Heat stress and air pollution in female reproductive health: from pathological alterations to molecular mechanisms

Background Female reproductive health is increasingly threatened by environmental degradation, particularly climate change and air pollution. This narrative review synthesizes epidemiological, pathophysiological, and mechanistic evidence on how these exposures affect female reproductive health.Discussion Epidemiological studies associate these exposures with diminished ovarian reserve, reduced implantation and live birth rates, increased pregnancy loss, and elevated risks of preterm birth and hypertensive disorders. Pathological evidence supports impaired follicular development, defective placental vascular remodeling, and reduced endometrial receptivity. Mechanistic studies implicate oxidative stress and inflammatory activation as initiating events, with epigenetic reprogramming and dysregulated apoptosis and autophagy as downstream mediators of persistent damage. However, current evidence is limited by heterogeneous exposure assessment methods, discrepancies between animal models and human pathology, insufficient characterization of susceptible windows, and predominant focus on female factors while neglecting male contributions. Despite these limitations, the convergence of epidemiological, pathological, and molecular evidence across diverse populations and experimental systems strengthens the biological plausibility of causal links.Conclusion(s) High temperature and air pollution adversely affect female reproductive health through interconnected epidemiological, pathological, and molecular pathways. Epidemiological evidence consistently links these exposures to clinical reproductive impairments, supported by pathological findings of disrupted follicular development, placental vascular remodeling, and endometrial receptivity. Mechanistic studies implicate oxidative stress, epigenetic dysregulation, and disrupted apoptosis and autophagy as potential mediators of these effects. Future research should prioritize standardized exposure assessment, long-term prospective cohorts to identify vulnerable populations and critical windows, and translational validation of preclinical findings to inform public health policies and clinical strategies.