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The effect of environmental oxidative stress on airway inflammation

Auerbach, Amy; Hernandez, Michelle L.

Current Opinion in Allergy and Clinical Immunology: April 2012 - Volume 12 - Issue 2 - p 133–139
doi: 10.1097/ACI.0b013e32835113d6
OCCUPATIONAL DISEASE: Edited by Susan M. Tarlo and Piero Maestrelli

Purpose of review Asthma is an inflammatory respiratory condition with significantly associated morbidity and mortality that is increasing in prevalence. Air pollution is an important factor in both the development of asthma and in asthma exacerbations. Oxidative stress as a result of exposure to air pollution and underlying genetic polymorphisms that may play a role in susceptibility to this oxidative stress are the subject of current investigation. This article reviews the data regarding the effects of air pollution on the innate immune response and potential clinical and treatment implications of how genetic polymorphisms affect this response.

Recent findings Recent investigation reveals how pollutant-induced oxidative stress impacts airway inflammatory responses. Work by our study group demonstrates that asthmatic patients have an exaggerated inflammatory response to air pollution-induced oxidative stress. New trials investigating antioxidants as potential therapeutic interventions may target this specific issue.

Summary Air pollution plays a critical role in asthma and may affect certain patients more than others. Further investigation into the genetic polymorphisms that affect inflammatory responses may help target patient populations at greatest risk for air pollution-induced asthma and may provide new therapeutic options for these patient populations.

aCenter for Environmental Medicine, Asthma and Lung Biology

bDepartment of Pediatrics, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA

Correspondence to Michelle L. Hernandez, MD, Center for Environmental Medicine, Asthma and Lung Biology, 104 Mason Farm Road, UNC School of Medicine, Chapel Hill, NC 27516, USA. Tel: +1 919 843 5383; fax: +1 919 966 9863; e-mail:

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