Low dose radiobiology: Mechanistic considerations

The question of whether very small doses of ionizing radiation really exert stochastic effects (i.e. induce harmful genetic effects, including cancer in a probablistic manner) has not been unequivocally settled. The much relied upon linear, no-threshold (LNT) hypothesis does not have convincing experimental evidence. As there are practical difficulties in generating data on genetic effects at very low doses and low dose rates, the conceptual development of the LNT hypothesis has depended upon background extrapolations from observations at high doses to low dose-regions. The dose, dose rate as well as the quality of radiation exposures in the case of atomicbomb survivors and their descendants are fraught with uncertainties. With data accumulating on radiation-induced gene expression, the basic concepts of how cell death is caused are undergoing significant changes. Many reported phenomena such as ‘radiation hormesis’ and ‘radioadaptive response’ could no more be outright rejected and these challenge the LNT hypothesis. The fact remains that the LNT is an over simplistic ‘biophysical model’ to explain radiation action on the DNA of living cells and organisms. It truly masks the whole lot of physical, physicochemical, biochemical and metabolic events involving not just the DNA but also the myriads of small and large molecules, which characterize the various organelles. Most fundamentally, the LNT ignores repair processes, immune reactions and the role of apoptosis. The purpose of this review is purely to address this issue from a scientific point of view and not to deal with implications for radiological protection standards.