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Amy H. Auchincloss,¹ Ana V. Diez Roux,¹ J. Timothy Dvonch,² Patrick L. Brown,³ R. Graham Barr,⁴ Martha L. Daviglus,⁵ David C. Goff Jr.,⁶ Joel D. Kaufman,⁷ and Marie S. O'Neill^1,2

¹Department of Epidemiology, and ²Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA; ³Department of Atmospheric Sciences, School of Engineering, University of Michigan, Ann Arbor, Michigan, USA; ⁴Departments of Medicine and Epidemiology, Columbia University Medical Center, New York, New York, USA; ⁵Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA; ⁶Department of Public Health Sciences, School of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA; ⁷Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, Washington, USA

Abstract
Background: Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter ≤ 2.5 µm in aerodynamic diameter ; PM_2.5) and BP: systolic (SBP) , diastolic (DBP) , mean arterial (MAP) , and pulse pressure (PP) .

Methods: The study sample included 5,112 persons 45–84 years of age, free of cardiovascular disease at the Multi-Ethnic Study of Atherosclerosis baseline examination (2000–2002) . Data from U.S. Environmental Protection Agency monitors were used to estimate ambient PM_2.5 exposures for the preceding 1, 2, 7, 30, and 60 days. Roadway data were used to estimate local exposures to traffic-related particles.

Results: Results from linear regression found PP and SBP positively associated with PM_2.5. For example, a 10-µg/m³ increase in PM_2.5 30-day mean was associated with 1.12 mmHg higher pulse pressure [95% confidence interval (CI) , 0.28–1.97] and 0.99 mmHg higher systolic BP (95% CI, –0.15 to 2.13) , adjusted for age, sex, race/ethnicity, income, education, body mass index, diabetes, cigarette smoking and environmental tobacco smoke, alcohol use, physical activity, medications, atmospheric pressure, and temperature. Results were much weaker and not statistically significant for MAP and DBP. Although traffic-related variables were not themselves associated with BP, the association between PM_2.5 and BP was stronger in the presence of higher traffic exposure.

Conclusions: Higher SBP and PP were associated with ambient levels of PM_2.5 and the association was stronger in the presence of roadway traffic, suggesting that impairment of blood pressure regulation may play a role in response to air pollution.

Key words: air pollution, blood pressure, cardiovascular disease, epidemiology, particulate matter. Environ Health Perspect 116:486–491 (2008) . doi:10.1289/ehp.10899 available via http://dx.doi.org/ [Online 24 January 2008]

Address correspondence to A.H. Auchincloss, Department of Epidemiology, School of Public Health, University of Michigan, 109 Observatory St., SPH Tower Room 3655, Ann Arbor, MI 48109-2029 USA. Telephone: (734) 615-9219. Fax: (734) 998-0006. E-mail: aauchinc@umich.edu

Supplemental Material is available online at http://www.ehponline.org/members/2008/10899/suppl.pdf

A.H.A. designed the study, analyzed data, and drafted the paper. A.V.D.R. contributed to study design and conceptualization, and edited drafts. J.T.D. assisted with conceptualization and commented on drafts. P.L.B. constructed data sets and commented on the paper. All other authors critically reviewed drafts and are listed in alphabetical order.

We thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org

MESA is supported by contracts N01-HC-95159 through N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood Institute. This work was supported by grants R830543 and RD831697 from the U.S. Environmental Protection Agency.

The authors declare they have no competing financial interests.

Received 19 September 2007 ; accepted 10 January 2008.