不吸烟女性肺癌危险因素病例-对照研究

目的：探讨不吸烟女性患肺癌的危险因素。方法：对沈阳市已确诊的126例不吸烟女性原发性肺癌进行1；1配对的病例对照研究。调查内容包括一般状况、家族史、疾病史、居住史、被动吸烟史、职业史、饮食史、烹饪史及室内微小环境等。结果：腺癌是女性肺癌的主要组织类型，占62．7％。生育次数越多，患肺癌的危险性越高（OR＝1．466，95％CI＝1．06－2．01）。肥胖指数（BMI）越小，肺癌的危险性越高（OR＝2．082，95％CI＝1．2－3．60）而且随着BMI的增加，肺癌的危险性降低。大量食用动物内脏（OR＝1．891，95％CI＝1．45－2．46）、玉米高梁（OR＝1．538，95％CI＝1．22－1．93）等能增加肺癌的危险性。使用液化石油作燃料（OR＝1．741，95％CI＝1．29－2．34）和室内燃煤（OR＝1．785，95％CI＝1．33－2．38）是不吸烟女性肺癌的危险因素。一级亲属中有肺癌患者，不吸烟女性的肺癌危险性增加（OR＝3．18，95％CI＝2．43－4．15）。结论：低BMI、多次生育、大量食用动物内脏及玉米高梁、室内燃煤、使用液化石油气作燃料均会增加不吸烟女性患肺癌的危险性。     

非吸烟女性肺癌危险因素的研究

背景与目的肺癌是世界上一个重大的公共卫生问题,在我国肺癌是大中城市中恶性肿瘤的第一死因,且发病率和死亡率增长迅速。其中女性肺癌死亡率正逐年上升,而病例中以非吸烟者占多数,其危险因素尚不清楚。本研究通过流行病学调查来研究女性肺癌发生的危险因素。方法采用以医院患者为基础的病例-对照研究方法,包括女性肺癌患者618人,对照872人,进行流行病学调查。内容包括人口特征、被动吸烟史、烹饪油烟暴露史、燃料种类、煤烟暴露、亲属患癌史、职业史与饮食史等。结果女性肺癌患者与对照组比较,儿童时期被动吸烟(OR=1.81,95%CI=1.46~2.24)、烹饪油烟暴露(OR=3.18,95%CI=2.55~3.97)、煤烟暴露(OR=2.56,95%CI=1.83~4.55)、肺部疾病史(OR=1.80,95%CI=1.43~2.27)、肺结核史(OR=1.63,95%CI=1.31~2.03)、肿瘤家族史(OR=2.09,95%CI=1.46~3.00)和肺癌家族史(OR=2.46,95%CI=1.55~3.90)是危险因素。结论本研究显示儿童时期被动吸烟、烹饪油烟暴露、煤烟暴露、肺部疾病史、肺结核史及肿瘤或肺癌家族史是非吸烟女性肺癌的危险因素。     

中国非吸烟人群被动吸烟与肺癌关系的meta分析

背景与目的 本研究旨在探讨中国非吸烟人群被动吸烟与肺癌的关系.方法 通过计算机检索Medline、PubMed、CENTRAL(theCochrane central register of controlled trials)、中国生物医学文献数据库系统(CBM)、中国期刊全文数据库(CNKI)、中文科技期刊全文数据库(VIP)等收集国内外1987年-2007年间公开发表的关于中国非吸烟人群被动吸烟与肺癌的研究文献,应用统计软件Stata 11.0进行数据分析,计算其合并优势比(odds ratio,OR)和95%置信区间(confidence interval,CI).采用Begg和Eggr法对发表偏倚进行量化检测.结果 纳入分析的文章共有16篇,合并分析结果表明:中国非吸烟人群被动吸烟与肺癌的关系有统计学意义(OR=1.13,95%CI:1.05-1.21,P=0.001).每日被动吸烟≥20支、成年时期被动吸烟、非吸烟女性被动吸烟、被动吸烟暴露于工作环境等与肺癌的发生关系具有统计学意义,P值、OR值及95%CI分别为:P=0.000 3、OR=1.78、95%CI: 1.30-2.43,P=0.000 1、OR=1.50、95%CI:1.23-1.83,P=0.000 7、OR=1.50、95%CI: 1.19-1.90,P＜0.000 1、OR=1.41、95%CI:1.19-1.66.结论 中国非吸烟人群中,被动吸烟是肺癌发生的一个重要危险因素,尤其是暴露量≥20支/日、成年时期被动吸烟、女性、工作环境的被动吸烟与肺癌的发生关系密切.     

