Radon and lung cancer risk.
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ABSTRACT:
SUBMITTER: Mema SC
PROVIDER: S-EPMC10281200 | biostudies-literature | 2023 Jun
REPOSITORIES: biostudies-literature
Publications
Radon and lung cancer risk.
Mema Silvina C SC Baytalan Greg G
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 20230601 24
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Project description:ObjectiveTo investigate the effect of reducing home ventilation as part of household energy efficiency measures on deaths from radon related lung cancer.DesignModelling study.SettingEngland.InterventionHome energy efficiency interventions, motivated in part by targets for reducing greenhouse gases, which entail reduction in uncontrolled ventilation in keeping with good practice guidance.Main outcome measuresModelled current and future distributions of indoor radon levels for the English housing stock and associated changes in life years due to lung cancer mortality, estimated using life tables.ResultsIncreasing the air tightness of dwellings (without compensatory purpose-provided ventilation) increased mean indoor radon concentrations by an estimated 56.6%, from 21.2 becquerels per cubic metre (Bq/m(3)) to 33.2 Bq/m(3). After the lag in lung cancer onset, this would result in an additional annual burden of 4700 life years lost and (at peak) 278 deaths. The increases in radon levels for the millions of homes that would contribute most of the additional burden are below the threshold at which radon remediation measures are cost effective. Fitting extraction fans and trickle ventilators to restore ventilation will help offset the additional burden but only if the ventilation related energy efficiency gains are lost. Mechanical ventilation systems with heat recovery may lower radon levels and the risk of cancer while maintaining the advantage of energy efficiency for the most airtight dwellings but there is potential for a major adverse impact on health if such systems fail.ConclusionUnless specific remediation is used, reducing the ventilation of dwellings will improve energy efficiency only at the expense of population wide adverse impact on indoor exposure to radon and risk of lung cancer. The implications of this and other consequences of changes to ventilation need to be carefully evaluated to ensure that the desirable health and environmental benefits of home energy efficiency are not compromised by avoidable negative impacts on indoor air quality.
| S-EPMC3898159 | biostudies-literature
Project description:BackgroundA determination of the risk of lung cancer at low levels of radon exposure is important for occupational radiation protection.MethodsThe risk of death from lung cancer at low radon exposure rates was investigated in the subcohort of 26,766 German uranium miners hired in 1960 or later.ResultsA clear association between lung cancer mortality (n=334 deaths) and cumulative exposure to radon in working level months (WLM) was found. The excess relative risk per WLM was 0.013 (95% confidence intervals: 0.007; 0.021).ConclusionsThe present findings provide strong evidence for an increased lung cancer risk after long-term exposure to low radon exposure rates among Wismut miners. The results are compatible to those from residential radon studies and miner studies restricted to low levels.
| S-EPMC4815799 | biostudies-literature
Project description:Radon is the number one cause of lung cancer in non-smokers. microRNA expression in human bronchial epithelium cells is altered by radon, with particular reference to upregulation of miR-16, miR-15, miR-23, miR-19, miR-125, and downregulation of let-7, miR-194, miR-373, miR-124, miR-146, miR-369, and miR-652. These alterations alter cell cycle, oxidative stress, inflammation, oncogene suppression, and malignant transformation. Also DNA methylation is altered as a consequence of miR-29 modification induced by radon. Indeed miR-29 targets DNA methyltransferases causing inhibition of CpG sites methylation. Massive microRNA dysregulation occurs in the lung due to radon expose and is functionally related with the resulting lung damage. However, in humans this massive lung microRNA alterations only barely reflect onto blood microRNAs. Indeed, blood miR-19 was not found altered in radon-exposed subjects. Thus, microRNAs are massively dysregulated in experimental models of radon lung carcinogenesis. In humans these events are initially adaptive being aimed at inhibiting neoplastic transformation. Only in case of long-term exposure to radon, microRNA alterations lead towards cancer development. Accordingly, it is difficult in human to establish a microRNA signature reflecting radon exposure. Additional studies are required to understand the role of microRNAs in pathogenesis of radon-induced lung cancer.
| S-EPMC7139524 | biostudies-literature
Project description: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.
| S-EPMC6192894 | biostudies-other
Project description:Introduction:Radon and its decay products may cause substantial health damage after long-term exposure. The aim of the study was to perform a spatial analysis of radon concentration in the Salento peninsula, province of Lecce (South-eastern Italy) in order to better characterize possible risk for human health, with specific focus on lung cancer. Methods:Based on previous radon monitoring campaigns carried out in 2006 on behalf of the Local Health Authority (ASL Lecce) involving 419 schools and through the application of kriging estimation method, a radon risk map was obtained for the province of Lecce, in order to determine if areas with higher radon concentrations were overlapping with those characterized by the highest pulmonary cancer incidence and mortality rates. Results:According to our data, areas at higher radon concentrations seem to overlap with those characterized by the highest pulmonary cancer mortality and incidence rates, thus indicating that human exposure to radon could possibly enhance other individual or environmental pro-carcinogenic risk factors (i.e. cigarette smoking, air pollution and other exposures). Conclusions:The radon risk should be further assessed in the evaluation of the causes resulting in higher mortality and incidence rates for pulmonary cancer in Salento area vs Italian average national data. For these reasons, ASL Lecce in cooperation with ARPA Puglia and CNR-IFC has included the monitoring of individual indoor radon concentrations in the protocol of PROTOS case-control Study, aimed at investigating the role of different personal and environmental risk factors for lung cancer in Salento.
