Purpose of Review <p>This review aims to elucidate the mechanisms by which air pollutants, such as particulate matter (PM), ozone, cigarette smoke, sulfur dioxide (SO₂) and nitrogen dioxide (NO₂) contribute to the development and progression of chronic rhinosinusitis (CRS) through their impact on nasal epithelial cells. We seek to understand the role of these cells as intermediaries in the pathogenesis of CRS and identify potential links between environmental exposures and disease outcomes.</p> Recent Findings <p>Recent studies have demonstrated a significant association between air pollution and CRS. Air pollutants significantly disrupt the barrier function of nasal epithelial cells, leading to increased permeability and impaired defense against pathogens and irritants. These pollutants also induce oxidative stress and inflammatory responses, impairing mucociliary clearance and exacerbating mucus accumulation. Additionally, they affect tissue repair and regeneration processes, contributing to chronic inflammation and tissue remodeling in CRS. These cellular changes are implicated in the complex pathogenesis of CRS, highlighting the importance of nasal epithelial cells as a key interface between environmental exposures and disease development.</p> Summary <p>Air pollutants play a significant role in CRS by compromising nasal epithelial cell homeostasis. Understanding these mechanisms highlights the need for targeted therapeutic strategies and reinforces the importance of environmental measures to reduce CRS burden.</p>