Claire L Leiser, Daniela Sotres-Alvarez, Haeyoon Chang, Elizabeth W Spalt, Barry E Hurwitz, Martha L Daviglus, Greg Talavera, Robert Kaplan, Bonnie E Shook-Sa, Carlos J Rodriguez, Joel D Kaufman
Our findings suggest that common air pollutant exposures are associated with longitudinal preclinical adverse changes in cardiac structure and function.
BACKGROUND: The effects of air pollutants on cardiac structure and function preceding the clinical diagnosis of heart failure are not well understood.
OBJECTIVES: The objective of the study was to determine if ambient pollutant concentrations are associated with longitudinal changes in cardiac structure and function.
METHODS: Measures of cardiac structure and function were serially assessed by echocardiogram at visits 1 (2008-2011) and 2 (2015-2018), respectively, with a median follow-up of 4.3 years (IQR: 4.0-4.4 years). Outdoor air pollution concentrations at residence were estimated from spatio-temporal models, as mean concentrations the year prior to each visit. We determined longitudinal relationships between air pollution and each echocardiographic measure, adjusted for baseline and time-varying covariates.
RESULTS: Echocardiographic data were available on 1,630 individuals; mean age was 55.3 years at visit 1. Per IQR of pollutant, higher mean residential concentrations of particulate matter air pollution <2.5 µm in aerodynamic diameter (particulate matter 2.5 [PM2.5]) and traffic-related air pollutant gas (nitrogen dioxide) were associated with a 0.52% (95% CI: 0.20-0.83) and 0.12% (95% CI: 0.03-0.20) increase in global longitudinal strain, respectively. Higher PM2.5 and nitrogen dioxide were associated with decreased left atrial volume index: -1.39 (95% CI: -2.25 to -0.54) and -0.94 (95% CI: -1.63 to -0.26) respectively. PM2.5 was associated with a decrease in left ventricular ejection fraction of -1.05% per year (95% CI: -1.73 to -0.37) and increase in relative wall thickness by 0.12 (95% CI: 0.05-0.19) unit.
CONCLUSIONS: Our findings suggest that common air pollutant exposures are associated with longitudinal preclinical adverse changes in cardiac structure and function.