Maternal mechanisms in air pollution exposure-related adverse pregnancy outcomes: A systematic review

Air pollution exposure is linked to various adverse health effects including cardiopulmonary, neurological and reproductive outcomes. Susceptible populations such as pregnant women and infants can be affected to a greater extent compared to healthy individuals. Thus, understanding air pollutant exposure-related toxicity pathways in pregnancy can provide information on developmental origin of health and diseases in both mothers and infants. The objective of this literature review was to explore maternal mechanisms underlying the association between air pollutant exposures and adverse maternal/infant health effects. A total of 209 articles published from 1996 until November 2024 were retrieved using PubMed, Scopus and Web of Science using relevant search terms (e.g. "Air Pollution" AND "Maternal" AND "Infant" AND "Health" AND "Biomarker"). After screening and removal of articles based on exclusion criteria, 36 observational studies were included for the final analysis. There were relatively fewer articles on air pollution exposure-related adverse maternal health effects compared to air-pollution-related adverse infant health effects. Of these articles selected for the final review, 32 studies compared the effects of particulate matter (PM), PM2.5, few on other (gaseous) pollutants and one study on effects of mixtures of air pollutants. Adverse maternal health effects included hypertensive disorders, gestational diabetes mellitus (GDM) and clinically recognized early pregnancy loss, while adverse infant health effects ranged from low birth weight, preterm birth, changes in fetal heart rate, crown rump length and fetal hyperinsulinism. Moreover, oxidative stress, inflammatory responses, endothelial and metabolic dysfunction were some of the mechanisms implicated in air pollution exposure-related adverse birth outcomes. These findings warrant further validation work and identification of maternal mechanism(s) constituting the causal pathway.