BEIR VI Report Research Articles

Simultaneous measurements of radon, thoron and their progeny for inhalation dose assessment in indoors of Srinagar, J&K, India

A variety of toxins are known to affect indoor air quality, thereby affecting the health of the inhabitants of that region. One such natural contaminant is radon, which is a dense, colourless, odourless and inert gas. As per BEIR-VI report (Chauhan and Chauhan in J Environ Radioact, 2015. https://doi.org/10.1016/j.jenvrad.2015.03.009), Radon alone contributes to more than 50% of the total natural background radiation and is the second leading element causing lung cancer after smoking. Therefore, its quantification is vital to assess any risk to human health. In order to assess health risks, a recently developed LR-115 detector based technique was employed for time-integrated passive measurements of radon, thoron and their progeny concentrations. The annual average radon concentration was found to be 35.6 Bq m−3 and thus lies well below the global average of 40 Bq m−3. However, thoron concentration exceeded the global average value of 10 Bq m−3.

Human lung cancer risks from radon: influence from bystander and adaptive response non-linear dose response effects

The book examines the aspects of human lung cancer risks from radon following the publication BEIR VI report. The topic is covered in eight chapters and two appendices along with the usual heads of preface, acknowledgments, references and index. It is apparent that Dr Leonard was motivated to perform the research, publish three peer-reviewed papers and write this book, by the large amount of case–control human lung cancer data that exhibit a very wide variation in human lung cancer risks from radon. The author previously had success in his adaptive response (AR) analysis using a microdosimetry model tailored after that proposed by the pioneers of microdosimetry, Victor Bond, Myron Pollycove, Ludwig Feinendegen and others. In all prior AR work, he found that a single low-LET radiation-induced charged particle traversal through the cell was sufficient to trigger the AR protective mechanism, and that AR protection is independent of radiation type or cell species. What is so remarkable is that he shows that an extremely small amount of energy per traversal is sufficient to trigger the protective mechanism.

Human Lung Cancer Risks from Radon – Part I - Influence from Bystander Effects - A Microdose Analysis

Since the publication of the BEIR VI report in 1999 on health risks from radon, a significant amount of new data has been published showing various mechanisms that may affect the ultimate assessment of radon as a carcinogen, at low domestic and workplace radon levels, in particular the Bystander Effect (BE) and the Adaptive Response radio-protection (AR). We analyzed the microbeam and broadbeam alpha particle data of Miller et al. (1995, 1999), Zhou et al. (2001, 2003, 2004), Nagasawa and Little (1999, 2002), Hei et al. (1999), Sawant et al. (2001a) and found that the shape of the cellular response to alphas is relatively independent of cell species and LET of the alphas. The same alpha particle traversal dose response behavior should be true for human lung tissue exposure to radon progeny alpha particles. In the Bystander Damage Region of the alpha particle response, there is a variation of RBE from about 10 to 35. There is a transition region between the Bystander Damage Region and Direct Damage Region of between one and two microdose alpha particle traversals indicating that perhaps two alpha particle "hits" are necessary to produce the direct damage. Extrapolation of underground miners lung cancer risks to human risks at domestic and workplace levels may not be valid.

Comparative risk assessment of residential radon exposures in two radon-prone areas, Ştei (Romania) and Torrelodones (Spain)

Radon and radon progeny are present indoors, in houses and others dwellings, representing the most important contribution to dose from natural sources of radiation. Most studies have demonstrated an increased risk of lung cancer at high concentration of radon for both smokers and nonsmokers. The work presents a comparative analysis of the radon exposure data in the two radon-prone areas, Ştei, Transylvania, (Romania), in the near of old Romanian uranium mines and in the granitic area of Torrelodones town, Sierra de Guadarrama (Spain). Measurements of indoor radon were performed in 280 dwellings (Romania) and 91 dwellings (Spain) by using nuclear track detectors, CR 39. The highest value measured in Ştei area was 2650 Bq m − 3 and 366 Bq m − 3 in the Spanish region. The results are computed with the BEIR VI report estimates using the age-duration model at an exposure rate below 2650 Bq m − 3 . We used the EC Radon Software to calculate the lifetime lung cancer death risks for individuals groups in function of attained age, radon exposures and tobacco consumption. A total of 233 lung cancer deaths were observed in the Ştei area for a period of 13 years (1994–2006), which is 116.82% higher than expected from the national statistics. In addition, the number of deaths estimated for the year 2005 is 28, which is worth more than 2.21 times the amount expected by authorities. In comparison, for Torrelodones was rated a number of 276 deaths caused by lung cancer for a period of 13 years, which is 2.09 times higher than the number expected by authorities. For the year 2005 in the Spanish region were reported 32 deaths caused by pulmonary cancer, the number of deaths exceeding seen again with a factor of 2.10 statistical expectations. This represents a significantly evidence that elevated risk can strongly be associated with cumulated radon exposure.

