Ethanol (Et) abusers may also be exposed to excessive amounts of cadmium (Cd). Thus, the study was aimed at estimating the influence of Et on the body turnover of Cd in a rat model reflecting excessive alcohol consumption in humans chronically exposed to moderate and relatively high levels of this metal. For this purpose, Cd apparent absorption, retention in the body and concentration in the blood, stomach, duodenum, liver, kidney, spleen, brain, heart, testis and femur as well as its fecal and urinary excretion in the rats exposed to 5 and 50mg Cd l−1 (in drinking water; for 16 weeks from the fifth week of the animal's life) and/or Et (5 g kg−1 b.w. per 24 h, by oral gavage; for 12 weeks from the ninth week of life) were estimated. Moreover, the duodenal, liver and kidney pool of the nonmetallothionein (Mt)-bound Cd was evaluated. The administration of Et during the exposure to 5 or 50mg Cd l−1 increased Cd accumulation in the gastrointestinal tract and its urinary excretion, and decreased Cd concentration in the blood, femur and numerous soft tissues (including liver and kidney) as well as the total pool of this metal in internal organs. Et modified or not the pool of the non-Mt-bound Cd, depending on the level of treatment with this metal. The results show that excessive Et consumption during Cd exposure may decrease the body burden of this metal, at least partly, by its lower absorption and increased urinary excretion. Based on this study, it can be concluded that Cd concentration in the blood and tissues of alcohol abusers chronically exposed to moderate and relatively high levels of this metal may be lower, whereas its urinary excretion is higher than in their nondrinking counterparts. However, since Et is toxic itself, the decreased body burden of Cd owing to alcohol consumption does not allow for the conclusion that the risk of health damage may be lower at co-exposure to these xenobiotics. In a further study, it will be investigated how the Et-induced changes in the body status of Cd influence the effects of its toxic action. Copyright © 2012 John Wiley & Sons, Ltd.