妊娠期空气污染物暴露与子代先天性心脏病的关联研究进展

Advances on associations of exposure to air pollutants during pregnancy with congenital heart disease in offspring

  • 摘要: 先天性心脏病(CHD)是最普遍的出生缺陷,全球平均患病率约为9.4‰,也是导致新生儿死亡的主要原因之一。本文回顾了现有的流行病学研究,发现妊娠期空气污染物暴露增加子代CHD发病风险,由于CHD不同亚型的发育和病因学存在异质性,空气污染物与CHD亚型的关联存在不一致性。妊娠期空气污染物暴露增加室间隔缺损、动脉导管未闭、肺动脉瓣狭窄、法洛四联症和大动脉转位的风险;然而,空气污染物与房间隔缺损(ASD)的关联性存在矛盾:母体可吸入颗粒物、二氧化氮暴露与ASD存在正向关联,细颗粒物、一氧化碳暴露则会对ASD起保护效应,而二氧化硫暴露与ASD的关联结果不一致。在暴露窗口期方面,空气污染物暴露影响心脏发育不仅限于第3—8周,妊娠早期颗粒物、氮氧化物暴露对胎儿心脏发育产生不利影响,妊娠早期一氧化碳暴露与心脏发育的关联强度则出现低谷,而二氧化硫和臭氧在整个妊娠期都会影响心脏发育。综上,基于妊娠期空气污染物暴露与CHD的关联研究进展,本文分析了现有研究存在的局限性,提出未来应该关注前瞻性队列研究和纵向研究、构建精确的暴露评估内容和方法、增加CHD亚型的独立研究,从而为减少环境暴露、预防CHD发病提供科学依据。

     

    Abstract: Congenital heart disease (CHD) is the most common birth defect and one of the major causes of neonatal death, with an average prevalence of 9.4‰ worldwide. We reviewed recent epidemiological studies and found that exposure to air pollutants is associated with increased CHD risks, but the associations are inconsistent between exposure to air pollutants and different subtypes of CHD due to developmental and etiological heterogeneity among different subtypes of CHD. It has been reported that air pollutants are associated with increased risks of ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, tetralogy of Fallot, and transposition of the great arteries. However, associations between maternal exposure to air pollutants and atrial septal defect (ASD) are contradictory, with significantly positive associations of inhalable particulate matter and nitrogen dioxide exposure, negative associations of fine particulate matter and carbon monoxide, and mixed associations of sulfur dioxide. Adverse effects of air pollutant on cardiac development cover a wide time window beyond 3-8 weeks during gestation; particulate matter and nitrogen oxide are more likely to affect fetal heart in early pregnancy, while the association strength of carbon monoxide shows a trough in early pregnancy, and sulfur dioxide and ozone affect cardiac health throughout pregnancy. In addition, we discussed the limitations of previous studies on the associations between maternal air pollutant exposure and CHD, and highlighted the application of precise assessment on exposure to air pollutants, the performance of prospective cohort studies and longitudinal studies, and the necessity of studies on CHD subtypes, in order to provide scientific evidence to control exposure to environmental pollutants and CHD occurrence.

     

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