妇女被动吸烟的健康影响

目的探讨被动吸烟对妇女的健康影响.方法于2002-2004年采用病例-对照的研究方法,对妇女被动吸烟与肺癌的关系、孕妇被动吸烟与足月出生小于胎龄儿的关系进行研究.妇女被动吸烟与肺癌的病例-对照研究收集北京、上海和成都指定医院经病理诊断确诊的肺癌新发住院病例157例,以1(肺癌病例):2(医院对照 人群对照)配对;孕妇被动吸烟与足月出生小于胎龄儿的病例-对照研究收集北京市足月分娩小于胎龄儿产妇155例,以1:1配对.结果妇女被动吸烟显著增加发生肺癌的相对危险性(OR=2.95),在24岁以前开始被动吸烟者发生肺癌的相对危险性显著增加(OR=4.12),经常吃动物内脏(OR=1.91)、职业接触有害物(OR=3.16)、职业接触粉尘(OR=3.41)、工作场所通风不良(OR=4.02)为非吸烟女性发生肺癌的危险因素.常吃蔬菜(OR=0.24)、常喝牛奶(OR=0.53)、经常服用维生素(OR=0.53)为非吸烟女性发生肺癌的保护因素.趋势性χ2检验显示,随着被动吸烟指数和被动吸烟年限的增加,肺癌的发生显著增加(P＜0.001).多因素条件Logistic逐步回归分析显示,被动吸烟指数≥50人·年、经常吃动物内脏、职业接触粉尘、工作场所通风不良是非吸烟女性发生肺癌的主要危险因素;常吃蔬菜、经常服用维生素是非吸烟女性发生肺癌的保护性因素.病例组与对照组在孕期体重增加少、孕期被动吸烟、工作场所通风不良、配偶身高较低和孕期进行胎教等方面的差异均有统计学意义(P＜0.01),产妇和配偶文化程度高、产妇孕前体重指数高、家庭总月收入高和孕期进行胎教等可能是足月出生小于胎龄儿的保护因素.多因素条件Logistic回归分析显示,产妇孕前体重低(OR=2.08)、孕期体重增加少(OR=2.83)、被动吸烟(OR=3.42)及孕期饮茶(OR=2.72)、孕期及怀孕之前3个月内进行染发、烫发或焗油(OR=5.67)、配偶身高较低(OR=2.92)等因素均使足月出生小于胎龄儿的相对危险性显著增加,是足月出生小于胎龄儿的主要危险因素;产妇孕前体重指数高使足月出生小于胎龄儿的相对危险性显著降低(OR=0.41),是足月出生小于胎龄儿的保护因素.结论被动吸烟是非吸烟女性发生肺癌的主要危险因素.孕期被动吸烟是足月出生小于胎龄儿的主要危险因素.     

被动吸烟与儿童哮喘关系的Meta分析

目的:探讨被动吸烟与儿童哮喘的关系。方法:采用ReviewManager4·2分析软件,对国内外15篇有关被动吸烟与儿童哮喘关系的病例对照结果进行了随机效应模型的Meta分析。结果:被动吸烟与儿童哮喘的发生关联明显(Z=4·93,P<0·00001),合并OR值为1·51,OR95%CI为1·28~1·77。结论:被动吸烟是儿童哮喘发生的一个危险因素。     

扬州市肺癌危险因素病例对照研究

目的探讨扬州市肺癌病人发病的危险因素,为肺癌病因研究提供线索。方法采用匹配病例对照研究方法,所有病例取自扬州市中医院2010年1月-2013年12月住院治疗的肺癌患者,均为病理诊断确诊病例,共425例,对照组为同期来院体检或探视病人的家属,共425例。采用自行设计的问卷进行调查,运用SPSS 13.0软件进行统计分析。结果非条件logistic回归多因素分析表明,扬州市人群肺癌的危险因素为吸烟(OR=1.831,95%CI:1.575~2.128)、负面情绪因素(OR=2.424,95%CI:1.865~3.151)、既往患有肺部疾病(OR=4.585,95%CI:3.146~6.681)、高血压(OR=1.404,95%CI:1.027~1.920);经常食用新鲜蔬菜瓜果(OR=0.426,95%CI:0.344~0.527)则是肺癌的保护因素。结论吸烟、不良情绪因素及某些慢性疾病是肺癌的危险因素,常吃新鲜瓜果蔬菜是保护因素。应大力提倡健康的生活方式,加强控烟力度,多吃新鲜蔬果,防治慢性病。     

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.     

