中国四川地区原发性非吸烟肺癌的病例对照研究

背景与目的近年来非吸烟人群的肺癌发病率有上升趋势,为了给临床工作提供更准确的依据,本研究分析了四川地区原发性非吸烟肺癌的主要危险因素。方法分别收集四川大学华西医院2009年3月-12月诊治的145例原发性非吸烟肺癌患者及145例非吸烟社区健康人群进行配对。结果单因素分析筛选出17个相关因素;多因素条件Logistic回归分析显示:被动吸烟史(OR=2.267,95%CI:1.231-4.177)、近10年内有搬入新近装修住房史(OR=5.080,95%CI:1.632-15.817)、非一级血缘亲属恶性肿瘤家族史(OR=7.937,95%CI:1.815-34.705)、无自我解压途径(OR=2.491,95%CI:1.230-4.738)、工作压力大(OR=5.769,95%CI:2.030-16.396)、睡眠质量差(OR=2.538,95%CI:1.277-4.861)为主要独立危险因素;体重指数较高(OR=0.419,95%CI:0.226-0.779)、喜食蔬菜水果(OR=0.344,95%CI:0.155-0.762)、经常参加体育锻炼(OR=0.507,95%CI:0.274-0.937)为可能的保护因素。结论四川地区原发性非吸烟肺癌的发生与被动吸烟史、有害环境接触史、恶性肿瘤家族史及精神心理因素等相关。     

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。     

尼古丁受体3基因启动子多态与被动吸烟者发生肺癌的易感性研究

目的:探讨被动吸烟人群尼古丁受体3基因(CHRNA3)启动子区遗传变异与肺癌发病的关系.方法:用病例一对照的研究方法,收集250例被动吸烟原发性肺癌患者和250例性别相同、年龄相差士1岁被动吸烟正常对照,采用PCR-RFLP技术检测CHRNA3基因启动子单核苷酸多态位点rs6495309(T>C)的基因型,用SAS 9.13软件进行非条件Logistic回归校正混杂因素的影响,分析基因变异与肺癌发病的关联.结果:基因型频率分析均符合Hardy-Wein-berg平衡,P=0.109 6;CHRNA3rs6495309(T>C)住点变异在肺癌与对照中的分布差异有统计学意义,P=0.043 2;携带CC基因型个体发生肺癌的危险性较TT基因型个体增加81%(95%CI=1.07～3.06;P=0.019);rs6495309C变异基因型(rs6495309TC和rs6495309CC)患肺癌的危险性增加(adjusted OR=1.63;95%CI=1.06～2.50;P=0.025).发现被动吸烟来自于父母人群时该位点变异在肺癌与对照中分布差异有统计学意义,P=0.047 9.结论:CHRNA3基因启动子rs6495309(T>C)变异的被动吸烟人群肺癌发病危险性较高,且其危害性主要表现为被动吸烟来源于父母的人群.     

非小细胞肺癌p53、FHIT、K-RAS基因突变与吸烟相关性Meta分析

目的:从循证医学的角度对非小细胞肺癌患者p53、FHIT、K-RAS基因突变异常表达与吸烟相关性进行Meta分析。方法:检索中国学术期刊网全文数据库(CNKI)、中国科技期刊数据库(维普资讯网)、美国国立图书馆PubMed数据库,美国临床肿瘤学会(ASCO)论文集,辅以手工检索;检索时间段为1990年-2010年。检索出p53、FHIT、K-RAS基因突变与吸烟关系研究的文献197篇,最终符合纳入标准的文献26篇。对纳入文献进行方法学质量评价,采用Meta分析专用软件Review Manager 5.0进行统计分析。结果:共纳入26个研究,分别对有相同统计内容且可以合并统计的p53、FHIT、K-RAS基因突变与吸烟关系合并OR值并计算95%CI。分别为:吸烟人群p53基因突变率较高,表现为低表达,[OR=3.50,95%CI(2.45-5.00),总体效应检验Z=6.88,P<0.0001];吸烟人群K-RAS基因突变率明显偏高,表现为高表达,[OR=4.50,95%CI(3.00-6.75),总体效应检验Z=7.26,P<0.0001];吸烟人群FHIT基因突变率较高,表现为低表达,[OR=2.99,95%CI(1.01-8.88),总体效应检验Z=1.98,P=0.005]。结论:吸烟与p53、FHIT、K-RAS基因突变率呈正相关,其中p53、FHIT基因高表达为保护性因素,K-RAS基因高表达为危险因素。     

