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MERCURY 116<br />

2. HEALTH EFFECTS<br />

Organic Mercury. Data on renal toxicity associated with ingestion of methylmercury in humans come from<br />

several case studies. An outbreak of ethylmercury fungicide-induced poisoning was reported by Jalili <strong>and</strong><br />

Abbasi (1961). Affected individuals exhibited polyuria, polydypsia, <strong>and</strong> albuminuria. Two boys who<br />

ingested meat from a hog that had consumed seed treated with ethylmercuric chloride also had increased<br />

blood urea, urinary protein, <strong>and</strong> urinary sediment (Cinca et al. 1979); an autopsy revealed nephritis. A<br />

13-month-old boy who ate porridge made from flour treated with an alkyl mercury compound (specific<br />

mercury compound not reported) experienced albuminuria, red <strong>and</strong> white cells, <strong>and</strong> casts in the urine<br />

(Engleson <strong>and</strong> Herner 1952). In autopsies carried out to evaluate the cause of death in 4 adults <strong>and</strong> 4 infants<br />

from the Iraqi epidemic of 1972, one case exhibited tubular degeneration in the kidneys (whether an adult or<br />

child was not specified) (Al-Saleem <strong>and</strong> the Clinical Committee on Mercury Poisoning 1976).<br />

Organic mercury-induced nephrotoxicity has been demonstrated in rodents following acute-, intermediate-,<br />

<strong>and</strong> chronic-duration exposure. The usefulness of results from subchronic studies may be limited because<br />

the pathological changes observed were often not distinguished as primary or secondary effects (i.e.,<br />

pathological changes secondary to induced shock). Nonetheless, they provide some useful indication of<br />

potential effects.<br />

Administration of methylmercuric chloride to mice in a single gavage dose of 16 mg Hg/kg resulted in<br />

decreased renal function (decreased phenolsulfonphthalein excretion), increased plasma creatinine, <strong>and</strong><br />

swelling of tubular epithelial cells, with exfoliation of the cells into the tubular lumen (Yasutake et al.<br />

1991b). Although no effects were observed after a single gavage dose of 8 mg Hg/kg (Yasutake et al.<br />

1991b), 5 daily gavage doses of 8 mg Hg/kg/day as methylmercuric chloride in rats resulted in vacuolization<br />

<strong>and</strong> tubular dilation in the proximal tubules with ongoing regeneration (Magos et al. 1985). Similar effects<br />

were observed after 5 doses of 8 mg Hg/kg/day as ethylmercuric chloride (Magos et al. 1985).<br />

In an intermediate-duration study, histopathological changes were observed in the kidneys of female rats<br />

exposed to 0.86, 1.68, or 3.36 mg Hg/kg/day as methylmercury dicyanidiamide by gavage 5 days a week <strong>for</strong><br />

3–12 weeks (Magos <strong>and</strong> Butler 1972). The low-dose group exhibited large foci of basophilic tubular<br />

epithelial cells, desquamation, fibrosis, <strong>and</strong> inflammation in the renal cortex; however, no control group was<br />

used in the study (Magos <strong>and</strong> Butler 1972). A 12-week diet containing 0.08 mg Hg/kg/day as methylmercury<br />

caused ultrastructural changes (cytoplasmic masses containing ribosomes <strong>and</strong> bundles of smooth<br />

endoplasmic reticulum) in kidney proximal tubule cells of female rats, despite the normal appearance of the

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