The efficacy of public health information for encouraging radon gas awareness and testing varies by audience age, sex and profession.

Radioactive radon inhalation is a leading cause of lung cancer and underlies an ongoing public health crisis. Radon exposure prevention strategies typically begin by informing populations about health effects, and their initial efficacy is measured by how well and how fast information convinces individuals to test properties. This communication process is rarely individualized, and there is little understanding if messages impact diverse demographics equally. Here, we explored how 2,390 people interested in radon testing differed in their reaction to radon's public health information and their subsequent decision to test. Only 20% were prompted to radon test after 1 encounter with awareness information, while 65% required 2-5 encounters over several months, and 15% needed 6 to > 10 encounters over many years. People who most delayed testing were more likely to be men or involved in engineering, architecture, real estate and/or physical science-related professions. Social pressures were not a major factor influencing radon testing. People who were the least worried about radon health risks were older and/or men, while negative emotional responses to awareness information were reported more by younger people, women and/or parents. This highlights the importance of developing targeted demographic messaging to create effective radon exposure prevention strategies.

Domestic radon exposure and risk of childhood leukemia: A meta-analysis.

PURPOSE: This meta-analysis evaluated the potential influence of environmental radon exposure on childhood leukemia. METHODS: We searched comprehensive electronic databases from PubMed, EMBASE, and Cochrane Library to identify studies evaluating the association between radon and leukemia. RESULTS: Ten eligible studies published from 1995 to 2014 were enrolled. Of these 10 studies, 8 were case-control studies (involving 10803 cases and 16202 controls) and 2 were cohort studies (involving 1,428 cases). Overall results as odds ratio (OR) with the corresponding 95% confidence intervals (95%CI) for case-control studies and fully adjusted hazard ratio (HR) with corresponding 95%CI for cohort studies were identified. A positive but weak association was found between radon exposure and childhood leukemia in case-control studies (summary OR 1.22, 95%CI 1.01-1.42) rather than cohort studies (summary HR 0.97, 95%CI 0.81-1.15). Heterogeneity or publication bias was not observed. Moreover, overall ORs were not changed by removing any single study, suggesting the stability and reliability of conclusions. CONCLUSIONS: Future prospective studies with well-controlled confounders are needed to verify the conclusion.

Radon, an invisible killer in Canadian homes: perceptions of Ottawa-Gatineau residents.

OBJECTIVES: Canadians have reason to care about indoor air quality as they spend over 90% of the time indoors. Although indoor radon causes more deaths than any other environmental hazard, only 55% of Canadians have heard of it, and of these, 6% have taken action. The gap between residents' risk awareness and adoption of actual protective behaviour presents a challenge to public health practitioners. Residents' perception of the risk should inform health communication that targets motivation for action. In Canada, research about the public perception of radon health risk is lacking. The aim of this study was to describe residents' perceptions of radon health risks and, applying a theoretical lens, evaluate how perceptions correlate with protection behaviours. METHODS: We conducted a mixed online and face-to-face survey (N = 557) with both homeowners and tenants in Ottawa-Gatineau census metropolitan area. Descriptive, correlation, and regression analyses addressed the research questions. RESULTS: Compared to the gravity of the risk, public perception remained low. While 32% of residents expressed some concern about radon health risk, 12% of them tested and only 3% mitigated their homes for radon. Residents' perceptions of the probability and severity of the risk, social influence, care for children, and smoking in home correlated significantly with their intention to test; these factors also predicted their behaviours for testing and mitigation. CONCLUSION: Health risk communication programs need to consider the affective aspects of risk perception in addition to rational cognition to improve protection behaviours. A qualitative study can explore the reasons behind the gap between testing and mitigation.

Indoor Radon and Lung Cancer: Estimation of Attributable Risk, Disease Burden, and Effects of Mitigation.

