吸烟和环境烟草烟雾暴露与膀胱癌关系的病例对照研究

目的研究分析吸烟及环境烟草烟雾暴露与膀胱癌的关系。方法自1996年1月~1999年6月,上海市区开展了一项大规模的基于全人群的膀胱癌病例对照研究,共访问到608例膀胱癌病例和607例健康人群对照。使用非条件logistic回归分析,调整可能的混杂因素,估计吸烟及环境烟草烟雾暴露对膀胱癌发生的比数比和95%可信区间。结果男性吸烟者患膀胱癌的危险性是不吸烟者的1.67倍(95%CI1.23~2.27),且随着每天吸烟量、累积吸烟量、吸烟年限和吸烟深度的增加而增加,吸烟开始年龄越小危险性越大;戒烟后膀胱癌危险性有所降低。吸烟也显著增加女性膀胱癌的危险性,调整OR为4.19(95%CI1.65~10.65)。吸烟者的调整人群归因危险度男性、女性分别为32.04%和15.61%。未发现环境烟草暴露增加非吸烟者膀胱癌的危险性。结论进一步证实吸烟是膀胱癌发生的重要危险因素。环境烟草烟雾暴露是否增加膀胱癌危险性尚难定论。     

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。     

上海市区慢性肺部疾病史与男性肺癌关系的前瞻性队列研究

目的:研究肺气肿、肺结核、慢性支气管炎和哮喘等慢性肺部疾病史与男性肺癌之间的关系.方法:建立2002-2006年上海市区61 500例男性队列调查资料,应用COX回归模型分析肺气肿、肺结核、慢性支气管炎和哮喘等慢性肺部疾病史与男性肺癌发生的风险比(hazard ratio,HR)及其95%可信区间(confidence interval, CI).结果:截至2008年12月31日,队列中共发生323例肺癌病例.调整了年龄、教育程度、家庭收入、吸烟状态和吸烟包-年等混杂因素后发现,慢性支气管炎可增加男性肺癌的危险性,其HR值为1.87(95%CI:1.35～2.57);进一步调整了体质指数(body mass index, BMI)、能量摄入和体力活动等因素后发现,慢性支气管炎仍可增加男性肺癌发生的危险性,与未患慢性支气管炎者相比差异有统计学意义(P<0.01).在排除了基线调查前3年内诊断为慢性肺部疾病的对象后发现,慢性支气管炎与肺癌危险性的关联强度没有明显变化.按吸烟史和BMI分层分析发现,在有吸烟史者中,慢性支气管炎增加了肺癌的危险性,其HR为1.58(95%CI:1.14～2.19);在从未吸烟者中,则未发现2者有关联.在非肥胖者(BMI<25)和肥胖者(BMI≥25)中,慢性支气管炎均可使肺癌的发病风险增加.同时各种分析均提示,肺气肿、肺结核和哮喘与肺癌的关联均无统计学意义.结论:慢性支气管炎可能增加了男性肺癌的发病风险.     

体质指数与非吸烟女性肺癌关系的前瞻性队列研究

目的:研究体质指数(body mass index, BMI)与非吸烟女性肺癌的关系.方法:建立1997-2000年上海市区74 942人(其中非吸烟者72 829人)、年龄40～70岁的女性队列,每2年随访1次,至2007年12月共收集271例非吸烟女性肺癌病例.用COX回归模型分析BMI与非吸烟女性肺癌发生的相对危险度(relative risk, RR)和95%可信区间(95% confidence interval,95%CI).结果:调整年龄、教育程度、绝经状态等因素后,基线BMI、20岁BMI与非吸烟女性肺癌危险均无关.基线BMI最高四分组与最低组比较,RR=0.95(95%CI:0.67～1.34);20岁BMI最高四分组与最低组比较,RR=0.77(95%CI:0.52～1.15).基线BMI和年龄与非吸烟女性肺癌之间关系的分层分析得到相似结果.结论:40岁以上非吸烟女性的BMI可能与其肺癌发生的危险性没有关联.     

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。     

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...     

