Acute Blood Pressure Responses in Healthy Adults During Controlled Air Pollution Exposures

Exposure to air pollution has been shown to cause arterial vasoconstriction and alter autonomic balance. Because these biologic responses may influence systemic hemodynamics, we investigated the effect of air pollution on blood pressure (BP). Responses during 2-hr exposures to concentrated ambient fine particles (particulate matter < 2.5 μm in aerodynamic diameter; PM(2.5)) plus ozone (CAP+O(3)) were compared with those of particle-free air (PFA) in 23 normotensive, non-smoking healthy adults. Mean concentrations of PM(2.5) were 147 ± 27 versus 2 ± 2 μg/m(3), respectively, and those of O(3) were 121 ± 3 versus 8 ± 5 ppb, respectively (p < 0.0001 for both). A significant increase in diastolic BP (DBP) was observed at 2 hr of CAP+O(3) [median change, 6 mm Hg (9.3%); binomial 95% confidence interval (CI), 0 to 11; p = 0.013, Wilcoxon signed rank test] above the 0-hr value. This increase was significantly different (p = 0.017, unadjusted for basal BP) from the small 2-hr change during PFA (median change, 1 mm Hg; 95% CI, −2 to 4; p = 0.24). This prompted further investigation of the CAP+O(3) response, which showed a strong association between the 2-hr change in DBP (and mean arterial pressure) and the concentration of the organic carbon fraction of PM(2.5) (r = 0.53, p < 0.01; r = 0.56, p < 0.01, respectively) but not with total PM(2.5) mass (r ≤ 0.25, p ≥ 0.27). These findings suggest that exposure to environmentally relevant concentrations of PM(2.5) and O(3) rapidly increases DBP. The magnitude of BP change is associated with the PM(2.5) carbon content. Exposure to vehicular traffic may provide a common link between our observations and previous studies in which traffic exposure was identified as a potential risk factor for cardiovascular disease.