Inhalation of increased levels of air pollutants generated in the workplace and environment may augment pulmonary infection and increase morbidity and mortality. The effect of exposure to different workplace particulates on lung defense responses was investigated using a rat bacterial infectivity model. Male Sprague- Dawley rats were pretreated by intratracheal instillation with 1.0 mg/ 100 g body wt of residual oil fly ash (ROFA), stainless steel welding fumes particulate matter (SS), or silica (Si) prior to bacterial inoculation with 5 x 103 or 5 x 105 Listeria monocytogenes. Particle-induced effects on pulmonary clearance of the bacteria, lung macrophage function (phagocytosis, oxidant production, and bacterial killing), and the secretion of lung cytokines, important in immune responses, were assessed. Pretreatment with ROFA and 55 significantly slowed the lung clearance of bacteria, increased animal morbidity, suppressed macrophage function, and altered IL-2, IL6, and IL-10 production after infection. The suppression observed for ROFA was due to soluble metals, whereas a combination of soluble and insoluble metals was responsible for the effect seen with SS. Conversely, Si pretreatment enhanced lung bacterial clearance and significantly upregulated non-specific lung defense responses (macrophage phagocytosis, oxidant production, and neutrophil activation) despite the presence of significant lung inflammation and fibrosis. In conclusion, inhalation of different workplace particulates may induce varied lung defense responses to infection. Chronic exposure to metal particles in the workplace may alter macrophage function and increase the susceptibility to lung infection in exposed workers.
The Toxicologist. Society of Toxicology 43nd Annual Meeting and ToxExpo, March 21-25, 2004, Baltimore, Maryland