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。     

硫酸基转移酶1E1基因单核苷酸多态性联合吸烟与肺癌易感性的关系

目的:研究硫酸基转移酶(sulfotransferase,SULT)1E1基因的单核苷酸多态性(single nucleotide polymorphism,SNP)联合吸烟与肺癌易感性的关系.方法:采用病例-对照研究,收集原发性肺癌患者351例和非肿瘤患者207例,应用AllGloTM探针结合实时荧光PCR方法分析肺癌组和对照组中SLUT1E1多态位点A-3037G(rs4149525)基因型分布情况,比较不同基因型联合吸烟与肺癌易感性的关系,以及对肺癌不同病理类型的影响. 结果:肺癌患者A-3037G多态位点的AA、AG、GG基因型和A、G等位基因频率分布与对照组比较,差异无统计学意义(P>0.05).吸烟≥30包年的野生型纯合子个体罹患肺癌的风险增加,调整比值比(odds ratio,OR)为2.307[95%可信区间(confidence interval,CI)为1.285～3.976,P<0.05];吸烟≥30包年携带突变等位基因G的个体患肺癌的风险可能增加,调整OR值为1.523(95%CI为0.987～2.961,P=0.05).3种基因型联合吸烟(≥30包年)可能增加了罹患肺鳞癌的风险,AA和AG+GG基因型的OR值分别为5.983(95%CI为2.786～12.850,P<0.01)和2.750(95%CI为1.245～6.075,P<0.05);而突变等位基因G对不吸烟个体似乎具有保护作用,OR值为0.296(95%CI为0.101～0.864,P<0.05);A-3037G多态性联合吸烟对肺腺癌的发病风险没有显著影响.结论:SULT1E1基因启动子区A-3037G多态性联合吸烟可能对肺癌的发病风险有一定影响.     

非小细胞肺癌p53、FHIT、K-RAS基因突变与吸烟相关性Meta分析

目的：从循证医学的角度对非小细胞肺癌患者p53、FHIT、K-RAS基因突变异常表达与吸烟相关性进行Meta分析。方法：检索中国学术期刊网全文数据库（CNKI）、中国科技期刊数据库（维普资讯网）、美国国立图书馆PubMed数据库,美国临床肿瘤学会（ASCO）论文集,辅以手工检索;检索时间段为1990年-2010年。检索出p53、FHIT、K-RAS基因突变与吸烟关系研究的文献197篇,最终符合纳入标准的文献26篇。对纳入文献进行方法学质量评价,采用Meta分析专用软件Review Manager 5.0进行统计分析。结果：共纳入26个研究,分别对有相同统计内容且可以合并统计的p53、FHIT、K-RAS基因突变与吸烟关系合并OR值并计算95%CI。分别为：吸烟人群p53基因突变率较高,表现为低表达,[OR=3.50,95%CI（2.45-5.00）,总体效应检验Z=6.88,P〈0.0001];吸烟人群K-RAS基因突变率明显偏高,表现为高表达,[OR=4.50,95%CI（3.00-6.75）,总体效应检验Z=7.26,P〈0.0001];吸烟人群FHIT基因突变率较高,表现为低表达,[OR=2.99,95%CI（1.01-8.88）,总体效应检验Z=1.98,P=0.005]。结论：吸烟与p53、FHIT、K-RAS基因突变率呈正相关,其中p53、FHIT基因高表达为保护性因素,K-RAS基因高表达为危险因素。     

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.     

