TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 1812. HEALTH EFFECTShyperplasia in the liver with either potassium dichromate or chromium(III) nitrate (Tandon et al. 1978).While these studies indicate that the liver is a target organ of chromium toxicity in animals, the methodsof administration may not be predictive of effects or doses by environmentally relevant routes. Whileoccupational exposure to chromium(VI) in the past may have caused adverse liver effects, they are notexpected to occur in humans currently exposed to chromium or its compounds occupationally or in peopleliving near hazardous waste sites. It is unlikely that oral exposure to the low levels of chromium(III) orchromium(VI) compounds detected in drinking water or in the ambient environment would cause hepaticeffects in humans.Renal Effects. Renal function has been studied in workers occupationally exposed to chromiumcompounds. Some studies of workers exposed to chromium(VI) and chromium(III) in the chromateproduction industry have found increased urinary levels of low molecular weight proteins indicative ofrenal damage, such as retinol binding protein and antigens, and white blood cell and red blood cell casts,in the urine (Franchini and Mutti 1988; Mutti et al. 1985a; PHS 1953). Other studies of renal function inworkers engaged in chromate production and manufacturing of chromium compounds found negative orinconclusive results (Sassi 1956; Satoh et al. 1981). Two studies of renal function in chrome platers,whose exposure is mainly to chromium(VI), reported elevated levels of β 2 -microglobulin in the urine ofcurrent platers (Lindberg and Vesterberg 1983b; Liu et al. 1998); an increase in N-acetyl-β-glucosaminadaselevels was also found (Liu et al. 1998). When the prevalence of elevated levels (defined ashigher than reference values) of these markers of potential kidney damage was compared to aluminumanode-oxidationworkers, only N-acetyl-β-glucosaminadase was significantly altered (Liu et al. 1998).No differences in levels of blood urea nitrogen, serum and urinary β 2 -microglobulin, and other proteinswere found between chrome platers and controls in another study (Verschoor et al. 1988). Studies instainless steel welders, whose exposure is mainly to chromium(VI) showed no indication of kidneydamage (Littorin et al. 1984; Verschoor et al. 1988). Occupational exposure to chromium(III) in theferrochromium production industry (Foa et al. 1988) and to chromium(0) in an alloy steel plant (Triebiget al. 1987) and in boilermakers (Verschoor et al. 1988) does not appear to be associated with renaleffects. Death records from a large cohort who worked in industries that produced chromium productsfrom chromite ore did not show signs of increases in urinary disease when compared to matched controlpopulations (Rosenman and Stanbury 1996). Examination of the urine of people who were lifetimeresidents of a contaminated area near chromium landfills where environmental exposures to chromiumdust occurred did not reveal evidence of tubular proteinurea or signs of preclinical kidney disease(Wedeen et al. 1996). Results of urinalysis revealed no difference between housewives who lived near achromium slag construction site and the control population (Greater Tokyo Bureau of Hygiene 1989).