Project at a Glance

Title: Effects of nitric acid vapor and ozone on the response to inhaled allergen in allergic asthmatic subjects.

Principal Investigator / Author(s): Balmes, John R

Contractor: UC San Francisco

Contract Number: A133-150

Research Program Area: Health & Exposure

Topic Areas: Acid Deposition, Health Effects of Air Pollution, Vulnerable Populations


Although epidemiologic data suggest that people with asthma are at increased risk of exacerbations due to elevated ozone levels, controlled human exposure studies have not consistantly shown asthmatic subjects to be more sensitive to ozone. A possible explanation for this discrepancy may be that ozone increases the response to the natural triggers of an asthma attack. Other factors, such as the presence of acidic pollutants, may also influence the respiratory effects of ozone. This study investigates whether exposure to ozone or the combination of ozone and nitric acid vapor enhances the response to inhaled allergen in allergic asthmatic subjects. In phase I of our study, 14 asthmatic subjects were exposed to 0.2 ppm ozone vs. filtered air for one hour while exercising with a minute ventilation of 25 L/min/m2 body surface area. Phase II consisted of ten subjects exposed to 0.2 ppm ozone combined with 150 mg/m3 nitric acid vapor vs. 0.2 ppm ozone for one hour under similar conditions. The ozone concentration used is similar to high ambient levels known to occur in some southern Californian urban centers, and although much higher than ambient conditions, a nitric acid vapor level of 150 mg/m3 was chosen to give definitive results as to whether its presence could effect the response to ozone. Following the 1 h exposure, subjects were challenged with doubling doses of dust mite D. Farinae allergen by inhalation until a drop in FEV1 of > 15% occurred (PC15). At 6 h post-allergen challenge, bronchoscopy with bronchoalveolar lavage (BAL), left mainstem proximal airway lavage, and endobronchial biopsy and brushings were done. The same subjects were restudied with the second exposure condition after 4 weeks. Although individual PC15 data for phase I revealed a trend toward an increase in sensitivity to inhaled allergen after ozone exposure compared to air, the results for the group as a whole did not reach statistical significance (p=0.42, sign-rank). Bronchoscopy during the late-phase response did show a near significant increase in neutrophils in proximal airway lavage fluid after ozone exposure (p=0.06, sign-rank), but no increase in markers of inflammation in BAL fluid. In phase II, no significant difference was seen in the response to allergen between the ozone/nitric acid vapor vs. ozone alone exposures (p=0.11, sign-rank). A significant increase in eosinophils (p=0.02, sign-rank) was seen in the bronchial fraction fluid after the combination exposure. In conclusion, the final results of this study can not confirm the hypothesis that exposure to ozone or the combination of ozone and nitric acid vapor significantly enhances the response to inhaled allergen in allergic asthmatic subjects.

For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 445-0753

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