Radon-induced Lung Cancer Risk Research Articles

Rural communities experience higher radon exposure versus urban areas, potentially due to drilled groundwater well annuli acting as unintended radon gas migration conduits

Repetitive, long-term inhalation of radioactive radon gas is one of the leading causes of lung cancer, with exposure differences being a function of geographic location, built environment, personal demographics, activity patterns, and decision-making. Here, we examine radon exposure disparities across the urban-to-rural landscape, based on 42,051 Canadian residential properties in 2034 distinct communities. People living in rural, lower population density communities experience as much as 31.2% greater average residential radon levels relative to urban equivalents, equating to an additional 26.7 Bq/m3 excess in geometric mean indoor air radon, and an additional 1 mSv/year in excess alpha radiation exposure dose rate to the lungs for occupants. Pairwise and multivariate analyses indicate that community-based radon exposure disparities are, in part, explained by increased prevalence of larger floorplan bungalows in rural areas, but that a majority of the effect is attributed to proximity to, but not water use from, drilled groundwater wells. We propose that unintended radon gas migration in the annulus of drilled groundwater wells provides radon migration pathways from the deeper subsurface into near-surface materials. Our findings highlight a previously under-appreciated determinant of radon-induced lung cancer risk, and support a need for targeted radon testing and reduction in rural communities.

Health Effects of Natural Environmental Radiation during Burning Season in Chiang Mai, Thailand.

This paper presents the first measurement of the investigation of the health impacts of indoor radon exposure and external dose from terrestrial radiation in Chiang Mai province during the dry season burning between 2018 and 2020. Indoor radon activity concentrations were carried out using a total of 220 RADUET detectors in 45 dwellings of Chiang Mai (7 districts) during burning and non-burning seasons. Results show that indoor radon activity concentration during the burning season (63 ± 33 Bq/m3) was significantly higher (p < 0.001) compared to the non-burning season (46 ± 19 Bq/m3), with an average annual value of 55 ± 28 Bq/m3. All values of indoor radon activity concentration were greater than the national (16 Bq/m3) and worldwide (39 Bq/m3) average values. In addition, the external dose from terrestrial radiation was measured using a car-borne survey during the burning season in 2018. The average absorbed rate in the air was 66 nGy/h, which is higher than the worldwide average value of 59 nGy/h. This might be due to the high activity concentrations of 238U and 323Th in the study area. With regards to the health risk assessment, the effective dose due to indoor radon exposure, external (outdoor) effective dose, and total annual effective dose were 1.6, 0.08, and 1.68 mSv/y, respectively. The total annual effective dose is higher than the worldwide average of 1.15 mSv/y. The excess lifetime cancer risk and radon-induced lung cancer risk during the burning season were 0.67% and 28.44 per million persons per year, respectively. Our results substantiate that indoor radon and natural radioactive elements in the air during the burning season are important contributors to the development of lung cancer.

A Mixed Methods Population Health Approach to Explore Radon-Induced Lung Cancer Risk Perception in Canada.

BackgroundRadon is a predominant indoor air pollutant and second leading cause of lung cancer in radon-prone areas. Despite the gravity of the health risk, residents in Canada have inadequate perception and taken minimal protective actions. Better perception of a risk motivates people to take preventive measures. Scholarship about radon health risk perception is lacking in Canada. We applied a mixed methods population health approach to explore the determinants shaping perception and actions of a resident population in Canada.MethodsWe conducted mixed surveys (n = 557) and qualitative bilingual interviews (n = 35) with both homeowners and tenants of Ottawa–Gatineau areas. The study explored residents' risk perception and adaptations factors. Descriptive, correlational and regression analyses described and established associations between quantitative variables. Thematic, inductive analyses identified themes in the qualitative data. A mixed methods analysis triangulated both results to draw a holistic perception of the health risk.ResultsResidents’ quantitative perceptions of radon health risk, smoking at home, synergistic risk perception, social influence and care for family were associated significantly with their intention to test for radon levels in their home, actual testing and mitigation. These results were explained further with the qualitative findings. Residents who had dual cognitive and emotional awareness of the risk were motivated enough to take preventive actions. Caring for family, knowing others who contracted lung cancer and financial capability were enablers, whereas lack of awareness and homeownership, cost of mitigation and stigma were obstacles to preventive actions. We also explored the dual subjective and objective aspects of risk perception that are influenced by micro- and macro-level determinants.ConclusionsInducing protective action to reduce risk requires comprehensive population-level interventions considering dual perceptions of the risk that can modify the risk determinants. Future research can explore the dual aspects of risk perception and unequal distribution of the risk factors.

