| Summary: | Fourteen smokers (S) underwent <SUP>99m</SUP>Tc-DTPA lung scans after refraining for 12 hours (chronic smoking, C) and after smoking until 1 hour before study (acute smoking, A). <SUP>99m</SUP>Tc-DTPA clearance was increased in C and further in A. Each smoker also underwent bronchoalveolar lavage (BAL) after either C or A and seven control non-smokers (NS) were also studied. Neutrophils in BAL were increased in A. Superoxide release (O<SUB>2</SUB><SUP>.-</SUP>) from mixed BAL leucocytes and plasma products of lipid peroxidation were increased in both smoking groups. In BAL fluid (BALF) and epithelial lining fluid (ELF) the latter doubled in C and increased 6 fold in A. Trolox equivalent anti-oxidant capacity (TEAC) decreased in plasma and increased in BALF. Reduced glutathione in the airspaces doubled in C. This increase was abolished in A. In a further study 15 healthy NS were exposed to filtered air (FA), or ozone 100 or 400ppb for 1 hour, during intermittent exercise. Ozone inhalation increased ELF volume overall. Neutrophils in BAL were increased 6 hours after ozone 400ppb compared to FA. Ozone inhalation decreased O<SUB>2</SUB><SUP>.- </SUP>release from mixed BAL leucocytes and products of lipid peroxidation in ELF, 1 and 6 hours after 400ppb. <I>In vitro</I> exposure of A549 cells to 1000ppb for 1 hour produced focal cell loss, with increased intracellular protein mixed disulphides, export of oxidized glutathione, and cytoskeletal disruption. In conclusion increased epithelial permeability and neutrophil influx in the airspaces, produced by oxidant inhalation are acute phenomena. In smokers they were associated with increased oxidant stress. In healthy non-smokers, in contrast, acute ozone inhalation was associated with decreased oxidant stress, at least as measured by the extent of lipid peroxidation and oxygen radical release from mixed BAL leucocytes, and in addition anti-oxidant levels were maintained. <I>In vitro</I> studies indicated the potential of ozone to increase oxidant stress in the respiratory epithelium and airspaces with profoundly damaging effects.
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