沈阳市女性肺癌危险因素的病例对照研究

对沈阳市区１９９１年４月至１９９４年１２月的３１３例、年龄３５～６９岁的女性肺癌患者进行了按年龄配比１：１的病例对照研究。结果显示，女性肺癌的危险因素为吸烟、烹饪油烟暴露，其ＯＲ值与９５％可信限分别为１．８６（１．３４～２．５７）和４．３１（３．０７～６．０５），其ＰＡＲ％分别为２２％与４６％。吸烟与油烟对肺癌的发生有交互作用，其相对超额危险度为３．１２。肺癌以腺癌为主，而吸烟仅与鳞癌有关。肺结核、慢性支气管炎增加肺癌发生危险性，但无显著意义。     

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.     

儿童被动吸烟与化脓性脑膜炎

笔者对６３例１～１２岁化脓性脑膜炎患儿进行了被动吸烟与化脓性脑膜炎关系的１：１病例对照研究。结果表明，被动吸烟儿童患化脓性脑膜炎的ＯＲ值为３．００，其９５％可信限大于１，Ｐ＜０．０５；并且家长的吸烟量与儿童患化脓性脑膜炎的相对危险性之间存在着显著的剂量效应关系，Ｐ＜０．００５。提示被动吸烟是儿童化脓性脑膜炎发病的危险因素之一。     

饮茶与肺癌发病风险的病例-对照研究

目的探讨饮茶与肺癌的关联。方法采用病例对照研究设计,收集确诊的肺癌新发病例1225例和按频数匹配的健康对照1234例。采用统一编制的调查表,面访收集研究对象的一般人口学特征、居住环境、饮食史、吸烟史、饮酒史、饮茶史、疾病及家族史等资料。非条件logistic回归模型估算饮茶与肺癌发病风险的调整比值比(OR)及其95%可信区间(95%CI),并分析饮茶与吸烟的交互作用。结果饮茶可显著降低非吸烟者肺癌的发病风险,调整OR值为0.465(95%CI 0.345～0.625);随着饮茶年数的增加,肺癌发生的危险性降低;红茶、绿茶、乌龙茶、其他类型茶的调整OR值分别为0.333(95%CI 0.154～0.720)、0.522(95%CI 0.356～0.767)、0.735(95%CI 0.424～1.274)和0.267(95%CI 0.143～0.497)。每周饮茶<3次和饮淡茶者与吸烟者肺癌有显著关联(P<0.05),调整OR值分别为0.453(95%CI 0.286～0.717)和0.518(95%CI 0.346～0.778)。结论饮茶是肺癌的保护因素,尤其可明显降低非吸烟肺癌的危险性。     

原发性肺癌致病因素的研究

本文对锦州100对原发性肺癌发病的高危因素进行1∶2配对病例对照研究。用MantelHaenszel法估计各危险因素OR及其95％可信限,用条件Logistic回归模型进行分析。结果表明:慢性气管炎、精神创伤史和吸烟为锦州男性肺癌发病的高危因素;吸烟、精神创伤史和室内煤烟污染为女性肺癌发病的主要危险因素。其他因素未见有显著意义。     

抚顺市职业暴露与肺癌关系的病例对照研究

本文着重评价职业暴露与肺癌的关系。研究结果表明,病例组与对照组的职业暴露史有显著差异,有职业暴露史者患肺癌的相对危险性为 OR_(MH)=3.84,95％CI 为1.58～9.30(调整吸烟后的 OR值)。且随职业暴露年限的延长患肺癌的危险性增大,存在剂量反应关系。据人群回归危险度估计,抚顺市大约有16.47％的肺癌是由职业暴露所致。吸烟与职业暴露存在正交互作用,符合相加模型     

太原市肺癌的危险性因素研究

1980年10月至1982年12月在太原进行了肺癌的病例对照研究,调查肺癌病例103人,每例配一名与吸烟无关的其它部位癌患者,其中71例肺癌同时配一名正常人对照。癌对照组吸烟的CRR为2.78(χ²=7.52 P<0.01),随吸烟量及吸烟年数增加,癌及正常对照组的CRR亦随之升高,戒烟后CRR下降,提示吸烟与肺癌有密切相关。在癌对照组慢支的CRR为2.27(χ²=5.70 P<0.05),正常对照组为4.81(χ²=13.39 P<0.01),慢支亦为肺癌的危险性因素。精神刺激与肺癌有相关关系。     

