EVIDENCE FOR DELAYED NEUROTOXICITY PRODUCED BY METHYLMERCURY

Delayed toxicity as a result of developmental methylmercury exposure w as identified in mice two decades ago by Spyker, who observed kyphosis , neuromuscular deficits, and other severe abnormalities as the mice a ged. Delayed neurotoxicity was also observed in monkeys treated with m ethylmercury from birth to seven years of age. When these monkeys reac hed 13 years of age, individuals began exhibiting clumsiness not prese nt previously. Further exploration revealed that treated monkeys requi red more time to retrieve treats than did nonexposed monkeys and displ ayed abnormalities on a clinical assessment of sense of touch in hands and feet, despite the fact that clinical examinations performed routi nely during the period of dosing had not yielded abnormal results. Ano ther 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 gro ups of monkeys exhibited impaired vibration sensitivity. These results are strongly suggestive of a delayed neurotoxicity manifested when th ese monkeys reached middle age. Data from persons with Minamata diseas e also provide evidence for delayed neurotoxicity. Perhaps the stronge st 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. Methylme rcury may represent the only environmental toxicant for wh ich there i s good evidence for delayed neurotoxicity that may be manifested many years after cessation of exposure. (C) 1996 Inter Press, Inc.