The dependence of the induction of cancer on the absorbed dose of ionizing radiations has been specified in terms of increasing complexity. The first notion of simple proportionality (the “linear hypothesis”) is now frequently replaced with a dependence of both the first and second powers of the dose (the “linear-quadratic model”), which implies proportionality at low doses only. Microdosimetric considerations, in particular the theory of dual radiation action, would be in accord with this relation if tumors were to arise from single cells as the result of a transformation that is autonomous (i.e., depends only on the radiation received by the cell). In this case, it most be expected that the linear portion of the dose-effect curve is dose rate independent, but that the quadratic component may decrease with decreasing dose rate because of repair during the interval between two events (energy depositions by individual particles). Various data appeared to be in agreement with this picture. However, it was shown some time ago that the dose-incidence relation of some neoplasms indicates a non-autonomous response because of departure from a linear dependence when the mean number of events in cells is much less than one in neutron irradiations. Another discrepancy is the repeated observation that reduction of dose rate, while resulting in the expected lessening of the effectiveness of low-LET radiation, increases the effectiveness of neutrons (especially in the case of oncogenic cell transformation). As will be shown, it is possible to account for this phenomenon, although at this point the limitations of the available data make the explanation semi-quantitative and therefore still somewhat hypothetical. However, it should be noted that it does not even require a nonautonomous response and thus is at least an example of the complexities that can arise in the earliest (biophysical) stage of radiation carcinogenesis.
©1988Health Physics Society