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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Relation of radon exposure and tobacco use to lung cancer among tin miners in Yunnan Province, China

We studied the relation of radon exposure and tobacco use to lung cancer among tin miners in Yunnan Province in the People's Republic of China. Interviews were conducted in 1985 with 107 living tin miners with lung cancer and an equal number of age-matched controls from among tin miners without lung cancer to obtain information on lung cancer risk factors including a detailed history of employment and tobacco use. Occupational history was combined with extensive industrial hygiene data to estimate cumulative working level months (WLM) of radon daughter exposure. Similar data were also used to estimate arsenic exposure for control in the analysis. Results indicate an increased risk of lung cancer for water pipe smoking, a traditional form of tobacco use practiced in 91% of cases and 85% of controls. Ever use of water pipes was associated with a twofold elevation in risk when compared with tobacco abstainers, and a dose-response relation was observed with increasing categories of pipe-year (dose times duration) usage. Estimated WLM of radon exposure varied from 0 to 1,761 among subjects but averaged 515 in cases versus only 244 in controls. Analyses indicated that the persons in the highest quarter of the radon exposure distribution had an odds ratio (OR) = 9.5 (95% confidence interval = 2.7-33.1) compared to persons without radon exposure after controlling for arsenic exposure and other potential confounders. Examination of duration and rate of radon exposure indicated higher risk associated with long duration as opposed to high rate of exposure. Cross-categorizations of radon exposure and tobacco use suggest greater risk associated with radon exposure than tobacco in these workers.     

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.     

The consequences of passive smoking: an overview.

Tobacco smoke contains a wide range of toxic vapors and particles that when inhaled are injurious to the smoker himself (active smoking) and to those around him (passive smoking). It is extremely difficult to define precisely the harmful effects of passive smoking on the individual's health because of the problems involved in quantifying the extent of exposure. A number of epidemiological studies indicate that exposure to passive smoking in public places is circumstantially but marginally linked to cardiovascular morbidity and mortality, as well as to benign and malignant pulmonary morbidity. There is an increased risk of cardiovascular and lung diseases among people living with spouses who smoke due to the exposure to tobacco smoke in the home. Passive smoking during pregnancy constitutes a health hazard for mother and fetus alike. Exposure to passive smoking during childhood may predispose the individual to benign and malignant pulmonary morbidity in both childhood and adulthood. For many people the worksite comprises the main exposure source. Many clinical conditions are further aggravated by exposure to a combination of tobacco smoke and industrial chemicals, mineral dust, or other carcinogens (asbestos, cadmium, radon daughters). Tobacco smoke exposure and the resultant morbidity can be reduced by regulations and legislation prohibiting smoking in public places and worksites.     

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.     

Indoor radon exposure and active and passive smoking in relation to the occurrence of lung cancer

Exposure to indoor radon and radon daughters is currently attracting great interest as a possible cause of lung cancer. This concern is supported by several studies, most of them relatively small in numbers or weak in the assessment of exposure. This study encompasses 177 persons with lung cancer and 677 noncancer referents, all deceased and with 30 years or more of residency in the same house in an area with radon-leaking alum shale deposits in the central part of southern Sweden. Exposure categories based on building material, type of house, and ground conditions were created, but measurements of the indoor radon daughter concentration were also made for 142 cases and 264 referents. Active and passive smoking was ascertained through questionnaires sent to the next-of-kin. Overall, the lung cancer risk was approximately twofold with regard to the categories of assumed radon daughter exposure for the rural sector of the population but not for the same categories of the urban sector, possibly because of less precise exposure assessment and influence from other factors. Occasional and passive smokers, as well as passive smokers alone, had a particularly increased risk of lung cancer in association with the increased exposure categories.     

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.     

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.     

Residential radon exposure and lung cancer risk: commentary on Cohen's county-based study

The large United States county-based study () in which an inverse relationship has been suggested between residential low-dose radon levels and lung cancer mortality has been reviewed. While this study has been used to evaluate the validity of the linear nonthreshold theory, the grouped nature of its data limits the usefulness of this application. Our assessment of the study's approach, including a reanalysis of its data, also indicates that the likelihood of strong, undetected confounding effects by cigarette smoking, coupled with approximations of data values and uncertainties in accuracy of data sources regarding levels of radon exposure and intensity of smoking, compromises the study's analytic power. The most clear data for estimating lung cancer risk from low levels of radon exposure continue to rest with higher-dose studies of miner populations in which projections to zero dose are consistent with estimates arising from most case-control studies regarding residential exposure.     

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.