Association of polymorphism &lt;i&gt;TP53&lt;/i&gt; Arg72Pro with radon-induced lung cancer in the Kazakh population

Lung cancer is a problem of great concern and one of the commonest cancer diseases worldwide and in the Republic of Kazakhstan in particular. Radon exposure is classified as the second most important cause of lung cancer. According to the experts, the contribution of natural sources to the average annual radiation dose of the Kazakh population currently stands at 80 %, including 50 % from radon. However, the effect of radon on human health in the Republic of Kazakhstan is almost unknown. The tumor suppressor gene TP53 is a key mediator of the DNA damage response cascade following cell exposure to ionizing radiation. The common polymorphism TP53 Arg72Pro (rs1042522) is a risk factor for lung cancer in the Asian population, but until now no genetic association studies have been done in the Kazakh population. No information on the synergistic carcinogenic effect of radon exposure and polymorphism TP53 Arg72Pro (rs1042522) is available either. This paper presents the results of the study of association between alteration in the TP53 gene and radon-induced lung cancer risk in the Kazakh population. Genetic association was assessed in a case-control study including 44 radon-exposed patients with lung cancer, 41 patients with lung cancer without radon exposure and 42 age/sex-matched healthy controls. We found that polymorphism TP53 Arg72Pro (rs1042522) was associated with lung cancer risk in the Kazakh population (OR = 6.95, 95 % CI = 2.41–20.05). Individuals with the Arg72Pro genotype also showed a significantly higher risk of radon-induced lung cancer (OR = 8.6, 95 % CI = 2.6–28.59).

First indoor radon mapping and assessment excess lifetime cancer risk in Iran

Radon (222Rn) is believed to be the main contributor to lung cancer second to smoking. The first national indoor radon map derived from some scattered regional radon surveys in Iran.The arithmetic mean of indoor radon concentration was calculated to 117.4 ± 97.7 Bq/m3. The mean excess life time cancer risk (ELCR) values were found to be in the range of 0.1%–4.26%, with an overall average value of 1.01%. The mean radon-induced lung cancer risk was 46.8 per million persons. Absence of sufficient indoor radon data showed that national wide monitoring programs should be activated in uncovered areas.Meanwhile, in order to provide further baseline values for radon mapping, we attempted to survey the radon levels inside 50 dwellings of Shabestar County in northwest of Iran. The investigation was also focused on the effects of some buildings related variables. The radon levels recorded varied from 3.92 to 520.12 Bq/m3, with a mean value of 56.19 ± 45.96 Bq/m3. In 9% of dwellings radon concentration exceeded 100 Bq/m3, the limit recommended by the World Health Organization. The average annual effective dose received by the residents of studied area was calculated to be 1.4 mSv. The ELCR was estimated to be 0.54%.

