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.     

The U.S. Environmental Protection Agency's assessment of risks from indoor radon

The U.S. Environmental Protection Agency has updated its assessment of health risks from indoor radon, which has been determined to be the second leading cause of lung cancer after cigarette smoking. This risk assessment is based primarily on results from a recent study of radon health effects (BEIR VI) by the National Academy of Sciences. In BEIR VI, the National Academy of Sciences fit empirical risk models to data from 11 cohorts of miners, and estimated that each year about 20,000 lung cancer deaths in the U.S. are radon related. A summary, abstracted from the technical report, is given of the EPA's risk assessment results and methods, including some modifications and extensions to the approach used in BEIR VI. Results include numerical estimates of lung cancer deaths per unit exposure, which had not been provided in BEIR VI.     

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.     

Lifetime risk of lung cancer due to radon exposure projected to Japanese and Swedish populations

Lifetime risk projections depend greatly on both background lung cancer rates and the selection of the risk model. Since background lung cancer rates differ from subject populations and the time, etiological risk of lifetime lung cancer mortality per unit radon exposure in WLM should be estimated for each subject population and the time of interest. To answer quantitatively how much are the differences among the projected risks for different populations, the Swedish case-control-study-based risk projection model was applied to the Japanese and Swedish populations from 1962 to 1997 as subject populations because of their distinct trends of lung cancer rates. To compare the results with the reference population and authorized risk projection models, U.S. population 1997 and the two risk projection models in BEIR VI report were applied, respectively. Lifetime risk of lung cancer mortality projected for Japanese, Swedish, and U.S. populations in 1997 per radon progeny exposure were estimated to range from 1.50 (0.40-3.19) x 10(-4) WLM(-1) to 9.86 (2.62-20.9) x 10(-4) WLM(-1), which could be compared to the detriment associated with a unit effective dose. Conclusive dose conversion coefficients in this study ranged from 2.05 (0.55-4.37) to 13.5 (3.59-28.6) mSv WLM(-1), and within this range the discrepancy between dosimetric and epidemiological approaches was included.     

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.     

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.     

Domestic radon risks may be dominated by bystander effects--but the risks are unlikely to be greater than we thought

Radon risks derive from exposure of bronchio-epithelial cells to alpha particles. Alpha-particle exposure can result in bystander effects when irradiated cells emit signals resulting in damage to nearby unirradiated bystander cells. Bystander effects can cause downwardly-curving dose-response relations and inverse dose-rate effects. We have extended a quantitative mechanistic model of bystander effects to include protracted exposure, with inverse dose-rate effects attributed to replenishment, during exposure, of a subpopulation of cells which are hypersensitive to bystander signals. In this approach, bystander effects and the inverse dose-rate effect are manifestations of the same basic phenomenon. The model was fitted to dose- and dose-rate dependent radon-exposed miner data; the results suggest that one directly-hit target cell can send bystander signals to about 50 neighboring cells and that, in the case of domestic radon exposures, the risk could be dominated by bystander effects. The analysis concludes that a naive linear extrapolation of radon miner data to low doses, without accounting for dose rate/bystander effects, would result in an underestimation of domestic radon risks by about a factor of approximately 4. However, recent domestic radon risk estimates (BEIR VI) have already applied a phenomenological correction factor of approximately 4 for inverse dose-rate effects, and have thus already implicitly taken into account corrections which we here suggest are due to bystander effects. Thus current domestic radon risk estimates are unlikely to be underestimates as a result of bystander effects.     

On power and sample size for studying features of the relative odds of disease

Estimates of sample size and statistical power are essential ingredients in the design of epidemiologic studies. Once an association between disease and exposure has been demonstrated, additional studies are often needed to investigate special features of the relation between exposure, other covariates, and risk of disease. The authors present a general formulation to compute sample size and power for case-control and cohort studies to investigate more complex patterns in the odds ratios, such as to distinguish between two different slopes of linear trend, to distinguish between two possible dose-response relations, or to distinguish different models for the joint effects of two important exposures or of one exposure factor adjusting for another. Such special studies of exposure-response relations may help investigators to distinguish between plausible biologic models and may lead to more realistic models for calculating attributable risk and lifetime disease risk. The sample size formulae are applied to studies of indoor radon exposure and lung cancer and suggest that epidemiologic studies may not be feasible for addressing some issues. For example, if the risk estimates from underground miners' studies are, in truth, not applicable to home exposures and overestimate the gradient of risk from home exposure to radon by, for example, a factor of 2, then enormously large numbers of subjects would be required to detect the difference. Furthermore, if the true interaction between smoking and radon exposure is less than multiplicative, only the largest investigations will have sufficient power to reject additivity. For the simple case of testing for no exposure effect, when exposure is either dichotomous or continuous, these methods yield well-known formulae.     

