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

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.

Human Lung Cancer Risks from Radon – Part III - Evidence of Influence of Combined Bystander and Adaptive Response Effects on Radon Case-Control Studies - A Microdose Analysis

“…It was found, at the world-wide mean radiation levels, that about 30% of the human lung cells should experience AR radioprotection and at the high UNSCEAR (2000) levels 100% of human lung cells should receive AR protection. From Parts I (Leonard et al 2010a) and II (Leonard et al 2010b), we show that the human lung cancer risk dose response should be non-linear from alpha particle cell damage and further, different ecological and geographical environments world-wide should impose a large range Adaptive Response radio-protection and a wide range of observed odds ratios of lung cancer risk as is indeed observed in the European (13 studies) and North American (8 studies) case-control studies as seen in Figure 1. This is supportive of the non-linear premises of Morgan (2006).…”

“…We believe that this three part study (Leonard et al 2010a, Leonard et al 2010b and this Part III) provides the first direct evidence of bystander and adaptive response effects on humans.…”

“…Conversely in the separate Part II (Leonard et al 2010b), we examined the potential influence of combined deleterious Bystander Effects and Adaptive Response radio-protection by assuming, based also on a very large amount of in vitro BE and AR data, that AR is operable for low LET ionizing radiations that humans routinely receive from natural background and man-made radiations. Significant to the Part II study of potential Adaptive Response effects on the human lung cancer risks from radon is the fact that single low LET radiation induced charged particle tracks through sensitive regions of cells induces an AR protection of 40 to 70 % against chromosome damage.…”

Calculations of the Radiation Dose for the Maximum Hormesis Effect

“…Radiation-adaptive responses have been reported as reductions of detrimental effects at low doses [19][20][21][22][23][24][25][26][27][28][29][30][31], and radiation hormesis as the hypothesis that low-dose radiation is beneficial to an organism [32][33][34][35][36][37][38][39][40]. The bystander effect [9,24,25,31,34,35,[41][42][43][44][45][46][47][48][49][50][51][52] and genomic instability [9,15,[24][25][26]30,31,34,[41][42]…”

“…In addition to LNT and hormesis, some possible models in the low-dose range (supra-linear, linear-quadratic, threshold, sigmoidal threshold, and hyper-radiosensitivity) have been proposed [52,56]. Biological findings and mathematical models at the molecular-cellular level have been studied to unravel the mysteries of low-dose exposure [32,[43][44][45][46][47][48][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68], and we have previously proposed a linear-hormesis coupling theory.…”