Adult Acute Blood Pressure Response to Controlled Air Pollution
Adult Acute Blood Pressure Response to Controlled Air Pollution
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; PM2.5) plus ozone (CAP+O3) were compared with those of particle-free air (PFA) in 23 normotensive, nonsmoking healthy adults. Mean concentrations of PM2.5 were 147 ± 27 versus 2 ± 2 µg/m, respectively, and those of O3 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+O3 [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+O3 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 PM2.5 (r = 0.53, p < 0.01; r = 0.56, p < 0.01, respectively) but not with total PM2.5 mass (r ≤ 0.25, p ≥ 0.27). These findings suggest that exposure to environmentally relevant concentrations of PM2.5 and O3 rapidly increases DBP. The magnitude of BP change is associated with the PM2.5 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.
Exposure to fine particulate air pollution [aerodynamic diameter < 2.5 µm (PM2.5)] is associated with increased cardiopulmonary mortality (Pope et al. 2002; Samet et al. 2000). Coronary ischemic events, occurring as rapidly as 1-2 hr after exposure, account for a major portion of this heightened mortality (Peters et al. 2001, 2004; Pope et al. 2004). In addition, an enhanced risk for acute cerebrovascular strokes has been linked to particulate air pollution (Hong et al. 2002; Tsai et al. 2003).
Several biologic mechanisms have been demonstrated that may in part explain these findings (Brook et al. 2003), including acute arterial vasoconstriction after exposure to concentrated ambient fine particles (CAP) with added ozone (Brook et al. 2002). In the latter study (Brook et al. 2002), subjects exposed to CAP with a higher organic carbon content had greater vasoconstriction than did those subjects exposed to CAP with less organic carbon content (Urch et al. 2004). Considering that PM2.5 has also been shown to alter autonomic balance (Devlin et al. 2003; Gold et al. 2000; Magari et al. 2001), it is reasonable to hypothesize that air pollution exposure can meaningfully affect blood pressure (BP). Using a randomized, sham [particle-free air (PFA) without added O3] controlled study, we investigated the effect of short-term inhalation of CAP with added O3 (CAP+O3) on BP and heart rate (HR) measured during exposure.
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; PM2.5) plus ozone (CAP+O3) were compared with those of particle-free air (PFA) in 23 normotensive, nonsmoking healthy adults. Mean concentrations of PM2.5 were 147 ± 27 versus 2 ± 2 µg/m, respectively, and those of O3 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+O3 [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+O3 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 PM2.5 (r = 0.53, p < 0.01; r = 0.56, p < 0.01, respectively) but not with total PM2.5 mass (r ≤ 0.25, p ≥ 0.27). These findings suggest that exposure to environmentally relevant concentrations of PM2.5 and O3 rapidly increases DBP. The magnitude of BP change is associated with the PM2.5 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.
Exposure to fine particulate air pollution [aerodynamic diameter < 2.5 µm (PM2.5)] is associated with increased cardiopulmonary mortality (Pope et al. 2002; Samet et al. 2000). Coronary ischemic events, occurring as rapidly as 1-2 hr after exposure, account for a major portion of this heightened mortality (Peters et al. 2001, 2004; Pope et al. 2004). In addition, an enhanced risk for acute cerebrovascular strokes has been linked to particulate air pollution (Hong et al. 2002; Tsai et al. 2003).
Several biologic mechanisms have been demonstrated that may in part explain these findings (Brook et al. 2003), including acute arterial vasoconstriction after exposure to concentrated ambient fine particles (CAP) with added ozone (Brook et al. 2002). In the latter study (Brook et al. 2002), subjects exposed to CAP with a higher organic carbon content had greater vasoconstriction than did those subjects exposed to CAP with less organic carbon content (Urch et al. 2004). Considering that PM2.5 has also been shown to alter autonomic balance (Devlin et al. 2003; Gold et al. 2000; Magari et al. 2001), it is reasonable to hypothesize that air pollution exposure can meaningfully affect blood pressure (BP). Using a randomized, sham [particle-free air (PFA) without added O3] controlled study, we investigated the effect of short-term inhalation of CAP with added O3 (CAP+O3) on BP and heart rate (HR) measured during exposure.