尼古丁乙酰胆碱受体基因CHRNA3的多态性和中国汉族人群肺癌风险关系的研究及其在晚期非小细胞肺癌中的预后分析

目的:研究编码尼古丁乙酰胆碱受体(nicotinic acetylcholine receptors,nAChRs)的候选基因CHRNA3的多态性与中国汉族人群肺癌风险的关系,进一步探讨其对晚期非小细胞肺癌(non-small celllung cancer,NSCLC)患者预后的影响.方法:对就诊于上海交通大学附属上海市胸科医院的547例肺癌患者,和上海市浦东新区和宝山区的567例健康人群进行病例.对照研究.选取候选基因CHRNA3上的3个SNPs位点(rs3743073,rs3743076和rs3743078),运用Taqman荧光定量基因分型技术,对该1114例中国汉族人进行基因型分析.采用非条件logistic回归分析法,比较各基因型在病例组与对照组中分布频率的差异,探讨其与肺癌的关系.进一步在101例不可手术ⅢB期/Ⅳ期NSCLC患者中探讨基因CHRNA3的多态性变化与预后的关系.结果:(1)候选基因CHRNA3上多态位点的频率分布在肺癌病例组和对照组之间的差异有统计学意义(P<0.05).调整了年龄、性别和吸烟后,证实候选基因CHRNA3上rs3743073位点的多态性变化与肺癌发病相关(OR=1.352,95%CI=1.116-1.640,P=0.002).rs3743073位点上携带TG者患肺癌的风险性是TT者的1.602倍(95%CI=1.150-2.232),携带GG者是TT者的1.824倍(95%CI=1.239-2.686).在非吸烟患者的分层分析中,同样证实rs3743073位点上的多态性变化与肺癌发生相关(OR=1.325,95%CI=1.048-1.674,P=0.019).(2)单因素生存分析(P=0.013)和Cox多因素生存分析(P=0.017)均证实,候选基因CHRNA3上rs3743078位点的多态性变化是影响不可手术ⅢB期/Ⅳ期NSCLC患者的独立预后因素.结论:nAChRs基因上CHRNA3的多态性与中国汉族人群的肺癌发病相关.是影响晚期NSCLC患者的独立预后因素     

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。     

The effects of passive smoking in the development of female lung cancer in the Nara district

Passive smoking in the development of lung cancer has been investigated in 25 female lung cancer patients in a case control study based on their histological type. Active smoking was notable squamous and small cell carcinoma, whereas passive smoking was notable in female lung cancer patients as a whole and current passive smoking being affected was the largest effect, but histological type was not notable. Adenocarcinoma was notable in cancer family aggregation. The female lung cancer patients as a whole was found the effect in the combination with passive smoking in each stage and cancer family aggregation.     

Active and passive smoking in relation to lung cancer incidence in the Women's Health Initiative Observational Study prospective cohort

BackgroundLung cancer is the leading cause of worldwide cancer deaths. While smoking is its leading risk factor, few prospective cohort studies have reported on the association of lung cancer with both active and passive smoking. This study aimed to determine the relationship between lung cancer incidence with both active and passive smoking (childhood, adult at home, and at work).Patients and methodsThe Women's Health Initiative Observational Study (WHI-OS) was a prospective cohort study conducted at 40 US centers that enrolled postmenopausal women from 1993 to 1999. Among 93 676 multiethnic participants aged 50–79, 76 304 women with complete smoking and covariate data comprised the analytic cohort. Lung cancer incidence was calculated by Cox proportional hazards models, stratified by smoking status.ResultsOver 10.5 mean follow-up years, 901 lung cancer cases were identified. Compared with never smokers (NS), lung cancer incidence was much higher in current [hazard ratio (HR) 13.44, 95% confidence interval (CI) 10.80–16.75] and former smokers (FS; HR 4.20, 95% CI 3.48–5.08) in a dose-dependent manner. Current and FS had significantly increased risk for all lung cancer subtypes, particularly small-cell and squamous cell carcinoma. Among NS, any passive smoking exposure did not significantly increase lung cancer risk (HR 0.88, 95% CI 0.52–1.49). However, risk tended to be increased in NS with adult home passive smoking exposure ≥30 years, compared with NS with no adult home exposure (HR 1.61, 95% CI 1.00–2.58).ConclusionsIn this prospective cohort of postmenopausal women, active smoking significantly increased risk of all lung cancer subtypes; current smokers had significantly increased risk compared with FS. Among NS, prolonged passive adult home exposure tended to increase lung cancer risk. These data support continued need for smoking prevention and cessation interventions, passive smoking research, and further study of lung cancer risk factors in addition to smoking.ClinicalTrials.govNCT00000611.     

