Lung cancer mortality attributable to residential radon: a systematic scoping review.

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.

A Novel Strategy for the Assessment of Radon Risk Based on Indicators.

Among the physical pollutants affecting indoor air, the radioactive gas radon may turn out to be the most hazardous. Health effects related to radon exposure have been investigated for several decades, providing major scientific evidence to conclude that chronic exposures can cause lung cancer. Additionally, an association with other diseases, such as leukemia and cancers of the extra-thoracic airways, has been advanced. The implementation of a strategy to reduce the exposure of the population and minimize the health risk, according to the European Directive 59/2013/Euratom on ionizing radiations, is a new challenge in public health management. Starting from an understanding of the general state-of-the-art, a critical analysis of existing approaches has been conducted, identifying strengths and weaknesses. Then, a strategy for assessing the radon exposure of the general population, in a new comprehensive way, is proposed. It identifies three main areas of intervention and provides a list of hazard indicators and operative solutions to control human exposure. The strategy has been conceived to provide a supporting tool to authorities in the introduction of effective measures to assess population health risks due to radon exposure.

Indoor radon exposure and excess of lung cancer mortality: the case of Mexico-an ecological study.

Radon is a radioactive gas that can migrate from soils and rocks and accumulate in indoor areas such as dwellings and buildings. Many studies have shown a strong association between the exposure to radon, and its decay products, and lung cancer (LC), particularly in miners. In Mexico, according to published surveys, there is evidence of radon exposure in large groups of the population, nevertheless, only few attention has been paid to its association as a risk factor for LC. The aim of this ecological study is to evaluate the excess risk of lung cancer mortality in Mexico due to indoor radon exposure. Mean radon levels per state of the Country were obtained from different publications and lung cancer mortality was obtained from the National Institute of Statistics, Geography and Informatics for the period 2001-2013. A model proposed by the International Commission on Radiological Protection to estimate the annual excess risk of LC mortality (per 105 inhabitants) per dose unit of radon was used. The average indoor radon concentrations found rank from 51 to 1863 Bq m-3, the higher average dose exposure found was 3.13 mSv year-1 in the north of the country (Chihuahua) and the mortality excess of LC cases found in the country was 10 ± 1.5 (range 1-235 deaths) per 105 inhabitants. The highest values were found mainly in the Northern part of the country, where numerous uranium deposits are found, followed by Mexico City, the most crowded and most air polluted area in the country. A positive correlation (r = 0.98 p < 0.0001) was found between the excess of LC cases and the dose of radon exposure. Although the excess risk of LC mortality associated with indoor radon found in this study was relatively low, further studies are needed in order to accurately establish its magnitude in the country.

EXPRESSION OF LIPOPROTEIN LIPASE AND c-MYC ONCOGENE IN PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA AFFECTED BY THE CHORNOBYL ACCIDENT. / EKSPRESIIa GENA LIPOPROTEÏNLIPAZY I ONKOGENA c-MYC U KhVORYKh NA KhRONIChNU LIMFOTsYTARNU LEIKEMIIu, IaKI POSTRAZhDALY VNASLIDOK AVARIÏ NA ChORNOBYL'S'KII AES.

OBJECTIVE: to determine the association between the expression of lipoprotein lipase (LPL) and c-MYC genes inperipheral blood cells of chronic lymphocytic leukemia (CLL) patients affected by the Chornobyl catastrophedepending on the mutational status of IGHV genes. METHODS: Analysis was performed in the group of 69 CLL patients irradiated due to the Chornobyl NPP accident (58clean-up workers of 1986 year, 6 inhabitants of radionuclide contaminated areas, and 5 evacuees). The IGHV genemutational status was studied by polymerase chain reaction (PCR) followed by direct sequencing. LPL and c-MYCexpression was evaluated by Quantitative Real-time PCR. Data were analyzed with the SPSS software package, version 20.0. RESULTS: Relative LPL expression levels in CLL samples ranged from 0 to 1663.5 (mean 138.47 ± 30.69, median 26.1).A strong correlation between individual LPL expression levels and IGHV mutational status was found (r = 0.684;p < 0.0001). The average relative c-MYC expression level was 5.7 ± 0.87 (median 2.86; range 0-48.5). No association between c-MYC expression and IGHV mutational status was found. Among unmutated IGHV cases, a correlationbetween LPL and c-MYC gene expression levels was identified: r = 0.351; p = 0.013. CONCLUSIONS: Our data confirm the dominant concept that unmutated IGHV CLL cases are more sensitive to the actionof proliferative stimuli compared to mutated IGHV CLL cases. This is manifested by an increase in the expression ofa functionally significant LPL gene, is one for the strongest negative prognostic markers in CLL.

