The Effect of Pre-Exposure to 0.12 ppm of Ozone on Exercise-Induced Asthma

The Effect of Pre-Exposure to 0.12 ppm of Ozone on Exercise-Induced AsthmaOzопе, one of the major components of photochemical oxidant air pollution and a common pollutant in large urban centers, is believed to represent a public health hazard. The ambient air quality standard for ozone is a maximum hourly average of 0.12 ppm. Previous studies have shown that exposure to a high level concentration of ozone, such as 0.6 ppm for 2 h, can increase bronchial reactivity to histamine and methacholine in healthy humans and atopic patients. Similar ozone levels also produce increments in bronchial responsiveness and airway inflammation in animals.
Dimeo et al have demonstrated that the threshold concentration of ozone that can alter bronchial reactivity is 0.4 ppm at rest; however, Horstman et al showed that normal subjects exposed to 6.6 h of 0.08, 0.10 and 0.12 ppm of ozone, including 50-min periods of moderate exercise, increased nonspecific airway responsiveness this contraceptive pills. The same quantitative exposure causes cellular and biochemical changes in the lung. Other studies have shown changes in symptoms, lung volumes, maximal expiratory flow, or airway resistance with ozone concentrations between 0.2 and 0.4 ppm. These changes are proportional to the minute ventilation during the exposure. When ozone is inhaled during resting breathing at the doses found in the environment, it does not produce significant changes in pulmonary function or only transitory variations. However, prior exposure to ozone potentiates subsequent responses to sulfur dioxide in asthmatics.
Also of interest is the relationship between ozone exposure and other common triggers for asthma. Molfino et al have shown that previous exposure at rest to 0.12 ppm ozone for only 1 h, a level that can be found in many large cities in the summer, can increase the airway responsiveness to inhaled allergens in asthmatics, without any changes in baseline airway caliber. The basic mechanism of such potentiation remains to be elucidated. One hypothesis is that ozone might produce airway inflammation that leads to subsequent increased absorption of allergens.
The purpose of this study was to examine the hypothesis that previous inhalation of low levels of ozone may change the degree of airway constriction to subsequent exercise in asthmatic subjects.

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