Oxidative stress in asthmatic and non‐asthmatic adolescent swimmers—A breathomics approach
The high prevalence of asthma among elite athletes has been related to bronchial epithelial damage. Oxidative stress is believed to contribute to the pathophysiology of asthma and, together with increased ventilation induced by exercise, may be a final common pathway leading to tissue damage.1 Swimmers are among the athletes with higher prevalence of asthma and present an increased risk for a specific phenotype,2 but the cause for it remains under debate. Trichloramine exposure in swimming pools may result in oxidative stress through reaction with substrates in the epithelial lining, therefore decreasing bronchial intrinsic antioxidants and producing subsequent inflammation, progression of bronchial hyper‐responsiveness, and a vicious cycle of continued airway oxidative stress and inflammation.3 Therefore, we hypothesized that exposure to chloramines during swimming would induce oxidative stress, which could be related to the etiopathogenesis of asthma in swimmers. In an exploratory study using metabolomic analysis of exhaled breath (EB) of elite swimmers, we aimed to assess the effect of a swimming training session on oxidative stress lipid peroxidation markers and to investigate whether the impact is similar across asthmatic and non‐asthmatic subjects.