Abstract

ISEE-141 Introduction: Particulate air pollution has been implicated as a cause of several adverse cardiovascular health outcomes, and people with diabetes may have special vulnerability. One potential pathway is inflammation and endothelial dysfunction, processes in which cell adhesion molecules play important roles. Levels of soluble intercellular adhesion molecule (ICAM) in the plasma have been shown to predict cardiovascular events, independent of other known risk factors. Aim: We examined whether levels of plasma ICAM were associated with particle exposure in a cross-sectional study of 92 Boston area residents with Type II diabetes. Methods: Integrated 24-hour ambient concentrations of particulate matter [(fine particles (PM2.5), black carbon (BC), and sulphates (SO42-)] were measured approximately 500 meters from the patient exam site. Pollutant concentrations were evaluated for associations with ICAMs. Linear regressions were fit to log-transformed ICAM concentration data with the particulate pollutant index, apparent temperature, season, age, race, sex, smoking history, body mass index, total cholesterol, and HbA1c, an indicator of longer-term glycaemic control, as predictors. Pollutant concentrations for the day of examination, one day previous, and moving averages up to six days previous, were evaluated in single pollutant models. Results: We express results as percent change in ICAM per interquartile range (IQR) increase in the pollutant at lag 0, which were: PM2.5: 7.5 mg/m3, BC: 0.7 mg/m3, SO4: 2.2 mg/m3. Point estimates for the associations of BC concentrations with ICAMs were positive at all averaging periods, and significantly so for the six day moving average [11.8% increase in plasma ICAM per IQR of BC, 95% confidence interval (CI): (1.0%, 23.8%)] and for the three day moving average [8.0%, 95% CI: (0.3%, 16.3%)]. Point estimates for the associations between PM2.5and SO4and plasma ICAM were all positive, but none significant. Conclusion: These results suggest that BC particle exposure may be involved in inflammatory pathways that increase the sensitivity of people with diabetes to air pollution. Further evaluation of these associations by using differing covariate specifications are planned to assess the robustness of the relationship. This work contributes to understanding of mechanisms behind associations of air pollution with cardiovascular events in vulnerable populations. Funding: 5 T32 ES07069-22, NIEHS ES00002, EPAR827353, 5P01ES09825, Robert Wood Johnson Foundation Health & Society Scholars Program, Pfizer Inc., American Diabetes Association; Parke Davis Inc., Pfizer, Inc., the Juvenile Diabetes Foundation International; NIH 2P30-DK-36836; NIH RR 01032, William Randolph Hearst Foundation; Iacocca Foundation

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