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| 2. |
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| 3. |
- Behndig, Annelie F, et al.
(författare)
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Antioxidant responses to acute ozone challenge in the healthy human airway
- 2009
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 21:11, s. 933-942
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the study was to characterize ozone-induced antioxidant responses in the human airway, including the resident leukocyte population, bronchial mucosa, and respiratory-tract lining fluids. Fifteen healthy subjects were exposed to 0.2 ppm ozone for 2 h, with bronchial wash, bronchoalveolar lavage, and biopsy sampling performed 6 h postexposure. Nasal lavage was also performed at multiple time points pre- and postexposure to evaluate responses during the actual exposure period. During the ozone challenge significant losses of nasal lining fluid urate and vitamin C were observed, which resolved 6 h postexposure. At this time point, increased numbers of neutrophils and enhanced concentrations of total glutathione, vitamin C, and urate were seen in bronchial airway lavages. In bronchoalveolar lavage, increased concentrations of total glutathione, vitamin C, urate, alpha-tocopherol, and extracellular superoxide dismutase occurred 6 h post ozone. In alveolar leukocytes significant losses of glutathione were observed, whereas ascorbate concentrations in endobronchial mucosal biopsies were elevated after ozone at this time. These data demonstrate that ozone elicits a broad spectrum of airway antioxidant responses, with initial losses of vitamin C and urate followed by a phase of augmentation of low-molecular-weight antioxidant concentrations at the air-lung interface. The temporal association between the increased RTLF glutathione following ozone and the loss of this thiol from macrophages implies a mobilization to the lung surface, despite the absence of a quantitative association. We propose this constitutes an acute protective adaptation to ozone.
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| 4. |
- Behndig, Annelie F, et al.
(författare)
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Augmentation of respiratory tract lining fluid ascorbate concentrations through supplementation with vitamin C.
- 2009
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Ingår i: Inhalation toxicology. - : Informa UK Limited. - 1091-7691 .- 0895-8378. ; 21:3, s. 250-8
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Tidskriftsartikel (refereegranskat)abstract
- Low molecular weight antioxidants within human respiratory tract lining fluids (RTLFs) have been proposed to confer protection against the damaging action of inhaled oxidant gases. There is therefore considerable interest in augmenting the concentrations of these moieties at the air-lung interface to protect against injury to the airway epithelium, the induction of inflammation, and declines in lung function. To determine whether RTLF ascorbate concentrations could be augmented through vitamin C supplementation, 24 healthy subjects with low plasma ascorbate (< 50 microM) were recruited into a double-blinded study. Subjects were divided into two groups, one receiving 60 mg/day of vitamin C for 14 days, the other placebo. On days 8 and 15 of this protocol, plasma, urine, and nasal lavage were obtained for ascorbate determination. After a 7-14-day non-intervention period, subjects previously on placebo received supplements containing 125 mg ascorbate, whilst the group previously on supplements received the placebo compound. This "switching" protocol was repeated three more times utilizing 250, 500, and 1000 mg/day ascorbate dosage regimens. Plasma ascorbate increased incrementally with vitamin C dose, as did its urinary excretion. Despite this, nasal lavage concentrations remained unaltered 24 h after the final supplement at all doses. Closer examination of this issue demonstrated that nasal lavage ascorbate concentrations increased acutely after ingestion of a high dose (1000 mg) supplement, peaking at 2-4 h (p < 0.05) before returning to baseline concentrations 24 h post-supplement. In the absence of a quantitative association between plasma and lavage ascorbate concentrations we contend that this response does not simply reflect ascorbate transudation from the plasma and interstitial space into the lavage medium. We therefore conclude that RTLF ascorbate can be augmented, albeit transiently, by oral vitamin C supplementation, with the transient nature of this response likely reflecting oxidative losses within the RTLF or its sequestration into airway cells.
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| 5. |
- Bosson, Jenny, et al.
