Activity concentrations of222Rn,220Rn,and their decay products in german dwellings,dose calculations and estimate of risk

Summary Measurements of the concentrations of²²²Rn, its short-lived decay products and of²¹²Pb -²¹²Bi were performed in 150 dwellings and in the open air in the Federal Republic of Germany. The concentration of²²²Rn was measured by electrostatic deposition of²¹⁸Po. The concentrations of the short-lived decay products were measured by air sampling and alpha-spectroscopy. It was found that inside dwellings the average potential alpha-energy concentration of the short-lived daughters is about three times higher than in the open air. The total potential alpha-energy concentration indoors amounts to 2.6 · 10^–3 Working Level (W. L.). Direct measurements of the equilibrium factor inside dwellings gave a mean value of 0.3. A strong dependence of the potential alpha energy concentration on the ventilation rate in dwellings has been observed. These ventilation effects exceed the effects caused by differences in the activity concentrations due to different building materials.The dose calculation results in an average dose to the whole lung due to the inhalation of short-lived radon daughters of about 0.05–0.2 mGy/a. An estimate of risk - based on the risk factors for uranium miners - shows an average lifetime risk of about 6 · 10^–4 for the incidence of lung cancer caused by inhalation of radon and thoron daughters in dwellings in the Federal Republic of Germany.The research programme was supported by the Bundesminister des Innern of the Federal Republic of Germany     

Quantitative health impact of indoor radon in France

Radon is the second leading cause of lung cancer after smoking. Since the previous quantitative risk assessment of indoor radon conducted in France, input data have changed such as, estimates of indoor radon concentrations, lung cancer rates and the prevalence of tobacco consumption. The aim of this work was to update the risk assessment of lung cancer mortality attributable to indoor radon in France using recent risk models and data, improving the consideration of smoking, and providing results at a fine geographical scale. The data used were population data (2012), vital statistics on death from lung cancer (2008–2012), domestic radon exposure from a recent database that combines measurement results of indoor radon concentration and the geogenic radon potential map for France (2015), and smoking prevalence (2010). The risk model used was derived from a European epidemiological study, considering that lung cancer risk increased by 16% per 100 becquerels per cubic meter (Bq/m³) indoor radon concentration. The estimated number of lung cancer deaths attributable to indoor radon exposure is about 3000 (1000; 5000), which corresponds to about 10% of all lung cancer deaths each year in France. About 33% of lung cancer deaths attributable to radon are due to exposure levels above 100 Bq/m³. Considering the combined effect of tobacco and radon, the study shows that 75% of estimated radon-attributable lung cancer deaths occur among current smokers, 20% among ex-smokers and 5% among never-smokers. It is concluded that the results of this study, which are based on precise estimates of indoor radon concentrations at finest geographical scale, can serve as a basis for defining French policy against radon risk.     

Lung cancer incidence attributable to residential radon exposure in Finland

This study aimed to estimate (1) the number of avoidable lung cancer cases attributable to residential radon in Finland in 2017, separately by age, sex, dwelling type and smoking status, (2) the impact of residential radon alone and the joint effect of residential radon and smoking on the number of lung cancers and (3) the potential decrease in the number of radon-attributable lung cancers if radon concentrations exceeding specified action levels (100, 200 and 300 Bq m^?3) would have been mitigated to those levels. Population-based surveys of radon concentrations and smoking patterns were used. Observed radon levels were contrasted with 25 Bq m^?3 representing a realistic minimum level of exposure. Lung cancer risk estimates for radon and smoking were derived from literature. Lastly, the uncertainty due to the estimation of exposure and risk was quantified using a computationally derived uncertainty interval. At least 3% and at most 8% of all lung cancers were estimated as being attributable to residential radon. For small cell carcinoma, the proportion of cases attributable to radon was 8–13%. Among smokers, the majority of the radon-related cases were attributable to the joint effect of radon and smoking. Reduction of radon exposure to 100 Bq m^?3 action level would eliminate approximately 30% of radon-attributable cases. Estimates were low compared with the literature, given the (relatively high) radon levels in Finland. This was mainly due to the lower radon levels and higher smoking prevalence in flats than in houses and a more realistic point of comparison, factors which have been ignored in previous studies. The results can guide actions in radon protection and in prevention of lung cancers.

