摘要
Background: Ultrafine particles (UFP) may contribute to the cardiovascular effects of exposure to particulate air pollution, partly because of their relatively efficient alveolar deposition and potential to enter the pulmonary vascular space. Objectives: This study tested the hypothesis that inhalation of elemental carbon UFP alters systemic vascular function. Methods: Sixteen healthy subjects (mean age, 26.9 ± 6.5 years) inhaled air or 50 μg/m 3 elemental carbon UFP by mouthpiece for 2 hr, while exercising intermittently. Measurements at preexposure baseline, 0 hr (immediately after exposure), 3.5 hr, 21 hr, and 45 hr included vital signs, venous occlusion plethysmography and reactive hyperemia of the forearm, and venous plasma nitrate and nitrite levels. Results: Peak forearm blood flow after ischemia increased 3.5 hr after exposure to air but not UFP (change from preexposure baseline, air: 9.31 ± 3.41; UFP: 1.09 ± 2.55 mL/min/100 mL; t-test, p = 0.03). Blood pressure did not change, so minimal resistance after ischemia (mean blood pressure divided by forearm blood flow) decreased with air, but not UFP [change from preexposure baseline, air: -0.48 ± 0,21; UFP: 0.07 ± 0.19 mmHg/mL/min; analysis of variance (ANOVA), p = 0.024]. There was no UFP effect an pre-ischemia forearm blood flow or resistance, or on total forearm blood flow after ischemia. Venous nitrate levels were significantly lower after exposure to carbon UFP compared with air (ANOVA, p = 0.038). There were no differences in venous nitrite levels. Conclusions: Inhalation of 50 μg/m 3 carbon UFP during intermittent exercise impairs peak forearm blood flow during reactive hyperemia in healthy human subjects.