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Experimentally determined human respiratory tract deposition of airborne particles at a busy street.

https://arctichealth.org/en/permalink/ahliterature94519
Source
Environ Sci Technol. 2009 Jul 1;43(13):4659-64
Publication Type
Article
Date
Jul-1-2009
Author
Löndahl Jakob
Massling Andreas
Swietlicki Erik
Bräuner Elvira Vaclavik
Ketzel Matthias
Pagels Joakim
Loft Steffen
Author Affiliation
Division of Nuclear Physics, Department of Physics, Lund University, PO Box 118, SE-221 00 Lund, Sweden. jakob.londahl@nuclear.lu.se
Source
Environ Sci Technol. 2009 Jul 1;43(13):4659-64
Date
Jul-1-2009
Language
English
Publication Type
Article
Keywords
Adult
Aerosols
Aged
Air Pollutants - analysis
Air Pollution
Bioelectric Energy Sources
Cities
Denmark
Environmental Monitoring - methods
Equipment Design
Female
Humans
Inhalation Exposure
Male
Middle Aged
Respiratory System - drug effects
Vehicle Emissions
Abstract
Traffic is one of the major sources of harmful airborne particles worldwide. To relate exposure to adverse health effects it is important to determine the deposition probability of the inhaled particles in the human respiratory tract. The size-dependent deposition of 12-580 nm particles was measured with a novel setup in 9 healthy subjects breathing by mouth on the windward side of a busy street in Copenhagen, Denmark. The aerosol was characterized both at the curbside and, to obtain the background concentration, at rooftop level. Particle hygroscopicity, a key parameter affecting respiratory tract deposition, was also measured at the same time of exposure. The total deposition fraction of the curbside particles in the range 12-580 nm was 0.60 by number, 0.29 by surface area, and 0.23 by mass. The deposition fractions of the "traffic exhaust" contribution, calculated as the hydrophobic fraction of the curbside particles, was 0.68, 0.35, and 0.28 by number, surface area, and mass, respectively. The deposited amount of traffic exhaust particles was 16 times higher by number and 3 times higher by surface area compared to the deposition of residential biofuel combustion particles investigated previously (equal inhaled mass concentrations). This was because the traffic exhaust particles had both a higher deposition probability and a higher number and surface area concentration per unit mass. To validate the results, the respiratory tract deposition was estimated by using the well-established ICRP model. Predictions were in agreement with experimental results when the effects of particle hygroscopicity were considered in the model.
PubMed ID
19673248 View in PubMed
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Exposure to wear particles generated from studded tires and pavement induces inflammatory cytokine release from human macrophages.

https://arctichealth.org/en/permalink/ahliterature82501
Source
Chem Res Toxicol. 2006 Apr;19(4):521-30
Publication Type
Article
Date
Apr-2006
Author
Lindbom John
Gustafsson Mats
Blomqvist Göran
Dahl Andreas
Gudmundsson Anders
Swietlicki Erik
Ljungman Anders G
Author Affiliation
Division of Occupational and Environmental Medicine, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden.
Source
Chem Res Toxicol. 2006 Apr;19(4):521-30
Date
Apr-2006
Language
English
Publication Type
Article
Keywords
Base Sequence
Cell Line
Cytokines - secretion
DNA Primers
Humans
Inflammation Mediators - metabolism
Macrophages - secretion
Microscopy, Electron, Scanning
Particle Size
Rubber - chemistry
X-Ray Diffraction
Abstract
Health risks associated with exposure to airborne particulate matter (PM) have been shown epidemiologically 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 the overall particle load, especially in the Nordic countries were studded tires are used. In this work, we investigated the inflammatory effect of PM10 generated from the wear of studded tires on two different types of pavement. As comparison, we also investigated PM10 from a traffic-intensive street, a subway station, 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-alpha into the culture medium was measured. The results show a significant release of cytokines from macrophages after exposure for all types of particles. When particles generated from asphalt/granite pavement were compared to asphalt/quartzite pavement, the granite pavement had a significantly higher capacity to induce the release of cytokines. The granite pavement particles induced cytokine release at the same magnitude as the street particles did, which was higher than what particles from both a subway station and DEP did. Exposure of epithelial cells to PM10 resulted in a significant increase of TNF-alpha secreted from BEAS-2B cells for all types of particles used (DEP was not tested), and the highest levels were induced by subway particles. None of the particle types were able to evoke detectable cytokine release from RPMI 2650 cells. The results indicate that PM10 generated by the wear of studded tires on the street surface is a large contributor to the cytokine-releasing ability of particles in traffic-intensive areas and that the type of pavement used is important for the level of this contribution. Furthermore, the airway inflammatory potential of wear particles from tires and pavement might be of a greater magnitude than that of DEP.
PubMed ID
16608163 View in PubMed
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