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Toxicity of engineered nanomaterials and their transformation products following wastewater treatment on A549 human lung epithelial cells.

ABSTRACT: Here we characterize the toxicity of environmentally-relevant forms of engineered nanomaterials (ENMs), which can transform during wastewater treatment and persist in aqueous effluents and biosolids. In an aerosol exposure scenario, cytotoxicity and genotoxicity of effluents and biosolids from lab-scale sequencing batch reactors (SBRs) to A549 human lung epithelial cells were examined. The SBRs were dosed with nanoAg, nano zero-valent iron (NZVI), nanoTiO₂ and nanoCeO₂ at sequentially increasing concentrations from 0.1 to 20 mg/L. Toxicities were compared to outputs from SBRs dosed with ionic/bulk analogs, undosed SBRs, and pristine ENMs. Pristine nanoAg and NZVI showed significant cytotoxicity to A549 cells in a dose-dependent manner from 1 to 67 ?g/mL, while nanoTiO₂ and nanoCeO₂ only exerted cytotoxicity at 67 ?g/mL. Only nanoAg induced a genotoxic response, at 9, 33 and 53 ?g/mL. However, no significant cytotoxic or genotoxic effects of the SBR effluents or biosolids containing nanomaterials were observed.

SUBMITTER: Ma Y

PROVIDER: S-EPMC5598501 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Toxicity of engineered nanomaterials and their transformation products following wastewater treatment on A549 human lung epithelial cells.

Ma Yanjun Y Elankumaran Subbiah S Marr Linsey C LC Vejerano Eric P EP Pruden Amy A

Toxicology reports 20140921

Here we characterize the toxicity of environmentally-relevant forms of engineered nanomaterials (ENMs), which can transform during wastewater treatment and persist in aqueous effluents and biosolids. In an aerosol exposure scenario, cytotoxicity and genotoxicity of effluents and biosolids from lab-scale sequencing batch reactors (SBRs) to A549 human lung epithelial cells were examined. The SBRs were dosed with nanoAg, nano zero-valent iron (NZVI), nanoTiO<sub>2</sub> and nanoCeO<sub>2</sub> at s ...[more]

PMID: 28962298

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Project description:Understanding the structure transformation of engineered nanomaterials (ENMs) is a grand measurement challenge, which impacts many aspects of ENMs applications, such as their efficacy, safety, and environmental consequence. To address the significant knowledge gap regarding the fundamental kinetic rate and extent of ENM transformation in the environment, we present a comprehensive and mechanistic structural investigation of the transformation, aggregation, and dissolution behavior of a polyvinylpyrrolidone-coated silver nanoparticle (AgNP) suspension upon sulfidation in moderately reduced hard water with fulvic acid and dissolved Na2S. This reaction is among the most prevalent and industrially and environmentally relevant ENMs transformation. Using ex situ transmission electron microscopy (TEM) and both in situ and ex situ synchrotron-based small angle X-ray scattering (SAXS) and X-ray diffraction (XRD), we find that sulfidation of faceted AgNPs strongly depends on the crystallographic orientation of the facets, with nanometer-scale passivation layers developed on {111} and {100} facets and continuous nucleation and growth on {110} facets. Nanobeam electron diffraction and atomic resolution imaging show Ag and Ag2S domains both possess a high degree of crystalline order, contradicting amorphous structures as previously reported. In situ SAXS/XRD allowed simultaneous determination of the morphological changes and extent of sulfidation of AgNPs. SAXS/XRD results strongly indicate sulfidation follows first-order reaction kinetics without any aggregation. Aided by their size monodispersity, for the first time, using direct, in situ morphology and atomic-structure probes whose results mutually corroborate, we unequivocally determined the sulfidation rate constant of AgNPs under an environmentally relevant condition (~0.013 min-1 for 68 nm diameter AgNPs). A rigorous analysis of the long-term sulfidation product of the AgNPs under different S/Ag ratios using ex situ SAXS/XRD clearly demonstrates that the silver mass in the original AgNP and transformed Ag/Ag2S NP is preserved. This result has important environmental implications, strongly suggesting that Ag+ ions, a known highly effective antimicrobial agent, are not leached into the solution during sulfidation of AgNPs. The combined nondestructive methodology can be extended to unfold the structure transformation pathway and kinetics in a broad range of ENM systems.

Project description:BackgroundThis study has investigated the ability of tobacco smoke, and ingredients of tobacco smoke, to induce apoptosis in the airway epithelial cell line A549.MethodA549 cells were treated with 80 microg/ml Tobacco smoke condensate (TSC), 10 mM Nicotine, 10 microM paraldehyde, 10 microM hydrogen peroxide, 1 microM Taxol (Paclitaxel), 100%, 50% and 25% cigarette smoke extract (CSE). Following 4-48 h incubation apoptosis was measured morphologically following staining of cells with DAPI. TUNEL staining was also used to assess DNA damage after 24 and 48 h incubation. In addition, loss of mitochondrial cytochrome C and activation of Bax-alpha, early events in the apoptotic process, were measured after 4 h of incubation.ResultsIncubation of A549 cells with vehicle, Taxol, TSC, nicotine, paraldehyde, hydrogen peroxide and CSE caused a time-dependent detachment of the cells from the flask between 6 and 48 h. DAPI staining revealed that the cells remaining adhered to the flask appeared healthy whereas some of those that had detached appeared to be either apoptotic or indeterminate. Treatment with Taxol, TSC, nicotine, paraldehyde, hydrogen peroxide and CSE caused a significant increase in the number of apoptotic cells. Similarly, treatment with Taxol, TSC, nicotine, hydrogen peroxide and CSE caused a significant increase in the number of apoptotic cells among the cells that had detached from the culture plate. After 4 h of incubation, Taxol, TSC, hydrogen peroxide and CSE caused a significant reduction in mitochondrial cytochrome C and an increase in cytosolic cytochrome C. At the same time point, hydrogen peroxide and CSE significantly increased the concentration of Bax-alpha in the mitochondria.ConclusionTobacco smoke initiates apoptosis in A549 airway epithelial cells as a result of mitochondrial damage and that this results in a cell detachment and full apoptosis. This effect appears to result from factors in tobacco smoke other than nicotine and may result from free radical activity. However, additional stable factors may also be involved since the free radical content of TSC is likely to be low.

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Toxicity of engineered nanomaterials and their transformation products following wastewater treatment on A549 human lung epithelial cells.

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Toxicity of engineered nanomaterials and their transformation products following wastewater treatment on A549 human lung epithelial cells.

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