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Ambient source-specific particles are associated with prolonged repolarization and increased levels of inflammation in male coronary artery disease patients.
Mutat. Res. -Fund. Mol. Mech. Mutag. 621, 50-60 (2007)
Ambient particulate air pollution has been associated with altered cardiac function and systemic inflammation. We reported repolarization changes and variations in markers of inflammation in association with ambient particulate exposure in a panel of male coronary artery disease (CAD) patients. The objective of this analysis was to identify the specific sources associated with these effects. A panel of male CAD patients participated in 12 clinical visits in Erfurt, Germany. We used 56 patients’ 5 min ECG recordings for the analysis of repolarization parameters QT interval and T wave amplitude, and 57 patients’ plasma samples to determine the biomarkers von Willebrand factor (vWF) and C-reactive protein (CRP). Linear and logistic regression models were used to analyze the associations between five particle source factors (airborne soil, local traffic-related ultrafine particles, combustion-generated aerosols, diesel traffic-related particles, and secondary aerosols) and these health parameters adjusting for trend, weekday and meteorological variables. An increase in QT interval and a decrease in T wave amplitude were observed in association with traffic-related particles exposure during 0–23 h before the ECG recordings. The inflammatory marker vWF increased in association with both traffic-related particles and combustion-generated aerosols at different exposure lags. All source particles had positive associations with CRP levels above the 90th percentile (8.5 mg/l). These results suggest that traffic-related and combustion-generated particles show stronger adverse health impact with regard to cardiac effects, and that particles from different sources induce an acute phase response in these patients.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Coronary artery disease; Fine particulate; Inflammation; Repolarization; Source apportionment
ISSN (print) / ISBN 0027-5107
Quellenangaben Volume: 621, Pages: 50-60
Reviewing status Peer reviewed
Institute(s) Institute of Epidemiology (EPI)