Effect of ozone on diesel exhaust particle toxicity in rat lung

Ambient particulate matter (PM) concentrations have been associated with mo rtality and morbidity, Diesel exhaust particles (DEP) are present in ambien t urban air PM. Coexisting with DEP (and PM) is ozone (O-3), which has the potential to react with some components of DEP. Some reports have shown inc reased lung injury in rats coexposed to PM and O-3, but it is unclear wheth er this increased injury was due to direct interaction between the pollutan ts or via of her mechanisms. To examine whether O-3 can directly react with and affect PM bioactivity, we exposed DEP to O-3 in a cell-free in vitro s ystem and then examined the bioactivity of the resultant DEP in a rat model of lung injury. Standard Reference Material 2975 (diesel exhaust PIM) was initially exposed to 0.1 ppm O-3 for 48 h and then instilled intratracheall y in Sprague-Dawley rats. Rat lung inflammation and injury was examined 24 h after instillation by lung lavage. The DEP exposed to 0.1 ppm O-3 was mor e potent in increasing neutrophilia, lavage total protein, and LDH activity compared to unexposed DEP, The increased DEP activity induced by the O-3 e xposure was not attributable to alteration by air that was also present dur ing the O-3 exposure. Exposure of DEP to a higher O-3 concentration (1.0 pp m) led to a decreased bioactivity of the particles. In contrast, carbon bla ck particles, low in organic content relative to DEP, did not exhibit an in crease in any of the bioactivities examined after exposure to 0.1 ppm O-3. DEP incorporated O-3 (labeled with O-18) in a linear fashion. These data su ggest that ambient concentrations of O-3 can increase the biological potenc y of DEP. The ozonized DEP may play a role in the induction of lung respons es by ambient PM.