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。     

吸烟与饮酒对肺癌发病的影响及交互作用

目的探讨吸烟与饮酒及其交互作用对肺癌发病的影响。方法在肿瘤高发地区开展以人群为基础的病例对照研究,通过调查问卷收集主要人口学、吸烟和饮酒等相关信息,采用非条件logistic回归分析计算比值比(OR)及95%CI,并分析吸烟与饮酒在肺癌发病中的交互作用。结果调整相关因素(包括饮酒)后,与不吸烟者相比,吸烟者患肺癌的风险增加(P0.05),吸烟≥40年者患肺癌的风险是不吸烟者的4.79倍,每日吸烟≥20支者患肺癌的风险是不吸烟者的4.44倍,吸烟至肺部者患肺癌风险是不吸烟者的4.44倍(P值均0.001)。调整变量(包括吸烟)后,饮酒和饮酒年限与肺癌发病之间无统计学关联(P0.05)。吸烟和饮酒相乘交互作用的OR值(95%CI)为0.90(0.47~1.70)。吸烟和饮酒相加交互作用的超额相对危险度(RERI)值及其95%CI为0.36(-0.92~1.64),交互作用归因比(AP)值及95%CI为0.09(-0.22~0.40),交互作用指数(SI)值及95%CI为1.13(0.71~1.80)。结论吸烟是肺癌发病的主要危险因素,且该风险随吸烟年限、吸烟量、吸烟深度的增加而显著增加,现有证据并不支持饮酒与肺癌发病之间存在关联,吸烟和饮酒在肺癌发病中也未见交互作用。     

环境低浓度石棉暴露与肺癌危险性的巢式病例对照研究

目的探讨云南省大姚县环境低浓度青石棉暴露与肺癌之间的关联以及肺癌高发的主要危险因素，为当地的肺癌防制提供依据。方法采用巢式病例对照研究方法，从队列中获得53例肺癌病例，按1：3的比例分别匹配以性别相同、年龄相当的对照。结果单因素条件logistic回归分析发现石棉环境污染、吸烟、饮酒、喝茶与肺癌有统计学关联，石棉环境污染的各种形式中，只有使用石棉炉对肺癌发生有显著性意义。用多因素条件logistic回归进一步分析，使用石棉炉和吸烟与肺癌有统计学关联，OR值分别是3．38(95％CI1．43～7．95)和2．62(95％CI1．08～6．56)．其他各因素对肺癌的影响未发现有显著性意义。对吸烟与使用石棉炉的交互作用进行相乘模型的拟合，未发现两因素存在相乘模型的交互作用(P=0．310)。相加模型交互作用分析结果显示，吸烟和使用石棉炉对肺癌发病的影响可能存在着相加模型的交互作用。结论吸烟和使用石棉炉是当地肺癌高发的主要危险因素，且两者存在着相加模型的交互作用。     

橡胶职业暴露与肺癌关系的前瞻性研究——Ⅲ肺癌危险因素联合作用方式

目的探讨橡胶工人中亚硝胺暴露、吸烟和经济收入低等主要危险因素对肺癌联合作用的模式。方法应用广义相对危险度模型拟合某橡胶厂队列随访资料。结果联合作用下,亚硝胺暴露与吸烟对肺癌危险度为相乘作用形式,亚硝胺暴露与经济收入为相加形式,吸烟与经济收入为相加形式。结论受样本限制,不同模型之间拟合优度的差别较小,但是,在公共卫生实践和生物学机理的认识方面,确定因素对疾病危险度的联合作用方式具有重要意义     

肺癌危险因素间交互作用的研究

本文利用７３５４名肺癌高危对象的队列研究资料，采用多元Ｌｏｇｉｓｔｉｃ回归和对数线性模型对肺癌高发的危险因素及因素间的交互作用进行了统计分析。结果表明：吸烟、慢性支气管炎史和接触粉尘、砷、氡子体等职业危险因子是当地肺癌高发的主要危险因素；Ｌｏｇｉｓｔｉｃ回归分析没有发现两因素之间有显著意义的交互作用；对数线性模型分析进一步提示上述因素间存在高阶的交互效应。     

吸烟在云锡矿工肺癌发病中的作用

本文以1975-1984年为时段,对云南锡业公司所属六个单位工人进行了吸烟情况的调查分析。结果表明,吸烟者的肺癌发病率是非吸烟者的3.65倍。吸烟者的SMR为29.41;非吸烟者为8.42。无论吸烟程度如何,其发病、死亡都是有井下史者高于无井下史者。吸烟与职业性因素的复合作用是:吸烟+井下>单纯井下>单纯吸烟>非吸烟无井下史者。     