身体质量指数和上海市男性肺癌关系的前瞻性队列研究

目的：研究身体质量指数(BMI)和男性肺癌之间的关系。方法：采用前瞻性队列研究方法，1986～1989年在上海市区建立了1个包括18000人的男性队列，以后每年随访1次，至2000年7月共收集到肺癌新发病例374人。结果：身体质量指数越高，患肺癌的危险性越低。以身体质量指数五分位的最低组作参比，调整了年龄、文化程度和吸烟情况等混杂因素后，其它4组的相对危险度依次为0．8、0．8、0．6和0．7，趋势检验P值=0．002。按吸烟状况进行分层分析后发现在当前吸烟者中，身体质量指数和患肺癌危险性的负相关关系依然存在，但是在从不吸烟组中，由于肺癌发病例数太少，目前还无法得出结论。按肺癌的不同组织学类型进行分析，发现身体质量指数和肺腺癌的关系较明显。结论：身体质量指数可能与上海男性肺癌危险性之间存在负相关关系。     

亚甲基四氢叶酸还原酶基因C677T多态性、生活习惯与贲门癌易感性的关系

[目的]研究亚甲基四氢叶酸还原酶(MTHFR)基因C677T多态性及其与烟酒茶嗜好相互作用与贲门癌易感性的关系.[方法]在上消化道癌高发区淮安市进行了病例-对照研究(贲门癌89例,对照人群223例),调查研究对象的生活习惯,采用PCR-RFLP技术检测研究对象的MTHFR基因型.应用SAS软件或EPI Info软件进行统计学分析.[结果]①男性吸烟者和女性饮酒者与男性不吸烟者和女性不饮酒者相比患贲门癌的风险增高;不饮茶者与饮茶者相比发生贲门癌的危险性升高.②贲门癌组中MTHFRC/T T/T基因型携带者占82.0%,显著高于对照组的70.3%.与携带MTHFRC/C基因型相比,C/T T/T基因型携带者发生贲门癌的危险性(OR)为2.12(95%CI 1.14～3.95),调整性别、年龄、吸烟、饮酒、饮茶及生蔬菜、水果、肉和豆制品摄取习惯后OR为2.05(95%CI 1.05～2.03).③在吸烟、每周饮酒≥2次和不饮茶者中,携带MTHFRC/T T/T基因型者发生贲门癌的危险性显著上升.[结论]MTHFR基因型与贲门癌的易感性有关;MTHFR基因多态性影响吸烟、饮酒和饮茶与贲门癌之间的关系.     

吸烟与肝癌前瞻性研究的荟萃分析

目的:探索吸烟与肝癌发生的病因学联系. 方法:利用MEDLINE数据库及中国生物医学文献数据库检索1989年1月-2009年9月国内外公开发表的关于吸烟与肝癌关系的前瞻性研究文献,利用R软件及Meta程序包对检索结果进行荟萃分析. 结果: 纳入本次荟萃分析的文献共19篇,随访队列总样本量为3 023 558人,累计肝癌病例数为9 525人.与不吸烟者相比,吸烟者经Meta分析综合后的相对危险度(relative risk,RR)值及其95%可信区间(confidence interval,CI)为1.49(1.17～1.92),提示吸烟与肝癌呈中等程度相关;亚组分析显示,男女性别经Meta分析综合后吸烟的RR值及其95%CI分别为1.53(1.29～1.83)和1.70(1.17～2.48),差异均有统计学意义. 结论:吸烟与男女性肝癌之间存在病因学联系,是肝癌发生的危险因素之一.     

牙齿缺失与上消化道肿瘤关系前瞻性研究

[目的]探讨牙齿缺失与食管癌、贲门癌、胃癌发病的关系.[方法]采用前瞻性队列的研究方法.研究对象为1986～1991年林州市营养干预试验研究中的普通人群组,随访11年,观察牙齿缺失与食管癌、贲门癌、胃癌发生的关系,资料采用SPPSSl0.0多因素非条件Logistic回归分析.[结果]男性牙齿缺失与食管癌、贲门癌发病有统计学关联,相对危险度(RR)分别为1.265(95%CI=1.115～1.435,P=0.000);1.170(95%CI=1.009～1.356),P=0.037.女性牙齿缺失与胃癌发病有统计学关联,RR值为1.470(95%CI=1.042～2.074),P=0.027.经调整年龄、吸烟、体质指数、家族史等混杂因素后,男性牙齿缺失增加食管癌发病、女性牙齿缺失增加胃癌发病的危险性.牙齿缺失与上消化道肿瘤发病存在剂量-反应关系.[结论]在林州市男性牙齿缺失增加食管癌、贲门癌发病的危险,女性牙齿缺失增加胃癌发病的危险.     