P2.10-15 RADON: #1 Cause of Lung Cancer in Non-Smokers

Radon, a known carcinogen, is a radioactive gas that occurs naturally when the uranium in soil and rock breaks down. It is invisible, odourless and tasteless. When radon is released from the ground into the outdoor air, it is diluted and is not a concern. However, in enclosed spaces, like homes, it can sometimes accumulate to high levels, which can be a risk to the health of you and your family. Radon gas breaks down or decays to form radioactive elements that can be inhaled into the lungs. In the lungs, decay continues, creating radioactive particles that release small bursts of energy. This energy is absorbed by nearby lung tissue, damaging the lung cells. The World Health Organization has identified radon exposure being the second leading cause of lung cancer after tobacco smoking. Recent epidemiological studies on indoor radon and lung cancer in Europe, North America and Asia provided strong evidence that radon causes a substantial number of lung cancers in the general population. Using the risk model developed by the US Environmental Protection Agency and with the radon distribution obtained from a recent cross-Canada radon survey in about 14,000 homes, the Canadian age-specific rates for overall and lung cancer mortality rates averaged over five years from 2008 to 2012 and the Canadian age specific smoking prevalence data in 2002, the Canadian population risk for radon induced lung cancer was assessed. The population risk of radon-induced lung cancer is assessed by an attributable risk (AR). The ARs for Canadian males are 0.15 for ever-smokers and 0.29 for never-smokers. For Canadian females, the ARs are 0.14 for ever-smokers and 0.28 for never-smokers. The detailed breakdown of AR in different radon ranges showed that the risk increases with increased radon concentration. Based on the more accurate radon distribution characteristics obtained from the recent cross-Canada radon survey, the Canadian population risk of radon-induced lung cancer was assessed. The theoretical estimates show that about 14 – 16% of lung cancer deaths among Canadians are attributable to indoor radon exposure. The results strongly suggest that it is important to test your homes for radon, and take actions as required to effectively prevent and reduce radon-induced lung cancer.

Genetic modifiers of radon-induced lung cancer risk: a genome-wide interaction study in former uranium miners.

Radon is a risk factor for lung cancer and uranium miners are more exposed than the general population. A genome-wide interaction analysis was carried out to identify genomic loci, genes or gene sets that modify the susceptibility to lung cancer given occupational exposure to the radioactive gas radon. Samples from 28 studies provided by the International Lung Cancer Consortium were pooled with samples of former uranium miners collected by the German Federal Office of Radiation Protection. In total, 15,077 cases and 13,522 controls, all of European ancestries, comprising 463 uranium miners were compared. The DNA of all participants was genotyped with the OncoArray. We fitted single-marker and in multi-marker models and performed an exploratory gene-set analysis to detect cumulative enrichment of significance in sets of genes. We discovered a genome-wide significant interaction of the marker rs12440014 within the gene CHRNB4 (OR = 0.26, 95% CI 0.11-0.60, p = 0.0386 corrected for multiple testing). At least suggestive significant interaction of linkage disequilibrium blocks was observed at the chromosomal regions 18q21.23 (p = 1.2 × 10-6), 5q23.2 (p = 2.5 × 10-6), 1q21.3 (p = 3.2 × 10-6), 10p13 (p = 1.3 × 10-5) and 12p12.1 (p = 7.1 × 10-5). Genes belonging to the Gene Ontology term "DNA dealkylation involved in DNA repair" (GO:0006307; p = 0.0139) or the gene family HGNC:476 "microRNAs" (p = 0.0159) were enriched with LD-blockwise significance. The well-established association of the genomic region 15q25 to lung cancer might be influenced by exposure to radon among uranium miners. Furthermore, lung cancer susceptibility is related to the functional capability of DNA damage signaling via ubiquitination processes and repair of radiation-induced double-strand breaks by the single-strand annealing mechanism.

A DISCUSSION ON DIFFERENT APPROACHES FOR ASSESSING LIFETIME RISKS OF RADON-INDUCED LUNG CANCER.

Lifetime risks of radon induced lung cancer were assessed based on epidemiological approaches for Canadian, Swiss and Chinese populations, using the most recent vital statistic data and radon distribution characteristics available for each country. In the risk calculation, the North America residential radon risk model was used for the Canadian population, the European residential radon risk model for the Swiss population, the Chinese residential radon risk model for the Chinese population, and the EPA/BEIR-VI radon risk model for all three populations. The results were compared with the risk calculated from the International Commission on Radiological Protection (ICRP)'s exposure-to-risk conversion coefficients. In view of the fact that the ICRP coefficients were recommended for radiation protection of all populations, it was concluded that, generally speaking, lifetime absolute risks calculated with ICRP-recommended coefficients agree reasonably well with the range of radon induced lung cancer risk predicted by risk models derived from epidemiological pooling analyses.

