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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.

inhalation toxicology

Decreased lung function after inhalation of ultrafine and fine particulate matter during exercise is related to decreased total nitrate in exhaled breath condensate.