(64) Although there are recognised exceptions, for the purposes of radiological protection the Commission judges that the weight of evidence on fundamental cellular processes coupled with dose-response data supports the view that, in the low dose range, below about 100 mSv, it is scientifically plausible to assume that the incidence of cancer or heritable effects will rise in direct proportion to an increase in the equivalent dose in the relevant organs and tissues.
(63) The accumulation of cellular and animal data relevant to radiation tumorigenesis has, since 1990, strengthened the view that DNA damage response processes in single cells are of critical importance to the development of cancer after radiation exposure. These data, together with advances in knowledge of the cancer process in general, give increased confidence that detailed information on DNA damage response/repair and the induction of gene/chromosomal mutations can contribute significantly to judgements on the radiation-associated increase in the incidence of cancer at low doses. This knowledge also influences judgements on relative biological effectiveness (RBE), radiation weighting factors, and dose and dose-rate effects. Of particular importance are the advances in understanding radiation effects on DNA such as the induction of complex forms of DNA double strand breaks, the problems experienced by cells in correctly repairing these complex forms of DNA damage, and the consequent appearance of gene/chromosomal mutations. Advances in microdosimetric knowledge concerning aspects of radiation-induced DNA damage have also contributed significantly to this understanding (see Annexes A and B).