Controlled exposure to particulate matter from urban street air is associated with decreased vasodilation and heart rate variability in overweight and older adults

Background: Exposure 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. Methods: Sixty healthy subjects 25 males, 35 females, age 55 to 83 years, body mass index > 25 kg/m(2)) 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 similar to 23.000 versus similar to 1800/cm(3) and PM2.5 levels of 24 versus 3 mu g/m(3), respectively. The PM contained similar fractions of elemental and black carbon (similar to 20-25%) in both exposure scenarios. Reactive hyperemia and nitroglycerin-induced vasodilation in finger arteries and heart rate variability (HRV) measured within 1h 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). Results: Nitroglycerin-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. Conclusions: This 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.