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

MERCURY 129
2. HEALTH EFFECTS
hypotonia, spasticity, mydriasis, horizontal nystagmus, agitation, and coma. Electroencephalography
showed decreased alpha activity and increased slow-wave activity. Autopsy showed nerve cell loss and
glial proliferation in the cerebral cortex (calcarine cortex, midbrain, bulbar reticular formation),
demyelination, granule cell loss in the cerebellum, and motor neuron loss in the ventral horns of the spinal
cord. Neurotoxic signs in the surviving family members were generally similar (ataxia, gait impairment,
spasticity, drowsiness, intentional tremor, agitation, hypoesthesia in the limbs, speech difficulties, and
visual disturbances); all but the narrowing of the visual fields resolved after termination of exposure.
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. Twentytwo
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. The inorganic mercury levels in different regions of the brain of the 29-yearold
patient ranged from 82 to 100% of the total mercury present. 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.
LeBel et al. (1996) studied early nervous system dysfunction in Amazonian populations exposed to low
levels of methylmercury. A preliminary study was undertaken in two villages on the Tapajos River, an
effluent of the Amazon, situated over 200 km downstream from the methylmercury extraction areas. The
study population included 29 young adults $35 years (14 women and 15 men) randomly chosen from a
previous survey. Hair analyses were conducted with cold vapor atomic fluorescence spectrophotometry.
Total hair Hg (THg) varied between 5.6 µg/g and 38.4 µg/g, with MeHg levels from 72.2% to 93.3% of