Smoking as a confounder in ecologic correlations of cancer mortality rates with average county radon levels

Cohen has reported a negative correlation between lung cancer mortality and average radon levels by county. In this paper, the correlation of U.S. county mortality rates for various types of cancers during the period 1970-1994 with Cohen's radon measurements is examined. In general, quantitatively similar, strongly negative correlations are found for cancers strongly linked to cigarette smoking, weaker negative correlations are found for cancers moderately increased by smoking, whereas no such correlation is found for cancers not linked to smoking. The results indicate that the negative trend previously reported for lung cancer can be largely accounted for by a negative correlation between smoking and radon levels across counties. Hence, the observed ecological correlation provides no substantial evidence for a protective effect of low level radon exposure.     

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.     

Health effects in underground uranium miners

The health effects associated with uranium miners have received much attention in the last 30 years. Although mortality rates are elevated for such causes as accidents and nonmalignant respiratory disease, lung cancer caused by exposure to radon decay products is the primary hazard to underground uranium miners. This review summarizes studies of eight cohorts of radium miners, and examines several pooled analyses that provide the best understanding of the radon/lung cancer relationship. The relative risk of lung cancer is linearly related to cumulative exposure to radon decay products. The excess relative risk decreases with attained age and time since exposure. An inverse exposure-rate effect exists, such that prolonged exposure at low levels of radon is more hazardous than shorter exposures to higher levels. The linear no-threshold model used in most epidemiologic studies has been attacked by some as overestimating risk at indoor radon levels. These arguments are rejected by this reviewer.     

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.     

Radon daughter exposure to uranium miners

Radon exposures to U.S. uranium miners under present conditions average about 1.3 WLM per year approximately or equal to 60 WLM per full working lifetime. This is intermediate between (a) the lowest exposures for which there have been excess lung cancers reported among U.S. miners (120-240 WLM) and (b) average environmental radon exposures (16 WLM), so models based on these two situations are used to estimate expected effects on present uranium miners. In Model A, the loss of life expectancy is 45 days, the SMR (standardized mortality ratio) for lung cancer is 1.10, and the SMR for all causes between ages 18 and 65 is 1.013. In Model B these are 10 days, 1.03 and 1.002 respectively. It is shown that the radon exposures to miners are similar to those to millions of Americans from environmental exposure, and that miner health risks are comparable to those of other radiation workers. Their lung cancer risk from radon is 7-50 times less than their job-related accident mortality risk, and represents 0.7-4% of their total risk in mining. Miners suffer from many diseases with SMR very much larger than that for radon-induced lung cancer, and there are many other occupations and industries with far higher SMR for lung cancer than that from radon exposure to miners.     

Mortality of a cohort of tin miners 1941-86.

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

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.     

Mortality of a cohort of tin miners 1941-86

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

Cancer risk modelling and radiological protection

Statistical models describing how the radiation-related risks of particular types of cancer vary with the doses of radiation received by specific tissues are derived from data gathered in epidemiological studies of exposed groups of people, guided by an incomplete understanding of radiobiological mechanisms gleaned from experimental studies. Cancer risk models have been developed for a dozen or so different types of cancer, and take account of the effect of important risk modifying factors such as age at exposure and time since exposure. Of primary importance in the development of cancer risk models is the experience of the Japanese atomic bomb survivors, but other exposed groups contribute information, including those exposed to radiation from internally deposited radioactive material, such as inhaled radon. Cancer risk models predict that at low doses or low dose rates the excess risk of cancer is directly proportional to the dose of radiation received, with no threshold dose--the linear no threshold (LNT) dose-response model--and the inferred summary estimate of the overall average lifetime excess risk of developing a serious cancer is ～ 5%/Sv. It is these cancer risk models and this inferred nominal risk estimate that provide the technical basis of radiological protection. Although it is difficult to definitively test the LNT model at low doses or low dose rates, because the predicted excess risk is small compared with fluctuations in the baseline risk, evidence exists that a small risk of cancer results from low-level exposure to radiation and that the excess risk is around that predicted by current risk models.     

