Fixed airflow obstruction (FAO) occurs in asthma despite adequate treatment and no or minimal smoking history. FAO in asthma is more common in older people or those with long-standing disease and associated with poor outcomes. Airflow obstruction occurs in the small airways and is thought to be due to airway remodelling and driven by inflammation. Changes to the lung tissue, which may result in alteration of the lungs elastic properties such as loss of lung elastic recoil, may also contribute. The underlying mechanisms leading to FAO in asthma are poorly understood.
To explore the physiological properties of both the airways and lung tissue and airway inflammation in older non-smokers with asthma, and to assess how they may contribute to FAO.
Non-smoking adults >40 years old with asthma were treated with two months of high dose inhaled corticosteroid/long-acting beta-agonist (ICS/LABA). Subsequently standard lung function and small airway function was measured using the forced oscillation technique (FOT) and the multiple breath nitrogen washout test (MBNW). Lung elastic recoil was measured using the oesophageal balloon technique. Airway inflammation was measured using bronchoalveolar lavage fluid obtained during bronchoscopy.
Non-smoking adults with asthma (n=19) demonstrated moderate FAO; small airway dysfunction, as measured by FOT and MBNW; increased lung compliance and loss of elastic recoil and variable airway inflammation. Worse airflow obstruction was associated with increased lung compliance. Increased airway resistance and small airway dysfunction in the acinar airways was associated with a loss of lung elastic recoil. Cross-sectional assessment of airway inflammation was not associated with lung function impairment.
Changes to the lungs elastic properties results in increased compliance or reduced lung elastic recoil and make a significant contribution to FAO and small airway dysfunction in older non-smokers with asthma. ‘Lung remodelling’ is a potential pathological process leading to lung tissue changes and may be an alternate asthma paradigm. Underlying cellular mechanisms need further investigation.