Radon - occurrence and impact on the health.

Radon is noble, monatomic, radioactive, heavier than the air gas. It is colorless, odorless, tasteless. It exists in natural environment as a result of the decay of radium, and emits mainly alpha radiation and less beta radiation. Residential radon concentrations vary widely by geographic area. The higher concentration of radon is expected globally in the grounds where uranium, radium and thoron are present. Radon may gather in caves, tunnels, mines as well as in other lowestlying spaces, such as basements, and cellars. In accordance with Atomic Law (2000), the reference level for the average annual concentration of radioactive radon in rooms intended for human habitation is 300 Bq/m3. The most dangerous damages caused by ionizing radiation i.e. radon and its derivatives are changes to DNA, which may disturb the functions of cells and in the consequence lead to induction of cancer of respiratory tract, mainly of lungs and also leukaemia. So, the main consequence of exposure to high amount of radon are cancers of respiratory system. Radon enters the human organism mainly through inhaled atmospheric air. Moreover, radon significantly increased a risk of induction cancer in smokers and vice versa, smoking promotes the development of lung cancer after the exposure to radon and its derivatives. Radon may also have beneficial effect on the human body. Therefore it is used in medicine; mainly in radonbalneotherapy i.e. bath treatments, rinsing the mouth and inhalation. Beneficial effects of radon confirms the validity of the theory of radiation hormesis, which assumes that low doses of radiation may stimulate the repair of DNA damage by activation of protective mechanisms, which neutralize free radicals.

Proteomic and miRNA profiling of radon-induced skin damage in mice: FASN regulated by miRNAs.

Radon is a naturally occurring radioactive gas and considered as a serious carcinogen to humans. Continuous radioactive decay of this gas emits high-energy alpha particles. Long-term radon exposure induces oxidative stress and inflammatory response, which results in chronic lung diseases. However, biological effects after radon exposure in other organs have been rarely reported. As the outermost organ of the human body, the skin suffers from environmental damage to agents such as air pollution. Epidemiological studies indicated that areas with high level of radon had a high incidence of skin cancer. However, whether radon exposure induces skin damage has not been reported yet. In this study, we established a radon-exposed mouse model and found that radon exposure affected the structure of skin tissues, which was manifested by inflammatory cell infiltration and skin atrophy. Using proteomic approach, we found 45 preferentially expressed proteins in 60 Working Level Months (WLM) group and 314 preferentially expressed proteins in 120 WLM group from radon-exposed skin tissues. Through microRNA (miRNA) sequencing profiling analysis, 57 dysregulated miRNAs were screened between the control and radon-treated mouse skin. By integrating the dysregulated proteins and miRNAs, radon-induced fatty acid synthase (FASN) was investigated in greater detail. Results showed that FASN was regulated by miR-206-3p and miR-378a-3p and involved in the pathogenesis of radon-induced skin damage. Overexpression of FASN inhibited the proliferation, and induced in WS1 cells. Our present findings illustrate the molecular change during radon-induced skin damage and the potential role of FASN during this process.

Interaction of MS prevalence, radon gas concentration, and patient nutrition: a case-control study.

In general, ecological findings indicate a positive correlation between MS and the intake of certain foods. This study aimed to investigate the relationship between radon (Rn) gas concentration and nutrition of patients in food groups with MS. Demographic information, diet, and building characteristics were collected by a questionnaire. Indoors Rn gas was measured using CR-39 detectors. Three models were used in the study of food intake. The interaction analysis between MS prevalence, diet, residential building characteristics, and Rn gas content was performed using SPSS 2020. The total Rn was significantly associated with cooling devices (P = 0.021). Buildings > 20 years had higher Rn concentrations than buildings < 20 years (P = 0.038). Also, no significant relationship was found between Rn-total and MS concentrations, but the total Rn concentration was higher in people homes with MS. Case group used more processed meat than the control (P < 0.001). The case group consumed more butter than the control, which was significant in Model III (P < 0.04). Tomato consumption in the case group was significantly higher than the control (P < 0.03). According to the results there was no interaction between Rn gas concentration in any of the food groups in each cases. However, future studies with larger sample sizes will be needed prospectively.

Estimation of radon excess lung cancer near some dumpsites in, Lagos, Nigeria.

