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Mice fed either (1) a pelleted rodent diet, (2) evaporated milk, or (3) a synthetic diet (high protein, low fat) exhibited different rates of whole body mercury elimination and fecal mercury excretion after exposure (per os) to methylmercuric chloride. The percentage of the total mercury body burden present as mercuric mercury was highest (35.3%) in mice fed the synthetic diet (which had the highest rate of mercury elimination) and lowest (6.6%) in the animals having the lowest mercury elimination rate (milk-fed mice). Mice fed the synthetic diet had lower mercury concentrations and had a higher proportion of mercuric mercury in their tissues than the mice from the other dietary groups. Treatment of the mice with antibiotics throughout the experimental period to suppress the gut flora reduced fecal mercury excretion and the dietary differences in whole body retention of mercury. Tissue mercury concentrations and proportion of organic mercury in feces, cecal contents, liver, and kidneys were increased by antibiotic treatment of mice fed the pelleted or synthetic diets. These results are consistent with the theory that demethylation of methylmercury by intestinal microflora is a major factor determining the excretion rate of mercury.

In a five-year longitudinal study of mothers and infants exposed to methylmercury during the Iraq epidemic of 1972, the frequencies of signs and symptoms exhibited by the mothers were typical of methylmercury poisoning. When blood concentrations of mercury are corrected to 1 March 1972, mothers with the most severe signs and symptoms had an average blood mercury concentration significantly higher (p less than 0.01) than either the milder or asymptomatic groups. Analytical data indicate that the predominant route of exposure for the infant was through breast milk in which approximately 60% of total mercury was determined, by cold vapor atomic absorption, to be organic mercury. Abnormal neurological signs in these infants became more obvious with time: hyperreflexia was observed in 8 of 22 infants at first examination, and in 17 of 22 at second examination. Delayed motor development became evident at the second and third examinations. The frequency of pathological reflexes and delayed motor developmental milestones was so high as to be considered significant even in the absence of a controlled study. There was no increase in mortality as compared to a control group.