Exposure to Concentrated Ambient Particles Does Not Affect Vascular Function in Patients with Coronary Heart Disease

Abstract

BackgroundExposure to fine particulate air pollution is associated with increased cardiovascular morbidity and mortality. We previously demonstrated that exposure to dilute diesel exhaust causes vascular dysfunction in humans.ObjectivesWe conducted a study to determine whether exposure to ambient particulate matter causes vascular dysfunction.MethodsTwelve male patients with stable coronary heart disease and 12 age-matched volunteers were exposed to concentrated ambient fine and ultrafine particles (CAPs) or filtered air for 2 hr using a randomized, double-blind cross-over study design. We measured peripheral vascular vasomotor and fibrinolytic function, and inflammatory variables—including circulating leukocytes, serum C-reactive protein, and exhaled breath 8-isoprostane and nitrotyrosine—6–8 hr after both exposures.ResultsParticulate concentrations (mean ± SE) in the exposure chamber (190 ± 37 μg/m3) were higher than ambient levels (31 ± 8 μg/m3) and levels in filtered air (0.5 ± 0.4 μg/m3; p < 0.001). Chemical analysis of CAPs identified low levels of elemental carbon. Exhaled breath 8-isoprostane concentrations increased after exposure to CAPs (16.9 ± 8.5 vs. 4.9 ± 1.2 pg/mL, p < 0.05), but markers of systemic inflammation were largely unchanged. Although there was a dose-dependent increase in blood flow and plasma tissue plasminogen activator release (p < 0.001 for all), CAPs exposure had no effect on vascular function in either group.ConclusionsDespite achieving marked increases in particulate matter, exposure to CAPs—low in combustion-derived particles—did not affect vasomotor or fibrinolytic function in either middle-aged healthy volunteers or patients with coronary heart disease. These findings contrast with previous exposures to dilute diesel exhaust and highlight the importance of particle composition in determining the vascular effects of particulate matter in humans.

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

“…After exposure to PM, there were increases in exhaled breath 8-isoprostane, in blood flow and in plasma tissue plasminogen activator (P < 0.005); but there were no significant changes in markers of systemic inflammation, and there was no effect on vascular function in either group of subjects (Mills et al, 2008). It was noted that most of the particulate mass consisted of sea salt, and far less PM was derived from combustion sources than was identified in the studies described above.…”

Circulating endothelial progenitor cells are not affected by acute systemic inflammation

“…ELISAs were used to quantify serum IL-6 (Invitrogen) (23), VEGF-A (Invitrogen) (6), and stromal derived factor-1 (SDF-1; R&D Systems) concentrations according to the manufacturer's instructions (Invitrogen). Serum high sensitivity CRP (hs-CRP) was quantified using an immunoturbidimetric method (Dade-Behring, Marburg, Germany) (28).…”

Inflammatory and Oxidative Stress Responses of Healthy Young Adults to Changes in Air Quality during the Beijing Olympics

“…However, observational and experimental studies in humans or animals have generated limited and somewhat inconsistent data supporting several postulated pathophysiologic pathways (6-10). One of these is the hypothesis that inhaled pollutants can react rapidly with extracelluar macromolecules or cell constituents in the airway epithelium to generate reactive oxygen or nitrogen species (e.g., free radicals and peroxides), inducing local and systemic oxidative or nitrosative stress and subsequent inflammation (11).Pulmonary inflammation and oxidative stress responses to air pollution have been examined in human studies using several noninvasive biomarkers in exhaled breath and exhaled breath condensate (EBC) (7,(12)(13)(14)(15)(16)(17)(18). Increased air pollution levels have been associated with increased levels of fractional exhaled nitric oxide (FE NO ), reflecting pulmonary inflammation, in children and the elderly (12)(13)(14)(15)(19)(20)(21)(22).…”

“…Traffic pollution exposure has been associated with increased airway acidity (lowered EBC pH) in persons with asthma (16), reflecting inhibition of local epithelial proton pumps during airway inflammation (23). Furthermore, several novel EBC biomarkers reflecting oxidative and nitrosative stress in the respiratory tract (e.g., EBC nitrite, nitrate and 8-isoprostane) have been associated with air pollution exposure (17,(24)(25)(26). Recent studies also suggest that an increased wholebody burden of oxidative stress may induce or exacerbate pulmonary or systemic inflammation.…”