gms | German Medical Science

Kongress Medizin und Gesellschaft 2007

17. bis 21.09.2007, Augsburg

Air pollution and inflammation (Il-6, Fibrinogen, CRP) in myocardial infarction survivors

Meeting Abstract

  • Regina Rückerl - GSF Forschungszentrum für Umwelt und Gesundheit, Institut für Epidemiologie, Neuherberg
  • Sonja Greven - Ludwig-Maximilians-Universität, Institut für Statistik, München
  • Petter Ljungman - Institute of Environmental Medicine, Karolinska Institute, Stockholm
  • Pasi Aalto - University of Helsinki, Department of Physical Sciences, Helsinki
  • Charalambos Antoniades - University of Athens, Department of Hygiene and Epidemiology, Athen
  • Tom Bellander - Karolinska Institute und Department of Occupational and Environmental Health, Stockholm County Council, Stockholm
  • Niklas Berglind - Institute of Environmental Medicine, Karolinska Institute, Stockholm
  • Christina Chrysohoou - University of Athens, Department of Hygiene and Epidemiology, Athen
  • Francesco Forastiere - Local Health Authority RM E, Department of Epidemiology ASL RME, Rom
  • Bénédicte Jacquemin - Municipal Institute of Medical Research (IMIM), Barcelona
  • Stephanie von Klot - GSF Forschungszentrum für Umwelt und Gesundheit, Institut für Epidemiologie, Neuherberg
  • Wolfgang Koenig - Department of Internal Medicine II, Cardiology, University of Ulm Medical Center, Ulm
  • Helmut Küchenhoff - Ludwig-Maximilians-Universität, Institut für Statistik, München
  • Timo Lanki - National Public Health Institute (KTL), Environmental Epidemiology Unit, Kuopio
  • Juha Pekkanen - National Public Health Institute (KTL), Environmental Epidemiology Unit, Kuopio

Kongress Medizin und Gesellschaft 2007. Augsburg, 17.-21.09.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. Doc07gmds334

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/gmds2007/07gmds334.shtml

Published: September 6, 2007

© 2007 Rückerl et al.
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Outline

Text

Background: Air pollution has been associated with cardiovascular disease exacerbation in numerous studies. The mechanisms linking the inhalation of ambient particles to adverse cardiovascular events are not completely understood. Based on previous findings, we hypothesised that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, a particularly vulnerable group.

Materials and Methods: A prospective longitudinal study of 1,003 MI survivors was performed in six cities between May 2003 and July 2004. Repeated measurements (average 5.8 per patient) of IL-6, fibrinogen and C-reactive protein (CRP) were compared to concurrent levels of air pollution. Hourly data on particle number concentrations (PNC), mass concentrations of less than 10 µm (PM10) and 2.5 µm (PM2.5) and meteorological data were collected at central monitoring sites in each city. City specific confounder models were built for each blood marker separately adjusting for meteorology and time-invariant covariates. Data were analyzed with mixed effects models.

Results: Pooled results show an increase in IL-6 when concentrations of PNC were elevated 12-17 hours before blood withdrawal [%change of geometric mean: 2.7, CI:1.0;4.6]. Five day cumulative exposure to PM10 was associated with increased fibrinogen concentrations [%change of arithmetric mean: 0.6, CI:0.1;1.1]. Results on PM10 were similar among non-smokers, patients with elevated levels of N-Terminal proB-type natriuretic peptide and HbA1c, used as indicators for left ventricular dysfunction and hyperglycaemia, respectively [%change of arithmetric mean: 1.03, CI:0.16;1.90, 0.70, CI:-0.02;1.42 and 1.92, CI:0.60;3.24, respectively]. No consistent associations were found for CRP.

Conclusion: To our knowledge no epidemiological study on air pollution of this size using repeated measurements has been conducted. Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute phase proteins, as seen in slightly increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.