| S-EPMC7225648 | biostudies-literature
Project description: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.
| S-EPMC7796069 | biostudies-literature
Project description:BackgroundRadon is the second most important cause of lung cancer, ranked by the World Health Organization as the fifth leading cause of mortality in 2010. An updated database of national radon exposures for 66 countries allows the global burden of lung cancer mortality attributable to radon to be estimated.ObjectiveOur goal was to estimate the global population attributable burden of lung cancer mortality in 2012 from residential radon.MethodsEstimates of the population attributable risk (PAR) of lung cancer mortality from radon were determined using the attributable fraction approach, using three models for excess relative risk of lung cancer from radon.ResultsThe estimates of the median PAR of lung cancer mortality from residential radon in 2012 for the 66 countries having representative national radon surveys were consistent, as 16.5%, 14.4%, and 13.6% for the exposure-age-concentration (EAC) model (BEIR VI), the Hunter model, and the Kreuzer model, respectively. The mean PAR using the EAC model ranged from 4.2% (95% CI: 0.9, 11.7) for Japan, to 29.3% (95% CI: 22.9, 35.7) for Armenia, with a median for the 66 countries of 16.5%. Radon-attributable lung cancer deaths for all 66 countries totaled 226,057 in 2012 and represent a median of 3.0% of total cancer deaths.ConclusionsConsistent findings between the three models used to estimate excess relative risks of lung cancer from radon, and between the attributable fraction methodology and the life table analysis, confirm that residential radon is responsible for a substantial proportion of lung cancer mortality worldwide. https://doi.org/10.1289/EHP2503.
| S-EPMC6072010 | biostudies-literature
Project description:This study aimed to estimate (1) the number of avoidable lung cancer cases attributable to residential radon in Finland in 2017, separately by age, sex, dwelling type and smoking status, (2) the impact of residential radon alone and the joint effect of residential radon and smoking on the number of lung cancers and (3) the potential decrease in the number of radon-attributable lung cancers if radon concentrations exceeding specified action levels (100, 200 and 300 Bq m-3) would have been mitigated to those levels. Population-based surveys of radon concentrations and smoking patterns were used. Observed radon levels were contrasted with 25 Bq m-3 representing a realistic minimum level of exposure. Lung cancer risk estimates for radon and smoking were derived from literature. Lastly, the uncertainty due to the estimation of exposure and risk was quantified using a computationally derived uncertainty interval. At least 3% and at most 8% of all lung cancers were estimated as being attributable to residential radon. For small cell carcinoma, the proportion of cases attributable to radon was 8-13%. Among smokers, the majority of the radon-related cases were attributable to the joint effect of radon and smoking. Reduction of radon exposure to 100 Bq m-3 action level would eliminate approximately 30% of radon-attributable cases. Estimates were low compared with the literature, given the (relatively high) radon levels in Finland. This was mainly due to the lower radon levels and higher smoking prevalence in flats than in houses and a more realistic point of comparison, factors which have been ignored in previous studies. The results can guide actions in radon protection and in prevention of lung cancers.
| S-EPMC9950193 | biostudies-literature
Project description:BackgroundLung cancer is the leading cause of cancer-related death worldwide, for which smoking is considered as the primary risk factor. The present study was conducted to determine whether genetic alterations induced by radon exposure are associated with the susceptible risk of lung cancer in never smokers.MethodsTo accurately identify mutations within individual tumors, next generation sequencing was conduct for 19 pairs of lung cancer tissue. The associations of germline and somatic variations with radon exposure were visualized using OncoPrint and heatmap graphs. Bioinformatic analysis was performed using various tools.ResultsAlterations in several genes were implicated in lung cancer resulting from exposure to radon indoors, namely those in epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), NK2 homeobox 1 (NKX2.1), phosphatase and tensin homolog (PTEN), chromodomain helicase DNA binding protein 7 (CHD7), discoidin domain receptor tyrosine kinase 2 (DDR2), lysine methyltransferase 2C (MLL3), chromodomain helicase DNA binding protein 5 (CHD5), FAT atypical cadherin 1 (FAT1), and dual specificity phosphatase 27 (putative) (DUSP27).ConclusionsWhile these genes might regulate the carcinogenic pathways of radioactivity, further analysis is needed to determine whether the genes are indeed completely responsible for causing lung cancer in never smokers exposed to residential radon.
| S-EPMC5751841 | biostudies-literature
Project description:Effective targeted treatment strategies resulted from molecular profiling of lung cancer with distinct prevalent mutation profiles in smokers and non-smokers. Although Rn is the second most important risk factor, data for Rn-dependent driver events are limited. Therefore, a Rn-exposed cohort of lung cancer patients was screened for oncogenic drivers and their survival and genetic profiles were compared with data of the average regional population. Genetic alterations were analysed in 20 Rn-exposed and 22 histologically matched non-Rn exposed LC patients using targeted Next generation sequencing (NGS) and Fluorescence In Situ Hybridization (FISH). Sufficient material and sample quality could be obtained in 14/27 non-exposed versus 17/22 Rn-exposed LC samples. Survival was analysed in comparison to a histologically and stage-matched regional non-exposed lung cancer cohort (n = 51) for hypothesis generating. Median overall survivals were 83.02 months in the Rn-exposed and 38.7 months in the non-exposed lung cancer cohort (p = 0.22). Genetic alterations of both patient cohorts were in high concordance, except for an increase in MET alterations and a decrease in TP53 mutations in the Rn-exposed patients in this small hypothesis generating study.
| S-EPMC9600309 | biostudies-literature