饮茶与膀胱癌关系的上海市区全人群病例对照研究

目的:研究饮茶与膀胱癌的关系。方法:1996年1月~1999年6月,在上海市区开展了一项基于全人群的膀胱癌病例-对照研究,共访问了608例膀胱癌病例和607例健康对照。采用非条件logistic回归模型计算比数比(OR)和95%可信区间(CI)来衡量饮茶与膀胱癌的关系。结果:饮茶对非吸烟男性膀胱癌有保护作用,OR=0.58(95%CI:0.33~1.00);且随着饮茶量的增加,膀胱癌的危险性降低。以从不饮茶者为参比组,每月饮茶<150 g、150~200 g和>200 g者的OR值分别为0.92(95%CI:0.40~2.15)、0.42(95%CI:0.16~1.12)和0.52(95%CI:0.27~1.00),趋势检验有统计学意义(P=0.027),分析中调整了年龄、职业、饮酒、膀胱感染和体质指数等混杂因素。在男性吸烟者中,由于吸烟因素本身的作用较强,未见饮茶的保护作用。由于样本量限制,未观察到饮茶对女性的保护作用。结论:饮茶(特别是绿茶)有可能是非吸烟男性膀胱癌的保护因素。     

吸烟和环境烟草烟雾暴露与女性肺癌的关系的病例──对照研究

在上海市区进行了女性肺癌病例—对照研究中共调查新病例649例，对照675例。资料分析表明各种组织学类型肺癌都与吸烟有联系．其中鳞癌和小细胞癌与吸烟关系非常密切．OR分别为5.6和9．9，吸烟使腺癌危险性略有增加，OR=1.195％可信阳=0.7～1.7,吸烟对肺癌总的相对危险度为2.4（95％可信限=1.8～3.3）。各类肺癌的危险性均随每日吸烟量的增加、吸烟年限的延长和开始吸烟年龄的提前而增加。鳞癌和小细胞癌危险性上升速度最快，腺癌危险性增加缓慢，且趋势不显著。本研究还发现工作环境中的环境烟草烟雾暴露使女性非吸烟者肺癌危险性增加到1.5倍，95％可信限=1．1～2.0。未发现儿童期父母吸烟和成年期丈夫吸烟增加女性非吸烟者肺癌危险性。     

GSTM1、GSTT1基因多态性和吸烟与膀胱癌关系的病例对照研究

目的:应用全人群为基础的病例对照研究探讨GSTM1、GSTT1基因多态性和吸烟与膀胱癌危险性的关系。方法:采用多重PCR方法对404例正常对照和414例膀胱癌病例的基因组DNA进行GSTM1和GSTT1基因分型,应用非条件logistic回归分析方法进行统计分析。结果:与携带GSTM1( )基因型者比,GSTM1(-)基因型的男、女性患膀胱癌危险性分别为1.66(95%CI:1.18～2.33)和1.08(95%CI:0.59～1.98)。同样携带GSTM1(-)基因型,吸烟者比不吸烟者患膀胱癌的危险性更加明显。与不吸烟且携带GSTM1( )基因型男性比,GSTM1(-)基因型的目前吸烟者的OR值为2.99(95%CI:1.56～5.74),而携带GSTM1(-)基因型同时吸烟年限≥40年者OR为4.33(95%CI:2.14～8.73)。尽管女性吸烟例数较少,但携带GSTM1(-)基因型的吸烟女性患膀胱癌危险性显著高于不吸烟的GSTM1( )基因型者,OR值为6.72(95%CI:1.69～26.80)。与不吸烟且携带GSTT1( )基因型男性相比,携带GSTT1(-)基因型的吸烟者患男性膀胱癌危险的OR值为1.38(95%CI:0.79～2.42)。携带GSTT1(-)基因型的吸烟女性患膀胱癌危险性是不吸烟的GSTT1( )基因型者的3.04倍(95%CI:0.77～12.01)。结论:GSTM1(-)基因型能显著增加男性患膀胱癌的风险,该基因型与吸烟可能有一定的联合作用。GSTT1基因型可能与上海市区男、女性膀胱癌无关。     

