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。     

1996年全国吸烟行为的流行病学调查

编者按这里向读者推荐中国吸烟与健康研究成果──1996年全国吸烟行为的流行病学调查，该项成果以书籍形式出版，卫生部陈敏章部长书写了序言，他说国内不少流行病学家和统计学家，美国JohnHopkins大学的流行病学家，对这次调查的设计、现场调查质量、数据管理和结果分析，进行了认真的评价。他们一致认为，这次调查的设计是严谨的，现场调查的质量是可靠的，结果分析也是令人信服的。毫无疑问，这次调查中获取的大量数据和从中得出的重要结论，将有助于我国制订进一步控制吸烟危害的策略，有助于在各种人群中开展有针对性的行为干预活动，…     

忻州市肺癌发病的流行病学调查

由忻州抗癌协会牵头,于1993年对忻州市肺癌的发病情况进行调查,现将该市肺癌的流行病学调查结果总结如下:     

核工业职工肺癌死亡的流行病学调查

环境化学致癌因子是肺癌的重要发病危险因素。核工业作业环境存在着放射性,在大多数情况下表现为小剂量、低剂量率的慢性职业照射,但其损伤效应和致癌效应已引起人们越来越多的关注。本文系在核工业全死因调查的基础上,重点对肺癌的流行病学资料进行总结分析,了解其死亡危险,初步探讨其发生规律,为加强核工业的肺癌防治提供依据。1材料和方法1．1调查对象、分组及人年计算调查对象为核工业11个企事业单位自组建至1990年底的在册职工,未进行调出人员的随访。从事放射性作业满3年以上者为放射组,而非放组指放射组之外人员。为进一步分…     

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。     

广州肺癌危险因素的流行病学研究

广州市肺癌死亡率居全国各大城市的第三位，为探讨其危险因素，对近２０年所收集到的资料进行了分析，内容包括：（１）１９７６～１９８９年广州前五位恶性肿瘤（肺、肝、胃、食道、鼻咽）死亡率的变动趋势；（２）对１９８０～１９８９年肺癌死者进行了逐年回顾性调查，并分析其与吸烟、职业及生活习惯的关系；（３）大气污染；（４）室内空气污染；（５）病例对照研究：１９８５年全部肺癌死者病例对照研究；１９８５年全部不吸烟肺癌死者病例对照研究；１９８６年不吸烟女性肺癌死者病例对照研究；（６）１０９３例肺癌病例细胞类型与某些危险因素联系的分析。结果表明，广州市肺癌死亡率居各种恶性肿瘤的首位，且每年以约２／１０万的速度在增长，１９８９年高达４７／１０万。吸烟是男、女肺癌的重要因素。大气污染与肺癌市区分布有一定联系。此外，生前接触有害物质的职业对男性肺癌，室内空气污染对女性肺癌具有较重要的意义。但这种差别可能只是生活方式不同的缘故。未发现被动吸烟与女性肺癌有联系，但不应忽视它对健康的危害。经常食用新鲜蔬菜和水果，对男、女肺癌具有保护作用。联系肺癌细胞类型，发现吸烟与鳞癌有密切联系，腺癌则以吸烟以外的因素为重要。目前，仍存在一些难于解释     

非吸烟女性肺癌危险因素的研究

背景与目的肺癌是世界上一个重大的公共卫生问题,在我国肺癌是大中城市中恶性肿瘤的第一死因,且发病率和死亡率增长迅速。其中女性肺癌死亡率正逐年上升,而病例中以非吸烟者占多数,其危险因素尚不清楚。本研究通过流行病学调查来研究女性肺癌发生的危险因素。方法采用以医院患者为基础的病例-对照研究方法,包括女性肺癌患者618人,对照872人,进行流行病学调查。内容包括人口特征、被动吸烟史、烹饪油烟暴露史、燃料种类、煤烟暴露、亲属患癌史、职业史与饮食史等。结果女性肺癌患者与对照组比较,儿童时期被动吸烟(OR=1.81,95%CI=1.46~2.24)、烹饪油烟暴露(OR=3.18,95%CI=2.55~3.97)、煤烟暴露(OR=2.56,95%CI=1.83~4.55)、肺部疾病史(OR=1.80,95%CI=1.43~2.27)、肺结核史(OR=1.63,95%CI=1.31~2.03)、肿瘤家族史(OR=2.09,95%CI=1.46~3.00)和肺癌家族史(OR=2.46,95%CI=1.55~3.90)是危险因素。结论本研究显示儿童时期被动吸烟、烹饪油烟暴露、煤烟暴露、肺部疾病史、肺结核史及肿瘤或肺癌家族史是非吸烟女性肺癌的危险因素。     

