A COPD flare may not be confined to the lungs. Italian pulmonary and ear, nose and throat specialists are proposing that some exacerbations reflect instability across a continuous airway extending from the nose and sinuses to the chest.
The argument appears in a clinical overview published July 6 in Expert Review of Respiratory
Medicine by Simone Lelo of San Donato Hospital in Arezzo and colleagues at Italian hospitals and medical schools. It does not prove that exacerbations begin in the nose. Instead, the team organizes existing evidence into a “pan-airway” model that researchers can now test.
COPD exacerbations are conventionally recognized by an acute increase in breathlessness, cough or sputum. The 2026 Global Initiative for Chronic Obstructive Lung Disease report describes these events as worsening over several days—typically no more than 14—while noting that other conditions can mimic or aggravate them. Lelo’s group asks whether assessment should also extend above the vocal cords, particularly in people who have repeated attacks.
The review focuses on three possible connections: inflammation throughout the airway; epithelial “alarm” signals and cytokines; and a respiratory microbiome that does not observe the boundaries between medical specialties. Chronic rhinitis and chronic rhinosinusitis often coexist with COPD and may add symptoms, impair quality of life and help identify frequent exacerbators. Barrier dysfunction, impaired antiviral defenses and altered microbial communities offer plausible biological links between upper- and lower-airway disease.
That framework may explain why a respiratory infection can produce symptoms across several compartments without establishing a simple nose-to-lung chain. Viral illness, pollution and other triggers can disturb airway defenses through different routes, and clinically similar exacerbations may have different underlying biology.
The evidence is still largely associative. An earlier clinical study of nasal symptoms and inflammation in people with COPD documented that upper-airway problems can accompany the disease, but coexistence does not show that one compartment drives an attack in the other. The new review calls for longitudinal and multi-omic studies that sample the airway before, during and after exacerbations.
For clinicians, the immediate change is more likely to be in the history than the prescription. Asking about persistent congestion, rhinitis and sinus disease may produce a fuller picture of patients with repeated exacerbations. It does not replace established COPD action plans, and sudden worsening of breathlessness or sputum still requires prompt clinical assessment.
The decisive experiment comes next: determine whether upper-airway symptoms or biomarkers predict a flare—and whether treating documented sinonasal disease changes its frequency or severity. Until those trials are completed, the whole-airway model is a research agenda with clinical
logic, not a new standard of care.
