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.     

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.     

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.     

Should radon be reduced in homes? A cost-effect analysis

BACKGROUND: Radon is a radioactive gas that may leak into buildings from the ground. Radon exposure is a risk factor for lung cancer. An intervention against radon exposure in homes may consist of locating homes with high radon exposure (above 200 Bq m(-3)) and improving these, and protecting future houses. The purpose of this paper is to calculate the costs and the effects of this intervention. METHODS: We performed a cost-effect analysis from the perspective of the society, followed by an uncertainty and sensitivity analysis. The distribution of radon levels in Norwegian homes is lognormal with mean = 74.5 Bq m(-3), and 7.6% above 200 Bq m(-3). RESULTS: The preventable attributable fraction of radon on lung cancer was 3.8% (95% uncertainty interval: 0.6%, 8.3%). In cumulative present values the intervention would cost $238 (145, 310) million and save 892 (133, 1981) lives; each life saved costs $0.27 (0.09, 0.9) million. The cost-effect ratio was sensitive to the radon risk, the radon exposure distribution, and the latency period of lung cancer. Together these three parameters explained 90% of the variation in the cost-effect ratio. CONCLUSIONS: The uncertainty in the estimated cost per life is large, mainly due to uncertainty in the risk of lung cancer from radon. Based on estimates from road construction, the Norwegian society has been willing to pay $1 million to save a life. This is above the upper uncertainty limit of the cost per life. The intervention against radon in homes, therefore, seems justifiable.     

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.     

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.     

Radon in homes--a possible cause of lung cancer

An earlier case-referent study [Scand j work environ & health 5 (1979) 10-15] has indicated a possible relationship between lung cancer and exposure to radon and radon daughters in dwellings. Indoor radon concentrations seem to depend on both building material and leakage of radon from the ground. This new study, in a rural area, is a further attempt to elucidate the etiology of lung cancer, taking into consideration type of house and ground conditions, as well as smoking habits. Although the choice of a rural study population helped to eliminate various confounding exposures in the urban environment, it limited the size of the study because of the rareness of lung cancer in rural populations. Long-term residents, 30 years or more in the same houses, were studied, and again an association was found between lung cancer and estimated exposure to radon and radon daughters in homes. The data also seem to indicate the possibility of a multiplicative effect between smoking and exposure to radon and radon daughters in homes, but there was also some confounding between these factors in the data.     

A case-referent study of lung cancer and incense smoke, smoking, and residential radon in Chinese men

Background: Burning incense generates large amounts of air pollutants, many of which are confirmed or suspected human lung carcinogens.Objectives: We conducted a population-based case-referent study to examine the effect of incense smoke exposure on lung cancer risk among Chinese males and explored the joint effect of cigarette smoking and exposure to residential radon.Methods: We recruited 1,208 male lung cancer incident cases and 1,069 community referents from 2004 to 2006 and estimated their lifetime exposures to incense smoke and other residential indoor air pollutants based on self-reported information collected during interviews. We performed unconditional multivariable logistic regression analysis to estimate the odds ratio (OR) for lung cancer associated with exposure to incense smoke after adjusting for possible confounders. We conducted stratified analyses by smoking status and exposures to incense burning and residential radon and explored the potential additive-scale interactions.Results: We observed an association between incense exposure and lung cancer that was limited primarily to smokers. Cigarette smoking and high cumulative incense exposure at home appeared to have a synergistic effect on lung cancer (compared with never-smokers who never used incense, the OR for lung cancer for smokers who used incense ≥ 60 day-years = 5.00; 95% confidence interval: 3.34, 7.51). Power was limited, but we also found preliminary evidence suggesting that radon exposure may increase risk among smokers using incense.Conclusion: Our study suggests that exposure to incense smoke in the home may increase the risk of lung cancer among smokers and that exposure to radon may further increase risk.     