饮酒与膀胱癌关系的全人群病例对照研究

目的探讨饮酒与膀胱癌发生的关系。方法采用全人群为基础的病例对照研究,共调查1996年1月1日~1998年12月31日期间确诊的上海市区膀胱癌新发病例608例,健康人群对照607例。采用非条件logistic回归分析,调整吸烟等可能的混杂因素,以估计饮酒对膀胱癌发生的危险度及其95%可信区间。结果与不饮酒者相比,男、女性饮酒者患膀胱癌相对危险度分别是1.22(95%CI0.94~1.59)、0.50(95%CI0.13~1.90)。男性随总酒精摄入量增加患膀胱癌的危险有增加趋势,OR值分别为1.10(1~80g/d)和1.56(>80g/d)(趋势检验P=0.043)。男性总酒精摄入量与饮酒年限的联合作用分析表明,与不饮酒者相比,总酒精摄入量超过80g/d、饮酒年限超过40年者患膀胱癌危险度为2.11(95%CI1.11~4.01)。将饮酒分3层、吸烟分4层进行男性饮酒与吸烟的联合作用分析,结果显示总酒精摄入量>80g/d且吸烟≥35包年者的OR值为2.78(95%CI1.46~5.28)。未发现各饮酒种类与男性膀胱癌有显著关联。在不吸烟男性组中的分析显示,饮酒习惯的OR值均没有统计学意义。结论饮酒可能与男性膀胱癌有一定联系,但作用较弱,似乎主要表现为对吸烟男性的作用。     

吸烟与原发性肝癌关系的巢式病例对照研究

目的 分析吸烟与上海市区中老年男性原发性肝癌的关系.方法 应用巢式病例对照研究方法,对一个18 244名男性队列随访11年,以队列中213例新发肝癌患者作为病例组,按照患者年龄、采样日期、同居住区等配对条件,从队列中随机抽取1094名健康人作为对照组.使用配对Logistic回归分析,调整可能的混杂因素,估计吸烟对肝癌发生的危险度和95%可信区间(CI).结果 调整肝炎、肝硬化、胆石症或其他胆囊病史及乙型肝炎病毒感染等可能的混杂因素后,男性吸烟者患肝痛的危险性是不吸烟者的1.91倍(95%CI为1.28～2.86),日随着每天吸烟量、吸烟年限和吸烟包年数的增加而增加.每天吸烟≥20支者、吸烟≥40年者和吸烟37包年者患肝癌的相对危险度分别为2.16(95%CI为1.37～3.40)、2.14(95%CI为1.18～3.87)和2.12(95%CI为1.21～3.74).吸烟开始年龄越小,危险性越大,吸烟开始年龄<20岁者患肝癌的危险性为2.57(95%CI为1.50～4.40).结论 吸烟是上海市区男性原发性肝癌的危险因素.     

上海市区非吸烟女性肺癌病例对照研究的多因素分析

目的：为了进一步探索、验证上海市区非吸烟女性肺癌的危险因素。方法：1992年2月－1993年12月在上海市区进行女性肺癌的病例对照研究,共调查非吸烟女性肺癌病例498例及人群对照595例。结果：烹调油烟、腌制品摄入、工作环境烟草烟雾和肺癌家族史增加上海市区非吸烟女性肺癌的危险性,而饮茶,尤其是饮绿茶和新鲜瓜果,蔬菜的摄入和非吸烟女性肺癌呈负相关关系。结论：烹调油烟、腌制品、工作环境烟草烟雾和肺癌家族史可能是上海市区非吸烟女性肺癌的主要危险因素,而饮茶、多吃新鲜瓜果蔬菜对非吸烟女性肺有保护作用。     

