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.

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.

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.

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.

[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.

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.

Assessment of personal airborne exposures and surface contamination from x-ray vaporization of beryllium targets at the National Ignition Facility.

This article presents air and surface sampling data collected over the first two years since beryllium was introduced as a target material at the National Ignition Facility. Over this time, 101 experiments with beryllium-containing targets were executed. The data provides an assessment of current conditions in the facility and a baseline for future impacts as new, reduced regulatory limits for beryllium are being proposed by both the Occupational Safety and Health Administration and Department of Energy. This study also investigates how beryllium deposits onto exposed surfaces as a result of x-ray vaporization and the effectiveness of simple decontamination measures in reducing the amount of removable beryllium from a surface. Based on 1,961 surface wipe samples collected from entrant components (equipment directly exposed to target debris) and their surrounding work areas during routine reconfiguration activities, only one result was above the beryllium release limit of 0.2 µg/100 cm2 and 27 results were above the analytical reporting limit of 0.01 µg/100 cm2, for a beryllium detection rate of 1.4%. Surface wipe samples collected from the internal walls of the NIF target chamber, however, showed higher levels of beryllium, with beryllium detected on 73% and 87% of the samples during the first and second target chamber entries (performed annually), respectively, with 23% of the samples above the beryllium release limit during the second target chamber entry. The analysis of a target chamber wall panel exposed during the first 30 beryllium-containing experiments (cumulatively) indicated that 87% of the beryllium contamination remains fixed onto the surface after wet wiping the surface and 92% of the non-fixed contamination was removed by decontaminating the surface using a dry wipe followed by a wet wipe. Personal airborne exposures assessed during access to entrant components and during target chamber entry indicated that airborne beryllium was not present in workers' breathing zones. All the data thus far have shown that beryllium has been effectively managed to prevent exposures to workers during routine and non-routine work.

Mechanistic study on lung cancer mortality after radon exposure in the Wismut cohort supports important role of clonal expansion in lung carcinogenesis.

Lung cancer mortality after radon exposure in the Wismut cohort was analyzed using the two-stage clonal expansion (TSCE) model. A total of 2996 lung cancer deaths among the 58,695 male workers were observed during the follow-up period between 1946 and 2003. Adjustment to silica exposure was performed to find a more accurate estimation of the risk of radon exposure. An additional analysis with the descriptive excess relative risk (ERR) model was carried out for comparison. The TSCE model that best describes the data is nonlinear in the clonal expansion with radon exposure and has a saturation level at an exposure rate of [Formula: see text]. The excess relative risk decreases with age and shows an inverse exposure rate effect. In comparison with the ERR model, the TSCE model predicts a considerably larger risk for low exposures rates below [Formula: see text]. Comparison to other mechanistic studies of lung cancer after exposure to alpha particles using the TSCE model reveals an extraordinary consistency in the main features of the exposure response, given the diversity in the characteristics of the cohorts and the exposure across different studies. This suggests that a nonlinear response mechanism in the clonal expansion, with some level of saturation at large exposure rates, may be playing a crucial role in the development of lung cancer after alpha particle irradiation.

Radon induced hyperplasia: effective adaptation reducing the local doses in the bronchial epithelium.

There is experimental and histological evidence that chronic irritation and cell death may cause hyperplasia in the exposed tissue. As the heterogeneous deposition of inhaled radon progeny results in high local doses at the peak of the bronchial bifurcations, it was proposed earlier that hyperplasia occurs in these deposition hot spots upon chronic radon exposure. The objective of the present study is to quantify how the induction of basal cell hyperplasia modulates the microdosimetric consequences of a given radon exposure. For this purpose, computational epithelium models were constructed with spherical cell nuclei of six different cell types based on histological data. Basal cell hyperplasia was modelled by epithelium models with additional basal cells and increased epithelium thickness. Microdosimetry for alpha-particles was performed by an own-developed Monte-Carlo code. Results show that the average tissue dose, and the average hit number and dose of basal cells decrease by the increase of the measure of hyperplasia. Hit and dose distribution reveal that the induction of hyperplasia may result in a basal cell pool which is shielded from alpha-radiation. It highlights that the exposure history affects the microdosimetric consequences of a present exposure, while the biological and health effects may also depend on previous exposures. The induction of hyperplasia can be considered as a radioadaptive response at the tissue level. Such an adaptation of the tissue challenges the validity of the application of the dose and dose rate effectiveness factor from a mechanistic point of view. As the location of radiosensitive target cells may change due to previous exposures, dosimetry models considering the tissue geometry characteristic of normal conditions may be inappropriate for dose estimation in case of protracted exposures. As internal exposures are frequently chronic, such changes in tissue geometry may be highly relevant for other incorporated radionuclides.

