Small airway dysfunction: a shared, early, measurable, and potentially treatable trait across COPD, asthma, and fibrotic lung disease

Small airway dysfunction (SAD) has emerged as a key but historically under-recognized component of chronic respiratory diseases, offering a potential explanation for the frequent mismatch between symptom burden and spirometric findings. Increasing evidence suggests that the distal airway compartment represents an early and clinically meaningful site of physiological disturbance across chronic obstructive pulmonary disease (COPD), asthma, and fibrotic interstitial lung disease (ILD). Characterized by elevated peripheral resistance, ventilation heterogeneity, and a tendency toward airway closure, SAD links distal pathology to gas trapping, dynamic hyperinflation, and activity-limiting dyspnea. In asthma, strong physiological and longitudinal data support SAD as a prevalent and clinically relevant phenotype associated with poor control and exacerbation risk, with partial reversibility through targeted therapy. In COPD, structural injury and loss of terminal bronchioles appear early and contribute to symptoms primarily through modifiable mechanical consequences such as hyperinflation. In fibrotic ILD, emerging structural and physiological studies indicate early distal involvement and distinct mechanical signatures, although evidence for therapeutic modification remains limited. Considered across diseases, SAD satisfies several key features of a treatable trait in that it is measurable, clinically meaningful, and closely connected to mechanisms that shape symptoms and functional limitation, even if its reversibility differs between conditions. Framing SAD within a "treatable trait" perspective may therefore provide a unifying approach to linking symptoms, physiology, and underlying pathology, and support more individualized strategies for assessment and management.