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BACKGROUND: Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined crosssectional associations between short-term ambient fine particles (particulate matter <= 2.5 [mu]m in aerodynamic diameter; PM2.5) 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 PM2.5 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 PM2.5 For example, a 10-[mu]g/m(3) increase in PM2.5 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 PM2.5 and BP was stronger in the presence of higher traffic exposure. CONCLUSIONS: Higher SBP and PP were associated with ambient levels of PM2.5 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. [ABSTRACT FROM AUTHOR]

Background: Air pollution exposures are hypothesized to impact blood pressure, yet few longitudinal studies exist, their findings are inconsistent, and different adjustments have been made for potentially distinct confounding by calendar time and age., Objective: We aimed to investigate the associations of long- and short-term [Formula: see text] and [Formula: see text] concentrations with systolic and diastolic blood pressures and incident hypertension while also accounting for potential confounding by age and time., Methods: Between 2000 and 2012, Multi-Ethnic Study of Atherosclerosis participants were measured for systolic and diastolic blood pressure at five exams. We estimated annual average and daily [Formula: see text] and [Formula: see text] concentrations for 6,569 participants using spatiotemporal models and measurements, respectively. Associations of exposures with blood pressure corrected for medication were studied using mixed-effects models. Incident hypertension was examined with Cox regression. We adjusted all models for sex, race/ethnicity, socioeconomic status, smoking, physical activity, diet, season, and site. We compared associations from models adjusting for time-varying age with those that adjusted for both time-varying age and calendar time., Results: We observed decreases in pollution and blood pressures (adjusted for age and medication) over time. Strong, positive associations of long- and short-term exposures with blood pressure were found only in models with adjustment for time-varying age but not adjustment for both time-varying age and calendar time. For example, [Formula: see text] higher annual average [Formula: see text] concentrations were associated with 2.7 (95% CI: 1.5, 4.0) and [Formula: see text] (95% CI: [Formula: see text] 1.0) mmHg in systolic blood pressure with and without additional adjustment for time, respectively. Associations with incident hypertension were similarly weakened by additional adjustment for time. Sensitivity analyses indicated that air pollution did not likely cause the temporal trends in blood pressure., Conclusions: In contrast to experimental evidence, we found no associations between long- or short-term exposures to air pollution and blood pressure after accounting for both time-varying age and calendar time. This research suggests that careful consideration of both age and time is needed in longitudinal studies with trending exposures. https://doi.org/10.1289/EHP2966.

Background: Although research has shown that low socioeconomic status (SES) and minority communities have higher exposure to air pollution, few studies have simultaneously investigated the associations of individual and neighborhood SES with pollutants across multiple sites., Objectives: We characterized the distribution of ambient air pollution by both individual and neighborhood SES using spatial regression methods., Methods: The study population comprised 6,140 participants from the Multi-Ethnic Study of Atherosclerosis (MESA). Year 2000 annual average ambient PM2.5 and NOx concentrations were calculated for each study participant's home address at baseline examination. We investigated individual and neighborhood (2000 U.S. Census tract level) SES measures corresponding to the domains of income, wealth, education, and occupation. We used a spatial intrinsic conditional autoregressive model for multivariable analysis and examined pooled and metropolitan area-specific models., Results: A 1-unit increase in the z-score for family income was associated with 0.03-μg/m3 lower PM2.5 (95% CI: -0.05, -0.01) and 0.93% lower NOx (95% CI: -1.33, -0.53) after adjustment for covariates. A 1-SD-unit increase in the neighborhood's percentage of persons with at least a high school degree was associated with 0.47-μg/m3 lower mean PM2.5 (95% CI: -0.55, -0.40) and 9.61% lower NOx (95% CI: -10.85, -8.37). Metropolitan area-specific results exhibited considerable heterogeneity. For example, in New York, high-SES neighborhoods were associated with higher concentrations of pollution., Conclusions: We found statistically significant associations of SES measures with predicted air pollutant concentrations, demonstrating the importance of accounting for neighborhood- and individual-level SES in air pollution health effects research.

Background: Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events., Objective: We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites., Methods: We assigned pollution exposure during two decades preceding a clinical exam (2000-2002) using observed PM10 from monitors nearest participants' residences and PM10 and PM2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young's modulus (YM) from carotid artery ultrasound and large (C1) and small (C2) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m3 increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C1 and C2 models were further adjusted for heart rate, weight, and height., Results: Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C1, or C2, and the few associations observed were not robust across metrics and adjustment schemes., Conclusions: Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.

Background: Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter ≤ 2.5 µm in diameter (PM2.5) and cardiovascular disease (CVD). We examined the associations of PM2.5 with heart rate variability, a marker of autonomic function, and whether metabolic syndrome (MetS) modified these associations., Methods: We used data from the Multi-Ethnic Study of Atherosclerosis to measure the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive differences (rMSSD) of 5,465 participants 45-84 years old who were free of CVD at the baseline examination (2000-2002). Data from the U.S. regulatory monitor network were used to estimate ambient PM2.5 concentrations at the participants' residences. MetS was defined as having three or more of the following criteria: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein cholesterol, high blood pressure, and high fasting glucose., Results: After controlling for confounders, we found that an interquartile range (IQR) increase in 2-day average PM2.5 (10.2 µg/m3) was associated with a 2.1% decrease in rMSSD [95% confidence interval (CI), -4.2 to 0.0] and nonsignificantly associated with a 1.8% decrease in SDNN (95% CI, -3.7 to 0.1). Associations were stronger among individuals with MetS than among those without MetS: an IQR elevation in 2-day PM2.5 was associated with a 6.2% decrease in rMSSD (95% CI, -9.4 to -2.9) among participants with MetS, whereas almost no change was found among participants without MetS (p-interaction = 0.005). Similar effect modification was observed in SDNN (p-interaction = 0.011)., Conclusion: These findings suggest that autonomic dysfunction may be a mechanism through which PM exposure affects cardiovascular risk, especially among persons with MetS.