Abstract
The relationship of exhaled ethane and n-pentane to exhaled NO, carbonylated proteins, and indoor/outdoor atmospheric pollutants were examined in order to evaluate ethane and n-pentane as potential markers of airway inflammation and/or oxidative stress. Exhaled NO and carbonylated proteins were found to have no significant associations with either ethane (p = 0.96 and p = 0.81, respectively) or n-pentane (p = 0.44 and 0.28, respectively) when outliers were included. In the case where outliers were removed n-pentane was found to be inversely associated with carbonylated proteins. Exhaled hydrocarbons adjusted for indoor hydrocarbon concentrations were instead found to be positively associated with air pollutants (NO, NO2 and CO), suggesting pollutant exposure is driving exhaled hydrocarbon concentrations. Given these findings, ethane and n-pentane do not appear to be markers of airway inflammation or oxidative stress.
Highlights
Oxidative stress is a physiological condition that occurs when there is an imbalance of oxidants and antioxidants, favouring the former, and can arise from oxidants produced within the body as well as exposure to atmospheric oxidants
For the following analyses, room air was subtracted from breath air, and breath hydrocarbons were normalized to exhaled CO2 to obtain an estimate of endogenously produced ethane and n-pentane
The present work investigates the associations between a biomarker of airway inflammation, a biomarker of oxidative stress as measured by protein oxidation, and two suspected biomarkers of oxidative stress
Summary
Oxidative stress is a physiological condition that occurs when there is an imbalance of oxidants and antioxidants, favouring the former, and can arise from oxidants produced within the body as well as exposure to atmospheric oxidants. The presence of the hydrocarbons ethane and n-pentane in exhaled breath as a result of lipid peroxidation is of particular interest to this study. Numerous studies have examined short chain alkanes in exhaled breath in attempts to demonstrate their potential use as biomarkers of oxidative stress (Dillard et al 1978, Drury et al 1997, Pryor & Godber 1991, Paredi et al 2000, Phillips et al 2000, Aghdassi & Allard 2000, Cope 2005, Kanoh et al 2005, Cope et al 2006, Solga et al 2006, Lärstad et al 2007). While clinical studies have found betweensubject differences in exhaled hydrocarbons, a methods development study by Drury et al (1997), is one of the few studies that examined within-subject changes
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