(författare)
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Early suppression of NFκB and IL-8 bronchial epithelium after ozone exposure in healthy human subjects
- 2009
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Ingår i: Inhalation Toxicology. - : Informa Healthcare. - 0895-8378 .- 1091-7691. ; 21:11, s. 913-919
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to elevated concentrations of ozone, a common air pollutant, has been associated with numerous adverse health effects. We have previously reported the time-course of ozone-induced airway inflammation, demonstrating an early up-regulation of vascular endothelial adhesion molecules in bronchial mucosa at 1.5 hours, followed by a neutrophilic infiltration 6 hours after exposure to 0.2 ppm ozone. We hypothesized that the neutrophilic infiltration in the bronchial mucosa would reflect an early increase in bronchial epithelial expression of redox-sensitive transcription factors and kinases regulating neutrophil chemoattractant expression. To test this hypothesis, endobronchial biopsies were obtained from healthy human subjects (n = 11) 1.5 hours after 0.2 ppm of ozone and filtered air exposures (lasting for 2 hours) and stained for mitogen-activated protein kinases (MAPKs), transcription factors, and neutrophil chemoattractants. Total epithelial staining was quantified, as well as the extent of nuclear translocation. Contrary to expectation, ozone significantly suppressed total and nuclear expression of nuclear factor κB (NFκB) in bronchial epithelial cells (p = 0.02 and p = 0.003 respectively). Similarly, the total staining for phosphorylated C-jun was suppressed (p = 0.021). Expression of interleukin 8 (IL-8) in the bronchial epithelium was likewise decreased after ozone (p = 0.018), while GRO-α, ENA-78, C-fos, p-p38, p-JNK, and p-ERK stainings were unchanged. These data suggest that the redox-sensitive NFκB and activator protein 1 (AP-1) pathways within the human bronchial epithelium do not seem to be involved in the early inflammatory cell recruitment pathways in healthy subjects exposed to ozone.
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| 6. |
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| 7. |
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| 8. |
- Freberg, B. I., et al.
(författare)
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Pulmonary function and serum pneumoproteins in professional ski waxers
- 2016
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 28:1, s. 7-13
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Tidskriftsartikel (refereegranskat)abstract
- Context: Professional ski waxers are exposed to particulate matter (PM) during work, but little is known about untoward pulmonary effects.Objectives: The aim was to study lung function and pneumoproteins in professional ski waxers before and during exposure to PM generated during ski waxing and ski preparation.Material and methods: Forty-five male professional ski waxers examined on an exposure-free day in the morning and at least 6h later were re-examined during ski waxing 2 d later in a cross-shift study. Pulmonary function and gas diffusion capacity were measured and Clara cell protein 16 (CC-16), surfactant protein A and D (SP-A and SP-D), and C-reactive protein (CRP) were determined in serum. PM was collected by personal sampling.Results: The mean PM concentrations in the respirable and in the inhalable aerosol fraction in air samples collected during waxing were 3.1mg/m(3) and 6.2mg/m(3), respectively. The mid expiratory flow (MEF75%) was significantly lower during exposure. The concentrations of CRP increased significantly by more than 100% during ski waxing, and SP-D and CC-16 were significantly lower during the exposed day as compared with the non-exposed day. The results further suggest that SP-D and CC-16 in serum are affected by diurnal variations. No significant alterations were observed for the lung diffusion capacity.Discussion and conclusions: The results suggest that exposure to PM generated during ski waxing may induce pulmonary inflammation with reduced flow in small airways. The increased CRP concentrations indicate the induction of systemic inflammation in ski waxers during exposure.
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| 9. |
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| 10. |
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| 11. |
- Gerlofs-Nijland, Miriam E., et al.
(författare)
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Inhalation toxicity profiles of particulate matter : a comparison between brake wear with other sources of emission
- 2019
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Ingår i: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 31:3, s. 89-98
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Tidskriftsartikel (refereegranskat)abstract
- Objective: There is substantial evidence that exposure to airborne particulate matter (PM) from road traffic is associated with adverse health outcomes. Although it is often assumed to be caused by vehicle exhaust emissions such as soot, other components may also contribute to detrimental effects. The toxicity of fine PM (PM2.5; <2.5 µm mass median aerodynamic diameter) released from brake pads was compared to PM from other sources.Materials and methods: PM2.5 of different types of brake pads (low-metallic, semi-metallic, NAO and ECE-NAO hybrid), tires and road pavement, poultry as well as the combustion of diesel fuel and wood (modern and old-fashioned stove technologies) were collected as suspensions in water. These were subsequently aerosolized for inhalation exposures. Female BALB/cOlaHsd mice were exposed for 1.5, 3, or 6 hours by nose-only inhalation up to 9 mg/m 3 .Results: Neither cytotoxicity nor oxidative stress was observed after exposure to any of the re-aerosolized PM2.5 samples. Though, at similar PM mass concentrations the potency to induce inflammatory responses was strongly dependent on the emission source. Exposure to most examined PM2.5 sources provoked inflammation including those derived from the poultry farm, wear emissions of the NAO and ECE-NAO hybrid brake pads as well as diesel and wood combustion, as indicated by neutrophil chemoattractant, KC and MIP-2 and lung neutrophil influx.Discussion and conclusions: Our study revealed considerable variability in the toxic potency of brake wear particles. Understanding of sources that are most harmful to health can provide valuable information for risk management strategies and could help decision-makers to develop more targeted air pollution regulation.
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| 12. |
- Gerlofs-Nijland, Miriam E, et al.
(författare)
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Toxicity of coarse and fine particulate matter from sites with contrasting traffic profiles.
