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

Tungsten trioxide (WO 3 )-based nanoparticles (NPs) are gaining popularity because of their exciting potential for photocatalytic applications; however, the toxic potential of WO 3 -based NPs remains a concern. In this study, we evaluated the toxic risk of WO 3 NPs and hydrated WO 3 NPs (WO 3 ·H 2 O NPs) using lung cells and explored the underlying mechanism. WO 3 NPs and WO 3 ·H 2 O 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 WO 3 NPs and WO 3 ·H 2 O 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 WO 3 NPs have higher cytotoxicity and oxidative potential than WO 3 ·H 2 O NPs. In addition, the WO 3 NP cellular uptake rate was significantly higher than the WO 3 ·H 2 O NPs uptake rate in pulmonary cells. The greater extent of oxidative adverse effects induced by WO 3 -based NPs appears to be related to the enhanced particle uptake. WO 3 NPs and WO 3 ·H 2 O 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 WO 3 NPs and WO 3 ·H 2 O NPs raises the risk of developing chronic obstructive pulmonary disease. Taken together, our findings indicate that the toxic risk of WO 3 NPs and WO 3 ·H 2 O NPs must be considered when manufacturing and applying WO 3 -based NPs. • WO 3 NPs are internalized more efficiently and has a higher cellular uptake rate. • WO 3 NPs induced severe cytotoxicity and oxidative responses. • WO 3 ·H 2 O NPs induced more severe inflammatory responses. • WO 3 NPs and WO 3 ·H 2 O NPs can stimulate the early progression of lung disease. • Long-term exposure to WO 3 NPs and WO 3 ·H 2 O NPs can affect pulmonary health.