Swine Confinement Facility (SCF) dust consists of a complex mixture of feed grain particles, bacterial components, organic particulates and gases. When these particles are inhaled they deposit along the respiratory tract and mediate respiratory symptoms and disease in swine farmers and facility workers. Macrophages ingest and eliminate microbes and debris under chronic conditions; however, the role of macrophages in agricultural-related respiratory disease has not been fully elucidated. The goal was to evaluate the hypothesis that chronic exposure to SCF dust causes inflammation by modulating pulmonary protein levels and macrophage function. Balb/c mice were exposed to 5, 12.5 and 25% SCF Dust Extract (DE) via nebulization 30 min/day five days a week, for eight weeks with weekends excluded. Bronchoalveolar Lavage Fluid (BALF) was collected and analyzed for protein concentration, leukocyte distribution and macrophage morphology. For comparison, THP-1 monocytic cells were exposed to 0.1-10% DE overnight and evaluated for phagocytosis and reactive oxygen species production. Repeated exposure to DE via nebulizer caused a significant increase in protein concentration and inflammatory cell number, namely macrophages, in a dose-dependent manner within the lung as compared to controls. Macrophages with pseudopods and vacuoles were the most abundant leukocytes within BALF of mice exposed to DE. Similarly, in vitro studies with 10% DE treated THP-1 cells revealed enhanced phagocytosis (p<0.05), pseudopodia and vacuolization following exposure to compared to control cells. In addition, there were time-and dose-dependent increases of intracellular ROS production by THP-1 cells exposed to 5 and 10% DE compared to control (p<0.01). These findings indicate repeated, long-term inhalation of swine confinement facility dust may mediate chronic airway and lung inflammation through modulation of protein concentration and macrophage function. The aerosolized dust-mouse inhalation model presented here may offer a good tool for studying particle mediated chronic inflammation of the tracheobronchial tree and lungs.

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