- 2007
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Ingår i: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 19:13, s. 1055-69
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Tidskriftsartikel (refereegranskat)abstract
- Residence in urban areas with much traffic has been associated with various negative health effects. However, the contribution of traffic emissions to these adverse health effects has not been fully determined. Therefore, the objective of this in vivo study is to compare the pulmonary and systemic responses of rats exposed to particulate matter (PM) obtained from various locations with contrasting traffic profiles. Samples of coarse (2.5 mu m-10 mu m) and fine (0.1 mu m-2.5 mu m) PM were simultaneously collected at nine sites across Europe with a high-volume cascade impactor. Six PM samples from various locations were selected on the basis of contrast in in vitro analysis, chemical composition, and traffic profiles. We exposed spontaneously hypertensive (SH) rats to a single dose (3 mg PM/kg body weight or 10 mg PM/kg body weight) of either coarse or fine PM by intratracheal instillation. We assessed changes in biochemical markers, cell differentials, and histopathological changes in the lungs and blood 24 h postexposure. The dose-related adverse effects that both coarse and fine PM induced in the lungs and vascular system were mainly related to cytotoxicity, inflammation, and blood viscosity. We observed clear differences in the extent of these responses to PM from the various locations at equivalent dose levels. There was a trend that suggests that samples from high-traffic sites were the most toxic. It is likely that the toxicological responses of SH rats were associated with specific PM components derived from brake wear (copper and barium), tire wear (zinc), and wood smoke (potassium).
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| 13. |
- Jeppsson, Marina, et al.
(författare)
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Methylhexahydrophthalic anhydride adducted albumin tryptic peptides in nasal lavage fluid.
- 2009
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 21:12, s. 1013-1020
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Tidskriftsartikel (refereegranskat)abstract
- Methylhexahydrophthalic anhydride (MHHPA) is a reactive, low molecular weight chemical used in products such as plastics, paints, and electronic components. Exposure to MHHPA may lead to work-related airway diseases such as rhinitis, conjunctivitis, and asthma. Twelve subjects employed at a plant manufacturing electrical capacitors using MHHPA were included in this study. Nasal lavages were collected from subjects before work Monday morning and after work Tuesday afternoon. The levels of MHHPA adducted to serum albumin were analyzed with a straightforward work-up method. The samples were trypsinated before being analyzed with a liquid chromatography-triple quadrupole mass spectrometer. The mass spectrometer was run using selected reaction monitoring for six adducted peptides. Also, some biomarkers of effect (albumin, total protein, eosinophil cationic protein, and tryptase) were analyzed in nasal lavages. Furthermore, the metabolite MHHP acid in urine after work on Tuesday was analyzed by gas chromatography-mass spectrometry. Symptoms from the airways and the eyes and sensitization were registered. The main result of this study is that protein adducts can be analyzed in vivo after low occupational exposures to MHHPA. The results also show a correlation between adducted peptides and albumin in nasal lavage. Furthermore, there may be a difference in the potential to induce hyperresponsiveness between adducts bound to different amino acids.
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| 14. |
- Johannesson, Sandra, 1975, et al.
(författare)
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Urban air pollution and effects on biomarkers of systemic inflammation and coagulation: a panel study in healthy adults
- 2014
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 26:2, s. 84-94
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Tidskriftsartikel (refereegranskat)abstract
- Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity. Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden. Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10>30 mu g/m(3)) or a day with low levels (PM10<15 mu g/m(3) and NO2 <35 mu g/m(3)). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model. Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high-and low-pollution days was five for PM10 (median: 49 and 10 mg/m(3)) and two for NO2 (median: 47 and 24 mg/m(3)). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels. Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers.
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| 15. |
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| 16. |
- Jonasson, Sofia, et al.
(författare)
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Inhalation exposure of nano-scaled titanium dioxide (TiO2) particles alters the inflammatory responses in asthmatic mice
- 2013
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Ingår i: Inhalation Toxicology. - : Informa Healthcare. - 0895-8378 .- 1091-7691. ; 25:4, s. 179-191
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Tidskriftsartikel (refereegranskat)abstract
- Context: Titanium dioxide (TiO2) nanoparticles (NPs) are regarded as relatively non-toxic in concentrations occurring in occupational environments. Nevertheless, it is conceivable that adverse health effects may develop in sensitive populations such as individuals with respiratory diseases.Objective: We investigated whether single or repeated exposure to TiO2 could aggravate inflammatory responses in naive mice and mice with ovalbumin (OVA)-induced airway inflammation.Methods: Exposure to aerosolized TiO2 was performed during OVA sensitization, before, or during the OVA challenge period. The effects on respiratory physiology, inflammatory cells in bronchoalveolar lavage (BAL) and inflammatory mediators in BAL and serum were assessed 24 h after the last OVA challenge or TiO2 exposure.Results: A single exposure of TiO2 had a marked effect on responses in peripheral airways and increasing infiltration of neutrophils in airways of naive animals. Marked aggravation of airway responses was also observed in animals with allergic disease provided that the single dose TiO2 was given before allergen challenge. Repeated exposures to TiO2 during sensitization diminished the OVA-induced airway eosinophilia and airway hyperresponsiveness but concomitant exposure to TiO2 during the OVA challenge period resulted in neutrophilic airway inflammation and a decline in general health condition as indicated by the loss of body weight.Conclusion: We conclude that inhalation of TiO2 may aggravate respiratory diseases and that the adverse health effects are highly dependent on dose and timing of exposure. Our data imply that inhalation of NPs may increase the risk for individuals with allergic airway disease to develop symptoms of severe asthma.