PURPOSE: Exposure to indoor radon is associated with lung cancer. This study aimed to estimate the number of lung cancer deaths attributable to indoor radon exposure, its burden of disease, and the effects of radon mitigation in Korea in 2010. MATERIALS AND METHODS: Lung cancer deaths due to indoor radon exposure were estimated using exposure-response relations reported in previous studies. Years of life lost (YLLs) were calculated to quantify disease burden in relation to premature deaths. Mitigation effects were examined under scenarios in which all homes with indoor radon concentrations above a specified level were remediated below the level. RESULTS: The estimated number of lung cancer deaths attributable to indoor radon exposure ranged from 1946 to 3863, accounting for 12.5-24.7% of 15623 total lung cancer deaths in 2010. YLLs due to premature deaths were estimated at 43140-101855 years (90-212 years per 100000 population). If all homes with radon levels above 148 Bq/m³ are effectively remediated, 502-732 lung cancer deaths and 10972-18479 YLLs could be prevented. CONCLUSION: These findings suggest that indoor radon exposure contributes considerably to lung cancer, and that reducing indoor radon concentration would be helpful for decreasing the disease burden from lung cancer deaths.

Utility gains from reductions in the modifiable burden of lung cancer attributable to residential radon in Canada.

RESEARCH QUESTION: The objective of this analysis is to estimate the modifiable burden of disease according to the annual number of lung cancer deaths prevented and the associated period gain in quality-adjusted life years (QALYs) for the 2012 populations in Canada from reductions in residential radon exposures. INTERVENTIONS: Two postulated interventions for residential radon mitigation in new construction are assessed, corresponding to a 50% reduction and an 85% reduction in radon nationally, in the provinces/territories, and in 17 census metropolitan areas in Canada. METHODS: Data were derived from two recent Canadian radon surveys conducted by the Radiation Protection Bureau, Health Canada, along with Canadian mortality and quality of life data. Analyses adopted a lifetime horizon and a discount rate of 1.5%. A period life-table analysis was conducted using age- and sex-specific all-cause and lung cancer mortality rates, adjusted for smoking, and the BEIR VI exposure-age-concentration model for radon-attributable risk of lung cancer mortality. RESULTS: A reduction in residential radon by 50% could prevent 681 lung cancer deaths, associated with a gain of 15,445 QALYs in the Canadian population at a discount rate of 1.5%; a reduction in radon by 85% could prevent 1263 lung cancer deaths, associated with a gain of 26,336 QALYs. On a per population basis, the Yukon was estimated to benefit most from radon mitigation. CONCLUSION: The magnitude of QALY gains in Canada estimated under the two radon mitigation scenarios is appreciable but varies considerably across provinces due to variability in indoor radon concentrations and smoking rates.

Residential radon and small cell lung cancer. A systematic review.

Residential radon exposure is considered the second cause of lung cancer and the first in never smokers. Nevertheless, the association between the different histological types of lung cancer and radon is not completely clear, and radon effect on small cell lung cancer is not completely understood. We aim to asses the effect of residential radon exposure on the risk of small cell lung cancer (SCLC) in general population and miners through a systematic review applying predefined inclusion and exclusion criteria. 16 studies were included. Most of them point to a relationship between indoor radon and SCLC, though some investigations show no association. When comparing the risk of SCLC due to radon exposure with NSCLC, it can be observed that an increased risk for SCLC is present. Small cell lung cancer seems to be the histological type of lung cancer most tightly related with residential radon.

Geographic variation in radon and associated lung cancer risk in Canada.

OBJECTIVE: Radon is an important risk factor for lung cancer. Here we use maps of the geographic variation in radon to estimate the lung cancer risk associated with living in high radon areas of Canada. METHODS: Geographic variation in radon was estimated using two mapping methods. The first used a Health Canada survey of 14,000 residential radon measurements aggregated to health regions, and the second, radon risk areas previously estimated from geology, sediment geochemistry and aerial gamma-ray spectrometry. Lung cancer risk associated with living in these radon areas was examined using a population-based case-control study of 2,390 lung cancer cases and 3,507 controls collected from 1994-1997 in eight Canadian provinces. Residential histories over a 20-year period were used in combination with the two mapping methods to estimate ecological radon exposures. Hierarchical logistic regression analyses were used to estimate odds ratios for lung cancer incidence, after adjusting for a comprehensive set of individual and geographic covariates. RESULTS: Across health regions in Canada, significant variation in average residential radon concentrations (range: 16-386 Bq/m3) and in high geological-based radon areas (range: 0-100%) is present. In multivariate models, a 50 Bq/m3 increase in average health region radon was associated with a 7% (95% CI: -6-21%) increase in the odds of lung cancer. For every 10 years that individuals lived in high radon geological areas, the odds of lung cancer increased by 11% (95% CI: 1-23%). CONCLUSIONS: These findings provide further evidence that radon is an important risk factor for lung cancer and that risks are unevenly distributed across Canada.

