ABSTRACT
To reassess the use of the linear-nonthreshold dose-response model in the light of advancing knowledge, the National Council on Radiation Protection and Measurements formed Scientific Committee 1-6 and charged it to evaluate the evidence for and against the linear-nonthreshold dose-response hypothesis without reference to any associated policy ramifications. To accomplish this task, the Committee reviewed the relevant theoretical, experimental, and epidemiological data on those effects of ionizing radiation that are generally postulated to be stochastic in nature (i.e., genetic and carcinogenic effects). From its review of the data, the Committee concluded that the weight of evidence suggests that lesions that are precursors to cancer (i.e., mutations and chromosome aberrations), and certain types of cancer as well, may increase in frequency linearly with the dose in the low-dose domain. On this basis, the Committee concluded that no alternative dose-response model is more plausible than the linear-nonthreshold model although other dose-response relationships cannot be excluded, especially in view of growing evidence that the dose-response relationship may be modified by adaptive responses, bystander effects, and other variables.
Subject(s)
Linear Models , Models, Biological , Radiation, Ionizing , Radiometry/methods , Radiometry/standards , Advisory Committees , Animals , Chromosome Aberrations , Chromosomes/radiation effects , DNA/radiation effects , DNA Damage , DNA Repair/radiation effects , Dose-Response Relationship, Radiation , Humans , National Academy of Sciences, U.S. , Neoplasms, Radiation-Induced/etiology , Risk Assessment/methods , Technology Assessment, Biomedical/methods , United StatesABSTRACT
For public health purposes, the overall risks of cancer are assumed to increase in proportion to the dose of ionizing radiation, without a threshold. Assessment of the risks that may be attributable to doses below the range in which empirical data are available, however, entails the use of models, the credibility of which depends on the extent to which the models are consistent with what is known about the occurrence and mechanisms of the effects in question. Although the weight of existing evidence is consistent with the hypothesis that the risks of genetic and carcinogenic effects of ionizing radiation increase as linear-nonthreshold functions of the dose, this concept is challenged by some observers in view of growing evidence that low doses of radiation may elicit adaptive responses that enhance the repair of DNA damage and protect in other ways as well. Further research is needed to resolve the issue.