The assumption of radon-induced cancer risk

We read with interest the article by Axelsson et al. [1] about the potential risk of lung cancer due to inhalation of radioactive radon gas. Indeed, this has been the subject of many scientific papers around the world for years without clarification of whether there is risk or there is no risk when the radon concentration is low. The paper by Axelsson et al. [1] states that ‘‘residential exposure to radon is considered to be the second cause of lung cancer after smoking.’’ The authors cite the publications of many well-known radon experts, especially the analysis of 13 European case–control studies by Darby et al. [2]. They underscore their basic argument that in Sweden, there is a 16 % increase in the risk of radoninduced lung cancer per 100 Bq/m. However, there appear to be logical mistakes in their reasoning, which are presented below. The first mistake concerns their chosen dose–response model. They determine the 16 % increase in risk per 100 Bq/m by using the linear no-threshold (LNT) hypothesis. According to this hypothesis, the excess risk increases linearly versus Bq/m (or vs. mSv effective dose) from zero to the maximum. There are no data that support the validity of this hypothesis over the whole range of doses. All existing studies are subject to a number of limitations. Moreover, there is a huge scatter in the results, so it is impossible to reach a coherent conclusion [3]. In fact, the LNT hypothesis has been criticized fundamentally in many independent studies [4]. The second fallacy—the ‘‘zero radon environment’’—is related to the previous one. The authors [1] widely invoke the value ‘‘0 Bq/m,’’ which makes no sense from both the All signers of this letter are members or associate members of SARI (Scientists for Accurate Radiation Information, http://radiationeffects. org/). The above letter represents the professional opinions of the signers and does not necessarily represent the views of their affiliated institutions.

Calculation of lifetime lung cancer risks associated with radon exposure, based on various models and exposure scenarios

The risk of lung cancer mortality up to 75 years of age due to radon exposure has been estimated for both male and female continuing, ex- and never-smokers, based on various radon risk models and exposure scenarios. We used risk models derived from (i) the BEIR VI analysis of cohorts of radon-exposed miners, (ii) cohort and nested case-control analyses of a European cohort of uranium miners and (iii) the joint analysis of European residential radon case-control studies. Estimates of the lifetime lung cancer risk due to radon varied between these models by just over a factor of 2 and risk estimates based on models from analyses of European uranium miners exposed at comparatively low rates and of people exposed to radon in homes were broadly compatible. For a given smoking category, there was not much difference in lifetime lung cancer risk between males and females. The estimated lifetime risk of radon-induced lung cancer for exposure to a concentration of 200 Bq m−3 was in the range 2.98–6.55% for male continuing smokers and 0.19–0.42% for male never-smokers, depending on the model used and assuming a multiplicative relationship for the joint effect of radon and smoking. Stopping smoking at age 50 years decreases the lifetime risk due to radon by around a half relative to continuing smoking, but the risk for ex-smokers remains about a factor of 5–7 higher than that for never-smokers. Under a sub-multiplicative model for the joint effect of radon and smoking, the lifetime risk of radon-induced lung cancer was still estimated to be substantially higher for continuing smokers than for never smokers. Radon mitigation—used to reduce radon concentrations at homes—can also have a substantial impact on lung cancer risk, even for persons in their 50 s; for each of continuing smokers, ex-smokers and never-smokers, radon mitigation at age 50 would lower the lifetime risk of radon-induced lung cancer by about one-third. To maximise risk reductions, smokers in high-radon homes should both stop smoking and remediate their homes.