膳食因素与吸烟者和非吸烟者舌癌发病的关系

目的探讨膳食因素对吸烟和非吸烟人群舌癌发病的影响。方法采用病例-对照研究方法,收集2011年12月—2016年3月福州市某医院经病理学确诊的舌癌新发病例251例,同期收集来自福州市某社区的健康对照1382例。面访调查研究对象的吸烟、饮酒史以及一年前的膳食情况等内容,应用非条件Logistic回归模型计算膳食因素与舌癌发病风险的调整OR值及其95%CI,并进行吸烟与食畜肉类之间的相乘交互作用分析。结果进食鱼类≥3次/周、海鲜类≥1次/周、奶类及奶制品≥1次/周、绿叶蔬菜和非绿叶蔬菜≥1次/天以及新鲜水果≥3次/周均可降低舌癌的发病风险。按是否吸烟分层后,鱼类、海鲜类以及绿叶蔬菜和非绿叶蔬菜对舌癌的保护作用在吸烟人群中更加显著。而进食畜肉类≥3次/周仅与吸烟者舌癌的发病相关(调整OR=1.55,95%CI 1.02~2.34),且吸烟与食畜肉类存在正相乘交互作用(OR相乘=2.08,95%CI 1.43~3.03)。结论适量摄入新鲜的蔬菜水果、鱼及海鲜类、奶类及奶制品,以及在吸烟者中减少畜肉类的过量摄入可减少舌癌的发生。     

不同来源的被动吸烟与肺癌关系的研究

作者对１０４名非吸烟肺癌和１６３名对照进行了非条件ＬＯＧＩＳＴＩＣ回归分析以估计不同来源的被动吸烟对非吸烟肺癌的危险性。分析发现在不同来源的被动吸烟中，父母吸烟和工作场所接触吸烟者均对患肺癌无明显的影响；而暴露于配偶吸烟可使非吸烟者患肺癌危险性增加１．７７倍。结果提示，在不同来源的被动吸烟中，暴露于配偶的被动吸烟是导致非吸烟者尤其是女性肺癌的主要危险因素。     

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.     

2001-2008年北京市居民被动吸烟情况分析

吸烟产生的支流烟雾中尼古丁等有害物质的含量是主流烟雾的5.1倍,主要由被动吸烟者吸入.被动吸烟越来越引起社会各界的关注,已被确认是患肺癌、冠心病、成人慢性呼吸系统疾病和儿童哮喘等疾病的危险因素^[1].主动吸烟的危害已为大多数公众所知,但被动吸烟的危害及在我国目前的严重状况,应当引起公众的普遍关注.     

Relation between exposure to asbestos and smoking jointly and the risk of lung cancer

OBJECTIVES—To review evidence about the joint relation of exposure to asbestos and smoking on the risk of lung cancer to answer three questions: (1) does asbestos increase risk in non-smokers; (2) are the data consistent with an additive model; and (3) are the data consistent with a multiplicative model?METHODS—Analysis of 23 studies reporting epidemiological evidence on the joint relation. Comparison of risk of lung cancer in subjects unexposed to asbestos or smoking, exposed to asbestos only, to smoking only, or to both. Estimation of the relative risk associated with asbestos exposure in non-smokers and of statistics testing for additivity and multiplicativity of risk.RESULTS—Eight of the 23 studies provided insufficient data on the risk of lung cancer in non-smokers to test for possible effects of asbestos. Asbestos exposure was associated with a significantly (p<0.05) increased risk in non-smokers in six of the remaining studies and with a moderately increased, but not significant, increase in a further six. In two of the three studies that found no increase, asbestos exposure was insufficient to increase risks in smokers. In 30 of 31 data sets analysed, risk in the combined exposure group was greater than predicted by the additive model. There was no overall departure from the multiplicative model, the proportional increase in risk of lung cancer with exposure to asbestos being estimated as 0.90 (95% confidence interval (95% CI) 0.67 to 1.20) times higher in smokers than non-smokers. For two studies significant (p<0.05) departures from a multiplicative relation were found in some, but not all, analyses. Reasons are presented why these may not indicate true model discrepancies.CONCLUSIONS—Asbestos exposure multiplies risk of lung cancer by a similar factor in non-smokers and smokers. The extent to which it multiplies risk varies between studies, no doubt depending on the type of asbestos involved, and the nature, extent, and duration of exposure.     

