Sampada K Gandhi, David Q Rich, Pamela A Ohman-Strickland, Howard M Kipen, Andrew Gow
Journal: Inhalation toxicology 2015;26(7):426-34
PMID: 24862977
CONTEXT
Endothelial dysfunction has been suggested as a potential mechanism by which ambient air pollution may cause acute cardiovascular events. Recently, plasma nitrite has been developed as a marker of endothelial dysfunction.
OBJECTIVES
We examined the changes in plasma nitrite concentration associated with increases in ambient air pollutant concentrations in the previous 7 d.
MATERIALS AND METHODS
We linked up to three measurements of plasma nitrite concentrations obtained from 49 students to 24-h average concentrations of five criteria air pollutants [particle mass < 2.5 µm in aerodynamic diameter (PM(2.5)), carbon monoxide (CO), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and ozone (O₃)] measured at two monitoring sites closest to Rutgers University campus (6-15 miles) in New Jersey during the years 2006-2009. We examined the change in plasma nitrite associated with each interquartile-range (IQR) increase in pollutant concentration in the previous 24 h and six preceding 24- h periods, using linear mixed models.
RESULTS
IQR increases in mean PM(2.5) (7.0 µg/m³) and CO (161.7 parts per billion) concentrations in the first 24 h before the plasma nitrite measurement were associated with increased plasma nitrite concentrations (PM(2.5): 15.5 nanomolar; 95% confidence interval (CI): 2.4, 28.5; CO: 15.6 nanomolar; 95% CI: 2.4, 28.9). Increased plasma nitrite associated with IQR increases in O₃ and SO₂ concentrations over longer lags were observed.
DISCUSSION AND CONCLUSION
Rapid increases in plasma nitrite following exposure to ambient air pollutants support the hypothesis that ambient air pollution is associated with inducible nitric oxide synthase-mediated systemic inflammation in humans.
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