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      Associations between Recent Exposure to Ambient Fine Particulate Matter and Blood Pressure in the Multi-Ethnic Study of Atherosclerosis (MESA)

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          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/m 3 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.

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          Most cited references45

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          Exposure measurement error in time-series studies of air pollution: concepts and consequences.

          Misclassification of exposure is a well-recognized inherent limitation of epidemiologic studies of disease and the environment. For many agents of interest, exposures take place over time and in multiple locations; accurately estimating the relevant exposures for an individual participant in epidemiologic studies is often daunting, particularly within the limits set by feasibility, participant burden, and cost. Researchers have taken steps to deal with the consequences of measurement error by limiting the degree of error through a study's design, estimating the degree of error using a nested validation study, and by adjusting for measurement error in statistical analyses. In this paper, we address measurement error in observational studies of air pollution and health. Because measurement error may have substantial implications for interpreting epidemiologic studies on air pollution, particularly the time-series analyses, we developed a systematic conceptual formulation of the problem of measurement error in epidemiologic studies of air pollution and then considered the consequences within this formulation. When possible, we used available relevant data to make simple estimates of measurement error effects. This paper provides an overview of measurement errors in linear regression, distinguishing two extremes of a continuum-Berkson from classical type errors, and the univariate from the multivariate predictor case. We then propose one conceptual framework for the evaluation of measurement errors in the log-linear regression used for time-series studies of particulate air pollution and mortality and identify three main components of error. We present new simple analyses of data on exposures of particulate matter < 10 microm in aerodynamic diameter from the Particle Total Exposure Assessment Methodology Study. Finally, we summarize open questions regarding measurement error and suggest the kind of additional data necessary to address them. Images Figure 1 Figure 2 Figure 3
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            Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults.

            Fine particulate air pollution and ozone are associated with increased cardiovascular events. To help explain the mechanism behind these observations, we investigated the effect of air pollution exposure on vascular function. Twenty-five healthy adults underwent a randomized, double-blind, crossover study comparing the vascular response to the 2-hour inhalation of approximately 150 microg/m(3) of concentrated ambient fine particles (CAP) plus ozone (120 ppb) versus the response to the inhalation of filtered air. High-resolution vascular ultrasonography was used to measure alterations in brachial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD). Exposure to CAP plus ozone caused a significant brachial artery vasoconstriction compared with filtered air inhalation (-0.09+/-0.15 mm versus +0.01+/-0.18 mm, P=0.03). There were no significant differences in FMD (+0.29+/-4.11% versus -0.03+/-6.63%, P=0.88), NMD (+3.87+/-5.43% versus +3.46+/-7.92%, P=0.83), or blood pressure responses between exposures. Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.
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              Ambient Air Pollution and Atherosclerosis in Los Angeles

              Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 μm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects’ residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 μg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 μg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1–11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9–4.3% (p-values, 0.05–0.1). Among older subjects (≥60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women ≥60 years of age (15.7%, 5.7–26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                April 2008
                24 January 2008
                : 116
                : 4
                : 486-491
                Affiliations
                [1 ] Department of Epidemiology and
                [2 ] Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA
                [3 ] Department of Atmospheric Sciences, School of Engineering, University of Michigan, Ann Arbor, Michigan, USA
                [4 ] Departments of Medicine and Epidemiology, Columbia University Medical Center, New York, New York, USA
                [5 ] Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
                [6 ] Department of Public Health Sciences, School of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA
                [7 ] Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, Washington, USA
                Author notes
                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@ 123456umich.edu

                The authors declare they have no competing financial interests.

                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.

                Article
                ehp0116-000486
                10.1289/ehp.10899
                2291007
                18414631
                1b4b6419-d30e-44aa-ab03-3f50696ab18a
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 19 September 2007
                : 10 January 2008
                Categories
                Research

                Public health
                particulate matter,epidemiology,air pollution,blood pressure,cardiovascular disease
                Public health
                particulate matter, epidemiology, air pollution, blood pressure, cardiovascular disease

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