吸烟和环境烟草烟雾暴露与女性肺癌的关系的病例──对照研究

在上海市区进行了女性肺癌病例—对照研究中共调查新病例649例，对照675例。资料分析表明各种组织学类型肺癌都与吸烟有联系．其中鳞癌和小细胞癌与吸烟关系非常密切．OR分别为5.6和9．9，吸烟使腺癌危险性略有增加，OR=1.195％可信阳=0.7～1.7,吸烟对肺癌总的相对危险度为2.4（95％可信限=1.8～3.3）。各类肺癌的危险性均随每日吸烟量的增加、吸烟年限的延长和开始吸烟年龄的提前而增加。鳞癌和小细胞癌危险性上升速度最快，腺癌危险性增加缓慢，且趋势不显著。本研究还发现工作环境中的环境烟草烟雾暴露使女性非吸烟者肺癌危险性增加到1.5倍，95％可信限=1．1～2.0。未发现儿童期父母吸烟和成年期丈夫吸烟增加女性非吸烟者肺癌危险性。     

吸烟与胰腺癌发生风险的病例对照研究

[目的]探讨吸烟与胰腺癌发生风险的关系。[方法]采用1：1配对病例对照研究,病例来源于2011年11月至2013年2月间河南省肿瘤医院住院治疗的新发胰腺癌病例,选取非胰腺癌患者家属为对照组,对病例组和对照组进行问卷调查。采用单因素和多因素条件Logistic回归进行数据分析。[结果]吸烟（OR=2．57,95％CI：1．07～6．16）、清晨吸烟（OR=5．50,95％CI：1．22～24．81）是胰腺癌的危险因素。调整BMI、糖尿病、胆囊疾病等混杂因素后,吸烟、清晨吸烟的相对危险度分别为3．53（95％CI：1．30—9．60）,13．14（95％CI：1．45～118．68）：吸烟年限、每天吸烟支数和吸烟指数与胰腺癌发生风险增大存在趋势关系（P趋势〈0．05）。[结论]吸烟、尤其是清晨吸烟是胰腺癌的危险因素,控制烟草是预防胰腺癌的重要措施。     

非吸烟人群肺癌危险因素的病例对照研究

目的探讨中国非吸烟人群肺癌的危险因素,为防癌措施提供依据。方法采用病例对照研究的方法,按频数匹配收集非吸烟肺癌新发病例306例及非吸烟对照306例,利用统一编制的调查表对调查对象进行面访,收集病例和对照危险因素的暴露史等。结果单因素分析发现25个因素与非吸烟人群肺癌的发病有关联;多因素分析后发现：非吸烟人群肺癌发病的危险因素是体重指数(body mass index,BMI)＜18.5,居住地周围有污染企业、装修刺激性气味、家庭被动吸烟、工作场所被动吸烟、使用农药、性格内向、食用油炸食品、肺部手术史、癌症家族史,而保护因素是BMI≥24、常吃蛋类、常吃水果、饮茶、常以散步作为锻炼(2年前),经广义多因子降维法（GWDR）拟合的最优的交互作用模型是居住地企业+装修刺激性气味+家庭被动吸烟+工作场所被动吸烟+农药接触史+癌症家族史。结论非吸烟者发生肺癌的影响因素较多,仍需进一步识别。     

