Journal of Neurodevelopmental Disorders ( IF 4.1 ) Pub Date : 2020-12-16 , DOI: 10.1186/s11689-020-09345-y Heather Volk 1, 2 , Margaret A Sheridan 3, 4
How do we define the environment? In this special issue of the Journal of Neurodevelopmental Disorders (JNDD), we take a broad view, publishing research linking psychosocial adversity to risk for neurodevelopmental disorders side by side with studies examining the effects of exposure to environmental toxicants, such as air pollution and heavy metals. This issue both reflects the scope of the conceptualization of the ‘environment’ and the breadth of methods used to investigate it with studies spanning preclinical research, clinical studies of patients, and epidemiological approaches. Each of these studies reflects research pursued within one of 14 Intellectual and Developmental Disabilities Research Centers (IDDRCs) and showcases the breadth and depth of work these centers support.
The link between psychosocial risk early in life and negative neurodevelopmental outcomes has been observed for decades. Increasingly research has documented the impact of these experiences on central nervous system function and structure while randomized control trials have revealed that some of these associations are driven by causal linkages between early psychosocial adversity and neural outcomes [1, 2]. At the same time, the field documenting the impact of environmental toxicants on neurobiology and health outcomes has also grown dramatically in recent years. Both large scale epidemiologic studies and animal models have revealed the long-term impact of early exposures to air pollution, pesticides, heavy metals, and malnutrition. Thus, recent research has revealed that multiple kinds of exposures are likely to impact the development of the function and structure of the central nervous system, yielding a common pathway which may transduce multiple kinds of risk into impairments in cognition, social processing, and emotional functioning that manifest as neurodevelopmental disorders. Importantly, exposure to both psychosocial and environmental risk is often differential by social class and race, concentrating exposure to both forms of risk in a specific population. Considering the developmental environment broadly including examining psychosocial adversity, environmental toxicants, and malnutrition in studies that are in conversation with each other can open up new avenues of discovery. This work can identify shared pathways leading to risk for neurodevelopmental disorders across exposure or reveal potential cross-exposure interactions. In addition, this concentration of risk is a call to action, focusing on the need to address the issue of environmental justice more broadly than in relation to the chemical environment.
The research in this issue spans multiple levels of analysis, from animal models to population-based studies to community level investigations—all with the goal of addressing the role of the environment, broadly defined. With regard to psychosocial adversity, Smith and Pollak contribute a review highlighting the link between psychosocial adversity (prenatal and postnatal stress) and developmental changes in neurobiology (Smith and Pollak, this issue). This paper considers many psychosocial risk factors together. In contrast, Humphrey and colleagues elegantly link exposure to deprivation, a specific psychosocial adversity, to receptive language. This two-sample study spans degrees of exposure and draws a line connecting two forms of psychosocial adversity, institutionalization, and low socioeconomic status, by identifying the common experience of deprivation within both exposures (Humphreys et al., this issue).
Other forms of environmental adversity are explored in subsequent papers. Several contributions included here seek to provide biological evidence of air pollution and pesticide exposures from mouse models (Silverman et al., Cole et al., Hashimoto-Torii et al., this issue) to neurodevelopmental outcomes. These animal studies are juxtaposed with population-based studies of prenatal air pollution exposure and maternal immune response on ASD risk and low-level lead exposure on cognitive ability (Volk et al., Mazumdar et al., this issue). In a review, Cristancho and Marsh highlight the role that epigenetics may play in linking prenatal hypoxia exposure to neurodevelopmental disorders identifying a potential final common pathway for many forms of environmental risk (Cristancho and Marsh, this issue). Finally, McGrath and colleagues describe an ecological analysis of sociodemographic factors and non-native English language speaking on ASD rates in New York state (McGrath et al., this issue). This final paper, which uses sociodemographic variables that cluster other forms of risk as a predictor, highlights that at the population level, many aspects of the environment may work together to increase risk for neurodevelopmental disorders.
