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Research over the past 30 years has identified mechanistic biochemical oxidation pathways that contribute to asthma pathophysiology. Redox imbalance is present in asthma and strongly linked to the pathobiology of airflow obstruction, airway hyperreactivity, and remodeling. High levels of reactive oxygen species, reactive nitrogen species, and oxidatively modified proteins in the lung, blood, and urine provide conclusive evidence for pathologic oxidation in asthma. Concurrent loss of antioxidants, such as superoxide dismutases and catalase, is attributed to redox modifications of the enzymes, and further amplifies the oxidative injury in the airway. The presence of high levels of urine bromotyrosine, an oxidation product of eosinophil peroxidase, identifies activated eosinophils, and shows promise for use as a noninvasive biomarker of poor asthma control.