Environmental Health volume 18 , Article number: 90 Cite this article. Metrics details. Evidences that oxidative stress plays a role in the associations between outdoor air pollution and asthma are growing. We aimed to study the role of plasma fluorescent oxidation products levels FlOPs; an oxidative stress-related biomarker , as potential mediators, in the associations between outdoor air pollution and persistent asthma.
Analyses were conducted in adult asthmatics followed up in the French case-control and family study on asthma EGEA; the Epidemiological study of the Genetic and Environmental factors of Asthma. We used a mediation analysis to assess the mediated effect by FlOPs levels and the interaction between FlOPs levels and air pollution. Our results add insights on the role of oxidative stress in the association between air pollution and persistent asthma.
Peer Review reports. Evidences that outdoor air pollution is associated with asthma incidence, and various asthma phenotypes as asthma control or asthma severity among asthmatics keep going up [ 1 , 2 ], but the associations between outdoor air pollution and persistent asthma are very scarcely studied in adults. To our knowledge, only one study has investigated the associations between nitrogen dioxide NO 2 exposure, traffic road and persistent asthma, and showed that living close to a major road was associated with persistent asthma in adults followed up over eight years [ 3 ].
The underlying biological mechanisms by which outdoor air pollution may affect respiratory health include inflammatory processes, immune response modulations, genetic modifications and oxidative stress damages, which are increasingly suggested. Asthma is an oxidative stress-related disease [ 4 ], and exposures to ozone O 3 , NO 2 and particulate matter PM have been found associated with oxidative stress [ 5 ].
Studying biomarkers is a useful approach to provide new insights into the biological mechanisms that drive the disease process, to predict the development and progression of a disease and to personalize intervention strategies [ 6 , 7 ].
