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The proper management of discarded electronic devices (E-waste) is an important issue for solid waste professionals because of the magnitude of the waste stream and because these devices often contain a variety of toxic metals (e.g., lead). While recycling of E-waste is developing, much of this waste stream is disposed in landfills. Leaching tests are frequently used to characterize the potential of a solid waste to leach when disposed in a landfill. In the United States, the Toxicity Characteristic Leaching Procedure (TCLP) is used to determine whether a solid waste is a hazardous waste by the toxicity characteristic. The TCLP is designed to simulate worse-case leaching in a landfill environment where the waste is co-disposed with municipal solid waste (MSW). While the TCLP is a required analysis from a regulatory perspective, the leachate concentrations measured may not accurately reflect the concentrations observed under typical landfill conditions. Another method that can be performed to assess the degree a pollutant might leach from a waste in a landfill is to use actual landfill leachate as the leaching solution. In this study, two lead-containing components found in electronic devices (printed wire boards from computers and cathode ray tubes from computers and televisions) were leached using the TCLP and leachates from 11 Florida landfills. California's Waste Extraction Test (WET) and the Synthetic Precipitation Leaching Procedure were also performed. The results indicated that the extractions using MSW landfill leachates resulted in lower lead concentrations than those by the TCLP. The pH of the leaching solution and the ability of the organic acids in the TCLP and WET to complex with the lead are factors that regulate the amount of lead leached.

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Cathode ray tubes (CRTs) in television and computer monitors are one of the most common components of discarded electronics in the solid waste stream. CRTs present a disposal problem because of their growing magnitude in municipal solid waste (MSW) and their role as a major source of lead in MSW. Using the EPA Toxicity Characteristic Leaching Procedure (TCLP), lead leachability from CRTs was studied. Lead leached from the CRT samples at an average concentration of 18.5 mg/L. This exceeded the regulatory limit of 5.0 mg/L. Several factors affected the lead concentrations of each CRT sample. These included the sample fraction of the CRTs, the particle size used in the tests, and the CRT type. The most significant quantities of lead were obtained from the funnel portion of the CRTs at an average lead concentration of 75.3 mg/L. The major source of lead in the funnel is the frit seal of color CRTs. Samples containing the frit seal had lead leaching levels nearly 50 times those without. Samples comprised of smaller particle sizes exposed a greater surface area resulting in higher lead leaching levels. While 21 of 30 color CRTs exceeded regulatory lead limits, none of the six monochrome CRTs did. Age of the CRTs was not a significant factor for lead leaching. These results provide useful information to the regulatory and waste management community for developing policies for managing discarded CRTs.

The potential for discarded electronic devices to be classified as toxicity characteristic (TC) hazardous waste under provisions of the Resource Conservation and Recovery Act (RCRA) using the toxicity characteristic leaching procedure (TCLP) was examined. The regulatory TCLP method and two modified TCLP methods (in which devices were disassembled and leached in or near entirety) were utilized. Lead was the only element found to leach at concentrations greater than its TC limit (5 mg/L). Thirteen different types of electronic devices were tested using either the standard TCLP or modified versions. Every device type leached lead above 5 mg/L in at least one test and most devices leached lead above the TC limit in a majority of cases. Smaller devices that contained larger amounts of plastic and smaller amounts of ferrous metal (e.g., cellular phones, remote controls) tended to leach lead above the TC limit at a greater frequency than devices with more ferrous metal (e.g., computer CPUs, printers).

Obesity contributes to systemic inflammation, which is associated with the varied pathogenesis of neurodegenerative diseases. Growing evidence has demonstrated that endurance exercise (EE) mitigates obesity-induced brain inflammation. However, exercise-mediated anti-inflammatory mechanisms remain largely unknown. We investigated how treadmill exercise (TE) reverses obesity-induced brain inflammation, mainly focusing on toll-like receptor-4 (TLR-4)-dependent neuroinflammation in the obese rat brain after 20 weeks of a high-fat diet (HFD). TE in HFD-fed rats resulted in a significant lowering in the homeostasis model assessment of insulin resistance index, the area under the curve for glucose and abdominal visceral fat, and also improved working memory ability in a passive avoidance task relative to sedentary behaviour in HFD-fed rats, with the exception of body weight. More importantly, TE revoked the increase in HFD-induced proinflammatory cytokines (tumour necrosis factor α and interleukin-1β) and cyclooxygenase-2, which is in parallel with a reduction in TLR-4 and its downstream proteins, myeloid differentiation 88 and tumour necrosis factor receptor associated factor 6, and phosphorylation of transforming growth factor β-activated kinase 1, IkBα and nuclear factor-κB. Moreover, TE reduced an indicator of microglia activation, ionised calcium-binding adapter molecule-1, and also decreased glial fibrillary acidic protein, an indicator of gliosis formed by activated astrocytes in the cerebral cortex and the hippocampal dentate gyrus, compared to HFD-fed sedentary rats. Finally, EE up-regulated the expression of anti-apoptotic protein, Bcl-2, and suppressed the expression of pro-apoptotic protein, Bax, in the hippocampus compared to HFD-fed sedentary rats. Taken together, these data suggest that TE may exert neuroprotective effects as a result of mitigating the production of proinflammatory cytokines by inhibiting the TLR4 signalling pathways. The results of the present study suggest that the unique combination of the beneficial effects of TE on the restoration of the blood profile and the anti-inflammatory and anti-apoptotic effects on cognitive function should inspire further investigations into its therapeutic potential for metabolic disorders and neurodegenerative diseases.

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