Environmental heat and pollution impact on placenta and perinatal outcomes: Systematic review

Rising global temperatures and worsening air pollution represent converging threats to maternal and fetal health. The placenta, as the critical interface between mother and fetus, is uniquely vulnerable to environmental insults. While previous reviews have examined either heat or pollution separately, no prior synthesis has comprehensively assessed their combined effects on placental function and perinatal outcomes. The objective of this review was to systematically synthesize evidence on the impacts of heat stress and air pollution – individually and in combination – on placental biology and perinatal outcomes. This systematic review, conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines, searched PubMed, Scopus, Web of Science, Embase, Cochrane Library, and Google Scholar through August 2025. Eligible studies included human and animal investigations linking heat stress or ambient air pollutants to placental or perinatal outcomes such as preterm birth, growth restriction, stillbirth, or preeclampsia. Studies without relevant exposures or outcomes, reviews, commentaries, and non-English articles were excluded. Study quality and risk of bias were evaluated using the Newcastle–Ottawa Scale, A MeaSurement Tool to Assess systematic Reviews, version 2, and risk of bias in systematic reviews tools. From 3546 records identified and 3317 screened, 45 studies met the inclusion criteria, of which 20 high-quality studies were prioritized for detailed synthesis. Findings show that heat stress consistently impairs uteroplacental perfusion and induces oxidative stress, increasing risks of preeclampsia, preterm birth, and stillbirth. Air pollution – particularly fine particulate matter ≤2.5 μ m in diameter, ozone, and polycyclic aromatic hydrocarbons – alters placental DNA methylation, disrupts vascular remodeling, and promotes trophoblast apoptosis, contributing to intrauterine growth restriction and small-for-gestational-age births. Critical exposure windows were identified during preconception, early placentation, and late gestation, with the greatest burdens in low- and middle-income regions. This synthesis underscores convergent biological pathways through which environmental stressors compromise placental health and fetal development. Recognizing the placenta as a sentinel organ for climate and pollution exposure highlights the need for integrated maternal–fetal health strategies and policy interventions. No funding was received, and the review was not registered.