Exposure to Wear Particles Generated from Studded Tires and Pavement Induces Inflammatory Cytokine Release from Human Macrophages
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- 作者：John Lindbom ; Mats Gustafsson ; Gö ; ran Blomqvist ; Andreas Dahl ; Anders Gudmundsson ; Erik Swietlicki ; and Anders G. Ljungman
- 刊名：Chemical Research in Toxicology
- 出版年：2006
- 出版时间：April 2006
- 年：2006
- 卷：19
- 期：4
- 页码：521 - 530
- 全文大小：342K
- 年卷期：v.19,no.4(April 2006)
- ISSN：1520-5010
文摘
Health risks associated with exposure to airborne particulate matter (PM) have been shownepidemiologically as well as experimentally, pointing to both respiratory and cardiovascular effects. Lately,wear particles generated from traffic have been recognized to be a major contributing source to theoverall particle load, especially in the Nordic countries were studded tires are used. In this work, weinvestigated the inflammatory effect of PM10 generated from the wear of studded tires on two differenttypes of pavement. As comparison, we also investigated PM10 from a traffic-intensive street, a subwaystation, and diesel exhaust particles (DEP). Human monocyte-derived macrophages, nasal epithelial cells(RPMI 2650), and bronchial epithelial cells (BEAS-2B) were exposed to the different types of particles,and the secretion of IL-6, IL-8, IL-10, and TNF-
into the culture medium was measured. The resultsshow a significant release of cytokines from macrophages after exposure for all types of particles. Whenparticles generated from asphalt/granite pavement were compared to asphalt/quartzite pavement, the granitepavement had a significantly higher capacity to induce the release of cytokines. The granite pavementparticles induced cytokine release at the same magnitude as the street particles did, which was higherthan what particles from both a subway station and DEP did. Exposure of epithelial cells to PM10 resultedin a significant increase of TNF- secreted from BEAS-2B cells for all types of particles used (DEP wasnot tested), and the highest levels were induced by subway particles. None of the particle types wereable to evoke detectable cytokine release from RPMI 2650 cells. The results indicate that PM10 generatedby the wear of studded tires on the street surface is a large contributor to the cytokine-releasing abilityof particles in traffic-intensive areas and that the type of pavement used is important for the level of thiscontribution. Furthermore, the airway inflammatory potential of wear particles from tires and pavementmight be of a greater magnitude than that of DEP.
into the culture medium was measured. The resultsshow a significant release of cytokines from macrophages after exposure for all types of particles. Whenparticles generated from asphalt/granite pavement were compared to asphalt/quartzite pavement, the granitepavement had a significantly higher capacity to induce the release of cytokines. The granite pavementparticles induced cytokine release at the same magnitude as the street particles did, which was higherthan what particles from both a subway station and DEP did. Exposure of epithelial cells to PM10 resultedin a significant increase of TNF- secreted from BEAS-2B cells for all types of particles used (DEP wasnot tested), and the highest levels were induced by subway particles. None of the particle types wereable to evoke detectable cytokine release from RPMI 2650 cells. The results indicate that PM10 generatedby the wear of studded tires on the street surface is a large contributor to the cytokine-releasing abilityof particles in traffic-intensive areas and that the type of pavement used is important for the level of thiscontribution. Furthermore, the airway inflammatory potential of wear particles from tires and pavementmight be of a greater magnitude than that of DEP.