TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 962. HEALTH EFFECTSAverage daily ingestion of chromium(VI) for males was 1, 3, 6, and 24 mg/kg/day and 1, 3, 7, and28 mg/kg/day for females. Although no indication of hepatic effects was found in mice exposed to#36.7 mg/kg/day in a multigeneration feeding study (NTP 1997), some indication of liver toxicity wasfound in a 9-week feeding study in mice exposed to 1.1, 3.5, 7.4, and 32 mg chromium(VI)/kg/day formales and 1.8, 5.6, 12, and 48 mg chromium(VI)/kg/day for females (NTP 1996a). Hepatocytecytoplasmic vacuolization occurred in 1/6 males at 3.5 mg/kg/day, 2/5 males at 7.4 mg/kg/day, and2/6 males at 32 mg/kg/day, and in 1/12 control females, 0/12 females at 1.8 mg/kg/day, 3/12 females at5.6 mg/kg/day, 2/12 females at 12 mg/kg/day, and 4/12 females at 48 mg/kg/day. The vacuoles weresmall, clear, and well demarcated, which is suggestive of lipid accumulation. The small number ofanimals and lack of a clear dose-response preclude a definitive conclusion as to whether this effect wastoxicologically significant. Rats orally exposed to chromium(III) compounds had no evidence of liverdamage. Histological examination revealed no morphological changes in the livers of rats exposed to2,040 mg chromium(III)/kg/day as chromium oxide in the diet 5 days/week for 2 years (Ivankovic andPreussmann 1975), of rats exposed to 2.7 mg chromium(III)/kg/day as chromium trichloride in thedrinking water for 1 year (MacKenzie et al. 1958), of rats exposed to 9 mg chromium(III)/kg/day aschromium chloride or chromium picolinate in the diet for 20 weeks (Anderson et al. 1997b), or of ratsexposed to 0.46 mg chromium(III)/kg/day as chromium acetate in the drinking water for 2–3 years(Schroeder et al. 1965).Renal Effects. Case studies were located regarding renal effects in humans after oral exposure tochromium(VI) compounds. Acute renal failure, characterized by proteinuria, hematuria, followed byanuria, developed in a chrome plating worker who had accidentally swallowed an unreported volume of aplating fluid containing 300 g chromium trioxide/L. He was treated by hemodialysis (Fristedt et al.1965). Necrosis of renal tubules was found upon autopsy of a 22-month-old boy who died after ingestingan unknown amount of sodium dichromate (Ellis et al. 1982) and of a 17-year-old boy who died afteringesting 29 mg chromium(VI)/kg as potassium dichromate (Clochesy 1984; Iserson et al. 1983). A fatalingestion of 4.1 mg chromium(VI)/kg as a chromic acid solution in a 44-year-old man resulted in acutetubular necrosis and renal failure (Saryan and Reedy 1988). A 14-year-old boy who ingested 7.5 mgchromium(VI)/kg as potassium dichromate died from renal failure 8 days after he was admitted to thehospital. Upon postmortem examination, the kidneys were pale, enlarged, and necrotic with tubularnecrosis and edema (Kaufman et al. 1970). Another case study of an 18-year-old woman who ingested afew grams of potassium dichromate reported proteinuria, oliguria, and destruction of the tubularepithelium of the kidneys. She regained renal function following dialysis (Sharma et al. 1978).