赣榆县肺癌流行危险因素病例对照研究

目的探讨赣榆县肺癌有关危险因素及保护因素。方法对新发肺癌病例及其健康对照者的相关因素进行调查,应用非条件Logistic回归方法分析其相关危险和保护因素。结果肺癌的主要危险因素为住地有污染(OR=2.83),进食热烫食物(OR=1.56)、不按时吃饭(OR=1.18),粮食霉变(OR=1.61),吸烟部位深(OR=1.80)、家庭成员吸烟(OR=1.92)、工作场所被动吸烟(OR=1.41),饮烫茶(OR=1.71),性格抑郁(OR=1.72),常使用农药(OR=1.37);主要保护因素为经常生吃大蒜(OR=0.76),经常饮茶(OR=0.80),用冰箱保存食品(OR=0.53),粮食贮存一定的时间(OR=0.97)。结论本次研究所发现的有关结果可以为赣榆县肺癌的防治工作提供参考。     

肺癌危险因素及交互作用研究

目的探讨肺癌的影响因素及其交互作用。方法采用病例对照研究设计,收集781例肺癌病例,并按性别、年龄(±3岁)进行1:1匹配,通过调查问卷获取生活饮食习惯等信息。构建决策树及非条件Logistic回归模型,计算OR值及其95%CI,分析影响因素间的交互作用。结果肺癌的危险因素有吸烟(轻度吸烟OR=1.67,重度吸烟OR=7.27)、被动吸烟(轻度被动吸烟OR=2.63,重度被动吸烟OR=6.25)、居住地污染(吸烟者OR=2.26,不吸烟者OR=1.72)、肺癌家族史(吸烟者OR=15.94);保护因素有常吃水果(吸烟者OR=0.69,不吸烟者OR=0.44)、锻炼(吸烟者OR=0.50)、饮茶(不吸烟者OR=0.57)。吸烟与居住地污染、肺癌家族史存在交互作用,重度吸烟与不锻炼存在交互作用。结论吸烟、被动吸烟、居住地污染、肺癌家族史可增加肺癌风险,常吃水果、锻炼、饮茶有助于预防肺癌。肺癌影响因素间的协同作用应予重视。     

中国人群肺癌发病危险因素的Meta分析

[目的]探讨中国人群肺癌发生的主要危险因素,为预防决策提供依据。[方法]利用Meta分析方法对我国1995～2007年间公开发表的有关肺癌危险因素病例对照研究的12篇文献资料进行定量综合分析。[结果]各因素合并OR值及95%CI分别为:吸烟OR=2.7820(2.3428～3.3035);油烟OR=2.6257(1.7312～3.9879);家族肿瘤史OR=1.8075(1.4745～2.2157);肺结核OR=2.6018(1.8946～3.5731);慢性支气管炎OR=2.3052(1.8013～2.9500);精神因素OR=2.2648(1.8364～2.7932);饮酒OR=1.4942(1.2491～1.7873);被动吸烟OR=1.7064(0.9109～3.1965);新鲜蔬菜OR=0.5376(0.4445～0.6503)。[结论]吸烟、饮酒、油烟、家族肿瘤史、肺结核、慢性支气管炎、精神因素是目前中国人群肺癌发病的危险因素;而多吃新鲜蔬菜是肺癌发生的保护性因素。     