Population attributable fraction for lung cancer due to residential radon in Switzerland and Germany

Studies on miners as well as epidemiological studies in the general population show an increased lung cancer risk after exposure to radon and its progeny. The European pooled analysis of indoor radon studies estimates an excess relative risk of 8% (16% after correction for measurement uncertainties) per 100 Bq m(-3) indoor radon concentration. Here, we determine the population attributable fraction (PAF) for lung cancer due to residential radon based on this risk estimate for Switzerland and Germany. Based on regionally stratified radon data, the PAF was calculated following the World Health Organization concept of global burden of disease, compared to a realistic baseline radon concentration equal to the outdoor concentration. Lifetable approaches were used taking smoking and sex into account. Measurement error corrections were applied to both risk estimates and the radon distribution. In Switzerland, the average indoor radon concentration is 78 Bq m(-3), resulting in a PAF of 8.3%. Therefore, 169 male lung cancer deaths and 62 deaths in women can be attributed to residential radon per year. For Germany, the average indoor radon concentration is 49 Bq m(-3), corresponding to a PAF of 5.0% (1,422 male and 474 female deaths annually). In both countries, a large regional variation in the PAF was observed due to regional differences in radon concentrations and population structure. Both calculations show a strong dependency on the risk model used. Risk models based on miner studies result in higher PAF estimates than risk models based on indoor radon studies due to different assumptions regarding exposures received more than 35 years ago. The use of a non-zero baseline radon concentration also contributes to the lower PAF estimates reported here. Although the estimates of the population attributable fraction of residential radon presented here are lower than previously reported estimates, the risk is still one of the most widespread environmental hazards. Radon monitoring and radon reduction programs are therefore important issues for environmental public health management.     

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.     

Implications of a two-stage clonal expansion model to indoor radon risk assessment

Spreadsheet macro programs for calculations of exact hazard and probability of having contracted cancer were used to study the implications of the lung cancer model of Moolgavkar et al. Excess lifetime risk ELR and loss of life expectancy LLE were calculated from the annual values of hazard and probability, using published life tables. The influence of various factors on ELR and LLE was studied, as well as the lifetime risk projection in epidemiological studies. At indoor concentrations, ELR and LLE are coarsely proportional to lifetime exposure. The main factors determining the proportionality coefficient are 1. Smoking status, 2. General life expectancy, 3. Exposure schedule, and 4. Sex. For constant domestic exposure, the sex is less important, because the longer life of women is compensated by the lower hazard. ELR and LLE for a population with 30% smokers and life expectancies of 72.1 y and 79.5 y for men and women, respectively, are 56 per million per WLM and 860 y per million per WLM, respectively. For an exposure schedule with one high radon period, the mean age during the period becomes important, and the age-specific values for men and women differ from each other. Furthermore, the model predicts that case-control epidemiological studies overestimate the lifetime risk by an amount which may arise to several tens of percent.     

Latency and the lung cancer epidemic among United States uranium miners

The latency of occupational cancer was a key factor in the recent epidemic of lung cancer among U.S. uranium miners. A review of the epidemic and analysis of latency periods with a near lifetime follow-up found that among former and nonsmokers, the mean mid-induction latent period is nearly a constant at about 25 y, regardless of age at starting or magnitude of exposure. Among cigarette smokers, the mean is shorter (about 19 y). It is not influenced by age at start of smoking, amount smoked, or magnitude of exposure, but there is a marked shortening as the age at start of radiation exposure rises. These latency variables affect lifetime risk models. By disregarding the European radon mine exposures and waiting for strong evidence of lung cancer among U.S. uranium miners (ignoring the exposures occurring while waiting during the latency period), the epidemic became inevitable.     

Multivariate analysis of the carcinogenic risk of radon

Epidemiological studies using the methods of multivariate analysis were conducted to assess the contribution of unprofessional of radon radiation to the development of lung malignancies in the population living in the area having the increased radon hazard potential. The subject of the study was the town of Lermontov in the Stavropol Territory, the houses of its dwellers were found to have higher radon accumulation levels and high lung cancer morbidity rates were recorded among its population. Systems analysis of the influence of 23 various risk factors on the development of lung malignancies, which made by image recognition techniques, has indicated that in the town's population the contribution of nonprofessional exposure to radon to the development of this pathology is little and amounts to about 2%. The calculations of cancer risks from exposure of the population of the town of Lermontov to radon in the houses, made using the multiplicative BEIR VI models to assess the radiation risk, have shown higher results - 30%. Discussing the results of work has advanced arguments in favor of the reliability and higher adequacy of using the methods of multivariate analysis to assess the radiation risk in the range of small doses of radiation as compared with the univariate analysis.     