Indoor radon exposure and lung cancer risk: a review of case-control studies

BACKGROUND: Radon is a radioactive gas that tends to accumulate in indoor environment. A causal relationship between lung cancer and radon exposure has been demonstrated in epidemiologic studies of miners. The objective of this paper is to present the results of case-control studies of lung cancer risk associated with indoor radon exposure. METHODS: Case-control studies published since 1990 are included in this review. This type of protocol is particularly well suited for studying the relationship between indoor radon exposure and lung cancer risk, taking into account possible confounding factors such as tobacco smoking. The characteristics and results of these studies are summarized. The limitations associated with each of these studies are also discussed. RESULTS: The results of available studies are relatively concordant and suggest a positive association between lung cancer risk and indoor radon exposure with an estimated excess relative risk of about 6 to 9% per 100Bq/m3 increase in the observed time-weighted average radon concentration. The order of magnitude of this estimation agrees with extrapolations from miners but some studies may suffer from inadequate statistical power. CONCLUSION: At present, efforts are underway to pool together the data from the existing studies of indoor radon. This pooling analysis with thousands of cases and controls will provide a more precise estimate of the lung cancer risk from indoor radon exposure and explore the effect of modifying factors, such as 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.     

Radon and lung cancer risk: taking stock at the millenium

Radon is a well-established human carcinogen for which extensive data are available, extending into the range of exposures experienced by the general population. Mounting epidemiologic evidence on radon and lung cancer risk, now available from more than 20 different studies of underground miners and complementary laboratory findings, indicates that risks are linear in exposure without threshold. Radon is also a ubiquitous indoor air pollutant in homes, and risk projections imply that radon is the second leading cause of lung cancer after smoking. Recommended control strategies in the United States and other countries, which include testing of most homes and mitigation of those exceeding guideline levels, have been controversial. Further research is needed, drawing on molecular and cellular approaches and continuing the follow-up of the underground miner cohorts, and scientists should work toward constructing mechanistically based models that combine epidemiologic and experimental data to yield risk estimates with enhanced certainty.     

The impact of declining smoking on radon-related lung cancer in the United States

Objectives. We examined the effect of current patterns of smoking rates on future radon-related lung cancer.Methods. We combined the model developed by the National Academy of Science''s Committee on Health Risks of Exposure to Radon (the BEIR VI committee) for radon risk assessment with a forecasting model of US adult smoking prevalence to estimate proportional decline in radon-related deaths during the present century with and without mitigation of high-radon houses.Results. By 2025, the reduction in radon mortality from smoking reduction (15 percentage points) will surpass the maximum expected reduction from remediation (12 percentage points).Conclusions. Although still a genuine source of public health concern, radon-induced lung cancer is likely to decline substantially, driven by reductions in smoking rates. Smoking decline will reduce radon deaths more that remediation of high-radon houses, a fact that policymakers should consider as they contemplate the future of cancer control.The Environmental Protection Agency (EPA) estimates that radon in the home is responsible for over 21 000 lung cancer deaths annually among Americans, making radon the major cause of lung cancer after tobacco use. The agency considers radon a major public health problem and, since 1986, has mounted an aggressive campaign urging the public to test their homes for radon and take remedial actions when airborne concentrations of radon exceed 4 picocuries per liter of air (4 pCi/L).¹For its most current risk assessment, the EPA employed the BEIR VI model, developed by the Committee on Health Risks of Exposure to Radon (the BEIR VI committee) of the National Academy of Sciences (NAS).² The BEIR VI model''s calculation of radon-related risk (as was the case for its predecessor, BEIR IV) was estimated from data on miners, who are subject to much higher levels of radon than is the average population and have shown a significant correlation between lung cancer risk and radon exposure. Although the extrapolation of the results from miners to the much less exposed general public initially caused controversy, the BEIR VI implications of risk have been validated by recent case–control studies at the population level.^3–5 The BEIR VI model is thus broadly accepted as a valid predictor of the radon-related risk for typical individuals.The available data suggest a strong interaction effect between radon exposure and smoking status in the determination of lung cancer risk, which means that smokers are at a much higher risk of dying from radon-induced lung cancer than are nonsmokers. This interaction is recognized in the BEIR VI model, which postulates a superadditive (but less than multiplicative) interaction between smoking and radon. To appreciate the magnitude of this interaction, consider the fact that the background lung cancer risk ratio between ever and never smokers is 13 to 1.⁶ A multiplicative interaction between radon and smoking would imply that, at the same level of radon exposure, the ratio of radon-induced excess risk between ever and never smokers would be the same as the ratio of background lung cancer risks between those 2 groups (i.e., 13 to 1). On the other hand, an additive relationship between radon and smoking would imply that radon would add the same extra risk to ever and never smokers exposed to the same dosage, making the excess risks ratio between the 2 groups equal 1 to 1. Using the BEIR VI model, the EPA calculates that, at a radon level of 4 pCi/L, the lifetime risk of radon-induced lung cancer death is 62 per 1000 for ever smokers and 7 per 1000 for never smokers, yielding an excess risk ratio of 8.86 to 1 between the 2 groups.¹ As 8.86 falls between 1 and 13, the BEIR VI model implies that radon adds more risk to ever smokers than to never smokers, but that excess risk is less than proportional to the lung cancer background risk of those 2 groups, suggesting a submultiplicative (but superadditive) relationship between smoking and radon. The BEIR VI model does not distinguish between current and former smokers.Given this implied superadditive interaction, the number of future radon deaths will heavily depend on population smoking rates. As smoking rates in the United States have been falling for several decades and are expected to continue declining, the overall magnitude of the radon death toll is likely to decline as well. The question we try to address is what is the magnitude of this expected decline?We extend the EPA''s analysis by examining the sensitivity of radon-related lung cancer in the United States to future smoking rates. We estimate the proportional decline in the number of lung cancer deaths caused by radon for the period 2006 through 2100, assuming a likely scenario for smoking rates. We do not forecast specific numbers of radon-induced lung cancer deaths because these numbers will depend on many factors likely to change over such a long period of time. Instead, we concentrate on the relative impact of the smoking decline on the overall radon death toll and also examine the benefits of remediating houses with high radon levels given the results of our analysis. Following the EPA''s approach, in our computations, we employ the BEIR VI model, thereby assuming a submultiplicative relationship between smoking and radon. In the remaining sections of the report, we discuss the assumptions, models, and data employed in our analysis, our findings, and the implications of the results for both the magnitude of radon-related risk to the population and the effectiveness of housing remediation in reducing such risk.     

