RESPONSE OF LUNG EPITHELIUM TO WELL CHARACTERIZED FINE PARTICLES

Diesel particles form a large component of the fine particle fraction (PM10) in urban air in the UK. During pollution episodes small increas es in PM10 have been linked to detrimental health effects. The compara tive toxicological effects of diesel exhaust and other well-characteri sed particles (carbon black, amorphous and crystalline silica) on rat respiratory epithelium were investigated in the present study. The eff ects of small masses of particles (1 mg) delivered by intratracheal in stillation were monitored by changes in components of lavage fluid. Re spirable, crystalline quartz, produced significant increases in lung p ermeability, persistent surface inflammation, progressive increases in pulmonary surfactant and activities of epithelial marker enzymes up t o 12 weeks after primary exposure. Ultrafine amorphous silica did not induce progressive effects but it promoted initial epithelial damage w ith permeability changes and these regressed with time after exposure. By contrast, ultrafine/fine carbon black had little, if any, effect o n lung permeability, epithelial markers or inflammation, despite being given at a dose which readily translocated the epithelium and which h as been reported to induce inflammation. Similarly, diesel exhaust par ticles produced only minimal changes in lavage components, although th ey were smaller individual particles and differed in surface chemistry from carbon black. It is concluded that diesel exhaust particles are less damaging to respiratory epithelium than silicon dioxide and that the surface chemistry of a particle is more important than ultrafine s ize in explaining its biological reactivity.