The Effect of Ozone Inhalation on the Thymus and Mediastinal Lymph Nodes of CD-1 Mice

Ozone is a gaseous oxidant pollutant which damages lung tissue when inhaled in high concentrations. In this report, we describe how cells and tissues of the immune system respond to ozone challenge. Groups of CD-I female mice were exposed to ozone at 0.7 ppm in Rochester-type inhalation chambers, or to a control environment consisting of identical housing conditions in the absence of ozone. At timed intervals, animals were removed from the exposure chambers, sacrificed, and the thymus and right tracheobronchial lymph node were removed. Measurement of wet weights and histopathologic examination of plastic embedded tissue revealed atrophy of the thymus and hypertrophy of the lymph node. Thymic atrophy was characterized by cellular depletion of the cortex and was resistant to prior adrenalectomy. On the other hand hypertrophy of the node was dose dependent and was characterized by the presence of mitotic figures and increased cell numbers. Autoradiographic analysis of node tissue from ozone-exposed animals treated with tritiated thymidine revealed increased thymidine uptake in the paracortical, T cell region of the node when conpared to controls. Blastic forms were also evident in this portion of the node. Coincubation of the lymph node lymphocytes with Concavalin A, a T cell mitogen, produced a 2-3 fold increase in the functional reactivity of lymphocytes from animals exposed to ozone for 21-28 days. We then attempted to determine whether a humoral product of T lymphocyte activation affects the lung response to ozone, pharmacologic modulation of the humoral T cell mediator, interferon, using an interferon inducer (poly I:C) or an anti-interferon antibody during ozone inhalation, decreased or increased, respectively the degree of damage produced by ozone as determined by his tologic examination of the lung tissue. This study indicated that T lymphocytes in the thymus and the lymh node were affected by ozone inhalation and that the lovel of a T cell lymphokine can alter the resistance of the lung to ozone damage.