     

Lung cancer and indoor radon exposure in the north of Portugal--an ecological study

BackgroundIndoor radon exposure is a well documented environmental factor as a leading cause of lung cancer. Objectives: The aim of this study was to assess the risk of lung cancer and estimate the number of deaths due to indoor radon exposure in the north of Portugal, between 1995 and 2004. Methods: The sixth Biological Effects of Ionizing Radiation Committee (BEIR VI) preferred models were applied to estimate the risk of developing lung cancer induced by indoor radon exposure, by age and level of exposure, and calculated the number of lung cancer deaths attributable to this exposure. Lung cancer mortality data were granted by the North Regional Health Administration and indoor radon concentrations resulted from a national survey conducted by the Portuguese Environmental Agency. The smoking habit was accounted with two methods. A submultiplicative interaction between smoking and indoor radon exposure was considered. Results: Depending on the model applied and the method used to account for the smoking habit, the estimated number of lung cancer deaths attributed to indoor radon exposure, in northern Portugal, ranges from 1565 to 2406, for the period between 1995 and 2004. This indicates that of the 8514 lung cancer deaths observed, from 18 to 28% could be associated with indoor radon exposure.ConclusionsThis was the first study realized in Portugal on the impact of indoor radon exposure in lung cancer mortality. The application of the BEIR VI models led to a high number of lung cancer deaths due to indoor radon exposure.     

Age-adjustment in experimental animal data and its application to lung cancer in radon-exposed rats

Procedures for age-adjustment of cancer fractions are proposed which do not require fixed age intervals. The full available information on survival times can then be used, which is especially important in small treatment groups. For incidental cancers a non-decreasing prevalence function and for fatal cancers the Kaplan-Meier estimator is used. In the latter case, the estimated competing risk of the control population is standardized, not its true survival. This makes the technique also applicable to treatment groups with high incidence, which otherwise may give adjusted rates above 100%. In the application part these age-adjustment techniques are used here to study lung cancer in radon-exposed Wistar and Sprague-Dawley rats. The data include a classification in fatal and incidental lung cancers. For fatal lung cancer, the lifetime excess absolute risk (LEAR) at 1 WLM averaged over all exposed groups is 0.67×10^–4 for the Wistar rats, while for the Sprague-Dawley rats it is 0.40×10^–4. For the Sprague-Dawley rats, there are several groups exposed later in life. When the averaging is restricted to animals with start of exposure prior to 150 days of age, the weighted average risk among the Sprague-Dawley rats is 0.79×10^–4. Compared to groups with similar exposures as young adults (up to about 150 days), animals exposed later in life have substantially lower lifetime risks. The Wistar rats include groups with roughly equal exposure rates and ages at start of exposure, but with increasing exposure duration. Within these groupings the LEAR at 1 WLM does not decrease with additional exposure at higher age, as would be expected if the risk from exposures at different ages would be additive.     

Case-control study of lung cancer and combined home and work radon exposure in the town of Lermontov

Relation between the risk of lung cancer and combined home and work indoor radon exposure was studied on the example of the population of Lermontov town (Stavropol Region, Russia). The town is situated in the former uranium mining area. Case (121 lung cancer cases) and control (196 individuals free of lung cancer diagnosis) groups of the study included both ex-miners and individuals that were not involved in the uranium industry. Home and work radon exposures were estimated using archive data as well as contemporary indoor measurements. The results of our study support the conclusion about the effect of radon exposure on the lung cancer morbidity.     

