| 1. |
- Dahl, Andreas, et al.
(author)
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Traffic-generated emissions of ultrafine particles from pavement-tire interface
- 2006
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In: Atmospheric Environment. - : Elsevier. - 1352-2310 .- 1873-2844. ; 40:7, s. 1314-1323
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Journal article (peer-reviewed)abstract
- In a road simulator study, a significant source of sub-micrometer fine particles produced by the road-tire interface was observed. Since the particle size distribution and source strength is dependent on the type of tire used, it is likely that these particles largely originate from the tires, and not the road pavement. The particles consisted most likely of mineral oils from the softening filler and fragments of the carbon-reinforcing filler material (soot agglomerates). This identification was based on transmission electron microscopy studies of collected ultrafine wear particles and on-line thermal treatment using a thermodesorber. The mean particle number diameters were between 15-50 nm, similar to those found in light duty vehicle (LDV) tail-pipe exhaust. A simple box model approach was used to estimate emission factors in the size interval 15-700 nm. The emission factors increased with increasing vehicle speed, and varied between 3.7 x 10(11) and 3.2 x 10(12) particles vehicle(-1) km(-1) at speeds of 50 and 70 km h(-1). This corresponds to between 0.1-1% of tail-pipe emissions in real-world emission studies at similar speeds from a fleet of LDV with 95% gasoline and 5% diesel-fueled cars. The emission factors for particles originating from the road-tire interface were, however, similar in magnitude to particle number emission factors from liquefied petroleum gas-powered vehicles derived in test bench studies in Australia 2005. Thus the road-tire interface may be a significant contributor to particle emissions from ultraclean vehicles. (c) 2005 Elsevier Ltd. All rights reserved.
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| 2. |
- Lindbom, John, 1960-, et al.
(author)
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Exposure to wear particles generated from studded tires and pavement induces inflammatory cytokine release from human macrophages
- 2006
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In: Chemical Research in Toxicology. - : American Chemical Society (ACS). - 0893-228X .- 1520-5010. ; 19:4, s. 521-530
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Journal article (peer-reviewed)abstract
- Health risks associated with exposure to airborne paniculate 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-α 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 PM 10 resulted in a significant increase of TNF-α 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.
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| 3. |
- Lindbom, John, 1960-, et al.
(author)
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Wear particles generated from studded tires and pavement induces inflammatory reactions in mouse macrophage cells
- 2007
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In: Chemical Research in Toxicology. - : American Chemical Society (ACS). - 0893-228X .- 1520-5010. ; 20:6, s. 937-946
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Journal article (peer-reviewed)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. These health risks are of increasing concern in society, and to protect public health, a clarification of the toxic properties of particles from different sources is of importance. Lately, wear particles generated from traffic have been recognized as a major contributing source to the overall particle load, especially in the Nordic countries where studded tires are used. The aim of this study was to further investigate and compare the ability to induce inflammatory mediators of different traffic-related wear particles collected from an urban street, a subway station, and studded tire-pavement wear. Inflammatory effects were measured as induction of nitric oxide (NO), IL-6, TNF-α, arachidonic acid (AA), and lipid peroxidation after exposure of the murine macrophage like cell line RAW 264.7. In addition, the redox potential of the particles was measured in a cell-free system. The results show that all particles tested induce IL-6, TNF-α, and NO, and those from the urban street were the most potent ones. In contrast, particles collected from a subway station were most potent to induce lipid peroxidation, A A release, and formation of ROS. Particles from studded tire-pavement wear, generated using a road simulator, were able to induce inflammatory cytokines, NO, lipid peroxidation, and ROS formation. Interestingly, particles generated from pavement containing granite as the main stone material were more potent than those generated from pavement containing quartzite as the main stone material.
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| 4. |
- Nosratabadi, Ali Reza, 1964-, et al.
