Lung Cancer in Chinese Women: Evidence for an Interaction between Tobacco Smoking and Exposure to Inhalants in the Indoor Environment

Background

Epidemiologic data suggest that Chinese women have a high incidence of lung cancer in relation to their smoking prevalence. In addition to active tobacco smoke exposure, other sources of fumes and airborne particles in the indoor environment, such as cooking and burning of incense and mosquito coils, have been considered potential risk factors for lung cancer.

Objectives

We used a case–control study to explore effects of inhalants from combustion sources common in the domestic environment on lung cancer and their modification by active tobacco smoking.

Methods

We analyzed 703 primary lung cancer cases and 1,578 controls. Data on demographic background and relevant exposures were obtained by face-to-face interviews in the hospital.

Results

We observed a positive relationship with daily exposure to incense or mosquito coils and to cooking fumes only among smokers, and no association among lifetime nonsmokers. Interactions between smoking and frequency of cooking, or exposure to incense or mosquito coils were statistically significant and consistent with synergistic effects on lung cancer. The odds ratio (OR) comparing smokers without daily incense or mosquito coil exposure with nonsmokers without daily exposure was 2.80 [95% confidence interval (CI), 1.86–4.21], whereas the OR comparing smokers with daily exposure to the same referent group was 4.61 (95% CI, 3.41–6.24). In contrast, daily exposure to incense or mosquito coils was not associated with lung cancer among nonsmokers (OR = 0.91; 95% CI, 0.72–1.16). We observed the same pattern of associations for smokers without (OR = 2.31; 95% CI, 1.52–3.51) and with (OR = 4.50; 95% CI, 3.21–6.30) daily cooking exposure compared with nonsmokers, with no evidence of an association with daily cooking exposure among nonsmokers.

Conclusion

Our results suggest that active tobacco smoking not only is an important risk factor for development of lung cancer, but also may cause smokers to be more susceptible to the risk-enhancing effects of other inhalants.     

Effects of radon mitigation vs smoking cessation in reducing radon-related risk of lung cancer.

OBJECTIVES: The purpose of this paper is to provide smokers with information on the relative benefits of mitigating radon and quitting smoking in reducing radon-related lung cancer risk. METHODS: The standard radon risk model, linked with models characterizing residential radon exposure and patterns of moving to new homes, was used to estimate the risk reduction produced by remediating high-radon homes, quitting smoking, or both. RESULTS: Quitting smoking reduces lung cancer risk from radon more than does reduction of radon exposure itself. CONCLUSIONS: Smokers should understand that, in addition to producing other health benefits, quitting smoking dominates strategies to deal with the problem posed by radon.     

Design issues in studies of radon and lung cancer: implications of the joint effect of smoking and radon.

Many case-control studies have been undertaken to assess whether and to what extent residential radon exposure is a risk factor for lung cancer. Nearly all these studies have been conducted in populations including smokers and nonsmokers. In this paper, we show that, depending on the nature of the joint effect of radon and tobacco on lung cancer risk, it may be very difficult to detect a main effect due to radon in mixed smoking and nonsmoking populations. If the joint effect is closer to additive than multiplicative, the most cost-effective way to achieve adequate statistical power may be to conduct a study among never-smokers. Because the underlying joint effect is unknown, and because many studies have been carried out among mixed smoker and nonsmoker populations, it would be desirable to conduct some studies with adequate power among never-smokers only.     

Clinical measures, smoking, radon exposure, and risk of lung cancer in uranium miners.

OBJECTIVES: Exposure to the radioactive daughters of radon is associated with increased risk of lung cancer in mining populations. An investigation of incidence of lung cancer following a clinical survey of Ontario uranium miners was undertaken to explore whether risk associated with radon is modified by factors including smoking, radiographic silicosis, clinical symptoms, the results of lung function testing, and the temporal pattern of radon exposure. METHODS: Miners were examined in 1974 by a respiratory questionnaire, tests of lung function, and chest radiography. A random selection of 733 (75%) of the original 973 participants was followed up by linkage to the Ontario Mortality and Cancer Registries. RESULTS: Incidence of lung cancer was increased threefold. Risk of lung cancer among miners who had stopped smoking was half that of men who continued to smoke. There was no interaction between smoking and radon exposure. Men with lung function test results consistent with airways obstruction had an increased risk of lung cancer, even after adjustment for cigarette smoking. There was no association between radiographic silicosis and risk of lung cancer. Lung cancer was associated with exposures to radon daughters accumulated in a time window four to 14 years before diagnosis, but there was little association with exposures incurred earlier than 14 years before diagnosis. Among the men diagnosed with lung cancer, the mean and median dose rates were 2.6 working level months (WLM) a year and 1.8 WLM/year in the four to 14 year exposure window. CONCLUSIONS: Risk of lung cancer associated with radon is modified by dose and time from exposure. Risk can be substantially decreased by stopping smoking.     