Radon and lung cancer risk: an extension of the mortality follow-up of the Newfoundland fluorspar cohort

Radon is a well-recognized cause of lung cancer, and studies of underground miners have provided invaluable insights on the mechanisms of radon carcinogenesis. Given the dramatic decreases in occupational exposures and the latent interval between the time of exposure and the development of lung cancer, continued follow-up of these cohorts is needed to address uncertainties in risk estimates. Here, we report on the relationship between radon and lung cancer mortality in a cohort of 1,742 Newfoundland fluorspar miners between 1950 and 2001; follow-up has been extended 11 y from previous analyses. The standardized mortality ratio (SMR) was used to compare the mortality experience of the cohort to similarly aged Newfoundland males. Poisson regression methods were used to characterize the radon-lung cancer relationship with respect to: age at first exposure, attained age, time since last exposure, interactions with cigarette smoking, and exposure rate. In total, 191 lung cancers were observed among underground miners (SMR = 3.09; 95% CI = 2.66, 3.56). ERR/WLMs decreased with attained age and time since last exposure. An inverse dose-rate effect was observed, while age at first exposure was not associated with lung cancer risk. An important strength of this study is that the effects of gamma radiation, thoron, and radioactive dust, common exposures in other miner studies, can be ruled out because the source of radon was from water running through the mine. However, the results should be interpreted cautiously due to uncertainties associated with the estimation of radon exposure levels before ventilation was introduced into the mine, and the relatively small number of lung cancer deaths that precluded joint modeling of multiple risk factors.     

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.     

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.     

Mortality from lung cancer in Ontario uranium miners.

Mortality from lung cancer was greater in Ontario uranium miners than in the general male population of Ontario (observed = 152, expected = 67.6, standardised mortality ratio 225, 95% confidence interval 191-264). Part of the excess of lung cancer may be because the proportion of men who are smokers or have smoked is greater in uranium miners than in Ontario men. Smoking does not explain the whole excess. Mortality from lung cancer in Ontario uranium miners is clearly related to exposure to short lived radon progeny. The excess relative risk of lung cancer from the same degree of exposure to short lived radon progeny is greatest five to 14 years after exposure and less subsequently. It is greater in men under the age of 55 years and less in older men. Part of the excess of lung cancer mortality in Ontario uranium miners is probably also due to exposure to arsenic that occurred earlier in gold mines. In Ontario uranium miners, the lung cancer mortality from exposure to arsenic increases as the intensity of exposure to short lived radon progeny increases. This finding is consistent with the hypothesis that the risk of lung cancer from exposure to arsenic is enhanced by exposure to other carcinogens. In Ontario uranium miners, the proportion of lung cancers that are small cell carcinomas is greater than in the general population. The proportion of small cell carcinomas is especially great five to 14 years after exposure to short lived radon progeny and in men who die from lung cancer at younger ages.     

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.     

Glass-based radon-exposure assessment and lung cancer risk

Lung cancer risk estimation in relation to residential radon exposure remains uncertain, partly as a result of imprecision in air-based retrospective radon-exposure assessment in epidemiological studies. A recently developed methodology provides estimates for past radon concentrations and involves measurement of the surface activity of a glass object that has been in a subject's dwellings through the period for exposure assessment. Such glass measurements were performed for 110 lung cancer subjects, diagnosed 1985 to 1995, and for 231 control subjects, recruited in a case-control study of residential radon and lung cancer among never-smokers in Sweden. The relative risks (with 95% confidence intervals) of lung cancer in relation to categories of surface-based average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m(-3), were 1.60 (0.8 to 3.4), 1.96 (0.9 to 4.2), and 2.20 (0.9 to 5.6), respectively, with average radon concentrations below 50 Bq m(-3) used as reference category, and with adjustment for other risk factors. These relative risks, and the excess relative risk (ERR) of 75% (-4% to 430%) per 100 Bq m(-3) obtained when using a continuous variable for surface-based average radon concentration estimates, were about twice the size of the corresponding relative risks obtained among these subjects when using air-based average radon concentration estimates. This suggests that surface-based estimates may provide a more relevant exposure proxy than air-based estimates for relating past radon exposure to lung cancer risk.     

Relation of arsenic exposure to lung cancer among tin miners in Yunnan Province, China.

The relation of mining and smelting exposure to arsenic and lung cancer was studied among tin miners in Yunnan Province in the People's Republic of China. Interviews were conducted in 1985 with 107 living tin miners who had lung cancer and an equal number of age matched controls from among tin miners without lung cancer to obtain information on risk factors for lung cancer including detailed history of employment and tobacco use. Occupational history was combined with industrial hygiene data to estimate cumulative arsenic exposure. Similar methods were also used to estimate radon exposure for simultaneous evaluation in this analysis. The results indicate that subjects in the highest quarter of cumulative arsenic exposure have a relative risk of 22.6 compared with subjects without exposure after adjusting for tobacco and radon exposure, and a positive dose response relation was observed. Simultaneous evaluation of arsenic and tobacco exposure indicates a greater risk for arsenic, whereas simultaneous assessment of arsenic and radon exposure suggests radon to be the greater risk. There is no evidence of synergism between arsenic and tobacco exposure. Among arsenic exposed individuals, cases of lung cancer have longer duration but lower average intensity of arsenic exposure than controls, indicating that duration of exposure to arsenic may be more important than intensity in the aetiology of lung cancer. Finally, risk of lung cancer among workers exposed to arsenic only in mining is only slightly less than for miners whose exposure to arsenic was limited to smelting, although risks are highest when workers were exposed to both mining and smelting.     