Cohort analysis of cigarette smoking and lung cancer incidence among Norwegian women

BACKGROUND: Cancer registries have for decades surveyed the development of cancer diseases. Data on incident cases includes demographic variables. Knowledge of the temporal distribution of risk factors on the same variables makes it possible to model the relationship between disease and risk factor. The results of such analyses might be difficult to interpret since they are based on aggregated data. But the availability of these data sources should encourage further exploration of its possibilities and limitations. METHODS: The temporal pattern of smoking habits in 5-year birth cohorts from 1890-1949 was established, with data on the proportions of current smokers, former smokers and non-smokers and estimated average daily consumption of tobacco and average duration of smoking. The lung cancer incidence among the cohorts in 1953-1992 was analysed by a model which included an additive excess risk for smokers that depended on daily dose and duration of smoking. RESULTS: The lung cancer incidence in later decades was adequately described by the model, which showed a simple relationship with smoking behaviour in the cohorts. For both current smokers and former smokers, the excess risk was about proportional to the daily amount smoked and the 4.5 power of duration of smoking. The age-specific rates for non-smokers were close to a fifth-power curve of age. CONCLUSIONS: Even if lung cancer incidence is not determined separately for groups with known smoking habits, plausible estimates of the effect of smoking can be derived if appropriate information is available on temporal smoking habits in the population.     

MISCLASSIFICATION OF SMOKING HABITS AS A SOURCE OF BIAS IN THE STUDY OF ENVIRONMENTAL TOBACCO SMOKE AND LUNG CANCER

The relationship of environmental tobacco smoke to lung cancer risk in lifelong non-smokers is commonly studied using marriage to a smoker as the index of exposure. As smokers tend to marry smokers, relative risk estimates will be biased if some current or former smokers are misclassified as lifelong non-smokers. This paper shows how various factors affect the magnitude of the bias and describes a method for obtaining misclassification-adjusted relative risk estimates. Application of the method to U.S. and Asian data for women suggests misclassification is an important determinant of the slight excess risk observed in non-smokers married to smokers. Reasons why our conclusions differ from those of others are discussed, as are other difficulties in interpreting the association between spousal smoking and lung cancer risk.     

The interaction of asbestos and smoking in lung cancer: a modified measure of effect

OBJECTIVES: The ratio of the relative risk of lung cancer due to asbestos exposure in non-smokers to that in smokers has been termed the relative asbestos effect (RAE). In a review, Liddell [Liddell FDK (2001) Ann Occup Hyg; 45: 341-56] estimated that the RAE was approximately 2. This measure is satisfactory when there is an appreciable relative risk due to asbestos but does not generalize to lower levels of exposure. A modified measure is proposed to overcome this difficulty. The modified measure, RAEm, is defined as the ratio of the excess relative risk (RR - 1) in non-smokers to that in smokers. METHODS: The cohort studies combined in Liddell's 2001 analysis have been used to give a combined estimate of the modified measure. RESULTS: The combined value of RAEm is 3.19 with 95% confidence interval 1.67-6.13. CONCLUSION: The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers. The modified measure has been placed within a more versatile model of interaction. If interaction is present the relative risk from asbestos exposure changes only slightly between light and heavy smokers, but is higher in very light smokers and non-smokers. The relative risk estimated from epidemiological studies of a mixed population of non-smokers and smokers applies to smokers.     

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。     

Residential radon exposure and lung cancer: risk in nonsmokers

Lung cancer is a disease that is almost entirely caused by smoking; hence, it is almost totally preventable. Yet there are a small percentage of cases, perhaps as many as 5 to 15%, where there are other causes. Risk factors identified for this other group include passive smoking, occupational exposure to certain chemicals and ionizing radiation, diet, and family history of cancer. In the United States cigarette smoking is on the decline among adults, occupational exposures are being reduced, and people are being made more aware of appropriate diets. These changes are gradually resulting in a reduced risk for this disease. Lung cancer in the U.S. may, therefore, eventually become largely a disease of the past. It remains important, however, to continue to study the cause(s) of lung cancer in non-smokers, particularly never smokers. Because of our interest in the effects of residential radon exposure on the development of lung cancer in non-smokers, we conducted a critical review of the scientific literature to evaluate this issue in detail. Strict criteria were utilized in selecting studies, which included being published in a peer reviewed journal, including non-smokers in the studied populations, having at least 100 cases, and being of case-control design. A total of 12 individual studies were found that met the criteria, with 10 providing some information on non-smokers. Most of these studies did not find any significant association between radon and lung cancer in non-smokers. Furthermore, data were not presented in sufficient detail for non-smokers in a number of studies. Based on the most recent findings, there is some evidence that radon may contribute to lung cancer risk in current smokers in high residential radon environments. The situation regarding the risk of lung cancer from radon in non-smokers (ex and never) is unclear, possibly because of both the relatively limited sample size of non-smokers and methodological limitations in most of the individual studies. A summary of these studies is provided concerning the state of knowledge of the lung cancer risk from radon, methodological problems with the residential studies, the need for the provision of additional data on non-smokers from researchers, and recommendations for future research in non-smokers.     