Preliminary Study of the GSTM1 Null Polymorphism and History of Tobacco Smoking among Oral Cancer Patients in Northeastern Thailand

Risks with GSTM1 genotypes and potential roles of smoking in the susceptibility to oral squamous cell carcinoma (OSCC) were studied in Northeastern Thailand. Study subjects were 79 histologically-confirmed OSCC cases (31 men, 48 women) and 79 age- and sex-matched healthy controls ranging in age from 25 to 84 years. GSTM1 genotyping was achieved by two independent PCR assays. The GSTM1 null allele and the homozygous genotype did not increase risk of OSCC vs the wild type allele and the remaining genotypes. When the focus was on the smoking habit, male subjects who smoked ≥10 or ≥35 years were at significantly increased risk for OSCC with adjusted ORs of 4.88 [95%CI, 1.41-16.87, p=0.012] or 4.94 [95%CI, 1.62-15.12, p=0.005], respectively. A higher risk for OSCC was found for smoking amount; those who smoked >5 or >10 pack-years were at a higher risk with adjusted OR of 4.46 [95%CI; 1.45-13.74, p=0.009] or 3.89 [95%CI; 1.34 11.28, p=0.012], respectively. There are certain smoking patterns that give greater risks and thus both smoking duration and pack-years should be taken into consideration in tobacco related cancer prevention.     

Cigarette and alcohol consumption and the risk of colorectal cancer in Shanghai, China.

The relation of cigarette smoking and alcohol drinking to colorectal cancer risk has been inconsistent in the epidemiological literature. In a population-based case-control study of colorectal cancer in Shanghai, China, where the incidence rates are rising sharply, we examined the association with tobacco and alcohol use. Cases were aged 30-74 years and newly diagnosed with cancers of the colon (N = 931) or rectum (N = 874) between 1990 and 1992. Controls (N = 1552) were randomly selected among Shanghai residents, frequency-matched to cases by gender and age. Information on lifetime consumption of tobacco and alcohol, as well as demographic and other risk factors, was obtained through in-person interviews. Associations with cigarette smoking and alcohol use were estimated by odds ratios (ORs) and 95% confidence intervals (CIs). Among women, the prevalence of smoking and alcohol drinking was low, and no significant association with colon or rectal cancer was observed. Although cigarette smoking among men was not related overall to colon or rectal cancer risk, there was a 50% excess risk of rectal cancer (OR 1.5, 95% CI 0.9-2.5) among those who smoked 55 or more pack-years. Among men, former alcohol drinkers had an increased risk of colon cancer (OR 2.3, 95% CI 1.4-3.7) but not rectal cancer, while current drinkers had a 30-50% excess risk of colon cancer only among those with long-term (30+ years) and heavy (>560 g ethanol/week) consumption. The excess risks were mainly associated with hard liquor consumption, with no material difference in risk between proximal and distal colon cancer. Although cigarette smoking and alcohol drinking in general were not risk factors for colorectal cancers in Shanghai, there were small excess risks for rectal cancer among heavy smokers and colon cancer among heavy drinkers.     

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.     

Cigarette smoking and alcohol consumption and the risk of pancreatic cancer: a case-control study in Shanghai,China

