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Regina Rückerl,¹* Sonja Greven,^1,2* Petter Ljungman,³ Pasi Aalto,⁴ Charalambos Antoniades,⁵ Tom Bellander,^3,6 Niklas Berglind,³ Christina Chrysohoou,⁵ Francesco Forastiere,⁷ Bénédicte Jacquemin,⁸ Stephanie von Klot,¹ Wolfgang Koenig,⁹ Helmut Küchenhoff,² Timo Lanki,¹⁰ Juha Pekkanen,^10,11 Carlo A. Perucci,⁷ Alexandra Schneider,¹ Jordi Sunyer,⁸ and Annette Peters,^1,12 for the AIRGENE Study Group

¹GSF National Research Centre for Environment and Health, Institute of Epidemiology, Neuherberg, Germany; ²Ludwig-Maximilians University, Department of Statistics, Munich, Germany; ³Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; ⁴Department of Physical Sciences, University of Helsinki, Helsinki, Finland; ⁵Department of Hygiene and Epidemiology, University of Athens, Athens, Greece; ⁶Department of Occupational and Environmental Health, Stockholm County Council, Stockholm, Sweden; ⁷Local Health Authority, Department of Epidemiology, Rome, Italy; ⁸Municipal Institute of Medical Research (IMIM), Barcelona, Spain; ⁹Department of Internal Medicine II, Cardiology, University of Ulm Medical Center, Ulm, Germany; ¹⁰Environmental Epidemiology Unit, National Public Health Institute (KTL), Kuopio, Finland; ¹¹School of Public Health and Clinical Nutrition, University of Kuopio, Kuopio, Finland; ¹²Focus-Network Aerosols and Health, GSF National Research Centre for Environment and Health, Neuherberg, Germany

Abstract
Background: Numerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation.

Objectives: Given previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles.

Methods: A prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6) , fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC) , mass concentrations of particulate matter (PM) < 10 µm (PM₁₀) and < 2.5 µm (PM_2.5) , gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time-varying 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 hr before blood withdrawal [percent change of geometric mean, 2.7 ; 95% confidence interval (CI) , 1.0–4.6]. Five day cumulative exposure to PM₁₀ was associated with increased fibrinogen concentrations (percent change of arithmetic mean, 0.6 ; 95% CI, 0.1–1.1) . Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP.

Conclusions: Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.

Key words: air pollution, C-reactive protein, CRP, epidemiology, fibrinogen, IL-6, inflammation, myocardial infarction, ultrafine particles. Environ Health Perspect 115:1072–1080 (2007) . doi:10.1289/ehp.10021 available via http://dx.doi.org/ [Online 18 April 2007]

Address correspondence to R. Rückerl, GSF National Research Centre for Environment and Health, Institute of Epidemiology, Building 56, Room 237, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Telephone: +49 89 3187 3211. Fax: 49 89 3187 3380. E-mail: rueckerl@gsf.de

Supplemental Material is available online at http://www.ehponline.org/docs/2007/10021/suppl.pdf

*These authors contributed equally.

The AIRGENE study was funded as part of the European Union's 5th Framework Programme, key action number 4: "Environment and Health," contract QLRT-2002-02236.

F. Nyberg, employed by AstraZeneca, is also Lecturer in Epidemiology at Karolinska Institute. AstraZeneca did not contribute any direct financing to this study.

The authors declare they have no competing financial interests.

Received 20 December 2006 ; accepted 18 April 2007.