Inhalation of dust accumulated on personal computer fans in the office may cause pathological effects by disrupting the metabolic activity of alveolar macrophages

Abstract

Considering that computer fans draw in dust from the office air, and that printers and copiers are typically placed near computers, we collected dust that accumulated on computer fans from three commercial personal computer centers to predict the health effects of inhaled office dust (OD). OD contained various types of microplastics and non-protein particles, and several hydrophilic elements were bound to the OD. When aspirated OD via the pharynx for 90 days, blood levels of IP and K significantly decreased in male mice, but not in female mice. Meanwhile, the total number of pulmonary cells increased, accompanied by increases in the proportions of lymphocytes and PMNs, as well as pulmonary levels of pro-inflammatory and anti-inflammatory mediators. Foamy alveolar macrophages and mucous cell hyperplasia were observed in the lung tissues, accompanied by increased levels of TGF-β1, IL-11, and IL-24. More importantly, structural disruption of mitochondria, mitophagy, and the formation of lamellar bodies and collagen fibers were frequently observed in the lung and heart tissues of OD-treated mice. In addition, LDH release and ATP production were not significantly affected in OD-treated alveolar macrophage cells, even at the highest concentration. Meanwhile, very interestingly, the activity of the NADPH-dependent cellular oxidoreductase enzyme decreased dramatically, even at the lowest concentration. Genes related to cytokine-cytokine receptor interaction and neutrophil extracellular trap formation were most significantly affected in cells exposed to OD, and Saa3, Cybb, Slc7a11, and CXCL2 were identified as the most upregulated genes. The expression of SOD-2, FeH, and COX-2 proteins was enhanced in OD-treated cells, along with increased NO production, whereas the expression of transferrin receptor and BAX protein was reduced in the same cells. Collectively, we suggest that OD exposure may increase the lung burden of foreign bodies by disrupting the metabolic activity of alveolar macrophages, ultimately resulting in chronic pulmonary diseases. We also hypothesize that impaired self-renewal capacity may contribute to the lung burden of OD.