Abstract
COPD is "a heterogeneous lung condition characterized by chronic respiratory symptoms due to abnormalities of the airways and/or alveoli that cause persistent, often progressive, airflow obstruction". COPD has been traditionally associated with tobacco smoking and accelerated lung function decline. However, our understanding of the pathogenesis of COPD has changed significantly over the past few years due to the recognition that different lung function trajectories starting in early life and progressing across the lifespan are also important pathways to COPD. Further, today, it is well accepted that there are multiple genetic, host and environmental factors (i.e., aetiotypes) that can cause COPD and contribute to its clinical heterogeneity. Here, we review current understanding of the environmental, genomic and immune factors associated with the early-life origins of COPD. We also discuss the current knowledge gaps and how this new knowledge can facilitate earlier detection and disease interception of COPD across the lifespan, thus reducing its disease burden and improving the well-being and prognosis of COPD patients.