环境卫生与监测

,91174,州半岛人群肺瘩与吸水烟关系的病例对照研究/苏汝好:.刀广东医学一1998,19(4)一287~288 雷州半岛地区人群有吸水烟的习惯,作者对1995年在广东医学院附属医院住院的全部雷州半岛籍肺癌病人进行了病例对照研究,着重了解吸水烟与肺癌的关系。研究结果表明,吸水烟者肺癌的相对危险性(2 .20)低于吸纸烟者肺癌的相对危险性(9 .22)。吸水烟者肺癌的相对危险性低的原因可能与吸水烟者的吸烟剂量少、水过滤有一定效果、水烟丝的有害成分偏少有关,值得进一步研究探讨。图。表4参3量与不吸烟者组比较分别为t~2.7118、尸<0.01;t=3 .1826、P<0.01…     

中国居民2000—2010年肺癌发病与吸烟的关系

目的探讨中国居民2000—2010年肺癌发病与吸烟关系的变迁,为进一步控烟决策提供理论依据。方法利用Me-ta分析对中国2000—2010年间公开发表的肺癌发病与吸烟关系的病例对照研究的文献资料进行定量综合分析。结果共6篇文献入选,累计肺癌病例1 644人,对照1 525人;异质性检验:χ2=10.66,Ω=5,P=0.06;吸烟与肺癌发病的合并OR值为1.7(95%CI:1.36～2.11)。结论尽管近10年吸烟致肺癌发病的危险性较以前降低,但控烟仍是肺癌防治工作的重点。     

沈阳肺癌的病因

在沈阳进行一项病例对照研究,包括1249例现症肺癌和1345名以全人口为基础的对照.研究证明吸烟仍是第一位病因,占男性病因(PAR)的55%及女性的37%,在家取暖烹饪所产生的室内空气污染(主要是煤烟)与肺癌有显著相关,估计占病因的10～20%.病例组报告其住宅周围有烟或二百米内有工厂大烟囱者比对照组多.住有色金属冶炼厂附近一公里内者在男性可见肺癌危险性升高(OR=3.0).其它显著相关因素还有冶金工业和化工制药职业暴露和慢性气管炎和肺结核.室内氡水平仅在小细胞型肺癌见到有轻微相关.     

Toenail nicotine level as a novel biomarker for lung cancer risk

The objective of this US study was to assess the association of toenail nicotine level as a novel biomarker with lung cancer risk independent of reported smoking history. A nested case-control study of 210 male lung cancer cases and 630 matched controls aged 40-75 years participating in the Health Professionals Follow-up Study was conducted. Toenail samples collected in 1987 were analyzed for nicotine levels, and incident lung cancer cases were diagnosed between 1988 and 2000. Mean toenail nicotine level among cases was 0.95 ng/mg compared with 0.25 ng/mg among controls (P < 0.0001). In univariate analyses, the relative risk of lung cancer for the highest versus lowest quintiles of toenail nicotine level was 10.50 (95% confidence interval: 5.61, 19.64; P for trend < 0.0001). When the authors adjusted for pack-years from reported smoking history in multivariate analyses, the relative risk for toenail nicotine levels in the highest quintile was still significant in predicting lung cancer risk: 3.57 (95% confidence interval: 1.73, 7.37; P for trend < 0.0001). In conclusion, the toenail nicotine biomarker was found to be a strong predictor of lung cancer independent of smoking history, suggesting that the adverse effects of cigarette smoke may be underestimated in studies based on smoking history only.     

Smoking and lung cancer in China: combined analysis of eight case-control studies.