非吸烟人群肺癌危险因素的病例对照研究

目的探讨中国非吸烟人群肺癌的危险因素,为防癌措施提供依据。方法采用病例对照研究的方法,按频数匹配收集非吸烟肺癌新发病例306例及非吸烟对照306例,利用统一编制的调查表对调查对象进行面访,收集病例和对照危险因素的暴露史等。结果单因素分析发现25个因素与非吸烟人群肺癌的发病有关联;多因素分析后发现：非吸烟人群肺癌发病的危险因素是体重指数(body mass index,BMI)＜18.5,居住地周围有污染企业、装修刺激性气味、家庭被动吸烟、工作场所被动吸烟、使用农药、性格内向、食用油炸食品、肺部手术史、癌症家族史,而保护因素是BMI≥24、常吃蛋类、常吃水果、饮茶、常以散步作为锻炼(2年前),经广义多因子降维法（GWDR）拟合的最优的交互作用模型是居住地企业+装修刺激性气味+家庭被动吸烟+工作场所被动吸烟+农药接触史+癌症家族史。结论非吸烟者发生肺癌的影响因素较多,仍需进一步识别。     

吸烟是肺癌最重要的致病因素

20世纪50年代以来,针对英国医务人员群体的研究得出一个令人震惊的结果：吸烟与肺癌的发生关系密切。此后,全球范围内多项研究证实,吸烟是导致肺癌的首要的危险因素。据估计,80%以上由环境因素导致的肺癌是因吸烟引起的。吸烟者因肺癌死亡的人数为不吸烟者的10倍以上。还有很多研究认为,被动吸烟可明显增加患肺癌的危险性。     

Cohort study on association of smoking and air pollution with lung cancer among 210,000 persons in shanghai

Survey on smoking habit and other related factors has been carried out among 110,000 persons in urban area and 100,000 persons in suburb and outer suburb area. The degrees of air pollution among three areas are different and the urban area is the one with the heaviest degree and the outer suburb with the lowest. Study on the relationship between smoking, air pollution and lung cancer has been carried out among the residents with the age of 40 years old and over in the three areas. The subjects were followed up for six years in urban area and five years in suburb and outer suburb. The total number of lung cancer death found in this period was 828. Most of these diagnosis were classified as group of high (I or II) degree. For nonsmokers, there were no significant differences of standardized mortality radio (SMR) of lung cancer among three areas. For male smokers, the highest SMR of lung cancer was seen in urban area, the lowest in outer suburb and these differences reached the significant lever. Cigarette smoking was significantly associated with increased risk of lung cancer by comparing the data between smokers and non-smokers in the three areas. Also, it was showed that the combiend effect of smoking with air pollution probably existed. The age-specific mortality rates for lung cancer among non-smokers in Shanghai urban were much higher than those in West Europe and North America, which indicated that risk factors other than smoking may exist.     

Gender differences in lung cancer risk by smoking: a multicentre case-control study in Germany and Italy

Several studies in the past have shown appreciably higher lung cancer risk estimates associated with smoking exposure among men than among women, while more recent studies in the USA report just the opposite. To evaluate this topic in a European population we conducted a case-control study of lung cancer in three German and three Italian centres. Personal interviews and standardized questionnaires were used to obtain detailed life-long smoking and occupational histories from 3723 male and 900 female cases and 4075 male and 1094 female controls. Lung cancer risk comparing ever-smokers with never-smokers was higher among men (odds ratios (OR) adjusted for age and centre = 16.1, 95% confidence interval (CI) 12.8-20.3) than among women (OR = 4.2, CI 3.5-5.1). Because the smoking habits of women were different from men, we conducted more detailed analyses using comparable levels of smoking exposure. After restriction to smokers and adjustment for other smoking variables, risk estimates did not differ appreciably between genders. The analysis of duration of smoking (0-19, 20-39, 40+ years) adjusted for cigarette consumption and time since quitting smoking revealed similar risk estimates in men (OR = 1.0, 3.3 [CI 2.6-4.2], 4.1 [CI 3.1-5.6]) and women (OR = 1.0, 2.7 [CI 1.7-4.1], 3.3 [CI 1.9-5.8]). The same was true of the analysis of average or cumulative smoking consumption, and also of analyses stratified by different histological types. We conclude that for comparable exposure to tobacco smoke, the risk of lung cancer is comparable in women and men.     

