In this review, we summarise the current epidemiological and experimental evidence on the association of ambient (outdoor) air pollution exposure and maternal cardiovascular health during pregnancy. This topic is of utmost clinical and public health importance as pregnant women represent a potentially susceptible group due to the delicate balance of the feto-placental circulation, rapid fetal development and tremendous physiological adaptations to the maternal cardiorespiratory system during pregnancy.
Several meta-analyses including up to 4 245 170 participants provide robust evidence that air pollutants, including particulate matter, nitrogen oxides and others, have adverse effects on the development of hypertensive disorders of pregnancy, gestational diabetes mellitus and cardiovascular events during labour. Potential underlying biological mechanisms include oxidative stress with subsequent endothelial dysfunction and vascular inflammation, β-cell dysfunction and epigenetic changes. Endothelial dysfunction can lead to hypertension by impairing vasodilatation and promoting vasoconstriction. Air pollution and the consequent oxidative stress can additionally accelerate β-cell dysfunction, which in turn triggers insulin resistance leading to gestational diabetes mellitus. Epigenetic changes in placental and mitochondrial DNA following air pollution exposures can lead to altered gene expression and contribute to placental dysfunction and induction of hypertensive disorders of pregnancy.
The maternal and fetal consequences of such cardiovascular and cardiometabolic disease during pregnancy can be serious and long lasting, including preterm birth, increased risk of type 2 diabetes mellitus or cardiovascular disease later in life. Acceleration of efforts to reduce air pollution is therefore urgently needed to realise the full health benefits for pregnant mothers and their children.
- diabetes mellitus
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Contributors FD drafted the manuscript. RT, DEN, MRM and RR reviewed and gave intellectual input.
Funding FD is supported by the Swiss National Science Foundation (P500PM_206634), the Bangeter-Rhyner Foundation. MRM and DEN are supported by the British Heart Foundation (FS/CRTF/20/24087, CH/09/002, RG/05/003, RG/10/9/28286, PG/03/017/15071, RG/16/10/32375, RE/18/5/34216, RG/F/22/110093). DEN is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA). RR acknowledges the support of the British Heart Foundation (RE/18/5/34216).
Competing interests DEN is on the Editorial Board for Heart.
Provenance and peer review Commissioned; externally peer reviewed.
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