产前和产后暴露于空气污染与临床诊断的注意缺陷多动障碍的关系:系统综述

Jinzhu Zhao, Tianyi He, Feng Wang, Wei Liu
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引用次数: 0

摘要

注意缺陷多动障碍(ADHD)是一种普遍存在于儿童中的神经发育障碍,它源于遗传、神经和环境因素的多方面相互作用。最近的研究越来越集中于环境因素,尤其是空气污染,以及它们对多动症发病风险的影响。此外,以往的研究常常将临床诊断为多动症的病例与仅有类似多动症症状的病例混为一谈,这种方法可能会产生偏差,并掩盖环境因素与多动症之间的真实关系。针对这一疏忽,我们的系统性综述细致地研究了产前和产后暴露于特定空气污染物与严格临床诊断的多动症之间的关系。我们的综合综述涵盖了 PubMed、Cochrane Library、Web of Science 和 Embase 数据库中的 801 项研究,其中有 8 项符合我们严格的纳入标准。我们采用纽卡斯尔-渥太华量表(NOS)来衡量研究的质量和偏差。我们的综述发现,产前暴露于PM2.5和氮氧化物与多动症风险升高之间存在联系,而产前暴露于PM10与多动症无关。这些研究结果表明,不同的颗粒物对健康的影响各不相同,而且不同性别的人对此类暴露的易感性也不尽相同。我们还发现了产后暴露于 PM2.5、PM10 和 NO2 与多动症风险增加之间的关系,强调了早期暴露于这些污染物对神经发育的潜在危害。这些关系看似错综复杂,而且可能与剂量有关,因此需要进行更详细的研究。我们这篇综述的独特价值在于详细探讨了特定空气污染暴露与临床诊断的多动症之间的关系。我们的研究结果为这一复杂领域提供了亟需的清晰度,并强调了未来研究的重要性,以规范暴露和结果指标、探究潜在机制并减少偏倚和异质性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association of prenatal and postnatal exposure to air pollution with clinically diagnosed attention deficit hyperactivity disorder: a systematic review
Attention deficit hyperactivity disorder (ADHD), a prevalent neurodevelopmental disorder in children, originates from a multifaceted interplay of genetic, neurological, and environmental factors. Recent studies have increasingly concentrated on environmental determinants, notably air pollution, and their impact on the risk of developing ADHD. Additionally, previous research has often conflated clinically diagnosed ADHD cases with instances of mere ADHD-like symptoms, a methodology that can introduce bias and obscure the true relationship between environmental factors and ADHD. To address this oversight, our systematic review meticulously investigates the relationship between both prenatal and postnatal exposures to particular air pollutants and strictly clinically diagnosed ADHD. Our comprehensive review encompassed 801 studies from PubMed, Cochrane Library, Web of Science, and Embase databases, out of which eight met our rigorous inclusion criteria. The Newcastle-Ottawa Scale (NOS) was utilized to gauge quality and bias. Our review found substantiated the connection between prenatal exposure to PM2.5 and NOx and a heightened risk of ADHD, while exposure to PM10 during the prenatal stage was not associated with ADHD. These findings hint at varied health impacts from different particulate matters and the prospect of gender-specific susceptibilities to such exposures. We also identified an association between postnatal exposure to PM2.5, PM10, and NO2 and an increased ADHD risk, underlining the potential neurodevelopmental harms from early exposure to these pollutants. These relationships, seemingly intricate and potentially dose-dependent, underscore the need for more detailed scrutiny. The unique value of our review is in its detailed exploration of the association between specific air pollution exposures and clinically diagnosed ADHD. Our findings offer much-needed clarity in this complex domain and emphasize the importance of future research to standardize exposure and outcome metrics, probe potential mechanisms, and reduce bias and heterogeneity.
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