Background: Urban environments expose pregnant women to a complex interplay of environmental and social stressors that disrupt placental immunology, contributing to adverse pregnancy outcomes such as preterm birth (PTB), preeclampsia, and intrauterine growth restriction (IUGR). Key stressors include air pollution, noise, heavy metals, socioeconomic disparities, infections, and maternal microbiome alterations.
Methods: This narrative review synthesizes findings from 39 peer-reviewed studies published between 2015 and 2025, focusing on urban populations and examining placental immune function and pregnancy outcomes. Studies were categorized into environmental exposures, social determinants, infections, and clinical outcomes.
Results: Air pollutants, notably PM2.5 and polycyclic aromatic hydrocarbons (PAHs), induce placental inflammation and oxidative stress, impairing trophoblast function and increasing PTB and IUGR risk. Heavy metals and urban noise disrupt maternal-fetal immune balance via elevated cortisol and altered cytokine profiles. Socioeconomic stressors, including poverty and systemic inequities, amplify pro-inflammatory placental responses and elevate preeclampsia risk. Infections like SARS-CoV-2 and cytomegalovirus (CMV) intensify placental immune activation, worsening adverse pregnancy outcomes. The maternal microbiome in urban environments shapes neonatal immune development. Mechanistically, these stressors converge on inflammatory pathways, impaired vascularization, and epigenetic modifications, with long-term implications for offspring health.
Conclusion: Urban stressors synergistically impair placental immunology, driving adverse pregnancy outcomes. Integrated interventions—improved air quality, equitable prenatal care, stress reduction, and microbiome-targeted strategies—are critical. Future research should focus on longitudinal, multi-exposure, and omics-based studies to develop targeted interventions for urban populations. |
