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

摘要

This study was designed to investigate PM1 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) PM1, 12 nonasthmatic males performed spirometry and eNO and EBC collection. Normal resting lung function did not change after low PM1 exercise. After high PM1 exercise, FEV1 and FEF25-75 fell significantly (p =.0005, p =.002) and was related to [PM1] (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 FEF25-75. NO3 did not change after low PM1 exercise (30.5% increase), but significantly decreased by 43.8% after high PM1 exercise, and correlated with lung function changes (r =.63, and r =.54 for FEV1 and FEF25-75, respectively; p =.001 and p =.007). No change in GSNO was observed. Alveolar NO decreased after high PM1 conditions (p =.02); eNO pre-to-post difference was related to changes in FEV1 (r =.60, p =.002). MDA increased 40% after low PM exercise (NS) and increased 208% after high PM exercise (p =.06). Thus, high PM1 inhalation during exercise caused a reduced alveolar contribution to eNO; NO3 and eNO variables were decreased and were related to impaired lung function. Decreased NO3 and eNO may be due to superoxide/NO formation of peroxynitrite, resulting in lipid peroxidation.