Human Lung Cancer Risks from Radon - Part II - Influence from Combined Adaptive Response and Bystander Effects - A Microdose Analysis

International Academy of Hi-Tech Services, Inc.
Dose-Response (Impact Factor: 1.22). 10/2011; 9(4):502-53. DOI: 10.2203/dose-response.09-058.Leonard
Source: PubMed


In the prior Part I, the potential influence of the low level alpha radiation induced bystander effect (BE) on human lung cancer risks was examined. Recent analysis of adaptive response (AR) research results with a Microdose Model has shown that single low LET radiation induced charged particles traversals through the cell nucleus activates AR. We have here conducted an analysis based on what is presently known about adaptive response and the bystander effect (BE) and what new research is needed that can assist in the further evaluation human cancer risks from radon. We find that, at the UNSCEAR (2000) worldwide average human exposures from natural background and man-made radiations, the human lung receives about a 25% adaptive response protection against the radon alpha bystander damage. At the UNSCEAR (2000) minimum range of background exposure levels, the lung receives minimal AR protection but at higher background levels, in the high UNSCEAR (2000) range, the lung receives essentially 100% protection from both the radon alpha damage and also the endogenic, spontaneously occurring, potentially carcinogenic, lung cellular damage.

    • "First one describes the observed object as a black box while the latter tries to find its integral separate elements. Both ways are used in the context of an influence of ionising radiation on the single cells or the cell colonies – as stochastic or deterministic computational models (UNSCEAR, 1986;Moolgavkar and Luebeck, 1990;Feinendegen et al., 2000;Feinendegen et al., 2010;Brenner et al., 2001;Calabrese and Baldwin, 2003;Feinendegen, 2005;Scott et al., 2007;Scott et al., 2013;Leonard, 2008;Shuryak et al., 2009;Bogen, 2011;Leonard et al., 2011a;Leonard et al., 2011b;Scott, 2011;Scott, 2013;Tavares and Tavares, 2013;Wodarz et al., 2014). In 2011 the fully stochastic and mechanistic approach using the Markov Chain Monte Carlo method was implemented to the virtual cells colony (Fornalski et al., 2011a;Fornalski et al., 2011b), and a significant development of the model was proposed afterwards (Fornalski, 2014b). "
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    ABSTRACT: In this paper full description of the mechanistic model of the cells irradiation is presented. The model is based on the computational Quasi-Markov Chain Monte Carlo method with a stochastic tree of probabilities and using the biophysical input. The biophysics of the cells is described by the probabilities and probability distributions provided as an input. Many biophysical aspects are implemented into the model, i.e. the adaptive response effect or the bystander effect. It results in the sigmoidal relationships for carcinogenic risk as a function of the irradiation. The methodology used makes the model universal and practical for the simulations of general processes. However, the presented theoretical model does not describe the real cells and tissues. Also the exposure geometry, type of radiation as well as microdosimetry are not taken into account in this model. The model is focused mainly on the creation of general and maximal wide mathematical description of irradiated hypothetical cells treated as complex physical systems.
    No preview · Article · Dec 2014 · International Journal of Low Radiation
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    ABSTRACT: 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.
    Full-text · Article · Apr 2011 · Dose-Response
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    ABSTRACT: Since the publication of the BEIR VI (1999) report 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, in particular the potentially deleterious Bystander Effect (BE) and the potentially beneficial Adaptive Response radio-protection (AR). The case-control radon lung cancer risk data of the pooled 13 European countries radon study (Darby et al 2005, 2006) and the 8 North American pooled study (Krewski et al 2005, 2006) have been evaluated. The large variation in the odds ratios of lung cancer from radon risk is reconciled, based on the large variation in geological and ecological conditions and variation in the degree of adaptive response radio-protection against the bystander effect induced lung damage. The analysis clearly shows Bystander Effect radon lung cancer induction and Adaptive Response reduction in lung cancer in some geographical regions. It is estimated that for radon levels up to about 400 Bq m(-3) there is about a 30% probability that no human lung cancer risk from radon will be experienced and a 20% probability that the risk is below the zero-radon, endogenic spontaneous or perhaps even genetically inheritable lung cancer risk rate. The BEIR VI (1999) and EPA (2003) estimates of human lung cancer deaths from radon are most likely significantly excessive. The assumption of linearity of risk, by the Linear No-Threshold Model, with increasing radon exposure is invalid.
    Full-text · Article · Jul 2012 · Dose-Response
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