lung cancer associated with smoking were calculated from the combined data which were obtained from a literature review. The eight case-control studies were conducted in Beijing, Shanghai, Shenyang, Nanjing, Harbin, Zhengzhou, Taiyuan, and Nanchang, yielding a total of 4081 lung cancer cases and 4338 controls. The summary OR of lung cancer associated with smoking was 2.17 (95% CI (confidence interval): 1.98-2.39). The OR were 3.09 (95% CI: 2.61-3.66) for males and 2.30 (95% CI: 1.96-2.69) for females. The AR were 38.2% for both sexes, 56.7% for males and 25.5% for females. Risks of 1.00, 1.03, 2.04, and 3.33 showed a dose-response relationship between lung cancer and number of cigarettes smoked per day. There were also significant dose-response relationships of lung cancer with duration of smoking (OR = 1.00, 1.02, 2.66), and age at start of smoking (OR = 1.00, 3.30, 2.36, 1.18). The OR and AR of lung cancer associated with smoking in China were much lower than those reported in Western countries and the possible reasons for this are discussed.     

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.     

EC-SOD和GSTM1基因多态性及吸烟与口腔癌风险关系研究

目的探讨细胞外超氧化物歧化酶(EC-SOD)和谷胱甘肽硫转移酶M1(GSTM1)基因多态性及吸烟与口腔癌风险之间的关系。方法利用病例-对照分子流行病学研究方法和聚合酶链反应技术对600例口腔癌患者和600健康正常对照者DNA进行EC-SOD和GSTM1基因分型,logistic回归方法估计基因、基因与吸烟的交互作用对口腔癌发病的危险度。结果 EC-SOD各基因型口腔癌病例组与对照组间的频率分别为在C/C型61.17%、78.50%,C/G型38.33%、21.50%,分布差异有显著性(P<0.01),EC-SOD(C/G)基因型使口腔癌的发生的危险性增加(OR=2.27,95%CI 1.73-4.02)。口腔癌组GSTM1(-)基因型频率(69.17%)显著高于对照组(44.17%)(P<0.01),GSTM1(-)基因型增加了口腔癌发生的危险性(OR=2.84,95%CI 1.95-4.47).基因突变的协同分析发现EC-SOD(C/G)/GSTM1(-)在口腔癌组和对照组中的分布频率分别为30.50%和6.67%,分布有显著性差异(P<0.01)。EC-SOD(C/G)/GSTM1(-)患口腔癌的风险性明显高于EC-SOD(C/C)/GSTM1(+)基因型者(OR=8.16,95%CI 3.73-12.91)。病例组的吸烟率显著高于对照组的吸烟率(P<0.01),吸烟显著提高口腔癌发生的危险性(OR=2.66,95%CI 1.45-4.36)。EC-SOD(C/G)及GSTM1(-)与吸烟有协同作用(OR=25.11,95%CI 12.37-36.62)。结论 EC-SOD(C/G)和GSTM1(-)是口腔癌的易患因素,二者对口腔癌的发生有协同作用,吸烟与口腔癌的易感性也有关,EC-SOD(C/G)和GSTM1(-)与吸烟在口腔癌的发生上具有相互促进作用。     

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

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

Meta- and pooled analysis of GSTT1 and lung cancer: a HuGE-GSEC review

Lung cancer is the most common malignancy in the Western world, and the main risk factor is tobacco smoking. Polymorphisms in metabolic genes may modulate the risk associated with environmental factors. The glutathione S-transferase theta 1 gene (GSTT1) is a particularly attractive candidate for lung cancer susceptibility because of its involvement in the metabolism of polycyclic aromatic hydrocarbons found in tobacco smoke and of other chemicals, pesticides, and industrial solvents. The frequency of the GSTT1 null genotype is lower among Caucasians (10-20%) than among Asians (50-60%). The authors present a meta- and a pooled analysis of case-control, genotype-based studies that examined the association between GSTT1 and lung cancer (34 studies, 7,629 cases and 10,087 controls for the meta-analysis; 34 studies, 7,044 cases and 10,000 controls for the pooled analysis). No association was observed between GSTT1 deletion and lung cancer for Caucasians (odds ratio (OR) = 0.99, 95% confidence interval (CI): 0.87, 1.12); for Asians, a positive association was found (OR = 1.28, 95% CI: 1.10, 1.49). In the pooled analysis, the odds ratios were not significant for either Asians (OR = 0.97, 95% CI: 0.83, 1.13) or Caucasians (OR = 1.09, 95% CI: 0.99, 1.21). No significant interaction was observed between GSTT1 and smoking on lung cancer, whereas GSTT1 appeared to modulate occupational-related lung cancer.     

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.     

GSTM1基因多态及膳食因素与肺癌关系的研究

目的 研究谷胱苷肽硫转移酶M1(GSTMl)基因多态性及膳食因素与广州地区肺癌发生的关系。方法 采用成组病例-对照研究方法，病例58例，对照62例，制定统一的调查表进行调查，用PCR检测GSTM1基因多态性。结果 GSTM1基因多态性与肺癌危险性关系无显著性差异(OR1．73，95％CI0．84～3．58)；Logistic单因素分析显示：胡萝卜摄入频率与肺癌发生的危险性呈负相关(OR0．24，95％CI0．10～0．58)，而用动物油脂炒菜与肺癌的发生呈正相关(OR5．34，95％CI1．13～20．16)。非条件logistic多因素回归分析校正吸烟等非膳食烹调因素后，胡萝卜摄入频率(OR0．18，95％C10．05～0．65)仍与肺癌发生负相关；不常吃胡萝卜联合GSTM1缺失发生肺癌的危险性显著增加(OR6．30，95％CI1．88～21．05)。结论 GSTM1基因单独作用时与肺癌关系不明显；用动物油脂炒菜显著增加肺癌发生的危险性。常摄入胡萝卜可显著降低肺癌发生危险性。GSTM1基因多态性与胡萝卜摄入间存在协同作用。     

Polymorphisms in CYP1A1, GSTM1, GSTT1 and lung cancer below the age of 45 years

BACKGROUND: A genetic component of early-onset lung cancer has been suggested. The role of metabolic gene polymorphisms has never been studied in young lung cancer cases. Phase 1 and Phase 2 gene polymorphisms are involved in tobacco carcinogens' metabolism and therefore in lung cancer risk. METHODS: The effect of metabolic gene polymorphisms on lung cancer at young ages was studied by pooling data from the Genetic Susceptibility to Environmental Carcinogens (GSEC) database. All primary lung cancer cases of both sexes who were Caucasian and 相似文献