Predicted reduction in lung cancer risk following cessation of smoking and radon exposure

Recently there has been considerable public and regulatory concern that radon, produced by the decay of naturally occurring uranium, can accumulate in homes, offices, and schools at levels that may substantially increase the risk of lung cancer. The major cause of lung cancer is smoking, and radon appears to interact multiplicatively with smoking in causing lung cancer. Thus, the most effective way to reduce the increased risk of lung cancer resulting from radon exposure is to cease smoking. In this paper, a model for the risks associated with radon exposure that was developed by a committee of the National Academy of Sciences is used to calculate the benefits, in terms of reduction in lifetime risk of lung cancer, of ceasing to smoke, ceasing radon exposure, or ceasing both. Ceasing to smoke is considerably more beneficial than ceasing radon exposure, and thus policymakers addressing the health effects of radon should place priority on encouraging individuals to stop smoking.     

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.     

Mentholated cigarette smoking and lung-cancer risk

PURPOSE: Menthol smoking may lead to a greater increase in lung-cancer risk than smoking of nonmentholated cigarettes. Mentholation of cigarettes adds additional carcinogenic components to cigarette smoke and increases retention times for cigarette smoke in the lungs. Only two epidemiologic studies have been conducted on menthol smoking and lung cancer, and their results are conflicting. Of note, African American males have much higher rates of lung cancer than Caucasian males despite smoking fewer cigarettes per day. Because the consumption of menthol cigarettes is much more frequent among African Americans, it is of interest to examine the possible association between menthol smoking and lung-cancer risk in this population. METHODS: We examined the association between menthol cigarette smoking and lung-cancer risk among smokers by comparing 337 incident cases of lung cancer with 478 population controls enrolled in a case-control study of lung cancer. Information on smoking history and other known and potential risk factors for lung cancer, including dietary intake, was obtained by in-person interviews. RESULTS: The adjusted odds ratios did not differ appreciably between smokers of mentholated cigarettes versus exclusive nonmentholated cigarette smokers in the overall study group of smokers. The odds ratio (OR) for 32 pack-years or more of mentholated vs. nonmentholated cigarettes was 0.90 (95% confidence interval (CI) = 0.38-2.12) in African Americans and 1.06 (95% CI = 0.47-2.36) in Caucasians, and did not differ for either ethnic group (p = 0.98). CONCLUSIONS: Our results suggest that the lung-cancer risk from smoking mentholated cigarettes resembles the risk from smoking non-mentholated cigarettes. Our data do not support the hypothesis that the increased risk of lung cancer among African Americans is due to the increased prevalence of menthol smoking.     

Lung cancer and indoor air pollution in rural china

PURPOSE: Indoor air pollution has been linked with lung cancer in China. In contrast to previous studies conducted in urban areas with high levels of industrial pollution, we undertook a lung cancer case-control study in a rural area of China, where residents live in underground dwellings. We evaluated the effects of radon, wood and coal combustion, cooking oil fumes, and environmental tobacco smoke on lung cancer risk.METHODS: We enrolled 886 lung cancer cases (656 males, 230 females) diagnosed between 1994-98, aged 30-75 years and 1765 frequency matched population-based controls from two prefectures in Gansu Province in Northwestern China. We conducted interviews with subjects or next of kin on smoking, housing characteristics, fuel use and cooking practices. Year-long radon detectors were placed in current and former homes of subjects.RESULTS: Subjects primarily used coal (22%), wood (56%) or a combination of both (22%) for heating. Odds Ratios (OR) for lung cancer rose with increasing percent of time that coal was used to heat homes over the past 30 years (ORs = 1.00, 1.17, 1.35, 1.23 compared to wood only, adjusted to smoking, P for trend = 0.025). Among non-smoking females and males, the OR for ever exposed to environmental tobacco smoke was 1.19, 95% CI = 0.7-2.0 with a significant trend for increasing years of exposure. Fumes from cooking with rapeseed oil increased the risk of lung cancer (OR = 1.56, 95% CI = 1.0-2.5) among non-smoking women. Among these women, occasional and frequent eye and throat irritation during cooking appeared to be associated with increased risk of lung cancer (ORs = 1.00, 1.42, 2.28, p trend < 0.01), whereas, increasing level of smokiness during cooking did not appear to affect risk.CONCLUSIONS: There is a suggestion that coal used for heating, environmental tobacco smoke, and cooking oil fumes contribute to the risk of lung cancer in this rural area of China.     

