Boischio A A, Henshel D S
School of Public and Environmental Affairs, Indiana University, Bloomington, USA.
Neurotoxicology. 1996 Spring;17(1):169-75.
Aquatic food chain mercury pollution is one of the consequences of the gold rush in the Amazon, which started in the late 1970s. This paper addresses the risks of methylmercury (MeHg) toxicity by a riverside population of heavy fish eaters along the Madeira river, in the Amazon, based on their hair mercury (Hg) concentration. Given the vulnerability of the developing nervous system, NOEL/LOEL values were used based on prenatal (LOELp = 0.7 microgram/ kg bw), and adult and childhood (LOELa = 3 micrograms/kg bw) Hg exposures. Based on hair Hg concentrations, we observed that approximately 95% of infants were at risk of absorbing Hg through the previous placental exposure, and/or by ingesting Hg from mother's milk, and/or fish consumption, at a level as great as the LOELp. The hazard quotient derived from the LOELp for neurobehavioral effects was 64 based on an estimated mean Hg daily intake of 4.5 micrograms/kg bw. Approximately 45% of the mothers of the infants and other women of child bearing age were at risk of ingesting Hg at a level equivalent to the LOELp. This also translates into a derived hazard quotient for neurobehavioral effects of 17 for all potential mothers in the population. The non-infant population at the highest risk was fish-eating children under 5 years old. This sub-population had a mean estimated Hg daily intake of 6.4 micrograms/kg bw. This resulted in a probability that almost 60% of this sub-population ingested Hg at a level equivalent to the LOELa or higher. For this sub-population, there was a hazard quotient of 21. These data strongly indicate that the young children of this riverside fish-eating population may be ingesting Hg doses that have been correlated with neurological damage from Hg poisoning.
水生食物链汞污染是始于20世纪70年代末的亚马逊淘金热的后果之一。本文基于马德拉河沿岸以大量食用鱼类为生的河边居民头发中的汞浓度,探讨了甲基汞(MeHg)毒性对亚马逊地区马德拉河沿岸居民的风险。鉴于发育中的神经系统较为脆弱,根据产前(最低观察到有害作用剂量[LOELp]=0.7微克/千克体重)以及成人和儿童(最低观察到有害作用剂量[LOELa]=3微克/千克体重)的汞暴露情况,采用了无明显有害作用水平(NOEL)/最低观察到有害作用剂量(LOEL)值。基于头发中的汞浓度,我们观察到,约95%的婴儿有通过先前的胎盘暴露、和/或通过摄入母乳中的汞、和/或食用鱼类而吸收汞的风险,其吸收水平高达最低观察到有害作用剂量[LOELp]。根据估计的每日平均汞摄入量4.5微克/千克体重,由最低观察到有害作用剂量[LOELp]得出的神经行为效应的危害商数为64。约45%的婴儿母亲及其他育龄妇女有摄入相当于最低观察到有害作用剂量[LOELp]水平汞的风险。这也意味着该人群中所有潜在母亲的神经行为效应的派生危害商数为17。风险最高的非婴儿人群是5岁以下以鱼类为食的儿童。该亚人群的估计每日平均汞摄入量为6.4微克/千克体重。这导致该亚人群中近60%的人摄入汞的水平相当于或高于最低观察到有害作用剂量[LOELa]。对于该亚人群,危害商数为21。这些数据有力地表明,这个以鱼类为食的河边人群中的幼儿可能正在摄入与汞中毒所致神经损伤相关的汞剂量。