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Exposure to radon gas is a leading cause of lung cancer. Testing homes for the gas is straightforward, yet most people do not undertake tests even when offered freely. We report a pre-registered randomised controlled trial of communications to encourage test uptake. Households ( N  = 3500) in areas at high risk of radon exposure were randomly assigned to receive (i) a the control letter from the national Environmental Protection Agency; (ii) a behaviourally-informed version of the control letter that incorporated multiple nudges, including reciprocity messages and numeric frequencies of risk; (iii) this same behaviourally-informed letter in a re-designed envelope; (iv) the behaviourally-informed letter in the re-designed enveloped with a radon risk map of the household’s county. The behaviourally-informed letter led to a large increase in test uptake, from 22% in the control condition to 33% (a 50% increase). There was no additional benefit of the re-designed envelope, which generated uptake of 30%. Including the map led some households to respond faster, but the overall uptake (26%) was weaker. The results have implications for public health communications with households and show the potential for techniques from behavioural science to help mitigate environmental risks.

Background. More radon-related lung cancers occur among those exposed to tobacco smoke. Objectives. To test the effects of a personalized environmental report back intervention on change in stage of action for air nicotine testing and adopting a smoke-free home and radon testing and mitigation from baseline to 3 months postintervention. Methods. The study design used a two-arm parallel groups randomized controlled trial with stratified quota sampling. The treatment group received free air nicotine and radon home test kits and a brief problem-solving phone intervention; the control group received a coupon for free test kits. A sample of 515 homeowners were enrolled; 319 completed the 3-month follow-up. Stage of action to test and remediate the home was measured consistent with the precaution adoption process model. Linear mixed modeling assessed whether the main and interaction effects of treatment and time were associated with the testing and remediation outcomes; multiple covariates were included in the models. Results. The models for the four stages of action outcomes (testing and remediating for radon and secondhand smoke) each had a significant treatment-by-time effect. The general pattern was an increase in stage of action from baseline to 3 months. The degree of change was generally larger among the treatment group participants relative to the controls, indicating that those in the treatment group were more ready to take action. For all the models, participants with higher self-efficacy for radon/air nicotine testing and radon/secondhand smoke remediation were more ready to take action to test and remediate. Synergistic risk perception was associated with stage of action for radon mitigation. Conclusions. Homeowners who were provided free radon and air nicotine test kits, given their results, and engaged in a brief telephonic problem-solving consultation tended to show a greater increase in readiness to take action to test and remediate by 3 months compared with those who received standard public health practice. Both groups showed an increase in stage of action for all four outcomes over time.

ObjectivesRadon is carcinogenic, but more studies are needed to understand relationships with lung cancer and extrathoracic cancers at low exposures. There are few studies evaluating associations with cancer incidence or assessing the modifying effects of smoking.MethodsWe conducted a case–cohort study with 16 434 underground uranium miners in the Czech Republic with cancer incidence follow-up 1977–1996. Associations between radon exposure and lung cancer, and extrathoracic cancer, were estimated with linear excess relative rate (ERR) models. We examined potential modifying effects of smoking, time since exposure and exposure rate.ResultsUnder a simple ERR model, assuming a 5-year exposure lag, the estimated ERR of lung cancer per 100 working level months (WLM) was 0.54 (95% CI 0.33 to 0.83) and the estimated ERR of extrathoracic cancer per 100 WLM was 0.07 (95% CI −0.17 to 0.72). Most lung cancer cases were observed among smokers (82%), and the estimated ERR of lung cancer per 100 WLM was larger among smokers (ERR/100 WLM=1.35; 95% CI 0.84 to 2.15) than among never smokers (ERR/100 WLM=0.12; 95% CI −0.05 to 0.49). Among smokers, the estimated ERR of lung cancer per 100 WLM decreased with time since exposure from 3.07 (95% CI −0.04 to 10.32) in the period 5–14 years after exposure to 1.05 (95% CI 0.49 to 1.87) in the period 25+ years after exposure.ConclusionsWe observed positive associations between cumulative radon exposure and lung cancer, consistent with prior studies. We observed a positive association between cumulative radon exposure and extrathoracic cancers, although the estimates were small. There was evidence that the association between radon and lung cancer was modified by smoking in a multiplicative or super-multiplicative fashion.