眉山市洪雅县老年人不良行为生活方式现状及其影响因素分析

目的了解眉山市洪雅县老年人不良行为生活方式的流行现状并探索相关影响因素。方法2018-08/10,采用多阶段整群随机抽样,对洪雅县15个乡镇60岁及以上常住居民进行调查,包括问卷调查和体格检查,共计纳入5079名60岁及以上老年人,并计算现在吸烟率、经常饮酒率、身体活动不足率和肥胖率,采用非条件Logistic回归进行多因素分析。结果洪雅县老年人现在吸烟率、经常饮酒率、身体活动不足率和肥胖率分别为27.1%、7.5%、38.6%和6.9%。经多因素分析显示,初中文化(文盲为参照,OR=1.620,95%CI:1.237~2.120)是现在吸烟的危险因素,农民职业(非农民为参照,OR=1.683,95%CI:1.342~2.112)是现在吸烟的危险因素;初中文化(文盲为参照,OR=1.863,95%CI:1.280~2.712)是经常饮酒的危险因素;高龄(70~79岁:OR=1.216,95%CI:1.074~1.378;≥80岁:OR=1.811,95%CI:1.508~2.176)是身体活动不足的危险因素,农民(OR=2.348,95%CI:1.937~2.848)是身体活动不足的危险因素;女性是发生肥胖的危险因素(OR=1.654,95%CI:1.321~2.072)。结论洪雅县老年人不良行为生活方式普遍存在,应加强老年人健康危险行为干预。     

青少年女性痛经危险因素的关联性研究

目的:探索我国青少年女性痛经危险因素的关联强度,为青少年女性痛经的预防提供依据,并推动相关研究的进展。方法:通过检索CNKI和万方数据库等国内数据库收集有关青少年女性痛经危险因素的文献,应用STATA12.0软件计算比值比OR及95%置信区间。结果:我国青少年女性痛经的发病率达到59.41%,与青少年女性痛经相关危险因素差异有统计学意义的危险因素OR及95%置信区间分别为:负性心理(OR=2.62,95%CI=1.76~3.90)、喜好或经常冷饮冷食(OR=1.34,95%CI=1.06~1.70)、睡眠质量不佳或熬夜(OR=2.65,95%CI=1.87~3.77)、初潮年龄>15岁(OR=1.74,95%CI=1.45~2.09)、月经失调(OR=1.45,95%CI=1.11~1.90)和经常吃早餐(OR=0.76,95%CI=0.59~0.96)。结论:负性心理、喜好或经常冷饮冷食、睡眠质量不佳或熬夜、初潮年龄>15岁、月经失调和经常吃早餐与我国青少年女性痛经的发生密切相关,经常吃早餐是青少年女性痛经的保护因素。     

武汉地区肺癌新病例危险因素病例对照研究

目的：探讨武汉地区肺癌主要危险因素。方法：对183例肺癌患者和183例对照进行1：1配比病例对照研究，并用Logistic回归对所获资料举行单因素和多因素分析。结果：单因素分析结果表明，呼吸系统疾病史(慢性支气管炎病史OR＝2．90，其他呼吸系统疾病OR＝3．65)，吸烟(OR＝2．33)、家庭被动吸烟(OR＝1．69)、工作场所被动吸烟(OR＝1．72)、处于精神压抑(OR＝2．07)是武汉地区肺癌主要危险因素；在单因素分析基础上，多因素分析结果仅发现慢性支气管炎(OR＝2．92)、吸烟(OR＝4．09)、工作场所被动吸烟(OR＝1．95)为肺癌主要危险因素。结论：调查结果提示，武汉地区肺癌应针对慢性支气管炎、吸烟和工作场所被动吸烟因素开展一级预防。     

A case-control study of malignant and non-malignant respiratory disease among employees of a fiberglass manufacturing facility. II. Exposure assessment.

