Morphologic Correlation of Physiologic Changes Caused by SO₂-induced Bronchitis in Dogs

Abstract

Chronic bronchitis was induced in 6 mongrel dogs by exposure to SO2 gas for 6 to 18 months. All of the dogs developed cough and mucus hypersecretion. Chronic airway obstruction and decreased airway responsiveness to inhaled histamine developed in 5 of the dogs. Histologic changes in dogs evaluated after SO2 exposure included significant mucous gland hypertrophy and hyperplasia, epithelial thickening, and a decrease in the number of luminal cells containing undischarged secretory granules. Acute and chronic inflammation were found in the dogs with airway obstruction and decreased responsiveness to histamine, but such inflammation was absent in the one dog that failed to develop physiologic changes. After a period of recovery from SO2 exposure of 9 to 21 months, inflammation regressed dramatically and the other histologic changes returned toward normal. Physiologic changes regressed somewhat in those dogs that had had changes. These findings suggest that inflammation may be an important factor influencing the development of airway obstruction and altered airway responsiveness in the setting of chronic bronchitis.

A thirteen-year follow-up of respiratory effects of acute exposure to sulfur dioxide

“…The preaccident level was never reached, however. Chronic obstructive pulmonary disease developed as a sequela of exposure to high concentrations of sulfur dioxide, as documented also in case reports (10,12,18) and as induced experimentally in animals (13,14,15,16). Bronchial hyperresponsiviness seems to persist for years in humans exposed to high concentrations of sulfur dioxide.…”

Murine Model for Non-IgE-Mediated Asthma

“…The airway inflammation, evaluated by the number of bronchoalveolar lavage cells and the percentage of neutrophils in bronchoalveolar cells, is closely paralleled by the development of airway hyperresponsiveness in the presented model. Although some studies have demonstrated that neutrophil infiltration into the airways is not necessary for an increase in airway responsiveness (25,26), the hypothesis that neutrophil infiltration alters airway function is, however, supported by a larger number of studies (27)(28)(29). We hypothesize that this leukocyte accumulation, dominated by the infiltration of neutrophils, will lead to the induction of in vivo airway hyperresponsiveness and in vitro tracheal hyperreactivity.…”

Respiratory Tract Mucin Genes and Mucin Glycoproteins in Health and Disease

“…Sulfur dioxide exposure induces superficial secretory cell hyperplasia in rats (145) and mucus gland hypertrophy in dogs (236). Ozone induces mucus cell metaplasia in rat nasal airway epithelium (106).…”