Particulate Oxidative Burden as a Predictor of Exhaled Nitric Oxide in Children with Asthma

<p><strong>BACKGROUND:</strong> Epidemiological studies have provided strong evidence that fine particulate matter (PM_2.5, aerodynamic diameter 2.5µm and lower) can exacerbate asthmatic symptoms in children. Pro-oxidant components of PM2.5 are capable of directly generating reactive oxygen species. Oxidative burden is used to describe the capacity of PM_2.5 to generate reactive oxygen species in the lung.</p> <p><strong>OBJECTIVE:</strong> This study investigated the association between airway inflammation in asthmatic children and oxidative burden of PM_2.5 personal exposure.</p> <p><strong>METHODS:</strong> Daily PM_2.5 personal exposure samples (<i>n</i>=249) of 62 asthmatic school-aged children in Montreal were collected over ten consecutive days. The oxidative burden of PM_2.5 samples was determined <i>in vitro</i> as the depletion of low molecular weight antioxidants (ascorbate and glutathione) from a synthetic model of the fluid lining the respiratory tract. Airway inflammation was measured daily as fractional exhaled nitric oxide (FeNO).</p> <p><strong>RESULTS:</strong> A positive association was identified between FeNO and glutathione-related oxidative burden exposure in the previous 24 hours (6.0% increase per IQR change in glutathione). Glutathione-related oxidative burden was further found to be positively associated with FeNO over 1-day lag and 2-day lag periods. Results further demonstrate that corticosteroids use may reduce the FeNO response to elevated glutathione-related oxidative burden exposure (no use: 15.8%; irregular use: 3.8%), while mould (22.1%), dust (10.6%) or fur (13.1%) allergies may increase FeNO compared to children without these allergies (11.5%). No association was found between PM_2.5 mass or ascorbate-related oxidative burden and FeNO levels.</p> <p><strong>CONCLUSIONS:</strong> Exposure to PM_2.5 with elevated glutathione-related oxidative burden was associated with increased FeNO.</p>