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.

Evaluation of toxicity of polystyrene microplastics under realistic exposure levels in human vascular endothelial EA.hy926 cells.

Microplastics (MPs) have emerged as a global concern, with a recent study being the first to detect them in the bloodstream of healthy people. However, precise information regarding the toxic effects of MPs on the human vascular system is currently lacking. In this study, we used human vascular endothelial EA. hy926 cells to examine the toxic potential of polystyrene MPs (PSMPs) under realistic blood concentrations. Our findings indicated that PSMPs can cause oxidative stress by reducing the expression of antioxidants, thereby leading to apoptotic cytotoxicity in EA. hy926 cells. Furthermore, the protective potential of heat shock proteins can be reduced by PSMPs. PSMP-induced apoptosis might also lower the expression of rho-associated protein kinase-1 and nuclear factor-κB expression, thus dampening LRR- and pyrin domain-containing protein 3 in EA. hy926 cells. Moreover, we observed that PSMPs induce vascular barrier dysfunction via the depletion of zonula occludens-1 protein. However, although protein expression of the nuclear hormone receptor 77 was inhibited, no significant increase in ectin-like oxidized low-density lipoprotein receptor-1 was noted in PSMP-treated EA. hy926 cells. These results demonstrate that exposure to PSMPs may not sufficiently increase the risk of developing atherosclerosis. Overall, our research signifies that exposure to realistic blood concentrations of PSMPs is associated with low atherosclerotic cardiovascular risk in humans.