(author)
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Airway contraction and cytokine release in isolated rat lungs induced by wear particles from the road and tire interface and road vehicle brakes
- 2023
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In: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 35:13-14, s. 309-323
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Journal article (peer-reviewed)abstract
- The dominant road traffic particle sources are wear particles from the road and tire interface, and from vehicle brake pads. The aim of this work was to investigate the effect of road and brake wear particles on pulmonary function and biomarkers in isolated perfused rat lungs. Particles were sampled from the studded tire wear of three road pavements containing different rock materials in a road simulator; and from the wear of two brake pad materials using a pin-on-disk machine. Isolated rat lungs inhaled the coarse and fine fractions of the sampled particles resulting in an estimated total particle lung dose of 50 μg. The tidal volume (TV) was measured during the particle exposure and the following 50 min. Perfusate and BALF were analyzed for the cytokines TNF, CXCL1 and CCL3. The TV of lungs exposed to rock materials was significantly reduced after 25 min of exposure compared to the controls, for quartzite already after 4 min. The particles of the heavy-duty brake pads had no effect on the TV. Brake particles resulted in a significant elevation of CXCL1 in the perfusate. Brake particles showed significant elevations of all three measured cytokines, and quartzite showed a significant elevation of TNF in BALF. The study shows that the toxic effect on lungs exposed to airborne particles can be investigated using measurements of tidal volume. Furthermore, the study shows that the choice of rock material in road pavements has the potential to affect the toxicity of road wear PM10.
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| 5. |
- Nosratabadi, Ali Reza, 1964-
(author)
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Novel Methods for Sampling, Characterization and Analysis of Airborne Street Particles in a Health Perspective
- 2022
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Licentiate thesis (other academic/artistic)abstract
- Over the last decades, there has been much attention on air quality, especially in urban environments. A significant factor effecting the air quality in the urban environment is airborne particulate matter (PM). Long-term exposure to PM causes increased risk for heart disease, decreased lung function, exacerbation of asthma, and lung cancer. Therefore, many countries have implemented exposure limits to the concentration of ambient PM in the urban environments. The toxicity of PM is dependent on several factors such as chemical composition, shape, adsorbed materials, and particle sizes (usually divided in ultrafine, fine and coarse particles). However, the relationship between different PM properties and developing health hazards are not clear. Therefore, further studies to investigate different properties of PM may contribute to understanding the influence of PM on human health. In the present work, different novel methods to investigate sampled airborne PM and to investigate potential health effects have been used to increase the knowledge regarding street and wear particles. In study I, a sampling plan involving collecting one filter from Tapered Element Oscillating Microbalance (TEOM) monitoring stations used for Environmental monitoring each month for 20 months were developed. Particles on the filters were extracted into a suspension. TEOM particles were then studied with respect to constituents and variables that reflect their toxicity. The constituent and toxicity was found to be spatial and seasonal dependent. As a follow-up, in study II, TEOM filters from three geographical different cities were collected once a month for a year. The variation in particle mass measured with TEOM monitor, cadmium and lead contents, as well as endotoxin levels between locations and time points over the year was studied. The correlation between studied variables and biological effect was investigated. The results show that the concentration of metals and endotoxin in TEOM particles have no relationship to particle mass, while endotoxin levels coincided with pro-inflammatory response. These studies show that results from analyzing different variables on obtained particles from TEOM filters in combination with information about the ambient particle concentration, could be helpful in the evaluation of differences in the risk of breathing air at various locations. The dominant road traffic particle sources are wear particles from the road and tyre interface, and from vehicle brake pads. The particle concentrations are highest in cities with high traffic amounts and a high frequency of braking. There are a few cell studies that have investigated the toxicological and biological effect of these wear particles, but there is a lack of knowledge regarding their effect on tissue level. Furthermore, the knowledge about importance of rock materials in pavement is deficient. To mitigate these knowledge gaps, the effect of different wear particles from pavement and brake pad were tested using a model with isolated perfused rat lungs in study III. The wear particles from the pavement showed a significant decrease of tidal volume compared to unexposed controls. The largest effect were found with quartzite stone material. Wear particles from brakes instead showed a larger effect on released proinflammatory cytokines. The study shows that the toxic effect on lungs exposed to airborne particles can be investigated using repetitive measurements of tidal volume. Furthermore, the study shows that the choice of rock material in road pavements has the potential to affect the toxicity of road wear particles. This should be considered in environments where the concentrations and exposures are high. The brake particles showed a different effect than stone particles, indicating the need to differentiate wear particles from different sources in relation to health effects. In summary, the present work have investigated different aspects of airborne particles collected from streets as well as generated wear particles. These indicate different important aspects of the particles that may be of importance to better understand their health effects.
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| 6. |
- Nosratabadi, Ali Reza, 1964-, et al.
