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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.

The purpose of this study was to investigate effects of PM1 (particulate matter with aerodynamic diameter 0.02-2 microm) inhalation on exercise performance in healthy subjects. Inhalation of internal combustion-derived PM is associated with adverse effects to the pulmonary and muscle microcirculation. No data are available concerning air pollution and exercise performance. Fifteen healthy college-aged males performed 4 maximal effort 6-min cycle ergometer trials while breathing low or high PM1 to achieve maximal work accumulation (kJ). Low PM1 inhalation trials 1 and 2 were separated by 3 days; then after a 7 day washout, trials 3 and 4 (separated by 3 days) were done while breathing high PM1 generated from a gasoline engine; CO was kept below 10 ppm. Lung function was done after trial 1 to verify nonasthmatic status. Lung function was normal before and after low PM1 exercise. PM1 number counts were not different between high PM1 trials (336,730 +/- 149,206 and 396,200 +/- 82,564 for trial 3 and 4, respectively) and were different from low PM1 trial number counts (2,260 +/- 500) (P < 0.0001). Mean heart rate was not different between trials (189 +/- 6.0, 188 +/- 7.6, 188 +/- 7.6, 187 +/- 7.4, for low and high PM1 trials; respectively). Work accumulated was not different between low PM1 trials (96.1 +/- 9.38 versus 96.6 +/- 10.83 kJ) and the first high PM1 trial (trial 3, 96.8 +/- 10.65 kJ). Work accumulated in the second high PM1 trial 4, 91.3 +/- 10.04 kJ) was less than in low PM1 trials 1 and 2, and high PM1 trial 3 (P = 0.004, P = 0.003, P = 0.0008; respectively). Acute inhalation of high (PM1) typical of many urban environments could impair exercise performance.