Across these studies, a common theme emerges, the impact of the environment, broadly construed, on the development of the central nervous system. What remains to be done is linking across these important areas of investigation, identifying the clustering of risk across the chemical and social environment, observing final common pathways impacted by multiple forms of environmental exposures, and most importantly considering the ways in which these forms of risk interact.
Together, this collection of research illustrates that we cannot view intellectual and developmental disabilities narrowly. Investigations from the IDDRCs, and beyond, are essential for fostering improved understanding of not only the risk for onset, but also impact on the trajectory of impairment, for individuals with intellectual and developmental disabilities. The work reported on herein displays the strengths of the individuals IDDRCs as well as the collective strength of this network in integrating multiple levels of analysis and areas of expertise that are a hallmark of these inter-disciplinary centers. Fostering such within and cross-institutional expertise in both the study of the environment and neurodevelopment is essential for improving the health and well-bring of affected individuals and their families.
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Bick J, Nelson CA. Early adverse experiences and the developing brain. Neuropsychopharmacology. 2016;41:177–96.
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Sheridan MA, Sarsour K, Jutte D, D'Esposito M, Boyce WT. The impact of social disparity on prefrontal function in childhood. PLoS One. 2012;7:e35744.
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NIA Network grant to MAS (R24), NIH Grants MH014592, OD023342, ES029511, ES026961 (to HV), and NICHD IDDRC HD103538 and HD103573.
Affiliations
Departments of Mental Health and Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, 624 N. Broadway, HH833, Baltimore, MD, 21205, USA
Heather Volk
Intellectual and Developmental Disabilities Research Center, Kennedy Krieger Institute, Baltimore, USA
Heather Volk
Department of Psychology and Neuroscience, University of North Carolina, 238 E. Cameron Street, Office 248, Chapel Hill, NC, 27599, USA
Margaret A. Sheridan
Carolina Institute for Developmental Disabilities at the University of North Carolina, Chapel Hill, Chapel Hill, USA
Margaret A. Sheridan
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MAS and HV jointly conceptualized, wrote, and edited the paper. The author(s) read and approved the final manuscript.
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Correspondence to Heather Volk.