The exposure to tobacco smoke of the employees of a telephone company]

Smoking habits were studied in a group of employees of a telephone company. The smokers were 34% of the subjects interviewed. The non-smokers said that they were bothered by other people smoking everywhere and also to a considerable extent at the workplace. Differences between smokers and non-smokers and between exposed and non-exposed non-smokers were studied by measuring expired CO and urinary cotinine. An expired CO concentration of 10 ppm discriminated between smokers and non-smokers. A mean urinary cotinine concentration of about 16 ng/mg was found in the exposed non-smokers, corresponding to the direct smoking of 1/10 of a cigarette per day. The search for the metabolic phenotype of destromethorphane, which was taken as an indicator of susceptibility to contract lung cancer due to IPA, showed that there were no differences between smokers and non-smokers since the rapid metabolizers, and therefore subjects potentially exposed to risk of lung cancer due to tobacco smoke, prevailed in both groups.     

The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers

Although it is well known that both cigarette smoke and microscopic airborne asbestos fibres can cause lung cancer, evidence as to how these two agents combine is nebulous. Many workers have believed in the multiplicative theory, whereby asbestos increases the risk in proportion to the risk from other causes. However, evidence against this theory is mounting: a recent review concluded that the multiplicative hypothesis was untenable, and that the relative risk of lung cancer from asbestos exposure was about twice as high in non-smokers as in smokers, a finding largely independent of type of asbestos fibre. The criteria for entry to the current study were met by 7279 men in the 1891-1920 birth cohort of Quebec chrysotile miners and millers. The data consisted of date of birth, place of employment, smoking habit, asbestos exposure accumulated to age 55 and, for those 5527 who died between 1950 and June 1992, date and cause of death; 533 of the deaths were from lung cancer. For the principal analyses, ex-smokers were excluded from the study cohort, which comprised 5888 men, of whom 473 died of lung cancer. The conventional form of analysis is simply of the double dichotomy: non-smokers of cigarettes, 'unexposed' and exposed; all others, 'unexposed' and exposed. The respective standardized lung cancer mortality ratios (SMRs) were 0.29 and 0.62; and 1.37 and 1.72. Thus, the differences in relative risk, due to exposure, were closely similar, 0.33 and 0.35. On the other hand, the effects of asbestos measured by the corresponding ratios, 2.12 and 1.25, did differ, being 1.7 times as high in non-smokers as in others. The principal analysis was much more penetrating: the method was to fit models to a 'disaggregated' 6 x 10 array, by smoking habit (excluding ex-smokers) and asbestos exposure, of lung cancer SMRs. Both linear and log-linear models were fitted: the former included the additive and linear-multiplicative; the latter embraced the more conventional multiplicative form. The additive model fitted much the best. The fit of each multiplicative model was improved by the introduction of an interaction term that implied a less than multiplicative relationship. Thus smoking and exposure to chrysotile appear to have acted independently in causing lung cancer, with 10 cigarettes a day having an effect roughly equivalent to exposure amounting to 700 million particles per cubic foot x years. The refutation of the multiplicative hypothesis in these data reinforces its inapplicability in general; but the additive hypothesis is not generally applicable either. Indeed, there seems to be no good reason to believe that interactions conform to any simple theory. The implications are important.     

Body mass index and waist circumference in relation to lung cancer risk in the Women's Health Initiative

Investigators in several epidemiologic studies have observed an inverse association between body mass index (BMI) and lung cancer risk, while others have not. The authors used data from the Women's Health Initiative to study the association of anthropometric factors with lung cancer risk. Over 8 years of follow-up (1998-2006), 1,365 incident lung cancer cases were ascertained among 161,809 women. Cox proportional hazards models were used to estimate hazard ratios adjusted for covariates. Baseline BMI was inversely associated with lung cancer in current smokers (highest quintile vs. lowest: hazard ratio (HR) = 0.62, 95% confidence interval (CI): 0.42, 0.92). When BMI and waist circumference were mutually adjusted, BMI was inversely associated with lung cancer risk in both current smokers and former smokers (HR = 0.40 (95% CI: 0.22, 0.72) and HR = 0.61 (95% CI: 0.40, 0.94), respectively), and waist circumference was positively associated with risk (HR = 1.56 (95% CI: 0.91, 2.69) and HR = 1.50 (95% CI: 0.98, 2.31), respectively). In never smokers, height showed a borderline positive association with lung cancer. These findings suggest that in smokers, BMI is inversely associated with lung cancer risk and that waist circumference is positively associated with risk.