Abstract
The effects of cigarette smoking on blood to airway pulmonary permeability to the low-molecular-weight solute urea were investigated, in an attempt to evaluate its use as a dilution marker for bronchoalveolar lavage (BAL) studies. Five healthy normal smokers who smoked a cigarette 10 min prior to undergoing a 3 x 60 mL bronchoalveolar lavage (BAL), and five nonsmokers who also underwent BAL but without cigarette smoke exposure were studied. Five minutes before bronchoscopy, 4 MBq 3H-water and 1 MBq 14C-urea were injected intravenously and biochemical urea assays and an indirect radiotracer method were used to evaluate permeability. It was shown that the smoking group had less urea in their BAL supernatants compared to nonsmokers the results using the radiotracer method being significant (p<0.005). Using both methods, it was shown that levels of urea increased in sequentially aspirated aliquots in both groups. The median directly assayed levels of urea in the smokers rose as follows: aliquot 1 0.05 micromol x mL(-1), (range 0.03-0.14), aliquot 2 0.10 micromol x mL(-1) (0.07-0.17), aliquot 3 0.12 micromol x mL(-1) (0.06-0.23) (p<0.05). This led to significantly increased calculated levels of epithelial lining fluid in the sequential aliquots (p<0.05). In addition, there were large but variable amounts of labelled water detected in both subject groups indicating a complex interaction between the BAL procedure and the circulation. Changing urea measurements during the bronchoalveolar lavage procedure confound the use of the urea (epithelial lining fluid) method for normalizing dilution factors. The use of epithelial lining fluid determinations in smokers ignores the additional and probably complex permeability changes. The present data suggest that acute exposure to cigarette smoke in smokers may decrease blood to airway permeability.
