Aim: To summarise evidence linking wildfire and air-pollutant exposure with ENT morbidity. Methods: Targeted overview of peer-reviewed studies (2010–early 2025) on wildfire smoke or high-pollution episodes reporting ENT outcomes, plus key mechanistic and guideline papers on mucociliary function, epithelial injury and exposure reduction. Results: Across multiple jurisdictions, including Australia's 2019-20 fires, spikes in fine particulates (<2.5 µm diameter, PM₂.₅) correspond with surges in upper-airway presentations. Paediatric populations show clear signals that higher PM₂.₅ exposures are linked to otitis media and irritant upper-airway symptoms. For chronic rhinosinusitis (CRS), epidemiological links are emerging but heterogeneous; however, mechanistic data demonstrate impaired ciliary function, epithelial barrier disruption, and inflammatory pathway activation after particulate exposure, providing strong biological plausibility for CRS flares. Practical mitigation includes properly fitted respirators (e.g., P2/N95) when outdoors during smoke events, high-efficiency indoor air filtration, and service-level clinic surge planning (triage, telehealth, priority access for high-risk patients). Conclusion: Wildfire and urban air pollution plausibly increase ENT burden, most clearly in paediatric ear disease and sinonasal symptom flares. Public health services can act now by embedding smoke-season pathways (patient education on masks/filtration, clinic surge plans) whilst recognising that individual-level measures cannot substitute for upstream climate and air-quality mitigation in the face of an ever-emerging global health issue.