工作环境烟草暴露与肺癌发生危险的系统评价

背景与目的已有的研究表明:工作环境烟草暴露与非吸烟人群肺癌发生有密切关系并不十分明确,本研究旨在探讨工作环境烟草暴露与非吸烟人群肺癌发生危险的关系。方法通过计算机检索Medline(1954年-2010年8月)、CENT L(the Cochrane central register of controlledtrials)(2010issue3)、EMBASE(1970年-2010年8月)中国生物医学文献数据库系统(CBM)(1978年-2010年8月)、中国期刊全文数据库(CNKI)(1979年-2010年8月)、中文科技期刊全文数据库(VIP)(1989年-2010年8月)等数据库,收集国内外公开发表的关于工作环境烟草暴露与非吸烟人群肺癌发生关系的研究文献,应用统计软件Stata11.0进行数据分析,计算其合并优势比(oddsratio,OR)和95%置信区间(con dence interval,CI)。采用Begg法对发表偏倚进行量化检测。结果最终纳入分析的文章共有22篇,合并分析结果表明工作环境烟草暴露使非吸烟人群肺癌发生率增加了25%(OR=1.25,95%CI:1.13-1.39,P<0.001),使非吸烟女性肺癌的发生率增加了22%(OR=1.22,95%CI:1.05-1.42,P=0.011);工作环境烟草暴露导致非吸烟男性肺癌的发生率增加了54%,但无统计学意义(OR=1.54,95%CI:0.74-3.18,P=0.247)。结论工作环境烟草暴露是非吸烟人群肺癌发生的一个危险因素,非吸烟女性工作环境的烟草暴露与肺癌的发生关系密切。     

吸烟与肺癌的研究进展

在1950年统计学上第一次证实吸烟与肺癌的联系。据研究一个吸烟成为人们的习惯的国家里，80％—95％的肺癌、75％的支气管炎、40％膀胱癌及肾癌、25％的缺血性心脏病的死亡是由于吸烟。非吸烟者因被动吸烟（吸入他人烟雾）患肺癌可能将上升25％—35％。吸烟与其他职业暴露也明显增加肺癌的发生（如石棉增加50倍），烟草燃烧时，释放出致癌物40多种，癌诱发物10多种，吸烟持续时间是引起肺癌的最重要因素，吸烟或每增加一倍，肺切发生的可能上升近20倍。香烟与烟雾中含8000多种化学物质。一、烟草使用据估计，工业化国家15岁以上41％男性、21…     

主动吸烟所致中国人群消化系统恶性肿瘤风险的meta分析

目的 探讨主动吸烟所致中国人群消化系统恶性肿瘤的风险大小,为制定中国控烟政策及评估烟草使用所致中国人群疾病负担提供必要参数。方法 在PubMed、Web of science、Embase、CNKI、维普、万方、Sinomed数据库中检索从建库至2021-06-31发表的关于吸烟与消化系统恶性肿瘤关系的文献,主题词包括烟草、吸烟、香烟、吸烟者、抽烟者、尼古丁、队列、病例对照、中国和中国人,使用Stata 16.0进行Meta分析,探究相对风险值(RR)。结果 共纳入88篇文献,相比不吸烟者,吸烟、现在吸烟、戒烟者消化系统恶性肿瘤合计的RR(95%CI)分别为1.94(1.77～2.13)、1.95(1.52～2.51)、2.06(1.41～3.02)。吸烟者男性RR(95%CI)为1.42(1.32～1.52),略高于女性的1.30(1.20～1.41);现在吸烟和戒烟者中女性文献仅1篇,且RR无统计学意义,男性均有统计学意义。吸烟者男性食管癌的RR(95%CI)为1.92(1.63～2.25),高于胃癌的1.30(1.19～1.41)、肝癌的1.25(1.14～1.36);女性食管癌...     

吸烟、饮酒与胃癌关系的病例对照研究

目的 探讨吸烟、饮酒与胃癌发生的关系。方法 采用全人群病例对照研究,共调查1999年4月－1999年10月期间诊断的上海市区新发胃癌病例311例,对照1579例（注：本课题为“九五”中乳腺癌、肺癌及胃癌病例－对照之一,对照共用）。采用非条件logistic回归分析,调整可能的混杂因素,以估计吸烟、饮酒对胃癌发生的比数比和95％的可信区间。结果 吸烟与男性胃癌发生有关,调整OR为1．67（95％CI：1．14－2．460,并且随着吸烟年龄的提前（P＜0．01）、吸烟年限的延长（P＜0．05）、每日吸烟量的增加（P＜0．05）和吸烟包－年（P＜0．01）,患胃癌的危险性显著增大;未发现女性吸烟与胃癌发生有显著性联系。进一步调整整烟,发现饮酒与胃癌无密切关系,但重度饮酒可能与女性胃癌发生有关。进一步研究饮酒的作用,分析吸烟与饮酒状况及吸烟支数与酒精克数不同剂量分层之间的交互作用,调整年龄、文化程度（仅女性）、腌制食品、新鲜水果及慢性胃炎后,发现男性饮酒与吸烟不同剂量之间有交互作用存在,交互项χ^2值为5．20,P＝0．02,即饮酒增加男性吸烟者患癌的危险。结论 进一步证实吸烟是胃癌发生的危险因素;单独饮酒与胃癌发生无明显关系,饮酒不是胃癌的一项独立危险因素;饮酒增加吸烟患胃癌的危险,两者有协同作用。     

