CIGARETTE-SMOKE INCREASES AMOSITE ASBESTOS FIBER BINDING TO THE SURFACE OF TRACHEAL EPITHELIAL-CELLS

Binding of asbestos fibers to the cell surface appears to be important in the initiation of intracellular signaling events as well as in ini tiation of particle uptake by the cell. We have previously shown that cigarette smoke increases the uptake of asbestos fibers by tracheal ep ithelial cells in explant culture. Whether smoke acts by increasing su rface binding of fibers is not known. In this study, we exposed rat tr acheal explants to air or cigarette smoke and then to a suspension of amosite asbestos. Explants were harvested after 1 or 24 h of dust expo sure and washed by repeated dips in culture medium to remove loosely b ound fibers, and the number of fibers adhering to the apical cell surf aces was determined by scanning electron microscopy. Smoke-exposed exp lants retained significantly more surface fibers than air-exposed expl ants. After four washes, binding levels were similar at 1 and 24 h. Th e smoke effect was still present when incubations were carried out at 4 degrees C, but binding was decreased similar to 25%. Preincubation o f the asbestos fibers with iron chloride to increase surface iron incr eased fiber binding in both air- and smoke-exposed explants, whereas p reincubation of the fibers with the iron chelator deferoxamine decreas ed binding after air exposure and completely eliminated the smoke effe ct. Inclusion of mannitol or catalase in the medium or preincubation o f the explants with GSH produced decreases in binding of 10-25% in air -exposed explants and generally greater decreases in smoke-exposed exp lants. We conclude that 1) amosite binding is a very rapid process tha t does not require active cellular metabolism, 2) cigarette smoke incr eases adhesion of fibers to the epithelial surfaces, and 3) iron on th e asbestos fiber appears to play an important role in binding, probabl y through an active oxygen species-mediated process.