Effect of Inhaled Carbon Ultrafine Particles on Reactive Hyperemia in Healthy Human Subjects

Abstract

BackgroundUltrafine 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.ObjectivesThis study tested the hypothesis that inhalation of elemental carbon UFP alters systemic vascular function.MethodsSixteen healthy subjects (mean age, 26.9 ± 6.5 years) inhaled air or 50 μg/m3 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.ResultsPeak 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 on 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.ConclusionsInhalation of 50 μg/m3 carbon UFP during intermittent exercise impairs peak forearm blood flow during reactive hyperemia in healthy human subjects.

Particulate Matter Air Pollution and Cardiovascular Disease

“…BP was also not affected. 407 Several recent studies have also shown that dilute diesel exhaust can impair peripheral resistance vessel responses to acetylcholine, bradykinin, and nitroprusside 6 hours after exposure. 384 The blunted responses to acetylcholine persisted for 24 hours in healthy adults.…”

Interaction of matrix metalloproteinases with pulmonary pollutants: Table 1–

“…In particular, exposure to traffic has been shown to be a stronger risk for acute myocardial infarction and proximity to roadways is more strongly associated with coronary artery calcification than are indices of particulate matter respiratory exposure [18,19]. Although particulate matter has a definite toxic effect on the systemic vasculature in rodent models and in controlled human studies [20,21], environmental exposure to particulate matter never occurs without concomitant exposure to numerous gaseous co-pollutants. Diseases of the systemic vasculature can manifest in many ways, and we have a growing appreciation that particulate matter air pollution may exacerbate atherosclerosis [22], hypertension [23] and diabetic vasculopathy [24].…”

Experimental evaluation of miniature plate DMAs (mini-plate DMAs) for future ultrafine particle (UFP) sensor network

“…It is because recent epidemiologic studies have shown UFPs are particularly relevant to pulmonary diseases, cancer, and mortality (Hoek et al 2002;Peters et al 2004;Delfino et al 2005Oberd€ orster et al 2005Br€ auner et al 2007;Shah et al 2008;Li et al 2010;Stewart et al 2010). The increased asthma prevalence is also found to often occur in the areas with high UFP level in ambient air or high motor vehicle traffic density, and in residence community nearby freeways (Samet et al 2000;Holguin 2008;Salam et al 2008;Patel and Miller, 2009).…”