Why do we need a new paradigm in radiobiology?

Over the past 20 or so years experimental evidence, which questions the fundamentals of some 50 years standing, of both biology and radiobiology has accrued. In order to accommodate this new evidence within a framework that encompasses existing knowledge, attention has to be paid to the organisational or epigenetic, features of the cell. In recent years the high dimensional dynamic attractor has emerged as a potential organisational or regulatory agent that represents phenotype. It is argued here that its limited robustness provides a modus operandi to account for stress induced genomic instability. When radiation deposition events act to overcome the robustness of a normal or "home" attractor in the cell of an established species and cause a transition to a variant attractor or phenotype, the consequences are unrelated to any specific molecular damage to the genomic DNA. Rather they correspond to the loss of evolutionarily acquired stability (genotypic replicative integrity) and robustness. Such processes are termed type B events and give rise to a separate category of effects and risk to those associated with the conventional effects of radiation, type A effects. How type B risks might be assessed is discussed.