Project at a Glance
Project Status: complete
Title: Airway hyperirritability induced by ozone II.
Principal Investigator / Author(s): Nadel, J. A.
Contractor: UC San Francisco
Contract Number: A8-053-30
Research Program Area: Health & Exposure
Topic Areas: Health Effects of Air Pollution
We have previously demonstrated that a Z-h exposure to 0.5-0.6 parts per million (ppm) of ozone increases bronchial reactivity to both histamine and methacholine in healthy non atopic and atopic human subjects (1 , 2 ). Studies completed within the past year have shown in 19 healthy adult subjects that a 2-h exposure to 0.4 ppm but not to 0.2 ppm of ozone significantly increased the rise in resistance provoked by inhalation of histamine. With three repeated 2-h exposures of 0.4 ppm of ozone on consecutive days, however, the bronchomotor response to histamine progressively decreased, ultimately returning to pre-exposure levels. Thus, we have shown that the threshold level of ozone causing an increase in bronchial reactivity in healthy human subjects is between 0.2 and 0.4 ppm and that tolerance to this effect of ozone develops with repeated exposures. We also studied the relationship between bronchomotor responsiveness to histamine and the response to inhalation of sulfur dioxide (S02). In three subjects we were unable to show any change in the response to 5 ppm of SO2 after a 2-h exposure to 0.6 ppm of ozone; but in a study of subjects with mild, asymptomatic asthma who had preexisting bronchial hyper reactivity to histamine, we showed a significant bronchomotor response to lomin inhalation of 1, 3, and 5 ppm of SO2 delivered via a mouthpiece, whereas normal and atopic subjects responded only to 5 ppm of S02. The response to SO2 was blocked by pre treatment with atropine, suggesting the involvement of postganglionic cholinergic pathways, but it did not correlate with the response to histamine. Our results indicate that subjects with asthma develop bronchoconstriction on exposure to levels of SO2 well below currently accepted standards for occupational exposure. The lack of correlation between responses to SO2 and to histamine suggests that these agents exert their effects via different pathways. This report was submitted in fulfillment of Contract Number A6-215-30 under the partial sponsorship of the California Air Resources Board. Work was completed on November 30, 1979.
For questions regarding this research project, including available data and progress status, contact: Heather Choi at (916) 322-3893
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