Acute Platelet Responses to Ambient Particulate Matter

Abstract

ISEE-0758 Background and Objective: Increases in ambient particulate air pollution (PM) have been associated with acute cardiovascular events over the following few hours and days in epidemiologic studies. Within 1–2 hours of intratracheal instillation of ultrafine PM, acute prothrombotic changes indicative of platelet activation have been corroborated in rodent models. We hypothesized that inhalation of ambient fine PM (PM2.5) leads to increases in platelet activation over the next few hours and days. Methods: We measured blood platelet surface activation markers in 37 healthy human subjects during 1–3 clinic visits per subject, 1 week apart (n = 85 measurements). Specific monoclonal antibodies (PAC1, CD62p, CD42b, and CD36) and flow cytometry were used to determine the mean fluorescence (MF) of each of four platelet surface markers. Using mixed regression models, we estimated the change in MF of each platelet marker associated with ambient PM2.5 concentration in the previous 24 hours, as well as moving averages out to 144 hours. Results: Each 7.56 μg/m3 increase in PM2.5 concentration in the 24 hours before the clinic visit was associated with a significant 0.34 unit (95% CI = 0.00, 0.68) increase in PAC1 and 2.45 unit (95% CI = 0.16, 4.75) increase in CD42b, with similar size changes related to PM2.5 over the previous 48 hours. Estimated PAC1 and CD42b changes for the longer moving averages were smaller and non-significant. Nonwhites had an approximately 50% greater PAC1 change than whites, but there was no difference by gender. We observed no association between CD62p or CD36 and PM2.5. Conclusion: These data suggest an acute platelet response to increases in ambient PM2.5 concentration. Further analyses will examine effect modification by specific genetic factors and specific periods of the day (e.g. rush hour), and examine whether PM2.5 effects are more acute than 24 hours.