福建省大肠癌发病危险因素的病例对照研究

 目的 探讨福建省大肠癌发生的危险因素。 方法 采用1∶1匹配的病例对照研究方法,应用统一制订的调查表进行流行病学调查。共调查286对病例和对照。对资料进行单因素和多因素条件Logistic回归分析。 结果 大肠癌的危险因素有饮用井水（OR=4.05,95%CI：1.50～10.94）和泉水（OR=7.73,95%CI：2.02～29.54）,每天吸烟量（OR=4.57,95%CI：2.19～9.54）,油腻饮食（OR=5.35,95%CI：2.21～12.99）,肿瘤家族史（OR=6.18,95%CI：3.05～12.51）,肠道疾病史（OR=6.78,95%CI：3.53～13.07）;保护因素有常吃粗粮（OR=0.31,95%CI：0.17～0.53）。 结论 福建省大肠癌与吸烟,膳食纤维缺乏,饮用井水、泉水,下消化道疾病和肿瘤家族史密切相关。     

吸烟、饮酒与胃癌关系的病例对照研究

目的 探讨吸烟、饮酒与胃癌发生的关系。方法 采用全人群病例对照研究,共调查1999年4月－1999年10月期间诊断的上海市区新发胃癌病例311例,对照1579例（注：本课题为“九五”中乳腺癌、肺癌及胃癌病例－对照之一,对照共用）。采用非条件logistic回归分析,调整可能的混杂因素,以估计吸烟、饮酒对胃癌发生的比数比和95％的可信区间。结果 吸烟与男性胃癌发生有关,调整OR为1．67（95％CI：1．14－2．460,并且随着吸烟年龄的提前（P＜0．01）、吸烟年限的延长（P＜0．05）、每日吸烟量的增加（P＜0．05）和吸烟包－年（P＜0．01）,患胃癌的危险性显著增大;未发现女性吸烟与胃癌发生有显著性联系。进一步调整整烟,发现饮酒与胃癌无密切关系,但重度饮酒可能与女性胃癌发生有关。进一步研究饮酒的作用,分析吸烟与饮酒状况及吸烟支数与酒精克数不同剂量分层之间的交互作用,调整年龄、文化程度（仅女性）、腌制食品、新鲜水果及慢性胃炎后,发现男性饮酒与吸烟不同剂量之间有交互作用存在,交互项χ^2值为5．20,P＝0．02,即饮酒增加男性吸烟者患癌的危险。结论 进一步证实吸烟是胃癌发生的危险因素;单独饮酒与胃癌发生无明显关系,饮酒不是胃癌的一项独立危险因素;饮酒增加吸烟患胃癌的危险,两者有协同作用。     

中国女性乳腺癌危险因素的Meta分析

[目的]评价中国女性乳腺癌部分危险因素的作用,探讨乳腺癌的病因。[方法]运用Meta分析方法对我国1996～2006年间公开发表的有关乳腺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值分别为：初潮年龄OR=1．5401（95％CI：1．3437～1．7654）;哺乳OR=0．6837（95％CI：0．4779—0．9782）;口服避孕药OR=1．3278（95％CI：1．0627—1．6589）;良性乳腺疾病史OR=2．6180（95％CI：2．0275—3．3804）;吸烟OR=1．8576（95％CI：1．5394—2．2415）;饮酒OR=0．8137（95％CI：0．6196～1．0686）;饮茶OR=0．8625（95％CI：0．7646～0．9728）。[结论]初潮年龄、口服避孕药、良性乳腺疾病史及吸烟是乳腺癌发生的危险因素,哺乳及饮茶则是乳腺癌的保护因素。     

CYP2D6基因G4268C和ERCC1基因C8092A位点的单核苷酸多态性与肺癌遗传易感性

目的：探讨辽宁地区CYP2D6基因G4268C和ERCC1基因C8092A位点的单核苷酸多态性对肺癌发生的影响。方法：采用病例-对照研究方法,选取肺癌患者和健康对照者各200例。应用KI法快速抽提人外周血基因组DNA,PCR-RFLP的方法检测CYP2D6基因G4268C和ERCC1基因C8092A位点的单核苷酸多态性。结果：G4268/G、G4268/C和C4268/C这3种基因型在病例和对照组的分布频率分别为1.50%、58.00%、40.50%和2.50%、44.00%、53.50%,非C4268/C基因型的个体发生肺癌的风险是C4268/C基因型个体的1.73倍（95%CI=1.02-2.95）,在腺癌中OR=2.75（95%CI=1.27-5.94）;按吸烟情况进行分层分析后发现不吸烟者及轻度吸烟者中携带非C4268/C基因型的个体患肺癌的风险显著增高,OR值为2.09（95%CI=1.09-4.25）和3.41（95%CI=1.24-9.93）;非A8092/A基因型的个体发生肺癌的风险是A8092/A基因型个体的0.98倍（95%CI=0.52-2.17）。结论：C4268/C基因型在不吸烟者和轻度吸烟者中可能作为保护因素而降低肺癌的易感性,ERCC1 C8092A多态性与肺癌易感性无相关性。     

