Interdisciplinary Brain Research Centre, JN Medical College, AMU, Aligarh, U.P., India.
Environ Toxicol Pharmacol. 2005 Sep;20(2):351-60. doi: 10.1016/j.etap.2005.03.007.
Post Minamata incident there has been awareness about mercury toxicity even among the general public. Previous researches contributed a vast amount of data regarding acute mercury exposure, but gradually information about the low dose [Ninomiya, T., Ohmori, H., Hashimoto, K., Tsuruta, K., Ekino, S., 1995. Expansion of methylmercury poisoning outside minamata: an epidemiological study on chronic methylmercury poisoninig outside of Minamata. Environ. Res. 70 (1) 47-50; Lebel, J., Mergler, D., Lucotte, M., Amorim, M., Dolbec, J., Miranda, D., Arantes, G., Rheault, I., Pichet, P., 1996. Evidence of early nervous system dysfunction in Amazonian populations exposed to low-levels of methylmercury. Neurotoxicology 17 (1) 157-167] of mercury toxicity has been trickling in. With mercury contaminating rain-, ground- and sea-water no one is safe. Polluted water leads to mercury laced fish, meat and vegetable. In aquatic environments, inorganic mercury is microbiologically transformed into lipophilic organic compound 'methylmercury'. This transformation makes mercury more prone to biomagnification in food chains. Consequently, populations with traditionally high dietary intake of food originating from fresh or marine environment have highest dietary exposure to mercury. Extensive research done on locals across the globe have already established this, persons who routinely consume fish or a particular species of fish are at an increased risk of methylmercury poisoning. The easy access of the toxicant to man through multiple pathways air, water, food, cosmetic products and even vaccines increase the exposure. Foetus and children are more susceptible towards mercury toxicity. Mothers consuming diet containing mercury pass the toxicant to foetus and to infants through breast milk. Decreased performance in areas of motor function and memory has been reported among children exposed to presumably safe mercury levels. Similarly, disruption of attention, fine motor function and verbal memory was also found in adults on exposure to low mercury levels. It is an occupational hazard for dental staff, chloralkali factory workers and goldminers, etc. Mercury has been found to be a causative agent of various sorts of disorders, including neurological, nephrological, immunological, cardiac, motor, reproductive and even genetic. Recently heavy metal mediated toxicity has been linked to diseases like Alzeihemer's, Parkinson's, Autism, Lupus, Amyotrophic lateral sclerosis, etc. Besides this, it poses danger to wildlife. Therefore, it becomes imperative to spread the information regarding the threat of mercury exposure amongst the scientists and masses.
在后水俣病事件之后，即使是普通大众也对汞毒性有了一定的认识。之前的研究提供了大量关于急性汞暴露的数据，但关于低剂量汞毒性的信息逐渐增多。[Ninomiya，T.，Ohmori，H.，Hashimoto，K.，Tsuruta，K.，Ekino，S.，1995. Minamata 以外甲基汞中毒的扩大： Minamata 以外慢性甲基汞中毒的流行病学研究。环境研究 70（1）47-50；Lebel，J.，Mergler，D.，Lucotte，M.，Amorim，M.，Dolbec，J.，Miranda，D.，Arantes，G.，Rheault，I.，Pichet，P.，1996. 暴露于低水平甲基汞的亚马逊人群中早期神经系统功能障碍的证据。神经毒理学 17（1）157-167]。随着汞污染雨水、地下水和海水，没有人是安全的。受污染的水导致汞含量高的鱼类、肉类和蔬菜。在水生环境中，无机汞在微生物的作用下转化为亲脂性有机化合物“甲基汞”。这种转化使汞更容易在食物链中生物放大。因此，传统上高摄入来自淡水或海洋环境的食物的人群对汞的饮食暴露最高。全球范围内对当地人进行的广泛研究已经证实，经常食用鱼类或某种特定鱼类的人患甲基汞中毒的风险增加。汞通过多种途径（空气、水、食物、化妆品甚至疫苗）很容易进入人体，增加了暴露的可能性。胎儿和儿童更容易受到汞毒性的影响。食用含汞饮食的母亲会通过胎盘和母乳将有毒物质传递给胎儿和婴儿。据报道，在接触假定安全的汞水平后，儿童的运动功能和记忆力等方面的表现下降。同样，在接触低水平汞时，成年人的注意力、精细运动功能和语言记忆也受到干扰。牙医、氯碱厂工人和采金人等都是职业危害者。汞已被发现是各种疾病的致病因子，包括神经、肾脏、免疫、心脏、运动、生殖甚至遗传疾病。最近，重金属介导的毒性与阿尔茨海默病、帕金森病、自闭症、狼疮、肌萎缩性侧索硬化症等疾病有关。此外，它对野生动物也构成威胁。因此，有必要在科学家和大众中传播有关汞暴露威胁的信息。
