Increased specific airway reactivity of persons with mild allergic asthma after 7.6 hours of exposure to 0.16 ppm ozone.
BACKGROUND
Exposure to ozone causes decrements in lung function, increased airway reactivity to nonspecific bronchoconstrictors, and lung inflammation. Epidemiology studies show an association between ambient oxidant levels and increased asthma attacks and hospital admissions.


OBJECTIVE
The purpose of our study was to evaluate the response of persons with mild asthma to inhaled allergen after ozone exposure conditions similar to those observed in urban areas of the United States.


METHODS
Using a double-blind, counter-balanced design, we exposed 9 (5 women and 4 men) subjects with mild atopic asthma (house dust mite sensitive) to clean air and to 0.16 ppm ozone for 7.6 hours; exposures were separated by a minimum of 4 weeks. During exposure, subjects performed light exercise (ventilation = 24 L/min) for 50 minutes of each hour, and pulmonary function was evaluated before and after exposures. The morning after exposure, subjects underwent bronchial challenge with inhaled house dust mite allergen (Dermatophagoides farinae). Using a series of doubling allergen concentrations, subjects inhaled 5 breaths of nebulized allergen (0.06 to 500 AU/mL) at 10-minute intervals until a minimum of a 20% decrement in FEV(1) was elicited.


RESULTS
Compared with the change in FEV(1) during air exposure, there was a mean 9.1% +/- 2.5% (SEM) decrement in FEV(1) observed because of ozone (P <.01). Seven of the 9 subjects required less allergen after ozone exposure than after air exposure; there was a 0.58 mean dose shift in the doubling concentration of allergen attributable to the ozone exposure (P =.03).


CONCLUSIONS
These findings indicate that exposure of subjects with mild atopic asthma to ozone at levels sufficient to cause modest decrements in lung function also increases the reactivity to allergen. To the extent that this effect occurs in response to ambient exposures, ozone may be contributing to the aggravation of asthma.
Kehrl
H R
HR
US Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Human Studies Division, Clinical Research Branch, Research Triangle Park, NC 27711, USA.
Peden
D B
DB
Ball
B
B
Folinsbee
L J
LJ
Horstman
D
D
D000328:Adult; D000485:Allergens; D000818:Animals; D039741:Antigens, Dermatophagoides; D001249:Asthma / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000139:chemically induced; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D008297:Male; D008925:Mites / Q000276:immunology; D010126:Ozone / Q000494:pharmacology*
D000485:Allergens; D039741:Antigens, Dermatophagoides; D006023:Glycoproteins; D010126:Ozone; D006632:Histamine