Exercise as an antidepressant: exploring its therapeutic potential.

The COVID-19 pandemic has increased the prevalence of depressive disorders worldwide, requiring alternative treatments beyond medication and psychotherapy. Exercise has positive effects on the brain; therefore, it has emerged as a promising therapeutic option for individuals with depression. Considerable research involving humans and animals offers compelling evidence to support the mental health benefits of physical activity or exercise mediated by the regulation of complex theoretical paradigms. However, challenges such as conducting long-term follow-up assessments and considering individual characteristics remain in human studies despite extensive efforts. While animal studies provide valuable insights into the potential benefits of exercise and its impact on outcomes related to depression and anxiety in rodents exposed to different stress paradigms, translating the findings to humans requires careful evaluation. More research is needed to establish precise exercise prescription guidelines and to better understand the complex relationship between exercise and depressive disorders. Therefore, this concise review explores the evidence supporting exercise intervention as an antidepressant treatment and its underlying mechanisms.

Post-consumer plastic packaging waste from online food delivery services in South Korea.

Along with the rapid growth of the food delivery industry, concerns are growing regarding the management of plastic packaging waste. This study estimates the amount of plastic packaging from online food delivery services in Korea and assesses its environmental effects using life cycle assessments. This study also compares the environmental impacts of the adoption of multi-use containers, the use of recycled materials, and the increase in recycling rates proposed by the Korean government for efficient plastic waste management. A total of 72.93 kt of plastic packaging was consumed by online food delivery in 2020, polypropylene and polyethylene terephthalate accounted for 81.48% of the packaging materials consumed. The adoption of multi-use containers is the most environmentally effective alternative, but its negative impact on terrestrial ecotoxicity is approximately 5 times higher than that of others. Although the other two alternatives are 2-6 times less efficient than adopting multi-use containers, they can still play an important role in plastic waste management. Overall, these results provide empirical information on food packaging waste and insights into the sustainable management of plastics. Keywords: Food packaging, Plastic waste, Online food delivery service, Waste management, Environmental impact.

Treadmill Exercise Alleviates Brain Iron Dyshomeostasis Accelerating Neuronal Amyloid-ß Production, Neuronal Cell Death, and Cognitive Impairment in Transgenic Mice Model of Alzheimer's Disease.

Brain iron increases with age and abnormal brain iron metabolism is proving increasingly likely to be involved in the pathology of Alzheimer's disease (AD). The iron-regulatory effect of furin, a ubiquitously expressed proconvertase, might play an important role in AD. Therefore, there is an urgent need to study the effect of furin on iron regulation in AD. For that purpose, we aimed to determine the role of physical exercise in AD associated with brain iron dyshomeostasis. Treadmill exercise attenuated the AD-related abnormal brain iron regulation by furin in vivo, as demonstrated via experiments in aged APP-C105 mice. Next, we examined whether treadmill exercise decreases excessive iron, directly affecting amyloid-ß (Aß) production through the regulation of α-secretase-dependent processing of amyloid protein precursor (APP) involved in the modulation of furin activity. We first observed that cognitive decline and Aß-induced neuronal cell death were induced by disruption of APP processing via excess iron-induced disruption of furin activity in aged APP-C105 mice. The induced cognitive decline and cell death were attenuated by treadmill exercise. This result suggests that treadmill exercise alleviated cognitive decline and Aß-induced neuronal cell death by promoting α-secretase-dependent processing of APP through low iron-induced enhancement of furin activity. This is concomitant with decreasing levels of lipid peroxidation products and promoting antioxidant defense enzyme capacities. Therefore, iron-targeted therapeutic strategies involving treadmill exercise might be useful for patients with AD.

Endurance Exercise-Induced Autophagy/Mitophagy Coincides with a Reinforced Anabolic State and Increased Mitochondrial Turnover in the Cortex of Young Male Mouse Brain.