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| 17. |
- Kaundal, Ankur, et al.
(författare)
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Numerical investigation of the effect of air supply on cook stove performance.
- 2021
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 33:5, s. 193-203
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: In a domestic biomass cook stove, the air supply plays a significant role in improving the overall combustion characteristics. The present research aims to numerically investigate the effect of air supply, division of air intake into primary and secondary air, and its optimization. > In a domestic biomass cook stove, the air supply plays a significant role in improving the overall combustion characteristics. The present research aims to numerically investigate the effect of air supply, division of air intake into primary and secondary air, and its optimization. Methods: The geometries of cook stove combustion chamber were prepared and simulated using species transport model with eddy-dissipation turbulent mixing. The stoichiometric amount of air was split into different ratios varying from 50:50 to 10:90 and simulations were carried out for each case. The computational model was validated and the concentration of CO2, H2O, O2, wood volatile and resultant temperature were compared and analyzed. Results: Species transport in the form of conservation of mass along with momentum conservation and energy conservation gave the spatial distribution of resultant species and spatial temperature distribution. The computational domain with feedstock inlet corresponding to the pyrolysis regime has yielded good results compared to that in the front. In this domain, the primary to secondary air ratio of 50:50 showed the best results due to the dominance of primary air utilization and, thus, less secondary air use even at higher elevations. With the maximum temperature near 1300 K, maximum relative CO2 production, and maximum feedstock utilization, the primary to secondary air ratio of 50:50 observed to be optimum. Conclusions: Due to the adequate intermixing of reactant species and uniform diffusion of product species along the combustion chamber's height, the computational domain with feedstock inlet corresponding to the pyrolysis regime has shown realistic conditions. The temperature profile and mole fraction of various species, thus obtained, can be used to design an efficient cook stove as the cross-section and dimensions of the combustion chamber and chimney relates to approach the desired division of air.
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| 18. |
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| 19. |
- Langrish, Jeremy, et al.
(författare)
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Exposure to nitrogen dioxide is not associated with vascular dysfunction in man
- 2010
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Ingår i: Inhalation Toxicology. - : Informa Healthcare. - 0895-8378 .- 1091-7691. ; 22:3, s. 192-198
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Tidskriftsartikel (refereegranskat)abstract
- Background: Exposure to air pollution is associated with increased cardiorespiratory morbidity and mortality. It is unclear whether these effects are mediated through combustion-derived particulate matter or gaseous components, such as nitrogen dioxide. Objectives: To investigate the effect of nitrogen dioxide exposure on vascular vasomotor and six fibrinolytic functions. Methods: Ten healthy male volunteers were exposed to nitrogen dioxide at 4 ppm or filtered air for 1 h during intermittent exercise in a randomized double-blind crossover study. Bilateral forearm blood flow and fibrinolytic markers were measured before and during unilateral intrabrachial infusion of bradykinin (100–1000 pmol/min), acetylcholine (5–20 μg/min), sodium nitroprusside (2–8 μg/min), and verapamil (10–100 μg/min) 4 h after the exposure. Lung function was determined before and after the exposure, and exhaled nitric oxide at baseline and 1 and 4 h after the exposure. Results: There were no differences in resting forearm blood flow after either exposure. There was a dose-dependent increase in forearm blood flow with all vasodilators but this was similar after either exposure for all vasodilators (p > .05 for all). Bradykinin caused a dose-dependent increase in plasma tissue-plasminogen activator, but again there was no difference between the exposures. There were no changes in lung function or exhaled nitric oxide following either exposure. Conclusion: Inhalation of nitrogen dioxide does not impair vascular vasomotor or fibrinolytic function. Nitrogen dioxide does not appear to be a major arbiter of the adverse cardiovascular effects of air pollution.
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| 20. |
- Larsson, Nirina, et al.
