D. O. Marsh

Dose-response analysis of infants prenatally exposed to methyl mercury: An application of a single compartment model to single-strand hair analysis

A new method of estimating fetal exposure is used in a dose-response analysis of data from the 1971 outbreak of methyl mercury poisoning in rural Iraq. An X-ray fluorescence instrument for the measurement of single strands of human hair was employed to obtain longitudinal profiles recapitulating fetal exposure. Logit and hockey-stick models as well as nonparametric smoothing are used to describe data on delayed development and central nervous system abnormality.

Dose-response relationship for human fetal exposure to methylmercury.

Eighty-four Iraqi mothers and their infants had been exposed to methylmercury during pregnancy. The methylmercury had been ingested as a fungicide. Peak maternal hair mercury concentrations were related to the frequency of maternal symptoms during pregnancy and to neurological effects in the infants. These include various degrees of psychomotor retardation. Severe neurological deficits were observed in five children whose maternal peak hair mercury concentrations were 165 to 320 ppm. Minimal symptoms were reported for mothers and children when peak maternal hair levels were below 68 ppm. Minimal clinical neurological signs occurred in children when peak maternal hair mercury concentrations were at an undetermined point between 68 and 180 ppm. Greater fetal risk appears to be associated with exposure during the second trimester. This exposure to methylmercury was acute and the results may not be extrapolated to a constant level of exposure throughout pregnancy. The effects of fetal exposure to methylmercury in marine fish may differ.

Dose-Response Relationships for Adult and Prenatal Exposures to Methylmercury

Public concern over the health hazards of methylmercury was aroused by the two outbreaks of poisoning in Japan: in Minamata in the 1950s and in Niigata Prefecture in the 1960s (for details, see reference 26). The cause of the mass poisoning was the consumption of fish that had been contaminated by industrial discharge of methylmercury compounds.

The Role of Methylmercury Toxicity in Mental Retardation

Publisher Summary This chapter presents the evidence that supports the presumption that a high intake of methylmercury in fish may be a major public health hazard. The organic form of methylmercury is especially toxic to the nervous system and causes severe mental retardation and motor delays. Experimentally, methylmercury can cause more subtle abnormalities in the nervous system, but the milder forms of methylmercury toxicity are rarely recognized in humans. The wide distribution of methylmercury in freshwater and oceanic fish and its rapid and total absorption through biological membranes can lead to elevated levels of methylmercury in people who eat fish. The developing fetal nervous system is particularly sensitive to methylmercury, which readily passes from the maternal to the fetal circulation. Consequently, the fetus may be seriously damaged, while the mother remains asymptomatic.