Radon Risk Communication Strategies: A Regional Story.

Risk communication on the health effects of radon encounters many challenges and requires a variety of risk communication strategies and approaches. The concern over radon exposure and its health effects may vary according to people's level of knowledge and receptivity. Homeowners in radon-prone areas are usually more informed and have greater concern over those not living in radon-prone areas. The latter group is often found to be resistant to testing. In British Columbia as well as many other parts of the country, some homes have been lying outside of the radon-prone areas have radon levels above the Canadian guideline, which is the reason Health Canada recommends that all homes should be tested. Over the last five years, the Environment Health Program (EHP) of Health Canada in the British Columbia region has been using a variety of different approaches in their radon risk communications through social media, workshops, webinars, public forums, poster contests, radon distribution maps, public inquiries, tradeshows and conference events, and partnership with different jurisdictions and nongovernmental organizations. The valuable lessons learned from these approaches are discussed in this special report.

Soil gas radon assessment and development of a radon risk map in Bolsena, Central Italy.

Vulsini Volcanic district in Northern Latium (Central Italy) is characterized by high natural radiation background resulting from the high concentrations of uranium, thorium and potassium in the volcanic products. In order to estimate the radon radiation risk, a series of soil gas radon measurements were carried out in Bolsena, the principal urban settlement in this area NE of Rome. Soil gas radon concentration ranges between 7 and 176 kBq/m(3) indicating a large degree of variability in the NORM content and behavior of the parent soil material related in particular to the occurrence of two different lithologies. Soil gas radon mapping confirmed the existence of two different areas: one along the shoreline of the Bolsena lake, characterized by low soil radon level, due to a prevailing alluvial lithology; another close to the Bolsena village with high soil radon level due to the presence of the high radioactive volcanic rocks of the Vulsini volcanic district. Radon risk assessment, based on soil gas radon and permeability data, results in a map where the alluvial area is characterized by a probability to be an area with high Radon Index lower than 20 %, while probabilities higher than 30 % and also above 50 % are found close to the Bolsena village.

Risk of leukaemia or cancer in the central nervous system among children living in an area with high indoor radon concentrations: results from a cohort study in Norway.

BACKGROUND: Over the past few years, there has been growing interest in assessing the relationship between exposure to radon at home and the risk of childhood cancer. Previous studies have produced conflicting results, probably because of limitations assessing radon exposure, too few cancer cases and poorly documented health statistics. METHODS: We used a cohort approach of 0-15-year-old children to examine whether residential radon exposure was associated with childhood leukaemia and cancer in the central nervous system in the Oslo region. The study was based on Norwegian population registers and identified cancer cases from The Cancer Registry of Norway. The residence of every child was geo-coded and assigned a radon exposure. RESULTS: In all, 712 674 children were followed from 1967 to 2009 from birth to date of cancer diagnosis, death, emigration or 15 years of age. A total of 864 cancer cases were identified, 437 children got leukaemia and 427 got cancer in the central nervous system.Conclusions or interpretation:No association was found for childhood leukaemia. An elevated nonsignificant risk for cancer in the central nervous system was observed. This association should be interpreted with caution owing to the crude exposure assessment and possibilities of confounding.

Occupational radon exposure and lung cancer mortality: estimating intervention effects using the parametric g-formula.

