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MERCURY 127<br />

2. HEALTH EFFECTS<br />

occurred is frequently limited because of difficulties in retracing prior exposure <strong>and</strong> uncertainties in<br />

estimating dose levels based on assumed food intake <strong>and</strong> contamination levels.<br />

Although isolated instances of alkyl mercury poisoning have been reported (Cinca et al. 1979; Engleson <strong>and</strong><br />

Herner 1952), the epidemic poisonings in Japan <strong>and</strong> Iraq focused attention on the neurotoxicity of these<br />

compounds. The first reported widespread outbreak of neurological disorders associated with the ingestion<br />

of methylmercury-contaminated fish occurred in the Minamata area of Japan (Kutsuna 1968). The<br />

neurological syndrome was characterized by a long list of symptoms including prickling, tingling sensation<br />

in the extremities (paresthesia); impaired peripheral vision, hearing, taste, <strong>and</strong> smell; slurred speech;<br />

unsteadiness of gait <strong>and</strong> limbs; muscle weakness; irritability; memory loss; depression; <strong>and</strong> sleeping<br />

difficulties (Kutsuna 1968; Tsubaki <strong>and</strong> Takahashi 1986). Elevated concentrations of methylmercury were<br />

observed in the hair <strong>and</strong> brains of victims (see Section 2.5). Epidemics of similar neurological disorders<br />

were reported in Iraq in 1956 <strong>and</strong> 1960 (Bakir et al. 1973; Jalili <strong>and</strong> Abbasi 1961) as the result of eating<br />

flour made from seed grain treated with ethylmercury p-toluene sulfonanilide. Affected individuals had an<br />

inability to walk, cerebellar ataxia, speech difficulties, paraplegia, spasticity, abnormal reflexes, restriction<br />

of visual fields or blindness, tremors, paresthesia, insomnia, confusion, hallucinations, excitement, <strong>and</strong> loss<br />

of consciousness. In the winter of 1971–1972 in Iraq, more than 6,530 patients required hospitalization <strong>and</strong><br />

459 deaths occurred, usually due to central nervous system damage, after the ingestion of contaminated<br />

bread prepared from wheat <strong>and</strong> other cereals treated with a methylmercury fungicide (Bakir et al. 1973).<br />

Al-Mufti et al. (1976) attempted to correlate symptoms of the poisoning incident with an estimate of<br />

methylmercury intake based on average levels found in grain <strong>and</strong> self-reported estimates of the number of<br />

loaves ingested. A number of assumptions were made in the estimates, <strong>and</strong> there were logistical constraints<br />

in surveying the widely spread rural population in Iraq. Moreover, only a total mercury intake was derived<br />

<strong>and</strong> compared with the results of a clinical evaluation <strong>and</strong> a survey <strong>for</strong> symptoms. Nonetheless, interesting<br />

<strong>and</strong> useful results were reported based on the 2,147 people surveyed. The mean period of exposure <strong>for</strong> the<br />

Iraqi population exposed to contaminated bread was 32 days, with some people consuming the bread <strong>for</strong> as<br />

long as 3 months. A mean of 121 loaves per person was eaten; the maximum was 480 loaves. Based on the<br />

mean number of loaves, the total intake of methylmercury was estimated at between 80 mg <strong>and</strong> 250 mg.<br />

However, those who had consumed the most loaves may have ingested up to 1,000 mg of methylmercury<br />

over a 3-month period. Of those with symptoms of alkylmercury poisoning at the time of the survey<br />

(October 1972–May 1973), 80% had eaten more than 100 loaves. Of the 75 people who had reported eating<br />

more than 200 loaves, 53 (71%) presented with some evidence of poisoning. The incidence rate <strong>for</strong>

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