Autophagy/mitophagy, a cellular catabolic process necessary for sustaining normal cellular function, has emerged as a potential therapeutic strategy against numerous obstinate diseases. In this regard, endurance exercise (EXE)-induced autophagy/mitophagy (EIAM) has been considered as a potential health-enriching factor in various tissues including the brain; however, underlying mechanisms of EIAM in the brain has not been fully defined yet. This study investigated the molecular signaling nexus of EIAM pathways in the cortex of the brain. C57BL/6 young male mice were randomly assigned to a control group (CON, n = 12) and an endurance exercise group (EXE, n = 12). Our data demonstrated that exercise-induced autophagy coincided with an enhanced anabolic state (p-AKT, p-mTOR, and p-p70S6K); furthermore, mitophagy concurred with enhanced mitochondrial turnover: increases in both fission (DRP1, BNIP3, and PINK1) and fusion (OPA1 and MFN2) proteins. In addition, neither oxidative stress nor sirtuins (SIRT) 1 and 3 were associated with EIAM; instead, the activation of AMPK as well as a JNK-BCL2 axis was linked to EIAM promotion. Collectively, our results demonstrated that EXE-induced anabolic enrichment did not hinder autophagy/mitophagy and that the concurrent augmentation of mitochondrial fusion and fusion process contributed to sustaining mitophagy in the cortex of the brain. Our findings suggest that the EXE-induced concomitant potentiation of the catabolic and anabolic state is a unique molecular mechanism that simultaneously contributes to recycling and rebuilding the cellular structure, leading to upholding healthy cellular environment. Thus, the current study provides a novel autophagy/mitophagy mechanism, from which groundbreaking pharmacological strategies of autophagy can be developed.

Endurance exercise-induced expression of autophagy-related protein coincides with anabolic expression and neurogenesis in the hippocampus of the mouse brain.

Autophagy and neurogenesis play a pivotal role in maintaining cellular homeostasis of neurons in the brain. Endurance exercise (EXE) serves as a potent regulator of both autophagy and neurogenesis in the hippocampus of the brain; however, the underlying molecular mechanisms of the dual expression remains unclear. Thus, we examined the signaling pathways of EXE-induced autophagy and neurogenesis-associated protein expression in the hippocampus. C57BL/6 male mice (10 weeks old) were randomly divided into two groups: control group (n = 10) and EXE group (EXE, n = 10). Our results showed that EXE increased expression of autophagy-related protein [LC3 II, BECLIN1, autophagy-related 7 (ATG7), p62, LAMP2, CATHEPSIN L and transcription factor EB] in the presence of anabolic signaling expression (AKT-mammalian target of rapamycin-ribosomal S6 kinase). Intriguingly, long-term EXE-mediated neurogenesis in the hippocampus was observed despite the downregulated expressions of canonical neurotrophic factors (e.g. brain-derived neurotrophic factor, glial cell line-derived neurotrophic factors and nerve growth factor); instead, upregulation of neuregulin-1 (NRG1)-mediated signaling cascades (e.g. NRG1-extracellular signal-regulated kinase-ribosomal s6 kinase-cyclic adenosine mono-phosphate response element-binding protein) were associated with EXE-induced hippocampal neurogenesis and synaptic plasticity. Our data, for the first time, show that EXE-mediated expression of autophagy-related protein coincides with anabolic expression and that NRG1 is involved in EXE-mediated neurogenesis and synaptic plasticity. Taken together, this study provides a novel mechanism of hippocampal autophagy and neurogenesis, which may provide potential insight into developing therapeutic neuroprotective strategies.

Elevation of hepatic autophagy and antioxidative capacity by endurance exercise is associated with suppression of apoptosis in mice.

