Radiation-induced cell inactivation as a cause for cancer promotion

In space research, estimates of health risks from high-LET radiation, as well as from mixed fields are needed. Features of several applications of the biologically based two step clonal expansion (TSCE) model on data with high-LET radiation, normally α-particles from radon and from Thorotrast, are reviewed. One conclusion is that radiation might not only influence the initiating event in carcinogenesis, but may also act as a promoter. A possible mechanism which gives a promoting action from cell inactivation is presented for the organs “lung”, with a two-dimensional arrangement of the cells at risk, and for “liver” where the sensitive cells are distributed in all three dimensions. Inferences for dose-response curves at low doses and dose rates are drawn. For liver, the number and size of premalignant clones is estimated from the cancer data.