CHRONIC MYELOID LEUKEMIA COURSE IN PERSONS EXPOSED TO IONIZING RADIATION AS A RESULT OF THE CHORNOBYL ACCIDENT. / PEREBIG KhRONIChNOÏ MIIeLOÏDNOÏ LEIKEMIÏ U OSIB, IaKI ZAZNALY DIÏ IONIZUIuChOGO VYPROMINIuVANNIa VNASLIDOK ChORNOBYL'S'KOÏ AVARIÏ.

OBJECTIVE: Describe and characterize the peculiarities of the chronic myeloid leukemia (CML) course and responseto treatment in patients irradiated as a result of the Chornobyl nuclear power plant (ChNPP) accident based on theassessment of clinical-laboratory and clinical parameters. MATERIALS AND METHODS: The CML patients (n = 33) exposed to ionizing radiation as a result of the ChNPP accidentwere enrolled. The comparison group consisted of CML patients (n = 725) with no history of radiation exposure. Allpatients were in the chronic phase of the disease. Clinical, hematological and molecular genetic research methodswere applied. RESULTS: Patients exposed to ionizing radiation as a result of the ChNPP accident had no differences in CML manifestation, as well as in classical genetic markers at the onset of the disease compared with patients with no historyof radiation exposure. Reduction of tumor clone on imatinib therapy was significantly less effective in the patientsexposed to ionizing radiation than in cases of no history of radiation exposure. Cases of primary resistance were statistically significantly prevalent in the ChNPP accident consequences clean-up workers while in the residents ofradiologically contaminated areas a statistically significant increase in probability of loss of complete cytogeneticresponse (development of secondary resistance) to imatinib therapy was found. An association was found betweenthe radiation exposure and probability of loss of complete cytogenetic response to imatinib therapy in this group ofpatients. CONCLUSION: The radiation exposure in the history even many years before the onset of CML is an unfavorable exogenous factor responsible for the development of resistance to imatinib therapy.

CHANGES IN GENE EXPRESSION ASSOCIATED WITH NON-CANCER EFFECTS OF THE CHORNOBYL CLEAN-UP WORKERS IN THE REMOTE PERIOD AFTER EXPOSURE. / ZMINY GENNOÏ EKSPRESIÏ, ASOTsIIOVANI Z NEPUKhLYNNYMY EFEKTAMY VIDDALENOGO PERIODU PISLIa OPROMINENNIa V UChASNYKIV LIKVIDATsIÏ NASLIDKIV AVARIÏ NA ChAES.

