Lung Cancer Risk from Radon in Marcellus Shale Gas in Northeast U.S. Homes

The amount of radon in natural gas varies with its source. Little has been published about the radon from shale gas to date, making estimates of its impact on radon‐induced lung cancer speculative. We measured radon in natural gas pipelines carrying gas from the Marcellus Shale in Pennsylvania and West Virginia. Radon concentrations ranged from 1,520 to 2,750 Bq/m³ (41–74 pCi/L), and the throughput‐weighted average was 1,983 Bq/m³ (54 pCi/L). Potential radon exposure due to the use of Marcellus Shale gas for cooking and space heating using vent‐free heaters or gas ranges in northeastern U.S. homes and apartments was assessed. Though the measured radon concentrations are higher than what has been previously reported, it is unlikely that exposure from natural gas cooking would exceed 1.2 Bq/m³ (<1% of the U.S. Environmental Protection Agency's action level). Using worst‐case assumptions, we estimate the excess lifetime (70 years) lung cancer risk associated with cooking to be 1.8×10^?4 (interval spanning 95% of simulation results: 8.5×10^?5, 3.4×10^?4). The risk profile for supplemental heating with unvented gas appliances is similar. Individuals using unvented gas appliances to provide primary heating may face lifetime risks as high as 3.9×10^?3. Under current housing stock and gas consumption assumptions, expected levels of residential radon exposure due to unvented combustion of Marcellus Shale natural gas in the Northeast United States do not result in a detectable change in the lung cancer death rates.     

Assessment of the Effectiveness of Radon Screening Programs in Reducing Lung Cancer Mortality

The present study was aimed at assessing the health consequences of the presence of radon in Quebec homes and the possible impact of various screening programs on lung cancer mortality. Lung cancer risk due to this radioactive gas was estimated according to the cancer risk model developed by the Sixth Committee on Biological Effects of Ionizing Radiations. Objective data on residential radon exposure, population mobility, and tobacco use in the study population were integrated into a Monte‐Carlo‐type model. Participation rates to radon screening programs were estimated from published data. According to the model used, approximately 10% of deaths due to lung cancer are attributable to residential radon exposure on a yearly basis in Quebec. In the long term, the promotion of a universal screening program would prevent less than one death/year on a province‐wide scale (0.8 case; IC 99%: –3.6 to 5.2 cases/year), for an overall reduction of 0.19% in radon‐related mortality. Reductions in mortality due to radon by (1) the implementation of a targeted screening program in the region with the highest concentrations, (2) the promotion of screening on a local basis with financial support, or (3) the realization of systematic investigations in primary and secondary schools would increase to 1%, 14%, and 16.4%, respectively, in the each of the populations targeted by these scenarios. Other than the battle against tobacco use, radon screening in public buildings thus currently appears as the most promising screening policy for reducing radon‐related lung cancer.     

Review of Radon and Lung Cancer Risk

Radon, a long-established cause of lung cancer in uranium and other underground miners, has recently emerged as a potentially important cause of lung cancer in the general population. The evidence for widespread exposure of the population to radon and the well-documented excess of lung cancer among underground miners exposed to radon decay products have raised concern that exposure to radon progeny might also be a cause of lung cancer in the general population. To date, epidemiological data on the lung cancer risk associated with environmental exposure to radon have been limited. Consequently, the lung cancer hazard posed by radon exposure in indoor air has been addressed primarily through risk estimation procedures. The quantitative risks of lung cancer have been estimated using exposure-response relations derived from the epidemiological investigations of uranium and other underground miners. We review five of the more informative studies of miners and recent risk projection models for excess lung cancer associated with radon. The principal models differ substantially in their underlying assumptions and consequently in the resulting risk projections. The resulting diversity illustrates the substantial uncertainty that remains concerning the most appropriate model of the temporal pattern of radon-related lung cancer. Animal experiments, further follow-up of the miner cohorts, and well-designed epidemiological studies of indoor exposure should reduce this uncertainty.     

Cancer Fatalities from Waterborne Radon (Rn-222)

A model of the biokinetics of radon in the human body following ingestion is developed from existing data. Calculations of the probability of cancer fatality from use of radon-laden water in the home then are presented. The pathways of emanation and ingestion are examined and shown to lead to roughly equal risks. The probability of fatal cancer resulting from lifetime use of water at a radon concentration of 1 pCi/L is shown to be 1 X 10(-6), with a reasonable range between 2 X 10(-7) and 5 X 10(-6). The allowed concentration consistent with an excess risk of 10(-4) then is approximately 100 pCi/L, which is exceeded in a significant fraction of U.S. water supplies. The lifetime number of premature deaths due to waterborne radon in the U.S. is estimated to lie between 5000 and 125,000, with a best estimate of 25,000.     

