Comment: Amalogam does not contain methylmercury!
MEDLINE: Biomedicine, 1990- @ Wed Sep 17 12:41:46 1997
Document 106
Accession No.: 97241079.
Author: Rice-D-C.
Title:
Evidence for delayed neurotoxicity produced by methylmercury.
Source: Neurotoxicology. 1996 Fall-Winter. 17(3-4). P 583-96.
Journal Title: NEUROTOXICOLOGY.
Abstract:
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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