The Effects of Ambient Air Pollution and Particle Radioactivity on Cardiovascular Health

Abstract

ABSTRACT Exposure to ambient air pollution is a well-recognized risk factor for cardiovascular morbidity and mortality. Studies have shown that air pollution, especially acute exposure to traffic and industrial sources, can influence the autonomic nervous system and in turn affect heart rate variability leading to arrhythmias. While some studies examine acute air pollution effects on ventricular arrhythmias or heart rate corrected QT interval (QTc), few have explored both acute and long-term effects in a mixture of components. Studies tend to focus on fine particulate matter, which can penetrate deep into the lungs due to its smaller size and deposit a large spectrum of organic and inorganic elements1. However, fewer studies have examined which specific elements of fine particulate matter can contribute to cardiovascular toxicity. This dissertation investigates how multiple components of ambient air pollution can impact cardiovascular health. We hypothesized that different components of fine particulate matter may have a direct impact on arrythmias and ventricular repolarization. In particular, we theorized that all the PM2.5 components would either increase the risk for ventricular arrythmias or prolong QT interval, but we expected PM2.5 mass, lead, nickel and elemental carbon to have the largest adverse effects based on past literature.

In our first study, we assessed the association of the onset of ventricular arrhythmias with 0-21 day moving averages of PM2.5 and particle radioactivity using time-stratified case-crossover analyses among 176 patients with dual-chamber implanted cardioverter-defibrillators in Boston, Massachusetts. We found that in this high-risk population, independently of particle radioactivity, 21-day PM2.5 exposure was associated with higher odds of a ventricular arrhythmia event onset among patients with known cardiac disease and indication for ICD implantation.

In our second study, we utilized time-varying linear mixed-effects regressions with a random intercept for each participant to analyze associations between QTc interval and moving averages (0 to 7 day moving averages) of 24-hour mean concentrations of PM2.5 metal components (vanadium, nickel, copper, zinc and lead) in the Normative Aging Study. We found that exposure to metals (especially lead and copper) contained in PM2.5 were associated with acute changes in ventricular repolarization as indicated by prolonged QT interval length.

Finally, we utilized time-varying linear mixed-effects regressions to examine associations between acute (0-3 day), intermediate (4-28 day) and long-term (1 year) exposure to components of fine particulate air pollution (PM2.5 mass, elemental carbon, organic carbon, nitrate, sulfate, ozone), temperature and heart-rate corrected QT interval (QTc). We also evaluated whether diabetic status would modify the association between the PM2.5 components and QTc interval. We found consistent results that higher sulfate levels were associated with significant longer QTc across all moving averages and that organic carbon also increased QTc interval, but for different time periods depending on the model. We found that diabetic status could amplify the association between certain PM2.5 components (elemental carbon, nitrate, organic carbon and sulfate) and QTc interval.