A case-control study of malignant and non-malignant respiratory disease among employees of the Owens-Corning Fiberglas Corporation's Newark, Ohio plant was undertaken. The aim was to determine the extent to which exposures to substances in the Newark plant environment, to non-workplace factors, or to a combination may play a part in the risk of mortality from respiratory disease among workers in this plant. A historical environmental reconstruction of the plant was undertaken to characterise the exposure profile for workers in this plant from its beginnings in 1934 to the end of 1987. The exposure profile provided estimates of cumulative exposure to respirable fibres, fine fibres, asbestos, talc, formaldehyde, silica, and asphalt fumes. Employment histories from Owens-Corning Fiberglas provided information on employment characteristics (duration of employment, year of hire, age at first hire) and an interview survey obtained information on demographic characteristics (birthdate, race, education, marital state, parent's ethnic background, and place of birth), lifetime residence, occupational and smoking histories, hobbies, and personal and family medical history. Matched, unadjusted odds ratios (ORs) were used to assess the association between lung cancer or non-malignant respiratory disease and the cumulative exposure history, demographic characteristics, and employment variables. Only the smoking variables and employment characteristics (year of hire and age at first hire) were statistically significant for lung cancer. For non-malignant respiratory disease, only the smoking variables were statistically significant in the univariate analysis. Of the variables entered into a conditional logistic regression model for lung cancer, only smoking (smoked for six months or more v never smoked: OR = 26.17, 95% confidence interval (95% CI) 3.316-206.5) and age at first hire (35 and over v less than 35: OR = 0.244, 95% CI 0.083-0.717) were statistically significant. There were, however, increased ORs for year of employment (first hired before 1945 v first hire after 1945: OR = 1.944, 95% CI 0.850-4.445), talc (cumulative exposure >1000 fibres/ml days v never exposed: OR = 1.355, 95% CI 0.407-5.515), and asphalt fumes (cumulative exposure >0.01 mg/m(3) days v never exposed: OR 1.131, 95% CI 0.468-2.730). For non-malignant respiratory disease, only the smoking variable was significant in the conditional logistic regression analysis (OR = 2.637, 95% CI 1.146-6.069). There were raised ORs for the higher cumulative exposure categories for respirable fibres, asbestos, silica, and asphalt fumes. For both silica and asphalt fumes, ORs were more than double the reference groups for all exposure categories. A limited number of subjects were exposed to fine fibres. The scarcity of cases and controls limits the extent to which analyses for fine fibre may be carried out. Within those limitations, among those who had worked with fine fibre, the unadjusted, unmatched OR for lung cancer was (1.0 (95% CI 0.229-4.373) and for non-malignant respiratory disease, the OR was 1.5 (95% CI 0.336-6.702). The unadjusted OR for lung cancer for exposure to fine fibre was consistent with that for all respirable fibre and does not suggest an association. For non-malignant respiratory disease, the unadjusted OR for fine fibre was opposite in direction from that for all respirable fibres. Within the limitations of the available data on fibre, there is o suggestion that exposure to fine fibre has resulted in an increase in risk of lung cancer. The increased OR for non-malignant respiratory disease is inconclusive. The results of this population, in this place and time, neither respirable fibres nor any of the substances investigated as part of the plant environment are statistically significant factors for lung cancer risk although there are increased ORs for exposure to talc and asphalt fumes. Smoking is the most important factors in risk for lung cancer in this population. The situation is less clear for non-malignant respiratory disease. Unlike lung cancer, non-malignant respiratory represents a constellation of outcomes and not a single well defined end point. Although smoking was the only statistically significant factor for non-malignant respiratory disease in this analysis, the ORs for respirable fibres, asbestos, silica, and asphalt fumes were greater than unity for the highest exposure categories. Although the raised ORs for these substances may represent the results of a random process, they may be suggestive of an increased risk and require further investigation.     

Passive smoking and lung cancer in nonsmoking women.

