阳江高本底地区肺癌与室内氡暴露巢式病例-对照研究

目的研究居室氡暴露与肺癌危险的关系。方法采用巢式病例-对照研究设计,病例与对照为1∶2个体配比。以面访的方式访问调查对象的家属或其他知情人。用固体核径迹探测器方法,对调查对象曾住房屋的氡浓度进行累积测量。结果成功访问了63例肺癌病例和125例对照,病例与对照的平均死亡年龄分别为60.1岁和60.6岁。病例和对照所在室内氡的平均浓度分别为40.1和39.2 Bq/m3。单因素条件logistic回归分析氡暴露与肺癌危险的关系,比值比[(OR)95%可信限(95%CI)]为1.25(0.63~2.52)。不同程度氡暴露,肺癌危险有增加趋势,但差异无统计学意义(P>0.05)。在100 Bq/m3氡浓度时,氡暴露的超额比值比(EOR)为0.30(95%CI:-0.53~14.93),调整钍射气贡献后,EOR=0.14。结论未发现室内氡暴露与肺癌危险有统计学意义的关联。     

铀矿工氡职业暴露与肺癌风险:巢式病例-对照研究

[目的]探讨铀矿工氡职业暴露与肺癌的关系。[方法]采用回顾性巢式病例-对照研究的方法,以1958—2000年在某铀矿山工作,且由当地省市级医院确诊为肺癌的72例男性死亡病例为病例组,以与病例组年龄相差不超过5岁、同性别、1∶4配比方法选取的288例铀矿工为对照组,采用条件logistic回归方法对职业性氡暴露与肺癌关系进行分析,并计算氡致肺癌的危险系数[每工作水平月(WLM)引起的肺癌风险增量]。[结果]病例组及对照组的氡暴露量几何均数分别为171.8 WLM和127.5 WLM。单因素条件logistic回归分析显示:病例组与对照组的首次下井年龄、坑龄、年龄差异无统计学意义;吸烟(OR=1.88,95%CI:1.07~3.31)和氡职业暴露(OR=1.61,95%CI:1.19~2.16)增加肺癌风险。多因素条件logistic回归分析显示:吸烟及氡暴露仍是矿工肺癌发生的主要危险因素,吸烟致肺癌的OR为2.27(95%CI:1.26~4.09),氡致肺癌的OR为1.62(95%CI:1.18~2.24)。使用OR=1.62计算出氡致肺癌的危险系数为0.36%WLM-1,即每WLM的职业氡暴露可使铀矿工患肺癌死亡的风险增加0.36%。[结论]除吸烟外,氡职业暴露是铀矿工肺癌的主要危险因素。     

氡暴露致肺癌相关基因研究的进展

氡是地壳中铀的天然衰变产物，普遍存在于环境空气中。近年来，随着建筑材料的广泛应用，普通人群对氡的接触机会和暴露水平明显增加。主要的职业性氡接触人群是铀矿工。矿工吸入高浓度氡(^222Rn)会增加患肺癌的危险性。利用矿工模型的外推表明，氡是第二位致肺癌因素。德国7％的肺癌、荷兰4％的肺癌、瑞典4％的肺癌以及美国10％～15％的肺癌由氧暴露引起。     

非吸烟人群肺癌与居住环境氡暴露的关系

为进一步证实非吸烟人群肺癌发生与居住环境氡暴露有关，从不吸烟的肺癌患者和不吸烟的对照人群进行了病例对照研究。对住所的氡浓度进行全面测量，结合前期开展的肺癌与居住环境氡暴露作了病例对照研究。结果表明，居住环境氡暴露对被动吸烟者更加有害。平均氡浓度每增加100Bqm^-3，肺癌的相对危险度大约增加10％，这一研究结果与截至目前为止所有氡研究结果大致相似。     

