An opportunity to study the effects of methylmercury
poisoning in humans was provided by the large outbreak in Iraq in 1971-2. In adults,
poisoning resulted from the ingestion of home-made bread prepared from methylmercury-treated seed grain and there was a highly significant correlation between the amount of bread ingested and blood
mercury levels.
Poisoning in infants resulted either from prior exposure in utero or from suckling or both. Blood
mercury levels were higher in infants and children than in adults. There was no increased incidence of
congenital defects. Symptoms and signs of
poisoning and histopathological changes were mainly confined to the CNS. Symptoms developed, on average, 1-2 months after exposure. In children there was
mental retardation with delayed onset of speech and impaired motor, sensory and autonomic function. Severely affected children were blind and deaf. In adults, the clinical picture could be classified as 1, mild (mainly of sensory symptoms) 2, moderate (sensory symptoms accompanied by cerebellar signs) and 3, severe (gross
ataxia with marked visual and
hearing loss which, in some cases, progressed to
akinetic mutism followed by
coma). Grades 1 and 2 carried a better prognosis thant grade 3. Interference with transmission at the myoneural junction was found in 14% of patients studied. There was no evidence of peripheral nerve involvement per se and sensory symptoms may be of central origin. The clinical differences between the Iraqi and Japanese outbreaks may be a result, in part at least, of the severe, prolonged and continuous exposure which occurred in the latter outbreak. Improvement was observed among the mild and moderate group. Treatment with
chelating agents,
thiol resin, haemodialysis and exchange transfusion lowered blood
mercury concentrations but produced no convincing clinical benefit. To be effective, treatment may need to be instituted soon after exposure.