武汉市城区居民肺癌危险因素研究

 目的 探讨武汉市肺癌主要危险因素,为采取切实可行的防治措施提供依据。方法 采用病例对照研究方法,收集370例肺癌病例和符合条件的对照740例进行问卷调查,应用条件Logistic回归分析方法进行单因素和多因素的分析,并计算每个危险因素的PAR%。结果 武汉市城区肺癌主要危险因素有室内化学物污染、吸烟、被动吸烟、精神压抑、肺部疾患史、新鲜蔬菜和水果摄入少等。男性肺癌归因于吸烟的比例为最高;女性肺癌主要归因于新鲜蔬菜摄入少、体重指数、体育锻炼、厨房油烟。结论精神压抑、室内化学物污染、吸烟、被动吸烟、新鲜蔬菜摄入少、呼吸系统疾病史、厨房油烟等因素可以解释武汉市城区90%左右的肺癌发病。而吃蔬菜较多、参加体育锻炼、心理健康等为肺癌发病的保护因素。     

Cigarette smoking and lung cancer risk according to histologic type in Japanese men and women

Although cigarette smoking is a well‐known risk factor for lung cancer, histology‐specific risk has not been fully clarified in Japan. This case‐control study evaluated the associations between smoking and lung cancer risk according to sex and histologic type. From among patients aged 30 years and over admitted to a single hospital in Japan between 1997 and 2009, 1670 lung cancer cases and 5855 controls were selected. History of smoking, quantity and duration of smoking, and passive smoking from spouses were assessed using a self‐administered questionnaire. Odds ratios (ORs) and 95% confidence intervals (CIs) for each exposure were estimated by unconditional logistic regression. Ever‐smoking was significantly associated with a higher risk of squamous cell and small cell carcinoma. The OR for these two histologic types combined was larger in women (OR = 24.98, 95% CI: 13.50–46.23) than in men (OR = 9.43, 95% CI: 5.73–15.51). Analysis of the quantity and duration of smoking showed that the OR for each exposure level tended to be larger in women than in men. For adenocarcinoma, clear positive associations with quantity and duration‐related factors were observed among men, and a significant positive association with passive smoking from spouses was found among non‐smoking women (OR = 1.44, 95% CI: 1.06–1.95). These results suggest sex‐ and histologic type‐ differences in the association of smoking with lung cancer risk. Although smoking control should be continued to prevent lung cancers, further studies are required to better clarify differences in smoking‐related lung cancer risk between the sexes and histologic types.     

天津地区肺癌危险因素研究

目的 探讨天津地区肺癌危险因素,进一步为肺癌危险因素的监测提供依据。方法 采用病例-对照研究方法,调查年龄在30-75岁之间的、原发性肺癌患者193例和正常对照组259例,内容包括一般情况、生活居住环境、生活习惯、既往病史和家族病史等。通过非条件logistic回归模型进行单因素和多因素分析。结果 单因素分析显示,吸烟、被动吸烟、饮酒和恶性肿瘤家族史、职业均与肺癌有关。多因素分析结果显示,影响肺癌发病的主要因素为吸烟、被动吸烟、10年前月人均收入、10年前人均住房面积和体质指数(OR分别为3．302,1．193,1．003,1．067和0．913)。结论 吸烟和被动吸烟为肺癌的独立危险因素;随着10年前月人均收入和10年前人均住房面积的增加,肺癌发生的危险性增大;较高的体质指数则为肺癌的保护性因素。     