An Analysis of the Uncertainties in Estimates of Radon-Induced Lung Cancer

A recent report by the National Academy of Sciences estimates that the radiation dose to the bronchial epithelium, per working level month (WLM) of radon daughter exposure, is about 30% lower for residential exposures than for exposures received in underground mines. Adjusting the previously published BEIR IV radon risk model accordingly, the unit risk for indoor exposures of the general population is about 2.2 x 10(-4) lung cancer deaths (lcd)/WLM. Using results from EPA's National Residential Radon Survey, the average radon level is estimated to be about 1.25 pCi/L, and the annual average exposure about 0.242 WLM. Based on these estimates, 13,600 radon-induced lcd/yr are projected for the United States. A quantitative uncertainty analysis was performed, which considers: statistical uncertainties in the epidemiological studies of radon-exposed miners; the dependence of risk on age at, and time since, exposure; the extrapolation of risk estimates from mines to homes based on comparative dosimetry; and uncertainties in the radon daughter levels in homes and in the average residential occupancy. Based on this assessment of the uncertainties in the unit risk and exposure estimates, an uncertainty range of 7000-30000 lcd/yr is derived.     

Lay Understanding of Synergistic Risk: The Case of Radon and Cigarette Smoking

The combination of radon and smoking produces a synergistic risk of lung cancer. Lay understanding of this risk was examined from the perspectives of mental models theory, the psychometric approach to risk perception, and optimistic bias. As assessed by interview, participants ( N = 50) had more extensive mental models for the risks of smoking than for the risks of radon or the combination of radon and smoking; 32% knew little or nothing about radon. Despite reading an informational brochure, their risk-perception ratings of the three hazards showed no perception of the synergy between smoking and radon risk, although the combined hazard was rated as less familiar but more controllable than the average of the single hazards ( p < .01). No evidence of optimistic bias for the health consequences of radon, or the combination of radon and smoking was observed. Participants appeared to be combining the single-hazard risks subadditively to arrive at their combined-hazard risk perceptions. Further research on the integration of perceived risks would be beneficial for designing optimal communications about synergistic risk.     

Awareness and Perceptions of the Risks of Exposure to Indoor Radon: A Population‐Based Approach to Evaluate a Radon Awareness and Testing Campaign in England and Wales

The current study aimed to evaluate the locally directed radon roll‐out program that was conducted between 2001 and 2005 in England and Wales to increase radon awareness and testing rates. A representative sample of 1,578 residents aged 16 and older were interviewed who lived in radon‐affected areas of 15 local authorities in England and Wales that were eligible for participation in the program. The study systematically sampled across participating and nonparticipating local authorities, “actionable” and “nonactionable” radon‐affected areas, and geographic regions with different campaign histories (Wales, Southwest England, and the rest of England). As a multistage sampling strategy was used, the data were analyzed from a multilevel perspective. This study found that participants living in participating local authorities had higher levels of awareness and were more likely to have tested their home for radon than participants living in nonparticipating local authorities. Similar results were found for participants living in “actionable” areas as compared to those living in “nonactionable” radon‐affected areas. The study further found that radon awareness and testing rates were the highest in Southwest England and the lowest in Wales. This study suggests that the radon roll‐out program has been effective in raising awareness and testing rates, and that ongoing domestic radon campaigns in Southwest England may have raised radon awareness and testing in these areas, showing important reinforcement effects of multiple risk communication campaigns.     

Residential Radon in Canada: An Uncertainty Analysis of Population and Individual Lung Cancer Risk

Following a comprehensive evaluation of the health risks of radon, the U.S. National Research Council (US-NRC) concluded that the radon inside the homes of U.S. residents is an important cause of lung cancer. To assess lung cancer risks associated with radon exposure in Canadian homes, we apply the new (US-NRC) techniques, tailoring assumptions to the Canadian context. A two-dimensional uncertainty analysis is used to provide both population-based (population attributable risk, PAR; excess lifetime risk ratio, ELRR; and life-years lost, LYL) and individual-based (ELRR and LYL) estimates. Our primary results obtained for the Canadian population reveal mean estimates for ELRR, PAR, and LYL are 0.08, 8%, and 0.10 years, respectively. Results are also available and stratified by smoking status (ever versus never). Conveniently, the three indices (ELRR, PAR, and LYL) reveal similar output uncertainty (geometric standard deviation, GSD approximately 1.3), and in the case of ELRR and LYL, comparable variability and uncertainty combined (GSD approximately 4.2). Simplifying relationships are identified between ELRR, LYL, PAR, and the age-specific excess rate ratio (ERR), which suggest a way to scale results from one population to another. This insight is applied in scaling our baseline results to obtain gender-specific estimates, as well as in simplifying and illuminating sensitivity analysis.     

