Radiation risk estimation: Modelling approaches for “targeted” and “non-targeted” effects

The estimation of the risks from low doses of ionizing radiation – including heavy ions - is still a debated question. In particular, the action of heavy ions on biological targets needs further investigation. In this framework, we present a mechanistic model and a Monte Carlo simulation code for the induction of different types of chromosome aberrations. The model, previously validated for gamma rays and light ions, has recently started to be extended to heavy ions such as Iron and Carbon, which are of interest both for space radiation protection and for hadrontherapy. Preliminary results were found to be in agreement with experimental dose-response curves for aberration yields observed following heavy-ion irradiation of human lymphocytes treated with the Premature Chromosome Condensation technique. During the last ten years, the “Linear No Threshold” hypothesis has been challenged by a large number of observations on the so-called “non targeted effects” including bystander effect, which consists of the induction of cytogenetic damage in cells not directly traversed by radiation, most likely as a response to molecular messengers released by directly irradiated cells. Although it is now clear that cellular communication plays a fundamental role, our knowledge on the mechanisms underlying bystander effects is still poor, and would largely benefit from further investigations including theoretical models and simulation codes. In the present paper we will review different modelling approaches, including one that is being developed at the University of Pavia, focusing on the assumptions adopted by the various authors and on their implications in terms of low-dose radiation risk, as well as on the identification of "critical" parameters that can modulate the model outcomes.