EFFECTS OF CIGARETTE-SMOKE ON EPITHELIAL UPTAKE OF NONASBESTOS MINERAL PARTICLES IN TRACHEAL ORGAN-CULTURE

Cigarette smoke is believed to increase the pulmonary retention of many different types of mineral dusts, but the mechanisms of this process are unclear. We have previously shown, using a tracheal organ culture system, that exposure to cigarette smoke directly increases the uptake of asbestos fibers by tracheal epithelial cells, and that this process is mediated by active oxygen species. To determine whether the same effects are seen with other types of mineral dust, we exposed rat tracheal explants to cigarette smoke or air (control) and then to a variety of dusts generally considered ''inert'' or of low pathogenicity. Explants were maintained in organ culture to allow dust uptake, and segments fixed and prepared for light microscopy at various times up to 1 wk; particle uptake was determined morphometrically. We observed that cigarette smoke significantly increased the epithelial uptake of nonfibrous titanium dioxide and talc, and of fibrous silicon carbide, but not of fibrous or nonfibrous iron oxide, nonfibrous silicon carbide, or fibrous wollastonite. Scavengers of active oxygen species (catalase) or agents that prevent the formation of active oxygen species (deferoxamine) blocked the effects of smoke in enhancing titanium dioxide uptake but did not block the effects of smoke on talc uptake. These observations indicate that cigarette smoke may potentiate the effects of many types of dust, including relatively inert dusts, by directly increasing the numbers of particles entering the tracheobronchial epithelium and eventually reaching the interstitium. However, smoke does not directly enhance the uptake of every dust. Active oxygen species derived from the smoke appear to be involved in enhanced uptake of some but not all types of dusts, implying that other mechanisms of smoke-enhanced particle uptake must exist.