Radon as a Tracer of Lung Changes Induced by Smoking

After smoking, exposure to radon and its progeny is the second leading cause of lung cancer. The probability of inducing lung carcinomas by inhaled radon progeny depends on the deposited radiation dose, and is significantly affected by physiological and morphometric changes induced by smoking. Due to irritation of the airways, the inhalation of cigarette smoke leads to the hyperproduction of mucus. Two concurrent processes occur: on one hand, increased production of mucus protects the target cells against radiation damage; on the other hand, in the case of long-term smokers, a chronic lung obstruction develops, causing an increase in the radiation dose to the lungs. Depending on the duration and intensity of smoking, these processes contribute to the final radiation dose with different weights. The primary objective of this study was to investigate to what extent these smoke-induced changes can modify the resulting absorbed dose of inhaled radon progeny relative to healthy nonsmokers. Since the bronchial dose depends on the degree of lung tissue damage, we have used this dose as a tool for detecting the effects of smoking on the lung epithelium. In other words, the biological effect of radon served as a tracer of changes induced by smoking.     

The Interplay of Science, Values, and Experiences Among Scientists Asked to Evaluate the Hazards of Dioxin, Radon, and Environmental Tobacco Smoke

To investigate the extent to which personal values and experiences among scientists might affect their assessment of risks from dioxin, radon, and environmental tobacco smoke (ETS), we conducted an experiment through a telephone survey of 1461 epidemiologists, toxicologists, physicians, and general scientists. Each participant was read a vignette designed to reflect the mainstream scientific thinking on one of the three substances. For half of the participants (group A) the substance was named. For the other half (group B), the substance was not named but was identified only as Substance X, Y, or Z. Knowing the name of the substance had little effect on the scientists' evaluation of dioxin, although those who knew the substance to be dioxin were more likely to rate the substance as a serious environmental health hazard (51% vs. 42%, p = 0.062). For radon, those who knew the substance by name were significantly more likely to consider it an environmental health hazard than were those who knew it as substance Z (91% vs. 78%, p less than 0.001). Participants who knew they were being asked about ETS rather than substance X were significantly more likely to consider the substance an environmental health hazard (88% vs. 66%, p less than 0.001), to consider the substance a serious environmental health hazard (70% vs. 33%, p less than 0.001), to believe that background exposure required public health intervention (85% vs. 41%, p less than 0.001), and to believe that above-background exposure required public health intervention (90% vs. 74%, p less than 0.001). These findings suggest that values and experiences may be influencing health risk assessments for these substances, and indicate the need for more study of this phenomenon.     

Radon Risk Information and Voluntary Protection: Evidence from a Natural Experiment

This study examines the perceived risks and mitigating behavior of Maine households who received new information on their exposures to significant health risks from indoor radon. The observed responses of these households illustrate conceptual issues related to designing an effective risk information program. Despite the involvement of generally well-motivated homeowners and well-intentioned researchers and government officials, we conclude that the risk information approach used in Maine failed to induce appropriate, cost-effective voluntary protection. The results indicate that, after receiving radon test results, information on associated health risks, and suggestions on how to reduce exposures: perceived risks tended to understate objective risks by orders of magnitude, and there was no statistically significant relationship between mitigating behavior and objective risks. These results suggest that the formation of risk perceptions and subsequent behavioral adjustments involve complex interactions among information, contextual, socioeconomic, and psychological variables. Therefore, government programs that seek to reduce health and safety risks with information programs, instead of using more conventional enforced standards, must be crafted very carefully to accommodate this complex process.     

The Perceived Health Risks of Indoor Radon Gas and Overhead Powerlines: A Comparative Multilevel Approach

Radon and overhead powerlines are two radiation risk cases that have raised varying levels of concern among the general public and experts. Despite both involving radiation—a typically feared and unseen health hazard—individuals' perceptions of the two risk cases may invoke rather different factors. We examined individual and geographic-contextual factors influencing public perceptions of the health risks of indoor radon gas and overhead powerlines in a comparative research design, utilizing a postal questionnaire with 1,528 members of the general public (response rate 28%) and multilevel modeling techniques. This study found that beliefs about the two risk cases mainly differed according to the level of "exposure"—defined here in terms of spatial proximity. We argue that there are two alternative explanations for this pattern of findings: that risk perception itself varies directly with proximity, or that risk is more salient to concerned people in the exposed areas. We also found that while people living in high radon areas are more concerned about the risks of indoor radon gas, they find these risks more acceptable and have more trust in authorities. These results might reflect the positive effects of successive radon campaigns in high radon areas, which may have raised awareness and concern, and at the same time may have helped to increase trust by showing that the government takes the health risks of indoor radon gas seriously, suggesting that genuine risk communication initiatives may have positive impacts on trust in risk management institutions.     

