吸烟、被动吸烟与肺癌发病风险的病例对照研究

目的 探讨吸烟、被动吸烟与肺癌的关联.方法 采用病例对照研究设计,面访肺癌新发病例1 303例和按性别、年龄(±2岁)频数匹配的健康对照1 303例.结果 吸烟是男性肺癌的重要危险因素(调整OR=4.974,95％ CI:3.933 ～6.291),随着开始吸烟年龄提前、吸烟年限延长、日吸烟量、吸烟包年以及吸烟深度的增加,患肺癌危险性增高,呈剂量反应关系(Ptrend＜0.001),戒烟≥10年患肺癌的危险性降低45.4％.男性吸烟患肺鳞癌的危险性比患肺腺癌大.被动吸烟是非吸烟者肺癌的危险因素(调整OR=1.912,95％CI:1.486～2.460),工作环境被动吸烟的男性非吸烟者患肺癌的调整OR为2.221(95％CI:1.361 ～3.625),家庭环境被动吸烟的女性非吸烟者患肺癌的调整OR为1.804(95％ CI:1.270～2.562).68.04％男性肺癌的发生可归因于吸烟,26.51％非吸烟者肺癌的发生可归因于被动吸烟.结论 吸烟是肺癌的重要危险因素,工作环境被动吸烟是男性非吸烟者肺癌的主要危险因素,家庭环境被动吸烟是女性肺癌的主要危险因素.戒烟具有重大的公共卫生学意义.     

吸烟及烟碱型乙酰胆碱受体亚单位α5基因rs17486278位点多态性对肺癌的交互作用

目的 探讨在中国男性人群中吸烟、烟碱型乙酰胆碱受体亚单位α5(CHRNA5)基因多态性与肺癌的关联及其交互作用.方法 采用成组病例对照研究设计,收集男性原发性肺癌病例204例,正常健康对照者821例.采用结构式问卷调查社会人口学特征、吸烟行为及健康状况等,采集静脉血检测CHRNA5 SNP位点rs17486278的多态性.应用多因素logistic回归模型分析吸烟、CHRNA5的基因多态性与肺癌的关系及其交互作用.结果 控制潜在混杂因素后,每天吸烟量＞15支者发生肺癌的风险高于不吸烟者(OR=3.49,95％CI:2.29～ 5.32),未发现CHRNA5上的rs17486278多态性与肺癌有统计学关联.进一步交互作用分析显示,每天吸烟量1～15支并携带rs17486278纯合变异基因型(CC)者对肺癌的发生存在正交互作用(OR=16.13,95％CI:1.27～205.33).根据rs17486278多态性和吸烟行为进行分层分析,与不吸烟并携带rs17486278野生基因型(AA)者相比,每天吸烟量1～15支并携带纯合变异基因型(CC)者、每天吸烟量＞15支并携带野生基因型(AA)者和每天吸烟量＞15支并携带杂合变异基因型(AC)者发生肺癌风险增高,OR直分别为8.14(95％CI:1.17 ～ 56.56)、3.84(95％CI:1.30～ 11.40)和5.32(95％CI:1.78 ～ 15.93).结论 在中国男性人群中CHRNA5的基因多态性与吸烟行为对肺癌的发生存在正交互作用.     

国内吸烟、饮酒与缺血性脑卒中关系的Meta分析

目的探讨吸烟、饮酒与缺血性脑卒中的关系.方法应用Meta分析方法对检索到的国内10个吸烟、饮酒与缺血性脑卒中关系的研究结果进行定量综合分析,一致性检验后,应用随机效应模型(D-L法)计算,合并比值比(OR)及其95%的可信区间(95% CI).结果吸烟、饮酒的合并OR(95% CI)分别为2.01(1.41～2.85)和2.36(1.87～2.98).吸烟、饮酒高危人群缺血性脑卒中的病因分值为50.25%和57.63%,一般人群归因危险百分比为26.66%和34.83%.结论吸烟、饮酒是我国缺血性脑卒中的重要危险因素,开展人群戒烟限酒干预是缺血性脑卒中病因预防的一项重要措施.     

