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Classifying the heterogeneity of asthma has been an ongoing challenge. Asthma phenotypes and endotypes have mainly been defined by clinical features, markers of atopy, airway immune cells and inflammatory markers.1 While clustering has helped the advancement of biologics specific targeting immune receptors or IgE, there has been less success in using clustering by other parameters such as genetics or environmental factors therapeutically.2 Despite a wealth of information on the detrimental effects of environmental factors such as air pollution and tobacco smoke exposure on asthma,3 their role in asthma pathogenesis is still unclear. The integration of environmental factors in host metabolic and inflammatory endotypes is of great interest and poorly understood.
The study by Wu and colleagues4 addresses this gap in knowledge by evaluating environmental exposures to small particulate matter (PM2.5) in six asthma endotypes from a data base of adults with asthma in Taiwan that included 209 837 emergency and 638 538 outpatient visits. In a case-control study, the authors further assessed markers for pollutant exposure and oxidative stress as well as metal concentrations in urine, blood cytokines and sphingolipids in adults with (n=365) and without (n=235) asthma. Monitoring …
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.