OBJECTIVE: to establish the connection of radiation-induced changes in gene expression with the realized pathology of the broncho-pulmonary and cardiovascular systems in Chornobyl clean-up workers. MATERIALS AND METHODS: We examined 314 male Chornobyl clean-up workers (main group; age (58.94 ± 6.82) years(M ± SD); min 33, max 79 years; radiation dose (411.82 ± 625.41) mSv (M ± SD); min 1.74, max 3600 mSv) with various nosological forms of cardiovascular and broncho-pulmonary pathology (BPP) and 50 subjects of the controlgroup: age (50.50 ± 5.73) years (M ± SD); min 41, max 67 years. The relative level of BCL2, CDKN2A, CLSTN2, GSTM1,IFNG, IL1B, MCF2L, SERPINB9, STAT3, TERF1, TERF2, TERT, TNF, TP53, CCND1, CSF2, VEGFA genes expression was determined inperipheral blood leukocytes by real-time PCR (7900 HT Fast Real-Time PCR System (Applied Biosystems, USA)). The«gene-disease¼ association was determined on statistical models stratified separately for each disease and gene.Logistic regression was used to calculate the odds ratio. RESULTS: Increased GSTM1 gene expression and no changes in angiogenesis-related VEGFA gene expression werefound in the main group of patients with coronary heart disease (CHD). It was established overexpression of TP53,VEGF and IFNG genes in the group of patients with arterial hypertension (AH). At combination of these diseases anincrease of expression of СSF2, TERF1, TERF2 genes was established. The detected changes demonstrate an activationof the antioxidative defense system in patients with CHD, while AH is associated with the expression of genes ofangiogenesis and immune inflammation. It was shown an increase in the expression of genes associated with apoptosis and kinase activity (BCL2, CLSTN2, CDKN2), immune inflammation (CSF2, IL1B, TNF) in Chornobyl clean-upworkers with BPP. Expression of TP53 and GSTM1 (gene, associated with the glutathione system) was significantlyupregulated in the group of individuals with chronic bronchitis, whereas in patients with chronic obstructive pulmonary disease, no increase was detected; the expression of SERPINB9 and MCF2L genes was downregulated. CONCLUSIONS: Changes in the expression of genes, associated with the development of somatic pathology in theremote period after irradiation, in particular the genes of the immune response and inflammatory reactions CSF2,IFNG, IL1B, TNF; expression of genes that regulate cell proliferation, aging and apoptosis TP53, BCL2, MCF2L, CDKN2A,SERPINB9, TERF1, TERF2, TERT; genes that regulate cell adhesion and angiogenesis CLSTN2, VEGF.

CONTRIBUTION OF THE G1691A ALLELE CARRYING OF THE COAGULATION FACTOR V GENE TO THE DEVELOPMENT OF THROMBOSES IN RADIATION-EXPOSED PATIENTS WITH REACTIVE CHANGES IN PERIPHERAL BLOOD. / VNESOK NOSIISTVA ALEL'NOGO VARIANTA G1691A GENA V FAKTORU KOAGULIaTsIÏ V ROZVYTOK TROMBOTYChNYKh USKLADNEN' V OSIB Z REAKTYVNYMY ZMINAMY U PERYFERIINII KROVI, ShchO ZAZNALY RADIATsIINOGO OPROMINENNIa.

Thrombosis triggers, in addition to «classic¼ risk factors (RFs) of cardiovascular events, includes the reactive changesof peripheral blood (RCPB), markers of the hereditary thrombophilia and radiation anamnesis. However, results ofmost studies suggest the «classic¼ RFs are able to neutralize the prothrombogenic potential of the hereditary thrombophilia and other, less powerful predictors of thrombosis. OBJECTIVE: to determine the influence of the G1691A allele of the proaccelerin gene carrying to the thrombosis development, taking into account the vascular type of their occurrence, the presence of RFs in individuals with RCPB (reactive leukocytosis and thrombocytosis, and secondary erythrocytosis), as well as with and without radiation anamnesis. MATERIAL AND METHODS: In general, it was analyzed the results of clinical and molecular-genetic data of 152 patientswith RCPB, 19 patients had radiation anamnesis, 133 - did not have. The thrombotic complications were detected in5 (26.31 %) of radiation-exposer patients and 25 (18.79 %) patients without radiation anamneses. The carrying ofthe G1691A allele proaccelerin gene (APG) (Leiden mutation (LM)) was detected using the allele-specific polymerasechain reaction. RESULTS: The LM was found in 5.9 % (9 carriers) of the general cohort (GC) of RPBC patients. There were no differencein the LM frequency between the groups of patients with and without radiation anamnesis (р = 0.312). In the groupof radiation-exposer patients (р = 0.017), as well as in the group without its (р = 0.031), venous thromboses only weremore frequently in the LM carriers. In the presence of a radiation anamnesis, G1691A APG carriers with RFs have thehigher frequency (р = 0.008) and the probability of the occurrence (relative risk [RR] = 25.00; CI 95 %: 1.56-399.68)of venous thrombosis. In the group without radiation anamnesis, the frequency of venues thrombosis in the LMcarriers is higher in the younger age subgroup (р = 0.001), without RFs (p = 0.044) and without RFs under 60 years(р = 0.023). The risk of venous thrombosis in the G1691A APG carriers of the group without radiation anamnesis is5.78 (95 % CI: 1.58-21.13). In LM carriers without radiation anamnesis and RFs, as well as under the 60 years of age,the probability of venous thrombosis was 6.85 (95 % CI: 1.86-25.22) and 19.40 (95 % CI: 4.64-81.09), respectively,and in the absence of both criteria - 9.57 (95 % CI: 2.49-36.73). CONCLUSIONS: In patients with and without radiation anamnesis, the risk of venues thrombosis are observed moreoften in carriers of LM. The carrying of the G1691A APG in patients with RPBC and without RA increased the risk ofvenues thrombosis development in subjects without FRs and below 60 years of age. In the radiation-exposure group,the frequency and the risk of venues thrombosis in the G1691A APG carriers was higher in the subgroup with RFs. It isprobably due to the peculiarity of the samples, or prothrombogenic interaction between LM and radiation-associated endothelial damage.

