Asthma/Obstructive Pulmonary Disease Overlap

Update on Definition, Biomarkers, and Therapeutics

August Generoso; John Oppenheimer

Disclosures

Curr Opin Allergy Clin Immunol. 2020;20(1):43-47. 

In This Article

Influencing Factors

Although the underlying mechanisms of inflammation influence the development of ACO, environmental factors such as tobacco smoking, infections, pollutants, and diet likely also play a role.[3] Two of the best studied of these exposures are cigarette smoke and pollution.

Though definitely a driving factor in COPD, smoking is a habit seen in asthma patients as well.[14] It is uncertain whether tobacco exposure contributes to irreversible airway remodeling in asthma as it does in COPD. Of note, even in COPD, similar amount of tobacco exposure does not necessarily lead to the same outcome with regard to decline in lung function in all patients.[3,15] Moreover, smoking not only leads to increased symptoms in asthmatics, but it also decreases corticosteroid responsiveness.[16–18] Furthermore, active smokers have a more rapid annual rate of lung function decline, which may be mitigated by smoking cessation.[19] Currently, it is unknown whether asthmatics who smoke and progress to ACO represent the same phenotype as their nonsmoking counterparts.[3]

As for air pollution, exposure has been linked to the development of asthma and COPD.[3] However, its role in the development of ACO is unknown. In their study of asthmatic adults (n = 6040), To et al.[20] did find that higher cumulative exposure to fine particulate matter and ozone had nearly a three-fold greater odds of developing ACO.

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