Our scientific community agrees that some patients present overlapping features of chronic obstructive pulmonary disease (COPD) and asthma. The Spanish COPD guidelines (GesEPOC)1 call this the mixed COPD–asthma phenotype, but it is known internationally as asthma–COPD overlap syndrome (ACOS). Its prevalence has not been well defined, and various studies report differences in sex and age.2 Variations in the prevalence of ACOS are primarily due to discrepancies among the consensus-based diagnostic criteria.2,3 Indeed, in a Canadian study, prevalence ranged between 5% and 27% depending on the diagnostic criteria applied.4 According to clinical guidelines, significant criteria for establishing a diagnosis of ACOS include a previous diagnosis of asthma and, particularly, early onset of respiratory symptoms.1,2

The studies cited above mainly focus on COPD caused by tobacco smoke. We know, however, that exposure to biomass smoke is a major cause of COPD, although the characteristics of this entity remain to be defined. Specifically, little information is available on the prevalence of ACOS in COPD caused by biomass smoke. In a study conducted by our group, we found a 21.3% prevalence of ACOS in patients with COPD caused by biomass smoke, compared to 5% in COPD caused by tobacco, but these differences may be related to an uneven gender distribution in study groups.5 In this study, we used modified GesEPOC criteria to diagnose ACOS; however, the retrospective nature of the study was a major limitation, and prevented us from systematically investigating all possible diagnostic criteria in each case. The diagnostic factor most frequently used was personal history of asthma, based primarily on onset of respiratory symptoms before the age of 40 years. However, this criterion may not be applicable to COPD caused by biomass smoke, since, unlike tobacco, exposure to this noxious substance typically begins in early childhood, a crucial stage in the development of the respiratory system. For this reason, early onset is a specific feature of COPD caused by biomass smoke, and does not constitute a reliable indicator of coexisting asthma in this population. ACOS, then, may have been overdiagnosed in our series, and we must question whether the usual diagnostic criteria are applicable in this COPD subtype.

We believe research should be undertaken to identify biomarkers that would allow ACOS to be reliably differentiated in populations with different risk factors for the disease. The clinical implications are obvious, because ACOS patients and particularly those with COPD caused by biomass smoke have typically been excluded from clinical studies, resulting in a scarcity of scientific evidence on which to base therapeutic decisions.