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。     

Passive smoking and diet in the etiology of lung cancer among non-smokets

A case-control study was undertaken in Athens to explore the role of passive smoking and diet in the causation of lung cancer, by histologic type, in non-smoking women. Among 160 women with lung cancer admitted to one of seven major hospitats in Greater Athens between 1987 and 1989, 154 were interviewed in person; of those interviewed, 91 were life-long non-smokers. Among 160 identified controls with fractures or other orthopedic conditions, 145 were interviewed in person; of those interviewed, 120 were life-long non-smokers. Marriage of a non-smoking woman to a smoket was associated with a relative risk for lung cancer of 2.1 (95% confidence interval [CI] 1.1–4.1); number of cigarettes smoked daily by the husband and years of exposure to husband's smoking were positively, but not significantly, related to lung cancer risk. There was no evidence of any association with exposure to smoking of other household members, and the association with exposure to passive smoking at work was small and not statistically significant. Dietary data collected through a semi-quantitative food-frequency questionnaire indicated that high consumption of fruits was inversely related to the risk of lung cancer (the relative risk between extreme quartiles was 0.27 (CI 0.10–0.74)). Neither vegetables nor any other food group had an additional protective effect; futthermore, the apparent protective effect of vegetables was not due to carotenoid vitamin A content and was only partly explained in terms of vitamin C. The associations of lung cancer risk with passive smoking and reduced fruit intake were independent and did not confound each other. Passive smoking was associated with an increase of the risk of all histologic types of cancer, although the elevation was more modest for adenocarcinoma.Drs kalandidi, Katsouyanni, Voropoulou, and Bastas are in the Department of Hygiene and Epidemiology, University of Athens Medical School, Athens, Greece. Dr Saracci is at the International Agency for Research on Cancer, Lyon, France. Dr Trichopoulos is in the Department of Epidemiology, Harvard School of Public Health. Reprint requests should be sent to Dr Trichopoulos at 655 Huntington Avenue, Boston, MA 02115, USA. The research was supported by the International Agency for Research on Cancer and the Commission of the European Communities. It is part of the EUROPASS collaborative EEC project.     

Passive smoking and lung cancer in Japanese non-smoking women: a prospective study

Although smoking is a major cause of lung cancer, the proportion of lung cancer cases among Japanese women who never smoked is high. As the prevalence of smoking in Japan is relatively high in men but low in women, the development of lung cancer in non-smoking Japanese women may be significantly impacted by passive smoking. We conducted a population-based prospective study established in 1990 for Cohort I and in 1993 for Cohort II. The study population was defined as all residents aged 40-69 years at the baseline survey. 28,414 lifelong non-smoking women provided baseline information on exposure to tobacco smoke from their husband, at the workplace and during childhood. Over 13 years of follow-up, 109 women were newly diagnosed with lung cancer, of whom 82 developed adenocarcinoma. Compared with women married to never smokers, hazard ratio (HR) [95% confidence interval (CI)] for all lung cancer incidence in women who lived with a smoking husband was 1.34 (95% CI 0.81-2.21). An association was clearly identified for adenocarcinoma (HR 2.03, 95% CI 1.07-3.86), for which dose-response relationships were seen for both the intensity (p for trend = 0.02) and amount (p for trend = 0.03) of the husband's smoking. Passive smoking at the workplace also increased the risk of lung cancer (HR 1.32, 95% CI 0.85-2.04). Moreover, a higher risk of adenocarcinoma was seen for combined husband and workplace exposure (HR 1.93, 95% CI 0.88-4.23). These findings confirm that passive smoking is a risk factor for lung cancer, especially for adenocarcinoma among Japanese women.     

Air pollution:a smoking gun for cancer

Once considered a taboo topic or stigma, cancer is the number one public health enemy in the world. Once a product of an almost untouchable industry, tobacco is indisputably recognized as a major cause of cancer and a target for anticancer efforts. With the emergence of new economic powers in the world, especially in highly populated countries such as China, air pollution has rapidly emerged as a smoking gun for cancer and has become a hot topic for public health debate because of the complex political, economic, scientific, and technologic issues surrounding the air pollution problem. This editorial and the referred articles published in this special issue of the Chinese Journal of Cancer discuss these fundamental questions. Does air pollution cause a wide spectrum of cancers？ Should air pollution be considered a necessary evil accompanying economic transformation in developing countries？ Is an explosion of cancer incidence coming to China and how soon will it arrive？ What must be done to prevent this possible human catastrophe？ Finally, the approaches for air pollution control are also discussed.     

