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MERCURY 326<br />

2. HEALTH EFFECTS<br />

at dosages of 1 mg/kg/day was reported by Bapu et al. (1994). Therapy with both B-complex vitamins<br />

<strong>and</strong> vitamin E was found to mobilize a significant amount of mercury from all tissues examined (brain,<br />

spinal cord, liver, <strong>and</strong> kidneys), with the maximum mobilization (about 63%, compared with controls)<br />

being recorded in the spinal cord following vitamin E treatment. NAHT treatment also produced<br />

significant mobilization of mercury from nervous tissue but caused an increase in mercury concentration<br />

in non-nervous tissue.<br />

Another group of compounds that combines with mercury (<strong>and</strong> other divalent cation species) is comprised<br />

by those used in chelation therapy to reduce the body burden of mercury by enhancing its elimination<br />

from the body. Such chelators include: ethylenediaminetetraacetic acid (EDTA); ethylene glycol<br />

bis(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA); 2,3-dimercaptopropane-1-sulphonate<br />

(DMPS); 2,3-dimercaptosuccoinic acid (DMSA); 2,3-dimercaptopropanol (British anti-Lewisite [BAL];<br />

sometimes called dimercaprol); <strong>and</strong> N-acetylpenicillamine (NAP). While these chelating agents have a<br />

very high affinity <strong>for</strong> Hg ++ , which makes them effective mercury chelators, they also have an affinity <strong>for</strong><br />

other divalent cations, many of which are essential <strong>for</strong> normal physiological function.<br />

BAL was the first chelating agent used <strong>for</strong> mercury toxicity, <strong>and</strong> it is still widely used today <strong>for</strong> inorganic<br />

mercury poisoning (ATSDR 1992). BAL is also believed to be effective in treating phenylmercury<br />

poisoning, because of the rapid in vivo oxidization of phenylmercuric acetate to Hg ++ , thereby rendering<br />

phenylmercury similar in behavior to inorganic mercury. BAL is contraindicated <strong>for</strong> cases of methylmercury<br />

poisoning, however, because it has been demonstrated to increase the concentration of methylmercury<br />

in the brain. Possible side effects of BAL include nausea, vomiting, headache, tachycardia,<br />

fever, conjunctivitis, blepharospasm, <strong>and</strong> lacrimation. As an adjunct or alternative to parenterally<br />

administered BAL, oral NAP may be used (ATSDR 1992). Side effects of NAP may include fever, rash,<br />

leukopenia, eosinophilia, <strong>and</strong> thrombocytopenia.<br />

DMPS <strong>and</strong> DMSA are derivatives of BAL, but they have been found to be more effective than BAL in<br />

experimental studies. Although still considered an investigational drug, DMPS decreased the mercury<br />

excretion half-life from 33.1 to 11.2 days in 2 workers exposed to high levels of mercury vapor (ATSDR<br />

1992). In a study of the influence of DMPS <strong>and</strong> DMSA on renal deposition of mercury in rats, both<br />

chelating agents were found to cause a significantly increased urinary excretion of mercury (Zalups<br />

1993), although significant differences in the extrarenal h<strong>and</strong>ling of these two chelators were found.<br />

DMPS was also shown to increase the urinary excretion of mercury 7.6-fold in a group of <strong>for</strong>mer chloralkali workers

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