Air Force Academy, United States
Air Force Academy, United States

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Leonard B.E.,International Academy of Hi Technology Services | Thompson R.E.,Johns Hopkins Medical Center | Beecher G.C.,International Academy of Hi Technology Services
Dose-Response | Year: 2011

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. © 2011 University of Massachusetts.


Leonard B.E.,International Academy of Hi Technology Services | Thompson R.E.,Johns Hopkins Medical Center | Beecher G.C.,International Academy of Hi Technology Services
Dose-Response | Year: 2011

Since the publication of the BEIR VI report in 1999 on health risks from radon, a significantamount of new data has been published showing various mechanisms that mayaffect the ultimate assessment of radon as a carcinogen, at low domestic and workplaceradon 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 etal. (1995, 1999), Zhou et al. (2001, 2003, 2004), Nagasawa and Little (1999, 2002), Hei etal. (1999), Sawant et al. (2001a) and found that the shape of the cellular response toalphas is relatively independent of cell species and LET of the alphas. The same alpha particletraversal dose response behavior should be true for human lung tissue exposure toradon progeny alpha particles. In the Bystander Damage Region of the alpha particleresponse, there is a variation of RBE from about 10 to 35. There is a transition regionbetween the Bystander Damage Region and Direct Damage Region of between one andtwo microdose alpha particle traversals indicating that perhaps two alpha particle "hits"are necessary to produce the direct damage. Extrapolation of underground miners lungcancer risks to human risks at domestic and workplace levels may not be valid. © 2011 University of Massachusetts.


PubMed | International Academy of Hi Technology Services
Type: Journal Article | Journal: Dose-response : a publication of International Hormesis Society | Year: 2012

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.


PubMed | International Academy of Hi Technology Services
Type: Journal Article | Journal: Dose-response : a publication of International Hormesis Society | Year: 2012

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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