(författare)
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Airway inflammatory responses to diesel exhaust in allergic rhinitics
- 2013
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 25:3, s. 160-167
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Tidskriftsartikel (refereegranskat)abstract
- Context: Proximity to traffic, particularly to diesel-powered vehicles, has been associated with inducing and enhancing allergies. To investigate the basis for this association, we performed controlled exposures of allergic rhinitics to diesel exhaust (DE) at a dose known to be pro-inflammatory in healthy individuals.Objective: We hypothesized that diesel-exhaust exposure would augment lower airway inflammation in allergic rhinitics.Materials and methods: Fourteen allergic rhinitics were exposed in a double-blinded, randomized trial to DE (100 mu g/m(3) PM10) and filtered air for 2 h on separate occasions. Bronchoscopy with endobronchial mucosal biopsies and airway lavage was performed 18 h post-exposure, and inflammatory markers were assessed.Results: No evidence of neutrophilic airway inflammation was observed post-diesel, however, a small increase in myeloperoxidase was found in bronchoalveolar lavage (p = 0.032). We found no increases in allergic inflammatory cells. Reduced mast cell immunoreactivity for tryptase was observed in the epithelium (p = 0.013) parallel to a small decrease in bronchial wash stem cell factor (p = 0.033). Discussion and conclusion: DE, at a dose previously shown to cause neutrophilic inflammation in healthy individuals, induced no neutrophilic inflammation in the lower airways of allergic rhinitics, consistent with previous reports in asthmatics. Although there was no increase in allergic inflammatory cell numbers, the reduction in tryptase in the epithelium may indicate mast cell degranulation. However, this occurred in the absence of allergic symptoms. These data do not provide a simplistic explanation of the sensitivity in rhinitics to traffic-related air pollution. The role of mast cells requires further investigation.
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| 21. |
- Löndahl, Jakob, et al.
(författare)
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Deposition of biomass combustion aerosol particles in the human respiratory tract.
- 2008
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 20:10, s. 923-933
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Tidskriftsartikel (refereegranskat)abstract
- Smoke from biomass combustion has been identified as a major environmental risk factor associated with adverse health effects globally. Deposition of the smoke particles in the lungs is a crucial factor for toxicological effects, but has not previously been studied experimentally. We investigated the size-dependent respiratory-tract deposition of aerosol particles from wood combustion in humans. Two combustion conditions were studied in a wood pellet burner: efficient ("complete") combustion and low-temperature (incomplete) combustion simulating "wood smoke." The size-dependent deposition fraction of 15-to 680-nm particles was measured for 10 healthy subjects with a novel setup. Both aerosols were extensively characterized with regard to chemical and physical particle properties. The deposition was additionally estimated with the ICRP model, modified for the determined aerosol properties, in order to validate the experiments and allow a generalization of the results. The measured total deposited fraction of particles from both efficient combustion and low-temperature combustion was 0.21-0.24 by number, surface, and mass. The deposition behavior can be explained by the size distributions of the particles and by their ability to grow by water uptake in the lungs, where the relative humidity is close to saturation. The experiments were in basic agreement with the model calculations. Our findings illustrate: (1) that particles from biomass combustion obtain a size in the respiratory tract at which the deposition probability is close to its minimum, (2) that particle water absorption has substantial impact on deposition, and (3) that deposition is markedly influenced by individual factors.
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| 22. |
- Löndahl, Jakob, et al.
(författare)
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Size-Resolved Respiratory Tract Deposition of Fine and Ultrafine Hydrophobic and Hygroscopic Aerosol Particles during Rest and Exercise
- 2007
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 19:2, s. 109-116
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Tidskriftsartikel (refereegranskat)abstract
- Airborne ultrafine particles (diameter <100 nm) are ubiquitous in the environment and have been associated with adverse health effects. The respiratory-tract deposition of these particles is fundamentally influenced by their hygroscopicity: their ability to grow by condensation of water in the humid respiratory system. Ambient particles are typically hygroscopic, to varying degrees. This article investigates the influence of hygroscopicity, exercise level, gender, and intersubject variability on size-dependent deposition of fine and ultrafine particles during spontaneous breathing. Using a novel and well-characterized setup, respiratory-tract deposition in the range 12-320 nm has been measured for 29 healthy adults (20 men, 9 women). Each subject completed four sessions: rest and light exercise on an ergometer bicycle while inhaling both hydrophobic (diethylhexylsebacate) and hygroscopic (NaCl) particles. The deposited fraction (DF) based on dry diameters was two to four times higher for the hydrophobic ultrafine particles than for the hygroscopic. The DF of hygroscopic ultrafine particles could be estimated by calculating their equilibrium size at 99.5% relative humidity. The differences in average DF due to exercise level and gender were essentially less than 0.03. However, the minute ventilation increased fourfold during exercise and was 18-46% higher for the men than for the women. Consequently the deposited dose of particles was fourfold higher during exercise and considerably increased for the male subjects. Some individuals consistently had a high DF in all four sessions. As an example, the results show that an average person exposed to 100-nm hydrophobic particles during exercise will receive a 16 times higher dose than a relaxed person exposed to an equal amount of hygroscopic (NaCl) particles.
