| Background: Substantial evidence links exposure to particulate matter air pollution with cardiovascular morbidity and mortality. Endothelial dysfunction has been recently investigated as a potential mechanism by which an exposure to air pollutants for a short period of time can cause adverse cardiovascular events.;Methods: We examined the intra-day reproducibility of EndoPAT measurements obtained 2.5 hours apart and the inter-day reproducibility of EndoPAT measurements obtained 1 week apart in a group of young and healthy volunteers. We also examined the acute changes in EndoPAT measurements and plasma nitrite concentration following a 2-hour exposure to diesel exhaust (DE) and secondary organic aerosol (SOA) compared to clean air (CA) in a controlled environmental facility as well as changes in these markers associated with increases in 5 ambient air pollutant concentrations, namely particulate matter less than 2.5 micrometers in diameter (PM2.5), carbon monoxide (CO), sulphur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3) on the preceding 7 days.;Results: In Aim 1, the intra-class correlation coefficients (ICC) for the PAT ratio obtained 2.5 hours apart were -0.07 and 0.40 in the pilot and CA exposure study, respectively, and the ICC for the PAT ratio obtained a week apart was 0.27, indicating a low intra-day and inter-day reproducibility. In Aim 2, the plasma nitrite concentration showed a greater decrease following the exposure to DE and SOA compared to CA. The mean PAT ratios showed an increase from pre to post-exposure to DE, SOA, and CA. In Aim 3, each interquartile range increase in the mean PM2.5 and CO concentration in the first 24 hours before the endothelial function measurement was associated with an increase in the plasma nitrite concentration (17.1 and 17.2% respectively).;Conclusions: The EndoPAT device does not produce reliable PAT ratios 2.5 hours apart and one week apart in a young population. The increase in the plasma nitrite associated with the increase in the ambient air pollutants in the first 24 hours suggests a potential role of systemic inflammation via stimulation of inducible nitric oxide synthase enzyme and generation of nitric oxide within a short period of time. |
