revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY 306
2. HEALTH EFFECTS
apparently normal infant was born, but the infant later displayed brain damage manifested by mental
retardation, incoordination, and inability to move (Engleson and Herner 1952). A 40-year-old woman,
3 months pregnant, consumed methylmercury-contaminated meat for an unspecified duration and
subsequently delivered a male infant with elevated urinary mercury levels (Snyder and Seelinger 1976). At
3 months, the infant was hypotonic, irritable, and exhibited myoclonic seizures. At 6 years of age, the child
displayed severe neurological impairment (e.g., blindness, myoclonic seizures, neuromuscular weakness,
inability to speak) (Snyder and Seelinger 1976).
Another incidence of neurodevelopmental effects occurring as a result of in utero exposure to methyl­
mercury was reported by Cox et al. (1989) and WHO (1990). The effect of concern was the delayed onset of
walking in offspring in Iraqi children whose mothers were exposed to methylmercury through the
consumption of seed grain treated with methylmercury as a fungicide (Al-Mufti et al. 1976; Bakir et al.
1973; Cox et al. 1989; Marsh et al. 1981, 1987).
A New Mexico family, including a pregnant woman, a 20-year-old female, and 2 children (a 13-year-old
male and an 8-year-old female) ate meat from a hog inadvertently fed seed grain treated with a fungicide
containing methylmercury and experienced severe, delayed neurological effects (Davis et al. 1994). Several
months after the exposures, the children developed symptoms of neurological dysfunction. The newborn
child of the exposed mother showed signs of central nervous system disorder from birth. Twenty-two years
after the 3-month exposure period, the people who were 20 and 13 years old at time of exposure had
developed cortical blindness or constricted visual fields, diminished hand proprioception, choreoathetosis,
and attention deficits. MRI examination of these two revealed residual brain damage in the calcarine
cortices, parietal cortices, and cerebellum. The brain of the person who was exposed at age 8 (who died of
aspiration pneumonia with a superimposed Klebsiella bronchopneumonia and sepsis at age 29) showed
cortical atrophy, neuronal loss, and gliosis, most pronounced in the paracentral and parieto-occipital regions.
Regional brain mercury levels correlated with the extent of brain damage. The youngest (in utero at the time
of exposure) developed quadriplegia, blindness, severe mental retardation, choreoathetosis, and seizures, and
died at age 21. Since inorganic mercury crosses the blood-brain barrier poorly, biotransformation of the
methylmercury to inorganic mercury may have occurred after the methylmercury crossed the blood-brain
barrier, accounting for its observed persistence in the brain and its possible contribution to the brain damage.