Radon is a leading cause of lung cancer in indoor public and mining workers. Inhaled radon progeny releases alpha particles, which can damage cells in the airway epithelium. The extent and complexity of cellular damage vary depending on the alpha particle’s kinetic energy and cell characteristics. We developed a framework to quantitate the cellular damage on the nanometer and micrometer scales at different intensities of exposure to radon progenies Po-218 and Po-214. Energy depositions along the tracks of alpha particles that were slowing down were simulated on a nanometer scale using the Monte Carlo code Geant4-DNA. The nano-scaled track histories in a 5 μm radius and 1 μm-thick cylindrical volume were integrated into the tracking scheme of alpha trajectories in a micron-scale bronchial epithelium segment in the user-written SNU-CDS program. Damage distribution in cellular DNA was estimated for six cell types in the epithelium. Deep-sited cell nuclei in the epithelium would have less chance of being hit, but DNA damage from a single hit would be more serious, because low-energy alpha particles of high LET would hit the nuclei. The greater damage in deep-sited nuclei was due to the 7.69 MeV alpha particles emitted from Po-214. From daily work under 1 WL of radon concentration, basal cells would respond with the highest portion of complex DSBs among the suspected progenitor cells in the most exposed regions of the lung epithelium.

Largely unnoticed, all life on earth is constantly exposed to low levels of ionizing radiation. Radon, an imperceptible natural occurring radioactive noble gas, contributes as the largest single fraction to radiation exposure from natural sources. For that reason, radon represents a major issue for radiation protection. Nevertheless, radon is also applied for the therapy of inflammatory and degenerative diseases in galleries and spas to many thousand patients a year. In either case, chronic environmental exposure or therapy, the effect of radon on the organism exposed is still under investigation at all levels of interaction. This includes the physical stage of diffusion and energy deposition by radioactive decay of radon and its progeny and the biological stage of initiating and propagating a physiologic response or inducing cancer after chronic exposure. The purpose of this manuscript is to comprehensively review the current knowledge of radon and its progeny on physical background, associated cancer risk and potential therapeutic effects.

Radon, a naturally occurring radioactive gas known for its health risks, has recently gained attention for its potential protective role against COVID-19 mortality. This cross-sectional ecological study examined the relationship between indoor radon exposure and COVID-19 mortality rates across eight countries, including several European nations, the United States, and the State of Kerala, India, during the pre-vaccination period. The analyzed data on the subject were derived from recent scientific publications. The environmental aspect was represented by the variable \"indoor radon concentration or probability of exceeding a radon concentration in indoor air,\" depending on data availability. Using national radon surveys and COVID-19 mortality statistics, statistical analyses, including Spearman's correlation and Kendall Tau, were conducted between March and December 2020. The findings revealed a consistent negative correlation between radon concentrations and COVID-19 mortality rates, indicating that higher radon concentrations were associated with lower mortality rates. Regions such as Finland and Sweden, where radon exposure was relatively high, experienced significantly lower mortality. With Sweden and Finland showing a mortality risk reduction factor of respectively 1,42 and 5,47 during the first wave compared to the UK where Radon levels are very low. Although the findings are not overwhelmingly strong, the data suggest that radon exposure may have a mitigating effect on COVID-19 mortality.

ObjectivesRadon is a ubiquitous occupational and environmental lung carcinogen. We aim to quantify the association between radon progeny and lung cancer mortality in the largest and most up-to-date pooled study of uranium miners.MethodsThe pooled uranium miners analysis combines 7 cohorts of male uranium miners with 7754 lung cancer deaths and 4.3 million person-years of follow-up. Vital status and lung cancer deaths were ascertained between 1946 and 2014. The association between cumulative radon exposure in working level months (WLM) and lung cancer was modelled as the excess relative rate (ERR) per 100 WLM using Poisson regression; variation in the association by temporal and exposure factors was examined. We also examined analyses restricted to miners first hired before 1960 and with <100 WLM cumulative exposure.ResultsIn a model that allows for variation by attained age, time since exposure and annual exposure rate, the ERR/100 WLM was 4.68 (95% CI 2.88 to 6.96) among miners who were less than 55 years of age and were exposed in the prior 5 to <15 years at annual exposure rates of <0.5 WL. This association decreased with older attained age, longer time since exposure and higher annual exposure rate. In analyses restricted to men first hired before 1960, we observed similar patterns of association but a slightly lower estimate of the ERR/100 WLM.ConclusionsThis new large, pooled study confirms and supports a linear exposure–response relationship between cumulative radon exposure and lung cancer mortality which is jointly modified by temporal and exposure factors.