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| 23. |
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| 24. |
- Mills, Nicholas L, et al.
(författare)
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Air pollution and atherothrombosis.
- 2007
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Ingår i: Inhal Toxicol. - : Informa UK Limited. - 1091-7691. ; 19 Suppl 1, s. 81-9
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Tidskriftsartikel (refereegranskat)
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| 25. |
- Nosratabadi, Ali Reza, et al.
(författare)
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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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Ingår i: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 35:13-14, s. 309-323
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Tidskriftsartikel (refereegranskat)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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| 26. |
- Ohlson, Carl-Goran, et al.
(författare)
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Inflammatory markers and exposure to occupational air pollutants
- 2010
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 22:13, s. 1083-1090
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Tidskriftsartikel (refereegranskat)abstract
- Methods: Total dust was sampled in the breathing zone of 73 subjects working with welding, cutting, grinding and in foundries such as iron, aluminium, and concrete. Stationary measurements were used to study different size fractions of particles including respirable dust, particulate matter (PM)(10) and PM2.5, the particle number concentration, the number of particles deposited in the alveoli, and total particle surface area concentration. Inflammatory markers such as interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, D-dimer, and urate were measured in plasma or serum before the first shift after the summer vacation and after the first, second, and fourth shift. Results: The mean level of total dust in the breathing zone was 0.93 mg/m
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| 27. |
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| 28. |
- Qvarfordt, Mikaela, et al.
(författare)
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Pulmonary translocation of ultrafine carbon particles in COPD and IPF patients
- 2022
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 34:1-2, s. 14-23
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Tidskriftsartikel (refereegranskat)abstract
- Objective Epidemiological studies indicate association between elevated air pollution and adverse health effects. Several mechanisms have been suggested, including translocation of inhaled ultrafine carbon (UFC) particles into the bloodstream. Previous studies in healthy subjects have shown no significant pulmonary translocation of UFC-particles. This study aimed to assess if UFC-particles translocate from damaged alveolar compartment in subjects suffering from chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Methods Eleven COPD and nine IPF subjects were exposed to a 100 nm UFC-particle-aerosol labeled with Indium-111. Activity in the body was followed up for 10 days using gamma camera planar-imaging as well as in blood and urine samples. Results The pulmonary central to periphery activity ratio was significantly higher for COPD as compared to IPF subjects at exposure, 1.8 and 1.4, respectively and remained constant throughout the test period. Ten days after exposure, the estimated median pulmonary translocation of UFC particles was 22.8 and 25.8% for COPD and IPF, respectively. Bound activity was present in blood throughout the test period, peaking at 24-h postinhalation with a median concentration of 5.6 and 8.9 Bq/ml for the COPD and IPF, respectively. Median bound activity excreted in urine (% of inhaled) after 10 days was 1.4% in COPD and 0.7% in IPF. Activity accumulation in liver and spleen could not be demonstrated. Conclusions Our results suggest that UFC particles leak through the damaged alveolar barrier to the bloodstream in COPD and IPF patients probably distributing in a wide spectrum of whole-body tissues.
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| 29. |
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| 30. |
- Sehlstedt, Maria, 1979-, et al.
(författare)
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Airway inflammatory response to diesel exhaust generated at urban cycle running conditions
- 2010
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 22:14, s. 1144-1150
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Tidskriftsartikel (refereegranskat)abstract
- DE generated under urban running conditions increased bronchial adhesion molecule expressions, together with the novel finding of bronchoalveolar eosinophilia, which has not been shown after exposure to DE at idling. Variations in airway inflammatory response to DE generated under diverse running condition may be related to differences in exhaust composition.
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| 31. |
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| 32. |
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| 33. |
- Stamyr, Kristin, et al.
(författare)
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Swedish forensic data 1992-2009 suggest hydrogen cyanide as an important cause of death in fire victims
- 2012
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Ingår i: Inhalation Toxicology. - : Informa Healthcare. - 0895-8378 .- 1091-7691. ; 24:3, s. 194-199
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Tidskriftsartikel (refereegranskat)abstract
- Between 60 and 80% of all deaths related to fire are attributed to toxic fumes. Carbon monoxide (CO) is commonly thought to be the major cause. However, hydrogen cyanide (HCN) is also formed. Still, the exact contribution of HCN to fire-related fatalities is unknown. The aim of the study was to investigate the impact of HCN in relation to CO as a cause of death in fire victims. Data on carboxyhemoglobin (COHb) and blood cyanide from deceased fire victims in the period 1992-2009 were collected from two Swedish nationwide forensic databases (ToxBase and RattsBase). The databases contain data on COHb and/or cyanide from 2303 fire victims, whereof 816 on both COHb and cyanide. Nonparametric statistical tests were used. Seventeen percent of the victims had lethal or life-threatening blood cyanide levels (andgt;1 mu g/g) and 32% had lethal COHb levels (andgt;50% COHb). Over 31% had cyanide levels above 0.5 mu g/g, an indication of significant HCN exposure. The percentages may be underestimates, as cyanide is quickly eliminated in blood also after death. Our results support the notion that HCN contributes more to the cause of death among fire victims than previously thought.
