Abstract

ISEE-733 Objective: The effects of particulate air pollution on cardiovascular diseases have been suggested to be mediated through inflammatory processes. However, the exact mechanisms are not known. Therefore, we evaluated the associations between personal exposure to fine particles (PM2.5; particles <2.5 μm) and serum levels of interleukin (IL)-12, a cytokine abundant in atherosclerotic plaques and capable of inducing T-helper (Th)1 type immune response. Materials and Methods: Persons with coronary artery disease were followed in the city of Kotka, Finland, for 6 months with biweekly clinic visits. During the visits, blood samples were collected for the determination of circulating levels of IL-12 and several other cytokines. The study participants carried PM2.5 samplers during the 24 hours preceding the clinic visit. Filter samples were weighed to calculate mass concentrations, and measured with a reflectometer to obtain the values of absorbance, an indicator of elemental carbon. Associations between particulate air pollution and log-transformed levels of IL-12 were evaluated using mixed models and penalized splines. Effect estimates are presented as percent changes of geometric mean per interquartile increase in exposure. Results: There were 49 study participants for whom at least 4 clinic visits were available and altogether 453 visits for which filter samples were also available. Personal exposures to both PM2.5 and absorbance were associated with IL-12; effect estimates (95% confidence interval) were 2.8% (−0.1; 5.7) and 6.1% (1.75; 10.4), respectively. Results for other cytokines will be presented for comparison. Conclusions: Our preliminary results suggest that exposure to fine particles, especially of combustion origin, is associated with increased levels of IL-12, which may contribute to plaque instability.

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