Smoking is well established as a principal risk factor for lung cancer. The risk of lung cancer is about ten times higher in smokers in Western countries. In China, a number of epidemiological studies have investigated the association between lung cancer and smoking and in the present paper, a combined analysis of eight such case-control studies is described. The summary odds ratio (OR), calculated by the Mantel-Haenszel method, and attributable risk (AR) of lung cancer associated with smoking were calculated from the combined data which were obtained from a literature review. The eight case-control studies were conducted in Beijing, Shanghai, Shenyang, Nanjing, Harbin, Zhengzhou, Taiyuan, and Nanchang, yielding a total of 4081 lung cancer cases and 4338 controls. The summary OR of lung cancer associated with smoking was 2.17 (95% CI (confidence interval): 1.98-2.39). The OR were 3.09 (95% CI: 2.61-3.66) for males and 2.30 (95% CI: 1.96-2.69) for females. The AR were 38.2% for both sexes, 56.7% for males and 25.5% for females. Risks of 1.00, 1.03, 2.04, and 3.33 showed a dose-response relationship between lung cancer and number of cigarettes smoked per day. There were also significant dose-response relationships of lung cancer with duration of smoking (OR = 1.00, 1.02, 2.66), and age at start of smoking (OR = 1.00, 3.30, 2.36, 1.18). The OR and AR of lung cancer associated with smoking in China were much lower than those reported in Western countries and the possible reasons for this are discussed.     

Menthol cigarettes and risk of lung cancer

The authors analyzed data from a multihospital case-control study in the eastern United States to evaluate the hypothesis that smoking menthol cigarettes increases lung cancer risk compared with smoking nonmenthol cigarettes. Subjects included cases with lung cancer and controls admitted for conditions unrelated to smoking who were aged 40-74 years, were interviewed from 1981 to 2000, and had smoked for >or=20 years. Information was available on the brand and type of cigarette smoked most recently and for the longest time. Analyses were based on 643 cases and 4,110 controls for whom brand information was available for >or=60% of the total duration of smoking. Logistic regression was used to estimate the relative risk of lung cancer according to number of years of menthol cigarette use (>15, 1-15, 0), adjusting for demographic and smoking-related factors. The lung cancer risk for long-term smokers of menthol cigarettes was similar to that for smokers of nonmenthol cigarettes (odds ratio = 0.97, 95% confidence interval: 0.70, 1.34). Odds ratios were also close to 1.0 in separate analyses of male, female, Black, and White subjects. The results of this study do not support the hypothesis that smoking menthol cigarettes increases the risk of lung cancer relative to smoking nonmenthol cigarettes.     

Serum retinol and retinol-binding protein levels do not predict subsequent lung cancer

Retinol and retinol-binding protein levels were measured in sera previously obtained, and stored in the frozen state, at multiphasic health checkups from 151 persons subsequently found to have lung cancer (cases) and 302 persons who remained free of cancer (controls). Two controls were matched to each case for sex, skin color, age, date of multiphasic health checkup, and aspects of the smoking habit. Mean levels in cases and controls were, respectively, retinol: 82.17 and 82.37 micrograms/dl (p = 0.93), and retinol-binding protein: 6.04 and 6.00 mg/dl (p = 0.81). Mean differences between cases and controls were, retinol: 0.195 micrograms/dl with 95% confidence limits, -3.91 and 4.30 micrograms/dl; retinol-binding protein: -0.033 mg/dl with 95% confidence limits, -0.31 and 0.24 mg/dl. No significant trend in relative risk of lung cancer was observed when the retinol or retinol-binding protein distribution was divided into quintiles. No significant associations were observed in subgroups based on age, sex, histologic type of cancer, cigarette consumption, or interval between blood drawing and cancer diagnosis. In this large study, retinol and retinol-binding protein levels were not useful in predicting the subsequent development of lung cancer.     