(author)
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Use of TEOM monitors for continuous long-term sampling of ambient particles for analysis of constituents and biological effects
- 2019
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In: Air quality, atmosphere and health. - : Springer. - 1873-9318 .- 1873-9326. ; 12:2, s. 161-171
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Journal article (peer-reviewed)abstract
- Many countries have implemented exposure limits for the concentration of ambient particular matter and do therefore have to monitor their concentration. This could be performed with TEOM monitors (Tapered Element Oscillating Microbalance-monitors) that contain a filter on which particles are collected. These filters are regularly exchanged for new ones. The aim of this study was to test the feasibility of collecting used filters from monitors at different locations and establishing a method to extract particles and then study them with respect to their ability to generate oxidants, their endotoxin content, and ability to activate inflammatory cells. Filters from nine geographically spread locations in Sweden were collected during a 21-month period by local technicians who then sent them to the laboratory where they were extracted and analyzed. The procedure to let local technicians perform the filter exchange and send used TEOM filters to the laboratory worked well. A method was established in which pyrogen-free water was used to extract particles that then were aliquoted and stored for later analysis. Particulate matter (PM 10 ) from different locations showed both a considerable seasonal and spatial-dependent difference with respect to oxidative potential (oxidize glutathione), endotoxin content, and ability to activate blood monocytes to release interleukin-1β. This study shows that, instead of discarding TEOM filters, they can be collected and extracted so that particles that have been sampled in a standardized way could be analyzed with respect to variables that reflect their toxicity. This could be done at a low cost. In combination with information about the ambient particle concentration, such information could be helpful in the evaluation of differences in the risk of breathing air at various locations.
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| 7. |
- Karlsson, Hanna L, et al.
(author)
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Comparison of genotoxic and inflammatory effects of particles generated by wood combustion, a road simulator and collected from street and subway
- 2006
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In: Toxicology Letters. - : Elsevier BV. - 0378-4274 .- 1879-3169. ; 165:3, s. 203-211
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Journal article (peer-reviewed)abstract
- The health effects of exposure to airborne particles are of increasing concern in society. In order to protect public health, a clarification of the toxic properties of particles from different sources is of importance. The aim of this study was to investigate and compare the genotoxicity and the ability to induce inflammatory mediators of nine different particle types from wood and pellets combustion, from tire–road wear and collected from an urban street and a subway station. The comet assay was used to assess genotoxicity after exposure of the human lung cell line A549. Inflammatory effects were measured as induction of IL-6, IL-8 and TNF-α after exposure of human macrophages. We found that all particles tested caused DNA damage and those from the subway caused more damage than the other particles (p < 0.001) likely due to redox-active iron. In contrast, particles collected from an urban street were most potent to induce inflammatory cytokines. Particles from tire–road wear collected using a road simulator were genotoxic and able to induce cytokines. Finally, more effective combustion of wood led to less emission of particles, but those emitted did not show less toxicity in this study.
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| 8. |
- Lindbom, John, 1960-, et al.
(author)
-
Expression of members of the phospholipase A2 family of enzymes in human nasal mucosa
- 2001
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In: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 18:1, s. 130-138
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Journal article (peer-reviewed)abstract
- Phospholipase A2 (PLA2) is a family of enzymes thought to play a key role in inflammation by releasing arachidonic acid for the synthesis of eicosanoids and lysophospholipid for the synthesis of platelet-activating factor. However, the precise contribution of different PLA2 types to the formation of inflammatory lipid mediators in the upper airways is not known and the expression of different PLA2 genes in the human nasal mucosa has not been examined.This study therefore investigated the occurrence of messenger ribonucleic acids (mRNAs) for different PLA2 forms (IB, IIA, IID, IIE, III, IVA, IVB, IVC, V, VI, VII, X, acid calcium-independent (aiPLA2), and calcium-independent membrane bound PLA2, (iPLA2-2)) in the nasal mucosa of five healthy human subjects.Using reversed transcription-polymerase chain reaction (RT-PCR) techniques it was found that all these PLA2 types except PLA2 V were expressed in all subjects, whereas PLA2 V was detected in only one individual on one single occasion. The relative abundance of the different PLA2 transcripts were aiPLA2>X≈IVA>IIA≈IIE≈IVB≈VI>IB≈IID≈III≈IVC≈VII≈iPLA2-2. To further quantify the mRNA-expression of PLA2 X, IVA and IIA, the samples were reanalysed with a quantitative PCR-technique utilizing competitive deoxyribonucleic acid (DNA) mimics as references. The amounts of PLA2 X, IVA and IIA mRNA were then estimated to 0.9±0.2, 1.1±0.7, and 0.0025±0.0021 amol (mean±se), respectively, confirming the relative abundance of these PLA2 transcripts and indicating that the recently described PLA2 X form is relatively strongly expressed.These findings demonstrate that a large number of PLA2 types are expressed in the normal human nasal mucosa. Moreover, this investigation demonstrates, for the first time, the presence of the newly discovered phospholipase A2 forms IID, IIE, III, IVB, IVC, X and calcium-independent membrane bound phospholipase A2 in the human nasal mucosa and raises the possibility that one or several of these may be involved in inflammatory reactions in the nose.
