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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.

This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 microm (noted as PM1) inhalation during exercise on conduit artery and microvascular function. Inhalation of internal combustion-derived PM is associated with cardiovascular mortality and morbidity. Direct action of PM on the vascular endothelium is likely, as a substantial fraction of ultrafine PM translocates from the alveoli to the circulatory system. Sixteen intercollegiate athletes performed 30 min of exercise while inhaling low or high PM1. Flow-mediated brachial artery dilation (FMD) using high-resolution ultrasonography with simultaneous measurements of forearm oxygen kinetics using near infrared spectrophotometry (NIRS) was done before and after exercise. Basal brachial artery vasoconstriction was found after high PM1 exercise (4.0%, 4.66 +/- 0.609 to 4.47 +/- 0.625 mm diameter; p = .0002), but not after low PM1 exercise (-0.3%, 4.66 +/- 0.626 to 4.68 +/- 0.613 mm diameter). FMD was impaired after high PM1 exercise (6.8 +/- 3.58% for preexercise FMD and 0.30 +/- 2.74% for postexercise FMD, p = .0001), but not after low PM1 exercise (6.6 +/- 4.04% for preexercise FMD and 4.89 +/- 4.42% for postexercise FMD). Reduction in forearm muscle reperfusion estimated by reoxygenation slope-to-baseline after 4 min cuff ischemia was observed for high PM1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM1] typical of urban environments impairs both systemic conduit artery function and microcirculation. The observed decrease reoxygenation slope-to-baseline after cuff release is consistent with reduced blood flow in the muscle microvasculature.

In spite of epidemiological evidence concerning vehicular air pollution and adverse respiratory/cardiovascular health, many athletic fields and school playgrounds are adjacent to high traffic roadways and could present long-term health risks for exercising children and young adults. Particulate matter (PM(1),0.02-1.0 microm diameter) number counts were taken serially at four elementary school athletic/playground fields and at one university soccer field. Elementary school PM1 measurements were taken over 17 days; measurements at the university soccer field were taken over 62 days. The high-traffic-location elementary school field demonstrated higher 17-day [PM1] than the moderate and 2 low traffic elementary school fields (48,890 +/- 34,260, 16,730 +/- 10,550, 11,960 +/- 6680, 10,030 +/- 6280, respective mean counts; p.05). The 62-day mean PM1 values at the university soccer field ranged from 115,000 to 134,000 particles cm(-3). Lowest mean values were recorded at measurement sites furthest from the highway (approximately 34,000 particles cm(-3)) and followed a second-order logarithmic decay (R2 = .999) with distance away from the highway. Mean NO2 and SO2 levels were below 100 ppb, mean CO was 0.33 +/- 1.87 ppm, and mean O3 was 106 +/- 47 ppb. Ozone increased with rising temperature and was highest in the warmer afternoon hours (R = .61). Although the consequence of daily recess play and athletic activities by school children and young athletes in high ambient [PM1] conditions has not yet been clearly defined, this study is a critical component to evaluating functional effects of chronic combustion-derived PM exposure on these exercising schoolchildren and young adults. Future studies should examine threshold limits and mechanistic actions of real-world particle exposure.