家庭二手烟暴露与城市女性结直肠癌的相关研究

[目的]探讨家庭二手烟暴露与女性结直肠癌的关系.[方法]从1986～1988年我国吸烟与人口死因调查数据库选取23个城市为研究地区,30～79岁女性为研究对象,分析结直肠癌死者丈夫的吸烟史与结直肠癌死亡率的关系.[结果]研究对象结直肠癌死亡率为7.90/10万～26.39/10万,平均14.19/10万.相关分析发现,丈夫吸烟年限≥40年与女性结直肠癌死亡率呈正相关(r=0.48,P=0.02).分层分析显示,丈夫吸烟指数≥20包年与30～39岁结直肠癌死亡率呈正相关(r=0.44,P=0.04);丈夫日吸烟量10～19支、吸烟年限＜30年与50～59岁结直肠癌死亡率相关系数分别为0.552、0.551,P＜0.05;丈夫开始吸烟年龄＜20岁、吸烟年限＜30年、吸烟指数＜10包年与70～79岁结直肠癌死亡率相关系数分别为0.51、0.46、0.60,P＜0.05.[结论]家庭二手烟暴露可能是女性结直肠癌的重要危险因素.     

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。     

江苏省昆山市2006~2015年膀胱癌发病趋势分析

[目的]分析江苏省昆山市2006～2015年膀胱癌的发病趋势.[方法]2006～2015年膀胱癌发病病例来源于昆山市肿瘤登记报告;计算历年膀胱癌粗发病率与年龄标化发病率(中标发病率).用平均年度变化百分比(APC)及其95％CI评价膀胱癌发病率在年份之间的变化趋势;用时间趋势与自回归模型结合的方法预测未来年份膀胱癌粗发病率.[结果] 2006～2015年登记膀胱癌519例,占同期新发恶性肿瘤的2.12％.膀胱癌中标发病率在男女合计(APC=1.6％,95％CI:-0.6％～3.8％)、男性(APC=1.3％,95％CI:-1.2％～3.8％)和女性(APC=5.3％,95％CI:-2.1％～12.7％)无明显趋势变化;但30～69岁人群膀胱癌中标发病率变化趋势在男女合计(APC =4.1％,95％CI:0.5％～7.7％)和女性(APC=9.5％,95％CI:1.0％～18.0％)人群中明显上升.时间趋势与自回归模型预测结果显示2016～2020年膀胱癌粗发病率在男性和女性人群中均呈现持续上升趋势.[结论]虽然膀胱癌中标发病率无明显趋势变化,但是膀胱癌发病数逐年增加,因膀胱癌造成的疾病负担逐年增加,特别在30～69岁女性人群中上升趋势最为显著.     

2003-2007年中国肿瘤登记地区膀胱癌的发病与死亡分析

目的:描述中国32个肿瘤登记地区2003-2007年膀胱癌和发病与死亡水平,并进行国际间的比较.方法:对全国32个肿瘤登记地区的数据进行汇总,计算膀胱癌的发病率和死亡率,参照GLOBOCAN 2008的数据进行国际间的比较.结果:膀胱癌总发病率为6.69/10万,城市地区为7.79/10万,农村地区为2.93/10万,城市是农村的2.7倍.膀胱癌总死亡率为2.53/10万,城市地区为2.82/10万,农村地区为1.52/10万,城市是农村的1.9倍.北京、上海和启东地区1988-2007年的年龄标化发病率都明显上升.发达国家膀胱癌年龄调整发病率为发展中国家的3倍.中国膀胱癌发病率高于发展中国家,但低于发达国家,在全球184个国家中男性位居第72位、女性位居第69位.结论:中国膀胱癌发病率城市高于农村,男性高于女性,目前处于发达国家和发展中国家之间,但呈逐渐上升趋势.     

上海市长宁区1988—2013年肾癌、膀胱癌发病和死亡趋势分析

摘 要：［目的］ 分析1988—2013年上海市长宁区居民肾癌、膀胱癌发病和死亡的现况和时间变化趋势。 ［方法］ 根据上海市长宁区1988—2013年的肾癌、膀胱癌发病、死亡人数,计算相应的粗率、世标率等指标。利用Joinpoint软件分析世标发病率/死亡率的时间变化趋势,计算年度变化百分比（APC）。应用年龄—时期—队列模型,评估这3个因素对发病率/死亡率变化的影响。［结果］ 1988—2013年期间,上海市长宁区肾癌世标发病率呈上升趋势,男、女性APC分别为7.11%和3.85%,男性肾癌死亡率显著上升（APC=3.64%）;膀胱癌中仅女性死亡率显著下降（APC=-3.29%）。年龄—时期—队列模型结果提示,随着年龄的增大,肾癌、膀胱癌的发病率和死亡率均呈上升趋势;肾癌发病率还同时受到时期、队列效应的影响（P值均<0.05）。［结论］ 1988—2013年上海市长宁区居民的肾癌、膀胱癌的发病率和死亡率均随年龄增加而逐渐上升,提示中老年人群是防治工作的重点。     

