TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 2272. HEALTH EFFECTS0.1 µg/mL culture medium chromium(VI) salts which gave optimum responses and cell growth ratios oftreated/nontreated cells from eight sensitive individuals ranging from 1.56 to 13.22,average=5.8 (chromium(III)), from 2.24 to11.43, average 5.4 sodium chromate and from 1.82 to 9.48,average 5.4potassiium dichromate. The nonsensitive individuals’ ratios were consistently lower withranges from 0.90 to 2.28 and average ratios of 1.14, 1.30, and 1.56. The authors felt that this in vitromethodology could be used diagnostically to assess chromium sensitive individuals.For more information on biomarkers for renal and hepatic effects of chemicals see ATSDR/CDCSubcommittee Report on Biological Indicators of Organ Damage (1990) and for information onbiomarkers for neurological effects see OTA (1990).2.9 INTERACTIONS WITH OTHER CHEMICALSPotassium dichromate (10 mg/kg) administered by subcutaneous injection potentiated the effects of thenephrotoxins, mercuric chloride, citrinin, and hexachloro-1,3-butadiene, in rats. Effects on renal functionincluded changes in urine volume, osmolality, electrolyte and glucose excretion, and a reduction in renalcortical slice organic ion transport. Chromium(VI) compounds potentiated the effect of mercuric chlorideon organic acid uptake but not organic base uptake by renal cortical slices (Baggett 1986; Haberman et al.1987). A similar experiment with another nephrotoxin, maleic acid, demonstrated the potentiating effectof potassium dichromate (10 mg/kg administered subcutaneously) (Christenson et al. 1989). Christensonet al. (1989) suggested that the combination of potassium dichromate with maleic acid might enhancedamage to the brush border of the renal proximal tubules or that damage to the luminal cells by potassiumdichromate might allow maleic acid to more easily enter the cells.Interactions between selenium in the diet and ammonium dichromate in the drinking water wereinvestigated in a study using rats. During the experiment, one rat died and the other rats had atrophy ofthe central liver lobe when given selenium alone. Dietary selenium and ammonium chromate incombination caused hepatic necrosis, resulting in the death of four rats (Moxon and DuBois 1939).Although the rats were not fed chromium alone, other studies indicate that the liver is a target forchromium exposure (see Section 2.2). The mechanism for the interaction was not discussed.A number of studies indicate an increase in the mutagenic effects of chromium(VI) compounds incombination with other chemicals. Synergism has been observed between chromium(VI) and9-aminoacridine, nitrilotriacetic acid, and azide (Bronzetti and Galli 1989; Gava et al. 1989a; LaVelle