Ultrafine particles and platelet activation in patients with coronary heart disease – results from a prospective panel study

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Abstract

Background

Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Toxicological studies have provided evidence for thrombogenic effects of particles.

A prospective panel study in a susceptible population was conducted in Erfurt, Germany, to study the effects of daily changes in ambient particles on various blood cells and soluble CD40ligand (sCD40L, also known as CD154), a marker for platelet activation that can cause increased coagulation and inflammation.

Blood cells and plasma sCD40L levels were repeatedly measured in 57 male patients with coronary heart disease (CHD) during winter 2000/2001. Fixed effects linear regression models were applied, adjusting for trend, weekday and meteorological parameters.

Hourly data on ultrafine particles (UFP, number concentration of particles from 0.01 to 0.1 μm), mass concentration of particles less than 10 and 2.5 μm in diameter (PM ₁₀, PM _2.5), accumulation mode particle counts (AP, 0.1–1.0 μm), elemental and organic carbon, gaseous pollutants and meteorological data were collected at central monitoring sites.

Results

An immediate increase in plasma sCD40L was found in association with UFP and AP (% change from geometric mean: 7.1; CI: [0.1, 14.5] and 6.9; CI: [0.5, 13.8], respectively). Platelet counts decreased in association with UFP showing an immediate, a three days delayed (lag 3) and a 5-day average response (% change from the mean: -1.8; CI: [-3.4,-0.2]; -2.4; CI: [-4.5,-0.3] and -2.2; CI: [-4.0,-0.3] respectively).

Conclusion

The increased plasma sCD40L levels support the hypothesis that higher levels of ambient air pollution lead to an inflammatory response in patients with CHD thus providing a possible explanation for the observed association between air pollution and cardiovascular morbidity and mortality in susceptible parts of the population.

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Most cited references 61

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CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells.

V Henn, J Slupsky, M. Gräfe … (1998)

CD40 ligand (CD40L, CD154), a transmembrane protein structurally related to the cytokine TNF-alpha, was originally identified on stimulated CD4+ T cells, and later on stimulated mast cells and basophils. Interaction of CD40L on T cells with CD40 on B cells is of paramount importance for the development and function of the humoral immune system. CD40 is not only constitutively present on B cells, but it is also found on monocytes, macrophages and endothelial cells, suggesting that CD40L has a broader function in vivo. We now report that platelets express CD40L within seconds of activation in vitro and in the process of thrombus formation in vivo. Like TNF-alpha and interleukin-1, CD40L on platelets induces endothelial cells to secrete chemokines and to express adhesion molecules, thereby generating signals for the recruitment and extravasation of leukocytes at the site of injury. Our results indicate that platelets are not only involved in haemostasis but that they also directly initiate an inflammatory response of the vessel wall.

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T-cell function and migration. Two sides of the same coin.

U von Andrian, C Mackay (2000)

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Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers.

S Salvi, A Blomberg, B Rudell … (1999)

Several epidemiologic studies have demonstrated a consistent association between levels of particulate matter (PM) in the ambient air with increases in cardiovascular and respiratory mortality and morbidity. Diesel exhaust (DE), in addition to generating other pollutants, is a major contributor to PM pollution in most places in the world. Although the epidemiologic evidence is strong, there are as yet no established biological mechanisms to explain the toxicity of PM in humans. To determine the impact of DE on human airways, we exposed 15 healthy human volunteers to air and diluted DE under controlled conditions for 1 h with intermittent exercise. Lung functions were measured before and after each exposure. Blood sampling and bronchoscopy were performed 6 h after each exposure to obtain airway lavages and endobronchial biopsies. While standard lung function measures did not change following DE exposure, there was a significant increase in neutrophils and B lymphocytes in airway lavage, along with increases in histamine and fibronectin. The bronchial biopsies obtained 6 h after DE exposure showed a significant increase in neutrophils, mast cells, CD4+ and CD8+ T lymphocytes along with upregulation of the endothelial adhesion molecules ICAM-1 and VCAM-1, with increases in the numbers of LFA-1+ cells in the bronchial tissue. Significant increases in neutrophils and platelets were observed in peripheral blood following DE exposure. This study demonstrates that at high ambient concentrations, acute short-term DE exposure produces a well-defined and marked systemic and pulmonary inflammatory response in healthy human volunteers, which is underestimated by standard lung function measurements.

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Author and article information

Journal

Journal ID (nlm-ta): Part Fibre Toxicol

Title: Particle and Fibre Toxicology

Publisher: BioMed Central (London )

ISSN (Electronic): 1743-8977

Publication date Collection: 2007

Publication date (Electronic): 22 January 2007

Volume: 4

Page: 1

Affiliations

[1 ]Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany

[2 ]Department of Environmental Medicine – Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA

[3 ]Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany

[4 ]Department of Medicine – Pulmonary and Critical Care Division, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA

[5 ]Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany and WZU – Environmental Science Centre of the University Augsburg, Augsburg, Germany

[6 ]Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA

[7 ]Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany; IBE Chair of Epidemiology, Ludwig-Maximilians-University of Munich, Munich, Germany and Focus-Network Aerosols and Health, GSF National Research Center for Environment and Health, Germany

[8 ]Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany and Focus-Network Aerosols and Health, GSF National Research Center for Environment and Health, Neuherberg, Germany

Article

Publisher ID: 1743-8977-4-1

DOI: 10.1186/1743-8977-4-1

PMC ID: 1790903

PubMed ID: 17241467

SO-VID: b136d9cc-3aab-4346-be7c-3445765e5c7b

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Ultrafine particles and platelet activation in patients with coronary heart disease – results from a prospective panel study

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Abstract

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Journal of the Netherlands Society of Toxicology

Most cited references 61

CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells.

T-cell function and migration. Two sides of the same coin.

Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers.

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