Abstract
BackgroundExposure to particulate matter (PM) is generally associated with elevated risk of cardiovascular morbidity and mortality. Elderly and obese subjects may be particularly susceptible, although short-term effects are poorly described.MethodsSixty healthy subjects (25 males, 35 females, age 55 to 83 years, body mass index > 25 kg/m2) were included in a cross-over study with 5 hours of exposure to particle- or sham-filtered air from a busy street using an exposure-chamber. The sham- versus particle-filtered air had average particle number concentrations of ~23.000 versus ~1800/cm3 and PM2.5 levels of 24 versus 3μg/m3, respectively. The PM contained similar fractions of elemental and black carbon (~20-25%) in both exposure scenarios. Reactive hyperemia and nitroglycerin-induced vasodilation in finger arteries and heart rate variability (HRV) measured within 1 h after exposure were primary outcomes. Potential explanatory mechanistic variables included markers of oxidative stress (ascorbate/dehydroascorbate, nitric oxide-production cofactor tetrahydrobiopterin and its oxidation product dihydrobiopterin) and inflammation markers (C-reactive protein and leukocyte differential counts).ResultsNitroglycerin-induced vasodilation was reduced by 12% [95% confidence interval: −22%; −1.0%] following PM exposure, whereas hyperemia-induced vasodilation was reduced by 5% [95% confidence interval: −11.6%; 1.6%]. Moreover, HRV measurements showed that the high and low frequency domains were significantly decreased and increased, respectively. Redox and inflammatory status did not change significantly based on the above measures.ConclusionsThis study indicates that exposure to real-life levels of PM from urban street air impairs the vasomotor function and HRV in overweight middle-aged and elderly adults, although this could not be explained by changes in inflammation, oxidative stress or nitric oxide-cofactors.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-015-0081-9) contains supplementary material, which is available to authorized users.
Highlights
Exposure to particulate matter (PM) is generally associated with elevated risk of cardiovascular morbidity and mortality
Exposure to particulate matter (PM) in terms PM2.5 in ambient air is associated with elevated risk of cardiovascular morbidity and mortality especially in risk groups with old age, obesity and/or diabetes [1,2]
The oxidized form of BH4, dihydrobiopterin (BH2), can cause endothelial nitric oxide synthase (eNOS) uncoupling with production of superoxide anion radicals, which react with nitric oxide (NO) forming peroxynitrite, a potent oxidant [5,6]
Summary
Exposure to particulate matter (PM) is generally associated with elevated risk of cardiovascular morbidity and mortality. Exposure to particulate matter (PM) in terms PM2.5 (mass of PM with aerodynamic diameter < 2.5 μm) in ambient air is associated with elevated risk of cardiovascular morbidity and mortality especially in risk groups with old age, obesity and/or diabetes [1,2]. An animal study indicated that exposure to diesel exhaust, the most important source of urban ultrafine particles, increased vasoconstriction through decreased NO bioavailability by uncoupling eNOS and decreased levels of BH4 [7]. Studies with controlled exposure to diesel exhaust in humans have indicated that vasodilation response was impaired both related to endothelial stimulation to NO production and to administration of an NO donor [3]
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