The Likelihood of Adverse Pregnancy Outcomes and Genetic Disease (Transgenerational Effects) from Exposure to Radioactive Fallout from the 1945 Trinity Atomic Bomb Test.

The potential health consequences of the Trinity nuclear weapon test of 16 July 1945 at Alamogordo, New Mexico, are challenging to assess. Population data are available for mortality but not for cancer incidence for New Mexico residents for the first 25 y after the test, and the estimates of radiation dose to the nearby population are lower than the cumulative dose received from ubiquitous natural background radiation. Despite the estimates of low population exposures, it is believed by some that cancer rates in counties near the Trinity test site (located in Socorro County) are elevated compared with other locations across the state. Further, there is a concern about adverse pregnancy outcomes and genetic diseases (transgenerational or heritable effects) related to population exposure to fallout radiation. The possibility of an intergenerational effect has long been a concern of exposed populations, e.g., Japanese atomic bomb survivors, survivors of childhood and adolescent cancer, radiation workers, and environmentally exposed groups. In this paper, the likelihood of discernible transgenerational effects is discounted because (1) in all large-scale comprehensive studies of exposed populations, no heritable genetic effects have been demonstrated in children of exposed parents; (2) the distribution of estimated doses from Trinity is much lower than in other studied populations where no transgenerational effects have been observed; and (3) there is no evidence of increased cancer rates among the scientific, military, and professional participants at the Trinity test and at other nuclear weapons tests who received much higher doses than New Mexico residents living downwind of the Trinity site.

Estimated Radiation Doses Received by New Mexico Residents from the 1945 Trinity Nuclear Test.

The National Cancer Institute study of projected health risks to New Mexico residents from the 1945 Trinity nuclear test provides best estimates of organ radiation absorbed doses received by representative persons according to ethnicity, age, and county. Doses to five organs/tissues at significant risk from exposure to radioactive fallout (i.e., active bone marrow, thyroid gland, lungs, stomach, and colon) from the 63 most important radionuclides in fresh fallout from external and internal irradiation were estimated. The organ doses were estimated for four resident ethnic groups in New Mexico (Whites, Hispanics, Native Americans, and African Americans) in seven age groups using: (1) assessment models described in a companion paper, (2) data on the spatial distribution and magnitude of radioactive fallout derived from historical documents, and (3) data collected on diets and lifestyles in 1945 from interviews and focus groups conducted in 2015-2017 (described in a companion paper). The organ doses were found to vary widely across the state with the highest doses directly to the northeast of the detonation site and at locations close to the center of the Trinity fallout plume. Spatial heterogeneity of fallout deposition was the largest cause of variation of doses across the state with lesser differences due to age and ethnicity, the latter because of differences in diets and lifestyles. The exposure pathways considered included both external irradiation from deposited fallout and internal irradiation via inhalation of airborne radionuclides in the debris cloud as well as resuspended ground activity and ingestion of contaminated drinking water (derived both from rivers and rainwater cisterns) and foodstuffs including milk products, beef, mutton, and pork, human-consumed plant products including leafy vegetables, fruit vegetables, fruits, and berries. Tables of best estimates of county population-weighted average organ doses by ethnicity and age are presented. A discussion of our estimates of uncertainty is also provided to illustrate a lower and upper credible range on our best estimates of doses. Our findings indicate that only small geographic areas immediately downwind to the northeast received exposures of any significance as judged by their magnitude relative to natural radiation. The findings presented are the most comprehensive and well-described estimates of doses received by populations of New Mexico from the Trinity nuclear test.

