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HERO ID
2613063
Reference Type
Journal Article
Subtype
Abstract
Title
Divergent airway inflammatory pathways of oxidative air pollutants
Author(s)
Damewood, JB; Pourazar, J; Stenfors, N; Blomberg, A; Frew, A; Kelly, F; Sandstrom, T
Year
2010
Is Peer Reviewed?
Yes
Journal
American Journal of Respiratory and Critical Care Medicine
ISSN:
1073-449X
EISSN:
1535-4970
Volume
181
Page Numbers
A1146
Language
English
DOI
10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A1146
Web of Science Id
WOS:000208771000147
Relationship(s)
is part of a larger document
3452678
Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Abstract
Rationale: In spite of stricter regulations, ambient air pollution still remains a global health issue. Ozone (O3) and diesel exhaust (DE), both key oxidative air pollutants, have been demonstrated through numerous studies to pose hazardous health effects. Exposure to O3, as well as DE, has been shown to produce significant neutrophilia in the airways. It has previously been demonstrated that DE triggers an increase in nuclear translocation of NFκB and AP-1. The aim of the present study was to assess the expression of these transcription factors in the bronchial epithelium at baseline and after exposure to ozone in healthy subjects.
Methods: 15 healthy subjects underwent two separate 2-hour exposures, to filtered air as well as 0.2 ppm of O3. Bronchoscopy with endobronchial mucosal biopsy sampling was completed 6 hours post-exposure. Biopsies were processed in glycolmethacrylate (GMA) resin and immunostained for transcription factors.
Results: No significant changes were found in the bronchial epithelial expression of NFκB, C-fos or p-c-Jun post-ozone exposure as compared to air. This was true for total stainings as well as nuclear staining.
Conclusion: The activation of redox sensitive transcription factors after DE exposure could denote an underlying oxidative stress. However, in the current study, no analogous upregulation of these transcription factors was observed after an O3 challenge. These new data, taken in conjunction with previous results, further suggests that the inflammatory pathway triggered in the airways by ozone differs from that of diesel exhaust.
Conference Name
American Thoracic Society 2010 International Conference
Conference Location
New Orleans, LA
Conference Dates
May 14-19, 2010
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