Association between Genetic Polymorphisms of N-acetyltransferase 2, Environmental Factors and Female Breast Cancer

目的 分析N-乙酰基转移酶-2( NAT2)基因多态性和环境因素与女性乳腺癌的关系.方法 采用以医院为基础的1:1配对的病例-对照研究,收集唐山市原发性乳腺癌新发女性患者48例与相应非肿瘤患者48例.以问卷调查收集各研究对象的饮食习惯和生活方式、生理生育、环境暴露和职业接触、既往病史、心理等信息.采用聚合酶链反应-限制性片段多态性(PCR-RFLP)技术检测NAT2的野生型等位基因WT、突变型等位基因M1、M2和M3突变频率,分析NAT2基因多态性和环境危险因素与女性乳腺癌的关系.结果 被动吸烟大于或等于10年(OR=3.957,95％CI:1.589～10.002)、居住地环境污染(OR=33.571,95％CI:4.270～263.967)、职业接触(OR=9.400,95％CI:1.127～78.405)、烹调时使用排油设备(OR=0.177,95％CI:0.060～0.529)、农药的使用(OR=28.200,95％CI:3.576～222.389)等是乳腺癌的环境危险因素.携带M2、M3等位基因可能是乳腺癌的危险因素,OR值分别为2.563(95％CI:1.155～5.707)和2.083(95％CI:1.068～4.062),而M1等位基因频率在病例组与对照组的分布差异无统计学意义(x2=0.447,P＞0.05).病例组与对照组突变杂合子基因型(WT/Mx)分布频率差异无统计学意义(x2=0.021,P＞0.05),而两组间突变纯合子(Mx/Mx)分布频率差异有统计学意义(OR=3.545,95％CI:1.141～11.015).慢乙酰化表型者患乳腺癌的风险是快乙酰化表型者的3.364倍(x2=7.599,P＜0.05).分层分析发现NAT2慢乙酰化表型与被动吸烟大于或等于10年存在交互作用(OR=9.917,95％CI:1.597～61.597).结论 NAT2基因多态性和部分环境危险因素与乳腺癌发病存在统计学关联.     

中国高校学生吸烟危险因素的Meta分析

目的 探讨影响中国高校学生吸烟的危险因素,为制定预防教育措施提供科学依据.方法 利用Meta分析方法综合分析公开发表的有关我国高校学生吸烟影响因素的17篇文献.结果 我国高校学生吸烟危险因素的单因素分析合并OR值及95％ CI分别为:朋友吸烟3.84(3.09 ～4.77)、教师吸烟2.21(1.60 ～3.07)、父母吸烟1.81(1.43 ～2.30);多因素分析合并OR值及95％ CI分别为:父母吸烟1.66(1.39～1.98)、教师吸烟1.48(1.21 ～1.82)、朋友吸烟2.39(1.96 ～2.91)、专业2.05(1.20 ～3.50)、吸烟态度2.89( 1.85 ～4.54)、每月生活费2.84(2.18 ～3.71)、低年级1.24(1.00～1.54)、同学吸烟1.40(1.02 ～1.91)、母亲文化程度0.34(0.18 ～0.62)、饮酒4.84(3.03～7.72).结论 饮酒、吸烟态度、月生活费、朋友吸烟、专业、父母吸烟、教师吸烟、同学吸烟是我国高校学生吸烟的危险因素.     

