Evidence for delayed neurotoxicity produced by
methylmercury.
Rice DC.
Toxicology Research Division, Bureau of Chemical Safety, Health Canada.
Delayed toxicity as a result of developmental methylmercury exposure was
identified in mice two decades ago by Spyker, who observed kyphosis,
neuromuscular deficits, and other severe abnormalities as the mice aged.
Delayed neurotoxicity was also observed in monkeys treated with methylmercury
from birth to seven years of age. When these monkeys reached 13 years of age,
individuals began exhibiting clumsiness not present previously. Further
exploration revealed that treated monkeys required more time to retrieve
treats than did nonexposed monkeys and displayed abnormalities on a clinical
assessment of sense of touch in hands and feet, despite the fact that clinical
examinations performed routinely during the period of dosing had not yielded
abnormal results. Another group of monkeys, dosed from in utero to four years
of age, also took longer to retrieve treats when assessed years after
cessation of exposure. These observations were pursued in both groups of
monkeys by objective assessment of somatosensory function in the hands: both
groups of monkeys exhibited impaired vibration sensitivity. These results are
strongly suggestive of a delayed neurotoxicity manifested when these monkeys
reached middle age. Data from persons with Minamata disease also provide
evidence for delayed neurotoxicity. Perhaps the strongest piece of evidence
comes from a study of over 1100 Minamata patients over 40 years old, in which
difficulty in performing daily activities increased as a function of age
compared to matched controls. Methylmercury may represent the only
environmental toxicant for which there is good evidence for delayed
neurotoxicity that may be manifested many years after cessation of exposure.
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