level, has motivated investigations to determine whether specific lung-cancers can be linked to radon; that is, is there a ''signature" that identifies a particular cancer as caused by radon? Demonstration of a signature would add specificity to risk assessments and even permit the designation of lung-cancers in individuals as caused by radon or some other factor. The committee reviewed the literature for evidence of signatures of radon-related lung-cancer


The committee's approach to assessing the risks associated with indoor radon had multiple components. Analysis of the miner data supplied a model describing the relationship between cumulative exposure to radon and lung-cancer risk; that model development is described in chapter 3 and appendix A. The greatest proportion of the population's exposure to radon is at the lower end of the distribution of residential concentrations (Figure 1-4), a distribution which results in exposures across the lifespan substantially lower than the cumulative exposures received by most of the miners in the epidemiologic studies.

As a basis for selecting the preferred exposure-response model, the committee reviewed relevant biologic information on mechanisms of DNA damage by alpha particles and the dosimetry of alpha particles at exposures relevant to environmental exposures. This review, described in chapter 2, led to the conclusion that, at typical indoor exposure levels and over a typical lifetime, target-cell locations in the respiratory tract would be traversed by no more than a single alpha particle. Even allowing for DNA repair and cellular lethality, such a single alpha-particle traversal is known to produce, with significant probability, large-scale damage to the DNA in surviving traversed cells. Thus, at low exposure levels, a further decrease in the exposure would result in a proportionate decrease in the number of target cells traversed by single alpha particles, and thus suffering large scale DNA damage. Each of these heavily damaged traversed cells would still be expected to show the same probability of initiating the sequence of events that ultimately lead to carcinogenesis. Taken together, these observations provide a rationale for the committee's assumption that the dose-response relationship for radon-induced lung-cancer is likely to be best described by a linear model with no threshold in dose.

The committee noted, as discussed elsewhere in this report, that statistical considerations preclude a direct investigation of low-dose thresholds for radon-induced carcinogenesis, at least in human populations. However, the view of the committee was that the mechanistic and experimental considerations were sufficiently compelling to support assumption of a linear/nonthreshold dose-response relationship at low radon exposures. It is also important to note that the linear/nonthreshold approach which the committee has adopted is based on mechanistic considerations relating to the nature of alpha-particle induced energy deposition

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