Asthma and Chronic Obstructive Pulmonary Disease: Just Old Friends or Relatives?

To the Editor:

There is broad consensus that asthma and tobacco smoke–related chronic obstructive pulmonary disease (COPD) are clinically, immunologically, and histopathologically distinct. However, recent evidence identified different trajectories that lead to chronic airflow limitation at different times of one’s life, starting from childhood (1). It is now well established that prenatal, perinatal, and early childhood factors affect lung development and function (2). The more we learn about these common etiologies, the more studies aimed at digging into the first years of life are needed to shed light on the roots of the structural and functional changes associated with airflow limitation.

We have read with great interest the study from Izadi and colleagues. By further analyzing the Childhood Asthma Management Program, an initial drug trial turned to a well-defined, long-term, ongoing cohort study. Izadi and colleagues unravel some knowledge gaps in the nature of childhood factors associated with persistent severe asthma in adult life (3). These authors reported that only two determinants among more than 22 explored, namely, reduced lung growth in childhood and maternal smoking during pregnancy, were predictors of persistent severe asthma later in life. Interestingly, this association was not maintained if the subjects had normal lung growth in childhood even in the presence of early lung function decline, suggesting that lung function in the first years of life is a major determinant of chronic airflow limitation regardless of how the lung function is going to develop and/or decline. These findings shed light on the gray transition area in which patients with asthma become progressively irreversible until they meet the spirometric criteria for COPD. Large cohort studies had previously found irreversible airflow obstruction to be associated with low lung function at birth, especially when modifiable early-life exposure such as first- or second-hand smoke, including maternal exposures, are present (4). Also, irreversible airflow obstruction compatible with COPD is common in those with severe asthma (5). Thus, this study serves as a bridge between early origins of asthma and COPD.

From a pathobiological standpoint, inflammatory processes contribute to small airway obstruction in both asthma and COPD. The nature of these processes and the extent to which they overlap in both conditions or evolve into each other are not well understood (6). We have missed for years the opportunity to explore, especially by longitudinal imaging, the lungs from younger subjects before they develop any spirometric criteria for COPD and/or after they surpassed the critical age to be studied as patients with asthma.

Altogether, these studies aimed at profiling the causes and the evolution of airflow obstruction are slowly shifting the focus toward younger individuals who have been so far overlooked, as COPD was wrongly considered a disease of the elderly. These long-term (life-long?) cohorts are crucial to further understand the determinants of lung function from birth; how small airway obstruction shapes into asthma, COPD, or both; and the potential long-term implications of these factors for the development of COPD later in life.

Here and now, there is a brand new window of opportunity to tackle the multifaceted aspects of airflow limitation. Let’s keep this window wide open to promote lung health starting from birth.