Radon,Smoking, and Lung Cancer: The Need to Refocus Radon Control Policy

Exposure to radon is the second leading cause of lung cancer, and the risk is significantly higher for smokers than for nonsmokers. More than 85% of radon-induced lung cancer deaths are among smokers. The most powerful approach for reducing the public health burden of radon is shaped by 2 overarching principles: public communication efforts that promote residential radon testing and remediation will be the most cost effective if they are primarily directed at current and former smokers; and focusing on smoking prevention and cessation is the optimal strategy for reducing radon-induced lung cancer in terms of both public health gains and economic efficiency. Tobacco control policy is the most promising route to the public health goals of radon control policy.It is estimated that 222 520 new cases of lung cancer were diagnosed and approximately 157 300 people died from this disease in the United States in 2010.1 Exposure to radon—an odorless radioactive gas that can be trapped in homes and other structures—is considered the second leading cause of lung cancer after smoking.2–5 The Environmental Protection Agency (EPA) estimates that residential radon causes approximately 21 000 lung cancer deaths in the United States each year.6,7 In response, the EPA and numerous organizations, including the National Radon Safety Board, promote wide-scale radon screening and remediation in domestic residences.8The strong synergism between radon exposure and smoking as risk factors is a critical aspect of the relationship between radon and lung cancer.2,4,9 That is, the absolute magnitude of the lung cancer risk associated with radon exposure is significantly higher for ever-smokers than for never-smokers. It is estimated that 86% of radon-related lung cancer deaths are in current and former smokers.7,10Angell recently claimed that radon research and remediation programs have “stalled” in the face of severe funding cuts over the past decade and that there has been little progress in testing and remediation in the US housing stock.11 With the recent economic downturn and the resource constraints most governmental health departments face, Angell’s concerns unfortunately will remain salient in the near term. Thus, we have argued that a concentrated policy focus on smoking prevention and cessation and on smokers as targets of both smoking cessation efforts and of radon testing and remediation programs currently provides the most powerful and cost-effective opportunity for reducing the public health burden of radon.Although some researchers have made this argument in the past, there is very little evidence in the United States of any significant radon control activities targeting smokers or of any coordinated efforts between tobacco control and radon control programs or initiatives.4,12 We have elucidated the evidence-based position that residential radon control policy will be most effective and efficient if it combines forces with tobacco prevention and control efforts. We have also offered strategic guidance about what a synergistic radon and tobacco control approach entails.     

Residential radon and risk of lung cancer in an Italian alpine area

To evaluate whether residential radon exposure explains the excess mortality for lung cancer in an Italian alpine valley with high natural radioactivity, the authors conducted a population-based case-control study on 138 deceased cases and 291 sex- and year-of-birth-matched controls. Year-long alpha-track measurements of radon were performed in the most recent residence, and information about occupational history and lifetime smoking habits was obtained. The authors adjusted for smoking, and radon was associated with lung cancer risk among men: compared with a radon level of < 40 becquerels (Bq) per cubic meter (m3), the odds ratios for 40-76 Bq/m3, 77-139 Bq/m3, 140-199 Bq/m3, and 200+ Bq/m3 were 2.1, 2.0, 2.7, and 1.4, respectively. The association between radon and lung cancer, as determined with a multiplicative model, was found only among male smokers.     