•Environmental exposures have been linked to neurocognitive dysfunction.•Home radon exposure’s impact on cognitive function has not been well characterized.•We examined links between radon exposure and dynamics of cognitive control in youth.•Youths with greater exposure showed aberrant oscillations with attentional control.•Radon exposure modulated expected neural and behavioral developmental trajectories. Radon is a prevalent, naturally occurring gas which contributes to radiation within the environment and is the second-leading cause of lung cancer worldwide. Although many environmental toxins have been linked to maladaptive neurodevelopmental outcomes in children and adolescents, radon has seldom been examined for its effects on the developing brain. This study aimed to investigate the effects of chronic home radon exposure on top-down neural processes of cognitive control in youths. Fifty-nine participants (aged 6–14 years) completed a Simon interference task during magnetoencephalography (MEG), and radon levels were measured in their homes. MEG data were transformed into time-frequency space and significant oscillatory responses relative to baseline were imaged condition-wise and then subtracted to isolate the Simon interference effect (i.e., Simon-control). Whole-brain linear regressions indicated that children with greater radon exposure exhibited aberrant oscillatory activity in widespread networks related to attentional control. We also found that radon exposure moderated the developmental trajectory of theta and gamma oscillations underlying selective attention in frontoparietal cortices and other regions. Further, mediation analyses showed that the neural interference effects within cerebellar and extended motor cortices mediated the relationship between radon exposure and behavioral outcomes. Additionally, we found the mediating effects of neural interference within the left superior frontal gyrus and precuneus on the relationship between age and task accuracy were dependent on radon exposure. These data are among the first to demonstrate radon-related disruptions to the normative development of the neural substrates supporting cognitive control processes. Further, these disruptions have direct implications on observable behavior.

We aim to provide an overview of the research available on indoor radon and lung cancer, with a special focus on Spanish investigations. Early studies on underground miners established the link between radon and lung cancer, which was later confirmed for the general population by residential case–control studies. Spain contributed with extensive evidence, including 5 multicentric, hospital-based, case–control studies in the last 30 years, exploring diverse aspects, such as radon's effect on never-smokers, molecular pathways linking radon exposure to lung cancer risk, survival rates, mortality burden, and occupational exposure. There is a well-established causal association between radon with lung cancer. Despite pioneering research performed in our country by the Galician Radon Laboratory, particularly on driver genes, the evidence on the potential molecular pathways which makes radon a carcinogen is sparse. Also, relevant questions on the potential association of radon exposure with the induction of other diseases are still pending.

After smoking, residential radon is the second risk factor of lung cancer in general population and the first in never-smokers. Previous studies have analyzed radon attributable lung cancer mortality for some countries. We aim to identify, summarize, and critically analyze the available data regarding the mortality burden of lung cancer due to radon, performing a quality assessment of the papers included, and comparing the results from different countries. We performed a systematic scoping review using the main biomedical databases. We included original studies with attributable mortality data related to radon exposure. We selected studies according to specific inclusion and exclusion criteria. PRISMA 2020 methodology and PRISMA Extension for Scoping Reviews requirements were followed. Data were abstracted using a standardized data sheet and a tailored scale was used to assess quality. We selected 24 studies describing radon attributable mortality derived from 14 different countries. Overall, 13 studies used risk models based on cohorts of miners, 8 used risks from residential radon case-control studies and 3 used both risk model options. Radon geometric mean concentration ranged from 11 to 83 Becquerels per cubic meter (Bq/m3) and the population attributable fraction (PAF) ranged from 0.2 to 26%. Studies performed in radon prone areas obtained the highest attributable mortality. High-quality publications reported PAF ranging from 3 to 12% for residential risk sources and from 7 to 25% for miner risk sources. Radon PAF for lung cancer mortality varies widely between studies. A large part of the variation is due to differences in the risk source used and the conceptual description of radon exposure assumed. A common methodology should be described and used from now on to improve the communication of these results.