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CARCINOGENIC EFFECTS OF LOW DOSES OF IONIZING RADIATION
Preston, R J. CARCINOGENIC EFFECTS OF LOW DOSES OF IONIZING RADIATION. Presented at American Association for the Advancement of Science, Seattle, Washington, February 12-16, 2004.
Carcinogenic Effects of Low Doses of Ionizing Radiation
R Julian Preston, Environmental Carcinogenesis Division, NHEERL, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
The form of the dose-response curve for radiation-induced cancers, particularly at low doses, is the subject of an ongoing and lively debate. For acute radiation exposures, epidemiological data are available for Japanese A-bomb survivors and for occupationally and medically exposed groups. These data allow for the conclusion that for solid cancers the best fit to the data is a linear response to exposures as low as 0.06Sv, with no evidence for a threshold below this dose. For leukemias, the form of the low dose response is less well defined - either no response at doses below about 0.2 Sv or some risk. These conclusions for solid cancers are broadly supported by data for radiation-induced tumors in laboratory animals, although the degree of consistency among the range of studies requires discussion Based upon current molecular knowledge of the mechanisms of carcinogenicity, it is reasonable to conclude that data for the induction of gene mutations and chromosomal alterations by ionizing radiations can be used to predict tumor outcomes in a qualitative sense. In general, the dose-response curves for both radiation-induced gene mutations and chromosomal alterations are linear at low doses (in the range of a few tens of mGy). Several epigenetic,cellular responses, especially induced in vitro, have recently been investigated in some detail. These include bystander responses, genomic instability and adaptive responses. It has been proposed that one or more of these might have a role to play in low dose radiation carcinogenesis, but it is too soon to tell if this is indeed the case. Such a role would not change the current radiation risk estimates because these are based directly on human tumor frequencies and not on mechanistic considerations. Clearly the debate will continue, and conducting the types of studies that can inform the mechanism of induction of cancers by radiation is essential. In this regard, whole genome studies (e.g. genomics and proteomics) should provide such a stimulus.(This abstract does not necessarily reflect EPA policy)