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Abstract

Residential radon has been found to be associated with lung cancer in epidemiological/ ecological studies and the researchers have inappropriately concluded that residential radon causes lung cancer. Their conclusion relates to the linear-no-threshold (LNT) hypothesisbased, risk-assessment paradigm; however, the LNT hypothesis has been invalidated in numerous studies. It is shown in this paper that our hormetic relative risk (HRR) model is consistent with lung cancer data where detailed measurements of radon in each home were carried out. Based on the HRR model, low-level radon radioactive progeny is credited for activated natural protection (ANP) against lung cancer including smoking-related lung cancer. The proportion B(x) (benefit function) of ANP beneficiaries increases as the average radon level x increases to near the Environmental Protection Agency’s action level of 4 picocuries/L (approximately 150 Bq m-3). As the average level of radon increases to somewhat above the action level, ANP beneficiaries progressively decrease to zero (B(x) decreases to 0), facilitating the occurrence of smoking-related lung cancers as well as those related to other less important risk factors. Thus, residential radon does not appear to cause lung cancer but rather to protect, in an exposure-level-dependent manner, from its induction by other agents (e.g., cigarette-smoke-related carcinogens).

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