Asthma Pathophysiology and Clinical Implications

Core Pathophysiologic Mechanisms

The European Respiratory Society suggests that asthma is fundamentally a chronic inflammatory disease of the airways characterized by bronchoconstriction, airway edema, and increased mucus production, with distinct inflammatory patterns that differ significantly between children and adults 1, 2
The primary pathologic feature of asthma is chronic airway inflammation that leads to bronchial hyperresponsiveness, variable airflow obstruction, and respiratory symptoms including wheezing, shortness of breath, chest tightness, and cough 1, 2
The inflammatory process involves airway edema, mucus hypersecretion, and infiltration of inflammatory cells into the bronchial walls, creating the characteristic obstructive pattern 1, 2

Children predominantly exhibit T2-high asthma characterized by eosinophilic airway inflammation driven by IgE-mediated allergic responses and cytokines including IL-4, IL-5, and IL-13 1, 2, 3
Adults more commonly exhibit T2-low asthma featuring either neutrophilic or paucigranulocytic airway inflammation sustained by IL-8, IL-17, IL-22, and other T-cell-related cytokines 1, 2, 3
Adult-onset asthma is generally less quiescent than childhood-onset disease, with more frequent relapses, fewer remissions, poorer treatment response, and worse overall prognosis 1, 2

Viral respiratory infections are the predominant trigger for asthma symptoms and exacerbations in children, especially those under 5 years of age 4
Genetic and perinatal risk factors include positive family history of asthma and atopy, genetic polymorphisms, and epigenetic markers 1, 2, 3
Early-life respiratory tract infections, allergic comorbidities (eczema, allergic rhinitis, food allergies), and lung function deficits are important determinants of persistent asthma from childhood into adulthood 1, 2, 3
Active smoking in adolescence significantly increases risk of persistent asthma symptoms 1, 2
Female gender, allergic sensitization and comorbidity, smoking, low socioeconomic status, and poor medication adherence (especially in the first years after diagnosis) are the most common risk factors for adult-onset asthma 1, 2

The shift from phenotype to endotype classification has enabled better understanding of clinical differences and identification of targeted biological therapies for severe asthma 1, 2, 3

Workplace exposures are responsible for approximately 15 %–25 % of new‑onset asthma cases that develop after age 40, highlighting the significant contribution of occupational factors to adult‑onset disease. 5, 6

Sensitization to high‑molecular‑weight (≥ 5 kDa) or low‑molecular‑weight (< 5 kDa) agents in the workplace can trigger new‑onset occupational asthma after months to years of exposure, underscoring the need for exposure assessment and possible removal from the offending environment. 5, 6

Cigarette smoking interacts with airway responsiveness and increases the likelihood of developing new‑onset asthma in adulthood, indicating that smoking cessation is a critical preventive strategy for at‑risk adults. 5, 6