Abstract
ObjectiveThe 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).MethodsUFPs 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.ResultsAll 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.ConclusionsMetal 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-015-0082-8) contains supplementary material, which is available to authorized users.
Highlights
Coarse particles are mostly deposited in the upper respiratory tract, whereas fine particles can be inhaled deep into the lung [1]
The lowest MTT ratio and highest Lactate dehydrogenase (LDH) activity were observed for nano-ZnO particles, and the highest intracellular reactive oxygen species (ROS) intensity and apoptotic percentage were produced by the soluble fraction of ambient fine particles (PM1.8) at 200 μg/mL
May be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and ultrafine particles (UFPs)
Summary
Coarse particles are mostly deposited in the upper respiratory tract, whereas fine particles can be inhaled deep into the lung [1]. UFPs could directly injure the lung, inducing lung inflammation or translocation of inhaled particles from lung airspaces into the systemic circulation, eventually reaching other organs [2,3,4,5]. A number of studies have investigated the toxicity of ambient particles [6,7]. Nanotoxicology has emerged as a new field for investigating the adverse biological outcomes of nanomaterials [2,8,9,10]. Current environmental laws and occupational health guidelines are based on the nominal chemical composition of the material and seldom specify special standards for ultrafine or nanosized particles. The potential occupational health and environmental effects of these nanosized particles are a public health concern [11]
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