Projected Cancer Risks to Residents of New Mexico from Exposure to Trinity Radioactive Fallout.

The Trinity nuclear test, conducted in 1945, exposed residents of New Mexico to varying degrees of radioactive fallout. Companion papers in this issue have detailed the results of a dose reconstruction that has estimated tissue-specific radiation absorbed doses to residents of New Mexico from internal and external exposure to radioactive fallout in the first year following the Trinity test when more than 90% of the lifetime dose was received. Estimated radiation doses depended on geographic location, race/ethnicity, and age at the time of the test. Here, these doses were applied to sex- and organ-specific risk coefficients (without applying a dose and dose rate effectiveness factor to extrapolate from a population with high-dose/high-dose rates to those with low-dose/low-dose rates) and combined with baseline cancer rates and published life tables to estimate and project the range of radiation-related excess cancers among 581,489 potentially exposed residents of New Mexico. The total lifetime baseline number of all solid cancers [excluding thyroid and non-melanoma skin cancer (NMSC)] was estimated to be 183,000 from 1945 to 2034. Estimates of ranges of numbers of radiation-related excess cancers and corresponding attributable fractions from 1945 to 2034 incorporate various sources of uncertainty. We estimated 90% uncertainty intervals (UIs) of excess cancer cases to be 210 to 460 for all solid cancers (except thyroid cancer and NMSC), 80 to 530 for thyroid cancer, and up to 10 for leukemia (except chronic lymphocytic leukemia), with corresponding attributable fractions ranging from 0.12% to 0.25%, 3.6% to 20%, and 0.02% to 0.31%, respectively. In the counties of Guadalupe, Lincoln, San Miguel, Socorro, and Torrance, which received the greatest fallout deposition, the 90% UI for the projected fraction of thyroid cancers attributable to radioactive fallout from the Trinity test was estimated to be from 17% to 58%. Attributable fractions for cancer types varied by race/ethnicity, but 90% UIs overlapped for all race/ethnicity groups for each cancer grouping. Thus, most cancers that have occurred or will occur among persons exposed to Trinity fallout are likely to be cancers unrelated to exposures from the Trinity nuclear test. While these ranges are based on the most detailed dose reconstruction to date and rely largely on methods previously established through scientific committee agreement, challenges inherent in the dose estimation, and assumptions relied upon both in the risk projection and incorporation of uncertainty are important limitations in quantifying the range of radiation-related excess cancer risk.

Solid cancer risk dependence on the Pasquill-Gifford atmospheric stability classes in a radiological event.

In a radiological event, the lack of preliminary information about the site of explosion and the difficulty in predicting the accurate path and distribution of radioactive plumes makes it difficult to predict expected health effects of exposed individuals. So far, in such a health evaluation, radiation-induced stochastic health effects such as cancer are not included. The Pasquill-Gifford atmospheric classes generally allow connecting atmospheric stability with dispersion of radioactive contaminants to the environment. In this work, an environmental release of radioactive Cs-137 was simulated and the resulting relative risk for solid cancer incidence among the affected population calculated. The HotSpot health physics code was used to simulate the radioactive atmospheric dispersion and calculate the Total Effective Dose Equivalent (TEDE), which was then used to estimate the relative risk of cancer incidence. The main results from this work suggest that the relative cancer risk and atmospheric stability classes are linked by differences in the TEDE. Such a finding may support triage, because it adds additional information on the potentially affected population at the early stages of an emergency response.

IDENTIFICATION OF NOVEL BIOMARKERS FOR LUNG CANCER RISK IN HIGH LEVELS OF RADON BY PROTEOMICS: A PILOT STUDY.