Generally, in Nigeria dumpsites are open and elevate the pollution by increasing the total environment contamination level. This affects not only the site of dumpsites but also the surrounding buildings and area. In the present work, indoor radon activity concentration is tested inside some buildings in the vicinity of dumpsites in Lagos, Nigeria. A passive technique with CR-39 detectors is used. Different buildings around different eight dumpsites were chosen. Radon concentration had ranged from 16.00 ± 3 to 931.00 ± 186 Bqm-3 in the dumpsites. With Mean concentrations range from 120 ± 24 at OKE-ODO to 334 ± 67, at Solus-4 respectively. The present results explain that 63% of the radon activity concentration in indoor air around the selected dumpsites at Lagos city in Nigeria is below the allowed limit from ICRP 200 Bq m-3 while 37% is more than this limit. Based on the measured radon concentration, the annual effective dose and cancer risk are evaluated. The range of ELC is from 242 to 14086 with mean value 3114 ± 1111.

The legacy of weapons grade plutonium production: Health status of Hanford complex workers who manage the waste.

The extent and etiology of health effects in workers who maintain underground storage tanks at the Hanford Nuclear Reservation (Hanford) have been subjects of controversy and concern for several decades. Hanford is a decommissioned nuclear production complex managed by the US Department of Energy in southeast Washington State. This integration-of-evidence review evaluates the relationship between exposure to vapors from mixed chemical and radioactive waste stored in underground storage tanks at Hanford and worker health. Hanford workers' health information was gathered from technical reports, media reports, and published literature, including the systematic search of seven databases. This review describes the health status and health concerns of Hanford tank farm workers based on the integration of the available health effects data from disparate sources. In interviews with external groups, Hanford workers reported both irritant-type symptoms and diseases that they believe are attributable to tank farm vapors. However, the results of this integration-of-evidence review indicated that no pervasive pattern of occupational disease was identified that can be associated with exposure to tank farm vapors. Inhalation exposure to asbestos and beryllium is associated with lung disease from various types of nuclear industry work but not from work on tank farms. This review concluded that while irritant-type symptoms and isolated cases of occupational disease are plausible under certain conditions, the currently available data do not support a pervasive pattern of occupational disease associated with vapor exposure.

[Radon exposure: also in this case it is better to open the window]. / Esposizione al Radon : anche in questo caso è meglio aprire la finestra.

Although many areas of the Italian territory are of volcanic origin, there is not much attention to the prevention of risks due to exposure to Radon gas. This gas is produced during the decay of uranium present in volcanic rocks and, if inhaled, its further decay produces radioactive radiation responsible for damage to lung tissues. It is estimated that these radiations are responsible for 10% of lung cancers. In conditions of poor air exchange, the concentration of Radon gas can easily reach high concentrations, particularly in underground rooms or on the ground floor that are in direct contact with the ground. In these territories, the designers of new buildings do not always consider this risk and the population is also poorly informed on the behavior to be adopted for prevention.

Protection of melatonin against long-term radon exposure-caused lung injury.

Radon is one of the major pathogenic factors worldwide. Recently, epidemiological studies have suggested that radon exposure plays an important role in lung injury, which could further cause cancer. However, the toxic effects and underlying mechanism on lung injury are still not clear. Here, we identified the detailed toxic effects of long-term radon exposure. Specifically, the manifestations were inflammatory response and cell apoptosis in dose- and time-dependent manners. In detail, it caused the mitochondrial dysfunction and oxidative stress as determined by the abnormal levels of mitochondrial DNA copy number, adenosine triphosphate, mitochondrial membrane potential, superoxide dismutase, and cycloxygenase-2. Furthermore, we found that melatonin treatment ameliorated mitochondrial dysfunction and attenuated the levels of oxidative stress caused by long-term radon exposure, which could further inhibit the lung tissue apoptosis as determined by the decreased levels of cleaved caspase 3. Our study would provide potential therapeutic application of melatonin on lung tissue injury caused by long-term radon exposure.

EXPOSURE LEVELS OF UKRAINIAN POPULATION IN THE CONTEXT OF AN ACTION PLAN TO REDUCE INDOOR RADON LEVELS. / RIVNI OPROMINENNIa NASELENNIa UKRAÏNY V KONTEKSTI PLANU DII ShchODO ZMENShENNIa RIVNIV RADONU V POVITRI PRYMIShchEN'.