Evaluation of radon induced lung cancer risk in occupants of the old and new dwellings of the Dera Ismail Khan City, Pakistan

In order to carry out indoor radon measurement in new and old buildings of the Dera Ismail Khan city, CR-39 based radon detectors were installed in bed rooms and sitting rooms/TV lounges in 25 (each) old and new houses and were exposed to indoor radon for 90 days. After processing, mean weighted average indoor radon concentrations in old and new houses were found to be 275 ± 33 and 86 ± 18 Bq m−3 whereas mean annual effective doses expected to be received by the occupants were 6.86 ± 0.79 and 2.1 ± 0.43 mSv year−1, respectively. From the measured weighted average indoor radon concentration, excess relative risk factor was calculated using the risk model of BEIR VI for the age group of 35 and 55 years. Average excess lung cancer risk was found to be 1.63 ± 0.19 and 1.35 ± 0.16 and 0.5 ± 0.10 and 0.4 ± 0.08 for old and new houses, respectively.

Modelling the effect of non-uniform radon progeny activities on transformation frequencies in human bronchial airways

The effects of radiological and morphological source heterogeneities in straight and Y-shaped bronchial airways on hit frequencies and microdosimetric quantities in epithelial cells have been investigated previously. The goal of the present study is to relate these physical quantities to transformation frequencies in sensitive target cells and to radon-induced lung cancer risk. Based on an effect-specific track length model, computed linear energy transfer (LET) spectra were converted to corresponding transformation frequencies for different activity distributions and source-target configurations. Average transformation probabilities were considerably enhanced for radon progeny accumulations and target cells at the carinal ridge, relative to uniform activity distributions and target cells located along the curved and straight airway portions at the same exposure level. Although uncorrelated transformation probabilities produce a linear dose-effect relationship, correlated transformations first increase depending on the LET, but then decrease significantly when exceeding a defined number of hits or cumulative exposure level.

Analysisof radon-induced lung cancer risk by a stochastic state-vectormodel of radiation carcinogenesis

A biologically based state-vector model (SVM) of radiationcarcinogenesis has been extended to incorporate stochasticityof cellular transitions and specific in vivoirradiation conditions in the lungs. Dose-rate-dependentcellular transitions related to the formation of double-stranded DNA breaks, repair of breaks, interactions(translocations) between breaks, fixation of breaks, cellularinactivation, stimulated mitosis and promotion through loss of intercellular communication are simulated by Monte Carlomethods. The stochastic SVM has been applied to the analysis oflung cancer incidence in uranium miners exposed toalpha-emitting radon progeny. When incorporating invivo features of cell differentiation, stimulated celldivision and heterogeneity of cellular doses into the model,excellent agreement between epidemiological data and modellingresults could be obtained. At low doses, the model predicts anon-linear dose-response relationship; e.g., computed lungcancer risk at 20 WLM is about half of current lung cancerestimates based on the linear hypothesis. The model alsopredicts a slight dose rate effect; e.g., at a cumulativeexposure of 20 WLM, calculated lung cancer incidence for anexposure rate 0.27 WLM/year (assuming an exposure time of 73 years) is smaller by a factor of 1.2 than that for anexposure rate of 10 WLM/year.

Influence of Exposure Rate on Lung Cancer Induction in Rats Exposed to Radon Progeny

Animal studies were used in addition to epidemiological studies to investigate the effects of exposure, exposure rate and other factors in predicting risks resulting from exposures to radon progeny. A trend toward increasing tumor risk with decreasing exposure rate was observed in rats exposed at a cumulative exposure varying from about 0.72 J h m(-3) (200 WLM) up to 10.8 J h m(-3) (3,000 WLM) and high exposure rates varying from 25 WLM per week to 500 WLM per week. In contrast, at low cumulative exposure, comparable to lifetime domestic indoor exposures or lifetime occupational exposure in uranium mines, no evidence of an inverse exposure-rate effect was found. Chronic radon exposure at 0.09 J h m(-3) (25 WLM), protracted over 18 months, at a potential alpha-particle energy concentration (PAEC) of 0.042 mJ m(-3) (2 WL), resulted in fewer lung carcinomas in rats than a similar cumulative exposure protracted over 4 to 6 months at a PAEC of 2.1 mJ m(-3) (100 WL). The preliminary results of a new series of experiments carried out at relatively low cumulative exposures of 0.36 J h m(-3) (100 WLM) and PAEC varying from 0.21 mJ m(-3) (10 WL) to 3.15 mJ m(-3) (150 WL) indicate that at cumulative exposures comparable to lifetime indoor or occupational exposures, the risk of lung cancer in rats decreases with decreasing PAEC, i.e. exposure rate. These data suggest that the risk of radon-induced lung cancer results from a complex interplay between cumulative exposure and exposure rate at a given exposure level.

