UBC Theses and Dissertations
Airway response to inhaled air pollutants--cigarette smoke & industrial dust & fume Kennedy, Susan Marguerite
Previous studies which identified inflammation in the peripheral airways of the lung as a potentially reversible early component in the development of chronic airflow obstruction led to the investigations reported here concerning the possible early diagnosis of airway inflammation using gallium-67; the relationship between airway inflammation, increased permeability and hyper-reactivity; and peripheral airway changes seen in persons exposed to mineral dust and fume contrasted with those seen in cigarette smokers. Aerosolized radiogallium was administered in two studies, first to guinea pigs exposed to cigarette smoke and then to human smokers and the retention and clearance compared to that in non-smoking controls, and in the guinea pigs, to the degree of polymorphonuclear infiltration of the airways. The results revealed no difference in clearance between smokers and non-smokers and prolonged retention of the tracer in the lungs. Autoradiography in guinea pigs and humans suggested that the gallium was taken up by macrophages, not by polymorphonuclear cells. This suggests that the use of radiogallium to mark polymorphonuclear infiltration is not useful. Increased respiratory epithelial permeability in human smokers was demonstrated by following the disappearance from the lungs of 99m technetium labelled diethylenetriame penta acetate. However, no relationship was seen between increased permeability and airway reactivity as measured by the degree of airflow obstruction following inhalation of increasing doses of histamine. This suggests that although airway inflammation may result in increased airway permeability, this does not directly induce hyper-reactivity. Finally, peripheral airway structural and functional changes were compared in two groups of patients undergoing lung resection: one with occupational mineral dust or fume exposure and the other, not exposed to dust or fume, individually matched to the first group for age and smoking history. The results indicated increased airflow obstruction in the exposed group and excess fibrous connective tissue deposition and goblet cell metaplasia in their peripheral airways, particularly in those patients exposed to mineral dust and fume in a non-mining occupation. No increase was seen in degree of inflammatory cell infiltration of the airway walls. These results suggest that the peripheral airway response to mineral dust or fume differs qualitatively from the response to cigarette smoke.