Cigarette smoking and risk of lung metastasis from esophageal cancer

BACKGROUND: Whereas extensive research has explored the effect of environmental factors on the etiology of specific cancers, the influence of exposures such as smoking on risk of site-specific metastasis is unknown. We investigated the association of cigarette smoking with lung metastasis in esophageal cancer. METHODS: We conducted a case-control study of esophageal cancer patients from two centers, comparing cases with lung metastases to controls without lung metastases. Information was gathered from medical records on smoking history, imaging results, site(s) of metastasis, and other patient and tumor characteristics. We used logistic regression to assess association. RESULTS: We identified 354 esophageal cancer cases; smoking status was known in 289 (82%). Among patients with lung metastases, 73.6% (39 of 53) were ever smokers, versus 47.8% (144 of 301) of patients without lung metastases [P=0.001; summary odds ratio (OR), 2.52; 95% confidence interval (95% CI), 1.17-5.45; stratified by histology]. Smoking was associated with a nonsignificant increased adjusted odds of lung metastasis (OR, 1.89; 95% CI, 0.80-4.46). Upper esophageal subsite (OR, 4.71; 95% CI, 1.20-18.5), but not histology (squamous OR 0.65,95% CI 0.27-1.60), was associated with lung metastasis. Compared with the combined never/unknown smoking status group, smoking was associated with a significantly increased odds of lung metastasis (OR, 2.35; 95% CI, 1.11-4.97). There was no association between liver metastasis and smoking (OR, 0.88; 95% CI, 0.42-1.83). CONCLUSIONS: Smoking is associated with increased odds of lung metastasis from esophageal cancer, and this relationship seems to be site specific. Future studies are needed to determine whether smoking affects the tumor cell or the site of metastasis, and whether this changes the survival outcome.     

CYP1A1 and GSTM1 polymorphisms in relation to lung cancer risk in Chinese women

We examined CYP1A1 (I462V) and GSTM1 null polymorphisms in 200 female cases and 144 female controls selected from a population-based case-control study of lung cancer conducted in northeast China, where the rates of lung cancer among Chinese women are especially high. The CYP1A1 codon 462 point mutation in exon 7 (I462V) causes an Ile-Val substitution near the heme binding site. This mutation correlates with inducibility of aryl hydrocarbon hydrolase (AHH) activity, which activates polycyclic aromatic hydrocarbons (PAHs) in tobacco smoke and in indoor air pollution from coal-burning stoves, a risk factor for lung cancer in this study population. We found that the CYP1A1 I462V genotype (combined ile/val and val/val) was significantly associated with lung cancer risk. The odds ratio (OR) was 2.5 (95% confidence interval [CI], 1.55-4.03) after adjustment for significant risk factors such as age, ever smoking status, family history of cancer, and eye irritation when cooking. The association was more pronounced among non-smokers (OR=3.67; 95% CI, 1.85-7.28) than among smokers (OR=1.74, 95% CI, 0.85-3.54). In contrast, we did not find a significant association with the GSTM1 null genotype. In summary, our case-control study of lung cancer among women in northeast China revealed an elevated risk associated with the CYP1A1 I462V genotype, but no interaction with smoking or indoor air pollution was found.     

Smoking and lung cancer in Harbin, northeast China.