氡及其子体的健康危害效应

地下矿工的队列研究和室内氡暴露的病例对照研究都证明氡及其子体是肺癌发生的危险因子,动物实验也证实了这样的危险增加。近年来地下矿工和室内氡暴露与肺癌关系的合并分析更有力地说明肺癌危险与氡及其子体暴露的相关性。氡致肺癌的细胞和分子机制的研究,包括抑癌基因和癌基因,以及常用的生物标志物或生物剂量计,如染色体畸变、红细胞血红糖蛋白A(GPA)、次黄嘌呤鸟嘌呤磷酸核糖转移酶基因(HPRT)的研究,有助于阐明氡致肺癌的机制,提出氡暴露危险评估的细胞和分子生物学依据。同时,进入呼吸道的氡的三分之一左右能进入血液分布至全身、血液和骨髓可能是肺之外氡及其子体作用的另一个靶器官,氡诱发白血病的危险也值得关注。     

云南锡矿工人肺癌高发的流行病学调查(1954～2002年)

[目的]分析云南锡矿工人职业性肺癌的流行特征，为预防与控制其高发提供科学依据。[方法]对1954-2002年矿工肺癌的发病、死亡及其相关工种和作业环境检测资料进行流行病学分析比较，评价暴露于职业环境中氡子体、砷的锡矿工职业性肺癌特征。[结果]云南锡矿的矿工暨冶炼工复合职业史男性肺癌标化死亡率高达1231．13／10^5，是当地普通男性居民肺癌标化死亡率（26．61／10^5）的46．27倍，其高发职业特征显著。作业环境中主要致肺癌危险因素砷、氡子体的暴露与肺癌发病之间存在剂量一效应关景。[结论]流行病学综合分析提示，预防和控制云南锡矿工人肺癌高发的关键是降低工作环境中的氡、砷浓度；其次是在矿工中加强戒烟教育并做好个人劳动保护。     

CYP1A1和GSTM1基因多态与肺癌发病关系的病例-对照研究

目的 探讨肺癌易感性标记物CYP1A1及GSTM1基因多态以及吸烟等其他环境暴露因素与肺癌发生的关系。方法 采用病例-对照研究的方法，收集原发性肺癌病例91例以及非肺部疾患的住院病例(对照)91例，所有的研究对象均采静脉血进行DNA抽提，并用PCR方法检测CYP1A1以及GSTM1基因多态，同时调查研究对象吸烟等其他环境暴露因素。应用Logistic回归分析方法进行单因素和多因素的分析。结果 无论是单因素分析还是多因素分析均未显示出CYP1A1和GSTM1基因多态与肺癌发病的关联。多因素分析结果表明：化程度的OR为0．63(95％CI：0．45～0．86)，吸烟量的OR为1．56(95％CI：1．14～2．14)，无抽油烟机的OR为3．77(95％CI：1．48～9．56)，食用动物油的OR为1．67(95％CI：1.25～2．24)，常吃胡萝卜的OR为0．47(95％CI：0．22～0．98)，饮酒的OR为6．58(95％CI：1.53～28．30)，家族肺癌史的OR为3．75(95％CI：1．64～8．58)。结论 CYP1A1和GSTM1基因多态与肺癌发病无明显的关联，吸烟、饮酒、食用动物油、家族肺癌吏以及无抽油烟机是肺癌的危险因素，而高化程度和常吃胡萝卜与降低肺癌风险有关。     

中国接触二氧化硅工人肺癌嵌套的病例—对照研究

试图对二氧化硅是否能引起肺癌进行评价,在中国中南五省,作者对陶器厂工人,钨、铜-铁、锡矿工,316例男性肺癌病例和1352名对照者进行了嵌套的病例-对照研究。对各研究对象粉尘和二氧化硅接触的定量评价是依据既往卫生学记录的累积接尘量;对混杂因素如无机砷、多环芳香烃(PAHs)和氡的含量亦是从工作场所收集而得;吸烟     

山东省黄金矿山氡及其子体浓度调查

调查并检测山东省主要黄金矿山井下,洗选厂房内,生活区居室内空气中氡及其子体浓度;估算井下矿工暴露在氡子体下的年有效剂量当量。氡浓度用气球法,氡子体α潜能浓度用库斯尼茨法测量。结果 井下,洗选厂房内,生活区居室内氡浓度平均值分别为３６７．０Ｂｑ．ｍ＾－３,９．７Ｂｑ．ｍ＾－３,１３．２Ｂｑ．ｍ＾－３;     

