Abstract
Air pollution has attracted widespread attention as one of the major environmental health problems worldwide. In recent years, recognized as one of the major environmental risk factors for the increased global burden of disease, fine particulate matter (PM2.5) increased risk of adverse pregnancy outcomes such as stillbirth. Stillbirths impose a substantial burden on both families and society. Although the existing evidence has revealed the association between PM2.5 exposure and stillbirth, the underlying mechanism behind this is a lack of clarity. In this review, epidemiological evidence regarding the effects of PM2.5 on stillbirth, as well as the sensitive windows of exposure, has been summarized. For the potential mechanism, the generation of reactive oxygen species was recognized as the molecular initiating event (MIE), and trigged oxidative stress, mitochondrial dysfunction, regulated cell death (RCD), inflammation and hyper coagulation, which can lead to pathological changes in the placenta and further lead to stillbirth. The purpose is to provide scientific evidence for developing early prevention strategies, reducing the stillbirth rate, and alleviating the social burdens of stillbirth.
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Research ethics: Not applicable.
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Informed consent: Not applicable.
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Author contributions: Zhan Li drafted the manuscript. Ruixia Liu and Enjie Zhang reviewed and edited. All authors contributed to the design and assisted in the preparation of the final version of the manuscript. All authors read and approved the final version of the manuscript.
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Use of Large Language Models, AI and Machine Learning Tools: None declared.
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Conflict of interest: The author states no conflict of interest.
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Research funding: None declared.
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Data availability: Not applicable.
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