Routine medicare and radiation exposure (3) biology about radiation exposure for its understanding

Radiation-induced biological responses are easily explained as follows. The process of cancer formation is on the hypothesis of multi-step carcinogenesis of the initiation, promotion and progression. Radiation is an exogenous physical initiator. Physical process of ionization in biomaterials by radiation occurs within the time of 10-12 sec order, which resulting in chemical process (10-6 sec) leading to tissue response or to cancerous change (several tens hours to several decades). Direct and indirect effects on DNA are yielded with the high LET (linear energy transfer) radiation and low, through OH-radical formation, respectively. Double strand break of DNA induced by radiation is repaired by the error-free homologous recombination or error-prone non-homologous end-joining. At the early phase of the damage, DNA damage response begins to work for repairing, and when the response is inoperable, cellular response is induced to lead radiation apoptosis as an exclusion mechanism of abnormal cells. The biological effects differ even at the same dose of different radiations when their LET is different, and relative biological effectiveness (RBE) is used. For correction of the stochastic radiation effect, the radiation weighting factor (WR) is used for conversion to the single photon beam dose that ICRP defines as the equivalent dose (HT, Sv). ICRP (Pub. 103) also recommends the use of RBE (Gy) for the definitive effect. Radiation effects are known to be modified by such phenomena as the bystander effect, cluster damage of DNA, radiation adaptation, hormesis, dose rate effect and non-tumor inducing dose. ICRP employs linear non-threshold (LNT) hypothesis for low dose and low dose rate carcinogenesis. (T.T.)