1. The difference between deterministic and stochastic effects.

Most adverse health effects of radiation exposure may be grouped in two general categories:

• deterministic effects (harmful tissue reactions) due in large part to the killing of cells following high doses;

• stochastic effects, i.e., cancer and heritable effects involving either cancer development in exposed individuals owing to mutation of somatic cells or heritable disease in their offspring owing to mutation of reproductive cells.

2. Threshold dose and tissue and cell clinically-fixed effects.

3. Radiation risk of cancer.

The accumulation of cellular and animal data relevant to radiation tumorigenesis has strengthened the view that DNA damage response processes in single cells are of critical importance to the development of cancer after radiation exposure. The practical system of radiological protection recommended by the Commission will continue to be based upon the assumption that at doses below about 100 mSv a given increment in dose will produce a directly proportionate increment in the probability of incurring cancer or heritable e?ects attributable to radiation. The Commission recognises that some biological factors, together with possible tumour-promoting e?ects of protracted irradiation, and immunological phenomena, may in?uence radiation cancer risk.

4. RBE

5. LNT

6. Radiation risk and heritable effects.

There continues to be no direct evidence that exposure of parents to radiation leads to excess heritable disease in offspring. The Commission prudently continues to include the risk of heritable e?ects in its system of radiological protection. The Commission has now adopted a new framework for the estimation of heritable risks that employs data from human and mouse studies. Mouse studies continue to be used to estimate genetic risks because of the lack of clear evidence in humans that germline mutations caused by radiation result in demonstrable genetic e?ects in o?spring. That direct data on spontaneous human mutation rates are used in conjunction with radiation-induced mutation rates derived from mouse studies. In the light of further knowledge the Commission judges that many of the underlying assumptions in such calculations are no longer sustainable. Accordingly, the Commission now expresses genetic risks up to the second generation only.

7. Genetic susceptibility to cancer.

Since 1990, there has been a remarkable expansion in knowledge of the various single gene human genetic disorders, where excess spontaneous cancer is expressed in a high proportion of gene carriers – the so-called high penetrance genes which can be strongly expressed as excess cancer. There is also a growing recognition, with some limited supporting data, that variant genes of lower penetrance through gene-gene and gene-environment interactions can result in a highly variable expression of cancer following radiation exposure.

8. Radiation effects on the induction of diseases other than cancer.

Since 1990 evidence has accumulated that the frequency of non-cancer diseases is increased in some irradiated populations. The strongest statistical evidence for the induction of these non-cancer e?ects at e?ective doses of the order of 1 Sv derives from the most recent mortality analysis of the Japanese atomic bomb survivors followed after 1968. That study has strengthened the statistical evidence for an association with dose – particularly for heart disease, stroke, digestive disorders, and respiratory disease. Additional evidence of the non-cancer e?ects of radiation, albeit at high doses, comes from studies of cancer patients receiving radiotherapy but these data do not clarify the issue of a possible dose threshold. It is also unclear what forms of cellular and tissue mechanisms might underlie such a diverse set of non-cancer disorders.