吸烟、饮酒及其交互作用对糖尿病发病的影响

目的:探讨吸烟和饮酒及其交互作用对糖尿病发病的影响.方法:研究数据为中国瑞慈医疗集团2010—2016年所有体检者的医疗记录.利用此数据进行回顾性队列研究.通过问卷调查进行资料收集,包括基本情况调查、身体测量和生化指标检测3个部分.采用相乘模型和相加模型分析吸烟与饮酒及其交互作用对糖尿病发病的影响.结果:根据筛选标准纳...     

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.     

吸烟、饮酒和吸烟饮酒协同作用对脑血流动力学的影响

目的比较吸烟、饮酒和吸烟饮酒协同作用对脑血流动力学的影响。方法采用经颅多普勒检测技术对吸烟组(每天吸烟量﹥10支),饮酒组(经常饮白酒或有色酒每天﹥100g或啤酒每天﹥1L),吸烟、饮酒混合组(达到以上两种标准)的3组473例病人的脑血流动力学进行观察和比较,并对吸烟、饮酒和吸烟饮酒混合组在3个年龄组(青年组、中年组、老年组)的脑血流动力学的改变进行比较。结果脑血管狭窄或闭塞以吸烟饮酒混合组最明显共61例、吸烟组次之34例、饮酒组相对较低共17例(χ2=26.38,P﹤0.05)。引起血流减慢原因也是吸烟饮酒混合组最突出(χ2=9.34,P﹤0.05),而单吸烟组和单饮酒组之间无明显差异。在青年组和中年组中导致血流减慢的主要因素是烟酒混合组(χ2=9.6,P﹤0.01,χ2=8.7,P﹤0.05);老年组中导致血流减慢吸烟、饮酒和混合组三者之间差异无统计学意义(χ2=4.77,P﹥0.05)。在青年组中导致血管狭窄或闭塞吸烟、饮酒和混合组三者之间无明显差异(χ2=4.27,P﹥0.05),但在中、老年组中导致血管狭窄或闭塞以吸烟饮酒混合组明显(χ2=12.30,P﹤0.05、χ2=8.76,P﹤0.05),吸烟和饮酒组之间无明显差异。结论吸烟比饮酒更易导致脑血管狭窄或闭塞,而吸烟饮酒对脑血管狭窄或闭塞的形成有协同作用,并促使脑血流减慢随着年龄的增加向脑血管狭窄或闭塞转化。     

职业紧张对吸烟及饮酒行为影响

目的 探讨职业紧张相关因素对吸烟、饮酒行为的影响.方法 采用横断面研究方法对115名男性机车调度员进行调查,采用职业紧张测量工具测试职业紧张因素、人格特征、心理性紧张反应,调查吸烟饮酒行为.结果 工作负荷、工作紧张、特质焦虑、内控性、状态焦虑、躯体抱怨和每日紧张感高评分组吸烟率高于低评分组,技术利用程度、积极的应对方式、工作中的人际关系和自尊感高评分组吸烟率低于低评分组,差异均有统计学意义(P ＜0.05或P＜0.01);工作负荷需求、A型行为、外控性、抑郁障碍、睡眠障碍及躯体抱怨高评分组饮酒率高于低评分组,社会支持、积极应对方式和自尊感高评分组饮酒率低于低评分组,差异均有统计学意义(P＜0.05).多因素logistic回归分析结果显示,特质焦虑(OR=1.485)和躯体抱怨(OR =2.135)是引发吸烟行为的危险因素,而工作中的人际关系(OR =0.044)和决定自由度(OR=0.153)是减少吸烟行为的保护因素,外控性是引发饮酒行为的危险因素(OR=1.549).结论 职业紧张因素和不利于应对应激的人格特征以及由此引发的心理紧张反应可能会引起吸烟、饮酒行为的改变.     

