Diverging airway inflammatory responses to diesel exhaust exposure in healthy and asthmatic subjects with and without inhaled corticosteroid treatment

A. F. Behndig, J. Brown, A. J. Frew, R. Helleday, F. J. Kelly, J. Pourazar, N. Stenfors, T. Sandström, A. Blomberg (Umeå, Sweden; Southampton, London, United Kingdom)

Source: Annual Congress 2002 - Effects of air pollution on lung cells
Session: Effects of air pollution on lung cells
Session type: Oral Presentation
Number: 264
Disease area: Airway diseases

Congress or journal article abstract

Abstract

Diesel exhaust (DE) is a major source of particulate matter (PM) pollution. Epidemiological data suggest asthmatics to be a sensitive group with respect to air pollution.
This study was performed to compare the airway inflammatory responses of subjects with asthma with (n=14) and without inhaled corticosteroids (ICS)(n=16) to that of healthy (n=24), when exposed to DE (PM10 100mg/m3) and air for 2 hours. Bronchoscopy with bronchial wash (BW) and bronchoalveolar lavage (BAL) was performed at 18 hours.
At baseline, asthmatics had sign. higher BW-eosinophils (p=0.015) and mast cells (p=0.001) vs. healthy.
In healthy, DE induced a neutrophilic airway inflammation in BW (p<0.01). In asthmatics without ICS, DE induced an increase in BAL-mast cell % (p=0.03) and decreased eosinophils (p=0.06). Asthmatics on ICS showed no sign. airway inflammatory changes after DE.
The DE induced responses, relative to the air responses, showed sign. higher % of BW-neutrophils in healthy compared to asthmatics without ICS(p=0.027), but no change compared to asthmatics with ICS. BAL-mast cell % after DE, relative to air exposure, were higher in the non-ICS treated group (p<0.01), whereas the ICS treated group of asthmatics showed no sign. changes.
In summary, DE exposure induced different responses in healthy and asthmatic subjects with and without inhaled corticosteroids. Healthy presented a neutrophilic inflammation and asthmatics without ICS showed a mastcell dominated inflammation. The data may suggest a protective effect against DE-induced airway inflammation by the inhaled corticosteroid treatment.


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A. F. Behndig, J. Brown, A. J. Frew, R. Helleday, F. J. Kelly, J. Pourazar, N. Stenfors, T. Sandström, A. Blomberg (Umeå, Sweden; Southampton, London, United Kingdom). Diverging airway inflammatory responses to diesel exhaust exposure in healthy and asthmatic subjects with and without inhaled corticosteroid treatment. Eur Respir J 2002; 20: Suppl. 38, 264

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