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Antioxidant airway responses following experimental exposure to wood smoke in man
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
Kings College London, MRC-HPA Centre for Environment and Health, School of Biomedical and Healthy Studies, King's College London, London, UK .
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik, Energiteknik och termisk processkemi.
Division of Aerosol Technology, Lund University, Lund, Sweden .
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2010 (Engelska)Ingår i: Particle and fibre toxicology, ISSN 1743-8977, Vol. 7, s. 21-Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Exposure of healthy subjects to wood smoke, derived from an experimental wood pellet boiler operating under incomplete combustion conditions with PM emissions dominated by organic matter, caused an increase in mucosal symptoms and GSH in the alveolar respiratory tract lining fluids but no acute airway inflammatory responses. We contend that this response reflects a mobilisation of GSH to the air-lung interface, consistent with a protective adaptation to the investigated wood smoke exposure.

Ort, förlag, år, upplaga, sidor
2010. Vol. 7, s. 21-
Identifikatorer
URN: urn:nbn:se:umu:diva-39427DOI: 10.1186/1743-8977-7-21ISI: 000282501800001PubMedID: 20727160OAI: oai:DiVA.org:umu-39427DiVA, id: diva2:392563
Tillgänglig från: 2011-01-27 Skapad: 2011-01-27 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
Ingår i avhandling
1. Respiratory effects of particulate matter air pollution: studies on diesel exhaust, road tunnel, subway and wood smoke exposure in human subjects
Öppna denna publikation i ny flik eller fönster >>Respiratory effects of particulate matter air pollution: studies on diesel exhaust, road tunnel, subway and wood smoke exposure in human subjects
2011 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Background:

Ambient air pollution is associated with adverse health effects, but the sources and components, which cause these effects is still incompletely understood. The aim of this thesis was to investigate the pulmonary effects of a variety of common air pollutants, including diesel exhaust, biomass smoke, and road tunnel and subway station environments. Healthy non-smoking volunteers were exposed in random order to the specific air pollutants and air/control, during intermittent exercise, followed by bronchoscopy.

Methods and results:

In study I, exposures were performed with diesel exhaust (DE) generated at transient engine load and air for 1 hour with bronchoscopy at 6 hours post-exposure. Immunohistochemical analyses of bronchial mucosal biopsies showed that DE exposure significantly increased the endothelial adhesion molecule expression of p-selectin and VCAM-1, together with increased bronchoalveolar lavage (BAL) eosinophils.

In study II, the subjects were exposed for 1 hour to DE generated during idling with bronchoscopy at 6 hours. The bronchial mucosal biopsies showed significant increases in neutrophils, mast cells and lymphocytes together with bronchial wash neutrophils. Additionally, DE exposure significantly increased the nuclear translocation of the aryl hydrocarbon receptor (AhR) and phosphorylated c-jun in the bronchial epithelium. In contrast, the phase II enzyme NAD(P)H-quinone oxidoreductase 1 (NQO1) decreased after DE.

In study III, the 2-hour exposures took place in a road tunnel with bronchoscopy 14 hours later. The road tunnel exposure significantly increased the total numbers of lymphocytes and alveolar macrophages in BAL, whereas NK cell and CD56+/T cell numbers significantly decreased. Additionally, the nuclear expression of phosphorylated c-jun in the bronchial epithelium was significantly increased after road tunnel exposure.

In study IV, the subjects were exposed to metal-rich particulate aerosol for 2 hours at a subway station with bronchial biopsy and BAL sampling at 14 hours. The subway exposure significantly increased the concentration of glutathione disulphide (GSSG) in BAL, with no airway inflammatory responses. In contrast, the number of neutrophils in the bronchial mucosa and the nuclear expression of phosphorylated c-jun in the bronchial epithelium tended to decrease after the subway exposure.

In study V, the exposure to biomass smoke lasted 3 hours. Bronchoscopy was conducted 24 hours post exposure. The investigated biomass combustion emissions resulted in a significant increase in total glutathione and reduced glutathione in BAL, without any evident acute airway inflammatory responses.

 

 

Conclusion:

The present thesis presents data from exposures of healthy subjects to a variety of common air pollutants, as compared with an air reference. Oxidative as well as bronchial mucosal and bronchoalveolar responses differed between these air pollutants, with the most pronounced airway effects seen after exposure to diesel exhaust. This may be due to differences in pulmonary deposition, physicochemical characteristics, toxicological pathways and potency. Additional studies will assist in addressing dose-response and time kinetic aspects of the airway responses.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå universitet, 2011. s. 110
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1394
Nyckelord
Airway inflammation, antioxidant, bronchoscopy, detoxification, immunohistochemistry, particulate matter
Nationell ämneskategori
Arbetsmedicin och miljömedicin
Identifikatorer
urn:nbn:se:umu:diva-39568 (URN)978-91-7459-130-9 (ISBN)
Disputation
2011-02-24, E04, Byggnad 6E, Norrlands Universitetssjukhus, Umeå, 09:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2011-02-04 Skapad: 2011-02-01 Senast uppdaterad: 2018-06-08Bibliografiskt granskad

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Sehlstedt, MariaBoman, ChristofferBosson, JennyBarath, StefanBehndig, Annelie FPourazar, JamshidSandström, ThomasBlomberg, Anders

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Sehlstedt, MariaBoman, ChristofferBosson, JennyBarath, StefanBehndig, Annelie FPourazar, JamshidSandström, ThomasBlomberg, Anders
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LungmedicinEnergiteknik och termisk processkemi

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