多环芳烃暴露与饮酒影响非吸烟人群心理健康状况的交互作用

目的  探讨多环芳烃(polycyclic aromatic hydrocarbons, PAHs)暴露与饮酒影响非吸烟人群心理健康的独立与交互作用。 方法  本研究对513名广西壮族自治区(简称广西)某大型企业非主动吸烟员工进行问卷调查、心理健康评估。使用一般心理健康问卷量表评估研究对象心理健康状况;尿中羟基多环芳烃(hydroxypolycyclic aromatic hydrocarbons, OH-PAHs)水平作为PAHs的内暴露指标;采用logistic回归分析模型和广义线性模型分析PAHs与饮酒的独立和交互作用对心理健康状况的影响。 结果  本组研究对象年龄为(39.60±6.60)岁,44.2%的职工饮酒,饮酒者多为未婚、男性、有二手烟暴露(均有P < 0.05)。logistic回归分析模型结果显示,总体研究对象尿液1-羟基萘(1-hydroxynaphthalene, 1-OHNAP)和总羟基萘(total hydroxynaphthalene, ∑OHNAPs)浓度增加会引起人群心理健康状况不良的发生风险增高(OR=1.23, 95% CI：1.01~1.49;OR=1.10,95% CI：1.00~1.21;均有P < 0.05)。交互分析结果显示,与不饮酒组及低水平尿OH-PAHs相比,尿中1-OHNAP、2-羟基萘(2-hydroxynaphthalene, 2-OHNAP)、∑OHNAPs和总羟基多环芳烃(total hydroxypolycyclic aromatic hydrocarbons, ∑OHPAHs)浓度与饮酒的交互作用增加中老年人发生心理健康状况不良的风险(OR=3.91, 95% CI: 1.01~15.11; OR=3.69, 95% CI: 1.05~12.98; OR=1.96, 95% CI: 1.01~3.80; OR=1.73, 95% CI: 1.06~2.93;均有P_int＜0.05)。 结论  PAHs暴露是非吸烟人群心理健康状况不良的危险因素,并且饮酒会增加PAHs对非吸烟中老年人不良心理健康状况的发生风险。     

饮酒与肺癌发病关联的Meta分析

目的探讨饮酒与肺癌的关系。方法全面检索相关文献,应用Meta分析方法对各研究进行数据合并与分析。结果纳入合并分析的文章共21篇,其中队列研究6篇,随访人数累计122288例,病例3053例;病例对照研究15篇,累计病例8838例,对照21591例。Meta分析饮酒与肺癌合并OR值为1.17(95%CI:0.96～1.42);男、女饮酒合并OR值分别为1.67(95%CI:0.61～4.59)和0.93(95%CI:0.51～1.68);男性饮啤酒合并OR值为1.46(95%CI:1.28～1.67);饮烈酒合并OR值为1.34(95%CI:1.02～1.74);饮酒≥7次/周与肺癌呈正相关(P<0.05)。结论饮用啤酒、烈酒和经常饮酒与肺癌有统计学关联。     

饮酒、吸烟与子宫内膜癌发病的危险关系

为研究饮酒、吸烟与子宫内膜癌的关系,开始于1986年的荷兰队列研究,以自我检测问卷方式调查了62573名妇女的饮食习惯以及其他的癌症危险因素的暴露情况.经过11.3年的随访,共有280名子宫内膜癌患者可供分析.经多因素分析,饮酒者相对于不饮酒者的RR为1.06(95%CI:0.78～1.43),并且所有类型的酒精饮料和子宫内膜癌之间都没有关联,也不存在剂量-反应关系.曾经吸烟和当前吸烟相对于非吸烟者的RR分别为0.83(95%CI:0.58～1.20)和0.59(95%CI:0.40～0.88).当把体重指数和绝经年龄加入分析模型后结果没有显著改变.研究认为,饮酒和子宫内膜癌之间没有关联;当前吸烟能降低子宫内膜癌的发病危险.这种关联不受体重指数和绝经年龄的影响.     

肥胖与吸烟的交互作用对糖尿病的影响分析

目的探讨肥胖与吸烟之间的交互作用对糖尿病的影响,为糖尿病的防治提供科学依据。方法采用多阶段分层整群抽样,以2014年北京市房山区18~79岁成人人群慢性病及其危险因素监测人群为基础扩大样本量,进行问卷调查,体格检查及实验室检查,纳入研究的调查对象共2 685名。采用R语言3.1.1版本软件,利用乘法模型和加法模型评价超重或肥胖、中心型肥胖与吸烟的交互作用对糖尿病的影响。结果将年龄、性别、文化程度和饮酒作为混杂因素纳入到logistic回归模型中,结果显示,超重或肥胖、中心型肥胖及吸烟均与糖尿病有关联性,其OR值分别为1.85(1.46~2.33),1.87(1.51~2.30),1.32(1.03~1.64)。交互作用分析结果显示,超重或肥胖与吸烟对糖尿病的加法交互作用有统计学意义,SI为2.33(95%CI:1.34~3.31),中心型肥胖与吸烟对糖尿病的交互作用均无统计学意义(P0.05)。结论降低体重及积极控烟有利于预防糖尿病的发生。     