OBJECTIVE: To analyze and evaluate the available information to indoor radon concentration in the context of theimplementation of the radon action plan. OBJECT OF STUDY: indoor radon-222 in dwellings by area and corresponding radiation risks of the population. Measurements were performed using passive track radonometry. The exposure time of the radonometers is atleast 30 days during heating season. Radiation risk calculations were performed according to the dose coefficientsand mathematical models of the ICRP. RESULTS: It was found that for the whole country, reference level 300 Bq/m3 (radon gas) is exceeded in 16 % ofcases. It was found that geometric mean of radon gas levels was 120 Bq/m3 and varies from 35 to 265 Bq/m3 bydifferent area, namely the difference between radon levels in different territories of the country can be up to 7.5times. Variability of radon levels at the district level is also significant. It was found, radon activity concentrationdiffering by almost 10 times by districts with lognormal distribution and a geometric mean of 75 Bq/m3. The analy-sis of radiation risks of the population has established that estimated annual number of lung cancer deaths due toradon in Ukraine is almost 8,900 cases; and а direct economic loss for the country are estimated at more than $450 million a year. CONCLUSIONS: Surveys of radon levels demonstrated significant variation in radon concentrations between different regions. For the whole country, reference level (300 Bq/m3) is exceeded on above 16 % of the dwellings, butpercentage of exceeding varies from 0.1 to 43.0 % by different area. Information on indoor radon concentrationsin almost a third of the country is non-available. For an effective implementation of the Action plan, it makes sense to introduce radon risk mapping.

Repeated radon exposure induced lung injury and epithelial-mesenchymal transition through the PI3K/AKT/mTOR pathway in human bronchial epithelial cells and mice.

Radon exposure is the most frequent cause of lung cancer in non-smokers. The high linear energy transfer alpha-particles from radon decay cause the accumulation of multiple genetic changes and lead to cancer development. Epithelial-mesenchymal transition (EMT) plays an important role in oncogenesis. However, the mechanisms underlying chronic radon exposure-induced EMT attributed to carcinogenesis are not understood. This study aimed to explore the EMT and potential molecular mechanisms induced by repeated radon exposure. The EMT model of 16HBE and BEAS-2B cells was established with radon exposure (20000 Bq/m3, 20 min each time every 3 days). We found repeated radon exposure facilitated epithelial cell migration, proliferation, reduced cell adhesion and ability to undergo EMT through a decrease in epithelial markers and an increase in mesenchymal markers. Radon regulated the expression of matrix metalloproteinase 2 (MMP2) and tissue inhibitors of metalloproteinase 2 (TIMP2) to disrupt the balance of MMP2/TIMP2. In vivo, BALB/c mice were exposed to 105 Bq/m3 radon gas for cumulative doses of 60 and 120 Working Level Months (WLM). Radon inhalation caused lung damage and fibrosis in mice, which was aggravated with the increase of exposure dose. EMT-like transformation also occurred in lung tissues of radon-exposure mice. Moreover, radon radiation increased p-PI3K, p-AKT and p-mTOR in cells and mice. Radon reduced the GSK-3ß level and elevated the active ß-catenin in 16HBE cells. The m-TOR and AKT inhibitors attenuated radon exposure-induced EMT by regulation related biomarkers. These data demonstrated that radon exposure induced EMT through the PI3K/AKT/mTOR pathway in epithelial cells and lung tissue.

A review of biological effects and treatments of inhaled depleted uranium aerosol.

Depleted uranium (DU) is primarily used for DU bombs and DU tanks in the military. Aerosol inhalation is considered the primary route of DU exposure. Although laboratory tests have confirmed that inhalation of DU aerosol can cause lung, kidney, and other organ damage, epidemiological studies have found no conclusive evidence that persons in areas with prolonged exposure to DU-containing bombs are affected. After the body inhaled DU aerosols, we first clear the insoluble DU through whole-lung lavage (WLL). Then we eliminate the soluble uranium by the chelating agent. Besides, reducing DU damage to tissues and cells through drugs is also an important treatment method. In future research, emphasis should be placed on the damage mechanism of DU aerosol, the laboratory and clinical research of DU chelating agents, the research on the combination of DU chelating agent and WLL, and the research and development of new drugs to prevent DU damage.

