Vascular responses to long- and short-term exposure to fine particulate matter: MESA Air (Multi-Ethnic Study of Atherosclerosis and Air Pollution)

Abstract

Objectives: This study evaluated the association of long- and short-term air pollutant exposures with flow-mediated dilation (FMD) and baseline arterial diameter (BAD) of the brachial artery using ultrasound in a large multicity cohort.

Background: Exposures to ambient air pollution, especially long-term exposure to particulate matter <2.5 μm in aerodynamic diameter (PM(2.5)), are linked with cardiovascular mortality. Short-term exposure to PM(2.5) has been associated with decreased FMD and vasoconstriction, suggesting that adverse effects of PM(2.5) may involve endothelial dysfunction. However, long-term effects of PM(2.5) on endothelial dysfunction have not been investigated.

Methods: FMD and BAD were measured by brachial artery ultrasound at the initial examination of the Multi-Ethnic Study of Atherosclerosis. Long-term PM(2.5) concentrations were estimated for the year 2000 at each participant's residence (n = 3,040) using a spatio-temporal model informed by cohort-specific monitoring. Short-term PM(2.5) concentrations were based on daily central-site monitoring in each of the 6 cities.

Results: An interquartile increase in long-term PM(2.5) concentration (3 μg/m(3)) was associated with a 0.3% decrease in FMD (95% confidence interval [CI] of difference: -0.6 to -0.03; p = 0.03), adjusting for demographic characteristics, traditional risk factors, sonographers, and 1/BAD. Women, nonsmokers, younger participants, and those with hypertension seemed to show a greater association of PM(2.5) with FMD. FMD was not significantly associated with short-term variation in PM(2.5) (-0.1% per 12 μg/m(3) daily increase [95% CI: -0.2 to 0.04] on the day before examination).

Conclusions: Long-term PM(2.5) exposure was significantly associated with decreased endothelial function according to brachial ultrasound results. These findings may elucidate an important pathway linking air pollution and cardiovascular mortality.

Trial registration: ClinicalTrials.gov NCT00005487.

Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1. Distribution of the PM2.5 Concentrations

(A) Long-term particulate matter <2.5 μm in aerodynamic diameter (PM2.5) concentrations estimated for the year 2000 annual average. (B) Short-term PM2.5 concentrations for 2 days before the brachial examination. Similar distribution pattern was seen for all other averaging time points.

Figure 2. Dose-Response Associations Between Brachial Outcomes and Modeled Long-Term Pollutant Concentrations After Controlling for Covariates

The values for (A) baseline arterial diameter (BAD) and (B) flow-mediated dilation (FMD) represent partial residuals from a final model controlled for age, gender, ethnicity, body surface area, sonographer, income, education, smoking, alcohol use, dietary fat intake, emotional distress, physical activity, waist to hip ratio, systolic blood pressure, diastolic blood pressure, total cholesterol, high-density lipoprotein, C-reactive protein, fibrinogen, homocysteine, fasting blood glucose, anti-inflammatory agents, antihypertensive agents, lipid-lowering drugs, and vitamin C. FMD% includes adjustment for 1/BAD. Data are plotted as penalized thin-plate regression splines with smoothness parameter selected by generalized cross-validation for BAD and FMD%.