It has been previously observed that exposure of rainbow trout to Cd from water or food did not result in a steady state for key compartments such as the gill, liver, and kidney. Further, during depuration, the mass of Cd in the kidney continued to increase. A seven-compartment pharmacokinetic model of the disposition of cadmium in the rainbow trout was constructed to obtain insight into these observations. The model considers exchange across the gill from exposure to dissolved (available) Cd in the water and exchange of Cd across the gut wall due to exposure to Cd in the food source. Internal distribution of Cd is via Cd in blood exchanging with aqueous phase Cd in kidney, liver, and a storage compartment. Equilibrium partitioning is assumed between the aqueous phase Cd and bound tissue Cd in each compartment. The model is applied to a data set where trout were exposed under two conditions: Cd primarily in water and primarily in food. The model parameters were obtained from other published exposure experiments as well as calibration to the data. The parameters were not altered between the two exposure pathways. High surface gill sorption and gut biliary transfer were necessary in order to obtain reasonable model calibration. Reproduction of the observed increase in kidney Cd during depuration is obtained with a relatively high partitioning, and model flux calculations indicate a net flux into the kidney during the depuration phase. Model simulations for both water and food exposure routes indicated that the whole body Cd concentration was calculated to reach equilibrium in about 50 d. However, Cd did not achieve a steady state in the kidney where it reached a maximum concentration at seven times whole body. For assessment of Cd risk to trout target tissues, it is concluded that a pharmacokinetic model may be necessary.