Dual home screening and tailored environmental feedback to reduce radon and secondhand smoke: an exploratory study.

Combined exposure to secondhand smoke (SHS) and radon increases lung cancer risk 10-fold. The authors assessed the feasibility and impact of a brief home screening and environmental feedback intervention to reduce radon and SHS (Freedom from Radon and Smoking in the Home [FRESH]) and measured perceived risk of lung cancer and synergistic risk perception (SHS x radon). Participants (N = 50) received home radon and SHS kits and completed baseline surveys. Test results were shared using an intervention guided by the Teachable Moment Model. Half of the participants completed online surveys two months later. Most (76%) returned the radon test kits; 48% returned SHS kits. Of the returned radon test kits, 26% were >4.0 pCi/L. Of the returned SHS kits, 38% had nicotine > .1 microg/m3. Of those with high radon, more than half had contacted a mitigation specialist or planned contact. Of those with positive air nicotine, 75% had adopted smoke-free homes. A significant increase occurred in perceived risk for lung cancer and synergistic risk perception after FRESH.

Residential radon and lung cancer in never smokers. A systematic review.

Radon exposure is considered the second cause of lung cancer and the first in never smokers. We aim to assess the effect of residential radon exposure on the risk of lung cancer in never smokers through a systematic review applying predefined inclusion and exclusion criteria. 14 Studies were included. Some of them point to a relationship between residential radon and lung cancer while others show no association. Further studies are necessary to test this association and to assess if other risk factors such as environmental tobacco smoke could modify the effect of residential radon exposure on lung cancer.

Lung cancer risk from radon in Ontario, Canada: how many lung cancers can we prevent?

PURPOSE: To calculate the burden of lung cancer illness due to radon for all thirty-six health units in Ontario and determine the number of radon-attributable lung cancer deaths that could be prevented. METHODS: We calculated the population attributable risk percent, excess life-time risk ratio, life-years lost, the number of lung cancer deaths due to radon, and the number of deaths that could be prevented if all homes above various cut-points were effectively reduced to background levels. RESULTS: It is estimated that 13.6 % (95 % CI 11.0, 16.7) of lung cancer deaths in Ontario are attributable to radon, corresponding to 847 (95 % CI 686, 1,039) lung cancer deaths each year, approximately 84 % of these in ever-smokers. If all homes above 200 Bq/m(3), the current Canadian guideline, were remediated to background levels, it is estimated that 91 lung cancer deaths could be prevented each year, 233 if remediation was performed at 100 Bq/m(3). There was important variation across health units. CONCLUSIONS: Radon is an important contributor to lung cancer deaths in Ontario. A large portion of radon-attributable lung cancer deaths are from exposures below the current Canadian guideline, suggesting interventions that install effective radon-preventive measures into buildings at build may be a good alternative population prevention strategy to testing and remediation. For some health units, testing and remediation may also prevent a portion of radon-related lung cancer deaths. Regional attributable risk estimates can help with local public health resource allocation and decision making.

[A cohort study on risk factors of lung cancer in Yunnan tin miners].

BACKGROUND: Smoking is a major cause of lung cancer. Studies of lung cancer among miners have shown that occupational exposure also played an important role. The aim of this study is to investigate radon, cigarette use and other risk factors of lung cancer in Yunnan tin miners and to provide a scientific basis for the prevention and control of occupational lung cancer. METHODS: A prospective cohort study was conducted among Yunnan tin miners, the associations between potential risk factors for lung cancer were analyzed by multivariate Cox regression model. Effects of age at first radon exposure and radon exposure rate on lung cancer risk were analyzed. The relationship between cumulative working level month and lung cancer was analyzed according to smoking status. The joint effect of tobacco use and cumulative radon exposure was analyzed based on additive and multiplicative models. RESULTS: Increased risk of lung cancer was associated with age at enrollment, tobacco use, prior bronchitis, and cumulative arsenic and radon exposure, while higher education level was associated with decreased lung cancer risk. An inverse effect of radon exposure rate was observed. There was no significant association between lung cancer risk and first radon exposure age. There was a significant additive interaction between tobacco use and radon exposure on lung cancer risk. CONCLUSIONS: Several risk factors may contribute to the high incidence of lung cancer in Yunnan tin miners. Further studies are warranted to evaluate joint effect of different risk factors.

