Chronic obstructive pulmonary disease (COPD) is a highly prevalent and heterogeneous chronic disease of the lower airways and lungs that is associated with huge morbidity, disability, and mortality worldwide and disproportionately affects poor and vulnerable people.¹ Pathologically, COPD is characterised by variable degrees of chronic inflammation and remodelling of small airways (bronchiolitis) and destruction of alveolar walls (emphysema). ² Diagnosis of COPD relies on respiratory symptoms and the presence of spirometric airflow limitation.³ COPD has long been considered a self-inflicted disease that occurs in adult cigarette smokers as a result of accelerated decline in lung function.⁴ However, epidemiological evidence has shown that many other factors, including indoor and outdoor air pollution, occupational exposures, and use of e-cigarettes and cannabis, also cause COPD. Furthermore, in addition to accelerated lung function decline in adulthood, several other lung function trajectories—characterised by impaired lung development in utero or impaired lung growth in early life—have been linked to COPD.⁵ Indeed, COPD can be elicited by early-life events such as prematurity, childhood asthma, and childhood respiratory infections. Importantly, tuberculosis and HIV—common chronic infections, especially in low-income and middle-income countries—can lead to airway obstruction and COPD. Finally, although COPD is a complex disease caused by multiple gene–environment interactions throughout the life course, it is mainly genetically determined in specific subgroups of patients with early-onset COPD or a positive family history (eg, people with α₁ antitrypsin deficiency).

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