Alterations of murine immunologic responses after silica dust inhalation

Due to the increasing concern that environmental pollution is a health hazard, the possible cytotoxic effects of particulate pollutants on cells of the immune system deserve close examination. The alteration of cell populations and functions related to immunologic responses were examined in the mouse after inhalation of silica dioxide (SiO₂). Such exposure produced changes in the T and B lymphocyte population, in the macrophages, and in functions associated with each of these cell types. The possible nature of the immunologic alterations induced by silica dust inhalation is discussed. Inhalation of silica dust enhanced the transformation of concanavalin A responsive cells, the T lymphocytes, in the spleens of exposed mice, while decreasing the response in the cells of the mediastinal lymph nodes (MLN). Mice exposed to silica dust by inhalation for 2 weeks before and 3 weeks after aerosol or subcutaneous immunization with Mycobacterium tuberculosis H37Ra exhibited enhanced uptake of ³H thymidine upon culture of their spleen lymphocytes with purified protein derivative (PPD) of tuberculin. The lipopolysaccharide (LPS) responsive cell population, B lymphocytes, of both spleen and MLN cultures exhibited decreased uptake of ³H thymidine at all times of assay after silica dust inhalation. Silica exposed mice also had much lower numbers of plaque forming cells (PFC) in the spleen, decreased serum agglutinin activity, and generally lower numbers of PFC in the MLN when assayed with Escherichia coli LPS coated sheep red blood cells after aerosol immunization with whole E. coli O55:B5. Similar immunodepression was noted in exposed mice immunized i.v. with whole E. coli, but to a lesser degree than via aerosol immunization. Depressed B lymphocyte immunocompetence was demonstrated with the adoptive transfer of spleen lymphocytes from exposed and control animals into irradiated recipients. Alveolar macrophages from silica exposed mice had less ability to phagocytize E. coli, in vitro. Both alveolar and spleen macrophages from exposed animals exhibited decreased capacity to phagocytize antigen and initiate antibody formation, when compared to control animals, upon transfer of in vitro antigen 'fed' macrophages from exposed mice to normal syngeneic recipients.