血、尿核黄素水平与肺癌危险性的嵌套病例-对照研究

用 1∶2配比的嵌套病例 -对照设计研究了云锡矿工血、尿核黄素水平与肺癌危险性的关系。病例为云锡肺癌高危人群普查队列中 1992～ 1995年新确诊的肺癌患者 ,对照以 1:2的比例从普查队列的非肺癌矿工中随机抽取 ,按职业暴露史、年龄、血、尿样本采集时间等因素与病例配对 ,所测生化指标为红细胞谷胱甘酞还原酶活性系数 (EGR AC)和尿核黄素 肌酐比值。在调整了混杂因素的影响后 ,两项指标以连续变量引入logistic回归方程 ,其OR值分别为 0 780 (EGR AC)和 1 0 0 0 ,均无显著意义 (P >0 0 5) ;以等级变量将两项指标引入方程 ,两指标各等级的OR值也无显著性意义 (P >0 0 5)。本研究没有观察到血、尿核黄素水平与云锡矿工肺癌危险性有相关关系     

Residential radon and risk of lung cancer: a combined analysis of 7 North American case-control studies

BACKGROUND: Underground miners exposed to high levels of radon have an excess risk of lung cancer. Residential exposure to radon is at much lower levels, and the risk of lung cancer with residential exposure is less clear. We conducted a systematic analysis of pooled data from all North American residential radon studies. METHODS: The pooling project included original data from 7 North American case-control studies, all of which used long-term alpha-track detectors to assess residential radon concentrations. A total of 3662 cases and 4966 controls were retained for the analysis. We used conditional likelihood regression to estimate the excess risk of lung cancer. RESULTS: Odds ratios (ORs) for lung cancer increased with residential radon concentration. The estimated OR after exposure to radon at a concentration of 100 Bq/m3 in the exposure time window 5 to 30 years before the index date was 1.11 (95% confidence interval = 1.00-1.28). This estimate is compatible with the estimate of 1.12 (1.02-1.25) predicted by downward extrapolation of the miner data. There was no evidence of heterogeneity of radon effects across studies. There was no apparent heterogeneity in the association by sex, educational level, type of respondent (proxy or self), or cigarette smoking, although there was some evidence of a decreasing radon-associated lung cancer risk with age. Analyses restricted to subsets of the data with presumed more accurate radon dosimetry resulted in increased estimates of risk. CONCLUSIONS: These results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted using miner data and consistent with results from animal and in vitro studies.     

Residential radon and lung cancer among never-smokers in Sweden.

In this study, we attempted to reduce existing uncertainty about the relative risk of lung cancer from residential radon exposure among never-smokers. Comprehensive measurements of domestic radon were performed for 258 never-smoking lung cancer cases and 487 never-smoking controls from five Swedish case-control studies. With additional never-smokers from a previous case-control study of lung cancer and residential radon exposure in Sweden, a total of 436 never-smoking lung cancer cases diagnosed in Sweden between 1980 and 1995 and 1,649 never-smoking controls were included. The relative risks (with 95% confidence intervals in parentheses) of lung cancer in relation to categories of time-weighted average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m(-3), were 1.08 (0.8--1.5), 1.18 (0.9--1.6), and 1.44 (1.0--2.1), respectively, with average radon concentrations below 50 Bq m(-3) used as reference category and with adjustment for other risk factors. The data suggested that among never-smokers residential radon exposure may be more harmful for those exposed to environmental tobacco smoke. Overall, an excess relative risk of 10% per 100 Bq m(-3) average radon concentration was estimated, which is similar to the summary effect estimate for all subjects in the main residential radon studies to date.     

