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Sökning: onr:cnj6m298989zqg5f > Ozone and diesel ex...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
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020 z 9789172642669
024a http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-10712 uri
024a urn:nbn:se:umu:diva-10712 urn
040 a MimerProde a
041a eng
042 9 EPLK
100a Bosson, Jenny,d 1975-4 aut
2451 0a Ozone and diesel exhausth [Elektronisk resurs]b airway signaling, inflammation and pollutant interactions
264 1a Umeå :b Umeå universitet,c 2007
300 a 83
490a Umeå University medical dissertations,x 0346-6612x 0346-6612
500 a Härtill 4 uppsatser
500 a doctorat en médecine
500 a Medicine doktorsexamen
500 a Doctor medicinae
500 a Doctor of Philosophy (PhD)
500 a Sal B, 9 trappor, Tandläkarhuset, Norrlands Universitetssjukhus, Umeå
502 a Diss. (sammanfattning) Umeå : Umeå universitet, 2007
506a gratis
520 a It is well established that air pollution has detrimental effects on both human health as well as the environment. Exposure to ozone and particulate matter pollution, is associated with an increase in cardiopulmonary mortality and morbidity. Asthmatics, elderly and children have been indicated as especially sensitive groups. With a global increase in use of vehicles and industry, ambient air pollution represents a crucial health concern as well as a political, economical and environmental dilemma. Both ozone (O3) and diesel exhaust (DE) trigger oxidative stress and inflammation in the airways, causing symptoms such as wheezing, coughing and reduced lung function. The aim of this thesis was to further examine which pro-inflammatory signaling pathways that are initiated in the airways by ozone, as compared to diesel exhaust. Furthermore, to study the effects of these two ambient air pollutants in a sequential exposure, thus mimicking an urban profile. In order to investigate this in healthy as well as asthmatic subjects, walk-in exposure chambers were utilized and various airway compartments were studied by obtaining induced sputum, endobronchial biopsies, or airway lavage fluids. In asthmatic subjects, exposure to 0.2 ppm of O3 induced an increase in the cytokines IL 5, GM-CSF and ENA-78 in the bronchial epithelium six hours post-exposure. The healthy subjects, however, displayed no elevations of bronchial epithelial cytokine expression in response to the ozone exposure. The heightened levels of neutrophil chemoattractants and Th2 cytokines in the asthmatic airway epithelium may contribute to symptom exacerbations following air pollution exposure. When examining an earlier time point post O3 exposure (1½ hours), healthy subjects exhibited a suppression of IL-8 as well as of the transcription factors NFκB and c-jun in the bronchial epithelium, as opposed to after filtered air exposure. This inhibition of early signal transduction in the bronchial epithelium after O3 differs from the response detected after exposure to DE. Since both O3 and DE are associated with generating airway neutrophilia as well as causing direct oxidative damage, it raises the query of whether daily exposure to these two air pollutants creates a synergistic or additive effect. Induced sputum attained from healthy subjects exposed in sequence to 0.2 ppm of O3 five hours following DE at a PM concentration of 300 µg/m3, demonstrated significantly increased neutrophils, and elevated MPO levels, as compared to the sequential DE and filtered air exposure. O3 and DE interactions were further investigated by analyses of bronchoalveolar lavage and bronchial wash. It was demonstrated that pre-exposure to DE, as compared to filtered air, enhances the O3-induced airway inflammation, in terms of an increase in neutrophil and macrophage numbers in BW and higher EPX expression in BAL. In conclusion, this thesis has aspired to expand the knowledge of O3-induced inflammatory pathways in humans, observing a divergence to the previously described DE initiated responses. Moreover, a potentially adverse airway inflammation augmentation has been revealed after exposure to a relevant ambient combination of these air pollutants. This provides a foundation towards an understanding of the cumulative airway effects when exposed to a combination of ambient air pollutants and may have implications regarding future regulations of exposure limits.
650 7a Medical and Health Sciences2 hsv
650 7a Clinical Medicine2 hsv
650 7a Respiratory Medicine and Allergy2 hsv
650 7a Medicin och hälsovetenskap2 hsv
650 7a Klinisk medicin2 hsv
650 7a Lungmedicin och allergi2 hsv
650 7a MEDICINE2 svep
650 7a Dermatology and venerology,clinical genetics, internal medicine2 svep
650 7a Internal medicine2 svep
650 7a Lung diseases2 svep
650 7a MEDICIN2 svep
650 7a Dermatologi och venerologi, klinisk genetik, invärtesmedicin2 svep
650 7a Invärtesmedicin2 svep
650 7a Lungsjukdomar2 svep
650 7a lungmedicin2 umu
650 7a Lung Medicine2 umu
653 a air pollution
653 a ozone
653 a diesel exhaust
653 a airway inflammation
653 a asthma
653 a immunohistochemistry
655 7a government publication2 marcgt
700a Blomberg, Anders4 ths
700a Sandström, Thomas4 ths
700a Ädelroth, Ellinor4 ths
700a Balmes, John4 opn
710a Umeå universitetb Medicinska fakulteten4 pbl
7720 8i channel recordw tc5g1zj51493sl0
7760 8i Annat formatz 9789172642669
830 0a Umeå University medical dissertations,x 0346-6612x 0346-6612
8564 0u http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1071
8564 0u http://umu.diva-portal.org/smash/get/diva2:140106/FULLTEXT01
8564 2u http://www.umu.se/z Värdpublikation
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