ABO血型及其和吸烟的交互作用与肺癌易感性

目的：探讨ABO血型及其与吸烟交互作用与肺癌的相关性。方法：肺癌病例143例,年龄、性别匹配的对照121例;血清学方法检测血型,面访或查阅病历调查,分层分析血型与吸烟的交互作用。结果：单B型血者与肺癌无显著性联系,单吸烟者则联系显著,OR值2．09,同时具有B型血并吸烟,则联系非常显著,其OR值达5．88。结论B型血是肺癌的可能是易感标志,并与吸烟具有协同作用。     

吸烟及饮酒对噪声作业工人听力的影响

目的：探讨吸烟及（或）饮酒对噪声作业工人听力的影响.方法：对某机械厂388名男性噪声作业人员的职业健康体检资料进行分析.结果：吸烟〉10支/d组高频听力异常的发生率明显高于吸烟≤10支/d组（χ^2=8.85,P〈0.01）;饮酒〉50 g/d组高频听力异常的发生率明显高于饮酒量≤50 g/d组（χ^2=11.62,P〈0.01）.结论：大量吸烟、饮酒对噪声作业工人的高频听力有影响,建议企业在加强个人防护、改善工艺、降低噪声的同时,应注意对工人进行健康教育,改变其不良生活习惯,控制噪声聋的发生.     

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.     

烟熏、油炸和腌制食品联合吸烟饮酒与原发性肺癌的关系

目的探讨腌制、油炸和烟熏食品联合吸烟、饮酒对原发性肺癌发病风险的影响。方法采用以医院为基础的病例-对照设计,于2006年1月—2013年12月面访福建医科大学附属协和医院、附属第一医院和南京军区福州总医院经组织病理确诊的1902例(24～90岁)原发性肺癌新发病例及同期按病例组相同性别、年龄(±3岁)匹配的2026例(23～87岁)社区人群。利用非条件Logistic回归分析腌制、油炸和烟熏食品与吸烟饮酒的联合作用、交互作用,探讨其与原发性肺癌发病风险的关系。结果非条件Logistic回归分析结果表示,油炸食品和烟熏食品的摄入均为肺癌发生的危险因素。油炸食品摄入≥3次/周者肺癌发病风险是油炸食品摄入<3次/周者的2. 954倍(95%CI 2. 065～4. 226);烟熏食品摄入≥3次/周者肺癌发病风险是烟熏食品摄入<3次/周者的6. 774倍(95%CI 3. 309～13. 866)。联合作用分析结果显示食品摄入得分为1且合并吸烟饮酒者肺癌发病风险是食品摄入得分为0且不吸烟不饮酒者的2. 108倍(95%CI 1. 551～2. 865);食品摄入得分≥2合并吸烟饮酒时肺癌发病风险是食品摄入得分为0且不吸烟不饮酒组的2. 191倍(95%CI 1. 377～3. 484)。此外,交互作用分析结果显示同时摄入(≥1次/周)腌制、油炸和烟熏食品中的两种或两种以上食品会导致原发性肺癌发病风险升高(OR=1. 309,95%CI1. 010～1. 696),并且多种危险食品的同时摄入也会增加吸烟者的原发性肺癌发病风险(OR=1. 625,95%CI 1. 162～2. 274),随着危险食品高频摄入种类的增加,吸烟者肺癌患病风险增大,呈剂量-反应关系(P趋势<0. 001)。结论油炸和烟熏这两种食品的摄入均为肺癌发生的独立危险因素。此外腌制、油炸和烟熏食品与吸烟和饮酒存在联合作用,这些危险因素同时存在时原发性肺癌的发病风险会增加。多种危险食品的摄入会增加吸烟者的原发性肺癌发病风险。     