OBJECTIVES. The causes of lung cancer among nonsmokers are not clearly understood. To further evaluate the relation between passive smoke exposure and lung cancer in nonsmoking women, we conducted a population-based, case-control study. METHODS. Case patients (n = 618), identified through the Missouri Cancer Registry for the period 1986 through 1991, included 432 lifetime nonsmokers and 186 ex-smokers who had stopped at least 15 years before diagnosis or who had smoked for less than 1 pack-year. Control subjects (n = 1402) were selected from driver's license and Medicare files. RESULTS. No increased risk of lung cancer was associated with childhood passive smoke exposure. Adulthood analyses showed an increased lung cancer risk for lifetime nonsmokers with exposure of more than 40 pack-years from all household members (odds ratio [OR] = 1.3; 95% confidence interval [CI] = 1.0, 1.8) or from spouses only (OR = 1.3; 95% CI = 1.0, 1.7). When the time-weighted product of pack-years and average hours exposed per day was considered, a 30% excess risk was shown at the highest quartile of exposure among lifetime nonsmokers. CONCLUSIONS. Ours and other recent studies suggest a small but consistent increased risk of lung cancer from passive smoking. Comprehensive actions to limit smoking in public places and worksites are well-advised.     

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.     

鞍钢工人的肿瘤危险度——肺癌病例-对照研究

对鞍钢男工中６１０例肺癌新发病例及９５９例对照进行了访问调查。经吸烟、其他肺疾患、家族肿瘤史、食用水果等非职业因素调整后，岗位工龄等于或超过１５年的下列工人的肺癌危险度显著增高：冶炼工和轧钢工（ＱＲ＝１．５，９５％ＣＩ＝１．１～２．２），耐火砖厂工（ＯＲ＝２．９，９５％ＣＩ＝１．４～５．９），装卸工（ＯＲ＝２．５，９５％ＣＩ＝１．０～６．１），焦炉工（ＯＲ＝３．４，９５％ＣＩ＝１．４～８．５）。各种粉尘和Ｂ［ａ］Ｐ暴露与肺癌危险性呈显著的剂量－反应关系，但与粉尘的特殊成分未见此种关联。长期暴露于污染物的钢铁工人的肺癌的危险度增加４０％。     

天津市区胃癌危险因素的配对病例对照研究

目的 进一步探讨各危险因素与胃癌的关系。方法 选取天津市市内六区1998年和1999年的189例新发胃癌病人并按性别、年龄、民族等配比条件选取该市189名健康人群进行1：1配对的病例对照研究,资料处理采用条件logistic回归分析。结果 多因素条件logistic回归分析显示胃癌的发病与下列4种因素关节密切：烟熏食品OR=2.34,95%CI：1.60-4.98;吸烟量OR=6.07,95%CI：1.26-7.16;喜食重盐饮食OR=1.95,95%CI：1.27-3.23;过量摄入动物肉类OR=1.46,95%CI：1.05-2.02。结论 经常食用烟熏食品、吸烟量大、喜食重盐饮食、过量摄入动物肉类可能是胃癌的危险因素。     

Association between asbestos exposure,cigarette smoking,myeloperoxidase (MPO) genotypes,and lung cancer risk

BACKGROUND: As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. METHODS: RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. RESULTS: Asbestos exposure was associated with a significantly elevated risk estimate (OR = 1.45; 95% CI 1.04-2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09-2.66), while A-allele carriers (G/A + A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56-1.44). The OR was further reduced to 0.73 (0.49-1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR = 2.19; 95% CI 1.16-4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR = 1.18; 95% CI 0.58-2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. CONCLUSIONS: For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer.     

Lung cancer and occupation: results of a multicentre case-control study.