BACKGROUND: Traditional regression analysis techniques used to estimate associations between occupational radon exposure and lung cancer focus on estimating the effect of cumulative radon exposure on lung cancer. In contrast, public health interventions are typically based on regulating radon concentration rather than workers' cumulative exposure. Estimating the effect of cumulative occupational exposure on lung cancer may be difficult in situations vulnerable to the healthy worker survivor bias. METHODS: Workers in the Colorado Plateau Uranium Miners cohort (n = 4,134) entered the study between 1950 and 1964 and were followed for lung cancer mortality through 2005. We use the parametric g-formula to compare the observed lung cancer mortality to the potential lung cancer mortality had each of 3 policies to limit monthly radon exposure been in place throughout follow-up. RESULTS: There were 617 lung cancer deaths over 135,275 person-years of follow-up. With no intervention on radon exposure, estimated lung cancer mortality by age 90 was 16%. Lung cancer mortality was reduced for all interventions considered, and larger reductions in lung cancer mortality were seen for interventions with lower monthly radon exposure limits. The most stringent guideline, the Mine Safety and Health Administration standard of 0.33 working-level months, reduced lung cancer mortality from 16% to 10% (risk ratio = 0.67 [95% confidence interval = 0.61 to 0.73]). CONCLUSIONS: This work illustrates the utility of the parametric g-formula for estimating the effects of policies regarding occupational exposures, particularly in situations vulnerable to the healthy worker survivor bias.

Chest X-ray screening examinations among French uranium miners: exposure estimation and impact on radon-associated lung cancer risk.

BACKGROUND: Medical surveillance of uranium miners can include periodic chest X-ray examinations. This study aimed to assess the X-ray exposure due to occupational health monitoring in the French cohort of uranium miners, and to test whether consideration of this additional radiation exposure impacts the excess risk of lung cancer death associated with radon exposure. METHOD: X-ray exposure due to occupational health monitoring was estimated retrospectively based on review of a sample of miners' medical records and bibliographic data. Four exposure scenarios were designed, differing in their assumptions about the type of procedures performed, their frequency, and the lung dose delivered. Radon exposure and lung doses from exposure to α-particle emitters and external γ rays have previously been individually assessed. Exposure-risk and dose-risk relations were estimated by Poisson regression with a linear excess relative risk (ERR) model. RESULTS: The cohort included 5086 miners with a mean follow-up duration of 30.1 years. The mean number of chest X-ray examinations ranged from 15.1 in the lowest to 34 in the highest-exposure scenario, and produced a mean cumulative lung dose ranging from 4.6 to 34.2 mGy. The role of occupation-related imaging screening X-ray procedures in total equivalent lung dose appeared insignificant compared to α-emitter exposure. X-ray exposure was not associated with lung cancer mortality risk. The ERR associated with radon remained significantly positive when X-ray exposure was included in the multivariate analysis. CONCLUSIONS: X-ray exposure did not confound the exposure-risk relation between radon and lung cancer.

Silica dust, radon and death from non-malignant respiratory diseases in German uranium miners.

OBJECTIVE: To quantify the relationship between death from non-malignant respiratory diseases (NMRD) and exposure to silica dust or radon in a cohort of 58,690 former German uranium miners. METHODS: In the follow-up period from 1946 to 2008, a total of 2336 underlying deaths from NMRDs occurred, including 715 deaths from chronic obstructive pulmonary diseases (COPD) and 975 deaths from silicosis or other pneumoconiosis. Exposure to respirable crystalline silica and radon was individually assessed by means of a comprehensive job-exposure matrix. Risk analyses were based on a linear Poisson regression model with the baseline stratified by age, calendar year and duration of employment. RESULTS: There was no increase in risk of death from COPDs or any other NMRDs in relation to cumulative exposure to silica (mean=5.9, max=56 mg/m(3)-years), except in the group of deaths from silicosis or other pneumoconiosis. Here, a strong non-linear increase in risk was observed. Cumulative radon exposure (mean=280; max=3224 Working Level Months) was not related to death from COPDs or any other NMRDs. CONCLUSIONS: The present findings do not indicate a relationship between mortality from COPD with silica dust or radon. However, validity of cause of death and lack of control for smoking remain potential sources of bias.

Radon-induced alterations in micro-RNA expression profiles in transformed BEAS2B cells.

Radon and its progeny are confirmed to be type I carcinogenic agents accounting for increased risks in 10% of observed lung cancers globally. However, the underlying carcinogenic mechanisms are largely unknown. In the present study, BEAS2B cells were directly exposed twice to 20,000 Bq/m(3) radon gas for 20 min once (first passage) and subsequently 10 times (fifth passage). The fifth-passage cells were then subcultured for 1 and 20 generations (named Rn5-1 and Rn5-20, respectively). Molecular mechanisms indicative of malignant transformation were assessed by determination of apoptosis, seroresistance, and microRNA (miRNA) expression profiles. The microRNA profiles were used to assess the functional annotations of the target genes. Data indicated an increased seroresistance and colony efficiency on soft agar, and enhanced apoptosis resistance in the Rn5-20 cells with significant differential expressions in some miRNA, including hsa-miR-483-3p, hsa-miR-494, hsa-miR-2115*, hsa-miR-33b, hsa-miR-1246, hsa-miR-3202, hsa-miR-18a, hsa-miR-125b, hsa-miR-17*, and hsa-miR-886-3p. Functional annotation demonstrated that these miRNA target genes were predominantly involved in the regulation of cell proliferation, differentiation, and adhesion during the process of malignant transformation, which is associated with signal pathways such as mitogen-activated protein kinase (MAPK), Int and Wg (Wnt), reactive oxygen species (ROS), nuclear factor κB (NF-κB), and other genes regulating cell cycles.