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。     

肺癌患者吸烟量与痰液细胞p53和Ki—ras基因突变的关系

目的　了解痰液细胞癌基因突变是否与肺癌患者的吸烟量有相关性。方法　将痰液 0 .5毫升加入痰处理液制备细胞沉淀液 ,酚氯仿提取DNA ;应用SSCP PCR银染和RFLP PCR方法对痰液中p5 3、K ras突变情况进行检测。统计肺癌患者的香烟消耗量 ,分析p5 3、K ras突变与吸烟量的关系。结果　在确诊的 110例肺癌中 ,存在p5 3或K ras基因突变者有 76例 ,突变率达 69.1% ,其中 16例为p5 3和K ras基因均有突变。全组中有 71例重度吸烟者吸烟指数 (≥ 40 0支·年 ) ,71例中 5 5例有p5 3或K ras基因突变 ,突变率达 77.5 % ,显著高于非吸烟组 (P <0 .0 0 1) ;p5 3和K ras突变患者的平均吸烟指数分别达到 861和 63 0支·年 ;而未突变的平均吸烟指数为 2 84和 5 5 4支·年 ,二者之间有显著性差异 ( χ2 =3 6.5 6,P =0 .0 0 2 ,双尾检验 )。结论　痰液细胞癌基因突变检测具有简便、实用、可行的特点 ,吸烟的肺癌患者中癌基因突变率显著高于非吸烟的肺癌患者 ,提示吸烟尤其是重度吸烟可能是支气管癌基因突变的主要原因之一 ,值得临床进一步开展深入的研究。     

SULT1A1 genotype, active and passive smoking, and breast cancer risk by age 50 years in a German case-control study

IntroductionSulfotransferase 1A1 (encoded by SULT1A1) is involved in the metabolism of procarcinogens such as heterocyclic amines and polycyclic aromatic hydrocarbons, both of which are present in tobacco smoke. We recently reported a differential effect of N-acetyltransferase (NAT) 2 genotype on the association between active and passive smoking and breast cancer. Additional investigation of a common SULT1A1 genetic polymorphism associated with reduced enzyme activity and stability might therefore provide deeper insight into the modification of breast cancer susceptibility.MethodsWe conducted a population-based case–control study in Germany. A total of 419 patients who had developed breast cancer by age 50 years and 884 age-matched control individuals, for whom risk factor information and detailed smoking history were available, were included in the analysis. Genotyping was performed using a fluorescence-based melting curve analysis method. Multivariate logistic regression analysis was used to estimate breast cancer risk associated with the SULT1A1 Arg²¹³His polymorphism alone and in combination with NAT2 genotype in relation to smoking.ResultsThe overall risk for breast cancer in women who were carriers of at least one SULT1A1*2 allele was not significantly different from that for women with the SULT1A1*1/*1 genotype (adjusted odds ratio 0.83, 95% confidence interval 0.66–1.06). Risk for breast cancer with respect to several smoking variables did not differ substantially between carriers of the *2 allele and noncarriers. However, among NAT2 fast acetylators, the odds ratio associated with passive smoking only (3.23, 95% confidence interval 1.05–9.92) was elevated in homozygous carriers of the SULT1A1*1 allele but not in carriers of the SULT1A1*2 allele (odds ratio 1.28, 95% confidence interval 0.50–3.31).ConclusionWe found no evidence that the SULT1A1 genotype in itself modifies breast cancer risk associated with smoking in women up to age 50 years. In combination with NAT2 fast acetylator status, however, the SULT1A1*1/*1 genotype might increase breast cancer risk in women exposed to tobacco smoke.     

Involuntary smoking and lung cancer: a case-control study

In a case-control study in 4 hospitals from 1971 to 1981, 134 cases of lung cancer and 402 cases of colon-rectum cancer (the controls) were identified in nonsmoking women. All cases and controls were confirmed by histologic review of slides, and nonsmoking status and exposures were verified by interview. Odds ratios (OR) increased with increasing number of cigarettes smoked by the husband, particularly for cigarettes smoked at home. The OR for women whose husbands smoked 20 or more cigarettes at home was 2.11 (95% confidence limits: 1.13, 3.95). A logistic regression analysis showed a significant positive trend of increasing risk with increased exposure to the husband's smoking at home, controlled for age, hospital, socioeconomic class, and year of diagnosis. Comparison of women classified by number of hours exposed a day to smoke in the last 5 years and in the last 25 years showed no increase in risk of lung cancer.