Article

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

ABSTRACT

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: 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.
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