Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 169, Issue -, Pages 248-254Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2018.10.109
Keywords
PM2.5 (particulate matter <= 2.5 mu m in aerodynamic diameter); Prenatal exposure; Adverse birth outcome; Oxidative stress; Mitochondrial DNA; Endocrine disruption
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Funding
- National Nature Science Foundation of China [81273111, 81703189]
- Scientific Projects of Zhejiang Province [2015C33148, 2015C37117]
- Ningbo Scientific Innovation Team for Environmental Hazardous Factor Control and Prevention [2016C51001]
- Zhejiang Key Laboratory of Pathophysiology [201703]
- KC Wong Magna Fund of Ningbo University
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PM2.5 (particulate matter <= 2.5 mu m in aerodynamic diameter) refers to atmospheric particulate matter (PM) with an aerodynamic diameter of equal and less than 2.5 mu m that tends to be suspended for long periods of time and travel over long distances in both outdoor and indoor atmospheres. PM2.5, along with the toxic compounds attached on it, may cause a wide range of disorders. The fetus is considered to be highly susceptible to a variety of toxicants including atmospheric pollutants such as PM2.5 through prenatal exposure. To better understand the relationship between maternal exposure to PM2.5 and adverse birth outcomes for reproduction and fetus development, we studied the published data on this issue including case-control studies, cohort studies and meta analyses studies, and summarized the basic impact of ambient particulate matter on adverse birth outcomes. Research evidence indicates that PM2.5 has a potential to induce low birth weight (LBW), preterm birth (PTB), and stillbirth. A further in-depth analysis shows that oxidative stress, DNA methylation, mitochondrial DNA (mtDNA) content alteration, and endocrine disruptions may all play an important role in PM2.5 induced adverse effects to pregnant women and fetuses. In addition, PM2.5 exposure can cause male reproductive toxicity, leading to associated adverse pregnancy outcomes.
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