DUAL THEORY OF ACTION IONIZING RADIATION AND SPONTANEOUS CANCER

A mathematical model for radiogenic increasing of mortality was proposed, taking into account spontaneous background damages of the genetic material, that always occur in cells due to the influence of non-radiation internal and environmental factors. The model is based on the representation of indistinguishability between radiogenic andspontaneous cancers and on the postulates of the Kellerer-Rossi dual action theory. It was proposed that duringformation of premalignant damages dual interactions occur both between primary radiation damages, and betweenradiation and spontaneous primary damages (hybrid interactions). The role of the latter is particularly important at low levels exposure that corresponds to a linear dependence of cancer incidence on dose. Their significance is indicated by the following factor: at the adopted value of the nominal (radiation) risk factor (0,05 Sv^-1) and cancer mortality share among the population (0,15–0,2), the contribution of non-radiative carcinogenic factors for the total life is equivalent to radiation dose of 3–4 Sv or radiation at a constant dose rate of 40–50 mSv / year.

The model assumes formation in DNA of both spaced apart (single) damages with high probability of recovery, and nearby (double) damages, which are more likely to interact, entering into the permanent state. Permanent damages being formed in certain portions of DNA can be inherited to daughter cells as premalignant defects. The relative role of spontaneous primary damages is greater the more single damages are formed as compared to double ones within the area of potential interaction.

It was shown within this model that the presence of background cancer mortality for initial and finite population in the used by ICRP expression for interpopulation risk transfer has logical and biophysical justifications. Accounting of spontaneous primary damages and hybrid interactions enhances the capabilities for development of radiation risk models.

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