This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 μm (noted as PM 1 ) 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 PM 1 . 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 PM 1 exercise (4.0%, 4.66 ± 0.609 to 4.47 ± 0.625 mm diameter; p = .0002), but not after low PM 1 exercise (−0.3%, 4.66 ± 0.626 to 4.68 ± 0.613 mm diameter). FMD was impaired after high PM 1 exercise (6.8 ± 3.58% for preexercise FMD and 0.30 ± 2.74% for postexercise FMD, p = .0001), but not after low PM 1 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 PM 1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM 1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM 1 ] 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.

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.

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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 µm diameter) number counts were taken serially at four elementary school athletic/playground fields and at one university soccer field. Elementary school PM 1 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 [PM 1 ] 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 PM 1 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 (∼34,000 particles cm −3 ) and followed a second-order logarithmic decay (R 2 = .999) with distance away from the highway. Mean NO 2 and SO 2 levels were below 100 ppb, mean CO was 0.33 ± 1.87 ppm, and mean O 3 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 [PM 1 ] 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.

This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 μm (noted as PM 1 ) 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 PM 1 . 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 PM 1 exercise (4.0%, 4.66 ± 0.609 to 4.47 ± 0.625 mm diameter; p = .0002), but not after low PM 1 exercise (−0.3%, 4.66 ± 0.626 to 4.68 ± 0.613 mm diameter). FMD was impaired after high PM 1 exercise (6.8 ± 3.58% for preexercise FMD and 0.30 ± 2.74% for postexercise FMD, p = .0001), but not after low PM 1 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 PM 1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM 1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM 1 ] 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.