Comparative lung immunotoxicity of inhaled quartz and coal combustion fly ash

Some inhaled particles that are deposited in the terminal airways and alveoli clear to the lung-associated lymph nodes, and insoluble particles have a long half-life in these tissues. Because the lung-associated lymph nodes are essential in the induction of immunity after lung immunization, the accumulation of inhaled particles in these tissues could alter immune responses that develop after lung immunization. This study evaluated the effects of inhaled insoluble fly ash particles or alpha quartz on the immune functions of lung-associated lymph nodes. F344 rats were exposed for 20 days by inhalation of fly ash from a fluidized bed combustor (FBC) or a pulverized coal combustor (PCC). Rats were similarly exposed to quartz particles (Min-U-Sil). Control rats were exposed to filtered air. Groups of ten exposed and ten control rats from each group were immunized by intratracheal instillation of 10(8) sheep red blood cells at 4, 6, 40, and 52 weeks after the start of exposures. The cellularity of the lung-associated lymph nodes and antibody-mediated immunity were evaluated at 7 days after immunization. Tissues from lung and lung-associated lymph nodes were taken for histopathology. The inhalation of FBC fly ash, PCC fly ash, and quartz particles all significantly increased the number of lymphoid cells in the lung-associated lymph nodes at each of the sacrifice times. However, FBC fly ash had no significant effect on antibody immunity, while both PCC fly ash and quartz caused suppression of antibody responses at 52 weeks after the start of exposure. Histopathology data showed that exposure to quartz and PCC fly ash caused significant cellular changes in lungs and lung-associated lymph nodes, while FBC fly ash had less effect. These data indicate that an acute exposure (20 days) to relatively insoluble particles significantly increased the cellularity of the lung-associated lymph nodes for up to 52 weeks after the start of the exposure, but the pulmonary toxicity of the particles inhaled appeared to influence the effects of the exposure on antibody immune responses.