ABSTRACT
Radionuclides which decay by electron capture accompanied by Auger electron cascades, or by beta emission are thought to be excessively damaging when incorporated into the molecular structure of mammalian cell nuclei and thereby pose a radiation hazard which is not assessable by conventional dosimetry. Survival data, from the literature, for 125I, 77Br, 3H and 131I have been re-analysed to extract cross sections for inactivation, by the slowing down charged particle fluence, as these are absolute specifications of the radiation quality. When comparison is made with results similarly expressed for external irradiation with heavy particle and photon beams, the qualities of the low-energy emitters 125I, 77Br and 3H are found to approach those for heavy particles. An explanation for the damage mechanism is sought in a recently developed model for radiation action. The results are consistent with the interpretation that electron damage is caused predominantly at the end of the tracks, and the actual incorporation simply ensures that the slowing down fluence of low-energy tracks interacts preferentially in the vicinity of the radiosensitive sites. The absolute biological effectiveness of these radiations can be expressed quantitatively in terms of the model parameters.
