ABSTRACT

Background: Particulate matter ≤ 2.5 µm (PM2.5) is increasingly linked to sinonasal disorders such as allergic rhinitis (AR) and chronic rhinosinusitis (CRS), yet the underlying mechanisms remain poorly defined. We systematically integrated experimental and clinical evidence to propose a unified model of PM2.5 induced nasal epithelial injury.

Methods: PubMed and Embase were searched from inception to March 2025 for in‑vitro, in‑vivo, and human studies examining PM2.5 effects on nasal tissue. Thirty‑two studies met the prespecified criteria. Sample sizes, exposure protocols, and outcomes related to oxidative stress, immune signaling, barrier integrity, and mucociliary function were extracted and qualitatively synthesized.

Results: Across models, PM2.5 consistently generated excessive reactive oxygen species (ROS) that overwhelmed Nrf2‑mediated antioxidant defenses, precipitated mitochondrial dysfunction, and initiated ferroptotic or pyroptotic cell death. ROS activation of NF‑κB/MAPK cascades drove IL‑6, IL‑8, and TNF‑α release. In AR/CRS settings, exposure amplified Th2 polarization, promoted eosinophil recruitment, and disrupted tight‑ and adherens‑junction proteins, compromising epithelial barriers. PM further impaired mucociliary clearance by damaging cilia and inducing IL‑13–dependent mucus hypersecretion. These convergent findings delineate a ROS‑centered cascade linking pollutant exposure to sinonasal pathology.

Conclusions: Current evidence positions ROS‑initiated, Nrf2‑modulated oxidative injury as the central driver of PM2.5sinonasal toxicity. Future studies should pinpoint the most hazardous PM constituents, explore epigenetic alterations, and evaluate antioxidant interventions to protect pollution‑exposed upper airways.