The diagnosis of mercury intoxication involves integration of the history and physical findings with confirmatory laboratory testing or other evidence of exposure. In the absence of occupational exposure, the urine mercury concentration is usually <5 mcg/L, and whole blood mercury is <5 mcg/L. In 1990, the Biological Exposure Index (BEI) Committee of the American Conference of Governmental Industrial Hygienists (ACGIH) recommended that workplace exposures should result in urinary mercury concentrations <35 mcg per gram of creatinine and end-of-work-week whole blood mercury concentrations <15 mcg/L. To minimize the risk of developmental neurotoxicity from methylmercury, the EPA and the US Food and Drug Administration (FDA) have advised A pregnant women, women who might become pregnant, nursing mothers, and young children to avoid consumption of fish with high mercury levels (eg, swordfish) and to limit consumption of albacore tuna to 6 ounces a week, but to otherwise consume 8–12 ounces of fish per week (see http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm393070.htm).
A. Acute Exposure
In addition to intensive supportive care, prompt chelation with oral or intravenous unithiol, intramuscular dimercaprol, or oral succimer may be of value in diminishing nephrotoxicity after acute exposure to inorganic mercury salts. Vigorous hydration may help to maintain urine output, but if acute renal failure ensues, days to weeks of hemodialysis or hemodiafiltration in conjunction with chelation may be necessary. Because the efficacy of chelation declines with time since exposure, treatment should not be delayed until the onset of oliguria or other major systemic effects.
B. Chronic Exposure
Unithiol and succimer increase urine mercury excretion following acute or chronic elemental mercury inhalation, but the impact of such treatment on clinical outcome is unknown. Dimercaprol has been shown to redistribute mercury to the central nervous system from other tissue sites, and since the brain is a key target organ, dimercaprol should not be used in treatment of exposure to elemental or organic mercury. Limited data suggest that succimer, unithiol, and N-acetyl-l-cysteine (NAC) may enhance body clear- ance of methylmercury.
Chelating agents are drugs used to prevent or reverse the toxic effects of a heavy metal on an enzyme or other cellular target, or to accelerate the elimination of the metal from the body. By forming a complex with the heavy metal, the chelating agent renders the metal unavailable for toxic interactions with functional groups of enzymes or other proteins, coenzymes, cellular nucleophiles, and membranes. Chelating agents contain one or more coordinating atoms, usually oxygen, sulfur, or nitrogen, which donate a pair of electrons to a cationic metal ion to form one or more coordinate-covalent bonds. Depending on the number of metal-ligand bonds, the complex may be referred to as mono-, bi-, or polydentate. Figure 57–2 depicts the hexadentate chelate formed by interaction of edetate (ethylenediaminetetraacetate) with a metal atom, such as lead.
In some cases, the metal-mobilizing effect of a therapeutic chelating agent may not only enhance that metal’s excretion—a desired effect—but may also redistribute some of the metal to other vital organs. This has been demonstrated for dimercaprol,