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Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. (Östersund Research Unit, Umeå University.)
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
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2004 (Engelska)Ingår i: Eur Respir J, ISSN 0903-1936, Vol. 23, nr 1, s. 82-6Artikel i tidskrift (Refereegranskat) Published
Ort, förlag, år, upplaga, sidor
2004. Vol. 23, nr 1, s. 82-6
Nyckelord [en]
Adult, Airway Resistance/drug effects, Asthma/*physiopathology, Bronchi/chemistry, Bronchoalveolar Lavage Fluid/chemistry, Cell Adhesion Molecules/analysis, Environmental Exposure, Female, Humans, Inflammation/chemically induced, Interleukin-10/analysis, Interleukin-8/analysis/genetics, Lymphocytosis/chemically induced, Male, Middle Aged, Neutrophils/pathology, RNA; Messenger/analysis, Respiratory Mucosa/chemistry, Respiratory System/*drug effects/pathology, Vehicle Emissions/*toxicity
Identifikatorer
URN: urn:nbn:se:umu:diva-13161PubMedID: 14738236OAI: oai:DiVA.org:umu-13161DiVA, id: diva2:152832
Tillgänglig från: 2007-05-03 Skapad: 2007-05-03 Senast uppdaterad: 2018-06-09Bibliografiskt granskad
Ingår i avhandling
1. Airway effects of diesel exhaust in healthy and asthmatic subjects
Öppna denna publikation i ny flik eller fönster >>Airway effects of diesel exhaust in healthy and asthmatic subjects
2002 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Several epidemiological studies have revealed an association between particulate matter (PM) pollution and various health effects. Importantly, there is evidence to suggest that individuals with pre-existing respiratory disease, such as asthma, are more sensitive to elevated ground levels of particulate matter as compared to healthy subjects. Among the various sources of PM pollution, diesel powered vehicles have been identified as important contributors.

The aim of this thesis was to investigate the airway effects of experimental chamber exposure to diesel exhaust (DE) in healthy and asthmatic subjects, focusing on airway responsiveness, airway inflammation and lung function. To achieve a comprehensive picture of the airway responses to DE, a number of different methods were used, including lung function measurements, methacholine inhalation tests, induced sputum and bronchoscopy. Each subject acted as his/her own control by being exposed both to filtered air and DE in a crossover design.

Short term exposure to DE, at a particle concentration (PMi0) of 300 ug/m3, was associated with a clinically significant increase in bronchial hyperresponsiveness in asthmatic subjects. In accordance with the epidemiological data suggesting a 1-4 day lag effect for most health outcomes to PM pollution, the increase was detected one day after DE exposure, indicating a long lasting response to DE in asthmatic airways.

Diesel exhaust induced a range of airway inflammatory changes as reflected in induced sputum, bronchoalveolar lavage and bronchial mucosal biopsies. In healthy subjects, DE exposure was associated with an increase in neutrophils and IL-6 in sputum, elevated levels of IL-8 and IL-6 in bronchial wash (BW), enhanced expression of IL-8 and GRO-a in the bronchial epithelium and with increases in P-selectin and VCAM-1 in the airway mucosa. In contrast, asthmatics responded with an increase in IL-6 in sputum and an enhanced expression of IL-10 in the bronchial epithelium following exposure DE. Thus, clear differences were identified between healthy and asthmatic subjects in the inflammatory response to DE.

Airway epithelial cells constitute the first line of cellular defence towards inhaled air pollutants and increasing evidence suggests that these cells contribute markedly to the initiation of airway inflammatory responses. The bronchial epithelium was identified to have an important regulatory role in response to diesel exhaust, including the capacity to produce chemoattractant and immunoregulatory proteins associated with development of airway inflammation and bronchial hyperresponsiveness.

Lung function measurements revealed that short-term exposure to DE induces an immediate bronchoconstrictive response in both healthy and asthmatic individuals, with significant increases in airway resistance (Raw) following DE exposure.

This thesis also investigated the effects of a lower concentration of DE (PMio 100 ug/m3) than previously studied. It was shown that exposure to DE at a concentration corresponding to a PM level that may be encountered in busy traffic situations, was still associated with potentially adverse airway responses in healthy and asthmatic subjects.

In summary, the results presented here indicate that short term exposure to diesel exhaust, at high ambient concentrations, has the potential to induce a range of biological events in the airways of healthy and asthmatic subjects.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå Universitet, 2002. s. 60
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 750
Nyckelord
air pollution, diesel exhaust, airway responsiveness, airway inflammation, lung function, asthmatics, immunohistochemistry, bronchial epithelium
Nationell ämneskategori
Lungmedicin och allergi
Identifikatorer
urn:nbn:se:umu:diva-96901 (URN)91-7305-172-1 (ISBN)
Disputation
2002-02-16, Sal B, 9 trappor, Byggnad ID (Tandläkarhögskolan), Norrlands Universitetssjukhus i Umeå, Umeå universitet, Umeå, 12:00
Handledare
Projekt
digitalisering@umu
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Diss. (sammanfattning) Umeå : Umeå universitet, 2002, härtill 4 uppsatser.

Tillgänglig från: 2015-01-26 Skapad: 2014-12-05 Senast uppdaterad: 2018-06-07Bibliografiskt granskad

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Stenfors, NikolaiBlomberg, AndersHelleday, RagnberthLevin, Jan-OlofSandström, Thomas

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