• P D Scanlon, J Seltzer, R H Ingram, L Reid, and J M Drazen.
• Am. Rev. Respir. Dis. 1987 Apr 1; 135 (4): 831-9.

AbstractSeven adult mongrel dogs were exposed to SO2 gas at 2 different concentrations (15 and 50 ppm) on a daily basis for 5 to 11 months. Mucous hypersecretion and airway obstruction (a sustained increase in pulmonary resistance) developed in 4 dogs exposed to 50 ppm SO2. Histologic examination of the dogs' airways demonstrated epithelial thickening and an increase in size of the mucous glands. No inflammatory cell infiltration of the airways was noted and, in addition, responsiveness to inhaled histamine and methacholine did not change. The increase in lung resistance correlated with increase in mucous gland volume and airway wall thickening, but not with any change in airway responsiveness. Dogs exposed to 15 ppm SO2 showed minimal histologic and physiologic changes compared with control dogs. Previous work with a similar model of chronic bronchitis, using higher level SO2 exposure, has demonstrated an association of airway inflammation with decreased responsiveness to inhaled bronchoconstrictors. In the present study, with a lower exposure level to SO2 (50 versus 200 ppm), we found similar histologic findings associated with airway obstruction, but in the absence of airway inflammation, responsiveness to inhaled bronchoconstrictors was unchanged. This supports the theory that chronic airway inflammation may be associated with decreased responsiveness to inhaled bronchoconstrictors. This contrasts with the hyperresponsiveness induced by acute exposure to irritant gases noted by others.

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