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。     

2013年中国膀胱癌发病和死亡流行状况分析

摘 要：［目的］ 分析2013年中国膀胱癌发病和死亡的流行状况。［方法］ 对全国肿瘤登记地区2013年的登记数据进行汇总,计算膀胱癌的发病率、死亡率、中国人口和Segi’s世界人口标化发病率和死亡率、35~64岁截缩率和0~74岁累积率。［结果］ 2013年中国膀胱癌发病率为5.46/10万,占所有新发肿瘤病例的2.02%,居恶性肿瘤发病第16位。2000年中国人口标化发病率为3.64/10万,世界人口标化发病率为3.58/10万,35~64岁截缩率为4.49/10万,0~74岁累积发病率为0.41%。城市人口膀胱癌发病率（6.47/10万）高于农村（4.30/10万）;男性膀胱癌发病率（8.40/10万）远高于女性（2.38/10万）。2013年中国膀胱癌死亡率为2.16/10万,占所有恶性肿瘤死亡病例的1.32%,居恶性肿瘤死亡第16位。2000年中国人口标化死亡率为1.31/10万,世界人口标化死亡率为1.31/10万,35~64岁截缩率为0.89/10万,0~74岁累积死亡率为0.12%。城市人口膀胱癌死亡率（2.41/10万）高于农村（1.86/10万）;男性膀胱癌死亡率（3.21/10万）高于女性（1.05/10万）。［结论］ 膀胱癌已成为中国男性常见的恶性肿瘤,尤其在城市地区负担严重,应加强重点人群膀胱癌的防治工作。     

2004～2005年广西膀胱癌死亡状况及减寿分析

目的了解广西膀胱癌死亡的流行病学特征及对居民健康的危害。方法收集、整理2004～2005年广西人口死因抽样调查中膀胱癌的死亡资料,统计分析其粗死亡率、标化死亡率、潜在减寿年数（PYLL）及减寿率（PYLLR）。结果 2004～2005年广西膀胱癌粗死亡率为0.97/10万,男性为1.33/10万,女性为0.56/10万,男性粗死亡率是女性的2.38倍,差异有统计学意义（u=3.60,P〈0.05）。2004～2005年广西膀胱癌死亡率比1990～1992年上升（u=1.97,P〈0.05）。男性PYLL为285人年,女性PYLL为60人年;男性PYLLR为0.07‰,女性PYLLR为0.02‰。结论 2004～2005年广西膀胱癌死亡率上升,男性膀胱癌死亡率高于女性,男性膀胱癌死亡危害程度高于女性。     

膀胱癌Survivin和VEGF的表达与血管生成关系的研究

目的:探讨膀胱癌组织中凋亡抑制基因存活素(Survivin)和血管内皮生长因子(VEGF)的表达与膀胱癌血管生成的关系。方法:应用免疫组化S-P法检测69例膀胱癌组织和8例正常膀胱粘膜组织(对照组)中Survivin和VEGF的表达,同时分析不同Survivin和VEGF表达状态下膀胱癌组织微血管密度(MVD)的变化。结果:膀胱癌组和对照组Survivin阳性率分别为71.0%(49/69)和0(0/8),二组比较差异亦有统计学意义(χ2=11.31,P<0.01);膀胱癌组和对照组VEGF阳性率分别为66.7%(46/69)和0(0/8),二组比较差异有统计学意义(χ2=10.62,P<0.01);膀胱癌组织中Survivin和VEGF的表达呈正相关(r=0.785,P<0.01)。将膀胱癌分为4组,A组(n=39)为Survivin /VEGF ,B组(n=13)为Survivin-/VEGF-,C组(n=7)为Survivin-/VEGF ,D组(n=10)为Survivin /VEGF-。4组MVD分别为46.69±11.28、30.72±5.10、36.18±8.62、34.47±7.98,A组MVD显著高于其他3组(P均<0.01)。结论:膀胱癌中Survivin可能通过信号传导网络参与调控VEGF的表达而促进血管生成,导致肿瘤恶性进展。     

Decrease in risk of lung cancer death in males after smoking cessation by age at quitting: findings from the JACC study.