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

Radiation and Environmental Biophysics - Indoor exposure to natural radon is a factor that influences lung cancer risk worldwide. The present study includes a meta-analysis of epidemiological data...     

The conversion of exposures due to radon into the effective dose: the epidemiological approach

The risks and dose conversion coefficients for residential and occupational exposures due to radon were determined with applying the epidemiological risk models to ICRP representative populations. The dose conversion coefficient for residential radon was estimated with a value of 1.6 mSv year^?1 per 100 Bq m^?3 (3.6 mSv per WLM), which is significantly lower than the corresponding value derived from the biokinetic and dosimetric models. The dose conversion coefficient for occupational exposures with applying the risk models for miners was estimated with a value of 14 mSv per WLM, which is in good accordance with the results of the dosimetric models. To resolve the discrepancy regarding residential radon, the ICRP approaches for the determination of risks and doses were reviewed. It could be shown that ICRP overestimates the risk for lung cancer caused by residential radon. This can be attributed to a wrong population weighting of the radon-induced risks in its epidemiological approach. With the approach in this work, the average risks for lung cancer were determined, taking into account the age-specific risk contributions of all individuals in the population. As a result, a lower risk coefficient for residential radon was obtained. The results from the ICRP biokinetic and dosimetric models for both, the occupationally exposed working age population and the whole population exposed to residential radon, can be brought in better accordance with the corresponding results of the epidemiological approach, if the respective relative radiation detriments and a radiation-weighting factor for alpha particles of about ten are used.     

Biologically Based Prediction of Empirical Nonlinearity in Lung Cancer Risk vs. Residential/ Occupational Radon Exposure

Ecologic U.S. county data suggest negative associations between residential radon exposure and lung cancer mortality (LCM) that are inconsistent with clearly positive ones revealed by individual data on underground miners. If this inconsistency is due to competing effects of induced cell killing vs. mutations in alpha-radiation exposed bronchial epithelium, then linear extrapolation from miner data may overestimate typical residential radon risks. To investigate the plausibility of this hypothesis, a biologically based “cytodynamic 2-stage” (CD2) cancer-risk model was fit to combined 1950 to 1954 age-specific person-year data on white females of age 40+ y in 2821 U.S. counties (～90% never-smokers), and on five cohorts of underground miners who never smoked, conditional on a realistic rate of alpha-radiation-induced killing of human lung cells, and on linear-no-threshold dose-response relations for both processes assumed to affect cancer risk (alpha-induced mutations and cell killing). As summarized previously (Bogen, K.T., Hum. Exper. Toxicol. 17:691-6, 1998), a good CD2 fit was obtained that involved biologically plausible parameter values and (without further optimization) also predicted inverse dose-rate effects observed in the nonsmoking miners. The present paper reports mathematical details of the CD2 model used, as well as additional modeling results involving the same combined data set. The results obtained are consistent with the hypotheses that low-level radon exposure is nonlinearly related to LCM risk, and that current linear no-threshold extrapolation models overestimate LCM risk associated with relatively low residential radon concentrations (<～200?Bq m^?3). Testing this hypothesis would require more extensive individual-level epidemiological data relating residential radon exposures to LCM than are currently available.     

The relative biological effectiveness of alpha-radiation during human lung exposure to irradiation

The assessment of the relative biological effectiveness (RBE) for alpha-radiation was held in the cases of inhalation of radon progeny and incorporation of plutonium in lungs. It is based on simulation of lung cancer radiation risk for different types of radiation. Specific radiation risk models developed according to the results of direct epidemiological studies are used for the simulation. These include two published risk models for uranium miners and nuclear workers of the Mayak facilities in the former Soviet Union. Additionally two lung cancer risk models are developed and described for the following cases: population indoor radon exposure and low-linear-energy-transfer reference radiation exposure. By the results of lifetime lung cancer risk simulation the RBE values range from 11 to 12 and from 1.7 to 4.9 for the cases of plutonium incorporation and of radon progeny exposure accordingly. The significant uncertainty of radiation risk models results in significant variation of RBE assessments. Rough estimations of RBE values 90% confidence interval are from unit fraction to 25 and from 2 to 50 for the cases of radon progeny exposure and plutonium incorporation accordingly.     