Quantitative aspects of radon daughter exposure and lung cancer in underground miners

Epidemiological studies have shown an excessive incidence of lung cancer in miners with exposure to radon daughters. The various risk estimates have ranged from six to 47 excess cases per 10(6) person years and working level month, but the effect of smoking has not been fully evaluated. The present study, among a group of iron ore miners, is an attempt to obtain quantitative information about the risk of lung cancer due to radon and its daughters among smoking and non-smoking miners. The results show a considerable risk for miners to develop lung cancer; even non-smoking miners seem to be at a rather high risk. An additive effect of smoking and exposure to radon daughters is indicated and an estimate of about 30-40 excess cases per 10(6) person years and working level month seems to apply on a life time basis to both smoking and non-smoking miners aged over 50.     

Effects of residential mobility on individual versus population risk of radon-related lung cancer.

The U.S. Environment Protection Agency (EPA) does not consider the effects of normal patterns of residential mobility in estimating individual radon-related lung cancer risks. As a consequence, the EPA's population risk estimates may have little bearing on individual risks, and remediation of high-radon homes may have only small health benefits for the individual who remediate their homes. Through a stimulation analysis, we examine the effects of residential mobility on random exposure and lung cancer risk. Given normal mobility, only 7% of eventual radon-related mortality among current 30 year old will occur in the 5% currently living in homes above pCi/l (the EPA's action level for remediation) in contrast with you estimate of 31% of deaths when mobility's ignored. About 10 pCi/l the no-mobility assumption implies 10.3% of deaths, compared to only 0.4% when mobility taken into account. We conclude that knowledge of one's current random exposure not necessarily a useful guide to one's risk, especially for residents of the high-radon homes targeted for remediation by the EPA. The risk of such individuals is like to be substantially lower than that implied in the EPA's risk charts. If people currently living in high radon homes remediate their houses, the majority of the resulting health benefits will accrue to future occupants of their homes.     

Quantitative aspects of radon daughter exposure and lung cancer in underground miners.

