Anticarcinogenicity in Rodent Bioassays: Relation to Observed Human Anticarcinogenicity. F. Pompei, Exergen Corporation, 51 Water Street, Watertown, MA 02172; R. Wilson and I. Linkov, Department of Physics, Harvard University, Cambridge, MA 02138; and L. R. Rhomberg and G. M. Gray, Harvard Center for Risk Analysis, Boston, MA 02115
Recent observations of anticarcinogenicity in humans related to such chemicals as tamoxifen, selenium, PCB and DDE, and dioxin have all been presaged by rodent bioassays, but the data has previously not been examined with a view to a causality model common to both species. A scaling apparatus has not been available to link the interspecies observations quantitatively. A model is discussed that provides a plausible biological mechanism based on combined toxicity with carcinogenicity that results in a calculated anticarcinogenic dose, which is then scaled from rodents to humans using a set of simple scaling rules. Examples of rodent anticarcinogenicity from the CBDS data base are scaled to compare to human results where human data is available, and predictions for other chemical anticarcinogenicity not yet observed in humans are made based on rodent data. Current thinking on the role of apoptosis as a cytotoxic mechanism in anticarcinogenicity neatly fits the modeling assumptions employed to calculate and scale anticarcinogenic doses.
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