Cancer of the pancreas has been rising in incidence in Shanghai, China since the early 1970s. In 1987–89, this malignancy ranked eighth in cancer incidence among men and ninth among women in Shanghai. To examine risk factors for this tumor in urban Shanghai, a population-based case-control study was conducted. Cases (n=451) were permanent residents of Shanghai, 30 to 74 years of age, newly diagnosed with pancreatic cancer between 1 October 1990 and 30 June 1993. Deceased cases (19 percent) were excluded from the study. Controls (n=1,552) were selected among Shanghai residents, frequency-matched to cases by gender and age. Cases and controls were interviewed about their demographic background and potential risk factors, including tobacco, alcohol and beverage consumption, diet, and medical history. Adjusted odds ratios (OR) and 95 percent confidence intervals (CI) were estimated using logistic regression models. Current cigarette smoking was associated with excess risk of pancreatic cancer in both men (OR=1.6, CI=1.1–2.2) and women (OR=1.4, CI=0.9–2.4). ORs increased significantly with number of cigarettes smoked per day, and with duration and packyears of smoking. Risk increased three-to sixfold among those in the highest categories of cigarette consumption, while risk decreased with increasing years since smoking cessation. Former smokers who stopped smoking for 10 or more years had risks comparable to nonsmokers. No association was found between alcohol use and pancreatic cancer. After adjustment for potential confounding factors, it was estimated that during the study period, nearly 25 percent of pancreatic cancer cases among men and six percent of cases among women could be attributed to smoking. Our findings add to the accumulating evidence linking smoking and pancreatic cancer, and suggest that the rising incidence of this malignancy in Shanghai may be related at least partly to the increasing prevalence of smoking.Dr Ji, formerly with the Shanghai Cancer InstituteDr McLaughlin, formerly with the National Cancer InstituteDr Hatch, formerly with Columbia University     

Association of cigarette smoking with the risk of ovarian cancer

Cigarette smoking may be associated with ovarian cancer risk. This association may differ by histological type. The authors conducted a population-based case-control study in Canada of 442 incident cases of ovarian cancer and 2,135 controls 20-76 years of age during 1994-1997 to examine this association, overall and by histological type. Compared to women who never smoked, those who smoked had higher odds (odds ratio [OR] = 1.22; 95% confidence interval [CI] = 0.98-1.53) of having ovarian cancer, and the OR was larger for ex-smokers (1.30; 95% CI = 1.01-1.67) than for current smokers (1.10; 95% CI = 0.81-1.49). The association with cigarette smoking was stronger for mucinous tumors (OR = 1.77; 95% CI = 1.06-2.96) than for nonmucinous tumors (OR = 1.13; 95% CI = 0.89-1.44). In addition, the odds of smokers having mucinous tumors increased with years of smoking (OR = 1.36, 1.88, 1.19, 4.89 for <20, 21-30, 31-40 and >40 years, respectively; p for trend = 0.002), number of cigarettes smoked per day (OR = 1.55, 1.89, 2.28 for <10, 11-20 and >20 cigarettes/day, respectively; p for trend = 0.014) and smoking pack-years (OR = 1.13, 2.65, 1.77 and 2.39 for <10, 11-20, 21-30 and >30 pack-years, respectively; p for trend = 0.004). Our data suggest that cigarette smoking is associated with an increased risk of ovarian cancer, especially for mucinous types.     

Cigarette smoking and risk of prostate cancer in the physicians' health study (United States)

To assess whether cigarette smoking is associated with prostate cancer incidence or mortality, we analyzed a large cohort of 22,071 men, aged 40-84 at baseline, in the Physicians' Health Study. During an average of 12.5 years of follow-up, we documented 996 cases of prostate cancer, including 113 fatal cases. Men were categorized according to smoking status, total pack-years smoked, and duration of smoking. We used Cox proportional hazard models to estimate the relative risks associated with smoking. Compared to never smokers, the age-adjusted relative risks (RR) of total prostate cancer were 1. 14 (95% confidence interval [CI] = 1.00-1.30) for past smokers, 1.10 (95% CI = 0.78-1.55) for current smokers of less than 20 cigarettes per day, and 1.10 (95% CI = 0.84-1.44) for current smokers of 20 or more cigarettes per day. Adjustment for body mass index, height, alcohol intake, and physical activity did not materially alter these findings. No significant association was observed in analyses of total pack-years smoked or duration of smoking. The results were similar for non-fatal and fatal prostate cancer. These data indicate no material association between cigarette smoking and prostate cancer incidence or mortality.     

Cigarette smoking and risk of prostate cancer in middle-aged men.