Urban air pollution and lung cancer in Stockholm

We conducted a population-based case-control study among men 40-75 years of age encompassing all cases of lung cancer 1985-1990 among stable residents of Stockholm County 1950-1990. Questionnaires to subjects or next-of-kin (primarily wives or children) elicited information regarding smoking and other risk factors, including occupational and residential histories. A high response rate (>85%) resulted in 1,042 cases and 2,364 controls. We created retrospective emission databases for NOx/NO2 and SO2 as indicators of air pollution from road traffic and heating, respectively. We estimated local annual source-specific air pollution levels using validated dispersion models and we linked these levels to residential addresses using Geographical Information System (GIS) techniques. Average traffic-related NO2 exposure over 30 years was associated with a relative risk (RR) of 1.2 (95% confidence interval 0.8-1.6) for the top decile of exposure, adjusted for tobacco smoking, socioeconomic status, residential radon, and occupational exposures. The data suggested a considerable latency period; the RR for the top decile of average traffic-related NO2 exposure 20 years previously was 1.4 (1.0-2.0). Little association was observed for SO2. Occupational exposure to asbestos, diesel exhaust, and other combustion products also increased the risk of lung cancer. Our results indicate that urban air pollution increases lung cancer risk and that vehicle emissions may be particularly important.     

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.     

Residential radon and risk of lung cancer in Eastern Germany

BACKGROUND: There is suggestive evidence that residential radon increases lung cancer risk. To elucidate this association further, we conducted a case-control study in Thuringia and Saxony in Eastern Germany during 1990-1997. METHODS: Histologically confirmed lung cancer patients from hospitals and a random sample of population controls matched on age, sex and geographical area were personally interviewed with respect to residential history, smoking, and other risk factors. One-year radon measurements were performed in houses occupied during the 5-35 years prior to the interview. The final analysis included a total of 1,192 cases and 1,640 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by logistic regression. RESULTS: Measurements covered on average 72% of the exposure time window, with mean radon concentrations of 76 Bq/m3 among the cases and 74 Bq/m3 among the controls. The smoking- and asbestos-adjusted ORs for categories of radon (50-80, 80-140 and >140 Bq/m*3, compared with 0-50 Bq/m3) were 0.95 (CI = 0.77 to 1.18), 1.13 (CI = 0.86 to1.50) and 1.30 (CI = 0.88 to 1.93). The excess relative risk per 100 Bq/m? was 0.08 (CI = -0.03 to 0.20) for all subjects and 0.09 (CI = -0.06 to 0.27) for subjects with complete measurements for all 30 years. CONCLUSIONS: Our data indicate a small increase in lung cancer risk as a result of residential radon that is consistent with the findings of previous indoor radon and miner studies.     

Radon progeny exposure and lung cancer risk among non-smoking uranium miners

Studies of miners provide the basis for public health efforts to reduce residential radon progeny exposure. Because the preponderance of households do not have members who smoke indoors, studies of non-smoking miners contribute essential data for risk assessments for residential radon progeny exposure. We studied a cohort of 2,209 never-smokers who were underground uranium miners employed in the western U.S. from 1956 to the early 1990's and who participated in a screening program for lung cancer conducted by Saccomanno and colleagues. After determining the vital status and cause of death in the cohort, we conducted a nested case-control study of 55 lung cancer deaths in males and 3 age-matched controls for each case. The relative risk of lung cancer was 29.2 (95% CI 5.1, 167.2) for miners with greater than 1,450 WLM compared with those exposed to less than 80 WLM. Temporal factors affected risk, including average dose rate, which was inversely associated with lung cancer risk, and the length of time since last exposure, which was directly associated with decreased risk. As in studies of non-smokers and smokers combined, the exposure response relationship in never-smokers was consistent with a decreased slope at higher WLM, which resulted, in part, from an inverse dose rate effect.     

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。     

Residential Radon and Risk of Lung Cancer in an Italian Alpine Area

To evaluate whether residential radon exposure explains the excess mortality for lung cancer in an Italian alpine valley with high natural radioactivity, the authors conducted a population-based case-control study on 138 deceased cases and 291 sex- and year-of-birth-matched controls. Year-long alpha-track measurements of radon were performed in the most recent residence, and information about occupational history and lifetime smoking habits was obtained. The authors adjusted for smoking, and radon was associated with lung cancer risk among men: compared with a radon level of < 40 becquerels (Bq) per cubic meter (m³), the odds ratios for 40–76 Bq/m³, 77–139 Bq/m³, 140–199 Bq/m³, and 200+ Bq/m³ were 2.1, 2.0, 2.7, and 1.4, respectively. The association between radon and lung cancer, as determined with a multiplicative model, was found only among male smokers.     

