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The natural activation ability of subsurface media to promote in-situ chemical oxidation of 1,4-dioxane.

ABSTRACT: The ability of soils and sediments to promote in-situ activation of persulfate and persulfate combined with hydrogen peroxide was investigated for treatment of 1,4-dioxane (dioxane). Experiments were conducted with both batch-reactor and column systems to examine reaction rates and activation mechanisms. Four soils and aquifer sediments were used. ICP-MS and XRD analyses were used to characterize geochemical properties of the solutions and sediments, while EPR spectroscopy was used to characterize radical formation. For the batch experiments, degradation of dioxane was significantly greater in the presence of each of the four subsurface geomedia compared to the controls with no geomedia. This indicates that all four geomedia induced oxidant activation, thereby enhancing dioxane degradation. Dioxane degradation was significantly enhanced by the addition of peroxide to the persulfate solution. It is hypothesized that iron associated with the geomedia is primarily responsible for activation, and that the degree of degradation enhancement relates in part to dissolved-phase iron content. EPR results indicate that manganese oxides and soil organic matter may also have contributed to some degree to persulfate activation, and that manganese oxides enhanced activation of peroxide under the study conditions. Approximately 10% of dioxane was degraded in the miscible-displacement experiments, consistent with the short residence time compared to dioxane's half-life. The pseudo first-order rate coefficients obtained from the batch and column experiments were similar. The results of this study indicate that subsurface geomedia can induce activation of persulfate and peroxide to enhance in-situ chemical oxidation applications.

SUBMITTER: Yan N

PROVIDER: S-EPMC6358466 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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The natural activation ability of subsurface media to promote in-situ chemical oxidation of 1,4-dioxane.

Yan Ni N Zhong Hua H Brusseau Mark L ML

Water research 20181114

The ability of soils and sediments to promote in-situ activation of persulfate and persulfate combined with hydrogen peroxide was investigated for treatment of 1,4-dioxane (dioxane). Experiments were conducted with both batch-reactor and column systems to examine reaction rates and activation mechanisms. Four soils and aquifer sediments were used. ICP-MS and XRD analyses were used to characterize geochemical properties of the solutions and sediments, while EPR spectroscopy was used to characteri ...[more]

PMID: 30471534

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Project description:1,4-Dioxane (1,4-DX) is an environmental contaminant found in drinking water throughout the United States (US). While it is a suspected liver carcinogen, there is no federal or state maximum contaminant level for 1,4-DX in drinking water. Very little is known about the mechanisms by which this chemical elicits liver carcinogenicity. In the present study, we performed chronic and short-term dosing studies in female BDF-1 mice to explore the toxic effects of 1,4-DX. Histopathology studies and a multi-omics approach (transcriptomics and metabolomics) were performed to investigate potential mechanisms of toxicity. Mice were exposed to various concentrations of 1,4-DX (0, 50, 500 and 5,000 mg/L) in their drinking water for one or four weeks. Immunohistochemical analysis of the liver revealed an increase in the number of H2AXγ-positive hepatocytes (a marker of DNA double strand breaks) in mice exposed to 5,000 mg/L 1,4-DX for one and four weeks. In addition, an expansion of precholangiocytes was observed after four weeks of 5,000 mg/L 1,4-DX exposure, as reflected by CK-7 immunostaining. An increase in these markers reflect both DNA damage and repair mechanisms. Liver transcriptomics profiling showed that exposure to 5,000 mg/L 1,4-DX for four weeks resulted in the differential expression of 65 genes compared to controls. Pathway analysis of the transcriptomic data revealed 1,4-DX-induced perturbations in multiple signaling pathways in the liver, including those involved in xenobiotic metabolism, nicotine degradation and glutathione-mediated detoxification. Changes to these pathways as a result of 1,4-DX exposure reflect would be predicted to impact the oxidative stress response, detoxification, and DNA damage. Liver, kidney, stool and urine metabolomics profiling revealed no effect of 5,000 mg/L 1,4-DX exposure for one or four weeks on metabolites. We speculate that this may be reflective of DNA damage being counterbalanced by the repair response, with the net result being a null overall effect on the systemic biochemistry of the exposed mice. Our results show a novel approach for the investigation of environmental chemicals that do not elicit cell death, but have activated the repair systems in response to 1,4-DX exposure

Dataset Information

The natural activation ability of subsurface media to promote in-situ chemical oxidation of 1,4-dioxane.

Publications

The natural activation ability of subsurface media to promote in-situ chemical oxidation of 1,4-dioxane.

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