A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder.
A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder.
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DOI：
10.1371/journal.pone.0161851
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Woodruff T
中科院分区：
文献类型：
--
作者：
Lam J;Sutton P;Kalkbrenner A;Windham G;Halladay A;Koustas E;Lawler C;Davidson L;Daniels N;Newschaffer C;Woodruff T
暴露于环境空气污染是普遍的，可能对人类大脑发育有害，并且是自闭症谱系障碍（ASD）的一个潜在风险因素。我们对关于ASD与暴露于所有空气污染物（包括颗粒物空气污染物及其他污染物，如农药和金属）之间关系的人类证据进行了系统综述。
为了回答“发育过程中暴露于空气污染是否与ASD相关？”这一问题，
我们对文献进行了全面检索，使用我们的研究方案中预先设定的纳入/排除标准确定了相关研究（在PROSPERO注册，注册号为CRD # 42015017890），评估了每项纳入研究的潜在偏倚风险，并确定了一个合适的研究子集用于荟萃分析。然后我们对所有空气污染物的证据总体质量和强度进行了评级。
在确定的1158篇参考文献中，有23项人类研究符合我们的纳入标准（17项病例对照研究、4项生态学研究、2项队列研究）。大多数领域的研究偏倚风险普遍较低；研究的局限性与潜在的混杂因素以及暴露评估方法的准确性有关。我们将所有空气污染物的证据体质量评为“中等”。通过我们的荟萃分析，我们发现PM10暴露量每增加10μg/m³，汇总优势比（OR）为1.07（95%置信区间：1.06，1.08）（n = 6项研究），PM2.5暴露量每增加10μg/m³，汇总优势比为2.32（95%置信区间：2.15，2.51）（n = 3项研究）。对于未纳入荟萃分析的污染物，我们综合评估了每项研究的证据，在对总体证据的强度和质量进行评级时考虑了不一致性、不精确性和剂量 - 反应证据等因素。所有纳入的研究总体上表明，随着暴露于空气污染的增加，ASD的风险增加，尽管并非在所有化学成分中都一致。
在考虑了研究体的优势和局限性之后，我们得出结论，对于生命早期整体暴露于空气污染与ASD诊断之间的关联，存在“有限的毒性证据”。最强的证据是产前暴露于颗粒物与ASD之间的关联。然而，荟萃分析中的研究数量较少，以及各个研究估计值之间无法解释的统计异质性意味着，实际影响可能比这些研究估计的更大或更小（包括不显著）。我们的研究支持制定健康保护公共政策以减少孕妇和儿童暴露于有害空气污染物的必要性，并为优化未来研究提供了契机。
Exposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals). To answer the question: “is developmental exposure to air pollution associated with ASD?” We conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants. Of 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as “moderate.” From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components. After considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.