Multiple Stressor Effects of Radon and Phthalates in Children: Background Information and Future Research.

The present paper reviews available background information for studying multiple stressor effects of radon (222Rn) and phthalates in children and provides insights on future directions. In realistic situations, living organisms are collectively subjected to many environmental stressors, with the resultant effects being referred to as multiple stressor effects. Radon is a naturally occurring radioactive gas that can lead to lung cancers. On the other hand, phthalates are semi-volatile organic compounds widely applied as plasticizers to provide flexibility to plastic in consumer products. Links of phthalates to various health effects have been reported, including allergy and asthma. In the present review, the focus on indoor contaminants was due to their higher concentrations and to the higher indoor occupancy factor, while the focus on the pediatric population was due to their inherent sensitivity and their spending more time close to the floor. Two main future directions in studying multiple stressor effects of radon and phthalates in children were proposed. The first one was on computational modeling and micro-dosimetric studies, and the second one was on biological studies. In particular, dose-response relationship and effect-specific models for combined exposures to radon and phthalates would be necessary. The ideas and methodology behind such proposed research work are also applicable to studies on multiple stressor effects of collective exposures to other significant airborne contaminants, and to population groups other than children.

SDHA-mediated Warburg effect in malignantly transformed human bronchial epithelial cells following long-term exposure to radon.

Radon and its progeny have been classified as human class I carcinogens by the IARC. However, the mechanisms by which radon induces lung and other cancers, especially the radon-induced Warburg effect, have not been fully elucidated. The aim of this study was to investigate the role of the succinate dehydrogenase subunit A (SDHA)-mediated Warburg effect in (human bronchial epithelial) BEAS-2B cells with malignant transformations induced by long-term radon exposure. Soft agar colony formation and MMP-9 were increased following radon-induced malignant transformation. Additionally, we observed the Warburg effect in BEAS-2B cells following long-term radon exposure, evidenced by increases in the levels of glucose uptake, lactate, and lactate dehydrogenase (LDH). Following radon exposure, the expression of SDHA was decreased, while the levels of HIF-1α and hexokinase-2 (HK2) were increased. Our findings suggested that the SDHA-associated pathway may be involved in mediating the Warburg effect in radon-induced malignant transformation of BEAS-2B.

Residential exposure to radon and levels of histone γH2AX and DNA damage in peripheral blood lymphocytes of residents of Kowary city regions (Poland).

INTRODUCTION: Radon-induced biological effects have been studied mainly through epidemiological investigations, and well-controlled in vitro and in vivo experiments. To provide data explaining radon exposure-induced harmful effects in natural environment, exposure assessment under these conditions is needed. The objective of the study was to examine the level of genetic damage assessed with biomarkers of DNA single- and double-strand breaks (SSBs and DSBs) in peripheral blood mononuclear cells obtained from individuals continuously exposed to Rn in homes. Naturally elevated Rn concentrations in homes can be found in the South of Poland, in Kowary city. METHODS: Measurements of expression of phosphorylated histone γH2AX was used as a marker of DNA double strand breaks. To detect DNA single and double-strand breaks and alkali labile sites, the alkaline comet assay was used. Oxidative damage of DNA was evaluated by formamidopyrimidyne (FPG)-modified comet assay. The blood was collected from 94 volunteers living in Kowary. Subjects were grouped according to their status of living in radon concentration ≥100 Bq/m3 (n = 67), and <100 Bq/m3 (n = 27). RESULTS: The statistically significant differences in levels of DNA damage in peripheral lymphocytes assessed with comet assay were found to be associated with levels of radon exposure in indoor air (p = 0.034). DNA damage in the comet assay was significantly correlated with DNA damage assessed with γH2AX staining. CONCLUSIONS: Results of the present study indicate the suitability of alkaline comet assay for the detection of DNA damage in peripheral blood lymphocytes of people environmentally exposed to radon.

[COMPLEX STUDY OF BIOLOGICAL EFFECT OF TSKHALTUBO RADON WATER INHALATION].

