Increased Particulate Air Pollution and Markers of Platelet Aggregation

Abstract

Background: Increased particulate air pollutant concentrations (PM) have previously been associated with platelet aggregation. Aspirin has been shown to protect against cardiovascular (CV) events. We hypothesized that increased ambient PM concentrations would be associated with increased markers of platelet aggregation, and that aspirin would lessen this response. Methods: We used data from a sequential therapy trial of aspirin and fish oil (n=30 subjects; 4 blood samples; 10/2010-3/2012) in type II diabetes patients. Using linear mixed models, we estimated changes in 3 platelet measures (aggregation induced by adenosine diphospate [ADP] or collagen, and thromboxane production) associated with interquartile range (IQR) increases in 1 to 96 hour mean concentrations of ambient PM2.5, black carbon, ultrafine particle (UFP; 10-100nm), and accumulation mode particle (AMP; 100-500nm) concentrations. Results: IQR increases in mean UFP and AMP concentrations were associated with significant decreases in platelet function, with the largest being a -1.7 ohm reduction in collagen-induced aggregation (95% CI= -3.1, -0.3) associated with each 2097 particles/cm3 increase in UFP, and a -0.43 decrease in log(thromboxane; pg/mL; 95% CI=-0.8, -0.1) associated with each 582 particles/cm3 increase in AMP, both in the previous 72 hours. We found no associations with PM2.5 or black carbon. Further, this UFP effect on thromboxane was greater when taking aspirin (-0.6; 95% CI = -1.0, -0.3) then when not (-0.0; 95% CI = -0.4, 0.3; interaction p=0.003). Conclusions: Inconsistent with our a priori hypothesis, we found that decreased platelet thromboxane production and collagen-induced aggregation were associated with increased UFP and AMP levels in the previous 3-4 days, with aspirin increasing this effect. The reason for this is unclear, but may be related to the disrupted lipid milieu and aspirin insensitivity in patients with type 2 diabetes.