2022
DOI: 10.1016/j.lfs.2022.121054
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Predisposed obesity and long-term metabolic diseases from maternal exposure to fine particulate matter (PM2.5) — A review of its effect and potential mechanisms

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Cited by 17 publications
(9 citation statements)
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“…31,44 As for O3 and NO2, we observed contrast results as a positive effect of O3 and NO2 but a negative effect of PM2.5. In addition, compared with the other two exposure windows, the impacts of particulate matter (PM) (PM2.5 and PM10) were more evident in Period 3, suggesting that long-term exposure to PM2.5 and PM10 is likely to cause biological changes such as systemic oxidative stress, endocrine dysfunction and epigenetic changes, 45 which may further lead to adverse maternal effects such as decreased placental function. 46 Interestingly, the correlation between O3 concentration and biochemical/clinical pregnancy is opposite to the results for other pollutants.…”
Section: Discussionmentioning
confidence: 99%
“…31,44 As for O3 and NO2, we observed contrast results as a positive effect of O3 and NO2 but a negative effect of PM2.5. In addition, compared with the other two exposure windows, the impacts of particulate matter (PM) (PM2.5 and PM10) were more evident in Period 3, suggesting that long-term exposure to PM2.5 and PM10 is likely to cause biological changes such as systemic oxidative stress, endocrine dysfunction and epigenetic changes, 45 which may further lead to adverse maternal effects such as decreased placental function. 46 Interestingly, the correlation between O3 concentration and biochemical/clinical pregnancy is opposite to the results for other pollutants.…”
Section: Discussionmentioning
confidence: 99%
“…However, emerging evidence suggests a link between prenatal exposure to PM 2.5 and fetal overdevelopment. Although the relevant biological mechanisms have not been fully understood, disorders of glucose and lipid metabolism have been suggested to play a role. Both epidemiological and toxicological evidence consistently shows that PM 2.5 may cause maternal metabolic dysfunction and disrupt normal lipid and glucose metabolic homeostasis, which significantly contribute to fetal overdevelopment. , Additionally, these findings have been confirmed by accumulating epidemiological studies. For instance, Shang et al and Li et al . found that prenatal exposure to PM 2.5 was significantly associated with an increased macrosomia risk in Xi’an and Yancheng, China, respectively.…”
Section: Introductionmentioning
confidence: 90%
“…Maternal exposure to ≤PM 2.5 predisposes adult male mice offspring to NAFLD and other long-term metabolic dysfunctions such as obesity, T2D, insulin resistance, hypertension, hyperlipidemia, and metabolic syndrome, likely affecting organogenesis and tissue functions [ 282 , 283 , 284 , 285 ]. In mice, prenatal exposure to diesel exhaust PM 2.5 (DEP) leads to increased lipogenesis and worsens fatty acid oxidation, favoring hepatic lipid deposition in the adult male offspring [ 286 ].…”
Section: Maternal Exposure To Pollutants and Developmental Origins Of...mentioning
confidence: 99%