Genetic variation in SIRT1 affects susceptibility of lung squamous cell carcinomas in former uranium miners from the Colorado plateau.

Epidemiological studies of underground miners suggested that occupational exposure to radon causes lung cancer with squamous cell carcinoma (SCC) as the predominant histological type. However, the genetic determinants for susceptibility of radon-induced SCC in miners are unclear. Double-strand breaks induced by radioactive radon daughters are repaired primarily by non-homologous end joining (NHEJ) that is accompanied by the dynamic changes in surrounding chromatin, including nucleosome repositioning and histone modifications. Thus, a molecular epidemiological study was conducted to assess whether genetic variation in 16 genes involved in NHEJ and related histone modification affected susceptibility for SCC in radon-exposed former miners (267 SCC cases and 383 controls) from the Colorado plateau. A global association between genetic variation in the haplotype block where SIRT1 resides and the risk for SCC in miners (P = 0.003) was identified. Haplotype alleles tagged by the A allele of SIRT1 rs7097008 were associated with increased risk for SCC (odds ratio = 1.69, P = 8.2 × 10(-5)) and greater survival in SCC cases (hazard ratio = 0.79, P = 0.03) in miners. Functional validation of rs7097008 demonstrated that the A allele was associated with reduced gene expression in bronchial epithelial cells and compromised DNA repair capacity in peripheral lymphocytes. Together, these findings substantiate genetic variation in SIRT1 as a risk modifier for developing SCC in miners and suggest that SIRT1 may also play a tumor suppressor role in radon-induced cancer in miners.

The performance of functional methods for correcting non-Gaussian measurement error within Poisson regression: corrected excess risk of lung cancer mortality in relation to radon exposure among French uranium miners.

A broad variety of methods for measurement error (ME) correction have been developed, but these methods have rarely been applied possibly because their ability to correct ME is poorly understood. We carried out a simulation study to assess the performance of three error-correction methods: two variants of regression calibration (the substitution method and the estimation calibration method) and the simulation extrapolation (SIMEX) method. Features of the simulated cohorts were borrowed from the French Uranium Miners' Cohort in which exposure to radon had been documented from 1946 to 1999. In the absence of ME correction, we observed a severe attenuation of the true effect of radon exposure, with a negative relative bias of the order of 60% on the excess relative risk of lung cancer death. In the main scenario considered, that is, when ME characteristics previously determined as most plausible from the French Uranium Miners' Cohort were used both to generate exposure data and to correct for ME at the analysis stage, all three error-correction methods showed a noticeable but partial reduction of the attenuation bias, with a slight advantage for the SIMEX method. However, the performance of the three correction methods highly depended on the accurate determination of the characteristics of ME. In particular, we encountered severe overestimation in some scenarios with the SIMEX method, and we observed lack of correction with the three methods in some other scenarios. For illustration, we also applied and compared the proposed methods on the real data set from the French Uranium Miners' Cohort study.

Quantitative relationship between silica exposure and lung cancer mortality in German uranium miners, 1946-2003.

BACKGROUND: In 1996 and 2009, the International Agency for Research on Cancer classified silica as carcinogenic to humans. The exposure-response relationship between silica and lung cancer risk, however, is still debated. Data from the German uranium miner cohort study were used to further investigate this relationship. METHODS: The cohort includes 58677 workers with individual information on occupational exposure to crystalline silica in mg m(-3)-years and the potential confounders radon and arsenic based on a detailed job-exposure matrix. In the follow-up period 1946-2003, 2995 miners died from lung cancer. Internal Poisson regression with stratification by age and calendar year was used to estimate the excess relative risk (ERR) per dust-year. Several models including linear, linear quadratic and spline functions were applied. Detailed adjustment for cumulative radon and arsenic exposure was performed. RESULTS: A piecewise linear spline function with a knot at 10 mg m(-3)-years provided the best model fit. After full adjustment for radon and arsenic no increase in risk <10 mg m(-3)-years was observed. Fixing the parameter estimate of the ERR in this range at 0 provided the best model fit with an ERR of 0.061 (95% confidence interval: 0.039, 0.083) >10 mg m(-3)-years. CONCLUSION: The study confirms a positive exposure-response relationship between silica and lung cancer, particularly for high exposures.