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Volk, H., Sheridan, M.A. Investigating the impact of the environment on neurodevelopmental disorder. J Neurodevelop Disord 12, 43 (2020). https://doi.org/10.1186/s11689-020-09345-y
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DOI: https://doi.org/10.1186/s11689-020-09345-y
中文翻译：
调查环境对神经发育障碍的影响
我们如何定义环境？在《神经发育障碍杂志》 (JNDD) 的这一特刊中，我们采取了广泛的观点，发表了将心理社会逆境与神经发育障碍风险联系起来的研究，以及检查暴露于环境毒物（如空气污染和重金属。这个问题既反映了“环境”概念化的范围，也反映了通过临床前研究、患者临床研究和流行病学方法进行研究的方法的广度。这些研究中的每一项都反映了在 14 个智力和发育障碍研究中心 (IDDRC) 之一内进行的研究，并展示了这些中心支持的工作的广度和深度。
几十年来，人们一直在观察生命早期社会心理风险与消极神经发育结果之间的联系。越来越多的研究记录了这些经历对中枢神经系统功能和结构的影响，而随机对照试验表明，其中一些关联是由早期心理社会逆境与神经结果之间的因果关系驱动的 [1, 2]。与此同时，近年来，记录环境毒物对神经生物学和健康结果影响的领域也急剧增长。大规模流行病学研究和动物模型都揭示了早期暴露于空气污染、杀虫剂、重金属和营养不良的长期影响。因此，最近的研究表明，多种暴露可能会影响中枢神经系统功能和结构的发展，产生一个共同的途径，可能将多种风险转化为认知、社会处理和情绪功能的损害，表现为作为神经发育障碍。重要的是，社会心理和环境风险的暴露通常因社会阶层和种族而异，在特定人群中集中暴露于两种形式的风险。广泛地考虑发展环境，包括在相互对话的研究中检查社会心理逆境、环境毒物和营养不良，可以开辟新的发现途径。这项工作可以确定导致神经发育障碍风险的共享途径或揭示潜在的交叉暴露相互作用。此外，这种风险的集中是行动的号召，重点是需要比化学环境更广泛地解决环境正义问题。
本期的研究跨越多个层次的分析，从动物模型到基于人群的研究再到社区层面的调查——所有这些都旨在解决广义上的环境作用。关于社会心理逆境，Smith 和 Pollak 发表了一篇综述，强调了心理逆境（产前和产后压力）与神经生物学发育变化之间的联系（Smith 和 Pollak，本期））。本文综合考虑了许多心理社会风险因素。相比之下，汉弗莱及其同事优雅地将暴露与剥夺（一种特定的心理社会逆境）与接受性语言联系起来。这项双样本研究跨越了暴露程度，并通过确定两种暴露中的普遍剥夺经历，将两种形式的社会心理逆境、制度化和低社会经济地位联系起来（Humphreys 等人，本期）。
其他形式的环境逆境将在后续论文中进行探讨。此处包含的几项贡献旨在为小鼠模型（Silverman 等人、Cole 等人、Hashimoto-Torii 等人，本期）提供空气污染和农药暴露对神经发育结果的生物学证据。这些动物研究与基于人群的产前空气污染暴露和母体免疫反应对 ASD 风险和低水平铅暴露对认知能力的研究并列（Volk 等人，Mazumdar 等人，本期）。在一篇综述中，Cristancho 和 Marsh 强调了表观遗传学在将产前缺氧暴露与神经发育障碍联系起来方面可能发挥的作用，从而确定了多种环境风险的潜在最终共同途径（Cristancho 和 Marsh，这个问题）。最后，McGrath 及其同事描述了关于纽约州 ASD 率的社会人口因素和非母语英语的生态分析（McGrath 等人，本期）。这篇最后的论文使用将其他形式的风险聚集在一起的社会人口学变量作为预测因子，强调在人口水平上，环境的许多方面可能会共同增加神经发育障碍的风险。
在这些研究中，出现了一个共同的主题，即广义上的环境对中枢神经系统发育的影响。剩下要做的是将这些重要的调查领域联系起来，确定化学和社会环境中的风险聚集，观察受多种环境暴露形式影响的最终共同途径，最重要的是考虑这些形式的风险的方式相互影响。
总之，这一系列研究表明我们不能狭隘地看待智力和发育障碍。来自 IDDRC 及其他机构的调查对于增进对智力和发育障碍个人的发病风险以及对损害轨迹的影响的理解至关重要。此处报告的工作展示了 IDDRC 个人的优势以及该网络在整合多层次分析和专业领域方面的集体实力，这是这些跨学科中心的标志。在环境和神经发育研究方面培养此类内部和跨机构专业知识对于改善受影响个人及其家庭的健康和福祉至关重要。
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比克 J，纳尔逊加利福尼亚州。早期的不良经历和发育中的大脑。神经精神药理学。2016 年；41：177-96。
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NIA Network 授予 MAS (R24)、NIH 授予 MH014592、OD023342、ES029511、ES026961（授予 HV）以及 NICHD IDDRC HD103538 和 HD103573。
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约翰霍普金斯大学彭博公共卫生学院心理健康和环境健康与工程系，624 N. Broadway, HH833, Baltimore, MD, 21205, USA
希瑟·沃尔克
美国巴尔的摩肯尼迪克里格研究所智力和发育障碍研究中心
希瑟·沃尔克
北卡罗来纳大学心理学和神经科学系，238 E. Cameron Street, Office 248, Chapel Hill, NC, 27599, USA
玛格丽特·A·谢里丹
北卡罗来纳大学卡罗莱纳发育障碍研究所，教堂山，美国教堂山
玛格丽特·A·谢里丹
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Volk, H., Sheridan, MA 调查环境对神经发育障碍的影响。J 神经发育障碍 12, 43 (2020)。https://doi.org/10.1186/s11689-020-09345-y
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