Meta-analysis of residential exposure to radon gas and lung cancer

OBJECTIVES: To investigate the relation between residential exposure to radon and lung cancer. METHODS: A literature search was performed using Medline and other sources. The quality of studies was assessed. Adjusted odds ratios with 95% confidence intervals (CI) for the risk of lung cancer among categories of levels of exposure to radon were extracted. For each study, a weighted log-linear regression analysis of the adjusted odds ratios was performed according to radon concentration. The random effect model was used to combine values from single studies. Separate meta-analyses were performed on results from studies grouped with similar characteristics or with quality scores above or equal to the median. FINDINGS: Seventeen case-control studies were included in the meta-analysis. Quality scoring for individual studies ranged from 0.45 to 0.77 (median, 0.64). Meta-analysis based on exposure at 150 Bq/m3 gave a pooled odds ratio estimate of 1.24 (95% CI, 1.11-1.38), which indicated a potential effect of residential exposure to radon on the risk of lung cancer. Pooled estimates of fitted odds ratios at several levels of randon exposure were all significantly different from unity--ranging from 1.07 at 50 Bq/m3 to 1.43 at 250 Bq/m3. No remarkable differences from the baseline analysis were found for odds ratios from sensitivity analyses of studies in which > 75% of eligible cases were recruited (1.12, 1.00-1.25) and studies that included only women (1.29, 1.04-1.60). CONCLUSION: Although no definitive conclusions may be drawn, our results suggest a dose-response relation between residential exposure to radon and the risk of lung cancer. They support the need to develop strategies to reduce human exposure to radon.     

A review of residential radon case-control epidemiologic studies performed in the United States.

Lung cancer is the leading cause of cancer death in the United States for both men and women. Although most lung cancer deaths are attributable to tobacco usage, even secondary causes of lung cancer are important because of the magnitude of lung cancer incidence and its poor survival rate. This review summarizes the basic features and major findings from the published U.S. large-scale residential radon case-control studies performed in New Jersey, Iowa, and Missouri (two studies). The methodology from an unpublished study covering Connecticut, Utah, and Southern Idaho is also presented. Overall, the higher categorical risk estimates for these published studies produced a positive association between prolonged radon exposure and lung cancer. Two studies (Missouri-II and Iowa) that incorporated enhanced dose estimates produced the most compelling evidence suggesting an association between prolonged residential radon exposure and lung cancer. The prevailing evidence suggests that the statistically significant findings may be related to improved retrospective radon exposure estimates. The general findings from the U.S. studies, along with extrapolations from radon-exposed underground miners, support the conclusion that after cigarette smoking, prolonged residential radon exposure is the second leading cause of lung cancer in the general population.     

Exposure to residential radon and lung cancer in Spain: a population-based case-control study

Although high radon concentrations have been linked to increased risk of lung cancer by both experimental studies and investigations of underground miners, epidemiologic studies of residential radon exposure display inconsistencies. The authors therefore decided to conduct a population-based case-control study in northwest Spain to determine the risk of lung cancer associated with exposure to residential radon. The study covered a total of 163 subjects with incident lung cancer and a population sample of 241 cancer-free subjects since 1992-1994. Odds ratios for radon were estimated using logistic regression adjusted for sex, age, lifetime tobacco use, family history, and habitat. The adjusted odds ratios for the second, third, and fourth quartiles of radon (breakpoints: 37.0, 55.2, and 148.0 Bq/m(3)) were 2.73 (95% confidence interval (CI): 1.12, 5.48), 2.48 (95% CI: 1.29, 6.79), and 2.96 (95% CI: 1.29, 6.79), respectively. An additive synergic effect between radon and tobacco was found. The results from this study suggest that, even at concentrations far below official guideline levels, radon may lead to a 2.5-fold rise in the risk of lung cancer. Furthermore, the synergy found between smoking and radon may prove useful when it comes to drafting public health recommendations.     

Residential radon exposure and lung cancer: variation in risk estimates using alternative exposure scenarios

The most direct way to derive risk estimates for residential radon progeny exposure is through epidemiologic studies that examine the association between residential radon exposure and lung cancer. However, the National Research Council concluded that the inconsistency among prior residential radon case-control studies was largely a consequence of errors in radon dosimetry. This paper examines the impact of applying various epidemiologic dosimetry models for radon exposure assessment using a common data set from the Iowa Radon Lung Cancer Study (IRLCS). The IRLCS uniquely combined enhanced dosimetric techniques, individual mobility assessment, and expert histologic review to examine the relationship between cumulative radon exposure, smoking, and lung cancer. The a priori defined IRLCS radon-exposure model produced higher odds ratios than those methodologies that did not link the subject's retrospective mobility with multiple, spatially diverse radon concentrations. In addition, the smallest measurement errors were noted for the IRLCS exposure model. Risk estimates based solely on basement radon measurements generally exhibited the lowest risk estimates and the greatest measurement error. The findings indicate that the power of an epidemiologic study to detect an excess risk from residential radon exposure is enhanced by linking spatially disparate radon concentrations with the subject's retrospective mobility.     

