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 reli
ed upon linear, no-threshold (LNT) hypothesis does not have convincing expe
rimental evidence. As there are practical difficulties in generating data o
n genetic effects at very low doses and low dose rates, the conceptual deve
lopment of the LNT hypothesis has depended upon background extrapolations f
rom observations at high doses to low dose-regions, The dose, dose rate as
well as the quality of radiation exposures in the case of atomic-bomb survi
vors and their descendants are fraught with uncertainties. With data accumu
lating on radiation-induced gene expression, the basic concepts of how cell
death is caused are undergoing significant changes. Many reported phenomen
a such as 'radiation hormesis' and 'radioadaptive response' could no more b
e outright rejected and these challenge the LNT hypothesis. The fact remain
s that the LNT is an over simplistic 'biophysical model' to explain radiati
on action on the DNA of living cells and organisms. It truly masks the whol
e lot of physical, physicochemical, biochemical and metabolic events involv
ing not just the DNA but also the myriads of small and large molecules, whi
ch 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 v
iew and not to deal with implications for radiological protection standards
.