The development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We tried to provide fundamental data to determine differences in cytotoxicity induced by ambient UFPs and engineered metal oxide NPs (ZnO, NiO, and CeO2). UFPs were sampled by using of a nano micro-orifice uniform deposit impactor. Physicochemical characterization of the UFPs and nano metal oxide particles were studied by scanning electron microscopy and transmission electron microscopy. Cellular toxicity induced by the different particles was assessed by using of comprehensive approaches and compared after A549 cells were exposured to the particles. All of the measured particles could damage A549 cells at concentrations ranging from 25 to 200 μg/mL. The lowest survival ratio and the highest lactate dehydrogenase level were caused by nano-ZnO particles, but the highest levels of intracellular reactive oxygen species (ROS) and percentages of apoptosis were observed in cells treated with the soluble fraction of ambient fine particles (PM1.8) at 200 μg/mL. Relatively high concentrations of anthropogenic metals, including Zn, Ni, Fe, and Cu, may be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and UFPs. The selected heavy metals (Zn, Ni, Fe, and Cu) were found to be located in the perinuclear and cytoplasmic areas of A549 cells. The distribution pattern of metals from ambient particles showed that distributions of the metals in A549 cells were not uniform and followed the pattern Cu > Zn > Fe > Ni, suggesting that Cu was absorbed by A549 cells more easily than the other metals. Metal nanoparticles oxides and UFPs at low concentration could damage to cells, but the manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles. The local concentration effect of heavy metals in A549 cells, as well as the induction of oxidative stress by the particles, may be responsible for the damage observed to the cells.

中文翻译：

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比较环境超细颗粒和工程金属氧化物纳米颗粒引起的细胞毒性。

纳米技术的发展引起了人们对暴露于纳米颗粒（NPs）和超细颗粒（UFPs）的健康影响的担忧。有关NP和UFP的毒理学数据可提供证据，以支持制定法规以减少颗粒暴露的风险。我们试图提供基础数据，以确定环境UFP和工程金属氧化物NP（ZnO，NiO和CeO2）诱导的细胞毒性差异。通过使用纳米微孔均匀沉积撞击器对UFP进行采样。通过扫描电子显微镜和透射电子显微镜研究了UFP和纳米金属氧化物颗粒的理化特性。通过使用综合方法评估由不同颗粒诱导的细胞毒性，并在将A549细胞暴露于颗粒后进行比较。所有测得的颗粒均可在25至200μg/ mL的浓度范围内破坏A549细胞。最低的存活率和最高的乳酸脱氢酶水平是由纳米ZnO颗粒引起的，但是在用可溶级分的环境细颗粒（PM1）处理的细胞中观察到了最高水平的细胞内活性氧（ROS）和凋亡百分比。 8）200μg/ mL。与周围的粗颗粒和UFP相比，较高浓度的人为金属（包括Zn，Ni，Fe和Cu）可能是导致周围细颗粒的毒性更高的原因。发现选定的重金属（Zn，Ni，Fe和Cu）位于A549细胞的核周和细胞质区域。周围颗粒中金属的分布模式表明，A549电池中金属的分布不均匀，并且遵循Cu> Zn> Fe> Ni的模式，这表明Cu比其他金属更容易被A549电池吸收。低浓度的金属纳米颗粒氧化物和UFP可能会损害细胞，但与环境颗粒相比，制造的金属氧化物纳米颗粒对肺细胞的毒性不高。重金属在A549细胞中的局部富集作用以及颗粒对氧化应激的诱导可能是对细胞造成的损害的原因。低浓度的金属纳米颗粒氧化物和UFP可能会损害细胞，但与环境颗粒相比，制造的金属氧化物纳米颗粒对肺细胞的毒性不高。重金属在A549细胞中的局部富集作用以及颗粒对氧化应激的诱导可能是对细胞造成的损害的原因。低浓度的金属纳米颗粒氧化物和UFP可能会损害细胞，但与环境颗粒相比，制造的金属氧化物纳米颗粒对肺细胞的毒性不高。重金属在A549细胞中的局部富集作用以及颗粒对氧化应激的诱导可能是对细胞造成的损害的原因。