TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 1802. HEALTH EFFECTSthe production of chromium compounds does not appear to be associated with long-term liver effects.Liver function parameters of Japanese workers engaged in the production of chromium compounds werewithin normal limits when tested 3 years after exposure (Satoh et al. 1981). Testing of workers employedin factories that produced chromium(III) compounds found no signs of liver disorders (Korallus et al.1974b), and testing of housewives who lived near a chromium slag construction site revealed no clinicalevidence of liver dysfunction (Greater Tokyo Bureau of Hygiene 1989). However, liver effects, such asjaundice, increased bilirubin, increased levels of serum lactic dehydrogenase, glutamic oxaloacetictransaminase and glutamic pyruvic transaminase, and necrosis have been reported in humans afteringestion of lethal doses of potassium dichromate or chromium trioxide (Fristedt et al. 1965; Kaufman etal. 1970).Only mild liver effects (increase in triglycerides and phospholipids) were observed in rats exposed to0.2 mg chromium(VI)/m 3 as sodium dichromate for 90 days (Glaser et al. 1985). These effects on theliver are minimal and were not observed in chronic exposure studies (Glaser et al. 1986, 1988). Effectson the liver of rats exposed orally to chromium(VI) compounds have been detected by biochemical andhistochemical techniques. These consisted of increased accumulations of lipids (Kumar and Rana 1982)and changes in levels and localization of enzymes (Kumar et al. 1985) in rats treated by gavage withpotassium chromate. Intermediate or chronic oral exposure of rats to chromium(III) compounds in thedrinking water (MacKenzie et al. 1958; Schroeder et al. 1965) or the diet (Anderson et al. 1997b;Ivankovic and Preussmann 1975) did not cause liver effects. Changes in liver enzymes indicative ofaltered carbohydrate metabolism were reported in rats after a single dermal application of 0.175%potassium dichromate (Merkur'eva et al. 1982). Although liver effects in animals exposed to chromiumcompounds by inhalation, oral, and dermal routes appear to be mild, studies in which animals wereexposed by other routes indicate more serious effects. Necrosis with regeneration occurred in ratsinjected subcutaneously with 3.5 mg chromium(VI)/kg as potassium dichromate (Baines 1965), lipidperoxidation occurred in rats injected intraperitoneally with 10 mg chromium/kg as chromium(III) nitrateor potassium dichromate (Ueno et al. 1988), and vacuolization of hepatocytes occurred in hamsters afterintravenous injection of 5.2 mg chromium(VI)/kg as chromium trioxide (Gale 1978). Rats injectedintraperitoneally with 2 mg chromium/kg/day, 3 days/week for 15–60 days developed liver necrosis withsodium chromate and vacuolization of hepatocytes with chromium(III) trichloride (Laborda et al. 1986).Cytochrome P450 activity in liver of rats was significantly increased after intraperitoneal injections ofpotassium dichromate(VI) (Witmer et al. 1994). P450 activity was measured by hydroxylation oftestosterone. Rabbits injected for 6 weeks intraperitoneally with 2 mg chromium/kg/day developedmarked congestion, large areas of focal necrosis, extensive hemorrhage, bile duct proliferation, and