Effect of ozone on bronchial mucosal inflammation in asthmatic and healthy subjects

• Published in: Respiratory medicine 2002-05, Vol.96 (5), p.352-358
• Main Authors: STENFORS, N., POURAZAR, J., BLOMBERG, A., KRISHNA, M.T., MUDWAY, I., HELLEDAY, R., KELLY, F.J., FREW, A.J., SANDSTRÖM, T.
• Format: Article
• Language: English
• Subjects: Adult; Air Pollutants - adverse effects; airways inflammation; asthma; Asthma - chemically induced; Asthma - pathology; Asthma - physiopathology; asthma, pollution, ozone, airways inflammation, neutrophil; Biological and medical sciences; Biopsy; Bronchi - drug effects; Bronchi - pathology; Bronchoalveolar Lavage Fluid - cytology; Chronic obstructive pulmonary disease, asthma; Female; Forced Expiratory Volume - drug effects; Humans; Inflammation Mediators - metabolism; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Middle Aged; neutrophil; Neutrophil Infiltration - drug effects; ozone; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Pneumology; pollution; Respiratory system; Sulfuric Acids - adverse effects; Vital Capacity - drug effects
• ISSN: 0954-6111; 1532-3064; 1532-3064
• DOI: 10.1053/rmed.2001.1265

Epidemiological studies suggest that asthmatics are more affected by ozone than healthy people. This study tested three hypotheses (1) that short-term exposure to ozone induces inflammatory cell increases and up-regulation of vascular adhesion molecules in airway lavages and bronchial tissue 6 h after ozone exposure in healthy subjects; (2) these responses are exaggerated in subjects with mild allergic asthma; (3) ozone exacerbates pre-existent allergic airways inflammation. We exposed 15 mild asthmatic and 15 healthy subjects to 0·2 ppm of ozone or filtered air for 2 h on two separate occasions. Airway lavages and bronchial biopsies were obtained 6 h post-challenge. We found that ozone induced similar increases in bronchial wash neutrophils in both groups, although the neutrophil increase in the asthmatic group was on top of an elevated baseline. In healthy subjects, ozone exposure increased the expression of the vascular endothelial adhesion molecules P-selectin and ICAM-1, as well as increasing tissue neutrophil and mast cell numbers. The asthmatics showed allergic airways inflammation at baseline but ozone did not aggravate this at the investigated time point. At 6 h post-ozone-exposure, we found no evidence that mild asthmatics were more responsive than healthy to ozone in terms of exaggerated neutrophil recruitment or exacerbation of pre-existing allergic inflammation. Further work is needed to assess the possibility of a difference in time kinetics between healthy and asthmatic subjects in their response to ozone.