Environmental tobacco smoke and bladder cancer risk in never smokers of Los Angeles County

Cigarette smoking is a major risk factor for bladder cancer and a prominent point source of 4-aminobiphenyl (4-ABP), a recognized human bladder carcinogen. 4-ABP-hemoglobin (Hb) adducts are established biomarkers of 4-ABP exposure in humans. The role of environmental tobacco smoke (ETS) in the etiology of bladder cancer is largely unknown. As part of a large population-based bladder cancer study in Los Angeles County, California, lifetime exposure to ETS was ascertained for 148 cases and 292 control subjects who had never used any tobacco products over their lifetime. 4-ABP-Hb adducts were quantitatively measured on 230 control subjects. Female lifelong nonsmokers living with two or more smokers during childhood were significantly related to risk of bladder cancer [odds ratio (OR), 3.08; 95% confidence interval (95% CI), 1.16-8.22]. During adulthood, approximately 2-fold risks were seen among women living with a spouse/domestic partner who smoked for > or =10 years or having a coworker who smoked in an indoor environment for > or =10 years. When all sources of ETS exposure were combined, a statistically significant, dose-dependent association (P for trend = 0.03) was noted in women, with the OR for the highest category of ETS exposure being 5.48 (95% CI, 1.06-28.36). Levels of 4-ABP-Hb adducts varied by ETS exposure status among female control subjects. Mean level was lowest in women never exposed to ETS (16.4 pg/g Hb) and highest in those with current ETS exposure (23.6 pg/g Hb). ETS exposure was associated with neither bladder cancer risk nor 4-ABP-Hb adduct levels in male lifelong nonsmokers. In conclusion, ETS is a risk factor for bladder cancer in women who were lifelong nonusers of any tobacco products.     

Environmental tobacco smoking, mutagen sensitivity, and head and neck squamous cell carcinoma.

Although active tobacco smoking has been considered a major risk factor for head and neck cancer, few studies have evaluated environmental tobacco smoke (ETS) and its interaction with mutagen sensitivity on the risk of head and neck cancer. We investigated the relationship between ETS and head and neck cancer in a case-control study of 173 previously untreated cases with pathologically confirmed diagnoses of squamous cell carcinoma of the head and neck and 176 cancer-free controls at Memorial Sloan-Kettering Cancer Center between 1992 and 1994. A structured questionnaire was used to collect ETS exposure and other covariates including a history of active tobacco smoking and alcohol use. ETS measures include a history of ETS exposure at home and at workplace. The associations between passive smoking and head and neck cancer were analyzed by Mantel-Haenszel methods and logistic regression models. Additive and multiplicative models were used to evaluate effect modifications between ETS and mutagen sensitivity. The crude odds ratio (OR) for ETS exposure was 2.8 [95% confidence intervals (CI), 1.3-6.0]. Controlling for age, sex, race, education, alcohol consumption, pack-years of cigarette smoking, and marijuana use, the risk of squamous cell carcinoma of the head and neck was increased with ETS (adjusted OR, 2.4; 95% CI, 0.9-6.8). Dose-response relationships were observed for the degree of ETS exposure; the adjusted ORs were 2.1 (95% CI, 0.7-6.1) for those with moderate exposure and 3.6 (95% CI, 1.1-11.5) for individuals with heavy exposure (P for trend = 0.025), in comparison with those who never had ETS exposures. These associations and the dose-response relationships were still present when the analysis was restricted to nonactive smoking cases and controls (crude OR, 2.2; 95% CI, 0.6-8.4). Crude odds ratios were 1.8 for those with moderate ETS exposure and 4.3 for individuals with heavy ETS exposure among nonsmoking cases and controls (P for trend = 0.008). More than multiplicative interaction was suggested between passive smoking and mutagen sensitivity. This study suggests that ETS exposure may increase the risk of head and neck cancer with a dose-response pattern. Our analysis indicated that passive smoking may interact with mutagen sensitivity and other risk factors to increase the risk of head and neck cancer. Our results need to be interpreted with caution because of potential residual confounding effects of active tobacco smoking and other methodological limitations. Future large-scale studies are warranted to confirm our findings.     

