TY - JOUR
T1 - Plasma nitrite is an indicator of acute changes in ambient air pollutant concentrations
AU - Gandhi, Sampada K.
AU - Rich, David Q.
AU - Ohman-Strickland, Pamela A.
AU - Kipen, Howard M.
AU - Gow, Andrew
N1 - Funding Information:
This work was supported by NIEHS Center grant P30ES0205022, EPA STAR grant R832144, and grant HL086621. Dr Ohman Strickland reports grants from Environmental Protection Agency, grants from NIEHS, during the conduct of the study; Drs Gandhi, Kipen, Rich and Gow report no declaration of interest.
PY - 2014/6
Y1 - 2014/6
N2 - 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<2.5μm in aerodynamic diameter (PM2.5), 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 24h and six preceding 24-h periods, using linear mixed models. Results: IQR increases in mean PM2.5 (7.0μg/m3) and CO (161.7 parts per billion) concentrations in the first 24h before the plasma nitrite measurement were associated with increased plasma nitrite concentrations (PM2.5: 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.
AB - 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<2.5μm in aerodynamic diameter (PM2.5), 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 24h and six preceding 24-h periods, using linear mixed models. Results: IQR increases in mean PM2.5 (7.0μg/m3) and CO (161.7 parts per billion) concentrations in the first 24h before the plasma nitrite measurement were associated with increased plasma nitrite concentrations (PM2.5: 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.
KW - Air pollution
KW - Ambient air pollutants
KW - Plasma nitrite concentration
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U2 - 10.3109/08958378.2014.913216
DO - 10.3109/08958378.2014.913216
M3 - Article
C2 - 24862977
AN - SCOPUS:84901492204
SN - 0895-8378
VL - 26
SP - 426
EP - 434
JO - Inhalation Toxicology
JF - Inhalation Toxicology
IS - 7
ER -