Occupational dust and radiation exposure and mortality from stomach cancer among German uranium miners, 1946-2003.

OBJECTIVES: 'Dusty occupations' and exposure to low-dose radiation have been suggested as potential risk factors for stomach cancer. Data from the German uranium miner cohort study are used to further evaluate this topic. METHODS: The cohort includes 58 677 miners with complete information on occupational exposure to dust, arsenic and radiation dose based on a detailed job-exposure matrix. A total of 592 stomach cancer deaths occurred in the follow-up period from 1946 to 2003. A Poisson regression model stratified by age and calendar year was used to calculate the excess relative risk (ERR) per unit of cumulative exposure to fine dust or from cumulative absorbed dose to stomach from α or low-LET (low linear energy transfer) radiation. For arsenic exposure, a binary quadratic model was applied. RESULTS: After adjustment for each of the three other variables, a statistically non-significant linear relationship was observed for absorbed dose from low-LET radiation (ERR/Gy=0.30, 95% CI -1.26 to 1.87), α radiation (ERR/Gy=22.5, 95% CI -26.5 to 71.5) and fine dust (ERR/dust-year=0.0012, 95% CI -0.0020 to 0.0043). The relationship between stomach cancer and arsenic exposure was non-linear with a 2.1-fold higher RR (95% CI 0.9 to 3.3) in the exposure category above 500 compared with 0 dust-years. CONCLUSION: Positive statistically non-significant relationships between stomach cancer and arsenic dust, fine dust and absorbed dose from α and low-LET radiation were found. Overall, low statistical power due to low doses from radiation and dust are of concern.

Oxidative damage in various tissues of rats exposed to radon.

Oxidative damage can be induced by many environmental stressors. 8-Hydroxydeoxyguanosine (8-OHdG) has been used as a biomarker of oxidative DNA damage in both in vitro and in vivo studies. In the present study, Wistar rats were exposed to radon gas at a concentration of 100,000Bq/m(3) for 12 h/d for 30, 60, and 120 d, equivalent to cumulative doses of 60, 120, and 240 working level months (WLM), respectively. Changes in levels of 8-OHdG, reactive oxygen species (ROS), and total antioxidant (T-AOC), as well as expressions of some DNA repair enzymes such as 8-oxoguanine DNA glycosylase (OGG1) and MutT homolog 1 (oxidized purine nucleoside triphosphatase, MTH1), were determined in rat urine, peripheral blood lymphocytes, and lung after exposure to radon. The results revealed an increase in 8-OHdG and ROS levels, a decrease in T-AOC levels, and reduced OGG1 and MTH1 expression levels. The elevated amount of 8-OHdG in urine or lymphocytes was positively correlated with the cumulative exposure dose, whereas OGG1 and MHT1 expression levels in lung were inversely correlated with cumulative exposure dose. These findings indicate that oxidative damage induced by radon may be involved in radon-induced carcinogenesis.

Response to "An unexpected mortality increase in the United States follows arrival of the radioactive plume from Fukushima: is there a correlation"?

The author responds to an article published in the Journal by Joseph J. Mangano and Janette D. Sherman suggesting that an increase in U.S. deaths shortly after Japan's Fukushima nuclear plant accident could be attributed to radiation from this accident arriving in the United States. The author writes that the cause of these deaths has not been analyzed and that there is no known mechanism for low-dose radiation to cause acute death in infants or adults. The author also notes that the cities under study with the lowest radiation fallout have the highest increases of death rates in the 14 weeks following Fukushima, while the Californian cities that would have received larger doses saw a decrease in death rate growth. He concludes that innumerable factors other than radiation likely are responsible for the bulk of the measured effect.