Non-DSB clustered damage is much more frequent than DSBs in galactic cosmic ray exposures.

In this paper for the first time the frequency of complex double strand breaks (DSB) and non-DSB clustered damage behind spacecraft and tissue shielding from exposure to galactic cosmic rays (GCR) and secondary radiation are predicted. Elementary DNA lesions produced by ionizing radiation include single strand breaks (SSB) and various forms of base damages (BD) (e.g. abasic or oxidative sites). Clustered DNA damage is defined by the occurence of 2 or more elementary lesions within 10 base-pairs (bp), and complex clustered damage as 3 or more elementary lesions within 10 bp. Clustered DNA damage is more difficult to repair compared to simple forms of DNA damage, while the relative contribution of clustered to simple DNA damage increases with ionization density or linear energy transfer (LET), and therefore imporant for space radiation exposures. The author has developed the multinominal model of clustered DNA damage that uses nanoscopic energy imparted spectra in DNA volumes and damage location probability operators to predict clustered DNA damage frequencies. In this paper, I combine the results of the multinomial model with GCR particle energy spectra to predict the probabilities of complex DSB, and tandem and bistranded non-DSB clustered damage. Predictions for the local interstellar (LIS), solar mininum, and solar maximum environments are discussed. Results show that the frequency of DSB and non-DSB clusters attenuates slowly with aluminum and tissue shielding, and that non-DSB clusters are >4 times more frequent than prompt DSBs. This is an important finding which quantifies a prediction of the dominance of delayed formation of DSBs created in non-DSB clusters repair processes over prompt DSBs in the initial GCR DNA damage in tissues.