Aim: To summarise evidence of inhaled micro-/nanoplastics (MNPs) in the human nasal cavity and evaluate potential links to sinonasal inflammation and olfactory dysfunction. Methods: Targeted summary overview of peer reviewed studies on MNP detection and mechanistic airway models. Results: MNPs are consistently detected in human nasal specimens, with higher concentrations reported in chronic rhinosinusitis and allergic rhinitis cohorts than in healthy controls; occupationally exposed workers likely experience greater inhalational burdens. Across nasal detection studies, commonly identified polymers include polyethylene, polypropylene, polyester and polyamide. In vitro and animal airway models show that MNP exposure can trigger processes overlapping with recognised CRS mechanisms, including: (i) generation of reactive oxygen species and oxidative injury to airway epithelium; (ii) disruption of tight junction proteins such as ZO-1 and occludin with increased epithelial permeability; (iii) altered mucus rheology and potential impairment of mucociliary clearance; (iv) upregulation of pro-inflammatory cytokines (e.g. IL-6, IL-8, TNF-α) with Th2-skewed responses in allergic models; and (v) activation of epithelial-to-mesenchymal transition pathways associated with tissue remodelling. Conclusions: MNPs represent a novel category of sinonasal irritant with demonstrated inflammatory mechanisms paralleling CRS pathophysiology. Microplastic pollution may pose an emerging environmental health crisis with potentially significant implications for otolaryngology. Global plastic production exceeds 400 million tonnes annually, fragmenting into micro- and nanoscale particles that pervade indoor and outdoor air. As atmospheric MNP concentrations continue rising and detection methods improve, the sinonasal mucosa, our primary interface with inhaled air, warrants close surveillance as a sentinel site for exposure-related disease.