To evaluate the impact of smoking cessation in individuals and populations, we examined the decrease in risk of lung cancer death in male ex-smokers by age at quitting in the Japan Collaborative Cohort Study for Evaluation of Cancer Risk Sponsored by Monbusho (JACC Study), which was initiated from 1988 to 1990 in Japan. For simplicity, subjects were limited to male non-smokers, and former / current smokers who started smoking at ages 18 - 22, and 33654 men aged 40 - 79 years were included. We modeled the mortality rates in non-smokers and current smokers, and compared the rates in ex-smokers with those expected from the model if they had continued smoking. During the mean follow-up of 8.0 years, 341 men died from lung cancer. The mortality rate ratio for current smokers, compared to non-smokers, was 5.16, and those for ex-smokers who had quit smoking 0 - 4, 5 - 9, 10 - 14, 15 - 19 and > or = 20 years before were 4.84, 3.19, 2.03, 1.29 and 0.99, respectively. The functions of 3.20 x 10(-7) x (age)(4.5) and 1.96 x 10(-5) x (age - 29.6)(4.5) fitted the observed mortality rates (per 100000 person-years) in non-smokers and continuing smokers, respectively. A greater decrease in lung cancer mortality was estimated among those who quit smoking at younger ages. Stopping smoking earlier in life appears preferable to keep the individual risk low. The absolute rate, however, substantially decreased after smoking cessation even in those who quit at ages 60 - 69, reflecting the high mortality rate among continuing smokers in the elderly.     

Decrease in Risk of Lung Cancer Death in Males after Smoking Cessation by Age at Quitting: Findings from the JACC Study

To evaluate the impact of smoking cessation in individuals and populations, we examined the decrease in risk of lung cancer death in male ex-smokers by age at quitting in the Japan Collaborative Cohort Study for Evaluation of Cancer Risk Sponsored by Monbusho (JACC Study), which was initiated from 1988 to 1990 in Japan. For simplicity, subjects were limited to male non-smokers, and former/current smokers who started smoking at ages 18-22, and 33 654 men aged 40-79 years were included. We modeled the mortality rates in non-smokers and current smokers, and compared the rates in ex-smokers with those expected from the model if they had continued smoking. During the mean follow-up of 8.0 years, 341 men died from lung cancer. The mortality rate ratio for current smokers, compared to non-smokers, was 5.16, and those for ex-smokers who had quit smoking 0-4, 5-9,10-14,15-19 and >20 years before were 4.84, 3.19, 2.03,1.29 and 0.99, respectively. The functions of 3.20×l0^-7×(age)⁴⁵ and 1.96×lO^-5×(age-29.6)^4.5 fitted the observed mortality rates (per 100 000 person-years) in non-smokers and continuing smokers, respectively. A greater decrease in lung cancer mortality was estimated among those who quit smoking at younger ages. Stopping smoking earlier in life appears preferable to keep the individual risk low. The absolute rate, however, substantially decreased after smoking cessation even in those who quit at ages 60-69, reflecting the high mortality rate among continuing smokers in the elderly.     

Smoking and mortality from esophageal cancer in China: a large case-control study of 19,734 male esophageal cancer deaths and 104,846 living spouse controls

An innovative population-based case-control study was conducted in a national mortality survey to assess the hazards of tobacco use on esophageal cancer among Chinese men. Cases were 19,734 males aged 35 years or older, who died of esophageal cancer during 1986-1988. Controls were 104,846 male living spouses of the same age when their wife died (of any cause) during the same period in the same county or city. The absolute esophageal cancer death rates were higher in smokers than those in nonsmokers in all geographical groups. The relative risks for esophageal cancer were 1.88 (95% CI: 1.73-2.05) and 1.39 (95% CI: 1.28-1.50) in urban and rural men, respectively, after adjustment for other relevant covariates including age group (5 years) and locality. When the calculation was restricted to men aged 35-69, the risk ratios for current cigarette smokers increased significantly with increasing number of cigarettes smoked daily and duration of smoking. Tobacco use, in any form, is an important risk factor for esophageal cancer in Chinese men. Selecting living spouses as controls is a unique and useful approach in the design of case-control studies of cigarette smoking.     