Radon and lung cancer in the American Cancer Society cohort.

BACKGROUND: Case-control studies conducted in North America, Europe, and Asia provided evidence of increased lung cancer risk due to radon in homes. Here, the association between residential radon and lung cancer mortality was examined in a large-scale cohort study. METHODS: Nearly 1.2 million Cancer Prevention Study-II participants were recruited in 1982. Mean county-level residential radon concentrations were linked to study participants according to ZIP code information at enrollment [mean (SD)=53.5 Bq/m3 (38.0)]. Cox proportional hazards regression models were used to obtain adjusted HR and 95% CI for lung cancer mortality associated with radon. Potential effect modification by cigarette smoking, ambient sulfate concentrations, and other risk factors was assessed on both the additive and multiplicative scales. RESULTS: Through 1988, 3,493 lung cancer deaths were observed among 811,961 participants included in the analysis. A significant positive linear trend was observed between categories of radon concentrations and lung cancer mortality (P=0.02). A 15% (95% CI, 1-31) increase in the risk of lung cancer mortality was observed per 100 Bq/m3 increase in radon. Participants with mean radon concentrations above the EPA guideline value (148 Bq/m3) experienced a 34% (95% CI, 7-68) increase in risk for lung cancer mortality relative to those below the guideline value. CONCLUSIONS: This large prospective study showed positive associations between ecological indicators of residential radon and lung cancer. IMPACT: These results further support efforts to reduce radon concentrations in homes to the lowest possible level.

Incidence of non-lung solid cancers in Czech uranium miners: a case-cohort study.

OBJECTIVES: Uranium miners are chronically exposed to radon and its progeny, which are known to cause lung cancer and may be associated with leukemia. This study was undertaken to evaluate risk of non-lung solid cancers among uranium miners in Príbram region, Czech Republic. METHODS: A retrospective stratified case-cohort study in a cohort of 22,816 underground miners who were employed between 1949 and 1975. All incident non-lung solid cancers were ascertained among miners who worked underground for at least 12 months (n=1020). A subcohort of 1707 subjects was randomly drawn from the same population by random sampling stratified on age. The follow-up period lasted from 1977 to 1996. RESULTS: Relative risks comparing 180 WLM (90th percentile) of cumulative lifetime radon exposure to 3 WLM (10th percentile) were 0.88 for all non-lung solid cancers combined (95% CI 0.73-1.04, n=1020), 0.87 for all digestive cancers (95% CI 0.69-1.09, n=561), 2.39 for gallbladder cancer (95% CI 0.52-10.98, n=13), 0.79 for larynx cancer (95% CI 0.38-1.64, n=62), 2.92 for malignant melanoma (95% CI 0.91-9.42, n=23), 0.84 for bladder cancer (95% CI 0.43-1.65, n=73), and 1.13 for kidney cancer (95% CI 0.62-2.04, n=66). No cancer type was significantly associated with radon exposure; only malignant melanoma and gallbladder cancer showed elevated but non-significant association with radon. CONCLUSIONS: Radon was not significantly associated with incidence of any cancer of interest, although a positive association of radon with malignant melanoma and gallbladder cancer cannot be entirely ruled out.

A hybrid model for reducing ecological bias.

A major drawback of epidemiological ecological studies, in which the association between area-level summaries of risk and exposure is used to make inference about individual risk, is the difficulty in characterizing within-area variability in exposure and confounder variables. To avoid ecological bias, samples of individual exposure/confounder data within each area are required. Unfortunately, these may be difficult or expensive to obtain, particularly if large samples are required. In this paper, we propose a new approach suitable for use with small samples. We combine a Bayesian nonparametric Dirichlet process prior with an estimating functions' approach and show that this model gives a compromise between 2 previously described methods. The method is investigated using simulated data, and a practical illustration is provided through an analysis of lung cancer mortality and residential radon exposure in counties of Minnesota. We conclude that we require good quality prior information about the exposure/confounder distributions and a large between- to within-area variability ratio for an ecological study to be feasible using only small samples of individual data.