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| 34. |
- Stenfors, Nikolai, et al.
(författare)
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Ozone exposure enhances mast-cell inflammation in asthmatic airways despite inhaled corticosteroid therapy.
- 2010
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Ingår i: Inhalation Toxicology. - : Informa Healthcare. - 0895-8378 .- 1091-7691. ; 22:2, s. 133-139
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Tidskriftsartikel (refereegranskat)abstract
- Asthmatics are recognised to be more susceptible than healthy individuals to adverse health effects caused by exposure to the common air pollutant ozone. Ozone has been reported to induce airway neutrophilia in mild asthmatics, but little is known about how it affects the airways of asthmatic subjects on inhaled corticosteroids. We hypothesised that ozone exposure would exacerbate the pre-existent asthmatic airway inflammation despite regular inhaled corticosteroid treatment. Therefore, we exposed subjects with persistent asthma on inhaled corticosteroid therapy to 0.2 ppm ozone or filtered air for 2 h, on 2 separate occasions. Lung function was evaluated before and immediately after exposure, while bronchoscopy was performed 18 h post exposure. Compared to filtered air, ozone exposure increased airway resistance. Ozone significantly enhanced neutrophil numbers and myeloperoxidase levels in airway lavages, and induced a fourfold increase in bronchial mucosal mast cell numbers. The present findings indicate that ozone worsened asthmatic airway inflammation and offer a possible biological explanation for the epidemiological findings of increased need for rescue medication and hospitalisation in asthmatic people following exposure to ambient ozone.
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| 35. |
- Stockfelt, Leo, 1981, et al.
(författare)
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A controlled chamber study of effects of exposure to diesel exhaust particles and noise on heart rate variability and endothelial function
- 2022
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Ingår i: Inhalation Toxicology. - : Taylor and Francis Ltd.. - 0895-8378 .- 1091-7691. ; 34:5-6, s. 159-170
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Tidskriftsartikel (refereegranskat)abstract
- Background: Adverse cardiovascular effects are associated with both diesel exhaust and road traffic noise, but these exposures are hard to disentangle epidemiologically. We used an experimental setup to evaluate the impact of diesel exhaust particles and traffic noise, alone and combined, on intermediary outcomes related to the autonomic nervous system and increased cardiovascular risk. Methods: In a controlled chamber 18 healthy adults were exposed to four scenarios in a randomized cross-over fashion. Each exposure scenario consisted of either filtered (clean) air or diesel engine exhaust (particle mass concentrations around 300 µg/m3), and either low (46 dB(A)) or high (75 dB(A)) levels of traffic noise for 3 h at rest. ECG was recorded for 10-min periods before and during each exposure type, and frequency-domain heart rate variability (HRV) computed. Endothelial dysfunction and arterial stiffness were assessed after each exposure using EndoPAT 2000. Results: Compared to control exposure, HRV in the high frequency band decreased during exposure to diesel exhaust, both alone and combined with noise, but not during noise exposure only. These differences were more pronounced in women. We observed no synergistic effects of combined exposure, and no significant differences between exposure scenarios for other HRV indices, endothelial function or arterial stiffness. Conclusion: Three-hour exposure to diesel exhaust, but not noise, was associated with decreased HRV in the high frequency band. This indicates activation of irritant receptor-mediated autonomic reflexes, a possible mechanism for the cardiovascular risks of diesel exposure. There was no effect on endothelial dysfunction or arterial stiffness after exposure. © 2022 The Author(s).
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| 36. |
- Stockfelt, Leo, 1981, et al.
(författare)
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Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.
- 2012
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Ingår i: Inhalation toxicology. - : Informa UK Limited. - 1091-7691 .- 0895-8378. ; 24:1, s. 47-59
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. Materials and Methods: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. Results: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. Conclusions: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.
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| 37. |
- Stockfelt, Leo, 1981, et al.
