By National Council on Radiation Protection

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Additional resources for Extrapolation of Radiation-induced Cancer Risks from Nonhuman Experimental Systems to Humans (N C R P Report Nro. 150)

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It is probable that the determination of the influence of these factors and estimates of the effects of high-LET radiations will continue to be derived mainly from the results on experimental animals. It is essential, therefore, to establish how the estimates of risk based on data from experimental animals, may be extrapolated to humans. 2 LESSONS LEARNED FROM GENETIC RISKS / 21 The extrapolation of biological effects across species can be addressed at empirical, mechanistic and theoretical levels.

For example, uncertainties have arisen concerning the validity of transferring cancer risks from the atomic-bomb survivors in Japan to other human populations exposed to radiation because of known differences in background rates for occurrence of specific tumor types (Land and Sinclair, 1991). Finally, since the factors that determine the occurrence of cancer in the majority of tissues of any species are not fully understood, empirical methods will remain (for now) the primary tool for estimating and extrapolating risks.

The additive model assumes that the average excess risk, in any population, given the same distribution by dose, gender and age at exposure will be the same for similar follow-up periods. The multiplicative model assumes that the ratio of excess risk to baseline risk at any age is invariant over populations with different baseline risks. The baseline risks for various cancers varies among populations. Studies of extrapolation across species are needed because there are insufficient data for humans to estimate: (1) hereditary effects; (2) the influence of dose rate, fractionation and protraction; (3) the effect of high-LET radiations, with the exception of alpha particles; and (4) how to transport risk estimates across populations as well as species.

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