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| 9. |
- Lindbom, John, 1960-, et al.
(author)
-
Increased gene expression of novel cytosolic and secretory phospholipase A2 types in human airway epithelial cells induced by tumor necrosis factor-α and IFN-γ
- 2002
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In: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 22:9, s. 947-955
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Journal article (peer-reviewed)abstract
- Phospholipase A2 (PLA2) is a growing family of enzymes that may play a major role in inflammation. We investigated the effect of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) on the gene expression of 19 different PLA2 types (IB, IIA, IID, IIE, IIF, III, IVA, IVB, IVC, V, VIA, VIB, VIIA, VIIB, VIIIA, VIIIB, X, XII, and XIII) in human bronchoepithelial (BEAS-2B) and nasal epithelial (RPMI 2650) cells. The cells were stimulated with TNF-α or IFN-γ for different lengths of time (1, 4, 18, and 48 h), and the mRNA levels of the different PLA2 types were determined by reverse transcriptase-PCR (RT-PCR) and normalized to those of the housekeeping gene, GAPDH. In both cell lines, TNF-α increased the expression of PLA2 IVA and IVC, and IFN-γ increased the expression of PLA2 IIA and IID. No influence on the gene expression of PLA2-activating protein (PLAP) was noted on cytokine stimulation. These findings indicate that TNF-α and IFN-γ induce gene expression of two novel cytosolic and secretory PLA2 types (IVC and IID, respectively) in human airway epithelial cells. The possibility that these PLA2 types are involved in cytokine-mediated inflammation in the respiratory tract is inferred.
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| 10. |
- Lindbom, John, 1960-, et al.
(author)
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Phospholipase A2 mRNA expression in the nasal mucosa of healthy subjects and patients with seasonal allergic rhinitis
- 2004
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In: Rhinology. - 0300-0729 .- 1996-8604. ; 42:2, s. 85-91
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Journal article (peer-reviewed)abstract
- Phospholipase A2 (PLA2) is a family of enzymes that play different role(s) in inflammation, but their importance in seasonal allergic rhinitis (SAR) has not been clarified. Here, we determined the levels of messenger ribonucleic acid (mRNA) for different PLA2 types in the nasal mucosa of SAR patients (n=6) and healthy controls (n=5). Nasal brush samples were taken both during pollen season, when the symptoms of the patients were severe, and off-season, when the patients were free of symptoms. We found that PLA2 IB, IIA, IID,IIE, IIF III, IVA, IVB, IVC, VIA, VIB, VIIA, VIIB, VIIIA, VIIIB, X, XII and XIII were all expressed in each subject at both occasions. The mRNA levels of PLA2 VIIA (platelet-activating factor (PAF) acetylhydrolase) were lower in SAR patients than controls, both during pollen season (p = 0.03) and off season (p = 0.03). These findings demonstrate that a large number of PLA2 types are expressed in the nasal mucosa, regardless of whether there is ongoing allergic inflammation or not. The observation that PAF acetylhydrolase mRNA expression in the nasal mucosa is lower in SAR patients than in healthy subjects suggests the possibility that impaired ability to inactivate PAF might be of importance in SAR. Further studies are required to clarify whether the decreased PAF acetylhydrolase mRNA expression in SAR is accompanied by decreased enzyme activity and whether aberrations in PAF acetylhydrolase are present in infectious rhinitis patients as well.
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| 11. |
- Ljungman, Anders, 1958-, et al.
(author)
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Examination involving students as peer examiners
- 2008
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In: Assessment & Evaluation in Higher Education. - : Informa UK Limited. - 0260-2938 .- 1469-297X. ; 33:3, s. 289-300
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Journal article (peer-reviewed)abstract
- The main interest in this article is students' involvement in assessment as a part of growth towards self-directedness in learning. In order to enhance students' development of autonomy in learning, a project involving 'older' students as peer examiners for 'younger' students was designed and carried out. Students in the sixth semester in a PBL-based Master's program of Medical Biology participated, together with faculty, as examiners of fifth-semester students. The examination and the assessment situation was carefully designed based on learning theories, empirical evidence and experiences underpinning student-centred learning, especially in the form of PBL used at the faculty. The project was evaluated and analysed in order to understand students' learning processes related to the responsibility for assessing peers. The situation of the peer examiners was interpreted based on their own experiences with statements from the students assessed and faculty involved in the assessment. Evaluations from six occasions, spring and fall, 2003-2005, were included in the study. The findings suggest that involving students in assessment as equal partners with faculty makes it is possible for students to apprehend the metacognitive competences needed to be responsible and autonomous in learning. The peer examiners experience motivation to learn about learning, they acquire tacit knowledge about assessment and they learn through being involved and trusted. The student-centred educational context, which requires responsibility throughout the programme, is recognized as very important.