Increased lung cancer risk due to residential radon in a pooled and extended analysis of studies in Germany

Residential radon has been shown to be a risk factor for lung cancer in several studies-but with limited power in each single study. The data of two case-control studies performed during 1990-1997 in Germany and used for previous publications have been extended and pooled. Both studies have identical study designs. In total, data of 2,963 incident lung cancer cases and 4,232 population controls are analyzed here. One-year radon measurements were performed in houses occupied during the 5-35 y prior to the interview. Conditional logistic and linear relative risk regression was used for the analysis. Measurements covered on average 70% of the exposure time window, with an average radon exposure of 61 Bq m(-3). The smoking and asbestos-adjusted ORs were 0.97 [95% confidence interval (CI) 0.85 to 1.11] for 50-80 Bq m(-3), 1.06 (95% CI 0.87 to 1.30) for 80-140 Bq m(-3) and 1.40 (95% CI 1.03 to 1.89) for radon concentrations above 140 Bq m(-3), compared to the reference category <50 Bq m(-3). The linear increase in the odds ratio per 100 Bq m(-3) was 0.10 (95% CI -0.02 to 0.30) for all subjects and 0.14 (95% CI -0.03 to 0.55) for less mobile subjects who lived in only one home in the last 5-35 y. The risk coefficients generally were higher when measurement error in the radon concentrations was reduced by restricting the population. With respect to histopathology, the risk for small cell carcinoma was higher than for other subtypes. This analysis strengthens the evidence that residential radon is a relevant risk factor for lung cancer.     

肺癌危险度与室内氡关系研究:中国两项研究的汇总分析结果

目的 居室氡暴露是导致肺癌死亡的第二位重要原因，这是地下矿工氡暴露研究的外推结果。本分析就是为了验证此预测的正确性。方法 中国进行的两项居室氡暴露肺癌病例-对照研究共包括1050肺癌病例和1996名对照，把这些数据汇总在一起进行分析。结果 根据线性模型，在95％置信区间情况下，每100Bq／m^3的附加比值比(EOR)为0．133(0．01，0．036)。对在现住所居住30a以上的调查对象进行分析，EOR值为0．315(0．07，0．91)。此估算值与矿工数据外推值及北美和欧洲室内氡研究结果类似。结论 在众多居室中普遍存在的氡浓度长期暴露，会使肺癌危险度增加。     

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.     

Mortality experience of haematite mine workers in China

The mortality risk of iron ore (haematite) miners between 1970 and 1982 was investigated in a retrospective cohort study of workers from two mines, Longyan and Taochong, in China. The cohort was limited to men and consisted of 5406 underground miners and 1038 unexposed surface workers. Among the 490 underground miners who died, 205 (42%) died of silicosis and silicotuberculosis and 98 (20%) of cancer, including 29 cases (5.9%) of lung cancer. The study found an excess risk of non-malignant respiratory disease and of lung cancer among haematite miners. The standardised mortality ratio for lung cancer compared with nationwide male population rates was significantly raised (SMR = 3.7), especially for those miners who were first employed underground before mechanical ventilation and wet drilling were introduced (SMR = 4.8); with jobs involving heavy exposure to dust, radon, and radon daughters (SMR = 4.2); with a history of silicosis (SMR = 5.3); and with silicotuberculosis (SMR = 6.6). No excess risk of lung cancer was observed in unexposed workers (SMR = 1.2). Among current smokers, the risk of lung cancer increased with the level of exposure to dust. The mortality from all cancer, stomach, liver, and oesophageal cancer was not raised among underground miners. An excess risk of lung cancer among underground mine workers which could not be attributed solely to tobacco use was associated with working conditions underground, especially with exposure to dust and radon gas and with the presence of non-malignant respiratory disease. Because of an overlap of exposures to dust and radon daughters, the independent effects of these factors could not be evaluated.