Alcohol drinking and tobacco smoking in gastric cancer. A case-control study

This study compares 210 cases of cancer of the stomach (138 males and 72 females) with 630 controls (414 males and 216 females) afflicted with a wide variety of diseases. All patients (cases and controls) were admitted for treatment at the University Hospital of Montevideo, Uruguay in the time period July 1985-December 1988. They were submitted to the same detailed questionnaire by 3 social workers unaware of the objectives of the study. The analysis was performed at the Louisiana State University of New Orleans, using multiple logistic regression. The variables analyzed were cigarette smoking, alcohol ingestion, salted meat intake, total vegetable consumption, total fruit consumption and "mate" ingestion. Strong positive associations were found in both sexes for low fruit and vegetable consumption, high intake of salted meat and "mate" ingestion. Only males showed significantly elevated OR's for tobacco smoking and alcohol drinking. Of the main tobacco variables, time-dependent one's (age at start, duration) displayed significant gradients of increasing risks. Thus, a prolonged exposure seems more important than the amount smoked per day for the risk of developing gastric carcinoma. Both wine and hard liquor carried increased OR's, but heavy drinkers of wine displayed a six-fold increase in risk, replicating previous reports from France.     

吸烟、危险职业与膀胱癌关系的病例对照研究

目的　探讨吸烟危险职业对我国人群膀胱癌发生作用。方法　应用 110例膀胱癌住院进行了病例对照研究。结果　吸烟者有显著升高的膀胱癌危险度 (OR =2 .13,95 %CI为 1.18— 3.84) ,尤其吸烟年限在 40年以上者 ,其危险度高达 4.10倍。开始吸烟年龄越小危险性越大 ,并随吸烟年限、吸烟量、吸烟深度的增加而增加 ,随戒烟年限的增加而减小 ,呈明显的剂量———反应关系。危险职业暴露者患膀胱癌的危险性增加 (OR =3.5 3) ,开始暴露年龄越早危险性越高 ,并随暴露年限的增加而增加。吸烟与危险职业暴露对膀胱癌的发生有交互作用 ,其相对超额危险度为 4.6 8。结论　吸烟对膀胱癌既是诱癌因素又是促癌因素 ,且吸烟者又暴露于危险职业则发生膀胱癌的危险性将显著增加     

A study of the interaction of alcohol drinking and tobacco smoking among French cases of laryngeal cancer.

Laryngeal cancer represents an important cause of cancer in France, and the individual effects of alcohol and tobacco on this cancer site are well known. However the problem of the interaction between these agents is less extensively documented, and the role of the high consumptions of alcohol has not been studied frequently. A case-control analysis was undertaken to investigate the joint effect of alcohol and tobacco by comparing 197 glottic and 214 supraglottic cancer cases to 4135 controls representative of the French general population. Heavy drinkers were available from the two groups of cases, the highest alcohol category being equivalent to a consumption of more than 2 litres of wine per day. The relative risks estimated for heavy drinkers and smokers were high, and the results indicated an even stronger effect of alcohol drinking and tobacco smoking on the upper part of the laryngeal region. Additive and multiplicative models were fitted to the data. The multiplicative hypothesis was found to be the most appropriate, implying that the risks associated with alcohol and tobacco multiply when the exposures occur simultaneously. The public health implications of this result and the contribution of heavy drinkers and smokers to the frequency of upper respiratory and digestive tract cancers are discussed.     

Learning the relationship between smoking,drinking alcohol and the risk of esophageal cancer

This study examined the effect of outcome feedback on learning the multiplicative relationship between daily intakes of tobacco and alcohol, and the risk of esophageal cancer. In the first of two experiments, 65 French adults judged the risk of esophageal cancer associated with combinations of five levels of intake of tobacco and five of wine. They made these judgments both before and after learning sessions in which they were shown the actual risk for each vignette. In the second experiment, 35 French adults underwent the same testing and learning, and were re-tested twice 1 month later. The study hypotheses were supported. First, prior to the learning sessions, the participants used a subadditive rule to combine the perceived risk of esophageal cancer from smoking and drinking. Second, they learned after only one training session to change to the multiplicative rule that is consistent with epidemiological data. Third, this learning persisted for 1 month. This methodology may prove useful in correcting people's underestimation of their health risks.     