Passive smoking and lung cancer in Chandigarh, India.

The aim of this study is to assess the relationship between exposure to environmental tobacco smoke (ETS) and lung cancer in non-smokers, a case-control study among lifetime non-smokers was conducted in Chandigarh, India. Cases consisted of 58 non-smoking histologically confirmed lung cancer patients; two controls for each case were selected, one among other patients admitted to the wards and one among the visitors to hospital patients. Subjects were asked about ETS exposure from different tobacco products in childhood and in adulthood at home, at the work place and in vehicles. Multivariate logistic regression analysis was used to assess the effects of the ETS exposure variables on lung cancer. Exposure to ETS during childhood was strongly associated with lung cancer (odds ratio (OR) = 3.9; 95% confidence interval (CI) = 1.9-8.2), the effect mostly arising from exposure to cigarettes smoke. The excess risk was observed with either a smoking father or mother. An increasing risk was found with increasing number of smokers and duration of exposure. Restricting the analysis to women produced higher estimates of the risk. No increased risk was found with exposure to a smoking spouse, except for those exposed only to cigarette smoke (OR = 5.1; 95% CI = 1.5-17). A weak association was seen between lung cancer and ETS exposure at the workplace, which increased with the number of years of exposure. Exposure in vehicles also was detected as a risk factor for lung cancer in non-smokers. This study suggests that ETS exposure may be a strong risk factor for lung cancer also in India, a country with low prevalence of smoking and, therefore, low rates of lung cancer. Other studies need to be conducted in similar settings to confirm the role played by ETS exposure early in life in the causation of lung cancer.     

Associations between smoking, passive smoking, GSTM-1, NAT2, and rectal cancer.

Cigarette smoking has been identified as a risk factor for colon cancer, however, much less is known about the association between cigarette smoking and rectal cancer. The purpose of this article is to evaluate the associations between rectal cancer and active and passive cigarette smoking and other forms of tobacco use. We also evaluate how genetic variants of GSTM-1 and NAT2 alter these associations. A population-based case-control study of 952 incident rectal cancer cases and 1205 controls was conducted. Detailed tobacco use information was collected as part of an interviewer-administered questionnaire. DNA was extracted from blood to examine genetic variants of GSTM-1 and NAT2. Cigarette smoking was associated with an increased risk of rectal cancer in men [odds ratio (OR)=1.5, 95% confidence interval (CI), 1.1-2.1 for current smokers; OR=1.7, 95% CI, 1.3-2.3 for smoking >20 pack-years of cigarettes relative to never-smokers]. After adjusting for active smoking, exposure to cigarette smoke of others also was associated with increased risk among men (OR=1.5, 95% CI, 1.1-2.0). Neither GSTM-1 genotype nor NAT2-imputed phenotype was independently associated with rectal cancer. However, the risk associated with smoking cigarettes among those who were GSTM-1 null relative to those who never smoked and had the GSTM-1 present genotype was OR=2.0 (95% CI, 1.2-3.3). This interaction was of borderline significance (P=0.08). Men who had the combined GSTM-1 present genotype and who were rapid acetylators had no increased risk from cigarette smoking. There were no significant associations between cigarette smoking and rectal cancer among women. This study shows that men who smoke cigarettes, especially those who smoke >20 pack-years, are at increased risk of rectal cancer. This association may be influenced by GSTM-1 genotype. Furthermore, exposure to cigarette smoke of others may increase risk of rectal cancer among men who do not smoke.     

