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Purpose of Review <p>Particulate matter (PM) exposure is increasingly associated with sinonasal disorders including allergic rhinitis (AR) and chronic rhinosinusitis (CRS), yet the mechanistic pathways linking PM to epithelial dysfunction remain incompletely defined. This review synthesizes experimental preclinical evidence to clarify the biologic mechanisms of PM-induced nasal epithelial injury and to propose an integrated model of PM-driven sinonasal pathology.</p> Recent Findings <p>We searched PubMed and Embase from inception to March 2025 for in vitro and in vivo studies examining PM effects on nasal tissue; 38 studies met prespecified inclusion criteria and were qualitatively synthesized. Across models, PM exposure consistently increased reactive oxygen species (ROS) and overwhelmed Nrf2-mediated antioxidant defenses, leading to mitochondrial dysfunction and autophagy associated cell death. Downstream ROS activation of NF-KB/MAPK signaling promoted proinflammatory cytokine release (including IL-6, IL-8, and TNF-a). In AR/CRS-relevant settings, PM amplified Th2-skewed inflammation, promoted eosinophilic recruitment, and disrupted epithelial tight junction proteins, impairing barrier integrity. PM also reduced mucociliary clearance through ciliary damage and IL-13-associated mucus hypersecretion.</p> Summary <p>Collectively, current experimental evidence supports an ROS-initiated, Nrf2-modulated cascade as a central mechanism of PM-related sinonasal toxicity, linking pollutant exposure to inflammation, barrier breakdown, and impaired mucociliary function relevant to AR and CRS. Key priorities for future work include identifying the most harmful PM constituents, clarifying persistent regulatory effects (including epigenetic mechanisms), and testing targeted antioxidant or cytoprotective interventions to mitigate pollution-associated upper airway disease.</p> <p><b>Level of Evidence</b>: Level 1 (Systematic Review).</p>

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Systematic Review of Particulate Matter-Induced Upper Respiratory Disease with Mechanistic Signaling Pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月17日

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  • Manwel Labib,
  • Christina Im,
  • Joah Lee,
  • Eri S. Srivatsan,
  • Saroj K. Basak,
  • Bhavani S. Gowda,
  • Jivianne T. Lee

摘要

Purpose of Review

Particulate matter (PM) exposure is increasingly associated with sinonasal disorders including allergic rhinitis (AR) and chronic rhinosinusitis (CRS), yet the mechanistic pathways linking PM to epithelial dysfunction remain incompletely defined. This review synthesizes experimental preclinical evidence to clarify the biologic mechanisms of PM-induced nasal epithelial injury and to propose an integrated model of PM-driven sinonasal pathology.

Recent Findings

We searched PubMed and Embase from inception to March 2025 for in vitro and in vivo studies examining PM effects on nasal tissue; 38 studies met prespecified inclusion criteria and were qualitatively synthesized. Across models, PM exposure consistently increased reactive oxygen species (ROS) and overwhelmed Nrf2-mediated antioxidant defenses, leading to mitochondrial dysfunction and autophagy associated cell death. Downstream ROS activation of NF-KB/MAPK signaling promoted proinflammatory cytokine release (including IL-6, IL-8, and TNF-a). In AR/CRS-relevant settings, PM amplified Th2-skewed inflammation, promoted eosinophilic recruitment, and disrupted epithelial tight junction proteins, impairing barrier integrity. PM also reduced mucociliary clearance through ciliary damage and IL-13-associated mucus hypersecretion.

Summary

Collectively, current experimental evidence supports an ROS-initiated, Nrf2-modulated cascade as a central mechanism of PM-related sinonasal toxicity, linking pollutant exposure to inflammation, barrier breakdown, and impaired mucociliary function relevant to AR and CRS. Key priorities for future work include identifying the most harmful PM constituents, clarifying persistent regulatory effects (including epigenetic mechanisms), and testing targeted antioxidant or cytoprotective interventions to mitigate pollution-associated upper airway disease.

Level of Evidence: Level 1 (Systematic Review).