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Neurotoxicants, Micronutrients, and Social Environments

机译:神经毒素,微量营养素和社会环境

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Systematic research evaluating the separate and interacting impacts of neurotoxicants, micronutrients, and social environments on children's cognition and behavior has only recently been initiated. Years of extensive human epidemiologic and animal experimental research document the deleterious impact of lead and other metals on the nervous system. However, discrepancies among human studies and between animal and human studies underscore the importance of variations in child nutrition as well as social and behavioral aspects of children's environments that mitigate or exacerbate the effects of neurotoxicants. In this monograph, we review existing research on the impact of neurotoxic metals, nutrients, and social environments and interactions across the three domains. We examine the literature on lead, mercury, manganese, and cadmium in terms of dispersal, epidemiology, experimental animal studies, effects of social environments, and effects of nutrition. Research documenting the negative impact of lead on cognition and behavior influenced reductions by the Center for Disease Control in child lead-screening guidelines from 30 micrograms per deciliter (μg/dL) in 1975 to 25 μg/dL in 1985 and to 10 μg/dL in 1991. A further reduction is currently being considered. Experimental animal research documents lead's alteration of glutamate-neurotransmitter (particularly N-methyl-D-aspartate) activity vital to learning and memory. In addition, lead induces changes in cholinergic and dopaminergic activity. Elevated lead concentrations in the blood are more common among children living in poverty and there is some evidence that socioeconomic status influences associations between lead and child outcomes. Micronutrients that influence the effects of lead include iron and zinc. Research documenting the negative impact of mercury on children (as well as adults) has resulted in a reference dose (RfD) of 0.1 microgram per kilogram of body weight per day (μg/kg/day). In animal studies, mercury interferes with glutamatergic, cholinergic, and dopaminergic activity. Although evidence for interactions of mercury with children's social contexts is minimal, researchers are examining interactions of mercury with several nutrients. Research on the effects of cadmium and manganese on child cognition and behavior is just beginning. Experimental animal research links cadmium to learning deficits, manganese to behaviors characteristic of Parkinson's disease, and both to altered dopaminergic functioning. We close our review with a discussion of policy implications, and we recommend interdisciplinary research that will enable us to bridge gaps within and across domains.
机译:评估神经毒物,微量营养素和社会环境对儿童的认知和行为的单独和相互作用的影响的系统研究直到最近才开始。多年的人类流行病学和动物实验研究证明了铅和其他金属对神经系统的有害影响。然而,人类研究之间以及动物与人类研究之间的差异强调了儿童营养变化以及减轻或加剧神经毒性作用的儿童环境的社会和行为方面的重要性。在此专着中,我们回顾了有关神经毒性金属,营养物质和社会环境以及跨这三个领域的相互作用的影响的现有研究。我们从扩散,流行病学,动物实验研究,社会环境影响以及营养影响方面研究了铅,汞,锰和镉方面的文献。疾病控制中心在儿童铅筛查指南中记录了铅对认知和行为的负面影响,影响了铅的减少,铅含量从1975年的30微克每分升(μg/ dL)下降到1985年的25μg/ dL和1985年的10μg/ dL 1991年。目前正在考虑进一步减少。动物实验研究文件表明,谷氨酸神经递质(特别是N-甲基-D-天冬氨酸)活性的改变对学习和记忆至关重要。另外,铅诱导胆碱能和多巴胺能活动的改变。血液中铅的浓度升高在贫困儿童中更为普遍,并且有一些证据表明,社会经济状况会影响铅与儿童结局之间的关联。影响铅影响的微量营养素包括铁和锌。研究记录了汞对儿童(以及成人)的负面影响,得出的参考剂量(RfD)为每天每千克体重0.1微克(μg/ kg /天)。在动物研究中,汞会干扰谷氨酸能,胆碱能和多巴胺能活动。尽管汞与儿童社交环境相互作用的证据很少,但研究人员正在研究汞与几种营养素的相互作用。镉和锰对儿童认知和行为影响的研究才刚刚开始。动物实验研究将镉与学习障碍联系在一起,将锰与帕金森氏病的特征行为联系在一起,并将二者与多巴胺能功能的改变联系起来。我们通过讨论政策含义来结束我们的评论,并建议进行跨学科研究,这将使我们能够弥合领域内和跨领域的差距。

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