母体接触污染物颗粒物质2.5与先天性心脏缺陷之间的关系:一项系统综述。

Katie C Hall, Jennifer C Robinson
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引用次数: 8

摘要

目的:本综述的目的是确定母亲在怀孕前三个月接触污染颗粒物2.5与出生后一年内先天性心脏缺陷之间是否存在关联。导言:环境被认为是个人和全体人民健康的一个重要决定因素。特别是空气污染是影响健康的主要环境风险因素,与哮喘、心脏病、肥胖和胎儿发育并发症有关。在通常监测的空气污染物中,颗粒物质2.5与健康有关,特别是对儿童和孕妇等弱势群体而言。先天性心脏缺陷是一种影响全球3430万婴儿的胎儿并发症,其中80%以上的诊断病因不明。虽然空气污染等环境危险因素被认为是诊断先天性心脏缺陷的一个危险因素,但流行病学研究证据有限。纳入标准:本综述考虑了评估孕妇在胎儿发育的前三个月(1-12周)暴露于空气污染物颗粒物2.5的研究。研究的主要结果是在婴儿出生后一年内诊断出先天性心脏缺陷。方法:本综述采用三步搜索策略,包括11个数据库和2个网站。2002年1月至2018年9月发表的研究符合纳入条件。仅收录了以英文发表的论文。合格的研究由两名独立的审稿人使用JBI的标准化关键评估工具进行严格评估。定量数据由两名审稿人独立地从纳入的研究中提取。比值比(ORs)和95%置信区间(CIs)分别用于单独的结果测量,特别是房间隔缺损、室间隔缺损和法洛四联症。在可能的情况下,在统计荟萃分析中识别和汇总缺陷。在无法进行统计汇总的情况下,以叙述方式报告调查结果。结果:5项研究符合纳入标准,包括3项队列设计和2项病例对照设计。每一项单独的研究都确定了至少一项统计上显著的颗粒物2.5与先天性心脏缺陷之间的增加或负相关。风险增加被确定为超过7个孤立和两组先天性心脏缺陷。两个孤立的和一组先天性心脏缺陷被确定为负风险。meta分析结果为:房间隔缺损,OR = 0.65 (95% CI, 0.37 ~ 1.15);室间隔缺损,OR = 1.02 (95% CI, 075 ~ 1.37);法洛四联症,OR = 1.16 (95% CI, 0.78 ~ 1.73),无统计学意义。结论:没有明显的证据支持空气污染物颗粒物质2.5与一岁先天性心脏缺陷之间的联系。然而,很少有研究符合严格的纳入标准,并且这些研究具有高度的异质性,这使得在如此有限的文章数量下完成荟萃分析变得困难。需要进一步的研究来规范结果和污染物监测方法,并提供可比较的分析结果,以便将来进行文献的综合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Association between maternal exposure to pollutant particulate matter 2.5 and congenital heart defects: a systematic review.

Objective: The objective of this review was to determine if there was an association between maternal exposure to pollutant particulate matter 2.5 during the first trimester of pregnancy and congenital heart defects within the first year of life.

Introduction: The environment is recognized as an important determinant of health for both the individual and population. Air pollution specifically is a major environmental risk factor impacting health with links to asthma, heart disease, obesity, and fetal developmental complications. Of the commonly monitored air pollutants, particulate matter 2.5 has associations with health, especially among vulnerable populations such as children and pregnant women. A congenital heart defect is a fetal complication that impacts 34.3 million infants globally, with more than 80% of the diagnoses having an unknown etiology. Although environmental risk factors such as air pollution are thought to be a risk factor in the diagnosis of a congenital heart defect, epidemiologic research evidence is limited.

Inclusion criteria: This review considered studies that evaluated maternal exposure to the air pollutant particulate matter 2.5 during the first trimester (weeks 1-12) of fetal development. The primary outcome was a diagnosis of a congenital heart defect in an infant within the first year of life.

Methods: A three-step search strategy was utilized in this review and included 11 databases and two websites. Studies published from January 2002 to September 2018 were eligible for inclusion. Only papers published in English were included. Eligible studies underwent critical appraisal by two independent reviewers using standardized critical appraisal instruments from JBI. Quantitative data were extracted from the included studies independently by two reviewers. Odds ratios (ORs) and 95% confidence intervals (CIs) were extracted for the individual outcome measures, specifically atrial septal defect, ventricular septal defect, and tetralogy of fallot, respectively. The defects were identified and pooled, where possible, in statistical meta-analysis. Where statistical pooling was not possible, findings were reported narratively.

Results: Five studies were identified that met the inclusion criteria, including three cohort and two case-control designs. Each individual study identified at least one statistically significant increase or inverse association between particulate matter 2.5 and a congenital heart defect. An increased risk was identified with more than seven isolated and two groupings of congenital heart defects. An inverse risk was identified with two isolated and one grouping of congenital heart defects. Meta-analysis results were: atrial septal defect, OR = 0.65 (95% CI, 0.37 to 1.15); ventricular septal defect, OR = 1.02 (95% CI, 075 to 1.37); and tetralogy of fallot, OR = 1.16 (95% CI, 0.78 to 1.73), indicating no statistically significant findings.

Conclusion: There was no significant evidence to support an association between air pollutant particulate matter 2.5 and a congenital heart defect in the first year of life. However, few studies met the rigorous inclusion criteria, and the studies that did had high heterogeneity, making it difficult to complete a meta-analysis with such a limited number of articles. Further research is needed to standardize the outcomes and pollutant monitoring methods, and provide comparable analysis results so that future synthesis of the literature can be conducted.

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