An analysis of some risk factors for lung cancer in Hong Kong

Lung cancer has been the major cause of cancer death in Hong Kong for more than a decade. Although it is known that some 95% of male cases can be attributed to smoking, the etiological factors in women remain elusive. Among "never-smoked" female cases, increases in attributable risk from passive smoking were limited to only some of the histological types of lung carcinomas, and an overall analysis of all types did not reveal any significant increase in relative risk from this source. Other environmental factors which encourage bronchial irritation are suspected. Methodological differences may explain the differences in proportional distributions of histological lung tumor types noted between previous reports, and the risk values attributed therein to active and passive smoking.     

Risk Factors for the Diagnosis of Lung Cancer in Poland: A Large-Scale,Population-Based Case-Control Study

Objective: Lung cancer is one of the most common and deadly malignant neoplasms. Currently, it is one of the main causes of cancer deaths worldwide. The study aimed to identify and evaluate patient characteristics, demographic and lifestyle factors that are associated with lung cancer at diagnosis. Methods: The study included 400 patients diagnosed with lung cancer and 400 within the control group. The research was based on a clinical, direct, individual, structured, in-depth and focused interview. Assessment of activity and BMI was used according to WHO recommendations, as well as the expert system. Results: The mean age of the patients was 74.53 ± 7.86 years, while in the control group 59.5 (7.93). There was a strong positive relationship between the incidence of tuberculosis and chronic obstructive pulmonary disease and the risk of lung cancer (p <0.001). The risk of lung cancer was significant in the case of smoking 20 or more than 20 cigarettes a day and smoking for more than 20 years (p = 0.01). Conclusions: Active and passive smoking, are a leading risk factor for lung cancer, which shows that understanding of the long-term and fatal effects of smoking is still very low in society.  No significant correlation has been found between lifestyle and risk of lung cancer. However, there was a strong positive correlation between tuberculosis and chronic obstructive pulmonary disease and the risk of lung cancer. Occupation is a predisposing factor for lung cancer occurrence.     

The fraction of lung cancer attributable to smoking in the Norwegian Women and Cancer (NOWAC) Study

Background We examined the association between active and passive smoking and lung cancer risk and the population attributable fraction (PAF) of lung cancer due to active smoking, in the Norwegian Women and Cancer Study, a nationally representative prospective cohort study.Methods We followed 142,508 women, aged 31–70 years, who completed a baseline questionnaire between 1991 and 2007, through linkages to national registries through December 2015. We used Cox proportional hazards models, to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). We calculated PAF to indicate what proportion of lung cancer cases could have been prevented in the absence of smoking.Results During the more than 2.3 million person-years of observation, we ascertained 1507 lung cancer cases. Compared with never smokers, current (HR 13.88, 95% CI 10.18–18.91) smokers had significantly increased risk of lung cancer. Female never smokers exposed to passive smoking had a 1.3-fold (HR 1.34, 95% CI 0.89–2.01) non- significantly increased risk of lung cancer, compared with never smokers. The PAF of lung cancer was 85.3% (95% CI 80.0–89.2).Conclusion More than 8 in 10 lung cancer cases could have been avoided in Norway, if the women did not smoke.Subject terms: Epidemiology, Oncology     

Smoking, passive smoking and lung cancer cell types among women in Poland.

A case-control study involving 242 women with histologically confirmed lung cancer and 352 healthy controls, was conducted in Cracow, Poland between 1991 and 1997. Subjects were interviewed about their exposure to smoking, passive smoking and other suspected risk factors, according to a structured questionnaire. Multivariate analysis has shown that cigarette smoking was the most strongly active risk factor in female lung cancer. The strongest influence of this factor was observed with reference to small cell carcinoma and squamous cell carcinoma. It has also been observed that passive smoking exposure during childhood before the age of 18, significantly increased risk of squamous cell carcinoma, small cell carcinoma and all cell types combined. A similar effect was observed for adenocarcinoma, but there was no statistical significance.