Published online before print July 20, 2009, doi: 10.1161/HYPERTENSIONAHA.109.130237
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(Hypertension. 2009;54:659.)
© 2009 American Heart Association, Inc.
Original Articles |
Insights Into the Mechanisms and Mediators of the Effects of Air Pollution Exposure on Blood Pressure and Vascular Function in Healthy Humans
From the Division of Cardiovascular Medicine (R.D.B., R.L.B.), School of Public Health (J.T.D., G.K., M.M., F.J.M., A.S.K.), Center for Human Growth and Development (N.K.), and Department of Biostatistics (N.K.), University of Michigan, Ann Arbor, Mich; Institute of Medical Science (B.U., F.S.), Dalla Lana School of Public Health (P.C., F.S.), and Department of Medicine (F.S.), University of Toronto, Toronto, Ontario, Canada; Gage Occupational and Environmental Health Unit (B.U., M.S., P.C., F.S., J.R.B.), Toronto, Ontario, Canada; School of Veterinary Medicine (J.H.), Michigan State University, East Lansing, Mich; Cardiovascular Epidemiology Research Unit (G.W., M.A.M.), Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Mass; Davis Heart Lung Research Institute, College of Medicine, Ohio State University (S.R.), Columbus, Ohio; Environment Canada (J.R.B.), Toronto, Ontario, Canada; Harvard Medical School (D.G.), Brigham and Women’s Hospital, Boston, Mass.
Correspondence to Robert D. Brook, University of Michigan, 24 Frank Lloyd Wright Dr, PO Box 322, Ann Arbor, MI 48106. E-mail robdbrok{at}umich.edu
Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 µg/m3) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor 
. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function, likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.
Key Words: hypertension • endothelium • sympathetic nervous system • inflammation • oxidative stress