Lung cancer attributable to indoor radon exposure in france: impact of the risk models and uncertainty analysis

OBJECTIVE: The inhalation of radon, a well-established human carcinogen, is the principal-and omnipresent-source of radioactivity exposure for the general population of most countries. Scientists have thus sought to assess the lung cancer risk associated with indoor radon. Our aim here is to assess this risk in France, using all available epidemiologic results and performing an uncertainty analysis. METHODS: We examined the exposure-response relations derived from cohorts of miners and from joint analyses of residential case-control studies and considered the interaction between radon and tobacco. The exposure data come from measurement campaigns conducted since the beginning of the 1980s by the Institute for Radiation Protection and Nuclear Safety and the Directorate-General of Health in France. We quantified the uncertainties associated with risk coefficients and exposures and calculated their impact on risk estimates. RESULTS: The estimated number of lung cancer deaths attributable to indoor radon exposure ranges from 543 [90% uncertainty interval (UI) , 75-1,097] to 3,108 (90% UI, 2,996-3,221) , depending on the model considered. This calculation suggests that from 2.2% (90% UI, 0.3-4.4) to 12.4% (90% UI, 11.9-12.8) of these deaths in France may be attributable to indoor radon. DISCUSSION: In this original work we used different exposure-response relations from several epidemiologic studies and found that regardless of the relation chosen, the number of lung cancer deaths attributable to indoor radon appears relatively stable. Smokers can reduce their risk not only by reducing their indoor radon concentration but also by giving up smoking.     

Personal exposure meets risk assessment: a comparison of measured and modeled exposures and risks in an urban community

Human exposure research has consistently shown that, for most volatile organic compounds (VOCs), personal exposures are vastly different from outdoor air concentrations. Therefore, risk estimates based on ambient measurements may over- or underestimate risk, leading to ineffective or inefficient management strategies. In the present study we examine the extent of exposure misclassification and its impact on risk for exposure estimated by the U.S. Environmental Protection Agency (U.S. EPA) Assessment System for Population Exposure Nationwide (ASPEN) model relative to monitoring results from a community-based exposure assessment conducted in Baltimore, Maryland (USA). This study is the first direct comparison of the ASPEN model (as used by the U.S. EPA for the Cumulative Exposure Project and subsequently the National-Scale Air Toxics Assessment) and human exposure data to estimate health risks. A random sampling strategy was used to recruit 33 nonsmoking adult community residents. Passive air sampling badges were used to assess 3-day time-weighted-average personal exposure as well as outdoor and indoor residential concentrations of VOCs for each study participant. In general, personal exposures were greater than indoor VOC concentrations, which were greater than outdoor VOC concentrations. Public health risks due to actual personal exposures were estimated. In comparing measured personal exposures and indoor and outdoor VOC concentrations with ASPEN model estimates for ambient concentrations, our data suggest that ASPEN was reasonably accurate as a surrogate for personal exposures (measured exposures of community residents) for VOCs emitted primarily from mobile sources or VOCs that occur as global "background" source pollutant with no indoor source contributions. Otherwise, the ASPEN model estimates were generally lower than measured personal exposures and the estimated health risks. ASPEN's lower exposures resulted in proportional underestimation of cumulative cancer risk when pollutant exposures were combined to estimate cumulative risk. Median cumulative lifetime cancer risk based on personal exposures was 3-fold greater than estimates based on ASPEN-modeled concentrations. These findings demonstrate the significance of indoor exposure sources and the importance of indoor and/or personal monitoring for accurate assessment of risk. Environmental health policies may not be sufficient in reducing exposures and risks if they are based solely on modeled ambient VOC concentrations. Results from our study underscore the need for a coordinated multimedia approach to exposure assessment for setting public health policy.     

