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Associations of endothelial dysfunction with exposure to ambient fine particles in diabetic subjects: are the effects modified by patient characteristics?
Citation:
Schneider, A., L. M. NEAS, M. HERBST, R. W. WILLIAMS, W. CASCIO, A. Hinderliter, F. Holguin, K. Dungan, M. Styner, A. Peters, AND R. B. DEVLIN. Associations of endothelial dysfunction with exposure to ambient fine particles in diabetic subjects: are the effects modified by patient characteristics? Presented at International Society for Environmental Epidemiology Annual Meeting, Pasadena, CA, October 12 - 16, 2008.
Impact/Purpose:
research results
Description:
Objective: Exposure to fme airborne particulate matter (PM2.5) has been shown to be responsible for cardiovascular and hematological effects, especially in older people with cardiovascular disease. Results of epidemiological studies suggest that subjects with diabetes may be a particularly susceptible population. The purpose of this study was to analyze the short-term effects ofPM2.5on markers ofendothelial function in diabetic patients with a focus on effect modification by patient characteristics. Methods: A prospective panel study was conducted on 22 people with diabetes in Chapel Hill, NC, from Nov 2004-Dec 2005. Each subject was studied for 4 consecutive days. Daily measurements ofPM2.5 were acquired from the Chapel Hill airport and meteorological data were measured on the rooftop ofthe patient exam site. Brachial artery flow mediated dilatation (FMD) measured by brachial artery ultrasound and small artery elasticity index (SAEI) measured by a pulsewave device were assessed during each subject visit. Potential effect modifiers such as body mass index (BMI), glycosylized haemoglobin (HbAlc), homocysteine, adiponectin, myeloperoxidase (MPO) as well as the intake ofstatins were examined. Moreover, gene¬environment interactions were analyzed with regard to the influence ofglutathione-S-transferases (GSTMl null and GSTPl), ofa polymorphism ofthe hemochromatosis gene HFE (H63D) and of the quinone oxidoreductase gene (NQ01) polymorphism P149S. Data were analyzed using random effects models adjusting for season, weekday and meteorology. Results: Results are presented for an increase of IOug/m" PM2.5 as percent changes ofmean outcome level with a 95% confidence interval. FMD decreased in association with PM2.5 exposure ofthe same day (-17.3% [-34.6%; 0.0%]). A similar reaction was found for SAEI but with a lag of 1 (-17.0% [-27.5%, -6.4%]) and 3 days (-15.1% [-29.3%, -0.9%]). Subjects with a BMI over 30 kg/m', with HbA 1cover 7%, with a homocysteine level over 12 umol/l or with adiponectin below 3700 ng/ml showed stronger effects. The FMD reaction was even more pronounced on days were the subject had an elevated MPO-level for same day exposure (-43.2% [-69.4%; -17.0%]), with a lag of 1 day (-30.7% [-59.9%; -1.4%]) and with a lag of2 days (-34.8% [-64.9%; -4.8%]). The intake ofstatins did not change the same day association ofFMD with PM. Subjects with the null polymorphism of GSTM1 showed a stronger association. The analysis indicated a trend for a stronger FMD effect with each copy of the valine-coding polymorphism of the GSTP 1 gene. Having one copy of the aspartic acid-coding variant ofthe HFE gene also seemed to slightly enhance endothelial dysfunction. Conclusion: These data demonstrate that PM exposure may cause immediate endothelial dysfunction and that certain patient characteristics, such as high BMI, elevated MPO or the presence of the null polymorphism ofGSTM1 may make some subjects more susceptible to PM exposure than others. This abstract of a proposed presentation does not necessarily represent EPA policy