Most of the studies linking
chronic obstructive pulmonary disease (
COPD) with oxidative stress are in vitro, using invasive techniques, or measuring systemic oxidative stress. The aim of this study was to quantify oxidative stress in the lungs in patients with
COPD and in healthy smokers, as reflected by
8-isoprostane concentrations in breath condensate. This is a noninvasive method to collect airway secretions.
8-Isoprostane is a prostaglandin-F(2alpha) isomer that is formed in vivo by
free radical-catalyzed peroxidation of
arachidonic acid. We also studied the acute effect of smoking on exhaled
8-isoprostane in healthy smokers. Exhaled
8-isoprostane was measured by a specific
enzyme immunoassay in 10 healthy nonsmokers and 12 smokers, 25
COPD ex-smokers, and 15
COPD current smokers.
8-Isoprostane concentrations were similar in
COPD ex-smokers (40 +/- 3.1 pg/ml) and current smokers (45 +/- 3.6 pg/ ml) and were increased about 1.8-fold compared with healthy smokers (24 +/- 2.6 pg/ml, p < 0.001), who had 2.2-fold higher
8-isoprostane than healthy nonsmokers (10.8 +/- 0.8 pg/ml, p < 0.05). Smoking caused an acute increase in exhaled
8-isoprostane by about 50%. Our study shows that
free radical production is increased in patients with
COPD and that smoking causes an acute increase in oxidative stress.