Permeability, inflammation and oxidant status in airspace epithelium exposed to ozone.
Avainsanat
Abstrakti
The aim of the study was to investigate possible mechanisms of epithelial injury in normal subjects exposed to environmentally relevant concentrations of ozone. Fifteen healthy non-smoking subjects (M:F 12:3) were studied. Five of the 15 subjects were exposed to filtered air, six were exposed to ozone 100 parts per billion (ppb) and seven were exposed to ozone 400 ppb with 99mtechnetium labelled diethylene-triamine-penta-acetate (99mTc-DTPA) or bronchoalveolar lavage (BAL) performed 1 or 6 h after exposure as indicated above. All the above studies were performed on different occasions at least 5 days apart. The subjects were exposed on each occasion for 1h during intermittent exercise at a ventilation of 40l min-1. 99mTc-DTPA lung clearance did not change after either level of ozone exposure, but neutrophils increased in BAL 6 h after exposure to 400 ppb. Superoxide anion release from mixed BAL leucocytes decreased 1 h after 100 ppb and 6 h after 400 ppb. Products of lipid peroxidation in epithelial lining fluid decreased both 1 and 6 h after 400 ppb. There was no change in anti-oxidant capacity or glutathione concentrations. Ozone exposure did not increase epithelial permeability, but was associated with neutrophil influx into the airspaces, without evidence of increased oxidative stress.