Breath condensate levels of 8-isoprostane and leukotriene B4 after ozone inhalation are greater in sensitive versus nonsensitive subjects

Ozone (O-3) inhalation induces pulmonary function decrements and inflammation. The present study was designed to determine if a relationship exists between O-3 induced pulmonary function changes and the presence of inflammatory markers as measured in exhaled breath condensates (EBCs) obtained from O-3-sensitive and nonsensitive human subjects. Eight healthy adult volunteers (4 malesl 4 ftmales, age 18 to 30 years) were studied, characterized as to their ozone sensitivity and placed into 2 groups (sensitive and nonsensilive) with each group having 2 males and 2ftmales. Subjects completed a 20-minute EBC collection and pulmonary function test (PFT) prior to a single 60-minute bout of cycle ergometer exercise (V-E = 50-55 L/min) while breathing filtered air (FA) or 0.35ppm O-3. Subjective symptom scores (SSSs) were collected at 6, 20, 40, and 60 minutes during exposure. An immediate postexposure RFTwas per/brined followed by an EBC collection. Subjective symptom scores, E2BCs, and PT-Fs were collected at 1, 4 and 8 hours post exposure. EBCs were analyzed for prostaglandin E-2 (PGE(2)), leukotriene B-4 (LTB4), 8-isoprostane, and total nit-tic oxide (NO) metabolites (nitrate+ nitrite con' tent). Sensitive subjects, breathing O-3, had significantly greaterfunctional decrements in PT7s, increased SSSs, and increased rapid shallow breathing as well as elevated Levels of 8-isoprostane and LTB4 in EBCs compared to those breathing FA. In addition, there were significant increases in nitrate+ nitrite content in both sensitive and nonsensitive subjects breathing O-3 compared to FA. These results indicate that sensitive subjects have elevated arachidonic acid metabolites in EBCs compared to nonsensitive subjects after O-3 inhalation.