Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential effect modification by nutrition.
Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential effect modification by nutrition.
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DOI：
10.1289/ehp.9081
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发表时间：
2006-11
影响因子：
10.4
通讯作者：
Krishnakumar A
中科院分区：
文献类型：
--
作者：
Kannan S;Misra DP;Dvonch JT;Krishnakumar A
具体目标有三个：描述接触颗粒物(PM)可能导致低出生体重(LBW)、宫内发育迟缓(IUGR)和早产(PTD)的不良围产儿结局的生物学上可信的机制；综述表明营养影响生物途径的证据；以及解释营养可能改变PM暴露对围产儿结局影响的机制。我们提出了一个跨学科的概念框架，将母婴营养、空气污染暴露评估以及心肺和围产期流行病学结合在一起。在新兴的环境科学文献中提出了五种可能的、尽管不是唯一的生物机制，并为拟议的框架提供了推论。保护母亲和婴儿的环境健康仍然是全球的首要任务。现有文献表明，PM对LBW、PTD和IUGR的影响可能通过氧化应激、炎症、凝血、内皮功能和血流动力学反应等心血管机制表现出来。PM暴露研究将机制途径与围产期结局联系起来，应考虑PM和非PM来源(如营养)可能同时产生的生物反应和不良分娩结局的可能性。在结论部分，我们提出了对所提出的模型进行实证测试和发展未来研究工作的策略。
The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.
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