CONCOMITANT EXPOSURE TO CARBON-BLACK PARTICULATES ENHANCES OZONE-INDUCED LUNG INFLAMMATION AND SUPPRESSION OF ALVEOLAR MACROPHAGE PHAGOCYTOSIS

The goal of this study was to investigate whether coexposures to carbo n black and O-3 result in a toxicologic interaction in the lungs as qu antitated by the inflammatory response and alveolar macrophage (AM) ph agocytosis. This aim was accomplished through inhalation coexposures o f Swiss mice for 4 h to target concentrations of 10 mg/m(3) of carbon black and 1.5 ppm O-3,, or exposure to either agent alone. As a contro l for the coexposure experiments, mice were also exposed for 4 h to ca rbon black, followed immediately thereafter by exposure for 4 h to O-3 , or vice versa. At 24 h after exposure, the lungs of the animals were lavaged for quantitation of total and differential cell counts and as sessment of AM Fc-receptor-mediated phagocytosis. Exposure to carbon b lack did not result in an inflammatory response, nor had it any effect on AM phagocytosis. Ozone exposure resulted in an inflammatory respon se in the lungs and suppression of AM phagocytosis. Both biologic para meters were significantly enhanced following combined exposure to the particle and the gas. Carbon black exposure either before or after O-3 had no significant effect on AM phagocytosis as compared to O-3 expos ure alone. These data demonstrate the toxicologic interaction of coexp osures to an inert particle and O-3 on well-accepted biologic markers pulmonary toxicity. The mechanism for the enhanced biologic effect may be that the carbon black particle acts as a carrier mechanism for O-3 to areas in the distal lung not accessible to O-3 in the gaseous phas e or that O-3 alters the physicochemistry of the particulate from a no ntoxic to a toxic form.