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| 12. |
- Ljungman, Anders, 1958-
(author)
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Mechanisms of inflammatory lung injury : Studies in isolated perfused rat lungs
- 1995
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Doctoral thesis (other academic/artistic)abstract
- Isolated perfused rat lungs (IPRLs) were used to study mechanisms andmediators of lung injury due to (i) ischemia-reperfusion (IR) and (ii) endotoxin. To investigate the role of polymorphonuclear neutrophils (PMNs) in IR injury, PMNs were added to the perfusate of IPRLs subjected to IR. PMNs did not contribute to the injury as assessed by albumin leak indices. Addition of erythrocytes or catalase attenuated the injury, indicating that IR injury is dependent on a non-PMN source of toxic 02 metabolites. Moreover, increased levels of 6-keto-PGE1o: and tromboxane B2 were found in the perfusate and cyclooxygenase and thromboxane synthase inhibitors (indomethacin and U 63557A) reduced the injury, suggesting that cyclooxygenase metabolites of arachidonic acid are involved in IR lung injury.To study PMN-dependent injury in IPRLs, phorbol ester-activated PMNs were added to the perfusate in the presence of Iloprost, a long-acting prostacyclin analog. Iloprost attenuated the lung injury and decreased PMN adherence to endothelial monolayers in vitro, indicating that prostacyclin is an important regulator of PMN-dependent injury in the lung. PMN-dependent lung injury was further explored by adding calcium ionophore-activatcd PMNs prestimulated with endotoxin to the perfusate and studying the increases in pulmonary arterial pressure and capillary permeability. Both these effects were attenuated by the Ginkgo biloba-derived platelet-activating factor (PAF) antagonist, BN 52021, suggesting that endotoxin-stimulated, calcium ionophore (A 23187)activated PMNs exert important parts of their pro-inflammatory action via generation of PAF. Furthermore, addition of endotoxin to the perfusate of IPRLs caused elevated levels of group-11 phospholipase A2 (PLAz), tumor necrosis factor alpha (TNF-o:) and interleukin-1 beta (Il-1~) mRNA in the lung tissue and release of PLA2 and TNF-o: activity into the perfusate. Increased TNF-a m RNA levels and increased TNF-o: activity release were also found in alveolar macrophages exposed in vitro to asbestos as well as man made mineral fibers. In conclusion, these observations illustrate the importance of PLA2 - related mediators in inflammatory lung injury and demonstrate that neutrophils are involved in some but not necessary for all types of lung injury to occur.
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| 13. |
- Nosratabadi, Ali Reza, 1964-, et al.
(author)
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Clara cell 10-KDA protein inhibits endotoxin-induced airway contraction in isolated perfused rat lungs
- 2003
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In: Experimental Lung Research. - : Informa UK Limited. - 0190-2148 .- 1521-0499. ; 29:7, s. 455-473
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Journal article (peer-reviewed)abstract
- Clara cell 10-kDa protein (CC10) is a major component of bronchoalveolar lavage fluid and is suggested to be a natural regulator of airway inflammation, possibly through its effects on theproin-flammatory enzyme(s), phospholipase A2. We examined the effect of recombinant human (rh) CC10 on endotoxin-induced airway contraction and cytokine release in isolated perfused rat lungs. We found that rhCC10 added to the lung perfusate abolished the endotoxin-induced airway contraction, and that it inhibited both the release of interleukin-1▀ and interleukin-6 into the lung perfusate and the release of tumor necrosis factors, into the pulmonary lavage fluid. By contrast, the levels of interferon-? were unaffected by CC10 administration. Rutin, a phospholipase A2 inhibitor, and N?-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, also attenuated the contraction induced by endotoxin. These findings demonstrate that rhCC10 inhibits endotoxin-induced airway contraction and the release of proinflammatory cytokines (interleukin-1▀, interleukin-6, and tumor necrosis factor-a) in isolated perfused rat lungs. The results also indicate that phospholipase A2 and nitric oxide are involved in the airway contraction in this model, possibly through their influence on the production of eicosanoids.
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