Comparing cancer risks between radiation and dioxin exposure based on two‐stage model

This study investigates the use of the Moolgavkar two-stage model to compare the biological and statistical nature of cancer risks from dioxin exposure and from radiation exposure. The two-stage model is a biologically based stochastic model for carrying out statistical inferences of cancer risks using biologically motivated hypothesis. This article briefly describes the conditional likelihood for the model recently developed by the authors and then presents results obtained from applying it to dioxin dietary data in rats (Kociba et al., 1978) and radiation exposure data in mice. Comparing the results following the two different types of exposures based on the two-stage model confirms that the radiation exposure increases the initiation rates while the dioxin exposure increases the net-proliferation rate. The results indicate that the effect of TCDD at 100ng/kg/day is an approximately 40 per cent increase in the net-proliferation rate in the intermediate cells. Portier et al. (1996b) and Moolgavkar et al. (1996) used the two-stage in-vivo initiation-promotion model in the rat liver. Measuring liver foci after administration of DEN followed by TCDD as a promoter, they observed an increase in proliferation rate in their initiated cells by 25-35 per cent. This closely agrees with our estimated increase of 40 per cent in the whole animal cancer incidence study of (Kociba et al., 1978). Another statistically important aspect obtained from the study is that the proportional hazards model is appropriate to apply to cancer incidence data following radiation exposure but is not appropriate for cancer risks following dioxin exposure.