母亲暴露于环境内分泌干扰物与后代先天性心脏病风险之间的关系:系统回顾与元分析

Kai Pan, Jie Xu, Chengxing Wang, Zhen Mao, Yuzhu Xu, Haoke Zhang, Jie Yu
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摘要

背景:先天性心脏病(CHD)是最常见的先天性畸形,也是新生儿死亡的主要原因。许多研究调查了母亲在怀孕期间接触环境内分泌干扰物(EEDs)与后代患先天性心脏病风险之间的关系。然而,目前还缺乏全面系统的研究来评估它们之间的关系。因此,本文旨在回顾过去 20 年中发表的有关孕期母体暴露于环境内分泌干扰物与子代罹患先天性心脏病风险的文献,并探讨两者之间的确切关系。研究方法检索了三个数据库(PubMed、Embase 和 Web of Science),共纳入 16 项研究,参与人数达 1068211 人。采用纽卡斯尔-渥太华量表(Newcastle Ottawa Scale,NOS)评价文献质量,采用Begg检验和Egger检验确定文献的发表偏倚,采用Q检验和I2统计量评价研究间的统计异质性,采用亚组分析考察各EEDs与CHD及其亚型之间的关系。结果显示结果表明,母体暴露于多环芳烃(PAHs)(OR = 1.34,95% CI:1.17-1.53)(例如:PAHs 和四联症)与先天性心脏病的发生有关、多环芳烃(PAHs)(OR = 1.34,95% CI:1.17-1.53)(例如,多环芳烃与法洛氏四联症(TOF)、室间隔缺损(SD)、圆锥角膜缺损(CD))、杀虫剂/杀虫剂(OR = 1.21,95% CI:1.05-1.40)、烷基酚化合物(OR = 1.46,95% CI:1.14-1.86)和重金属(砷、镉、汞、铅)(OR = 2.09,95% CI:1.53-2.86)会增加后代患先天性心脏病的风险。结论本研究表明,母体在怀孕期间接触 EEDs 可能是增加后代罹患先天性心脏病风险的一个重要因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association Between Maternal Exposure to Environmental Endocrine Disruptors and The Risk of Congenital Heart Diseases in Offspring: A Systematic Review and Meta-analysis
Background: Congenital heart diseases ( CHD ) are the most common type of congenital malformation and are the leading cause of death in newborns. Many studies have investigated the relationship between maternal exposure to environmental endocrine disruptors ( EEDs ) during pregnancy and the risk of CHD in offspring. However, there is a lack of comprehensive and systematic research to assess their relationship. Therefore, the purpose of this paper is to review the literature published in the past 20 years on maternal EEDs exposure during pregnancy and the risk of CHD in offspring, and to explore the exact relationship between them. Methods: Three databases ( PubMed, Embase, and Web of Science ) were searched, and 16 studies with 1068211 participants were included. The Newcastle Ottawa Scale ( NOS ) was used to evaluate the quality of the literature, Begg's test and Egger's test to determine the publication bias of the literature, Q test and I2 statistics to evaluate the statistical heterogeneity among the studies, and subgroup analysis to examine the association between each EEDs and CHD and its subtypes. Results: The results showed that maternal maternal exposure to polycyclic aromatic hydrocarbons ( PAHs ) ( OR = 1.34, 95% CI: 1.17-1.53 ) ( e.g., PAHs and Tetralogy of Fallot ( TOF ), Septal defects ( SD ), Conotruncal defects ( CD ) ), pesticides/insecticides ( OR = 1.21, 95% CI: 1.05 - 1.40 ), alkylphenolic compounds ( OR = 1.46, 95% CI: 1.14 - 1.86 ) and Heavy metals ( Arsenic, Cadmium, Mercury, Lead ) ( OR = 2.09, 95% CI: 1.53 - 2.86 ) during pregnancy increased the risk of CHD in offspring. Conclusion: This study suggests that maternal exposure to EEDs during pregnancy may be an important factor for increasing the risk of CHD in offspring.
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