Residential radon exposure and lung cancer in Swedish women.

A case-control study was undertaken to investigate the role of residential radon exposure for lung cancer. The study included 210 women with lung cancer diagnosed from 1983-1986 in the county of Stockholm and 191 hospital and 209 population controls. Interviews provided information on lifetime residences and smoking. Radon concentrations measured in 1,573 residences of the study subjects showed a lognormal distribution with arithmetic and geometric means of 127.7 and 96.0 Bq m-3, respectively. Lung cancer risks tended to increase with estimated radon exposure, reaching a relative risk of 1.7 (95% confidence interval: 1.0-2.9) in women having an average radon level exceeding 150 Bq m-3 (4 pCi L-1). Stronger associations were suggested in younger persons and risk estimates appeared to be within the same range as those projected for miners. However, further studies are needed to clarify the level of risk associated with exposure to residential radon.     

Canadian individual risks of radon-induced lung cancer for different exposure profiles

BACKGROUND: Indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. There is an increasing need among radiation practitioners to have numerical values of lung cancer risks for men and women, ever-smokers and never-smokers exposed to radon in homes. This study evaluates individual risks for the Canadian population exposed to radon in homes at different radon concentrations and for different periods of their lives. METHODS: Based on the risk model developed recently by U.S. Environmental Protection Agency (EPA), individual risks of radon-induced lung cancers are calculated with Canadian age-specific rates for overall and lung cancer mortalities (1996-2000) as well as the Canadian smoking prevalence data in 2002. RESULTS: Convenient tables of lifetime relative risks are constructed for lifetime exposures and short exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 50 to 1000 Bq/m3. CONCLUSIONS: The risk of developing lung cancer from residential radon exposure increases with radon concentration and exposure duration. For short exposure periods, such as 10 or 20 years, risks are higher in middle age groups (30-50) compared especially to the later years. Individuals could lower their risks significantly by reducing radon levels earlier in life. The tables could help radiation protection practitioners to better communicate indoor radon risk to members of the public.     

Radon-222 concentration in groundwater and cancer mortality in North Carolina

Summary In a geographic correlation study, we explored the possibility that residential exposure to radon in groundwater may be related to cancers other than lung cancer. Measurements of radon in groundwater and 1978–1982 cancer mortality data from North Carolina, USA were used to investigate this relationship. Counties were categorized in two levels of radon exposure according to measured radon concentration and geology. In the lower exposure group (unexposed) county mean radon concentrations ranged from 0–228 pCi/1 (0–8436 Bq/m³), and in the upper group (potentially exposed) the range of county average concentrations was 229–10892 pCi/1 (8473–403004 Bq/m³), (median 1375 pCi/1 (50875 Bq/m³)). Adjusted mortality ratios and 95% confidence intervals were calculated for selected cancers, including leukemias, gastro-intestinal tract cancers, and respiratory tract cancers excluding lung cancer. In contrast to other ecologic studies, we found no consistent association between radon level and cancer mortality.     

Residential randon exposure and lung cancer risk in Misasa, Japan: a case-control study

In order to investigate an association between residential radon exposure and risk of lung cancer, a case-control study was conducted in Misasa Town, Tottori Prefecture, Japan. The case series consisted of 28 people who had died of lung cancer in the years 1976-96 and 36 controls chosen randomly from the residents in 1976, matched by sex and year of birth. Individual residential radon concentrations were measured for 1 year with alpha track detectors. The average radon concentration was 46 Bq/m3 for cases and 51 Bq/m3 for controls. Compared to the level of 24 or less Bq/m3, the adjusted odds ratios of lung cancer associated with radon levels of 25-49, 50-99 and 100 or more Bq/m3, were 1.13 (95% confidence interval; 0.29-4.40), 1.23 (0.16-9.39) and 0.25 (0.03-2.33), respectively. None of the estimates showed statistical significance, due to small sample size. When the subjects were limited to only include residents of more than 30 years, the estimates did not change substantially. This study did not find that the risk pattern of lung cancer, possibly associated with residential radon exposure, in Misasa Town differed from patterns observed in other countries.