The effects of sidestream cigarette smoke (SSCS) (a 15-min exposure per day for 20 days) were determined on markers of lung injury in New Zealand white rabbits (n = 9) and a control group (n = 6). The SSCS consisted of air and smoke which were aspirated by syringe from a funnel inverted over a lit cigarette. The rabbits were placed in an environmental chamber into which 3 liters of SSCS were injected over a 15-min period each day. Chronic SSCS caused an increase (p < 0.05) in pulmonary epithelial clearance (k) of technetiumlabeled diethylenetriamine pentaacetate (^99mTcDTPA); k = 0.83 (±0.07) for the SSCS-exposed group and 0.66 ( ± 0.02) for the control group. This increase in lung permeability was accompanied by an increase in bronchoalveolar lavage (BAL) white cell count; SSCS = 83,353 ( ± 11,954) cells/mm3 BAL fluid versus control = 16,450 ( ± 6,683) cells/mm3 BAL fluid and an increase in BAL leukotriene E4; SSCS = 742 ( ± 285) pg/ml BAL fluid compared with 76 ( ± 2)pg/ml BAL fluid for controls. Cultured SSCS alveolar macrophages (AMs)produced more superoxide (O(2)); 2.4 (±0.8) nmol O(2)/10^6 AMs versus 0.4( ± 0.2) nmol O2/IO6 AMs for controls after incubation for 18 h with 10 pg/ml lipopolysaccharide. Electron microscopy demonstrated that the airway mucosa of SSCS rabbits was infiltrated by eosinophils,

Keywords:
Eicosanoids, Alveolar macrophages, Lung permeability, Passive smoke exposure
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1992
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