Modeling the Modification of the Risk of Radon-Induced Lung Cancer by Environmental Tobacco Smoke

The presence of environmental tobacco smoke (ETS) in homes has been implicated in the causation of lung cancer. While of interest in its own right, ETS also influences the risk imposed by radon and its decay products. The interaction between radon progeny and ETS alters the exposure, intake, uptake, biokinetics, dosimetry, and radiobiology of those progeny. The present paper details model predictions of the various influences of ETS on these factors in the U.S. population and provides estimates of the resulting change in the risk from average levels of radon progeny. It is predicted that the presence of ETS produces a very small (perhaps unmeasurable) increase in the risk of radiation-induced tracheobronchial cancer in homes with initially very high particle concentrations for both active and never-smokers, but significantly lowers the risk in homes with initially lower particle concentrations for both groups when generation 4 of the lung is considered the target site. For generation 16, the presence of ETS generally increases the radon-induced risk of lung cancer, although the increase should be unmeasurable at high initial particle concentrations. The net effect of ETS on human health is suggested to be a complicated function of the initial housing conditions, the concentration of particles introduced by smoking, the target generation considered, and the smoking status of exposed populations. This situation precludes any simple statements concerning the role of ETS in governing the incidence of lung cancer in a population.     

Evaluating Risk Communication: Narrative vs. Technical Presentations of Information About Radon

This paper reports on an experiment to test the hypothesis that people respond better to risk communication that reflects more closely the conditions of their social and cultural lives. The experiment used the case of radon to determine whether technical or narrative forms of risk communication were more effective at drawing people's attention, imparting information, and modifying behavior. Two series of articles on radon were placed in the local newspapers of two Massachusetts communities. Homeowner attitudes, knowledge, and responses were monitored in baseline and follow-up telephone surveys. A third community was selected for comparison. The newspaper series were developed on the basis of previous research and six focus groups conducted with homeowners. The technical series presented authoritative, factual risk information, in the scientific style of the passive voice with generalized and impersonal language. The narrative series consisted of dramatized accounts of individuals making decisions about radon testing and mitigation, written in a more personal style. The findings from the focus groups confirm the results of previous studies, but the small size of the follow-up samples was a limiting factor in drawing definitive conclusions about the relative effectiveness of the two formats. The experiment demonstrates the difficulty of any risk communication effort on radon and underscores the need for good research design.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modeling Lung Carcinogenesis in Radon‐Exposed Miner Cohorts: Accounting for Missing Information on Smoking

Epidemiological miner cohort data used to estimate lung cancer risks related to occupational radon exposure often lack cohort‐wide information on exposure to tobacco smoke, a potential confounder and important effect modifier. We have developed a method to project data on smoking habits from a case‐control study onto an entire cohort by means of a Monte Carlo resampling technique. As a proof of principle, this method is tested on a subcohort of 35,084 former uranium miners employed at the WISMUT company (Germany), with 461 lung cancer deaths in the follow‐up period 1955–1998. After applying the proposed imputation technique, a biologically‐based carcinogenesis model is employed to analyze the cohort's lung cancer mortality data. A sensitivity analysis based on a set of 200 independent projections with subsequent model analyses yields narrow distributions of the free model parameters, indicating that parameter values are relatively stable and independent of individual projections. This technique thus offers a possibility to account for unknown smoking habits, enabling us to unravel risks related to radon, to smoking, and to the combination of both.     

The Indoor Radiological Problem in Perspective

Measures to tighten homes to conserve energy, as are being encouraged and subsidized by federal and state governments, may reduce air infiltration by 20% or more. Standard prudent risk-assessment methodologies predict that, due to increased levels of indoor radon caused by this reduction in ventilation, the added lifetime lung cancer risk to members of the public is of order 200/million people exposed. In situations where the radon source term is unusually high, or extreme reductions in ventilation are made, the added risk can be more than an order of magnitude greater. While these imputed risks are far outside the range that is normally tolerated, no systematic efforts are in progress to mitigate or limit the risk in any way. Furthermore, efforts to determine better the variations in radon source term and the health effects of indoor radon are being deemphasized. The technical background is presented in some detail, and implications with regard to management of risks to the public are discussed.     

