The biological effects of ionizing radiation exposure are the result of a complex sequence of physical, chemical, biochemical, and physiological interactions which are modified by characteristics of the radiation, the timing of its administration, the chemical and physical environment, and the nature of the biological system. However, it is generally agreed that the health effects in animals originate from changes in individual cells, or possibly small groups of cells, and that these cellular changes are initiated by ionizations and excitations produced by the passage of charged particles through the cells. One way to begin a search for an understanding of health effects of radiation is through the development of phenomenological models of the response. Many models have been presented and tested in the slowly evolving process of characterizing cellular response. Different phenomena (LET dependence, dose rate effect, oxygen effect etc.) and different end points (cell survival, aberration formation, transformation, etc.) have been observed, and no single model has been developed to cover all of them. Instead, a range of models covering different end points and phenomena have developed in parallel. Many of these models employ similar assumptions about some underlying processes while differing about the nature of others. An attempt is made to organize many of the models into groups with similar features and to compare the consequences of those features with the actual experimental observations. It is assumed that by showing that some assumptions are inconsistent with experimental observations, the job of devising and testing mechanistic models can be simplified.
