Research

Long-Term Air Pollution in Relation to Cardiac Structure, Function, and Supraventricular Arrhythmias

Thomas Austin | 2020

Advisor: Susan R. Heckbert

Research Area(s): Cardiovascular & Metabolic Disease, Environmental & Occupational Health


Background: Air pollution is an important contributor to cardiovascular morbidity, including risk of heart failure. Acute exposure is associated with inflammation, elevation of blood pressure, and episodes of atrial fibrillation (AF). However, less is understood about how long-term exposures may influence measures of atrial and ventricular structure and function, including supraventricular arrhythmias. No large longitudinal analyses have investigated these associations. Methods: In the setting of the Multi-Ethnic Study of Atherosclerosis (MESA), we investigated associations of participant-specific, spatiotemporal model-estimated concentrations of fine particulate matter (PM2.5), oxides of nitrogen (NOX), and ozone (O3) with both cardiac magnetic resonance imaging-derived measures of left atrial (LA) and left ventricular (LV) structure and function, as well as with supraventricular arrhythmias identified from 14-day ambulatory electrocardiography (ECG) monitors worn by participants. Multivariable linear regression and generalized estimating equations were used, adjusting for potential confounders including MESA study site. Results: Among 2,250 participants at MESA Exam 5 (2010-2012), five-year average exposure to PM2.5, NOX, and O3 was not significantly associated with measures of left atrial structure and contractility. Among 1,324 MESA participants with ambulatory ECG monitoring at MESA Exam 6 (2016–2018), five-year average concentration of pollutants was not associated with supraventricular arrhythmias, though high two-week average concentration of PM2.5 was associated with increased rates of supraventricular tachycardia (23% higher per 5ug/m3, 95% CI: 4%-46%). Higher one-year average pollutant concentration prior to MESA Exam 1 (2000-2002) was associated with greater left-ventricular mass index (LVMI) for NOX (1.8% per 40 parts per billion [ppb] NOX, 95% CI: 0.3, 3.3) and PM2.5 (1.6% per 5ug/m3 higher PM2.5, 95% CI: 0.3, 2.9), and lower LVMI for O3 (-3.5% per 10ppb O3). Greater ten-year average NOX concentration between Exams 1 and 5 was associated with reduced LV contractility as measured by left-ventricular circumferential strain, though this association was only marginally significant. All analyses were sensitive to adjustment for MESA study site. Conclusions: Our study offers mixed evidence for an association of long-term concentrations of PM2.5, NOX, and O3 with cardiac structure and function. We did not find evidence of associations between pollutants and LA structure, and the association of PM2.5 with supraventricular tachycardia was minimal and confined to two-week pollutant concentrations. We identified significant associations between long-term pollutant concentrations and cross-sectional LVMI in the direction hypothesized for PM2.5 and NOX, and opposite that hypothesized for O3, though the strong inverse correlation between O3 and both PM2.5 and NOX may influence this finding. These findings suggest a role for NOX, PM2.5, and O3 in influencing cardiac structure in MESA. Additional work is needed to clarify that role and better understand the biological underpinnings of these associations.