环氧化酶2遗传变异与吸烟交互作用影响肺癌易感性

目的 探讨环氧化酶2(COX2)启动子区-1195G＞A遗传变异与肺癌遗传易感性的关系以及与吸烟的交互作用.方法 以2000年1月至2008年12月在中国医学科学院肿瘤医院就诊的956例肺癌患者作为病例组;健康对照来自同期北京市健康体检个体,以无肿瘤病史和体征者作为对照组,共994名.研究对象均为汉族,无年龄、性别限制.对照组与病例组相匹配.经知情同意,每名研究对象均采集2 ml外周血,以PCR-限制性片断长度多态性方法对研究对象进行基因分型,并且调查了对象的吸烟情况.以logistic回归法计算COX2-1195G＞A变异各基因型影响肺癌发病风险的OR值及95％ CI.结果 对照组、病例组基因分型为COX2-1195AA者分别占24.9％ (247/994)、28.3％ (271/956).与-1195GG基因型携带者相比,-1195AA基因型携带者肺癌的发病风险增加1.36倍(95％ CI:1.03～ 1.79).以吸烟进行分层分析,在吸烟人群中,携带COX2-1195AA基因型者,肺癌的发病风险明显增高,其OR(95％ CI)为1.56(1.08 ～2.25);在非吸烟组,未发现肺癌发病风险在不同基因型之间的差异(OR=1.17;95％ CI:0.77 ～ 1.61).在重度吸烟者(＞20包/年)中,-1195AA和-1195AG基因型携带者发生肺癌风险分别是-1195GG携带者的1.85倍(95％ CI:1.16 ～2.95)和1.62倍(95％CI:1.08 ～2.43);在轻度吸烟者(≤20包/年)中,-1195AG和AA基因型携带者发生肺癌风险的OR(95％ CI)分别为0.78(0.47 ～ 1.30)和1.08(0.60～1.94).结论 COX2启动子区遗传变异对肺癌发病风险的相关性和环境因素密切相关.     

上海市社区人群高血压危险因素聚集与患病关系的研究

目的 <\b>研究超重与中心型肥胖、家族遗传史、不适量饮酒、吸烟、血脂异常和高血糖6项危险因素的聚集与高血压患病间的关系.方法 <\b>利用2008-2011年对15 158名35 ～ 74岁上海市社区居民进行的心脑血管疾病社区综合防治研究项目数据,采用单因素和多因素统计方法,描述危险因素聚集与高血压之间的相关性,使用纵向队列进一步对因果关系进行探讨.结果 <\b>基线调查高血压总现患率为41.9％.随着高血压危险因素聚集数目的增加,与高血压患病关联的OR值(按年龄调整)增大.聚集数目为1～5项及以上的男性其OR值依次为3.157 (95％CI:2.152 ～ 4.630)、6.428 (95％CI:4.435 ～ 9.319)、11.797 (95％CI:8.135～ 17.105)、19.723 (95％CI:13.414 ～ 29.000)、33.051 (95％ CI:21.449～50.930),聚集数目为1～4项的女性其OR值依次为2.917 (95％CI:2.374～ 3.585)、6.499 (95％CI:5.307～ 7.959)、15.717 (95％CI:12.609～ 19.591)、31.719(95％CI:21.744～ 46.270).在纵向队列中,男性和女性的2年发病率分别为1.9％和1.6％.同无危险因素人群相比,聚集数目较多的人群2年发病率较高,女性中当聚集数目为2及3项时其RR值分别为2.111(95％CI:1.024 ～ 4.350)、3.000(95％CI:1.287 ～ 6.995),差异有统计学意义.结论 <\b>随着危险因素聚集数目的增加,高血压患病风险升高,应对危险因素进行综合防控.     

CYP1A1和GSTM1基因多态与肺癌发病关系的病例-对照研究

目的 探讨肺癌易感性标记物CYP1A1及GSTM1基因多态以及吸烟等其他环境暴露因素与肺癌发生的关系。方法 采用病例-对照研究的方法，收集原发性肺癌病例91例以及非肺部疾患的住院病例(对照)91例，所有的研究对象均采静脉血进行DNA抽提，并用PCR方法检测CYP1A1以及GSTM1基因多态，同时调查研究对象吸烟等其他环境暴露因素。应用Logistic回归分析方法进行单因素和多因素的分析。结果 无论是单因素分析还是多因素分析均未显示出CYP1A1和GSTM1基因多态与肺癌发病的关联。多因素分析结果表明：化程度的OR为0．63(95％CI：0．45～0．86)，吸烟量的OR为1．56(95％CI：1．14～2．14)，无抽油烟机的OR为3．77(95％CI：1．48～9．56)，食用动物油的OR为1．67(95％CI：1.25～2．24)，常吃胡萝卜的OR为0．47(95％CI：0．22～0．98)，饮酒的OR为6．58(95％CI：1.53～28．30)，家族肺癌史的OR为3．75(95％CI：1．64～8．58)。结论 CYP1A1和GSTM1基因多态与肺癌发病无明显的关联，吸烟、饮酒、食用动物油、家族肺癌吏以及无抽油烟机是肺癌的危险因素，而高化程度和常吃胡萝卜与降低肺癌风险有关。     