Lung Cancer in French and Czech Uranium Miners: Radon-Associated Risk at Low Exposure Rates and Modifying Effects of Time since Exposure and Age at Exposure

Radon is recognized as a public health concern for indoor exposure. Precise quantification derived from occupational exposure in miners is still needed for estimating the risk and the factors that modify the dependence on cumulated exposure. The present paper reports on relationship between radon exposure and lung cancer risk in French and Czech cohorts of uranium miners (n = 10,100). Miners from these two cohorts are characterized by low levels of exposure (average cumulated exposure of less than 60 WLM) protracted over a long period (mean duration of exposure of 10 years) and by a good quality of individual exposure estimates (95% of annual exposures based on radon measurements). The modifying effect of the quality of exposure on the risk is analyzed. A total of 574 lung cancer deaths were observed, which is 187% higher than expected from the national statistics. This significantly elevated risk is strongly associated with cumulated radon exposure. The estimated overall excess relative risk per WLM is 0.027 (95% CI: 0.017-0.043, related to measured exposures). For age at exposure of 30 and 20 years since exposure, the ERR/WLM is 0.042, and this value decreases by approximately 50% for each 10-year increase in age at exposure and time since exposure. The present study emphasizes that the quality of exposure estimates is an important factor that may substantially influence results. Time since exposure and simultaneously age at exposure were the most important effect modifiers. No inverse exposure-rate effect below 4 WL was observed. The results are consistent with estimates of the BEIR VI report using the concentration model at an exposure rate below 0.5 WL.

ESTIMATED RISKS OF RADON-INDUCED LUNG CANCER FOR DIFFERENT EXPOSURE PROFILES BASED ON THE NEW EPA MODEL

Radon is a naturally occurring radioactive gas. When inhaled, radon can cause mutations that lead to lung cancer. Some new epidemiologic studies indicate that indoor radon is a public health problem. The BEIR VI report outlined its preferred two risk models for the combined effects of smoking and exposure to radon progeny, and listed the estimated risk to ever-smokers and never-smokers of both sexes due to lifetime exposure. However, exposures for shorter periods of time are of practical interest since exposure to elevated levels of radon may occur and end at any age. This study aims to produce practical tables of lifetime relative risks for exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 100 to 1,000 Bq m(-3). The calculations are based on the risk model developed recently by U.S. Environmental Protection Agency. The EPA's risk model is a single model that gives risk values midway between those obtained from the two BEIR VI preferred models. The detailed tables provide a clearer view of the age groups at higher risk and the effect of exposure duration. The results will help radiation protection practitioners to better communicate indoor radon risk to members of the public.

Lung cancer risk due to radon exposure for 10 or 20 years

Lung cancer risks due to lifetime radon exposure are given in the BEIR VI report. However, exposures for shorter periods of time are of practical interest since exposure to elevated levels of radon may occur and end at any age. This study aims to produce practical data of lifetime relative risks due to radon exposures for 10 or 20 years, and at various radon concentrations found in most homes from 50 to 500 Bq/m 3.

Comparative dosimetry of BEIR VI revisited.

