which crosses shorter distances through the nucleus. Lethality can be related to the net absorption of a particular amount of total energy per cell, measured along a total path length through the nucleus—either a single track through a spherical nucleus or several shorter tracks through a flat nucleus. Calculations indicate a constant probability of 0.03–0.08 for a lethal event per micrometer of track (Jostes 1996). All radon alpha-particle effects at the low doses associated with environmental exposure from water occur from the passage of single particles through a small proportion of the cells in a tissue, so the dose-effect relationship will be a linear function of dose, with no dose-rate effects. This is true because variations in exposure change the number of cells hit by an alpha particle, rather than the amount of damage per cell. To calculate cancer risk it is then necessary to know the probability that a hit cell will undergo transformation, and the latent period and its age distribution before transformation to malignancy is complete. The latent period for single cells exposed to single tracks of alpha particles is unknown, but if it were long compared to the lifespan of the individual, the cancer risk would be correspondingly reduced, as suggested by Raabe (1987).

The important cellular subpopulation for carcinogenesis is not that of the rare cells killed by alpha-particle damage, but that of the cells that survive either with direct damage to their genetic material or with altered genomic stability. Because the calculated D37 is more than one alpha particle per cell in very low exposures, such as to ambient air or water, most exposed cells should survive, because it is extremely rare for any cell to be hit more than once. That might also account for the strong synergism displayed between radon exposure and cigarette-smoking: initial radon exposure leaves a viable, damaged cell, which is then stimulated further by the carcinogens found in cigarette smoke (Moolgavkar and others 1993; Brenner and Ward 1992).

Low-dose exposure also raises the question of whether radon alpha particles can give rise to radiation hormesis—the phenomenon whereby very low radiation doses are stimulatory and beneficial (Ueno and others 1996). If hormesis occurs through a stimulation of some kind of repair, the low stimulating dose must induce an excess repair capacity that can mend not only the damage caused by the initial dose, but also pre-existing endogenous cellular damage. That has been observed for repair of mitochondrial oxidative damage (Driggers and others 1996) but, evidence generally is indirect and difficult to obtain. Evidence of radiation hormesis is consequently controversial and will not be further considered here. Although extranuclear damage and extracellular ionization might play a role in some biologic effects (known as bystander effects), they are unlikely to play an important role in cell-killing (Hickman and others 1994; Dendy and others 1967). The flow of events that follow the production of DNA damage and other forms of cellular damage is therefore critical in understanding the development of malignancies.

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