浅析重症感染患者ICU治疗时间危险影响因素

目的:分析重症感染患者ICU治疗时间的危险影响因素.方法:以120名重症感染患者为研究对象,并按照治疗时间合理分为研究组(超过48小时,56名患者)以及对照组(不超过48小时,64名患者).收集2组患者的临床资料[心率(HR)、平均动脉压(MAP)、血清乳酸(LA)水平及急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分、多器官功能障碍综合征(MODS)发生率、序贯器官衰竭评估(SO-FA)评分和弥散性血管内凝血(DIC)发生率],并对重症感染ICU治疗时间较长的危险因素使用多因素非条件Logistic回归分析.结果:研究组患者HR值、SOFA评分和DIC发生率、血清LA水平及APACHEⅡ评分、MODS发生率结明显要比对照组高(均P<0.05).HR(OR=4.683,95％CI2.977～12.4534,P<0.05)、血清LA水平(95％CI1.442～3.769,OR=3.521,P<0.05)、DIC发生率(95％CI1.025～1.663,OR=1.039,P<0.05)、MODS发生率(95％CI1.035～1.784,OR=7.655,P<0.05)、APACHEⅡ评分(95％CI1.256～1.795,OR=3.110,P<0.05)、SOFA评分(95％CI1.271～1.973,OR=2.879,P<0.05)都是致使重症感染ICU治疗时间长的危险因素.结论:重症感染患者ICU治疗时间的影响因素较多,临床上必须要加强重视这些影响因素[1].     

老年人吸烟、饮酒与脑卒中的流行病学研究

目的 研究吸烟、饮酒及其他危险因素与脑卒中及其分型的关系。方法 对象为北京市万寿路地区60岁以上老年人群的分层随机抽样样本。共调查2096人，分析吸烟、饮酒及其他危险因素与脑卒中的关系。结果 单因素分析时吸烟的OR值为1.17(95％CI:1.01～1.35)。饮酒在男性脑卒中及脑梗塞的OR值(95％CI)分别是0.69(0.51～0.94)、0.71(0.52～0.98)；调整其他主要因素后，吸烟致脑卒中、脑出血的相对危险性OR值(9596CI)分别为1.19(1.02～1.39)、1.53(1.03～2.27)；饮酒似为脑卒中的保护因素，OR值(95％CI)为0.78(0.61～0.99)。另外与脑卒中有显著相关的危险因素包括年龄、收缩压、高密度脂蛋白、高血压、冠心病、糖尿病、高血脂、脑卒中家族史。结论 吸烟是脑卒中的危险因素，适量饮酒对其似有保护作用。     

脑溢血术后复发影响因素分析

目的了解脑溢血术后复发的相关因素,为健康教育策略的制定提供科学依据。方法采用方便抽样方法选取2012年1月—2014年1月进行微创颅脑穿刺术治疗的脑溢血复发患者75例;同期选取脑溢血未复发患者75例,调查既往病史、手术、高血压控制情况等资料,分析脑溢血复发的危险因素。结果调查对象复发比例中,文化程度中小学及以下最高（56.52%）;病史中患有高血压最高（51.49%）;术后血压偏高（61.70%）高于血压正常（30.36%）;酗酒（61.02%）高于不酗酒（42.86%）;吸烟（59.49%）高于不吸烟（39.44%）;术后从不康复训练最高（61.54%）;术后抑郁（64.91%）高于不抑郁（40.86%）,均P〈0.05。多因素分析显示发病至手术时间〈6 h（OR=1.87,95%CI：1.34～5.48）、术中抽吸量≥60%（OR=3.03,95%CI：1.09～6.04）、术后高血压偏高（OR=3.42,95%CI：1.40～8.31）、术后抑郁（OR=2.81,95%CI：1.22～6.50）是脑溢血复发的危险因素,大专及以上文化（OR=0.31,95%CI：0.14～0.69）、经常进行康复训练（OR=0.39,95%CI：0.17～0.92）是脑溢血复发的保护因素。结论脑溢血术后患者复发的危险因素复杂,增强患者对脑溢血复发相关知识的了解,可减少术后复发率;应加强对脑溢血术后患者复发的防治工作,通过健康教育提高患者对复发危险因素的认识并提高自我防护能力。     

