Residential Radon Exposure and Cigarette Smoking in Association with Lung Cancer: A Matched Case-Control Study in Korea.
ABSTRACT: Residential radon exposure and cigarette smoking are the two most important risk factors for lung cancer. The combined effects thereof were evaluated in a multi-center matched case-control study in South Korea. A total of 1038 participants were included, comprising 519 non-small cell lung cancer cases and 519 age- and sex- matched community-based controls. Residential radon levels were measured for all participants. Multivariate logistic regression was used to calculate odds ratios (OR) for lung cancer according to radon exposure (high ? 100 Bq/m3 vs. low < 100 Bq/m3), smoking status, and combinations of the two after adjusting for age, sex, indoor hours, and other housing information. The median age of the participants was 64 years, and 51.3% were women. The adjusted ORs (95% confidence intervals [CIs]) for high radon and cigarette smoking were 1.56 (1.03-2.37) and 2.53 (1.60-3.99), respectively. When stratified according to combinations of radon exposure and smoking status, the adjusted ORs (95% CIs) for lung cancer in high-radon non-smokers, low-radon smokers, and high-radon smokers were 1.40 (0.81-2.43), 2.42 (1.49-3.92), and 4.27 (2.14-8.52), respectively, with reference to low-radon non-smokers. Both residential radon and cigarette smoking were associated with increased odds for lung cancer, and the difference in ORs according to radon exposure was much greater in smokers than in non-smokers.
Project description:Residential radon exposure is known to be an important risk factor for the development of lung cancer. The objective of this study was to calculate the disease burden of lung cancer attributable to residential radon exposure in Korea.We calculated the national exposure level using Korean national radon survey data from 2011 to 2014, and house structure distribution data from each administrative region. Using the exposure-risk function, the population attributable fraction (PAF) was calculated and applied to calculate the disease burden for lung cancer attributable to residential radon exposure.Residential radon exposure levels were the highest, at 116.4 ± 50.4 Bq/m3 (annual mean radon concentration ± standard deviation) in detached houses, followed by 74.1 ± 30.0 Bq/m3 in the multi-family dwellings, and 55.9 ± 21.1 Bq/m3 in apartments. The PAF for lung cancer, due to long-term radon exposure in Korean homes, was 6.6% and 4.7% in men and women, respectively. The total disease burden of lung cancer attributable to residential radon exposure was 14,866 years of life lost (YLL) and 1,586 years lost due to disability (YLD) in 2013. Overall, 1,039 deaths occurred due to residential radon exposure, of which 828 were in men and 211 in women.The smoking rate of men in Korea exceeded 70% in the 1990s, and is still near 40%. Although the size of the effect varies depending on the estimation method, it is a critical aspect as a risk factor of lung cancer because of the synergistic relationship between smoking and radon exposure. Because the Korean society is rapidly aging, population who were formerly heavy-smokers are entering a high-risk age of lung cancer. Therefore, it is necessary to inform the public about the health benefits of reduced radon exposure and to strengthen the risk communication.
Project description:Radon is carcinogenic, and exposure to radon has been shown to increase the risk of lung cancer. The objective of this study was to quantify the proportion and number of lung cancer cases in Alberta in 2012 that could be attributed to residential radon exposure.We estimated the population attributable risk of lung cancer for residential radon using radon exposure data from the Cross-Canada Survey of Radon Concentrations in Homes from 2009-2011 and data on all-cause and lung cancer mortality from Statistics Canada from 2008-2012. We used cancer incidence data from the Alberta Cancer Registry for 2012 to estimate the total number of lung cancers attributable to residential radon exposure. Estimates were also stratified by sex and smoking status.The mean geometric residential radon level in Alberta in 2011 was 71.0 Bq/m3 (geometric standard deviation 2.14). Overall, an estimated 16.6% (95% confidence interval 9.4%-29.8%) of lung cancers were attributable to radon exposure, corresponding to 324 excess attributable cancer cases. The estimated population attributable risk of lung cancer due to radon exposure was higher among those who had never smoked (24.8%) than among ever smokers (15.6%). However, since only about 10% of cases of lung cancer occur in nonsmokers, the estimated total number of excess cases was higher for ever smokers (274) than for never smokers (48).With about 17% of lung cancer cases in Alberta in 2012 attributable to residential radon exposure, exposure reduction has the potential to substantially reduce Alberta's lung cancer burden. As such, home radon testing and remediation techniques represent important cancer prevention strategies.