The BEIR VI Committee applied recent developments in the comparative dosimetry of radon exposures in mines and homes to evaluate the so-called K-factor used to extrapolate the excess relative risk of lung cancer determined for underground uranium miners to exposures in homes. This paper describes methodological aspects of these developments that were specified ambiguously in the BEIR VI report. Specifically, in the section dealing with dosimetry (Appendix B of the BEIR VI report), the K-factor was unusually defined in terms of exposure to radon gas (K(gas)), and not in terms of exposure to potential alpha energy (K). An incorrect value of unity was calculated for K(gas). This implies a value of 0.44 for K. In this paper, we describe how application of the ICRP Publication 66 lung and dosimetric models to evaluate the regional lung dose per unit exposure to potential alpha-energy in mines and homes yields the value of K = unity. This confirms the BEIR VI Committee's choice of K = 1 for application in their risk extrapolation model. The paper also reviews the use of doses to specific sub-cellular targets in the evaluation of K. This yields a somewhat greater divergence in the corresponding estimates of K, but again an overall average value of K = unity. The paper describes the methods used to calculate alpha particle hit probabilities for specific subcellular targets, and the resulting estimates of single- and multiple-hit probabilities obtained for exposures in mines and homes, as a function of the respective exposure rates.

Residential radon and the LNT hypothesis

The question whether radon in aboveground situations represents a health hazard is important not only because of the high economic and social costs associated with radon surveys and the reduction of radon levels in homes, in the remediation of former uranium mining areas (e.g. in Saxony, Eastern Germany), etc., but—perhaps more importantly—because the radon controversy became an important test case for the validity of the linear-no-threshold (LNT) hypothesis, the collective dose concept, current relative biological effectiveness (RBE) estimates, and other central issues of legislation and regulatory control of low radiation doses. On the one hand, some institutions claim, based on miners' and a few case-control epidemiological studies (see, e.g., the BEIR VI report), that large numbers of additional lung cancers in the population are due to residential radon. On the other hand, various recent studies, for example, with never-smoking women in high-radon areas, as well as animal and cell experiments, indicate thresholds, perhaps even biopositive effects including the reduction of other types of cancer in areas with increased residential radon levels.

Do low dose-rate bystander effects influence domestic radon risks?

Purpose : Radon risks derive from exposure of bronchio-epithelial cells to high-linear energy transfer (LET) α -particles. α -particle exposure can result in bystander effects, where irradiated cells emit signals resulting in damage to nearby unirradiated bystander cells. This can result in non-linear dose-response relations, and inverse dose-rate effects. Domestic radon risk estimates are currently extrapolated from miner data, which are at both higher doses and higher dose-rates, so bystander effects on unhit cells could play a large role in the extrapolation of risks from mines to homes. Therefore, we extend an earlier quantitative mechanistic model of bystander effects to include protracted exposure, with the aim of quantifying the significance of the bystander effect for very prolonged exposures. Materials and methods : A model of high-LET bystander effects, originally developed to analyse oncogenic transformation in vitro, is extended to low dose-rates. The model considers radiation response as a superposition of bystander and linear direct e It attributes bystander effects to a small subpopulation of hypersensitive cells, with the bystander contribution dominating the direct contribution at very low acute doses but saturating as the dose increases. Inverse dose-rate effects are attributed to the replenishment of the hypersensitive subpopulation during prolonged irradiation. Results : The model was fitted to dose- and dose-rate-dependent radon-exposed miner data, suggesting that one directly hit target bronchio-epithelial cell can send bystander signals to about 50 neighbouring target cells. The model suggests that a naïve linear extrapolation of radon miner data to low doses, without accounting for dose-rate, would result in an underestimation of domestic radon risks by about a factor of 4, a value comparable with the empirical estimate applied in the recent BEIR-VI report on radon risk estimation. Conclusions : Bystander effects represent a plausible quantitative and mechanistic explanation of inverse dose-rate effects by high-LET radiation, resulting in non-linear dose-response relations and a complex interplay between the effects of dose and exposure time. The model presented provides a potential mechanistic underpinning for the empirical exposure-time correction factors applied in the recent BEIR-VI for domestic radon risk estimation.

Lifetime risk of lung cancer due to radon exposure projected to Japanese and Swedish populations.