Cigarette smoking may increase the risk of prostate cancer by affecting circulating hormone levels or through exposure to carcinogens. Although there are plausible mechanisms that could explain an association between smoking and prostate cancer, previous studies are inconsistent. The goal of this population-based case-control study was to assess this association in middle-aged men. Cases (n = 753) were men ages 40-64 years diagnosed with prostate cancer from 1993 to 1996 identified using the Seattle-Puget Sound Cancer Registry. Age-matched controls without prostate cancer from the same region (n = 703) were identified using random digit dialing. Participants completed detailed in-person interviews. Logistic regression was used to compute adjusted odds ratios (ORs) and 95% confidence intervals (CIs) to assess the prostate cancer-cigarette smoking relationship. Current smokers had an increased risk (OR = 1.4, 95% CI 1.0-2.0) relative to nonsmokers. A dose-response relationship was noted between number of pack-years smoked and prostate cancer risk (trend P = 0.03). The OR = 1.6 (95% CI 1.1-2.2) for men with >40 pack-years of smoking, with a stronger association observed in men with more aggressive disease (OR = 2.0, 95% CI 1.3-3.1). Smoking cessation resulted in a decline in risk (trend P = 0.02). Smoking is associated with a moderately increased relative risk of prostate cancer. Furthermore, a dose-response relationship exists between number of pack-years smoked and cancer risk. Given that smoking cessation seems to reduce these risks, results from this study have public health ramifications and suggest that prostate cancer should be added to the list of tumors for which cigarette smoking is a risk factor.     

Lung cancer and cigarette smoking in women: a multicenter case-control study in Europe

The association between cigarette smoking and lung cancer risk in women was investigated within the framework of a case-control study in 9 centres from 6 European countries. Cases were 1,556 women up to 75 years of age with histologically confirmed primary lung cancer; 2, 450 controls with age distribution similar to cases were selected. The predominant cell type was adenocarcinoma (33.5%), with similar proportions for squamous-cell type (26.4%) and small-cell carcinoma (22.3%). Overall, smoking cigarettes at any time was associated with a 5-fold increase in lung cancer risk (odds ratio 5.21, 95% confidence interval 4.49-6.04); corresponding figures for current smoking habits were 8.94, 7.54-10.6. The association showed a dose-response relationship with duration of the habit and daily and cumulative lifetime smoking. A significant excess risk of 70% was associated with every 10 pack-years smoked. After 10 years of smoking cessation, the relative risk decreased to 20% compared to current smokers. The following characteristics were associated with a higher relative risk: inhalation of smoke, smoking non-filter cigarettes, smoking dark-type cigarettes and starting at young age. The association was observed for all major histological types, being the strongest for small-cell type carcinoma, followed by squamous-cell type and the lowest for adenocarcinoma. The proportion of lung-cancer cases in the population attributable to cigarette smoking ranged from 14% to 85%. We concluded that women share most features of the association between cigarette smoking and lung cancer observed in men.     

Risk of lung cancer among cigarette and pipe smokers in southern China.

Studies in Shanghai and in north-east China indicate that cigarette smoking is a major contributor to the high rates of lung cancer in those areas, but doubts persist regarding the influence of cigarette use on lung cancer rates in other areas of China. In addition, the risk of lung cancer associated with other methods of tobacco consumption--in particular, the use of bamboo water-pipes and long-stem pipes--is uncertain. A population-based case-control study of 427 male lung cancer patients residing in a mining area of Southern China and 1,011 controls was carried out to address this and other issues. Of these patients, 63% smoked cigarettes and (water and long-stem) pipes; 17% and 14% smoked only cigarettes or pipes, respectively; and 6% did not smoke. Compared to non-smokers, smokers of cigarettes only, smokers of pipes only and mixed smokers were at increased risk; OR = 2.6 (95% CI 1.1-6.2), 1.8 (95% CI 0.8-4.2) and 4.1 (95% CI 2.3-9.2), respectively. Risk increased with duration of tobacco use; however, the rate of increase with years of cigarette use was significantly greater than for years of pipe use (p = 0.03). In addition, risks increased 8-fold in the highest quartile of number of cigarettes per day compared to non-cigarette smokers vs. 2.3-fold for the highest quartile of number of liang (50 g) smoked per month compared to non-pipe-smokers; the trends in the ORs differed significantly (p less than 0.001). Results suggest that, in this area of China, tobacco use is an important cause of lung cancer, and that smoking cigarettes may be more deleterious than smoking pipes (primarily water pipes).