Long-term exposure to ambient air pollution and measures of central hemodynamics and arterial stiffness among multiethnic Chicago residents

Abstract

Objectives: To examine whether air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters.

Methods: We assessed central hemodynamic parameters, brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes.

Results: The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013-2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-μg/m³ increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01).

Conclusion: This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans.

Figure 1:

Stratified analysis on associations between long-term PM2 5 (A) and N02 (B) exposure (unit increments, 1 μg/m³ fox PM2.5. and 1 ppb for N02) and systolic blood pressure (cSBP). and pulse pressure (cPP). Effect estimates (coefficients) are derived from mixed effect analysis, and bars cover 95% confidence intervals. Results were obtained from final models with participants having stable residence history and adjusted for age (not in age-stratified analysis), BMI (not in BMI-stratified analysts), race (not in race-stratified analysis), sex (not in sex-stratified analysis), smoking status (not in smoking status-stratified analysis), waist, alcohol consumption, education, income, marital status, season, Type 2 diabetes, and hypertension.

Figure 2:

Stratified analysis on associations between long-term PM2.5 (A) and N02 (B) exposure (unit increments, 1 μg/m³ for PM2.5, and 1 ppb for N02) and brachial artery distensibility (BAD), brachial artery compliance (BAC) and systemic vascular compliance (SVC). Effect estimates (coefficients) are derived from mixed effect analysis, and bars cover 95% confidence intervals. Results were obtained from final models with participants having stable residence history and adjusted for age (not in age-stratified analysis). BMI (not in BMI-stratified analysis), race (not in race-stratified analysis), sex (not in sex-stratified analysis), smoking status (not in smoking status-stratified analysis), waist, alcohol consumption, education, income, marital status, season. Type 2 diabetes, and hypertension.