Lifetime risk projections depend greatly on both background lung cancer rates and the selection of the risk model. Since background lung cancer rates differ from subject populations and the time, etiological risk of lifetime lung cancer mortality per unit radon exposure in WLM should be estimated for each subject population and the time of interest. To answer quantitatively how much are the differences among the projected risks for different populations, the Swedish case-control-study-based risk projection model was applied to the Japanese and Swedish populations from 1962 to 1997 as subject populations because of their distinct trends of lung cancer rates. To compare the results with the reference population and authorized risk projection models, U.S. population 1997 and the two risk projection models in BEIR VI report were applied, respectively. Lifetime risk of lung cancer mortality projected for Japanese, Swedish, and U.S. populations in 1997 per radon progeny exposure were estimated to range from 1.50 (0.40-3.19) x 10(-4) WLM(-1) to 9.86 (2.62-20.9) x 10(-4) WLM(-1), which could be compared to the detriment associated with a unit effective dose. Conclusive dose conversion coefficients in this study ranged from 2.05 (0.55-4.37) to 13.5 (3.59-28.6) mSv WLM(-1), and within this range the discrepancy between dosimetric and epidemiological approaches was included.

The Radon Equilibrium Factor and Comparative Dosimetry in Homes and Mines

The equilibrium factor, a measure of the degree of radioactive equilibrium between radon and its short-lived radioactive decay products, is often assumed to be 0.4 for risk assessment. While this is usually a reasonable assumption, there are important exceptions. In particular, in active mines where ventilation rates are high, the equilibrium factor can be much less than 0.4. In such cases, if lung dose rate is computed based on measured activity size distributions and normalised to radon concentrations, comparisons to lung dose rate in other environments must take into account possible differences in the equilibrium factor. In the comparative dosimetry section of the BEIR VI Report, this critical step was omitted. Thus, the ratio of home lung dose rate to diesel miner lung dose rate is actually 0.44, not 1 as stated in the Report. This oversight may have major public policy implications.

Testing a BEIR-VI suggestion for explaining the lung cancer vs. radon relationship for U.S. counties.

The BEIR-VI Report suggests that the large discrepancy between the observed lung cancer rate vs. radon exposure relationship for U.S. counties, and the predictions of linear no-threshold theory, may be explained by a strong negative correlation between smoking intensity and radon exposure. It proposes a model for testing that suggestion. We apply that model to the detailed data for U.S. counties; analysis shows that even a perfect negative correlation explains little more than half of the discrepancy, and the largest not-implausible correlation can explain less than a quarter of the discrepancy. We then extend the BEIR-VI suggestion to include a strong negative correlation between both the prevalence of smoking and the intensity of smoking. The largest not-implausible correlations can explain no more than 30% of the discrepancy. It is concluded that the previous interpretation of these data, that linear no-threshold theory fails this test, is sustained.

Letter to the Editor - Is Indoor Radon a Public Health Hazard? - the BEIR VI Report by K.L. Mossman

Letter to the Editor - Is Indoor Radon a Public Health Hazard? - the BEIR VI Report by K.L. Mossman

Biologically Based Analysis of the Data for the Colorado Uranium Miners Cohort: Age, Dose and Dose-Rate Effects

This study is a comprehensive analysis of the latest follow-up of the Colorado uranium miners cohort using the two-stage clonal expansion model with particular emphasis on effects related to age and exposure. The model provides a framework in which the hazard function for lung cancer mortality incorporates detailed information on exposure to radon and radon progeny from hard rock and uranium mining together with information on cigarette smoking. Even though the effect of smoking on lung cancer risk is explicitly modeled, a significant birth cohort effect is found which shows a linear increase in the baseline lung cancer risk with birth year of the miners in the cohort. The analysis based on the two-stage clonal expansion model suggests that exposure to radon affects both the rate of initiation of intermediate cells in the pathway to cancer and the rate of proliferation of intermediate cells. However, in contrast to the promotional effect of radon, which is highly significant, the effect of radon on the rate of initiation is found to be not significant. The model is also used to study the inverse dose-rate effect. This effect is evident for radon exposures typical for mines but is predicted to be attenuated, and for longer exposures even reversed, for the more protracted and lower radon exposures in homes. The model also predicts the drop in risk with time after exposure ceases. For residential exposures, lung cancer risks are compared with the estimates from the BEIR VI report. While the risk estimates are in agreement with those derived from residential studies, they are about two- to fourfold lower than those reported in the BEIR VI report.

Editorial - Is Indoor Radon a Public Health Hazard? - The BEIR VI Report

Editorial - Is Indoor Radon a Public Health Hazard? - The BEIR VI Report