others 1990; Nagasawa and Little 1992; Deshpande and others 1996). Again, both intercellular communication and tissue-culture factors could be involved in these changes. It is important to note here, however, that SCE formation is unlikely to be relevant in carcinogenesis.

Brooks and his colleagues (1990a) have demonstrated that when cells were exposed simultaneously to very low doses of alpha particles (6 cGy) and x rays, the response to the x rays with respect to both cell killing and induction of micronuclei was markedly increased. That suggests that the alpha particles change the responsiveness of the whole cell population, even though only a small percentage of the total cell population was traversed by alpha particles. The studies were conducted with confluent lung epithelial cells, so the damaged cells could potentially transmit information to neighboring cells. Clastogenic factors have also been isolated from the blood of Chernobyl accident victims; these factors remained in the blood for years after the exposure (Emerit and others 1995).

The significance of cellular responses in "bystander" cells in the development of radiation-related disease and risk cannot be defined at this time. However, since cellular changes can be induced in more cells than are traversed by alpha particles, it might be necessary to redefine target size for alpha particles to include a much larger volume than the cell nucleus through which the radiation traverses.

Thus, the long-accepted assumption that causing a heritable effect, such as cancer, requires a track to pass through the nucleus of affected cells is no longer unequivocal, in that now there is limited evidence that an ionizing event in 1 cell can affect its neighbor(s). The data are intriguing, but there is no real evidence that cells that are adjacent to traversed cells are damaged in such a way as to be transformed to a malignant state, nor has a cellular or molecular mechanism been proposed for how this could occur. In any case, the so-called bystander effect is unlikely to affect the concept of linearity. For a low dose-rate alpha-particle exposure, the number of cells traversed, say per year, is a small fraction of the total and doubling the dose approximately doubles the number of cells traversed by a track (rather than doubling the number of tracks in each cell, as with x rays). Consequently, the linear relationship between dose and effect is still the most tenable, whether the carcinogenic event results from a direct effect on the cell concerned or from an indirect effect from damage to a neighboring cell.


Alpha particles, which produce a high density of ionizations along their path (high-LET), differ greatly from sparsely ionizing (low-LET) radiations, such as x rays in their microscopic, spatial, and temporal patterns of interactions with cells,

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