Associations between cardiac-specific troponin concentrations and short-term ambient PM2.5 among myocardial infarction survivors
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Background/Aim: Fine particulate matter (PM2.5) is associated with cardiovascular disease. One potential mechanism is via cardiac tissue damage. Here, we study the association between ambient PM2.5 and troponin I, a biomarker for cardiac muscle damage, among myocardial infarction (MI) survivors. Methods: Our data was taken from electronic health records from University of North Carolina affiliated hospitals and comprised individuals seen between 2004 and 2016 who had a prior MI. Daily ambient PM2.5 (µg/m3) was estimated using a neural network at 1km resolution. After excluding troponin I measurements within 7 days of a clinically indicated MI, we assessed daily ambient PM2.5 concentrations with troponin I blood concentrations using linear mixed effect models adjusted for age, race, sex, socioeconomic status, temperature, relative humidity, and time trend. Associations were estimated per 1 µg/m3 increase in PM2.5 for daily lags (up to 4 days prior) and the 2-day rolling average. Results: There were 71,970 troponin I measurements from 12,019 individuals that occurred outside a clinically diagnosed MI. Same day and prior day PM2.5 concentrations were both associated with elevated troponin with stronger associations on the prior day (0.062 ng/mL per 1 µg/m3 increase in PM2.5; 95 % Confidence Interval [CI]: 0.04, 0.08). Associations weakened with increasing lags and no association was seen at 3 and 4-day prior PM2.5 concentrations. Two day rolling averages showed a similar pattern with associations strongest for the same day and day prior average (0.05 ng/mL higher troponin per 1 µg/m3 PM2.5; 95% CI: 0.03, 0.07). Conclusions: We observed that short-term changes in PM2.5 were associated with increased blood troponin concentrations among MI survivors. These results suggest that short-term elevations in ambient PM2.5 may be directly associated with cardiac tissue damage, and present a mechanism for PM2.5-induced cardiovascular events. This abstract does not reflect EPA policy.