Radon, smoking and lung cancer risk: results of a joint analysis of three European case-control studies among uranium miners

A combined analysis of three case-control studies nested in three European uranium miner cohorts was performed to study the joint effects of radon exposure and smoking on lung cancer death risk. Occupational history and exposure data were available from the cohorts. Smoking information was reconstructed using self-administered questionnaires and occupational medical archives. Linear excess relative risk models adjusted for smoking were used to estimate the lung cancer risk associated with radon exposure. The study includes 1046 lung cancer cases and 2492 controls with detailed radon exposure data and smoking status. The ERR/WLM adjusted for smoking is equal to 0.008 (95% CI: 0.004-0.014). Time since exposure is shown to be a major modifier of the relationship between radon exposure and lung cancer risk. Fitting geometric mixture models yielded arguments in favor of a sub-multiplicative interaction between radon and smoking. This combined study is the largest case-control study to investigate the joint effects of radon and smoking on lung cancer risk among miners. The results confirm that the lung carcinogenic effect of radon persists even when smoking is adjusted for, with arguments in favor of a sub-multiplicative interaction between radon and smoking.     

Occurrence of radon in some schools of Parma and Reggio Emilia (Northern Italy)

Summary Forty-seven measurement of radon concentration were made in some schools of Parma, Reggio Emilia, Albinea and Borzano. The method used was that of activated carbon canisters, which were placed in classrooms, laboratories, libraries and headmaster's offices for at least 48 hours in the period November '90–March '91. It was possible to determine the amount of radon in each canister counting the Pb-214 and Bi-214 gamma emitters by means of NaI (Tl) and Ge (I) detectors. The mean radon concentrations were: 20 Bq/m³ in Parma; 24 Bq/m³ in Reggio Emilia; 46 Bq/m³ in Borzano and 52 Bq/m³ in Albinea. The values recorded in schools are similar to the values previously recorded in dwellings of Parma and Reggio Emilia.     

NOTCH1, HIF1A and Other Cancer-Related Proteins in Lung Tissue from Uranium Miners—Variation by Occupational Exposure and Subtype of Lung Cancer

Background

Radon and arsenic are established pulmonary carcinogens. We investigated the association of cumulative exposure to these carcinogens with NOTCH1, HIF1A and other cancer-specific proteins in lung tissue from uranium miners.

Methodology/Principal Findings

Paraffin-embedded tissue of 147 miners was randomly selected from an autopsy repository by type of lung tissue, comprising adenocarcinoma (AdCa), squamous cell carcinoma (SqCC), small cell lung cancer (SCLC), and cancer-free tissue. Within each stratum, we additionally stratified by low or high level of exposure to radon or arsenic. Lifetime exposure to radon and arsenic was estimated using a quantitative job-exposure matrix developed for uranium mining. For 22 cancer-related proteins, immunohistochemical scores were calculated from the intensity and percentage of stained cells. We explored the associations of these scores with cumulative exposure to radon and arsenic with Spearman rank correlation coefficients (r_s). Occupational exposure was associated with an up-regulation of NOTCH1 (radon r_s = 0.18, 95% CI 0.02–0.33; arsenic: r_s = 0.23, 95% CI 0.07–0.38). Moreover, we investigated whether these cancer-related proteins can classify lung cancer using supervised and unsupervised classification. MUC1 classified lung cancer from cancer-free tissue with a failure rate of 2.1%. A two-protein signature discriminated SCLC (HIF1A low), AdCa (NKX2-1 high), and SqCC (NKX2-1 low) with a failure rate of 8.4%.