Radon is the second most important risk factor for lung cancer after tobacco smoking. In Chiang Mai, Thailand, the values of indoor radon activity concentrations are considerably higher than global average values and it is a highest level among East Asian countries. The aim of our study is to identify novel biomarkers for lung cancer risk in high radon areas using a proteomic approach. In our transitional study, a total of 81 participants of non-smokers were examined, consist of 25 lung cancer patients (LC), 16 healthy controls from low levels of natural radiation areas (LLNRA) and 40 healthy controls from high levels of natural radiation areas (HLNRA). The results showed that a total of 799 differentially expressed proteins were identified. Among these, a total of 25 proteins were observed in both LC and HLNRA, but not in LINRA. Owing to the results obtained from this study, we also point out the research direction regarding the validation of some new candidate protein as a biomarker to screen population with high risk for lung cancer in the area with high levels of radon.

DOSIMETRIC AND EPIDEMIOLOGICAL APPROACHES TO RADON LUNG CANCER RISK ASSESSMENT.

The two principal approaches used to assess the risk of lung cancer due to radon exposure are those based on dosimetric modelling and on epidemiology. Outline accounts are given of the main features of dosimetric models that have evolved over past decades. The main results of some occupational and residential epidemiological studies are also discussed. The doubling of the ICRP radon dose conversion factors estimated using the epidemiological based dose conversion convention in the period 1993-2010 are discussed. Also discussed is the more recent ICRP approach in which it is recommended that in future the doses should be estimated on the basis of dosimetric and biokinetic models thereby treating radon and its progeny as other radionuclides within its system of protection.

SURVEY OF INDOOR RADON LEVELS IN SOME UNIVERSITIES IN SOUTH WESTERN NIGERIA.

Indoor radon investigation was carried out in offices of three university campuses located in South-Western part of Nigeria; Federal University of Technology Akure (FUTA), Ekiti State University (EKSU) and Federal University Oye-Ekiti (FUOYE) using CR39 detectors. The mean activity concentration of indoor radon for the investigated offices of all three university campuses was estimated to be 222 ± 44 Bq m-3, which was below the reference level of 300 Bq m-3 recommended by the International Commission on Radiological Protection (ICRP 115). For the three institutions, the probability of lung cancer induction at age 70 years with respect to age of exposure (40, 50, and 60 years) ranged between 1.06 × 10-7 and 6.24 × 10-5. The expected mortality rate due to exposure to a radon activity concentration ranging from 7 to 1358 Bq m-3 was estimated to range from 0 to 44 deaths among a population of 10,000 persons.

Indoor radon exposure increases tumor mutation burden in never-smoker patients with lung adenocarcinoma.

OBJECTIVES: Radon, a natural radiation, is the leading environmental cause of lung cancer in never-smokers. However, the radon exposure impact on the mutational landscape and tumor mutation burden (TMB) of lung cancer in never-smokers has not been explored. The aim of this study was to investigate the mutational landscape of lung adenocarcinoma in never-smokers who were exposed to various degrees of residential radon. MATERIALS AND METHODS: To investigate the effect of indoor radon exposure, we estimated the cumulative exposure to indoor radon in each house of patients with lung cancer with a never-smoking history. Patients with at least 2 year-duration of residence before the diagnosis of lung adenocarcinoma were included. Patients were subgrouped based on the median radon exposure level (48 Bq/m3): radon-high vs. radon-low and targeted sequencing of tumor and matched blood were performed in all patients. RESULTS: Among 41 patients with lung adenocarcinoma, the TMB was significantly higher in the radon-high group than it was in the radon-low group (mean 4.94 vs. 2.6 mutations/Mb, P = 0.01). The recurrence rates between radon-high and radon-low group did not differ significantly. Mutational signatures of radon-high tumors showed features associated with inactivity of the base excision repair and DNA replication machineries. The analysis of tumor evolutionary trajectories also suggested a series of mutagenesis induced by radon exposure. In addition, radon-high tumors revealed a significant protein-protein interaction of genes involved in DNA damage and repair (P < 0.001). CONCLUSIONS: Indoor radon exposure increased the TMB in never-smoker patients with lung adenocarcinoma and their mutational signature was associated with defective DNA mismatch repair.

DOMESTIC RADON EXPOSURE AND CHILDHOOD LEUKAEMIA AND LYMPHOMA: A POPULATION-BASED STUDY IN CANADA.

