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 03 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 03, 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 03, 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 03 had no significant effect on AM phagocytosis as compared to 03 exposure alone. These data demonstrate the toxicologic interaction of coexposures to an inert particle and 03 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 03 to areas in the distal lung not accessible to 03 in the gaseous phase or that 03 alters the physicochemistry of the particulate from a nontoxic to a toxic form.