Abstract
BackgroundExposure to traffic-related air pollution (TRAP) is considered a trigger for acute cardiovascular events. Diesel Exhaust (DE) is a major contributor to TRAP in the world. We evaluated the effect of DE inhalation on circulating blood cell populations, hematological indices, and systemic inflammatory cytokines in humans using a specialized facility.MethodsIn a randomized double-blind crossover study balanced to order, 17 metabolic syndrome (MetS) and 15 healthy subjects inhaled filtered air (FA) or DE exposure in two-hour sessions on different days with a minimum 2-week washout period. We collected blood pre-exposure, 7, and 22 hours after exposure initiation and measured the complete blood count and differential. We performed multiplex cytokine assay to measure the changes in the systemic inflammatory cytokines, and endothelial adhesion molecules (n=15). A paired analysis compared the effect of DE and FA exposures for the change from pre-exposure to the subsequent time points.ResultsA significant increase in the hematocrit was noted 7 hrs after DE [1.4% (95% CI: 0.9 to 1.9%)] compared to FA exposure [0.5% (95% CI: -0.09 to 1.0%); p=0.008. The hemoglobin levels increased non-significantly at 7 hrs post DE [0.3 gm/dL (95% CI: 0.2 to 0.5 gm/dL)] versus FA exposure [0.2 gm/dL (95% CI: 0 to 0.3 gm/dL)]; p=0.06. Furthermore, the platelet count increased 22 hrs after DE exposure in healthy, but not in MetS subjects [DE: 16.6 (95% CI: 10.2 to 23) thousand platelets/mL versus [FA: 3.4 (95% CI: -9.5 to 16.3) thousand platelets/mL)]; p=0.04. No DE effect was observed for WBC, neutrophils, lymphocytes or erythrocytes. Using the multiplex assay, small borderline significant increases in matrix metalloproteinase-9, interleukins (IL)-1beta, 6 and 10 occurred 7 hrs post exposure initiation, whereas E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule -1, and myeloperoxidase 22 hrs post exposure.ConclusionsOur results suggest that short-term DE exposure results in hemoconcentration and thrombocytosis, which are important determinants of acute cardiovascular events. Multiplex assay showed a non-significant increase in IL-1β and IL-6 immediately post exposure followed by myeloperoxidase and endothelial activation molecules. Further specific assays in a larger population will improve our understanding of the systemic inflammatory mechanisms following acute exposure to TRAP.Clinical trials registration numberStudy was conducted between 2004 to 2006, prior to expectation for registration.
Highlights
Exposure to traffic-related air pollution (TRAP) is considered a trigger for acute cardiovascular events
Effects of diesel exhaust on endothelial adhesion molecules and inflammatory cytokines: results from the multiplex cytokine assay Using the multiplex assay, we found that the endothelial cell adhesion molecules E- selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) showed a small trend toward increase in the plasma following Diesel Exhaust (DE) exposure when compared to filtered air (FA) exposure at 22 hours, but variability in measurements was very high and no significant findings were detected (Table 3)
We found that the mean change in the IL-6 level following DE exposure was increased at 7 hours following DE [0.6 pg/mL,]; but not following FA [0.1 pg/mL,] at 7 hours post-exposure
Summary
Exposure to traffic-related air pollution (TRAP) is considered a trigger for acute cardiovascular events. Exposure to traffic related air pollution has been shown to trigger acute cardiovascular events and deaths primarily due to myocardial infarction [1,2,3,4]. Air pollutant components may induce these responses through vascular endothelial cells, leukocytes, and/or platelets, with expression of inflammatory cytokines, cellular adhesion molecules, viscosity of blood, and coagulation factors [7]. Activation of these inflammatory pathways potentially lead to increased vascular reactivity or vasoconstriction, [8,9] endothelial dysfunction, [10] and possibly plaque rupture triggering acute myocardial infarction or ischemia. We hypothesized that DE would affect peripheral blood cell counts, hematological indices, and systemic cytokine production in healthy and metabolic syndrome subjects
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