Decrease in risk of lung cancer death in Japanese men after smoking cessation by age at quitting: pooled analysis of three large-scale cohort studies

To evaluate the impact of smoking cessation on individuals and populations, we examined the decrease in risk of lung cancer death in male ex-smokers by age at quitting by pooling the data from three large-scale cohort studies in Japan. For simplicity, subjects were limited to male never smokers and former or current smokers who started smoking at ages 18-22 years, and 110,002 men aged 40-79 years at baseline were included. During the mean follow-up of 8.5 years, 968 men died from lung cancer. The mortality rate ratio compared to current smokers decreased with increasing attained age in men who stopped smoking before age 70 years. Among men who quit in their fifties, the cohort-adjusted mortality rate ratios (95% confidence interval) were 0.57 (0.40-0.82), 0.44 (0.29-0.66) and 0.36 (0.13-1.00) at attained ages 60-69, 70-79 and 80-89 years, respectively. The corresponding figures for those who quit in their sixties were 0.81 (0.44-1.48), 0.60 (0.43-0.82) and 0.43 (0.21-0.86). Overall, the mortality rate ratio for current smokers, relative to non-smokers, was 4.71 (95% confidence interval 3.76-5.89) and those for ex-smokers who had quit smoking 0-4, 5-9, 10-14, 15-19, 20-24 and >or=25 years before were 3.99 (2.97-5.35), 2.55 (1.80-3.62), 1.87 (1.23-2.85), 1.21 (0.66-2.22), 0.76 (0.33-1.75) and 0.67 (0.34-1.32), respectively. Although earlier cessation of smoking generally resulted in a lower rate of lung cancer mortality in each group of attained age, the absolute mortality rate decreased appreciably after stopping smoking even in men who quit at ages 60-69 years.     

Declining lung cancer mortality of young Australian women despite increased smoking is linked to reduced cigarette 'tar' yields

Lung cancer data were examined to determine whether the mortality rates of young Australian women have continued to increase in line with the proportions of them who have smoked tobacco. Trends in annual age-specific lung cancer mortality were estimated for 1965-1998. Age-specific mortality rates and age-adjusted ratios of mortality rates were calculated for birth cohorts. Proportions of smokers in those cohorts were estimated from results of eight national surveys of smoking, and their mean ages of commencement and years of smoking were assessed from surveys of smokers in two states. Lung cancer mortality rates of 20-44-year-old Australian women peaked in 1986. Age-adjusted mortality rates are lower for women born in the 1950s and 1960s than for women born in the 1940s, despite higher proportions of smokers, younger age of commencement and longer duration of smoking by age 30 years in the more recent cohorts. Increased smoking has not resulted in higher lung cancer mortality for Australian women born in the 1950s and 1960s. Reductions in tar yields of Australian-made cigarettes, which would have affected primarily those born after the 1940s, may be responsible.     

Cigarette smoking and colorectal cancer mortality in the cancer prevention study II

BACKGROUND: Recent studies suggest that long-term cigarette smoking is associated with an increased risk of colorectal cancer. Whether the association is causal or due to confounding remains unclear. METHODS: We examined cigarette smoking in relation to colorectal cancer mortality, evaluating smoking duration and recency and controlling for potential confounders in the Cancer Prevention Study II. This prospective nationwide mortality study of 1 184 657 adults (age > or =30 years) was begun by the American Cancer Society in 1982. After exclusions, our analytic cohort included 312 332 men and 469 019 women, among whom 4432 colon or rectal cancer deaths occurred between 1982 and 1996 among individuals who were cancer free in 1982. Rate ratios (RRs) and 95% confidence intervals (CIs) were estimated by fitting Cox proportional hazards models. All statistical tests were two-sided. RESULTS: Multivariate-adjusted colorectal cancer mortality rates were highest among current smokers, were intermediate among former smokers, and were lowest in lifelong nonsmokers. The multivariate-adjusted RR (95% CI) for current compared with never smokers was 1.32 (1.16-1.49) among men and 1.41 (1.26-1.58) among women. Increased risk was evident after 20 or more years of smoking for men and women combined as compared with never smokers. Risk among current and former smokers increased with duration of smoking and average number of cigarettes smoked per day; risk in former smokers decreased significantly with years since quitting. If the multivariate-adjusted RR estimates in this study do, in fact, reflect causality, then approximately 12% of colorectal cancer deaths among both men and women in the general U.S. population in 1997 were attributable to smoking. CONCLUSIONS: Long-term cigarette smoking is associated with increased risk of colorectal cancer mortality in both men and women. Clear reduction in risk is observed with early smoking cessation.     

