Weiss Bernard, Clarkson Thomas W, Simon William
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Environ Health Perspect. 2002 Oct;110 Suppl 5(Suppl 5):851-4. doi: 10.1289/ehp.02110s5851.
This article discusses three examples of delay (latency) in the appearance of signs and symptoms of poisoning after exposure to methylmercury. First, a case is presented of a 150-day delay period before the clinical manifestations of brain damage after a single brief (<1 day) exposure to dimethylmercury. The second example is taken from the Iraq outbreak of methylmercury poisoning in which the victims consumed contaminated bread for several weeks without any ill effects. Indeed, signs of poisoning did not appear until weeks or months after exposure stopped. The last example is drawn from observations on nonhuman primates and from the sequelae of the Minamata, Japan, outbreak in which low chronic doses of methylmercury may not have produced observable behavioral effects for periods of time measured in years. The mechanisms of these latency periods are discussed for both acute and chronic exposures. Parallels are drawn with other diseases that affect the central nervous system, such as Parkinson disease and post-polio syndrome, that also reflect the delayed appearance of central nervous system damage.
本文讨论了接触甲基汞后中毒体征和症状出现延迟(潜伏期)的三个例子。首先,介绍了一个案例,单次短暂(<1天)接触二甲基汞后,150天出现脑损伤临床表现的延迟期。第二个例子来自伊拉克甲基汞中毒事件,受害者食用受污染面包数周却未出现任何不良影响。事实上,中毒体征直到接触停止数周或数月后才出现。最后一个例子来自对非人类灵长类动物的观察以及日本水俣病疫情的后遗症,其中低剂量慢性甲基汞在数年时间内可能未产生可观察到的行为影响。本文讨论了急性和慢性接触情况下这些潜伏期的机制。还将其与其他影响中枢神经系统的疾病进行了对比,如帕金森病和小儿麻痹后遗症,这些疾病也反映了中枢神经系统损伤的延迟出现。