The effect of EMF of high frequencies (mobile phones and computers) and the action of radon therapeutic procedures (phenomenological and influencing therapeutic factors) is not still generally known. In addition, we are constantly under the influence of different EMF frequencies, the study of which also deserves attention. The aim of the work is detailed analysis of alpha radiation Tskhaltubo water effect. The subject of the study was 25 patients. The group took the inhalation procedure of air radon baths which was 36-370C, and radon concentration 37.0 Bq/m3. The conducted quantities and qualitative analyses show, that radon inhalation takes an active part in metabolism of biological active components: catecholamine's, amines and free amino acids. Biochemical experiments showed the normalization tendency of composition of these necessary blood-components after 10th day radon-therapeutic inhalation procedure.

QUANTITATIVE ANALYSIS OF THE POTENTIAL ROLE OF BASAL CELL HYPERPLASIA IN THE RELATIONSHIP BETWEEN CLONAL EXPANSION AND RADON CONCENTRATION.

Applying the two-stage clonal expansion model to epidemiology of lung cancer among uranium miners, it has been revealed that radon acts as a promoting agent facilitating the clonal expansion of already mutated cells. Clonal expansion rate increases non-linearly by radon concentration showing a plateau above a given exposure rate. The underlying mechanisms remain unclear. Earlier we proposed that progenitor cell hyperplasia may be induced upon chronic radon exposure. The objective of the present study is to test whether the induction of hyperplasia may provide a quantitative explanation for the plateau in clonal expansion rate. For this purpose, computational epithelium models were prepared with different number of basal cells. Cell nucleus hits were computed by an own-developed Monte-Carlo code. Surviving fractions were estimated based on the number of cell nucleus hits. Cell division rate was computed supposing equilibrium between cell death and cell division. It was also supposed that clonal expansion rate is proportional to cell division rate, and therefore the relative increase in cell division rate and clonal expansion rate are the same functions of exposure rate. While the simulation results highly depend on model parameters with high uncertainty, a parameter set has been found resulting in a cell division rate-exposure rate relationship corresponding to the plateau in clonal expansion rate. Due to the high uncertainty of the applied parameters, however, further studies are required to decide whether the induction of hyperplasia is responsible for the non-linear increase in clonal expansion rate or not. Nevertheless, the present study exemplifies how computational modelling can contribute to the integration of observational and experimental radiation protection research.

Recent exposure to particle radioactivity and biomarkers of oxidative stress and inflammation: The Framingham Heart Study.

BACKGROUND: Decay products of radioactive materials may attach to ambient fine particles and form radioactive aerosol. Internal ionizing radiation source from inhaled radioactive aerosol may contribute to the fine particulate matter (PM2.5)-inflammation pathway. However, few studies in humans have examined the associations. OBJECTIVES: To examine the associations between particle radioactivity and biomarkers of oxidative stress and inflammation among participants from the Framingham Offspring and Third Generation cohorts. METHODS: We included 3996 participants who were not current smokers and lived within 50 km from our central air pollution monitoring station. We estimated regional mean gross beta radioactivity from monitors in the northeastern U.S. as a surrogate for ambient radioactive particles, and calculated the 1- to 28-day moving averages. We used linear regression models for fibrinogen, tumor necrosis factor α, interleukin-6, and myeloperoxidase which were measured once, and linear mixed effect models for 8-epi-prostaglandin F2α, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, and tumor necrosis factor receptor-2 that were measured up to twice, adjusting for demographics, individual- and area-level socioeconomic positions, time, meteorology, and PM2.5. We also examined whether the associations differed by median age, sex, diabetes status, PM2.5 levels, and black carbon levels. RESULTS: The mean age was 54 years and 54% were women. An interquartile range (3 × 10-3 pCi/m3) higher beta radioactivity level at the 7-day moving average was associated with 5.09% (95% CI: 0.92, 9.43), 2.65% (1.10, 4.22), and 4.71% (95% CI: 3.01, 6.44) higher levels of interleukin-6, MCP-1, and P-selectin, but with 7.01% (95% CI: -11.64, -2.15) and 2.70% (95% CI: -3.97, -1.42) lower levels of 8-epi-prostaglandin F2α and ICAM-1, respectively. CONCLUSIONS: Regional mean particle radioactivity was positively associated with interleukin-6, MCP-1, and P-selectin, but negatively with ICAM-1 and 8-epi-prostaglandin F2α among our study participants.

