This study was designed to investigate PM(1) inhalation during exercise on lung function, exhaled nitric oxide (eNO), and total nitrate (NO3), S-nitrosoglutathione (GSNO), and malondialdehyde (MDA) in exhaled breath condensate (EBC). Inhalation of combustion-derived PM is associated with adverse respiratory health. A mechanistic action of PM on lung function is not defined; however, nitrosative/oxidative stress is likely. Prior to and after two 30-min exercise bouts 4-5 days apart, inhaling low (7382 +/- 1727 particles cm(- 3)) or high (252,290 +/- 77,529 particles cm(- 3)) PM(1), 12 nonasthmatic males performed spirometry and eNO and EBC collection. Normal resting lung function did not change after low PM(1) exercise. After high PM(1) exercise, FEV(1) and FEF(25-75) fell significantly (p = .0005, p = .002) and was related to [PM(1)] (r = -.55, p = .005 and r =-.61, p = .002; respectively); 11- and 52-ml decreases were calculated for each 20,000 particles cm(- 3) increase for FEV and FEF(25-75). NO3 did not change after low PM(1) exercise (30.5% increase), but significantly decreased by 43.8% after high PM(1) exercise, and correlated with lung function changes (r = .63, and r = .54 for FEV(1) and FEF(25-75), respectively; p = .001 and p = .007). No change in GSNO was observed. Alveolar NO decreased after high PM(1) conditions (p = .02); eNO pre-to-post difference was related to changes in FEV(1) (r = .60, p = .002). MDA increased 40% after low PM exercise (NS) and increased 208% after high PM exercise (p = .06). Thus, high PM(1) inhalation during exercise caused a reduced alveolar contribution to eNO; NO3 and eNO variables were decreased and were related to impaired lung function. Decreased NO(3) and eNO may be due to superoxide/NO formation of peroxynitrite, resulting in lipid peroxidation.