Exposure to mosquito coil smoke may be a risk factor for lung cancer in Taiwan

Background

About 50% of lung cancer deaths in Taiwan are not related to cigarette smoking. Environmental exposure may play a role in lung cancer risk. Taiwanese households frequently burn mosquito coil at home to repel mosquitoes. The aim of this hospital-based case-control study was to determine whether exposure to mosquito coil smoke is a risk for lung cancer.

Methods

Questionnaires were administered to 147 primary lung cancer patients and 400 potential controls to ascertain demographic data, occupation, lifestyle data, indoor environmental exposures (including habits of cigarette smoking, cooking methods, incense burning at home, and exposure to mosquito coil smoke ), as well as family history of cancer and detailed medical history.

Results

Mosquito coil smoke exposure was more frequent in lung cancer patients than controls (38.1% vs.17.8%; p<0.01). Risk of lung cancer was significantly higher in frequent burners of mosquito coils (more than 3 times [days] per week) than nonburners (adjusted odds ratio = 3.78; 95% confidence interval: 1.55-6.90). Those who seldom burned mosquito coils (less than 3 times per week) also had a significantly higher risk of lung cancer (adjusted odds ratio = 2.67; 95% confidence interval: 1.60-4.50).

Conclusion

Exposure to mosquito coil smoke may be a risk factor for development of lung cancer.Key words: Air Pollutants, Lung Neoplasms, Mosquito Coil, Smoke     

Occupational exposure to diesel motor exhaust and risk of lung cancer by histological subtype: a population-based case–control study in Swedish men

We investigated occupational exposure to diesel motor exhaust (DME) and the risk of lung cancer by histological subtype among men, using elemental carbon (EC) as a marker of DME exposure. 993 cases and 2359 controls frequency-matched on age and year of study inclusion were analyzed by unconditional logistic regression in this Swedish case–control study. Work and smoking histories were collected by a questionnaire and telephone interviews. DME was assessed by a job-exposure matrix. We adjusted for age, year of study inclusion, smoking, occupational exposure to asbestos and combustion products (other than motor exhaust), residential exposure to radon and exposure to air pollution from road traffic. The OR for lung cancer for ever vs. never exposure to DME was 1.15 (95% CI 0.94–1.41). The risk was higher for squamous and large cell, anaplastic or mixed cell carcinoma than for alveolar cell cancer, adenocarcinoma and small cell carcinoma. The OR in the highest quartile of exposure duration (≥34 years) vs. never exposed was 1.66 (95% CI 1.08–2.56; p for trend over all quartiles: 0.027) for lung cancer overall, 1.73 (95% CI 1.00–3.00; p: 0.040) for squamous cell carcinoma and 2.89 (95% CI 1.37–6.11; p: 0.005) for the group of undifferentiated, large cell, anaplastic and mixed cell carcinomas. We found no convincing association between exposure intensity and lung cancer risk. Long-term DME exposure was associated with an increased risk of lung cancer, particularly to squamous cell carcinoma and the group of undifferentiated, large cell, anaplastic or mixed carcinomas.     

Toward a more realistic appraisal of the lung cancer risk from radon: the effects of residential mobility.

OBJECTIVES: A consideration of the effects of residential mobility produces much more realistic estimates of typical individuals' radon exposures and mortality risks than those of the Environmental Protection Agency (EPA). METHODS: A model linking residential mobility, the distribution of radon in US homes, and lung cancer risk is used to simulate lifetime radon exposure, with and without mitigation of high-radon homes, for typical mobile individuals. Radon-related lung cancer mortality risks are then estimated for smokers and never-smokers. RESULTS: Most individuals residing in high-radon homes have equivalent lifelong radon exposures well below those they are currently experiencing. Consequently, actual lung cancer risks are generally well below those implied in the EPA's radon risk charts. For most people who mitigate high-radon homes, risk reduction is modest. CONCLUSIONS: Radon may indeed be responsible for as large a population risk of lung cancer as the EPA estimates. However, caution must be used in interpreting the EPA's risk assessment for individuals; in many cases, mitigation will have little effect on residents' health risks.