Key result
Personal NO2 exposure impairs vascular function, while airborne potassium is linked to lower diastolic BP.
Cohort (n=65)
No
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This work explored the association between nitrogen dioxide (NO(2)) and PM(2.5) components with changes in cardiovascular function in an adult non-smoking cohort. The cohort consisted of 65 volunteers participating in the US EPA's Detroit Exposure and Aerosol Research Study (DEARS) and a University of Michigan cardiovascular sub-study. Systolic and diastolic blood pressure (SBP, DBP), heart rate (HR), brachial artery diameter (BAD), brachial artery flow-mediated dilatation (FMD) and nitroglycerin-mediated arterial dilatation (NMD) were collected by in-home examinations. A maximum of 336 daily environmental and health effect observations were obtained. Daily potassium air concentrations were associated with significant decreases in DBP (-0.0447 mmHg/ng/m(3) ± 0.0132, p = 0.0016, lag day 0) among participants compliant with the personal monitoring protocol. Personal NO(2) exposures resulted in significant changes in BAD (e.g., 0.0041 mm/ppb ± 0.0019, p = 0.0353, lag day 1) and FMD (0.0612 ± 0.0235, p = 0.0103, lag day 0) among other findings.
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Williams et al. (2011) conducted a cohort in Cardiovascular function in relation to air pollution exposure (n=65). Personal and ambient exposures to nitrogen dioxide (NO2) and PM2.5 components (including potassium) was evaluated on Changes in cardiovascular function including systolic and diastolic blood pressure (SBP, DBP), heart rate (HR), brachial artery diameter (BAD), flow-mediated dilatation (FMD), and nitroglycerin-mediated arterial dilatation (NMD) (DBP: -0.0447 ± 0.0132 mmHg/ng/m3 (potassium, lag 0); BAD: 0.0041 ± 0.0019 mm/ppb (NO2, lag 1); FMD: 0.0612 ± 0.0235 (NO2, lag 0), p=0.0016 (DBP); 0.0353 (BAD); 0.0103 (FMD)). Personal NO2 exposure significantly altered brachial artery diameter (0.0041 mm/ppb, p=0.0353) and FMD (p=0.0103), while daily airborne potassium decreased DBP (-0.0447 mmHg/ng/m3, p=0.0016).
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