Patterns and predictors of tobacco smoking cessation: A hospital-based study of pregnant women in Lebanon

OBJECTIVES: To describe patterns of cigarette and narghile (hubble-bubble or water-pipe) smoking before and during pregnancy and identify predictors of successful smoking cessation. METHODS: A survey was conducted on 4660 pregnant women who delivered single live births between September 1st, 2001 and December 31st, 2002 at five hospitals in Beirut, Lebanon. Women were classified into four groups according to patterns of tobacco use before and during pregnancy: 1) consistent non-users, 2) successful quitters, 3) unsuccessful quitters and 4) consistent users. RESULTS: High education (OR = 2.03, 95% CI: 0.99-4.15), adequate prenatal care (OR = 1.72, 95% CI: 1.02-2.91) and mild smoking at baseline (OR = 2.35, 95% CI: 1.36-4.09) were main determinants of successful cigarette smoking cessation, whereas successful quitters of narghile use were more likely to be nulliparous (OR = 1.80, 95% CI: 1.08-2.99) or to have a nonsmoking partner (OR = 7.57, 95 % CI: 2.31-24.78). CONCLUSIONS: Different populations should be targeted when designing smoking cessation interventions for cigarette and narghile users.     

吸烟量与CHRNA7基因多态性对高血糖症的联合作用

目的探讨吸烟量与CHRNA7基因多态性对高血糖症的联合作用。方法调查909名男性吸烟者的社会人口学特征及吸烟行为等信息,并采集静脉血检测空腹血糖及CHRNA7上SNP位点rs2337980的多态性。在控制年龄、职业和糖尿病家族史后,应用多因素Logistic回归模型,分析吸烟量和CHRNA7基因多态性对高血糖症的联合作用。结果 909名男性吸烟者中,有166人（18.3%）为高血糖症,743人（81.7%）为正常血糖者。在控制年龄、职业和糖尿病家族史后,吸烟量〉15支/天的男性比吸烟量为1～15支/天者患高血糖症的风险增高（OR=1.51,95%CI：1.06～2.14）,携带变异基因型（CC＋CT）的个体较携带rs2337980野生基因型（CC）患高血糖症的危险性增高（OR=1.74,95%CI：1.22～2.48）。在控制年龄、职业、糖尿病家族史和吸烟年数后,进一步根据CHRNA7上SNP位点rs2337980的多态性和每日吸烟量进行分层分析,以携带野生基因型（CC）且吸烟量1～15支/天者为参照组,携带野生基因型（CC）且吸烟量〉15支/天者、携带变异基因型（CT＋TT）且每日吸烟1～15支/天者和携带变异基因型（CT＋TT）且吸烟者量〉15支/天者患高血糖症的危险性呈递增趋势,OR值分别为1.81（95%CI：1.07～3.07）、2.06（95%CI：1.26～3.38）和2.52（95%CI：1.52～4.17）。但未发现每日吸烟量和rs2337980多态性对高血糖症有交互作用。结论每日吸烟量与CHRNA7基因多态性对高血糖症有联合作用。     

北京市部分区县公务员吸烟行为及其影响因素调查

目的 描述北京市部分区县公务员吸烟情况,探讨吸烟行为的影响因素.方法 从北京市5个区县的3个级别机关单位中抽取公务员1230名,采取问卷调查的方法收集资料.用非条件Logistic回归方法分析公务员吸烟的影响因素.结果 公务员的吸烟率为23.7％,男性吸烟率为45.8％.男性较女性吸烟率高（OR=108.869,95％CI：43.819～270.488）.年龄（OR=1.026,95％CI：1.008～ 1.044）,机构类别（OR =2.406,95％ CI：1.210～ 4.786）,机构级别（OR=1.502,95％CI：1.112 ～2.028）,家里禁烟规定（OR=2.535,95％CI：1.976 ～ 3.252）,烟草危害认同度（OR=0.800,95％CI：0.702 ～0.913）,公众场所禁烟态度（OR =0.833,95％CI：0.753 ～0.920）等因素是吸烟的主要影响因素.结论 北京市公务员的吸烟率有所下降,但仍需有针对性的进行健康教育,进一步降低其吸烟率.     