Lung cancer risk associated to exposure to radon and smoking in a case-control study of French uranium miners

A case-control study nested in the cohort of French uranium miners took smoking information into account in investigating the effect of radon exposure on lung cancer risk. This study included 100 miners who died of lung cancer and 500 controls matched for birth period and attained age. Data about radon exposure came from the cohort study, and smoking information was retrospectively determined from a questionnaire and occupational medical records. Smoking status (never vs. ever) was reconstructed for 62 cases and 320 controls. Statistical analyses used conditional logistic regression. The effect of radon exposure on lung cancer risk was assessed with a linear excess relative risk model, and smoking was considered as a multiplicative factor. Mean cumulative radon exposures were 114.75 and 70.84 Working Level Months (WLM) among exposed cases and controls, respectively. The crude excess risk of lung cancer per 100 WLM was 0.98 (95% CI: 0.18-3.08%). When adjusted for smoking, the excess risk was 0.85 per 100 WLM (95% CI: 0.12-2.79%), which is still statistically significant. The relative risk related to smoking was equal to 3.04 (95% CI: 1.20-7.70). This analysis shows a relative risk of lung cancer related to smoking similar to that estimated from previous miners' cohorts. After adjustment for smoking, the effect of radon exposure on lung cancer risk persists, and its estimated risk coefficient is close to that found in the French cohort without smoking information.     

Case-control study of exposure to carbon black in the occupational setting and risk of lung cancer

Although it has been hypothesized that carbon black exposure may carry an excess risk of lung cancer, evidence to date is insufficient to assess the hypothesis properly. The relationship between workplace exposure to carbon black and lung cancer risk was examined in a population-based case-control study carried out in Montreal, Canada. Detailed job histories were elicited from 857 incident cases with histologically confirmed lung cancer as well as from 1,360 cancer controls and 533 population controls. Job histories were evaluated by a team of hygienists and chemists for evidence of exposure to a host of occupational substances, including carbon black. Logistic regression analyses adjusting for smoking and other nonoccupational and occupational potential confounders suggested no significant increase in risk with relatively low exposure to carbon black. Some increase in risk for all lung cancers was apparent with relatively high exposure using cancer controls (OR = 2.17; 95% CI = 0.95–4.91) and population controls (OR = 1.52; 95% CI = 0.58–3.97). Individuals with relatively high exposure had a significantly greater risk of oat-cell carcinoma using either control series (OR = 5.05; 95% CI = 1.72–14.87 using cancer controls and OR = 4.82; 95% CI = 1.36–17.02 using population controls). These results provide some evidence for an association between exposure to carbon black and lung cancer. © 1996 Wiley-Liss, Inc.     

Smoking and the risk of lung cancer: susceptibility with GSTP1 polymorphisms

BACKGROUND: GSTP1 is a gene that helps detoxify foreign substances in the body. Functional polymorphisms of GSTP1 have been studied as risk factors for lung cancer. Past studies have compared the effect of the "at risk" polymorphism in two strata of smoking pack-years (usually defined by the median among controls). We examined the interaction between GSTP1 polymorphisms and cumulative exposure to smoking and their association with lung cancer risk. METHODS: Data are from a large hospital-based case-control study of persons treated for primary lung cancer at the Massachusetts General Hospital since 1992. Controls were drawn from friends and nonrelated family members. We genotyped 1,042 cases and 1,161 controls for GSTP1 using polymerase chain reaction-restriction fragment length polymorphism techniques. FINDINGS: The GSTP1 GG genotype approximately doubled the lung cancer risk associated with pack-years. This interaction was stronger among current smokers. At 26 pack-years (median among controls with a smoking history), the adjusted odds ratio for the association between pack-years and lung cancer risk was 13 (95% confidence interval = 6.5-25) among current smokers with the GSTP1 GG genotype compared with 6.1 (95% confidence interval = 4.9-7.5) among those with the GSTP1 AA genotype. CONCLUSIONS: GSTP1 GG increases the lung cancer risk associated with pack-years of smoking.     