Project description:Human-made buildings can artificially concentrate radioactive radon gas of geologic origin, exposing occupants to harmful alpha particle radiation emissions that damage DNA and increase lung cancer risk. We examined how North American residential radon exposure varies by modern environmental design, occupant behaviour and season. 11,727 residential buildings were radon-tested using multiple approaches coupled to geologic, geographic, architectural, seasonal and behavioural data with quality controls. Regional residences contained 108?Bq/m3 geometric mean radon (min?<?15?Bq/m3; max 7,199?Bq/m3), with 17.8%???200?Bq/m3. Pairwise analysis reveals that short term radon tests, despite wide usage, display limited value for establishing dosimetry, with precision being strongly influenced by time of year. Regression analyses indicates that the modern North American Prairie residential environment displays exceptionally high and worsening radon exposure, with more recent construction year, greater square footage, fewer storeys, greater ceiling height, and reduced window opening behaviour all associated with increased radon. Remarkably, multiple test approaches reveal minimal winter-to-summer radon variation in almost half of properties, with the remainder having either higher winter or higher summer radon. This challenges the utility of seasonal correction values for establishing dosimetry in risk estimations, and suggests that radon-attributable cancers are being underestimated.
Project description:The inhalation of naturally occurring radon (222Rn) gas from indoor air exposes lung tissue to ?-particle bombardment, a highly mutagenic form of ionizing radiation that damages DNA and increases the lifetime risk of lung cancer. We analyzed household radon concentrations and risk factors in southern Alberta, including Calgary, the third-largest Canadian metropolis.A total of 2382 residential homes (2018 in Calgary and 364 in surrounding townships) from an area encompassing 82% of the southern Alberta population were tested for radon, per Health Canada guidelines, for at least 90 days (median 103 d) between 2013 and 2016. Participants also provided home metrics (construction year, build type, foundation type, and floor and room of deployment of the radon detector) via an online survey. Homes that were subsequently remediated were retested to determine the efficacy of radon reduction techniques in the region.The average indoor air radon level was 126 Bq/m3, which equates to an effective absorbed radiation dose of 3.2 mSv/yr. A total of 1135 homes (47.6%) had levels of 100 Bq/m3 or higher, and 295 homes (12.4%) had levels of 200 Bq/m3 or higher; the range was less than 15 Bq/m3 to 3441 Bq/m3. Homes built in 1992 or later had radon levels 31.5% higher, on average, than older homes (mean 142 Bq/m3 v. 108 Bq/m3). For 90 homes with an average radon level of 575 Bq/m3 before mitigation, radon suppression successfully reduced levels to an average of 32.5 Bq/m3.Our findings show that radon exposure is a genuine public health concern in southern Alberta, suggest that modern building practices are associated with increased indoor air radon accumulation, legitimatize efforts to understand the consequences of radon exposure to the public, and suggest that radon testing and mitigation are likely to be impactful cancer prevention strategies.
Project description:Background:Lung cancer in never smokers (LCINS) differs etiologically and clinically from lung cancer attributed to smoking. After smoking, radon exposure is the second leading cause and the primary risk factor of lung cancer among never smokers. Exposure to radon can lead to genetic and epigenetic alterations in tumor genomes affecting genes and pathways involved in lung cancer development. The present study sought to explore genetic alterations associated with LCINS exposed to radon gas indoors. Methods:Genetic associations were assessed via a case-control study of LCINS (39 cases and 30 controls) using next generation sequencing. Associations between genetic mutations and high exposure to radon were investigated by OncoPrint and heatmap graphs. Bioinformatic analysis was conducted using various tools. According radon exposure levels, we divided subjects in two groups of cases and controls. Results:We found that ABL2 rs117218074, SMARCA4 rs2288845, PIK3R2 rs142933317, MAPK1 rs1803545, and androgen receptor (AR) rs66766400 were associated with LCINS exposed to high radon levels. Among these, Chromodomain helicase DNA-binding protein 4 (CHD4) rs74790047, TSC2 rs2121870, and AR rs66766408 were identified as common exonic mutations in both lung cancer patients and normal individuals exposed to high levels of radon indoor. Conclusion:We identified that CHD4 rs74790047, TSC2 rs2121870, and AR rs66766408 are found to be common exonic mutations in both lung cancer patients and normal individuals exposed to radon indoors. Further analysis is needed to determine whether these genes are completely responsible for LCINS exposed to residential radon.
Project description:Epidemiological studies on residential radon exposure and the risk of histological types of lung cancer have yielded inconsistent results. We conducted a meta-analysis on this topic and updated previous related meta-analyses. We searched the databases of Cochrane Library, Embase, PubMed, Web of Science and Chinese National Knowledge Infrastructure for papers published up to 13 November 2018. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed and random effects models. Subgroup and dose?response analyses were also conducted. This study was registered with PROSPERO (No. CRD42019127761). A total of 28 studies, which included 13,748 lung cancer cases and 23,112 controls, were used for this meta-analysis. The pooled OR indicated that the highest residential radon exposure was significantly associated with an increased risk of lung cancer (OR = 1.48, 95% CI = 1.26-1.73). All histological types of lung cancer were associated with residential radon. Strongest association with small-cell lung carcinoma (OR = 2.03, 95% CI = 1.52-2.71) was found, followed by adenocarcinoma (OR = 1.58, 95% CI = 1.31-1.91), other histological types (OR = 1.54, 95% CI = 1.11-2.15) and squamous cell carcinoma (OR = 1.43, 95% CI = 1.18-1.74). With increasing residential radon levels per 100 Bq/m3, the risk of lung cancer, small-cell lung carcinoma and adenocarcinoma increased by 11%, 19% and 13%, respectively. This meta-analysis provides new evidence for a potential relationship between residential radon and all histological types of lung cancer.