In this paper, we revisit the possibility, first raised using a data set collected in the 1970s, that there is a link between average radon concentrations and the incidence of childhood leukaemia and lymphoma in Canada. Following the launch of the National Radon Program in 2007, Health Canada completed a long-term radon survey in 33 census metropolitan areas (CMAs), which covers about 70% of the Canadian population. We used this data, together with leukaemia and lymphoma incidence rates among children (0-14 years of age) in the past decade (2006-15), and tried to link the city-level average radon concentrations to the leukaemia and lymphoma incidence rates in 33 major Canadian cities. Analyses were conducted for six subtypes (ALL, AML, CMD, HL, NHL and BL) of leukaemia and lymphoma. Estimated doses to red bone marrow from domestic radon exposure were low and we did not find any association between radon exposure at home and the increased risk for developing leukaemia among children under 15 years of age living in the CMAs. The results indicate a slight positive association for AML among 1-4 year males in CMAs of Peer Group C and NHL among 5-9 year females in CMAs of Peer Group A; however, these should be interpreted with caution owing to the crude exposure assessment and possibilities of other confounding factors.

RISK ASSESSMENT FOR RADON EXPOSURE IN VARIOUS INDOOR ENVIRONMENTS.

Using data from a number of radon surveys, it was assessed that on average, radon progeny concentrations in Canadian homes are about three times higher than in school buildings, 4.7 times higher than in public buildings and indoor workplaces, and 12 times higher than in outdoor air. Canadian statistics show that most Canadians spend ~70% of their time indoors at home, 20% indoors away from home and 10% in outdoors. Due to relatively higher radon concentration in residential homes and longer time spent indoors at home, the exposure at home contributes to 90% of the radon-induced lung-cancer risk.

EVALUATION OF DOSE IN SLEEP BY MATTRESS CONTAINING MONAZITE.

Some companies in Korea have sold beds which contain a processed product containing monazite powder. Consumers may receive external exposure by radiation emitted by progeny radionuclides in uranium and thorium, and internal exposure through the breathing of radon progeny radionuclides produced in the decay chain. Thus, in this study, age specific dose conversion factors (mSv y-1 Bq-1) by external exposure and dose conversion factors by internal exposure (mSv y-1 per Bq m-3) were derived. Besides, a dose assessment program were developed to calculate dose by taking into account real conditions. And the age specific dose was evaluated using the radioactive concentration measured by the NSSC. As a results, external exposure was assessed to get effective doses in the range of 0.00086 to 0.0015 mSv y-1 by external exposure and a committed effective doses in the range of 1.3 to 12.26 mSv y-1 by internal exposure for all age groups.

ASSESSMENT OF INDOOR GAMMA RADIATION AND DETERMINATION OF EXCESS LIFETIME CANCER RISK IN TEHRAN IN WINTER AND SPRING 2017.

Natural radiation is a feature of the environment in which we live. One of the contributions of human exposure to ionizing radiation due to natural sources arises from gamma radiation. Therefore, present study was aimed to evaluate and map indoor gamma dose rate in Tehran. The corresponding annual effective dose (AED) and excess lifetime cancer risk (ELCR) were also calculated. All measurements were performed by a Geiger Muller detector in 43 dwellings in Tehran. The average indoor gamma dose rate in Tehran was appointed as 343.2 nGy/h. AED and ELCR were calculated as 2.4 mSv and 10.3 × 10-3, respectively. The evaluated indoor gamma dose rate and calculated AEDs and lifetime cancer risk were found higher than the world average value.

Meta-analysis of case-control studies on the relationship between lung cancer and indoor radon exposure.

Indoor exposure to natural radon is a factor that influences lung cancer risk worldwide. The present study includes a meta-analysis of epidemiological data on the relationship between lung cancer and indoor radon. Altogether, 31 case-control studies with 20,703 cases, 34,518 controls and 140 individual odds ratio (OR) estimates are included in the meta-analysis. Weighted median OR was calculated for five radon intervals. The following parameters were used for the weighting: standard error of OR, duration of radon concentration measurement, and relative number of controls in reference intervals. The dependence of the weighted median OR on the radon concentration was estimated applying linear non-threshold and threshold models. The results obtained suggest a significant linear no-threshold exposure-effect relationship for radon concentrations above 100 Bq/m3, with a slope of 0.14 (95% confidence interval 0.08-0.21) per 100 Bq/m3.