Protective Responses to Household Risk: A Case Study of Radon Mitigation

This study analyzes the effectiveness of a mass-media radon information and testing campaign conducted in the Washington, D.C. area in the winter of 1988. Although an impressive number of test kits (approximately 100,000) were sold, the ultimate mitigation rates resulting from the campaign were extremely low. Analyses show that low mitigation rates cannot be explained by postulating that people's responses to radon are insensitive to the level of objective risk. They may instead be due to characteristics of the protective response required to reduce radon risk. Radon may be thought of as one of a family of household risks which have risk response profiles that make them particularly difficult for people to manage and remediate. Traditional information campaigns for such risks are likely to be ineffective; instead, they may require regulatory strategies or programs which provide active guidance and assistance.     

Reanalysis of the DEMS Nested Case‐Control Study of Lung Cancer and Diesel Exhaust: Suitability for Quantitative Risk Assessment

The International Agency for Research on Cancer (IARC) in 2012 upgraded its hazard characterization of diesel engine exhaust (DEE) to “carcinogenic to humans.” The Diesel Exhaust in Miners Study (DEMS) cohort and nested case‐control studies of lung cancer mortality in eight U.S. nonmetal mines were influential in IARC's determination. We conducted a reanalysis of the DEMS case‐control data to evaluate its suitability for quantitative risk assessment (QRA). Our reanalysis used conditional logistic regression and adjusted for cigarette smoking in a manner similar to the original DEMS analysis. However, we included additional estimates of DEE exposure and adjustment for radon exposure. In addition to applying three DEE exposure estimates developed by DEMS, we applied six alternative estimates. Without adjusting for radon, our results were similar to those in the original DEMS analysis: all but one of the nine DEE exposure estimates showed evidence of an association between DEE exposure and lung cancer mortality, with trend slopes differing only by about a factor of two. When exposure to radon was adjusted, the evidence for a DEE effect was greatly diminished, but was still present in some analyses that utilized the three original DEMS DEE exposure estimates. A DEE effect was not observed when the six alternative DEE exposure estimates were utilized and radon was adjusted. No consistent evidence of a DEE effect was found among miners who worked only underground. This article highlights some issues that should be addressed in any use of the DEMS data in developing a QRA for DEE.     

Risk assessment methodologies for passive smoking-induced lung cancer

Risk assessment methodologies have been successfully applied to control societal risk from outdoor air pollutants. They are now being applied to indoor air pollutants such as environmental tobacco smoke (ETS) and radon. Nonsmokers' exposures to ETS have been assessed based on dosimetry of nicotine, its metabolite, continine, and on exposure to the particulate phase of ETS. Lung cancer responses have been based on both the epidemiology of active and of passive smoking. Nine risk assessments of nonsmokers' lung cancer risk from exposure to ETS have been performed. Some have estimated risks for lifelong nonsmokers only; others have included ex-smokers; still others have estimated total deaths from all causes. To facilitate interstudy comparison, in some cases lung cancers had to be interpolated from a total, or the authors' original estimate had to be adjusted to include ex-smokers. Further, all estimates were adjusted to 1988. Excluding one study whose estimate differs from the mean of the others by two orders of magnitude, the remaining risk assessments are in remarkable agreement. The mean estimate is approximately 5000 +/- 2400 nonsmokers' lung cancer deaths (LCDSs) per year. This is a 25% greater risk to nonsmokers than is indoor radon, and is about 57 times greater than the combined estimated cancer risk from all the hazardous outdoor air pollutants currently regulated by the Environmental Protection Agency: airborne radionuclides, asbestos, arsenic, benzene, coke oven emissions, and vinyl chloride.     

Bounding Poorly Characterized Risks: A Lung Cancer Example

For diseases with more than one risk factor, the sum of probabilistic estimates of the number of cases caused by each individual factor may exceed the total number of cases observed, especially when uncertainties about exposure and dose response for some risk factors are high. In this study, we outline a method of bounding the fraction of lung cancer fatalities not due to specific well-studied causes. Such information serves as a "reality check" for estimates of the impacts of the minor risk factors, and, as such, complements the traditional risk analysis. With lung cancer as our example, we allocate portions of the observed lung cancer mortality to known causes (such as smoking, residential radon, and asbestos fibers) and describe the uncertainty surrounding those estimates. The interactions among the risk factors are also quantified, to the extent possible. We then infer an upper bound on the residual mortality due to "other" causes, using a consistency constraint on the total number of deaths, the maximum uncertainty principle, and the mathematics originally developed of imprecise probabilities.