• Florence Chau-Etchepare, Joshua L Hoerger, Brooks T Kuhn, Amir A Zeki, Angela Haczku, Samuel Louie, Nicholas J Kenyon, Cristina E Davis, and Michael Schivo.
• Pulmonary, Critical Care, and Sleep Medicine, University of California Davis, Sacramento, California, USA.
• J. Investig. Med. 2019 Oct 1; 67 (7): 102910411029-1041.

AbstractAsthma is a complex inflammatory disease with many triggers. The best understood asthma inflammatory pathways involve signals characterized by peripheral eosinophilia and elevated immunoglobulin E levels (called T2-high or allergic asthma), though other asthma phenotypes exist (eg, T2-low or non-allergic asthma, eosinophilic or neutrophilic-predominant). Common triggers that lead to poor asthma control and exacerbations include respiratory viruses, aeroallergens, house dust, molds, and other organic and inorganic substances. Increasingly recognized non-allergen triggers include tobacco smoke, small particulate matter (eg, PM2.5), and volatile organic compounds. The interaction between respiratory viruses and non-allergen asthma triggers is not well understood, though it is likely a connection exists which may lead to asthma development and/or exacerbations. In this paper we describe common respiratory viruses and non-allergen triggers associated with asthma. In addition, we aim to show the possible interactions, and potential synergy, between viruses and non-allergen triggers. Finally, we introduce a new clinical approach that collects exhaled breath condensates to identify metabolomics associated with viruses and non-allergen triggers that may promote the early management of asthma symptoms.© American Federation for Medical Research 2019. No commercial re-use. See rights and permissions. Published by BMJ.

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