Influence of smoking and snuff cessation on risk of preterm birth

The mechanisms by which antenatal smoking exposure increases the risk of preterm birth remain unknown. Swedish oral moist snuff contains quantities of nicotine comparable to those typically absorbed from cigarette smoking, but does not result in exposure to the products of combustion, for example carbon monoxide. In a nation-wide study of 776,836 live singleton births in Sweden from 1999 to 2009, the authors used multiple logistic regression models to examine associations between cessation of smoking and Swedish snuff use early in pregnancy and risk of preterm birth (before 37 weeks). Compared with non-tobacco users both before and in early pregnancy, the adjusted odds ratios (OR), 95% confidence interval (CI) were OR=0.92, 95% CI 0.84-1.01, for women who stopped using snuff, and OR=0.90, 95% CI 0.87-0.94, for women who stopped smoking. In contrast, continued snuff use and smoking were associated with increased risks of preterm birth (adjusted OR=1.29, 95% CI 1.17-1.43, adjusted OR=1.30, 95% CI 1.25-1.36, respectively). The snuff and smoking-related risks were, if anything, higher for very (before 32 weeks) than moderately (32-36 weeks) preterm birth, and also higher for spontaneous than induced preterm birth. These findings suggest that antenatal exposure to nicotine is involved in the mechanism by which tobacco use increase the risk of preterm birth.     

Cigarette smoking and breast cancer.

An epidemiological case-control study was conducted in New York State, with 1617 primary breast cancer patients and an equal number of controls, to examine the relationship between cigarette smoking and breast cancer. Results showed no overall association between ever smokers versus never smokers and breast cancer risk (odds ratio [OR] = 1.03, 95% confidence interval [CI]: 0.90-1.19), nor was there any dose response trend observed with increased levels of smoking. In addition, no association was found with risk and age started smoking, age stopped smoking, amount smoked or total years smoked. Controlling for previously identified risk factors for breast cancer in the analysis did not significantly alter these relationships. Previous studies have found a difference in menopausal age among smokers compared to nonsmokers. The mean menopausal age was only slightly lower in smokers than in never smokers for both cases and controls. Breast cancer risk was observed to be close to unity for premenopausal women (OR = 0.97, 95% CI: 0.74-1.34) and postmenopausal women (OR = 1.06, 95% CI: 0.91-1.26). A recent study suggested breast cancer risk was more strongly related to starting smoking at a young age among women who smoked at least 25 or more cigarettes per day in the most recent year of smoking. This hypothesis was not supported by these data.     

Cigarette smoking and male lung cancer risk with special regard to type of tobacco.

BACKGROUND: The mortality rate from lung cancer (LC) increased sharply in Spain between 1957 and 1986. This increase has been related to a previous increase in cigarette smoking. Certain features of cigarette smoking which were frequent among Spanish smokers (use of black tobacco and use of cigarettes without filter) have been related to a higher risk of LC. METHODS: A hospital-based case-control study was conducted between December 1986 and June 1990. The 325 male patients with lung cancer included in the study (cases) were compared with 325 age-matched male controls without LC. Occupation and lifetime tobacco consumption were requested using a structured questionnaire. The LC odds ratios (OR) and 95% CI were estimated with multiple logistic regression. RESULTS: Lung cancer risk increased with cigarette consumption and duration of the habit. After adjusting for lifetime cigarette consumption and for socioeconomic level, LC risk was greater among black tobacco smokers than among exclusive blond tobacco smokers (OR = 5.0, 95% CI: 2.0-12.7); LC risk among long-term (> or =20 years) filter-tipped cigarette users was lower compared to all other smokers (OR = 0.4, 95% CI: 0.2-0.7). CONCLUSIONS: The main results of the study (a higher LC risk among black tobacco users than in exclusive blond tobacco users, and a lower LC risk among long-term filter-tipped cigarette smokers than all other smokers) have been consistent with previous case-control studies and with ecologic studies which took into account past exposure levels.     