A case–control study of lung cancer and environmental tobacco smoke among nonsmoking women living in Shanghai, China

Introduction: The incidence of lung cancer in women living in China is among the highest in the world but it does not appear that tobacco smoking is a major risk factor for lung cancer. As tobacco smoking is highly prevalent in Chinese men, exposure to environmental tobacco smoke (ETS) may play an important role in the development of lung cancer in Chinese women who never smoked. We conducted the present investigation because previous studies did not account for dietary habits or indoor air pollution from Chinese-style cooking and they did not assess the effect of occupational exposure to ETS.Methods: A population-based, case–control study was conducted to evaluate the relationship between lung cancer and exposure to ETS among nonsmoking women living in Shanghai, China. Five-hundred and four women diagnosed with incident, primary lung cancer between February 1992 and 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 was approximately frequency-matched to the age distribution of the lung cancer cases. Information on lifetime domestic and occupational exposure to ETS was obtained through face-to-face interviews. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression.Results: The OR for ever exposed to ETS from spouses was 1.1 (95% CI: 0.8–1.5), and the OR for ever exposed to ETS at work was 1.7 (95% CI: 1.3–2.3). Furthermore, the OR increased with increasing number of hours of daily exposure to ETS in the workplace and with increasing number of smoking co-workers. No associations were found for exposure to ETS during childhood.Conclusions: The main findings of the present study are that long-term occupational exposure to ETS, both alone or in combination with exposures at home, conferred an increased risk of lung cancer among women who never smoked. The inconsistency of the results regarding exposure to ETS at home and at work may have been due to lower exposures at home.     

Smoking and bladder cancer in Spain: effects of tobacco type, timing, environmental tobacco smoke, and gender.

We examined the effects of dose, type of tobacco, cessation, inhalation, and environmental tobacco smoke exposure on bladder cancer risk among 1,219 patients with newly diagnosed bladder cancer and 1,271 controls recruited from 18 hospitals in Spain. We used unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association between bladder cancer risk and various characteristics of cigarette smoking. Current smokers (men: OR, 7.4; 95% CI, 5.3-10.4; women: OR, 5.1; 95% CI, 1.6-16.4) and former smokers (men: OR, 3.8; 95% CI, 2.8-5.3; women: OR, 1.8; 95% CI, 0.5-7.2) had significantly increased risks of bladder cancer compared with nonsmokers. We observed a significant positive trend in risk with increasing duration and amount smoked. After adjustment for duration, risk was only 40% higher in smokers of black tobacco than that in smokers of blond tobacco (OR, 1.4; 95% CI, 0.98-2.0). Compared with risk in current smokers, a significant inverse trend in risk with increasing time since quitting smoking blond tobacco was observed (> or =20 years cessation: OR, 0.2; 95% CI, 0.1-0.9). No trend in risk with cessation of smoking black tobacco was apparent. Compared with men who inhaled into the mouth, risk increased for men who inhaled into the throat (OR, 1.7; 95% CI, 1.1-2.6) and chest (OR, 1.5; 95% CI, 1.1-2.1). Cumulative occupational exposure to environmental tobacco smoke seemed to confer increased risk among female nonsmokers but not among male nonsmokers. After eliminating the effect of cigarette smoking on bladder cancer risk in our study population, the male-to-female incidence ratio decreased from 8.2 to 1.7, suggesting that nearly the entire male excess of bladder cancer observed in Spain is explained by cigarette smoking rather than occupational/environmental exposures to other bladder carcinogens.     

Gender, smoking, glutathione-S-transferase variants and bladder cancer incidence: a population-based study

