umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Respiratory effects of particulate matter air pollution: studies on diesel exhaust, road tunnel, subway and wood smoke exposure in human subjects
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
2011 (English)Doctoral thesis, comprehensive summary (Other academic)
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.

Place, publisher, year, edition, pages
Umeå: Umeå universitet , 2011. , 110 p.
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 1394
Keyword [en]
Airway inflammation, antioxidant, bronchoscopy, detoxification, immunohistochemistry, particulate matter
National Category
Environmental Health and Occupational Health
Identifiers
URN: urn:nbn:se:umu:diva-39568ISBN: 978-91-7459-130-9 (print)OAI: oai:DiVA.org:umu-39568DiVA: diva2:394200
Public defence
2011-02-24, E04, Byggnad 6E, Norrlands Universitetssjukhus, Umeå, 09:00 (English)
Opponent
Supervisors
Available from: 2011-02-04 Created: 2011-02-01 Last updated: 2011-02-04Bibliographically approved
List of papers
1. Airway inflammatory response to diesel exhaust generated at urban cycle running conditions
Open this publication in new window or tab >>Airway inflammatory response to diesel exhaust generated at urban cycle running conditions
Show others...
2010 (English)In: Inhalation Toxicology, ISSN 0895-8378, E-ISSN 1091-7691, Vol. 22, no 14, 1144-1150 p.Article in journal (Refereed) Published
Abstract [en]

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.

Keyword
Air pollution, adhesion molecules, airway inflammation, particulate matter.
Identifiers
urn:nbn:se:umu:diva-5164 (URN)10.3109/08958378.2010.529181 (DOI)000284889300002 ()21110774 (PubMedID)
Available from: 2006-05-11 Created: 2006-05-11 Last updated: 2017-12-14Bibliographically approved
2. Diesel exhaust exposure increases nuclear translocation of AhR and supresses the detoxification enzyme NQO1 in human airways
Open this publication in new window or tab >>Diesel exhaust exposure increases nuclear translocation of AhR and supresses the detoxification enzyme NQO1 in human airways
Show others...
(English)Manuscript (preprint) (Other academic)
Identifiers
urn:nbn:se:umu:diva-39563 (URN)
Available from: 2011-02-01 Created: 2011-02-01 Last updated: 2011-02-04Bibliographically approved
3. Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects
Open this publication in new window or tab >>Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects
Show others...
2007 (English)In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 29, no 4, 699-705 p.Article in journal (Refereed) Published
Abstract [en]

Traffic-related air pollution is associated with adverse respiratory effects. The aim of the present study was to investigate whether exposure to air pollution in a road tunnel causes airway inflammatory and blood coagulation responses.

A total of 16 healthy subjects underwent bronchoscopy with bronchial mucosal biopsies and bronchoalveolar lavage (BAL) on two occasions, in random order: once at 14 h after a 2-h exposure to air pollution in a busy road tunnel, and once after a control day with subjects exposed to urban air during normal activities. Peripheral blood was sampled prior to bronchoscopy.

The road tunnel exposures included particulate matter with a 50% cut-off aerodynamic diameter of 2.5 μm, particulate matter with a 50% cut-off aerodynamic diameter of 10 μm and nitrogen dioxide which had median concentrations of 64, 176 and 230 µg·m−3, respectively. Significantly higher numbers of BAL fluid total cell number, lymphocytes and alveolar macrophages were present after road tunnel exposure versus control. Significantly higher nuclear expression of the transcription factor component c-Jun was found in the bronchial epithelium after exposure. No upregulation of adhesion molecules or cellular infiltration was present and blood coagulation factors were unaffected.

In conclusion, exposure of healthy subjects to traffic-related air pollution resulted in a lower airway inflammatory response with cell migration, together with signs of an initiated signal transduction in the bronchial epithelium.

Keyword
Adult, Air Pollutants/*toxicity, Air Pollution, Bronchi/*pathology, Bronchoalveolar Lavage Fluid, Female, Humans, Inflammation/*chemically induced/*etiology, Male, Middle Aged, Particulate Matter, Pulmonary Alveoli/*pathology, Respiratory Hypersensitivity/*chemically induced, Respiratory Mucosa/pathology, Vehicle Emissions
National Category
Environmental Health and Occupational Health
Identifiers
urn:nbn:se:umu:diva-6850 (URN)10.1183/09031936.00035706 (DOI)17251238 (PubMedID)
Available from: 2007-12-19 Created: 2007-12-19 Last updated: 2017-12-14Bibliographically approved
4. Short-term exposure to a train-derived metal rich particulate aerosol in a subway microenvironment induces oxidative stress in the distal airways
Open this publication in new window or tab >>Short-term exposure to a train-derived metal rich particulate aerosol in a subway microenvironment induces oxidative stress in the distal airways
Show others...
(English)Manuscript (preprint) (Other academic)
Identifiers
urn:nbn:se:umu:diva-39565 (URN)
Available from: 2011-02-01 Created: 2011-02-01 Last updated: 2011-02-04Bibliographically approved
5. Antioxidant airway responses following experimental exposure to wood smoke in man
Open this publication in new window or tab >>Antioxidant airway responses following experimental exposure to wood smoke in man
Show others...
2010 (English)In: Particle and fibre toxicology, ISSN 1743-8977, Vol. 7, 21- p.Article in journal (Refereed) 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.

Identifiers
urn:nbn:se:umu:diva-39427 (URN)10.1186/1743-8977-7-21 (DOI)000282501800001 ()20727160 (PubMedID)
Available from: 2011-01-27 Created: 2011-01-27 Last updated: 2011-02-04Bibliographically approved

Open Access in DiVA

fulltext(1346 kB)886 downloads
File information
File name FULLTEXT03.pdfFile size 1346 kBChecksum SHA-512
7e196e0bf67b08ba3e610257f6c82f0f7aade513f1dfc85f18c188d827bff96437ea2b9aa55eab28367ec85130dbd36e3f636fa135fa22ef6e04f9fb2b005a87
Type fulltextMimetype application/pdf

Search in DiVA

By author/editor
Sehlstedt, Maria
By organisation
Pulmonary Medicine
Environmental Health and Occupational Health

Search outside of DiVA

GoogleGoogle Scholar
Total: 886 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

isbn
urn-nbn

Altmetric score

isbn
urn-nbn
Total: 865 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf