Abstract P067: Left Ventricular Hypertrophy And Inflammation Modify The Harmful Effects Of Fine Particulate Matter On Sudden Death

Abstract

Sudden death accounts for approximately 10% of deaths among working age adults and is associated with poor air quality. We hypothesize that clinical risk factors for sudden death would modify the relationship of fine particulate matter (PM 2.5 ) to sudden death. Sudden death victims in Wake County, NC from 3/1/2013 - 2/28/2015 were identified by screening Emergency Medical Services (EMS) reports and adjudicated based on EMS, medical, and death records (n=399). Daily PM 2.5 concentrations for Wake County from the Air Quality Data Mart were linked to event and control periods for each individual. Using a case-crossover design, conditional logistic regression estimated OR (95%CI) for sudden death for a 5μg/m 3 increase in PM 2.5 with a 1-day lag, adjusted for temperature and humidity, across risk factor strata. Sensitivity analysis assessed consistency of main effects. Left ventricular hypertrophy (LVH) and neutrophil to lymphocyte ratio (NLR) were included as estimates of arrhythmic potential and inflammation, respectively. Low concentrations of PM 2.5 are potential risk factors for sudden death (Table 1). However, no clinical risk factors for sudden death modify that association. LVH and NLR, in contrast to clinical risk factors, are associated PM 2.5 and sudden death. Sensitivity analysis had no effect on the direction and minimal effect on the magnitude of the associations. Left ventricular hypertrophy and inflammation may be the final step in the mechanism whereby poor air quality and clinical risk factors trigger arrhythmia or myocardial ischemia and sudden death. This abstract does not necessarily reflect EPA policy.