GSTM1, smoking and lung cancer: a case-control study

BACKGROUND: We conducted a case-control study to examine the risk of lung cancer in relation to GSTM1 polymorphism and cigarette smoking (primarily of black tobacco) in a French population. METHODS: The 611 subjects were 301 incident lung cancer cases and 310 hospital controls. We were able to constitute a DNA bank for 547 subjects (89.5%) and gather detailed information on smoking history for all of them. Results presented here concern 247 cases and 254 controls. RESULTS: Taking non- or light smokers as the reference category, we estimated odds ratios (OR) of 4.2 (95% CI: 2.6-6.7) and 5.2 (95% CI: 3.3-8.3) for the medium and heavy smokers respectively. On the other hand we estimated that the crude OR associating GSTM1 with lung cancer was 1.3 (95% CI: 0.9-1.8). Furthermore our data do not depart significantly from a multiplicative model of the combined effects of smoking and GSTM1 deficiency. CONCLUSIONS: We conclude that smoking and the GSTM1 gene are each a risk factor for lung cancer, and that their combined effect does not differ significantly from that of a multiplicative model.     

Oesophageal cancer mortality: relationship with alcohol intake and cigarette smoking in Spain.

STUDY OBJECTIVE--The aim of the study was to explore temporal changes in mortality from oesophageal cancer that could be related to tobacco and alcohol consumption. DESIGN--The study used mortality trends from oesophageal cancer over the period 1951-1985. In addition, available trends on per capita consumption of alcohol and cigarettes are also presented. SETTING--Data for this study were derived from Spain's National Institute for Statistics. MAIN RESULTS--Age standardised mortality rates from oesophageal cancer have increased significantly among men in Spain from 1951 to 1985 (p less than 0.01). Mortality rates in women have not changed significantly during the same period, although there is evidence of a certain decrease in recent years. Trends of per capita cigarette consumption from 1957 to 1982 related positively with oesophageal cancer mortality among men, whereas no significant relationship was observed in women. Trends of beer, spirits, and total alcohol consumption were also positively correlated with oesophageal cancer mortality in men. Among women, a weaker relationship was found. Wine consumption showed no relationship with oesophageal cancer mortality either in men or women. CONCLUSIONS--These results are similar to those found in other studies, supporting a role of alcohol (spirits and beer) and cigarette consumption in causation of oesophageal cancer. No relationship was observed with wine consumption.     

吸烟与缺血性脑卒中关系的病例-对照研究

目的探讨吸烟与缺血性脑卒中的关系。方法采用病例-对照研究的方法,通过调查问卷收集缺血性脑卒中患者及对照者的研究信息。在哈尔滨医科大学附属第二医院神经内科收集的缺血性脑卒中住院患者1037例作为病例组,同期在黑龙江省电力医院体检中心参加健康体检的自愿者1205例作为对照组。统计分析采用Logistic回归,分析吸烟与缺血性脑卒中的关系。结果吸烟与缺血性脑卒中有关联,OR=1.368,95%CI 1.158~1.616。调整年龄、体质指数、腰臀比、血压、血糖、血脂、脑卒中家族史和饮酒因素后,吸烟与缺血性脑卒中仍存在关联,OR=2.158,95%CI 1.293~3.600。随着吸烟量的增加,患缺血性脑卒中的危险性也在增加,与不吸烟者相比,1~9支/天、10~19支/天和20~支/天的OR值分别为1.097、1.168和2.950。结论吸烟是缺血性脑卒中的危险因素。     

Arsenic exposure, smoking, and lung cancer in smelter workers--a case-control study

A cohort of 3,916 Swedish copper smelter workers employed for at least 3 months between 1928 and 1967 was followed up through 1981. Arsenic exposure was estimated for different time periods at each workplace within the smelter. Detailed job records were linked to the exposure matrix, thus forming individual cumulative arsenic exposure measures for each smelter worker. Smoking history was collected for 107 lung cancer cases and 214 controls from the cohort. Lung cancer risks were positively related to cumulative arsenic exposure with smoking standardized relative risks ranging from 0.7 to 8.7 in different exposure groups. A negative confounding by smoking was suggested in the higher exposure categories. The interaction between arsenic and smoking for the risk of developing lung cancer was intermediate between additive and multiplicative and appeared less pronounced among heavy smokers.