A Survey of Radon Levels in Jordanian Dwellings During an Autumn Season

Previously calibrated dosemeters containing CR-39 plastic detectors were used to measure radon levels in Jordanian cities during the autumn. The averages of radon concentrations in the different cities obtained in this work range from 29.3 to 99.7 Bq.m -3 . It was found that the city of Karak possesses the highest radon concentrations and the city of Aqaba possesses the lowest. Thus, the calculated average radon levels in Jordanian dwellings as a whole was found to be 56.7 Bq.m -3 . The average radon induced lung cancer risk during a lifetime for dwellers of the cities under study was found to range from 0.12% to 0.41%.

Errors in Exposure Assessment, Statistical Power and the Interpretation of Residential Radon Studies

To date, epidemiological studies of risk from residential radon have not convincingly demonstrated an association with lung cancer. These case-control studies, however, have inherent limitations due to errors in estimates of exposure to indoor radon. These errors take on special significance because the level of residential risk predicted from studies of underground miners is relatively low and possibly at the limit detectable by current epidemiological methods. To illustrate the problem caused by errors in exposure assessment, a series of case-control studies were simulated and resulting dose-response relationships evaluated. For each of four assumed error distributions for exposure to radon progeny, 10 indoor radon studies of 700 cases and 700 controls were generated randomly from a population with a risk of radon-induced lung cancer based on extrapolations from studies of underground miners. When exposures were assumed as known without error, 6 of 10 studies failed to find a significant dose response, in accord with the theoretical power of the study of 0.47. For simulations in which exposures were measured with error, the situation was worse, as the power of the study was reduced further and it was even less likely that a single study would result in a significant finding. For each error scenario, combining data from the 10 simulated studies did result in a significant dose response. However, the pooled results are somewhat misleading, because the effects of mobility, missing radon measurements, residential occupancy and potential confounding variables such as cigarette smoking were not taken into account. Empirical estimates of power were computed using 1,000 simulated case-control studies. When mobility and missing radon measurements in prior homes were incorporated into the design, the power of the study decreased, reducing the chance of detecting a significant effect of exposure. Enlarging study size to 2,000 cases and 2,000 controls increased the power of the study to 0.90 when exposure error was absent and subjects lived in one home only, but power was below 0.40 under realistic conditions for exposure error and mobility. When studies were generated under an assumption that exposure does not increase risk, up to 15% of simulated studies with 700 cases and 700 controls resulted in an estimated dose-response parameter in excess of the dose response from studies of miners. With increasing mobility and exposure error, it became virtually impossible to distinguish between the distributions of risk estimates from simulated studies based on an underlying excess relative risk of 0.015/working level month from estimates based on no risk from exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

Modelling the modification of the risk of radoninduced lung cancer by environmental tobacco smoke.

Modelling the modification of the risk of radoninduced lung cancer by environmental tobacco smoke.

A Dose Rate Model Predicting Radon-Induced Lung Cancer Risk in Rats

A Dose Rate Model Predicting Radon-Induced Lung Cancer Risk in Rats

A Dose Rate Model Predicting Radon-Induced Lung Cancer Risk in Rats

A Dose Rate Model Predicting Radon-Induced Lung Cancer Risk in Rats

Radon risk assessment: The effect of voluntary sampling distributions and bias

This paper examines the problem of estimating indoor radon concentrations for radon-induced lung cancer risk assessment. Previous authors have identified various problems and possible corrections for the use of generally available radon screening measurements. Bias evident in data collected from volunteers is described; regional databases developed from voluntary data generally exhibit higher mean values than those obtained from random samples. Tools are developed to better characterize the differences in voluntary and random concentration distributions. Application is demonstrated using voluntary and random radon survey data for the state of North Dakota.