Gender- and smoking-related bladder cancer risk

BACKGROUND: There is growing evidence that, when smoking habits are comparable, women incur a higher risk of lung cancer than men. Because smokers are also at risk for bladder cancer, we investigated possible sex differences in the susceptibility to bladder cancer among smokers. METHODS: A population-based, case--control study was conducted in Los Angeles, CA, involving 1514 case patients with bladder cancer and 1514 individually matched population control subjects. Information on tobacco use was collected through in-person interviews. Peripheral blood was collected from study participants to measure 3- and 4-aminobiphenyl (ABP)-hemoglobin adducts, a marker of arylamine exposure. Data were analyzed to determine whether the risk of bladder cancer differs between male and female smokers and whether female smokers exhibit higher levels of ABP-hemoglobin adducts than male smokers with comparable smoking habits. All statistical tests were two-sided. RESULTS: Cigarette smokers had a statistically significant 2.5-fold higher risk (95% confidence interval = 2.1 to 3.0) of bladder cancer than never smokers. Use of filtered versus nonfiltered cigarettes, low-tar versus higher tar cigarettes, or the pattern of inhalation did not modify the risk. The risk of bladder cancer in women who smoked was statistically significantly higher than that in men who smoked comparable numbers of cigarettes (P =.016 for sex-lifetime smoking interaction). Consistent with the sex difference in smoking-related bladder cancer risk, the slopes of the linear regression lines of the 3- and 4-ABP--hemoglobin adducts by cigarettes per day were statistically significantly steeper in women than in men (P values for sex differences <.001 and.006, respectively). CONCLUSION: The risk of bladder cancer may be higher in women than in men who smoked comparable amounts of cigarettes.     

Smoking and bladder cancer. The modifying effect of cigarettes on other factors

A population-based, incidence case-control study was used to assess the effect of cigarette smoking on other risk factors for the development of bladder cancer. White men (n = 332) between the ages of 21 and 84 with bladder cancer were compared with 686 population-based controls. Cigarette smokers were classified by current smoking status as well as by amount, duration, inhalation patterns, age at first having smoked, and years since having stopped smoking. These variables were associated with a change in the risk for bladder cancer. The population-attributable risk associated with cigarette smoking was 48.5%. Risks from the use of other tobacco products such as cigars, pipes, snuff, and chewing tobacco, and from caffeinated coffee, tea, and alcoholic beverages were evaluated in light of cigarette smoking status. Cigarette smoking was shown to be both a confounder and an effect modifier. Risk estimates for bladder cancer associated with caffeinated coffee and alcoholic beverages were decreased after controlling for the effects of cigarette smoking. However, an increased risk of developing bladder cancer from cigar smoking (Odds ratio [OR] = 2.46) and tea drinking (OR = 3.14) was only seen in men who never smoked cigarettes. An increased but not significant risk was also seen for pipe, snuff, and chewing tobacco use in noncigarette smokers. The population-attributable risk from cigars and tea in the population of white men who had never smoked was 6.3% and 18.9%, respectively. Our results suggest that cigarette smoking may obscure other risk factors unless those who never smoked are separately studied.     

Smoking and Cancer Risk in Korean Men and Women

OBJECTIVE: In Korea, male smoking prevalence is among the world's highest, and mortality rates from smoking-caused cancers, particularly lung cancer, are escalating. This cohort study examined the effects of cigarette smoking on the risk of cancer mortality and incidence, and characterized the relationship of cancer risk with the amount and duration of cigarette smoking. METHOD: A nine-year prospective cohort study was carried out on 1,212,906 Koreans, 30-95 years of age. The study population includes participants in a national insurance program, who completed a questionnaire on smoking and other risk factors. The main outcome measures were death from cancer and cancer incidence, obtained through record linkage. At baseline, 472,970 men (57.0%) and 20,548 (5.4%) women were current cigarette smokers. RESULTS: In multivariate Cox proportional hazards models, controlling for age, current smoking among men increased the risks of mortality for cancer of the lung (relative risk (RR), 4.6; 95% confidence interval (CI), 4.0-5.3) and other cancers, including larynx, bile duct, esophagus, liver, stomach, pancreas, bladder, and also leukemia. Current smoking among women increased the risk of lung cancer mortality (RR = 2.5, 95% CI = 2.0-3.1). Similar results were found for incidence among men and women. CONCLUSION: In Korea, smoking is an independent risk factor for a number of major cancers. The findings affirm the need for aggressive tobacco control in Korea in order to minimize the epidemic of smoking-caused disease.