Dark tobacco and lung cancer in Cuba

A retrospective case control study of lung cancer was conducted in Havana, Cuba to investigate whether Cuban high lung cancer mortality rates could be explained by cigarette and cigar consumption habits, including the smoking of dark tobacco cigarettes. The cases were drawn from patients admitted from 1978 to 1980 to the city's 12 main general hospitals with a tentative diagnosis of lung cancer. Only patients whose final diagnosis was confirmed by cytology and/ or histology according to the World Health Organization's Classification of Lung Cancer were included. A hospital control selected from patients with a current admission for a nonsmoking-related disease was matched to each case by sex, age, hospital of admission, and admission date. Data on 826 confirmed lung cancer cases (219 females and 607 males), 979 hospital controls, and 539 neighborhood controls were analyzed with procedures for matched and unmatched studies. Lung cancer patients ranged in age from 23 to 89 years; approximately 1/2 were females and 2/3 of the males were 60 years or older at diagnosis. Education level was similar in all groups. 167 of the 219 female cases (76.3%) and 595 of the 607 male cases (98%) ever smoked regularly, compared with 31% and 80.3%, respectively, of female and male controls. The corresponding proportions for female hospital and neighborhood controls were 30.5 and 31.8%, whereas for males they were 80.5% and 80.1%. The overall relative risk (RR) of lung cancer in cigarette smokers was 7.3 for females and 14.1 for males. Most smokers consumed the local dark tobacco ciagrettes exclusively. There were increased risks of lung cancer in both sexes associated with smoking both tobaccos, but the excess was greater for dark tobacco. The differences were reduced after adjustment for amount smoked. With either dark or light tobacco, the longer the duration of smoking or the greater the total number of cigarettes consumed, the higher the risk, all trends being highly significant. Cigarette smoking was associated with all 4 histologic types of lung cancer. A separate analysis was done on the 216 male cases and 389 controls who smoked either cigars only or cigars plus cigarettes. The risk of lung cancer in both groups was greater than those in nonsmokers. Based on attributable risk, it is estimated that a maximum of 66% of female and 91% of male lung cancer cases in Cuba are due to smoking.     

Lung cancer risk of workers in shoe manufacture and repair

BACKGROUND: The occupational lung cancer risk in manufacturing and repair of shoes was studied by pooling of two major case-control studies from Germany. METHODS: Some 4184 incident hospital-based cases of primary lung cancer and 4253 population controls, matched for sex, age, and region of residence were intensively interviewed with respect to their occupational and smoking history. Based on the occupational coding and a free text search, all individuals who had ever worked in shoe manufacturing or repair for at least half a year were identified. Shoemaker-years were calculated as the cumulated duration of working in shoe manufacturing or repair. Odds ratios (OR) and 95% confidence intervals (CI) were calculated via conditional logistic regression. Additional adjustment for smoking and occupational asbestos exposure was used. RESULTS: Seventy-six cases and 42 controls who had ever worked in shoe manufacture or repair (OR = 1.89, 95% CI: 1.29-2.78). After adjustment for smoking, this risk was lowered to 1.69 (95% CI: 1.09-2.62). Further adjustment for asbestos exposure only slightly changed the risk estimates upwards. The smoking adjusted OR in males was 1.50 (95% CI: 0.93-2.41) and 2.91 (95% CI: 0.90-9.44) in females. Logistic regression modeling showed a positive dose-effect relationship between duration of exposure in shoe manufacture and repair and lung cancer risk. The odds ratio for 30 years of exposure varied between 1.98 and 2.24 depending on the model specified. CONCLUSIONS: The study demonstrates an increased lung cancer risk for shoemakers and workers in shoe manufacturing. The risk seems to double after being 30 years in these occupations.     

核苷酸切除修复基因表达水平与肺癌易感性的关系

[目的]探讨核苷酸切除修复基因表达水平与肺癌易感性关系。[方法]采用病例一对照分子流行病学方法，以RT-PCR技术检测98例原发性肺癌患者和112名健康者外周血淋巴细胞核苷酸切除修复基因(XPB、XPC、XPG、ERCCl)表达水平，比较基因表达水平与肺癌易感性的关系。[结果]肺癌病例组4种基因的表达水平均低于健康对照组，其中XPB和XPC表达水平在两组之间有显著性差异，吸烟人群中病例与对照组基因表达水平差异大于非吸烟人群与对照组的差异，低表达XPB和XPC的人群患肺癌的相对危险度分别是高表达人群的2．06和2．27倍。[结论]低表达XPB和XPC的人群肺癌发病风险增高。