Abstract Introduction Recent advances in environmental health research have underscored the potential impact of fine particulate matter 2.5 (PM2.5) on sleep-disordered breathing. Emerging evidence suggests that PM2.5 may contribute to the pathogenesis of obstructive sleep apnea (OSA) through inflammatory, oxidative, and autonomic mechanisms affecting upper airway stability. Although the cardiopulmonary consequences of PM2.5 exposure are well documented, findings regarding its relationship with OSA remain methodologically inconsistent and inconclusive. Given the biologically plausible pathways connecting PM2.5 exposure to sleep-related respiratory impairment and the significant public health burden of both air pollution and OSA, a rigorous synthesis of the current evidence is warranted. A meta-analytic evaluation can better delineate the magnitude and consistency of this association. Methods This study involved a systematic literature search across PubMed, Scopus, and Web of Science for studies published up to December 2025. Study selection proceeded in two stages, with titles and abstracts screened first, followed by full-text assessment. Studies were considered eligible if they included quantitative assessments of ambient PM2.5 exposure and evaluated OSA using polysomnography or validated diagnostic criteria. Data on exposure metrics and OSA-related outcomes were extracted according to a standardized protocol. Heterogeneity and methodological quality were assessed using established criteria, and the review adhered to PRISMA guidelines. Results The meta-analysis revealed heterogeneity in the reported associations between PM2.5 exposure and both the risk and severity of OSA. Several studies observed that higher ambient PM2.5 concentrations corresponded with elevated apnea–hypopnea index values, supporting a potential dose-related relationship between particulate pollution and increased OSA severity. Conclusion Our findings indicate that exposure to ambient and indoor PM2.5 might be associated with an increased risk and greater severity of obstructive sleep apnea. These results underscore the importance of considering microenvironmental air quality as a potential modifier of sleep-disordered breathing and highlight the need for studies that integrate refined exposure metrics and mechanistic evaluations. Future research may help clarify causal pathways linking particulate pollution to upper airway dysfunction and may inform public health strategies aimed at mitigating pollution-related sleep and cardiometabolic consequences. Support (if any)
Maide Gözde İnam (Fri,) studied this question.