Extension of a generalized state-vector model of radiation carcinogenesis to consideration of dose rate.
Mathematical models for radiation carcinogenesis typically employ transition rates that either are a function of the dose to specific cells or are purely empirical constructs unrelated to biophysical theory. These functions either ignore or do not explicitly model interactions between the fates of cells in a community. This paper extends a model of mitosis, cell transformation, promotion, and progression to cases in which interacting cellular communities are irradiated at specific dose rates. The model predicts that lower dose rates are less effective at producing cancer when irradiation is by X- or gamma rays but are generally more effective in instances of irradiation by alpha particles up to a dose rate in excess of 0.01 Gy/day. The resulting predictions are compared with existing experimental data.
Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina, Chapel Hill 27599-7400.
D J
DJ
Crawford-Brown
W
W
Hofmann
D000818:Animals; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008433:Mathematics; D008938:Mitosis; D008954:Models, Biological; D009381:Neoplasms, Radiation-Induced / Q000453:epidemiology / Q000503:physiopathology*