Dose-response data for the induction of angiosarcoma in rats exposed to various levels of vinyl chloride (VC) together with attendant biotransformation data were used to estimate the risk of developing angiosarcoma in persons exposed to VC. Since a biotransformation product of VC, not VC per se, is responsible for the induction of angiosarcoma, the body surface area of people relative to rats was used to estimate the dose of the carcinogen biotransformed from VC by the former. Four models were used to extrapolate the data. Using a probit model, 10 hepatic angiosarcomas were predicted to occur in a recently reported epidemiological cohort of 9677 workers whereas five have occurred. Linear models and that based on the equation, Risk = 1 - e-βx, where x = dose, do not appear as reliable. For an 8-hr day, 5 days/week, 35-year time-weighted-average exposure of 1 ppm, the predicted incidence of hepatic angiosarcoma using the probit model is 1.5 × 10-8. © 1979.