The objective of the current study was to estimate the risk of lung cancer attributable to occupational factors and not due to tobacco. At 24 hospitals in nine metropolitan areas in the United States, 1793 male lung cancer cases were matched for race, age, hospital, year of interview, and cigarette smoking (never smoker, ex-smoker, smoker (1-19 and > or = 20 cigarettes per day)) to two types of controls (cancer and non-cancer hospital patients). Information on usual occupation, exposure to specific potential carcinogens, and cigarette smoking was obtained by interview. Risk of lung cancer was increased significantly for electricians; sheetmetal workers and tinsmiths; bookbinders and related printing trade workers; cranemen, derrickmen, and hoistmen; moulders, heat treaters, annealers and other heated metal workers; and construction labourers. All of these occupations are potentially exposed to known carcinogens. Odds ratios (ORs) were increased for exposure to coal dust (adjusted OR = 1.5; 95% confidence interval (95% CI) 1.1-2.1). After stratification, this association was statistically significant only after 10 or more years of exposure. Lung cancer was also related to exposure to asbestos (adjusted OR = 1.8; 95% CI 1.5-2.2). The ORs increased with increasing duration of exposure to asbestos for all smoking categories except for current smokers of 1-19 cigarettes per day. The statistical power to detect ORs among occupations that were previously reported to be at increased risk of lung cancer but that failed to show an OR of at least 1.5 in the current study was small. The cumulative population attributable risk (PAR) of lung cancer due to occupation was 9.2%. It is concluded that occupational factors play an important part in the development of lung cancer independently of cigarette smoking. Because occupations at high risk of lung cancer were under-represented, the cumulative PAR of the present study is likely to be an underestimate of the true contribution of occupation to risk of lung cancer.     

A population-based case-control study of lung cancer and green tea consumption among women living in Shanghai, China.

Epidemiologic evidence regarding the association between the consumption of green tea and lung cancer is limited and inconclusive, although experimental studies have shown consistently that tea preparations and tea polyphenols may inhibit the induction of a variety of cancers, including lung cancer. In this population-based case-control study, we examined the association between past consumption of green tea and the risk of lung cancer. We identified 649 incident cases of primary lung cancer among women diagnosed from February 1992 through January 1994 using the population-based Shanghai Cancer Registry. We randomly selected a control group of 675 women from the Shanghai Residential Registry, frequency-matched to the expected age distribution of the cases. Green tea consumption was ascertained through face-to-face interviews. We estimated adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) using unconditional logistic regression. Among nonsmoking women, consumption of green tea was associated with a reduced risk of lung cancer (OR = 0.65; 95% CI = 0.45-0.93), and the risks decreased with increasing consumption. We found little association, however, among women who smoked (OR = 0.94; 95% CI = 0.40-2.22). The inconsistency in the association between drinking tea and the risk of lung cancer reported in previous studies may in part be due to inadequate control of confounding of active smoking.     

Exposure to nickel compounds and smoking in relation to incidence of lung and nasal cancer among nickel refinery workers.

OBJECTIVES: To investigate the relation between occupational hazards among nickel refinery workers and their exposure to different forms of nickel over time and the interaction between smoking and total exposure to nickel. METHODS: The cohort consisted of 379 workers with first employment 1916-40 and at least three years of employment and 4385 workers with at least one year of employment 1946-83. Data on smoking (ever or never) were available for almost 95% of the cohort. Two analyses were used, indirect standardisation from observed and expected numbers and Poisson regression. RESULTS: During the follow up 1953-93, 203 new cases of lung cancer were observed v 68 expected (standardised incidence ratio (SIR) 3.0, 95% confidence interval (95% CI) 2.6-3.4) and 32 cases of nasal cancer were observed v 1.8 expected (SIR 18.0, 95% CI 12-25). The Poisson regression analysis showed an excess risk of lung cancer in association with exposure to soluble forms of nickel, with a threefold increase in relative risk (RR) (P < 0.001) and a multiplicative effect of smoking and exposure to nickel. The RRs were 1.1 (95% CI 0.2-5.1) for exposed workers who had never smoked and 5.1 (95% CI 1.3-20.5) for exposed workers who smoked. CONCLUSION: It is not possible to state with certainty which specific nickel compounds are carcinogenic, but a significant excess risk was found for workers exposed to soluble nickel alone or in combination with other forms of nickel. The present study suggests a multiplicative effect of smoking and nickel exposure.