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 carbon black and O3 result in a toxicologic interaction in the lungs as quantitated by the inflammatory response and alveolar macrophage (AM) phagocytosis. This aim was accomplished through inhalation coexposures of Swiss mice for 4 h to target concentrations of 10 mg/m3 of carbon black and 1.5 ppm O3, or exposure to either agent alone. As a control for the coexposure experiments, mice were also exposed for 4 h to carbon black, followed immediately thereafter by exposure for 4 h to O3, or vice versa. At 24 h after exposure, the lungs of the animals were lavaged for quantitation of total and differential cell counts and assessment of AM Fc-receptor-mediated phagocytosis. Exposure to carbon black did not result in an inflammatory response, nor had it any effect on AM phagocytosis. Ozone exposure resulted in an inflammatory response in the lungs and suppression of AM phagocytosis. Both biologic parameters were significantly enhanced following combined exposure to the particle and the gas. Carbon black exposure either before or after O3 had no significant effect on AM phagocytosis as compared to O3 exposure alone. These data demonstrate the toxicologic interaction of coexposures to an inert particle and O3 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 O3 to areas in the distal lung not accessible to O3 in the gaseous phase or that O3 alters the physicochemistry of the particulate from a nontoxic to a toxic form.