Lipfert F W, Moskowitz P D, Fthenakis V, Saroff L
Department of Applied Science, Brookhaven National Laboratory, Upton, New York 11973, USA.
Neurotoxicology. 1996 Spring;17(1):197-211.
This paper describes a probabilistic assessment of neurological risks incurred from consuming fish containing methylmercury (MeHg), focusing on the incremental effects of Hg deposited from local coal combustion. A Monte Carlo model is used to simulate a "worst case" scenario in which a population of 5000 fish eaters in the upper midwestern United States derive the freshwater fish portion of their diet from local waters near a hypothetical large coal-fired power plant. This population is characterized by distributions of body mass, half-life of MeHg, and the ratios of blood to body burden and hair to blood MeHg. Each person's diet consists of varying amounts of tuna fish, freshwater sportfish, and marine fish and shellfish, the MeHg contents of which are characterized by national distribution statistics, as are the consumption rates for marine fish. The consumption rates for freshwater fish are specific to the region. The fish portion size is linked to body mass by a variable correlation. Each meal is assumed to be an independent sample; thus, as metabolic equilibrium is approached, each person's body burden of MeHg tends to approach the value corresponding to the mean MeHg intake for the population. Predictions of MeHg levels in hair by this model compared well with an observed distribution of 1437 women. Two neurological endpoints were examined: adult paresthesia, as related to MeHg body burden, and congenital neurological effects, as associated with average concentrations of MeHg in maternal hair during pregnancy. Two exposure scenarios are considered: a "baseline" in which the source of the mercury in fish is from background atmospheric deposition, and an "impact" scenario, in which local Hg deposition and concentrations in fish are roughly doubled to represent additional deposition from the hypothetical nearby power plant. For both scenarios, the 99th percentile of MeHg body burden was more than an order of magnitude below the lowest level at which increased transient adult paresthesia was experienced in an acute MeHg poisoning incident in Iraq. We thus conclude that neurological risks to adults from MeHg resulting from atmospheric Hg deposition are trivial. Based on three epidemiological studies of congenital neurological risks, we find that fetal effects appear to be more critical and that there is a smaller margin of safety for pregnant consumers of freshwater sportfish. However, the margin of safety is still considerable and may have been diminished by uncertainties in the relationships between maternal hair Hg and the actual fetal exposures.
本文描述了食用含甲基汞(MeHg)鱼类所带来的神经学风险的概率评估,重点关注当地煤炭燃烧所沉积汞的增量影响。使用蒙特卡罗模型模拟一种“最坏情况”情景,即美国中西部上游地区的5000名食鱼者群体从假设的大型燃煤电厂附近的当地水域获取其饮食中的淡水鱼部分。该群体的特征在于体重分布、甲基汞半衰期以及血液与身体负荷之比和头发与血液甲基汞之比。每个人的饮食由不同数量的金枪鱼、淡水游钓鱼类以及海鱼和贝类组成,其甲基汞含量以全国分布统计数据为特征,海鱼的消费率也是如此。淡水鱼的消费率因地区而异。鱼的份量大小通过可变相关性与体重相关联。每餐被假定为独立样本;因此,随着代谢平衡的接近,每个人体内甲基汞的负荷往往会接近该群体甲基汞平均摄入量对应的数值。该模型对头发中甲基汞水平的预测与1437名女性的观察分布情况吻合良好。研究了两个神经学终点:与甲基汞身体负荷相关的成人感觉异常,以及与孕期母亲头发中甲基汞平均浓度相关的先天性神经学影响。考虑了两种暴露情景:一种是“基线”情景,即鱼类中汞的来源是背景大气沉积;另一种是“影响”情景,即当地汞沉积和鱼类中的浓度大致翻倍,以代表来自假设的附近电厂的额外沉积。对于这两种情景,甲基汞身体负荷的第99百分位数比伊拉克一次急性甲基汞中毒事件中出现成人短暂感觉异常增加的最低水平低一个数量级以上。因此,我们得出结论,大气汞沉积导致的甲基汞对成年人的神经学风险微不足道。基于三项关于先天性神经学风险的流行病学研究,我们发现胎儿影响似乎更为关键,对于食用淡水游钓鱼类的孕妇来说安全边际较小。然而,安全边际仍然相当可观,并且可能因母亲头发汞含量与实际胎儿暴露之间关系的不确定性而有所减小。