On the relationship between radiation standards for the general public and limitation of lifetime risk

This paper discusses the relationship between standards for limiting radiation exposures of individuals in the general public and limitation of lifetime risk. Most current radiation standards for the public in the United States specify limits on dose for each year of exposure. Particularly for internal exposures, we show that such standards may correspond poorly with a limit on lifetime risk when the age dependence of radionuclide intakes and dose is taken into account. We then show that standards which specify limits on annual dose averaged over a lifetime, with a subsidiary limit on dose in any year, correspond more closely with a limit on lifetime risk. Finally, we discuss standards for public exposures that are expressed directly as limits on lifetime risk. The development of risk standards would require consideration of age-dependent radiogenic risks and competing risks from all other causes as well as age-dependent dosimetry. We present sample calculations of lifetime risks from acute and chronic intakes that would support such a standard. We suggest that implementation of a standard for lifetime risk would require modification or abandonment of several radiation protection practices embodied in standards which specify limits on dose.     

Exposure to atmospheric radon.

We measured radon (222Rn) concentrations in Iowa and Minnesota and found that unusually high annual average radon concentrations occur outdoors in portions of central North America. In some areas, outdoor concentrations exceed the national average indoor radon concentration. The general spatial patterns of outdoor radon and indoor radon are similar to the spatial distribution of radon progeny in the soil. Outdoor radon exposure in this region can be a substantial fraction of an individual's total radon exposure and is highly variable across the population. Estimated lifetime effective dose equivalents for the women participants in a radon-related lung cancer study varied by a factor of two at the median dose, 8 mSv, and ranged up to 60 mSv (6 rem). Failure to include these doses can reduce the statistical power of epidemiologic studies that examine the lung cancer risk associated with residential radon exposure.     

Risk assessment of exposure to volatile organic compounds in different indoor environments

The lifetime cancer risks of exposure of cooks and food service workers, office workers, housewives, and schoolchildren in Hong Kong to volatile organic compounds (VOCs) in their respective indoor premises during normal indoor activities were assessed. The estimated cancer risk for housewives was the highest, and the second-highest lifetime cancer risk to VOC exposure was for the groups of food service and office workers. Within a certain group of the population, the lifetime cancer risk of the home living room was one to two orders of magnitude higher than that in other indoor environments. The estimated lifetime risks of food service workers were about two times that of office workers. Furthermore, the cancer risks of working in kitchen environments were approximately two times higher than the risks arising from studying in air-conditioned classrooms. The bus riders had higher average lifetime cancer risks than those travelling by Mass Transit Railway. For all target groups of people, the findings of this study show that the exposures to VOCs may lead to lifetime risks higher than 1 x 10(-6). Seven indoor environments were selected for the measurement of human exposure and the estimation of the corresponding lifetime cancer risks. The lifetime risks with 8-h average daily exposures to individual VOCs in individual environments were compared. People in a smoking home had the highest cancer risk, while students in an air-conditioned classroom had the lowest risk of cancer. Benzene accounted for about or more than 40% of the lifetime cancer risks for each category of indoor environment. Nonsmoking and smoking residences in Hong Kong had cancer risks associated with 8-h exposures of benzene above 1.8 x 10(-5) and 8.0 x 10(-5), respectively. The cancer risks associated with 1,1-dichloroethene, chloroform, methylene chloride, trichloroethene, and tetrachloroethene became more significant at selected homes and restaurants. Higher lifetime cancer risks due to exposure to styrene were only observed in the administrative and printing offices and air-conditioned classrooms. Higher lifetime cancer risks related to chloroform exposures were observed at the restaurant and the canteen.     

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.     

Modeling joint exposures and health outcomes for cumulative risk assessment: the case of radon and smoking

Community-based cumulative risk assessment requires characterization of exposures to multiple chemical and non-chemical stressors, with consideration of how the non-chemical stressors may influence risks from chemical stressors. Residential radon provides an interesting case example, given its large attributable risk, effect modification due to smoking, and significant variability in radon concentrations and smoking patterns. In spite of this fact, no study to date has estimated geographic and sociodemographic patterns of both radon and smoking in a manner that would allow for inclusion of radon in community-based cumulative risk assessment. In this study, we apply multi-level regression models to explain variability in radon based on housing characteristics and geological variables, and construct a regression model predicting housing characteristics using U.S. Census data. Multi-level regression models of smoking based on predictors common to the housing model allow us to link the exposures. We estimate county-average lifetime lung cancer risks from radon ranging from 0.15 to 1.8 in 100, with high-risk clusters in areas and for subpopulations with high predicted radon and smoking rates. Our findings demonstrate the viability of screening-level assessment to characterize patterns of lung cancer risk from radon, with an approach that can be generalized to multiple chemical and non-chemical stressors.