Comparative pulmonary toxicity assessment of tungsten trioxide and tungsten trioxide hydrate nanoparticles

Tungsten trioxide (WO₃)-based nanoparticles (NPs) are gaining popularity because of their exciting potential for photocatalytic applications; however, the toxic potential of WO₃-based NPs remains a concern. In this study, we evaluated the toxic risk of WO₃ NPs and hydrated WO₃ NPs (WO₃·H₂O NPs) using lung cells and explored the underlying mechanism. WO₃ NPs and WO₃·H₂O NPs significantly decreased the number of viable cells (59.5 %-85.8 % of control) and promoted apoptosis in human alveolar basal epithelial A549 cells after a 24-h exposure. Both WO₃ NPs and WO₃·H₂O NPs reduced the expression of heme oxygenase-1 (0.15-0.33 folds of control) and superoxide dismutase 2 (0.31-0.66 folds of control) and increased reactive oxygen species production (1.4-2.6 folds of control) and 8-hydroxy-2'-deoxyguanosine accumulation (1.22-1.43 folds of control). The results showed that WO₃ NPs have higher cytotoxicity and oxidative potential than WO₃·H₂O NPs. In addition, the WO₃ NP cellular uptake rate was significantly higher than the WO₃·H₂O NPs uptake rate in pulmonary cells. The greater extent of oxidative adverse effects induced by WO₃-based NPs appears to be related to the enhanced particle uptake. WO₃ NPs and WO₃·H₂O NPs exposure led to the secretion of inflammatory factor interleukin 6 (1.63-3.42 folds of control). Decreases in serpin family A member 1 gene expression (0.28-0.58 folds of control) and increases in the oxidation of neutrophil elastase inhibitor (1.34-1.62 folds of control) in pulmonary cells also suggest that exposure to WO₃ NPs and WO₃·H₂O NPs raises the risk of developing chronic obstructive pulmonary disease. Taken together, our findings indicate that the toxic risk of WO₃ NPs and WO₃·H₂O NPs must be considered when manufacturing and applying WO₃-based NPs.