title: Acute blood pressure responses in healthy adults during controlled air pollution exposures.
abstract: 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 microm 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 microg/m3, 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 < or = 0.25, p > or = 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.
authors.affiliation: Gage Occupational and Environmental Health Unit, St. Michael's Hospital, Toronto, Ontario, Canada. bruce.urch@utoronto.ca
authors.forename: Bruce
authors.initials: B
authors.lastname: Urch
authors.forename: Frances
authors.initials: F
authors.lastname: Silverman
authors.forename: Paul
authors.initials: P
authors.lastname: Corey
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Brook
authors.forename: Karl Z
authors.initials: KZ
authors.lastname: Lukic
authors.forename: Sanjay
authors.initials: S
authors.lastname: Rajagopalan
authors.forename: Robert D
authors.initials: RD
authors.lastname: Brook
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D000397:Air Pollution / Q000009:adverse effects*; D001794:Blood Pressure / Q000187:drug effects*; D002244:Carbon / Q000032:analysis; D002248:Carbon Monoxide / Q000032:analysis / Q000633:toxicity; D004391:Dust / Q000032:analysis; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D019570:Inhalation Exposure; D008297:Male; D008875:Middle Aged; D009589:Nitrogen Oxides / Q000032:analysis / Q000633:toxicity; D010083:Oxidants, Photochemical / Q000032:analysis / Q000633:toxicity*; D010126:Ozone / Q000032:analysis / Q000633:toxicity*; D010316:Particle Size; D013458:Sulfur Dioxide / Q000032:analysis / Q000633:toxicity; D001335:Vehicle Emissions
chemical_list: D000393:Air Pollutants; D004391:Dust; D009589:Nitrogen Oxides; D010083:Oxidants, Photochemical; D001335:Vehicle Emissions; D013458:Sulfur Dioxide; D010126:Ozone; D002244:Carbon; D002248:Carbon Monoxide