Effect of ozone exposure on airway responses to inhaled allergen in asthmatic subjects.
BACKGROUND
Controlled human exposure studies have produced conflicting results regarding the effect of ozone on the early bronchoconstrictor response to inhaled allergen in specifically sensitized asthmatic subjects. Spirometric parameters do not necessarily reflect the airway inflammatory effects of inhaled ozone or allergen.


OBJECTIVE
This study was designed to investigate whether exposure to ozone enhances the late airway inflammatory response, as well as the early bronchoconstrictor response, to inhaled house dust mite allergen in sensitized asthmatic subjects.


METHODS
Randomized, counter-balanced, cross-over study.


METHODS
Human exposure laboratory.


METHODS
Fourteen subjects were exposed to 0.2 ppm O(3) or filtered air, on separate days, for 1 h during exercise. After each exposure, the subjects were challenged with doubling doses of Dermatophagoides farinae (DF) allergen (provocative concentration of DF causing a 15% decrease in FEV(1) [PC(15)]). At 6 h after allergen challenge, bronchoscopy with BAL, proximal airway lavage (PAL), and endobronchial biopsy were performed. The second exposure/allergen challenge/bronchoscopy sequence was performed at least 4 weeks after the first sequence.


RESULTS
No significant difference in cellular or biochemical markers of the late inflammatory response after allergen was found between the ozone and air exposures (although a trend toward increased neutrophils was noted after ozone exposure in the PAL fluid, p = 0.06). For the group as a whole, no significant difference in PC(15) was demonstrated after ozone exposure compared to air exposure. However, subjects with the greatest ozone-induced decrements in FEV(1) tended to have lower PC(15) values after ozone exposure.


CONCLUSIONS
Exposure to a relatively low-level concentration of ozone does not enhance the late inflammatory or early bronchoconstrictor response to inhaled antigen in most allergic asthmatic subjects. Our results do suggest, however, that a subgroup of asthmatics may acquire increased sensitivity to aeroallergens after exposure to ozone.
Chen
Lisa L
LL
Lung Biology Center, Center for Occupational and Environmental Health, Cardiovascular Research Institute, and Medical Service, San Francisco General Hospital, University of California, San Francisco, CA, USA.
Tager
Ira B
IB
Peden
David B
DB
Christian
Dorothy L
DL
Ferrando
Ronald E
RE
Welch
Barbara S
BS
Balmes
John R
JR
D000280:Administration, Inhalation; D000293:Adolescent; D000328:Adult; D039741:Antigens, Dermatophagoides / Q000009:adverse effects*; D001249:Asthma / Q000175:diagnosis / Q000276:immunology* / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D018592:Cross-Over Studies; D004784:Environmental Monitoring; D006801:Humans; D008297:Male; D009946:Organothiophosphorus Compounds; D010126:Ozone / Q000494:pharmacology*; D011336:Probability; D012016:Reference Values; D012129:Respiratory Function Tests; D012680:Sensitivity and Specificity; D018709:Statistics, Nonparametric
D039741:Antigens, Dermatophagoides; D009946:Organothiophosphorus Compounds; D010126:Ozone; C009680:VX-agent