BACKGROUND: We studied the relationship between smoking and lung cancer risk in Harbin, Heilongjiang province, northeast China, an area with a very high baseline risk of lung cancer in both sexes, using data from a case-control study of lung cancer conducted between 1987 and 1990. PATIENTS AND METHODS: Cases were 218 patients with incident, histologically confirmed lung cancer and controls were 436 patients admitted to the same hospital with non-neoplastic and non-lung diseases. RESULTS: Compared with never-smokers, the multivariate odds ratio (OR) for current smokers was 3.47 [95% confidence interval (CI) 2.31--5.20], and for ex-smokers 1.53 (95% CI 0.81--2.87). Lung cancer risk increased by 20% (95% CI 14% to 28%) for an increment of 5 years in smoking duration, and by 29% (95% CI 15% to 45%) for an increment of five cigarettes per day. The OR for smokers reporting occupational exposure to selected known or likely lung carcinogens was 7.22, compared with non-smokers without occupational exposure. CONCLUSIONS: This study further confirms that cigarette smoking is a strong determinant of lung cancer also in this high-risk area of northeast China.     

Household air pollution and risk of incident lung cancer in urban China: A prospective cohort study

Household air pollution (HAP) is associated with the development of lung cancer, yet few studies investigated the exposure patterns and joint associations with tobacco smoking. In our study, we included 224 189 urban participants from China Kadoorie Biobank (CKB), 3288 of which diagnosed with lung cancer during the follow-up. Exposure to four HAP sources (solid fuels for cooking/heating/stove and environmental tobacco smoke exposure) was assessed at baseline. Distinct HAP patterns and their associations with lung cancer were examined through latent class analysis (LCA) and multivariable Cox regression. A total of 76.1% of the participants reported regular cooking and 52.2% reported winter heating, of which 9% and 24.7% used solid fuels, respectively. Solid fuel heating increased lung cancer risk (Hazards ratio [HR]: 1.25, 95% confidence interval [CI]: 1.08-1.46). LCA identified three HAP patterns; the “clean fuel cooking and solid fuel heating” pattern significantly increased lung cancer risk (HR: 1.25, 95% CI: 1.10-1.41), compared to low HAP pattern. An additive interaction was observed between heavy smoking and “clean fuel cooking and solid fuel heating” (relative excess risk [RERI]: 1.32, 95% CI: 0.29-2.47, attributable proportion [AP]: 0.23, 95% CI: 0.06-0.36). Cases resulting from solid fuel account for ~4% of total cases (population attribute fraction [PAF]_overall: 4.31%, 95% CI: 2.16%-6.47%, PAF_{ever smokers}: 4.38%, 95% CI: 1.54%-7.23%). Our results suggest that in urban China, solid fuel heating increased the risk of lung cancer, particularly among heavy smokers. The whole population could benefit from cleaner indoor air quality by reducing using solid fuels, especially smokers.     

Gender differences in lung cancer risk by smoking: a multicentre case-control study in Germany and Italy

Several studies in the past have shown appreciably higher lung cancer risk estimates associated with smoking exposure among men than among women, while more recent studies in the USA report just the opposite. To evaluate this topic in a European population we conducted a case-control study of lung cancer in three German and three Italian centres. Personal interviews and standardized questionnaires were used to obtain detailed life-long smoking and occupational histories from 3723 male and 900 female cases and 4075 male and 1094 female controls. Lung cancer risk comparing ever-smokers with never-smokers was higher among men (odds ratios (OR) adjusted for age and centre = 16.1, 95% confidence interval (CI) 12.8-20.3) than among women (OR = 4.2, CI 3.5-5.1). Because the smoking habits of women were different from men, we conducted more detailed analyses using comparable levels of smoking exposure. After restriction to smokers and adjustment for other smoking variables, risk estimates did not differ appreciably between genders. The analysis of duration of smoking (0-19, 20-39, 40+ years) adjusted for cigarette consumption and time since quitting smoking revealed similar risk estimates in men (OR = 1.0, 3.3 [CI 2.6-4.2], 4.1 [CI 3.1-5.6]) and women (OR = 1.0, 2.7 [CI 1.7-4.1], 3.3 [CI 1.9-5.8]). The same was true of the analysis of average or cumulative smoking consumption, and also of analyses stratified by different histological types. We conclude that for comparable exposure to tobacco smoke, the risk of lung cancer is comparable in women and men.     

