Methyl mercury neurological effect

Organic Mercury. Only two case histories were located regarding cardiovascular effects in persons exposed by inhalation to organic mercury compounds. No cardiovascular effects were reported in four men hospitalized for neurological symptoms after inhaling an unspecified concentration of methyl-mercury dust for at least several months (Hunter et al. 1940). Elevated blood pressure was reported in two men exposed occupationally to methylmercury compounds (dose not known) (Hook et al. 1954). 

Mercury is unusual in its ability to induce delayed neurological effects. This is especially prevalent with exposure to alkyl mercury compounds. In such cases, the onset of adverse effects may be delayed for months after the initial exposure. The delayed effects of methyl- and dimethylmercury reported in human poisonings are thought, in part, to result from binding to red blood cells, and subsequent slow release. Methylmercury also forms a complex in plasma with the amino acid cysteine, which is structurally similar to the essential amino acid methionine (Aschner and Clarkson 1988). Clarkson (1995) proposed that methylmercury can cross the blood-brain barrier "disguised" as an amino acid via a carrier-mediated system (i.e., transport is not solely the result of methylmercury s lipid solubility). 

Many of the observed Great Lakes region toxic effects are attributed to persistent toxic chemical compounds. TCDD is associated with human thyroid hormone fluctuation, problems in male reproductive function, and neurological malfunction. Hexachlorobenzene (HCB) and methyl mercury (MeHg) are associated with human thyroid hormone fluctuation, problems in female reproductive function, neurological and neurodevelopmental problems. These effects, summarized in Table 13.1, illustrate the difficulty in attributing a particular toxic effect to a single chemical, particularly when one considers the potential impacts of thousands of other chemicals. 

Alkyl compounds of mercury (RHgX) and other organomercury compounds (i.e., methyl mercury) are strong irritants (eye, mucous membranes and skin), the latter with a direct effect on chromosomes. In fact, Minamata disease is termed after the methyl mercury intoxication incidence observed in the fish meat in Minamata, Japan, which produced neurological damage and mental retardation in newborn babies [42]. 

Mathews T, Fisher NS (2008) Evaluating the trophic transfer of cadmium, polonium, and methyl-mercury in an estuarine food chain. Environ Toxicol Chem 27 1093-1101 McAlpine D, Araki S (1959) Minamata disease late effects of an unusual neurological disorder caused by contaminated fish. AM A Arch Neurol 1 522-530 McGeer J, Brix KV, Skeaff JM, Deforest DK, Brigham SI, Adams WJ, Green AS (2003) The inverse relationship between bioconcentration factor and exposiure concentration for metals implications for hazard assessment of metals in the aquatic environment. Environ Toxicol Chem 22 1017-1037... 

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