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

MERCURY 128
2. HEALTH EFFECTS
poisoning was estimated at 271 per 1,000; this includes a mortality of 59 per 1,000, a severe disability rate
of 32 per 1,000, a rate of mild or moderate disability of 41 per 1,000; and a rate for those with only a
subjective evidence of poisoning of 138 per 1,000. Based on estimates of total intake, dose-related
increases were observed in the incidence and severity of paresthesia, astereognosis (loss of the ability to
judge the form of an object by touch), persistent pain in the limbs, persistent headaches, difficulty walking,
difficulty using the arms, and changes in speech, sight, and hearing. The most commonly observed
symptom was paresthesia, most frequently involving the extremities but also on the trunk and the
circumoral region. Difficulty walking and a feeling of weakness were the next most common symptoms.
The total estimated intake in total milligrams associated with the four categories (no evidence of poisoning,
subjective evidence, mild to moderate evidence, and severe symptoms) is as follows for all ages combined
(number of persons in parentheses): 95 mg (n=59), 141 mg (n=131), 160 mg (n=35), 173 mg (n=22). This
dose range is small for such dramatically different health states, and does not widen when the data are
evaluated by age group. Interestingly, the total intake associated with severity of symptoms decreases on a
mg/kg body weight basis with increasing age in contrast with what would be expected if children were more
susceptible. For example, intakes (mg/kg over the total exposure period) associated with severe symptoms
are as follows for the age groups 5–9 years, 10–14 years, and 15 years and older, respectively: 7.8 mg/kg
(n=9), 4 mg/kg (n=7), and 3.6 mg/kg (n=6). Comparable numbers are for the mild/moderate symptoms and
the subjective symptoms (shown): 6 mg/kg (n=19), 3.4 mg/kg (n=20), and 2.4 mg/kg (n=92). It is possible
that child sensitivity may not be as large a factor when exposures reach the levels experienced in Iraq.
Neurotoxic effects seen in the Minamata (Japan) and Iraqi poisonings have been associated with neuronal
degeneration and glial proliferation in the cortical and cerebellar gray matter and basal ganglia (Al-Saleem
and the Clinical Committee on Mercury Poisoning 1976), and 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). In the brain, Purkinje, basket, and stellate cells were severely affected. Granule cells
were variably affected. Sural nerves removed from two women with neurotoxicity associated with the
Minamata incident also showed evidence of peripheral nerve degeneration and regeneration (Miyakawa et
al. 1976).
Similar effects have been observed in persons ingesting meat contaminated with ethylmercuric chloride
(Cinca et al. 1979). Neurotoxic signs observed in two boys who ultimately died as the result of the
exposure included gait disturbance, ataxia, dysarthria, dysphagia, aphonia, hyperreactive tendon reflexes,