TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 2332. HEALTH EFFECTSpotassium dichromate dermally (Samitz 1970). An antichrome powder consisting of a mixture of 40%sodium metabisulfite, 20% ammonium chloride, 20% tartaric acid, and 20% sucrose as a 10% aqueoussolution was effective in reducing the healing time of chrome sores on the skin of guinea pigs to whichpotassium dichromate had been applied (Samitz and Epstein 1962). In cases of severe dermal exposure,excision of the skin has been recommended to prevent chrome sores (HSDB 1998). Thorough irrigationwith water has been recommended if the eyes have been exposed (HSDB 1998).Both the cytotoxic effects of chromium(III) chloride, chromium(III) nitrate, sodium chromate, sodiumdichromate, potassium dichromate(VI), and chromium(V) potassium sulfate dodecahydrate and the abilityof ascorbic acid, glutathione 4-acetamido-4'-isothiocyanato-2,2-stibenedisolphonic acid (SITS) to preventchromium toxicity in transformed human keratinocytes were examined (Little et al. 1996). This cell linewas used because histopathological studies have shown that dichromate compounds have causedkeratinocyte necrosis. Cells were exposed to the chromium salts for 24 hours, and the viability of thecultures was examined for their ability to take up neutral red dye and release lactate dehydrogenase intothe media. None of the chromium(III) or chromium(V) salts seemed toxic to the cells at concentrationsup to about 100 µM. The chromium(VI) salts showed toxicity at about 8 µM and there was little cellsurvival at 100 µM. The dose-response curves were similar for all chromium(VI) salts tested. Similarexperiments were conducted with normal human keratinocytes obtained from abdominoplasties or breastreductions from six donors and treated with sodium dichromate. The toxicity to normal cells overallseemed to be less than in the transformed line. Ascorbic acid at 500 µM completely inhibited the celltoxicity caused by chromium(VI), whereas glutathione and SITS were less effective. Ascorbate probablyprotected cells by reducing chromium(VI) and chelation to the reduced complex. Glutathione may haveformed complexes with the chromium(VI) which eventually led to chromium(III), whereas SITS mayhave inhibited the cellular uptake of the chromate by altering the non-specific membrane anion carrier.The authors conclude that these available drugs provide protection against cytotoxicity to keratinocytesinvolved in dermatitis and may be useful to prevent toxic reactions to metals contacting the skin.The effect of decreasing the concentration of water-soluble chromium in cement from about 10 to below2 ppm on the incidences of chromium-induced dermatitis was examined among construction workers inFinland (Roto et al. 1996). After 1987, when the decrease occurred, allergic dermatitis caused bychromium in the industry was reduced by 33% from previous levels, whereas irritant contact dermatitisremained unchanged.