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

MERCURY 141
2. HEALTH EFFECTS
dysarthria; hyperkinesia; hypersalivation; atrophy and hypoplasia of the cerebral cortex, corpus callosum,
and granule cell layer of the cerebellum; dysmyelination of the pyramidal tracts; and an abnormal neuronal
cytoarchitecture. It has been suggested that the widespread damage involved derangement of basic
developmental processes, such as neuronal migration (Choi et al. 1978; Matsumoto et al. 1965) and
neuronal cell division (Sager et al. 1983).
Large-scale poisonings also occurred in Iraq in 1956 and 1960 (Bakir et al. 1973). Thirty-one pregnant
women were victims of poisoning; 14 women died from ingesting wheat flour from seeds treated with
ethylmercury p-toluene sulfonanilide (Bakir et al. 1973). Infants were born with blood mercury
concentrations of 250 µg/100 mL and suffered severe brain damage. Similar cases of severe brain damage
resulting from prenatal exposure to methylmercury were reported in an outbreak of methylmercury
poisoning in Iraq occurring in 1971–1972 (Amin-Zaki et al. 1974). Attempts to correlate symptoms with
exposure levels have shown that a dose-response relationship exists between the severity of the neurological
symptoms in offspring and the maternal intake of methylmercury (as determined using analysis of hair for
mercury content) (Cox et al. 1989; Marsh et al. 1980, 1981, 1987). Delays in walking and talking were
more often associated with lower peak hair levels during pregnancy than were mental retardation and
seizures (Marsh et al. 1981, 1987). These studies showed that the most severely affected children had been
exposed to methylmercury during the second trimester of pregnancy. Male offspring were more severely
affected than female offspring. Neurological abnormalities have also been observed among offspring of
Cree Indians in Quebec, Canada, exposed to methylmercury in fish (McKeown-Eyssen et al. 1983).
A significant correlation was observed between male offspring with abnormal muscle tone or reflexes and
maternal prenatal exposure (as determined using hair levels). An analysis of peak hair mercury levels
during pregnancy in mothers exposed during the 1971–1972 outbreak in Iraq has led to an estimated
population threshold of 10 ppm (highest value during pregnancy, for total mercury in hair) associated with
delays in the onset of walking in infants (Cox et al. 1989). However, this estimated threshold for the Iraqi
population depends heavily on the assumed background frequency for abnormal onset of walking time, as
well as the threshold chosen to define onset of walking as abnormal. Furthermore, most of the positive
responses (i.e., reported delays in onset of walking or talking) were observed for maternal hair levels above
about 60 ppm. Only 3 of 24 children with positive responses were born to mothers with hair levels below
59 ppm. The peak total mercury hair levels during pregnancy for the mothers of those 3 children were 14,
18, and 38 ppm (WHO 1990). A maternal exposure level of 0.0012 mg/kg/day, corresponding to a hair