Epidemiological studies have shown an excessive incidence of lung cancer in miners with exposure to radon daughters. The various risk estimates have ranged from six to 47 excess cases per 10(6) person years and working level month, but the effect of smoking has not been fully evaluated. The present study, among a group of iron ore miners, is an attempt to obtain quantitative information about the risk of lung cancer due to radon and its daughters among smoking and non-smoking miners. The results show a considerable risk for miners to develop lung cancer; even non-smoking miners seem to be at a rather high risk. An additive effect of smoking and exposure to radon daughters is indicated and an estimate of about 30-40 excess cases per 10(6) person years and working level month seems to apply on a life time basis to both smoking and non-smoking miners aged over 50.     

Estimated risks of radon-induced lung cancer for different exposure profiles based on the new EPA model

Radon is a naturally occurring radioactive gas. When inhaled, radon can cause mutations that lead to lung cancer. Some new epidemiologic studies indicate that indoor radon is a public health problem. The BEIR VI report outlined its preferred two risk models for the combined effects of smoking and exposure to radon progeny, and listed the estimated risk to ever-smokers and never-smokers of both sexes due to lifetime exposure. However, exposures for shorter periods of time are of practical interest since exposure to elevated levels of radon may occur and end at any age. This study aims to produce practical tables of lifetime relative risks for exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 100 to 1,000 Bq m(-3). The calculations are based on the risk model developed recently by U.S. Environmental Protection Agency. The EPA's risk model is a single model that gives risk values midway between those obtained from the two BEIR VI preferred models. The detailed tables provide a clearer view of the age groups at higher risk and the effect of exposure duration. The results will help radiation protection practitioners to better communicate indoor radon risk to members of the public.     

Epidemiological associations among lung cancer,radon exposure and elevation above sea level--a reassessment of Cohen''s county level radon study

Inhalation of radon (222Rn) decay products by persons living in homes has been associated with increased risk of lung cancer. Some epidemiological studies have shown a positive association between radon exposure and lung cancer rates. However, a large U.S.-wide ecological study (Cohen 1995) has shown a clear inverse association between average county radon concentration in homes and average lung cancer rates in the county. Cohen's strong inverse association between radon and lung cancer is surprising since there is no plausible biological reason for an inverse causal relationship between the two. We plot the county average lung cancer rate vs. the elevation above sea level (altitude) and show an inverse association between county average lung cancer rate and elevation. The elevation used for each county is the altitude of the most populous place in the county. We postulate that the decrease in lung cancer rates with higher elevations is caused by the carcinogenic effect of higher absolute oxygen concentration in the inspired air at lower elevations. Stratifying Cohen's lung cancer vs. radon data into ten groups of counties with similar elevations removes some, but not all, of his inverse association between radon and lung cancer.     

Indoor radon and lung cancer in France

BACKGROUND: Several case-control studies have indicated an increased risk of lung cancer linked to indoor radon exposure; others have not supported this hypothesis, partly because of a lack of statistical power. As part of a large European project, a hospital-based case-control study was carried out in 4 areas in France with relatively high radon levels. METHODS: Radon concentrations were measured in dwellings that had been occupied by the study subjects during the 5- to 30-year period before the interview. Measurements of radon concentrations were performed during a 6-month period using 2 Kodalpha LR 115 detectors (Dosirad, France), 1 in the living room and 1 in the bedroom. We examined lung cancer risk in relation to indoor radon exposure after adjustment for age, sex, region, cigarette smoking, and occupational exposure. RESULTS: We included in the analysis 486 cases and 984 controls with radon measures in at least 1 dwelling. When lung cancer risk was examined in relation to the time-weighted average radon concentration during the 5- to 30-year period, the estimated relative risks (with 95% confidence intervals) were: 0.85 (0.59-1.22), 1.19 (0.81-1.77), 1.04 (0.64-1.67), and 1.11 (0.59-2.09) for categories 50-100, 100-200, 200-400, and 400+ becquerels per cubic meter (Bq/m), respectively (reference <50 Bq/m). The estimated relative risk per 100 Bq/m was 1.04 (0.99-1.11) for all subjects and 1.07 (1.00-1.14) for subjects with complete measurements. CONCLUSIONS: Our results support the presence of a small excess lung cancer risk associated with indoor radon exposure after precise adjustment on smoking. They are in agreement with results from some other indoor radon case-control studies and with extrapolations from studies of underground miners.     

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.     

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.