Strengthened dewaterability of coke-oven plant oily sludge by altering extracellular organics using Fe(II)-activated persulfate oxidation.

Although oily sludge has tremendous resource recovery value, its high water content has hindered its treatment and reuse. This study systematically explored the technical feasibility of using Fe(II)-activated persulfate oxidation (Fe2+/S2O82-) to enhance the dewaterability of oily sludge. To identify the main factors controlling sludge dewatering, this study measured changes in chemical oxygen demand, ammonia nitrogen (NH4+-N) and extracellular polymeric substances (EPS). Results showed that at 0.1 mmol-Fe2+/g-VSS and 0.08 mmol-S2O82-/g-VSS, capillary suction time (s) was reduced by roughly 36.1% within 1 min and dewaterability was strengthened strongly. Sulfate radicals originating from Fe2+/S2O82- oxidized a large amount of EPS, leading to liberation of EPS-bound water. A similar declining trend in NH4+-N was evident as a result of the strong oxidizing ability of sulfate radicals. Further analysis via scanning electron microscopy and thermogravimetric-Fourier transform infrared spectrometry revealed that Fe2+/S2O82- oxidation destroyed the water-oil-gel-like structure of the oily sludge, thereby accelerating the separation of solids and water while reducing CO2 emissions during the subsequent pyrolysis. Therefore, oily sludge dewatering was enhanced significantly by the Fe2+/S2O82- process.

Behavioral deficits and neural damage of Caenorhabditis elegans induced by three rare earth elements.

Rare earth elements (REEs) are widely used in industry, agriculture, medicine and daily life in recent years. However, environmental and health risks of REEs are still poorly understood. In this study, neurotoxicity of trichloride neodymium, praseodymium and scandium were evaluated using nematode Caenorhabditis elegans as the assay system. Median lethal concentrations (48 h) were 99.9, 157.2 and 106.4 mg/L for NdCl3, PrCl3 and ScCl3, respectively. Sublethal dose (10-30 mg/L) of these trichloride salts significantly inhibited body length of nematodes. Three REEs resulted in significant declines in locomotor frequency of body bending, head thrashing and pharyngeal pumping. In addition, mean speed and wavelength of crawling movement were significantly reduced after chronic exposure. Using transgenic nematodes, we found NdCl3, PrCl3 and ScCl3 resulted in loss of dendrite and soma of neurons, and induced down-expression of dat-1::GFP and unc-47::GFP. It indicates that REEs can lead to damage of dopaminergic and GABAergic neurons. Our data suggest that exposure to REEs may cause neurotoxicity of inducing behavioral deficits and neural damage. These findings provide useful information for understanding health risk of REE materials.