(författare)
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Short-term chamber exposure to low doses of two kinds of wood smoke does not induce systemic inflammation, coagulation or oxidative stress in healthy humans
- 2013
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 25:8, s. 417-425
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Air pollution increases the risk of cardiovascular diseases. A proposed mechanism is that local airway inflammation leads to systemic inflammation, affecting coagulation and the long-term risk of atherosclerosis. One major source of air pollution is wood burning. Here we investigate whether exposure to two kinds of wood smoke, previously shown to cause airway effects, affects biomarkers of systemic inflammation, coagulation and lipid peroxidation. Methods: Thirteen healthy adults were exposed to filtered air followed by two sessions of wood smoke for three hours, one week apart. One session used smoke from the start-up phase of the wood-burning cycle, and the other smoke from the burn-out phase. Mean particle mass concentrations were 295 mu g/m(3) and 146 mu g/m(3), and number concentrations were 140 000/cm(3) and 100 000/cm(3), respectively. Biomarkers were analyzed in samples of blood and urine taken before and several times after exposure. Results after wood smoke exposure were adjusted for exposure to filtered air. Results: Markers of systemic inflammation and soluble adhesion molecules did not increase after wood smoke exposure. Effects on markers of coagulation were ambiguous, with minor decreases in fibrinogen and platelet counts and mixed results concerning the coagulation factors VII and VIII. Urinary F-2-isoprostane, a consistent marker of in vivo lipid peroxidation, unexpectedly decreased after wood smoke exposure. Conclusions: The effects on biomarkers of inflammation, coagulation and lipid peroxidation do not indicate an increased risk of cardiovascular diseases in healthy adults by short-term exposure to wood smoke at these moderate doses, previously shown to cause airway effects.
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| 38. |
- Sällsten, Gerd, 1952, et al.
(författare)
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Experimental wood smoke exposure in humans
- 2006
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 18:11, s. 855-864
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Tidskriftsartikel (refereegranskat)abstract
- Experimental studies are used to evaluate effects of human exposure to diesel exhaust and concentrated ambient particles. This article describes a system for studying exposure of humans to wood smoke. Wood smoke was generated using a wood stove placed outside an exposure chamber that can hold at least 10 subjects. A partial flow of the generated wood smoke from the stove was mixed with filtered indoor air. Personal and stationary measurements were performed of PM2.5 and PM1 mass concentrations and various volatile organic compounds (VOCs): 1,3-butadiene, benzene, and aldehydes. In addition, particulate matter ( PM) mass, number concentrations, and size distributions of particles (0.007 - 6.7 mu m), as well as nitrous oxides, CO2, and CO, were measured online. Filters were analyzed for trace elements and black smoke. Polycyclic aromatic compounds, toluene, and xylenes were determined in stationary samples. Results of the first experiment showed no differences between personal and stationary measurements for particles or VOCs. Consequently, stationary measurements can be used to predict personal exposure. All PM mass ( about 250 mu g/m(3)) was in the PM1 fraction. Subjective symptoms were generally weak, while clear objective signs were found, for example, in biomarkers of inflammation. With careful control of the combustion process, relatively constant mass and number concentrations were obtained over each exposure session. By varying the combustion and dilution of the wood smoke, different exposure scenarios can be achieved and thus, knowledge about which of the properties of particles and gaseous compounds are crucial for the effects.
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| 39. |
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| 40. |
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| 41. |
- Wigenstam, Elisabeth, 1980-, et al.
(författare)
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Treatment with dexamethasone or liposome-encapsuled vitamin E provides beneficial effects after chemical-induced lung injury.
- 2009
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 21:11, s. 958-964
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Tidskriftsartikel (refereegranskat)abstract
- The pathogenesis of lung injury by exposure to highly toxic sulfur and nitrogen mustards involves alkylating damage of the respiratory epithelium followed by an acute inflammatory response and lung edema. The acute phase is followed by long-term respiratory complications characterized by bronchitis, lung fibrosis, and airway hyperreactivity. In this study, we utilized a mouse model for airway inflammation induced by inhalation exposure to the alkylating nitrogen mustard melphalan, in order to investigate possible beneficial treatment effects by the corticosteroid dexamethasone. In addition, we investigated therapeutic efficacy of liposome-encapsuled vitamin E, an antioxidant formulation previously shown to be efficient in counteracting inflammatory conditions. Influx of inflammatory cells to airways, edema formation, and expression of different cytokines were analyzed 6 and 18 hours after exposure to melphalan. In order to evaluate long-term lung effects, we also investigated collagen deposition and accumulation of lymphocytes at 2 and 4 weeks after exposure. A single intraperitoneal injection of dexamethasone (10 mg/kg body weight) 1 hour after melphalan exposure significantly reduced interleukin (IL)-1 and IL-6 in bronchoalveolar lavage fluid (BALF) and diminished the acute airway inflammation. Our results also indicate that early single-dose treatment with dexamethasone protects against long-term effects observed 2-4 weeks after melphalan exposure, as indicated by reduced lymphocytic response in airways and decreased collagen deposition. Furthermore, our results indicate that also vitamin E (50 mg/kg) reduces acute inflammatory cell influx, and suppresses collagen formation in lung tissue, indicating that this drug could be used in combination with corticosteroids for protection against chemical-induced lung injury.
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| 42. |
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