Cigar and pipe smoking and lung cancer risk: a multicenter study from Europe

BACKGROUND: Because limited information is available on the quantitative association between consumption of tobacco products other than cigarettes and lung cancer risk, we undertook a case-control study of this relationship. METHODS: We investigated lung cancer risk among smokers of cigars and/or cigarillos only and of pipes only and compared these risks with the risk of smokers of cigarettes only in a case-control study conducted in seven European areas. Our study population consisted of 5621 male case patients with lung cancer and 7255 male control subjects. Each subject or his proxy was interviewed with respect to the subject's smoking history and other risk factors for lung cancer. RESULTS: The odds ratio (OR) for smoking cigars and cigarillos only was 9.0 (95% confidence interval [CI] = 5.8-14.1), based on 43 exposed case patients and 77 exposed control subjects, and the OR for smoking a pipe only was 7.9 (95% CI = 5.3-11.8), representing 61 case patients and 129 control subjects. The OR for smoking cigarettes only was 14.9 (95% CI = 12.3-18.1), based on 4204 case patients and 3930 control subjects. A dose-response relationship was present for duration of use and cumulative consumption both for cigars and cigarillos and for pipe tobacco. An effect was also suggested for inhalation of cigar and cigarillo smoke. The dose-response relationships between lung cancer risk and either duration of smoking or average and cumulative consumption were similar for cigar and cigarillo smoking, pipe smoking, and cigarette smoking. CONCLUSION: Our results suggest that smoking of European cigars, cigarillos, and pipe tobacco might exert a carcinogenic effect on the lung comparable to that of cigarettes.     

Fumes from meat cooking and lung cancer risk in Chinese women.

Chinese women are recognized to have a high incidence of lung cancer despite a low smoking prevalence. Several studies have implicated domestic exposure to cooking fumes as a possible risk factor, although the exact carcinogens have yet to be identified. Heterocyclic amines are known carcinogens, which have been identified in cooked meat, and also in fumes generated during frying or grilling of meats. We conducted a case-control study of 303 Chinese women with pathologically confirmed, primary carcinomas of the lung and 765 controls to examine the association between exposure to meat cooking and lung cancer risk. Data on demographic background, smoking status, and domestic cooking exposure, including stir-frying of meat, were obtained by in-person interview while in hospital. The response rates among eligible cases and controls were 95.0 and 96.9%, respectively. The proportion of smokers (current or ex-smokers) among cases and controls was 41.7 and 13.1%, respectively. Adenocarcinomas comprised 31.5% of cancers among smokers and 71.6% among nonsmokers. When cases were compared with controls, the odds ratio (OR) for lung cancer (all subtypes) among ex-smokers was 4.3 [95% confidence interval (CI) 2.7-6.8] and that among current smokers was 5.0 (95% CI, 3.4-7.3). Among smokers, women who reported that they stir-fried daily in the past had a significantly increased risk of lung cancer (adjusted OR, 2.0; 95% CI, 1.0-3.8) and among these women, risk was enhanced for those who stir-fried meat daily (OR, 2.7; 95% CI, 1.3-5.5). Women who stir-fried daily but cooked meat less often than daily did not show an elevated risk (OR, 1.0. 95% CI, 0.5-2.4). Risk was further increased among women stir-frying meat daily who reported that their kitchen was filled with oily fumes during cooking (OR, 3.7; 95% CI, 1.8-7.5). These cooking practices on their own did not increase risk among nonsmokers in our study population. Our results suggest that inhalation of carcinogens, such as heterocyclic amines generated during frying of meat, may increase the risk of lung cancer among smokers. Further studies in different settings are warranted to examine this possibility, which may also help to explain the higher risk observed among women smokers compared with men.     

