Influence of Ozone on Pulmonary Defense Mechanisms of Silicotic Mice

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Abstract
Respiratory illnesses are consequences of exposure to atmospheric pollutants. Whether or not anatomic damage due to pneumoconiosis increases susceptibility to infection following exposure to pollutants is unknown. Silicosis was induced in mice by intratracheal infection of 10 mg of silica. Seventy days later, silicotic and latex-injected controls were infected with aerosols of Staphylococcus aureus labelled with phosphorus 32, and then exposed for four hours either to ozone (0.4 to 1.6 ppm) or air containing 21% oxygen. Following this, murine pulmonary bactericidal activity rates were determined. An equivalently progressive decrease in pulmonary bactericidal activity occurred with exposure to increasing ozone concentrations for silicotic and control mice. Silicosis, itself, did not inhibit bactericidal activity, since the silicotic and control mice which were exposed to the oxygen had normal bactericidal activity, it is concluded that anatomic abnormalities due to silicosis do not enhance ozone-induced inhibition in pulmonary bactericidal activity.