Research Projects

Project at a Glance

Project Status: complete

Title: Airway responses to atmospheric pollutants: sulfur dioxide and ozone.

Principal Investigator / Author(s): Nadel, J. A.

Contractor: Cardiovascular Research Institute, UC San Francisco

Contract Number: A1-133-33


Research Program Area: Health & Exposure

Topic Areas: Health Effects of Air Pollution


Abstract:

Although our previous finding that people with asthma have greater bronchomotor sensitivity to sulfur-dioxide than healthy people was widely accepted, the relevance of the finding to standards regulating atmospheric concentrations of sulfur dioxide was disputed on the grounds that our exposure conditions (use of mouthpiece or facemask) did not mimic those of ordinary exposure, especially in that they altered the fraction of ventilation passing through the nose, a highly efficient filter for removing sulfur dioxide. The greater part of the studies conducted under this contract were aimed at examining the validity of this criticism, In a study of ten subjects with mild asthma exposed to sulfur dioxide while performing moderate exercise and breathing freely in an exposure chamber, We found that 0.50 ppm of sulfur dioxide caused significant bronchoconstriction, similar in degree to that induced with breathing the same concentration through a facemask. This result establishes the relevance of our earlier work, for it shows that people with asthma performing moderate exercise and breathing without encumbrance may develop bronchoconstriction on inhaling levels of sulfur dioxide that are occasionally exceeded in ambient air. In a study of 19 subjects with mild asthma we found no significant bronchoconstriction due to exposure to 0.215 ppm of sulfur dioxide even when the subjects exercised vigorously. Thus, the threshold values for the bronchomotor effect of sulfur dioxide in people with mild asthma lies between 0.25 and 0.50 ppm. We next examined the importance of another of our earlier findings, that the airway effects of sulfur dioxide are potentated when it is inhaled in cold, dry air. In our study of eight subjects we confirmed that this effect was statistically significant even for law concentrations of sulfur dioxide (0.1-0.25 ppm), but the magnitude of the potentiation was so small as to be of doubtful clinical importance. Thus, even when inhaled in cold, dry air, the threshold of sulfur dioxide causing symptomatic bronchoconstriction in people with mild asthma is probably greater than 0.25 ppm but less than 0.50 ppm. The final study of human subjects in this contract examined whether anesthetizing the upper airway (pharynx and larynx) by injecting xylocaine around the superior laryngeal nerves would alter the response to inhalation of sulfur dioxide, as would be predicted from animal studies showing that sulfur dioxide stimulates afferent nerve endings in the larynx, Our initially promising results later are to be largely due to the placebo effect of the injection. but the ultimately negative result of the study is difficult to interpret in the absence of a "gold standard" allowing the conclusion that conduction in the superior laryngeal nerves was indeed blocked. Studies of laboratory animals constituted a small part of the research effort, but these studies established that inhalation of sulfur dioxide provokes an increase in secretion of mucus from bronchial submucosal glands-- an effect that may be important in people with diseases associated with a disturbance in mucus secretion (cystic fibrosis, asthma, chronic bronchitis) -- and that sulfur dioxide alters the pattern of breathing as well as the caliber of airways. In summary, the work done under this contract extends the work done in previous contract periods and establishes the fact that under real worlds.


 

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