Conclusions/Significance

These results suggest that the radiation-sensitive protein NOTCH1 can be up-regulated in lung tissue from uranium miners by level of exposure to pulmonary carcinogens. We evaluated a three-protein signature consisting of a physiological protein (MUC1), a cancer-specific protein (HIF1A), and a lineage-specific protein (NKX2-1) that could discriminate lung cancer and its major subtypes with a low failure rate.     

Long-term variation of outdoor radon equilibrium equivalent concentration

Long-term variation of outdoor radon equilibrium equivalent concentration was investigated from 1982 to 1992 at a semi-natural location 10 km north of Munich, southern Germany. For this period the continuous measurement yielded a long-term average of 8.6 Bq·m^–3 (arithmetic mean) and 6.9 Bq·m^–3 (geometric mean), from which an average annual effective dose of 0.14 mSv due to outdoor radon can be derived. A long-term trend of the radon concentration was not detectable over the whole period of observation. However, by time series analysis, a long-term cyclic pattern was identified with two maxima (1984–1986, 1989–1991) and two minima (1982–1983, 1987–1988). The seasonal pattern is characterized by an autumn maximum and an early summer minimum. On average, the seasonal maximum in October was found to be higher by a factor of 2 than the June minimum. The diurnal variation of the radon concentration shows a maximum in the early morning and a minimum in the afternoon. On average, this maximum is a factor of 2 higher than the minimum. In the long term a seasonal pattern was observed for diurnal variation, with an average diurnal maximum to minimum ratio of 1.5 in winter compared with 3.5 in the summer months. The radon concentration is correlated with a meteorological parameter (stagnation index) which takes into account horizontal and vertical exchange processes and the wash-out of aerosols in the lower atmosphere.Dedicated to Prof. F. Waschsmann on the occasion of this 90th birthday     

Estimation of dose rate for indoor radon from building materials

The internal dose rate due to indoor radon (Rn) emissions from building materials is estimated. It is observed that the contribution from building materials to the dose rate is very small. The average indoor radon concentration in 75 different rooms is found to be 55 ± 12 Bq. m^–3. Assuming an occupancy factor of 0.8, the annual average effective dose equivalent is 1.7 mSv. It seems that soil gas is mainly responsible for the internal exposure from indoor Rn.     

Radon sources and impacts: a review of mining and non-mining issues

Radon is a ubiquitous natural carcinogen derived from the three primordial radionuclides of the uranium series (²³⁸U and ²³⁵U) and thorium series (²³²Th). In general, it is present at very low concentrations in the outdoor or indoor environment, but a number of scenarios can give rise to significant radiological exposures. Historically, these scenarios were not recognised, and took many centuries to understand the links between the complex behaviour of radon and progeny decay and health risks such as lung cancer. However, in concert with the rapid evolution in the related sciences of nuclear physics and radiological health in the first half of the twentieth century, a more comprehensive understanding of the links between radon, its progeny and health impacts such as lung cancer has evolved. It is clear from uranium miner studies that acute occupational exposures lead to significant increases in cancer risk, but chronic or sub-chronic exposures, such as indoor residential settings, while suggestive of health risks, still entails various uncertainties. At present, prominent groups such as the BEIR or UNSCEAR committees argue that the ‘linear no threshold’ (LNT) model is the most appropriate model for radiation exposure management, based on their detailed review and analysis of uranium miner, residential, cellular or molecular studies. The LNT model implies that any additional or excess exposure to radon and progeny increases overall risks such as lung cancer. A variety of engineering approaches are available to address radon exposure problems. Where high radon scenarios are encountered, such as uranium mining, the most cost effective approach is well-engineered ventilation systems. For residential radon problems, various options can be assessed, including building design and passive or active ventilation systems. This paper presents a very broad but thorough review of radon sources, its behaviour (especially the importance of its radioactive decay progeny), common mining and non-mining scenarios which can give rise to significant radon and progeny exposures, followed by a review of associated health impacts, culminating in typical engineering approaches to reduce exposures and rehabilitate wastes.