Project description:BACKGROUND: Radon gas is considered as a main risk factor for lung cancer and found naturally in rock, soil, and water. The objective of this study was to determine the radon level in the drinking water sources in Nablus city in order to set up a sound policy on water management in Palestine. METHODS: This was a descriptive study carried out in two phases with a random sampling technique in the second phase. Primarily, samples were taken from 4 wells and 5 springs that supplied Nablus city residents. For each source, 3 samples were taken and each was analyzed in 4 cycles by RAD 7 device manufactured by Durridge Company. Secondly, from the seven regions of the Nablus city, three samples were taken from the residential tap water of each region. Regarding the old city, ten samples were taken. Finally, the mean radon concentration value for each source was calculated. RESULTS: The mean (range) concentration of radon in the main sources were 6.9 (1.5-23.4) Becquerel/liter (Bq/L). Separately, springs and wells' means were 4.6 Bq/L and 9.5 Bq/L; respectively. For the residential tap water in the 7 regions, the results of the mean (range) concentration values were found to be 1.0 (0.9-1.3) Bq/L. For the old city, the mean (range) concentration values were 2.3 (0.9-3.9) Bq/L. CONCLUSIONS: Except for Al-Badan well, radon concentrations in the wells and springs were below the United State Environmental Protection Agency maximum contaminated level (U.S EPA MCL). The level was much lower for tap water. Although the concentration of radon in the tap water of old city were below the MCL, it was higher than other regions in the city. Preventive measures and population awareness on radon's exposure are recommended.
Project description:Lung 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.To 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.Alterations 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).While 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.
Project description:Background: Radon (and its decay products) is a known human carcinogen and the leading cause of lung cancer in never-smokers and the second in ever-smokers. The carcinogenic mechanism from radiation is a combination of genetic and epigenetic processes, but compared to the genetic mechanisms, epigenetic processes remain understudied in humans. This study aimed to explore associations between residential radon exposure and DNA methylation in the general population. Methods: Potential residential radon exposure for 75-metre area buffers was linked to genome-wide DNA methylation measured in peripheral blood from children and mothers of the Accessible Resource for Integrated Epigenomic Studies subsample of the ALSPAC birth cohort. Associations with DNA methylation were tested at over 450,000 CpG sites at ages 0, 7 and 17 years (children) and antenatally and during middle-age (mothers). Analyses were adjusted for potential residential and lifestyle confounding factors and were determined for participants with complete data (n = 786 to 980). Results: Average potential exposure to radon was associated in an exposure-dependent manner with methylation at cg25422346 in mothers during pregnancy, with no associations at middle age. For children, radon potential exposure was associated in an exposure-dependent manner with methylation of cg16451995 at birth, cg01864468 at age 7, and cg04912984, cg16105117, cg23988964, cg04945076, cg08601898, cg16260355 and cg26056703 in adolescence. Conclusions: Residential radon exposure was associated with DNA methylation in an exposure-dependent manner. Although chance and residual confounding cannot be excluded, the identified associations may show biological mechanisms involved in early biological effects from radon exposure.
Project description:OBJECTIVE:Exposure to radon causes lung cancer. The scope and impact of exposure among Canadian workers have not been assessed. Our study estimated occupational radon exposure in Canada and its associated lung cancer burden. METHODS:Exposed workers were identified among the working population during the risk exposure period (1961-2001) using data from the Canadian Census and Labour Force Survey. Exposure levels were assigned based on 12,865 workplace radon measurements for indoor workers and assumed to be 1800 mg/m3 for underground workers. Lung cancer risks were calculated using the Biological Effects of Ionizing Radiation (BEIR) VI exposure-age-concentration model. Population attributable fractions were calculated with Levin's equation and applied to 2011 Canadian lung cancer statistics. RESULTS:Approximately 15.5 million Canadian workers were exposed to radon during the risk exposure period. 79% of exposed workers were exposed to radon levels?<?50 Bq/m3 and 4.8% were exposed to levels?>?150 Bq/m3. We estimated that 0.8% of lung cancers in Canada were attributable to occupational radon exposure, corresponding to approximately 188 incident lung cancers in 2011. CONCLUSIONS:The lung cancer burden associated with occupational radon exposure in Canada is small, with the greatest burden occurring among those exposed to low levels of radon.