Risk factors for lung cancer in Iowa women: implications for prevention

BACKGROUND: Multiple risk factors possibly associated with lung cancer were examined as part of a large-scale residential radon case-control study conducted in Iowa between 1994 and 1997. We were particularly interested in stratifying risk factors by smoking status. Relatively little risk factor information is available for Midwestern rural women. METHODS: Four hundred thirteen female lung cancer cases and 614 controls aged 40-84, who were residents of their current home for at least 20 years, were included. Risk factors examined included cigarette smoking, passive smoking, occupation, chemical exposure, previous lung disease, family history of cancer, and urban residence. Multiple logistic regression analysis was conducted after adjusting for age, education, and cumulative radon exposure. RESULTS: As expected, active cigarette smoking was the major risk factor for lung cancer. While cessation of smoking was significantly associated with a reduced risk for lung cancer, the risk remained significantly elevated for 25 years. Among all cases, asbestos exposure was a significant risk. Among ex-smokers, pack-year history predominated as the major risk. Among never smokers, a family history of kidney or bladder cancer were significant risk factors (OR=7.34, 95% CI=1.91-28.18; and OR=5.02, 95% CI=1.64-15.39, respectively), as was a history of previous lung disease (OR=2.28, 95% CI=1.24-4.18) and asbestos exposure. No statistically significant increase in lung cancer risk was found for occupation or urban residence. CONCLUSIONS: Smoking prevention activities are urgently needed in rural areas of the United States. Relatives of individuals with smoking-related cancers are potentially at increased risk. Genetic risk factors should be more fully investigated in never smokers.     

Home kitchen ventilation,cooking fuels,and lung cancer risk in a prospective cohort of never smoking women in Shanghai,China

Indoor air pollution (IAP) caused by cooking has been associated with lung cancer risk in retrospective case–control studies in developing and rural countries. We report the association of cooking conditions, fuel use, oil use, and risk of lung cancer in a developed urban population in a prospective cohort of women in Shanghai. A total of 71,320 never smoking women were followed from 1996 through 2009 and 429 incident lung cancer cases were identified. Questionnaires collected information on household living and cooking practices for the three most recent residences and utilization of cooking fuel and oil, and ventilation conditions. Cox proportional hazards regression estimated the association for kitchen ventilation conditions, cooking fuels, and use of cooking oils for the risk of lung cancer by hazard ratios (HR) with 95% confidence intervals (95% CI). Ever poor kitchen ventilation was associated with a 49% increase in lung cancer risk (HR: 1.49; 95% CI: 1.15–1.95) compared to never poor ventilation. Ever use of coal was not significantly associated. However, ever coal use with poor ventilation (HR: 1.69; 95% CI: 1.22–2.35) and 20 or more years of using coal with poor ventilation (HR: 2.03; 95% CI: 1.35–3.05) was significantly associated compared to no exposure to coal or poor ventilation. Cooking oil use was not significantly associated. These results demonstrate that IAP from poor ventilation of coal combustion increases the risk of lung cancer and is an important public health issue in cities across China where people may have lived in homes with inadequate kitchen ventilation.     

Smoky coal,tobacco smoking,and lung cancer risk in Xuanwei,China

Objectives

Lung cancer rates in Xuanwei are the highest in China. In-home use of smoky coal has been associated with lung cancer risk, and the association of smoking and lung cancer risk strengthened after stove improvement. Here, we explored the differential association of tobacco use and lung cancer risk by the intensity, duration, and type of coal used.

Materials and methods

We conducted a population-based case-control study of 260 male lung cancer cases and 260 age-matched male controls. Odds ratios (OR) and 95% confidence interval (CI) for tobacco use was calculated by conditional logistic regression.

Results

Use of smoky coal was significantly associated with an increased risk of lung cancer, and tobacco use was weakly and non-significantly associated with lung cancer risk. When the association was assessed by coal use, the cigarette-lung cancer risk association was null in hazardous coal users and elevated in less hazardous smoky coal users and non-smoky coal users. The risk of lung cancer per cigarette per day decreased as annual use of coal increased (>0–3 tons: OR: 1.09; 95% CI: 1.03–1.17; >3 tons: OR: 0.99; 95% CI: 0.95–1.03). Among more hazardous coal users, attenuation occured at even low levels of usage (>0–3 tons: OR: 1.02; 95% CI: 0.91–1.14; >3 tons: OR: 0.94; 95% CI: 0.97–1.03).

Conclusion

We found evidence that smoky coal attenuated the tobacco and lung cancer risk association in males that lived in Xuanwei, particularly among users of hazardous coal where even low levels of smoky coal attenuated the association. Our results suggest that the adverse effects of tobacco may become more apparent as China's population continues to switch to cleaner fuels for the home, underscoring the urgent need for smoking cessation in China and elsewhere.