围孕期有害环境暴露与子代先天性心脏病关联的研究进展

    Research progress on the association between adverse environmental exposure during the periconceptional period and offspring congenital heart disease

    • 摘要: 围孕期有害环境暴露是子代先天性心脏病(congenital heart disease, CHD)重要环境危险因素。本文纳入97篇相关文献, 系统梳理近五年围孕期环境暴露与子代CHD的流行病学及机制研究进展。现有证据表明, 母体围孕期接触大气污染物、多环芳烃、重金属、农药、环境内分泌干扰物等化学污染物, 会升高子代CHD患病风险; 光污染、极端气温等物理环境刺激亦可损害胎儿心脏发育。各类污染物可通过诱发氧化应激、炎症反应、线粒体损伤、内分泌失调及表观遗传异常, 干扰胚胎心脏正常形态发育。现阶段研究尚存短板: 多污染物联合暴露交互作用、污染物胎盘转运分子机制及不同CHD亚型专属敏感暴露窗口均有待深入探究。后续需构建多污染物共暴露评估模型, 结合分子生物学手段解析致病通路, 为CHD孕前及孕期防控提供理论依据。

       

      Abstract: Harmful periconceptional environmental exposure is a critical environmental risk factor for congenital heart disease (CHD) in offspring. This paper incorporates 97 relevant literatures to systematically review epidemiological and mechanistic research advances regarding the correlation between periconceptional environmental exposure and offspring CHD over the past five years. Current evidence indicates that maternal exposure to chemical contaminants including air pollutants, polycyclic aromatic hydrocarbons, heavy metals, pesticides and environmental endocrine disruptors during the periconceptional period elevates the risk of CHD in offspring; physical environmental stressors such as light pollution and extreme temperatures also impair fetal cardiac development. Various pollutants disrupt normal morphological development of embryonic hearts by inducing oxidative stress, inflammatory responses, mitochondrial damage, endocrine disorders and epigenetic abnormalities. Existing research has several limitations: the interaction of combined multi-pollutant exposure, molecular mechanisms underlying placental transport of pollutants, and exposure-sensitive windows specific to distinct CHD subtypes remain to be further explored. Future studies should establish assessment models for co-exposure to multiple pollutants and elucidate pathogenic pathways via molecular biological techniques, so as to provide theoretical evidence for the preconceptional and antenatal prevention and control of CHD.

       

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