OBJECTIVE: Male gender, tobacco smoking and occupational exposure to arylamines and polycyclic aromatic hydrocarbons are the primary risk factors for bladder cancer. Emerging, and consistent data indicate that risk may be modified by polymorphisms in carcinogen metabolism genes, including those involving the glutathione-S-transferases. Recent work further suggests that susceptibility to the carcinogenic effects of tobacco on the bladder may differ among men and women. METHOD: We investigated the gender specific risk of bladder cancer associated with glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms in a population-based case-control study of 354 bladder cancer cases and 542 controls. RESULTS: We found an increased risk of bladder cancer associated with GSTM1 null genotype among women (OR 1.7; 95% CI 1.0-3.0), but not men (OR 0.9; 95% CI 0.7-1.3). Among women, the GSTM1 null genotype was associated with an elevated bladder cancer risk only among smokers (OR 2.3; 95% CI 1.1-4.5 in ever smokers versus OR 0.9; 95% CI 0.3-2.5 in never smokers). There was no apparent association between bladder cancer and the GSTT1 null polymorphism in either men or women, and we did not detect evidence of any GSTT1-smoking or GSTT1-GSTM1 gene-gene interaction. CONCLUSION: Our data suggest that a subset of women may be particularly susceptible to tobacco-induced bladder cancer.     

A prospective study on active and environmental tobacco smoking and bladder cancer risk (The Netherlands)

Objective: In a prospective cohort study among 120,852 adult subjects the authors investigated the associations between cigarette, cigar, pipe, environmental tobacco smoking (ETS), and bladder cancer. Methods: In 1986 all subjects completed a questionnaire on cancer risk factors. Follow-up for incident bladder cancer was established by linkage to cancer registries until 1992. The case–cohort analysis was based on 619 cases and 3346 subcohort members. Results: Compared with lifelong non-smokers the age- and sex-adjusted incidence rate ratios (RR) for ex- and current cigarette smokers were 2.1 (95% CI 1.5–3.0) and 3.3 (95% CI 2.4–4.6), respectively. The RR for smoking duration was 1.03 (95% CI: 1.02–1.04) per 1-year increment. The RR per 10 cigarettes/day was 1.3 (95% CI 1.2–1.4). Tar and nicotine exposure increased bladder cancer risk only weakly. It appeared that associations of cigarette smoking characteristics with bladder cancer risk were largely attributable to cigarette smoking duration only. Smoking cessation, age at first exposure, filter-tip usage, cigar and pipe smoking, and ETS were no longer associated with bladder cancer risk after adjustment for frequency and duration of smoking. Conclusions: The authors conclude that current cigarette smokers have a three-fold higher bladder cancer risk than non-smokers. Ex-smokers experience a two-fold increased risk. About half of male bladder cancer and one-fifth of female bladder cancer was attributable to cigarette smoking. Other smoking types (cigar, pipe, or ETS) were not associated with increased risks.     

Tobacco smoking, GSTP1 polymorphism, and bladder carcinoma

BACKGROUND: Although cigarette smoking is considered a major risk factor for bladder carcinoma, little is known about the interaction between metabolic genes such as glutathione-S-transferase P1 and tobacco smoking in this process. GSTP1 may play a role in detoxification of tobacco-related carcinogens. METHODS: In this case-control study of 145 cases with bladder carcinoma (male:female = 7.5:1) and 170 noncancer controls (male:female = 3.7:1), the relation between genetic polymorphisms of GSTP1 and susceptibility to bladder carcinoma was investigated and the gene-environment interaction between tobacco smoking and GSTP1 polymorphism was evaluated. Epidemiological data were collected for all cases and controls by a standard questionnaire. Polymorphisms of GSTP1 were measured by polymerase chain reaction-restriction fragment length polymorphism. The logistic regression model in SAS was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). RESULTS: Cigarette smoking was confirmed as a risk factor of bladder carcinoma with an OR of 3.1 (95% CI: 1.7-5.9) after controlling for potential confounding factors. The OR for pack-years of smoking as a continuous variable was 2.4 (95% CI: 2.0-2.8). The ORs were 7.6 (95% CI: 1.18-49.51) for isoleucine/valine (Ile/Val) and 6.5 (95% CI: 1.01-41.56) for Ile/Ile when the homozygous Val/Val was considered as comparison group after adjusting for age, gender, race, and education. The adjusted OR for interaction between smoking and the GSTP1 (any Ile genotype) was 11.42 (95% CI: 0.53-248.15). CONCLUSIONS: The results indicate that the Ile 105 allele is associated with an increased risk of bladder carcinoma and suggest that individuals who smoke and possess the Ile allele might be at increased risk for bladder carcinoma.