Rapid reduction in coronary risk for those who quit cigarette smoking

The objective of this study was to determine the rate of the decline in risk of a major coronary event after quitting cigarette smoking. It was a population-based case-control study of men and women aged 35 to 69 years in Newcastle, Australia, and men and women aged 35 to 64 years in Auckland, New Zealand, between 1986 and 1994. Cases were 5,572 people identified in population registers of coronary events and controls were 6,268 participants in independent community-based risk factor prevalence surveys from the same study populations. There was a rapid reduction in risk after quitting cigarette smoking. The risk of suffering a major coronary event for men who were current cigarette smokers was 3.5 (95% CI 3.0–4.0) times higher than the risk for never smokers but this fell to 1.5 (95% CI 1.1–1.9) for men who had quit for 1–3 years. Women who were current cigarette smokers were 4.8 (95% CI 4.0–5.9) times more likely to suffer a major coronary event than never smokers and this fell to 1.6 (95% CI 1.0–2.5) for women who had quit for 1–3 years. Those who had quit cigarette smoking for 4–6 years or more had a similar risk to never smokers. These results reinforce the importance of smoking cessation. The public health message is that the benefit of giving up smoking occurs rapidly.     

中国人群吸烟与喉癌关系的Meta分析

目的综合评价中国人群吸烟与喉癌之间的关系及关联强度,为我国喉癌的防治策略提供依据。方法在CNKI、万方、维普、PubMed、ScienceDirect、SpringerLink、Wiley、ProQuest等数据库中系统检索截止2013年1月之前国内外发表的相关研究文献。所有文献检索、文献选取、文献信息的提取及文献质量评价均由两人独立进行。根据研究之间的异质性大小采用合适的方法来合并相关结果。结果纳入合格研究文献16篇,喉癌患者2730例,对照3224例。吸烟与喉癌发病关系的合并0尺值为4．08（95％CI：2．90—5．26;r=86．7％,P〈0．001）。很少吸烟者及经常吸烟者发生喉癌的OR值为分别为5．90（95％CI：3．05～11．41）及13．30（95％CI：8．03～22．03）。结合漏斗图的结果,尚不能认为目前纳入的研究存在发表偏倚（Egger,P=0．402;Begg,P=0．784）。结论在中国,吸烟会显著增加喉癌的发病风险,而且随着吸烟量的增加,喉癌的风险可能更高。     

Cigarette smoking and risk of breast carcinoma in situ

BACKGROUND: Although the associations with cigarette smoking have been explored extensively for invasive breast cancer, the relation to in situ cancer has not previously been examined in depth. METHODS: We analyzed data from a population-based case-control study of women living in Wisconsin, Massachusetts, and New Hampshire. Eligible cases of incident breast carcinoma in situ were reported to statewide registries in 1997-2001 (n = 1878); similarly aged controls (n = 8041) were randomly selected from population lists. Smoking history and other risk factor information were collected through structured telephone interviews. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated from logistic regression models adjusting for potential confounders. RESULTS: In multivariate models, the OR for breast carcinoma in situ among current smokers was 0.8, compared with never-smokers (95% CI = 0.7-1.0). Risk estimates increased towards the null with greater time since smoking cessation. Odds ratios were also less than 1.0 among women who initiated smoking in adolescence (OR = 0.8) or after a full-term birth (OR = 0.7), relative to women who never smoked. The reduced odds ratios associated with current smoking were strongest among women with annual screening mammograms (OR = 0.7; 95% CI = 0.6-0.9). Odds ratios were not less than 1.0 among current smokers without a recent screening mammogram (1.3; 0.9-2.0). CONCLUSIONS: Our findings suggest an inverse association between current smoking and risk of breast carcinoma in situ among women undergoing breast cancer screening.