Project at a Glance

Title: Studies on air pollution: effects of nitrogen dioxide on airway caliber and reactivity in asthmatic subjects; effects of nitrogen dioxide on lung lymphocytes and macrophage products in healthy subjects; nasal and bronchial effects of sulfur dioxide in asthmatic subjects

Principal Investigator / Author(s): Btoushey, H

Contractor: Cardiovascular Research Institute and Department of Medicine, UC San Francisco

Contract Number: A6-200-33

Research Program Area: Health & Exposure

Topic Areas: Health Effects of Air Pollution, Vulnerable Populations


We performed three studies of the effects of NO2 and SO2 on airway function in human subjects. In the first study, we found in nine exercising asthmatic subjects that a 30 min exposure to 0.3 ppm nitrogen dioxide did not alter specific airway resistance, maximal expiratory flow, or the slope of phase Ill on the single breath test of nitrogen distribution and had no effect on airway hyper responsiveness to sulfur dioxide. In the second study, we found that repeated exposure of five healthy subjects to nitrogen dioxide (0.60 ppm x 2 h on four different days in a six-day period) was associated neither with any significant change in pulmonary function nor in the levels of secretary products of lung macrophages (interleukin 1, tumor necrosis factor) in bronchoalveolar lavage fluid. Analysis of the numbers and types of lymphocytes in venous blood and bronchoalveolar lavage fluid revealed no change apart from a small, possibly artifactual increase in natural killer cells in bronchoalveolar lavage fluid after NO2 exposure. Our third study examined whether brief exposures to moderately high concentrations of SO2 caused acute increases in nasal symptoms and nasal resistance in 8 subjects with a history of both asthma and allergic rhinitis and with demonstrable bronchial hyperactivity to S02. In this group of subjects we did not find a greater change in nasal resistance and nasal symptoms after ten minutes of nasal inhalation of a concentration of SO2 more than twice that required to provoke symptomatic bronchoconstriction when inhaled by mouth than we found after a similar inhalation of conditioned room air.

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