Short Telomere Length as a Biomarker Risk of Lung Cancer Development Induced by High Radon Levels: A Pilot Study.

Long-term exposure to radon has been determined to be the second leading cause of lung cancer after tobacco smoking. However, an in-depth study of this topic has not been explicitly carried out in Chiang Mai (Thailand). This paper presents the results of an indoor radon level measurement campaign in dwellings of Chiang Mai using total of 110 detectors (CR-39) during one year. The results show that the average radon levels varied from 35 to 219 Bq/m³, with an overall average of 57 Bq/m³. The finding also shows that the average value is higher than the global average value of 39 Bq/m³. In addition, to examine the cause of lung cancer development among people with risk of chronic exposure to radon during their lifetime, 35 non-smoker lung cancer patients and 33 healthy nonsmokers were analyzed for telomere length. As expected, telomere length was significantly shorter in lung cancer patients than in healthy nonsmokers. Among healthy nonsmokers, the telomere length was significantly shorter in a high radon group than in an unaffected low radon group. To the best of our knowledge, our research provides the first attempt in describing the shortened telomeres in areas with high levels of environmental radon that might be related to lung cancer development.

Estimates of the Lung Cancer Cases Attributable to Radon in Municipalities of Two Apulia Provinces (Italy) and Assessment of Main Exposure Determinants.

Indoor radon exposure is responsible for increased incidence of lung cancer in communities. Building construction characteristics, materials, and environmental determinants are associated with increased radon concentration at specific sites. In this study, routine data related to radon measurements available from the Apulia (Italy) Regional Environmental Protection Agency (ARPA) were combined with building and ground characteristics data. An algorithm was created based on the experience of miners and it was able to produce estimates of lung cancer cases attributable to radon in different municipalities with the combined data. In the province of Lecce, the sites with a higher risk of lung cancer are Campi Salentina and Minervino, with 1.18 WLM (working level months) and 1.38 WLM, respectively, corresponding to lung cancer incidence rates of 3.34 and 3.89 per 10 × 10³ inhabitants. The sites in the province of Bari with higher risks of lung cancer are Gravina di Puglia and Locorotondo, measuring 1.89 WLM and 1.22 WLM, respectively, which correspond to an incidence rate of lung cancer of 5.36 and 3.44 per 10 × 10³ inhabitants. The main determinants of radon exposure are whether the buildings were built between 1999 and 2001, were one-room buildings with porous masonry, and were built on soil consisting of pelvis, clayey sand, gravel and conglomerates, calcarenites, and permeable lithotypes.

DNA damage in oral epithelial cells of individuals chronically exposed to indoor radon (222Rn) in a hydrothermal area.

Hydrothermal areas are potentially hazardous to humans as volcanic gases such as radon (222Rn) are continuously released from soil diffuse degassing. Exposure to radon is estimated to be the second leading cause of lung cancer, but little is known about radon health-associated risks in hydrothermal regions. This cross-sectional study was designed to evaluate the DNA damage in the buccal epithelial cells of individuals chronically exposed to indoor radon in a volcanic area (Furnas volcano, Azores, Portugal) with a hydrothermal system. Buccal epithelial cells were collected from 33 individuals inhabiting the hydrothermal area (Ribeira Quente village) and from 49 individuals inhabiting a non-hydrothermal area (Ponta Delgada city). Indoor radon was measured with Ramon 2.2 detectors. Chromosome damage was measured by micronucleus cytome assay, and RAPD-PCR was used as a complementary tool to evaluate DNA damage, using three 10-mer primers (D11, F1 and F12). Indoor radon concentration correlated positively with the frequency of micronucleated cells (r s = 0.325, p = 0.003). Exposure to radon is a risk factor for the occurrence micronucleated cells in the inhabitants of the hydrothermal area (RR = 1.71; 95% CI, 1.2-2.4; p = 0.003). One RAPD-PCR primer (F12) produced differences in the banding pattern, a fact that can indicate its potential for detecting radon-induced specific genomic alterations. The observed association between chronic exposure to indoor radon and the occurrence of chromosome damage in human oral epithelial cells evidences the usefulness of biological surveillance to assess mutations involved in pre-carcinogenesis in hydrothermal areas, reinforcing the need for further studies with human populations living in these areas.