INTRODUCTION AND OBJECTIVES: Endurance exercise (EXE) has emerged as a potent inducer of autophagy essential in maintaining cellular homeostasis in various tissues; however, the functional significance and molecular mechanisms of EXE-induced autophagy in the liver remain unclear. Thus, the aim of this study is to examine the signaling nexus of hepatic autophagy pathways occurring during acute EXE and a potential crosstalk between autophagy and apoptosis. MATERIALS AND METHODS: C57BL/6 male mice were randomly assigned to sedentary control group (CON, n=9) and endurance exercise (EXE, n=9). Mice assigned to EXE were gradually acclimated to treadmill running and ran for 60min per day for five consecutive days. RESULTS: Our data showed that EXE promoted hepatic autophagy via activation of canonical autophagy signaling pathways via mediating microtubule-associated protein B-light chain 3 II (LC3-II), autophagy protein 7 (ATG7), phosphorylated adenosine mono phosphate-activated protein kinase (p-AMPK), CATHEPSIN L, lysosome-associated membrane protein 2 (LAMP2), and a reduction in p62. Interestingly, this autophagy promotion concurred with enhanced anabolic activation via AKT-mammalian target of rapamycin (mTOR)-p70S6K signaling cascade and enhanced antioxidant capacity such as copper zinc superoxide dismutase (CuZnSOD), glutathione peroxidase (GPX), and peroxiredoxin 3 (PRX3), known to be as antagonists of autophagy. Moreover, exercise-induced autophagy was inversely related to apoptosis in the liver. CONCLUSIONS: Our findings indicate that improved autophagy and antioxidant capacity, and potentiated anabolic signaling may be a potent non-pharmacological therapeutic strategy against diverse liver diseases.

Endurance Exercise Attenuates Doxorubicin-induced Cardiotoxicity.

PURPOSE: Endurance exercise (EXE) preconditioning before DOX treatment confers cardioprotection; however, whether EXE postconditioning (i.e., EXE intervention after the completion of DOX treatment) is cardioprotective remains unknown. Thus, the aim of the present study was to investigate if EXE postconditioning provides cardioprotection by testing the hypothesis that EXE-autophagy upregulation and NADPH oxidase 2 (NOX2) downregulation would be linked to cardioprotection against DOX-induced cardiotoxicity. METHODS: C57BL/6 male mice were assigned into three groups: control (CON, n = 10), doxorubicin (DOX, n = 10), and doxorubicin + endurance exercise (DOX + EXE, n = 10). Animals assigned to DOX and DOX + EXE groups were intraperitoneally injected with DOX (5 mg·kg each week for 4 wk). Forty-eight hours after the last DOX treatment, the mice assigned to DOX + EXE performed EXE on a motorized treadmill at a speed of 13-15 m·min for 60 min·d for 4 wk. RESULTS: EXE prevented DOX-induced apoptosis and mitigated tissue damages. Although DOX did not modulate auto/mitophagy, EXE significantly enhanced its flux (increased LC3-II levels, reduced p62 levels, and increased autophagosomes with mitochondria) along with increased mitochondrial fission (DRP1) and reduced fusion markers (OPA1 and MFN2). Interestingly, EXE-induced autophagy against DOX occurred in the absence of alterations of autophagy inducer AMPK or autophagy inhibitor mTOR signaling. EXE prohibited DOX-induced oxidative damages by suppressing NOX2 levels but without modulating other key antioxidant enzymes including MnSOD, CuZnSOD, catalase, and GPX1/2. CONCLUSION: Our data provide novel findings that EXE-induced auto/mitophagy promotion and NOX2 downregulation are linked to cardioprotection against DOX-induced cardiotoxicity. Importantly, our study shows that EXE postconditioning intervention is effective and efficacious to prevent DOX-induced cardiac injuries.

Endurance Exercise Prevents Metabolic Distress-induced Senescence in the Hippocampus.

PURPOSE: Metabolic disorder such as obesity and type 2 diabetes caused by excess caloric intake is associated with an increased risk of neurodegenerative diseases. Endurance exercise (EXE) has been suggested to exert neuroprotective effects against the metabolic distress. However, the exact underlying molecular mechanisms responsible for the exercise-induced neuroprotection have not been fully elucidated. In this study, we investigated whether EXE-induced neuroprotection is associated with cellular senescence, neuroinflammation, and oxidative stress using a mouse model of obesity induced by a high-fat/high-fructose diet. METHODS: C57BL/6 female mice (10 wk old) were randomly divided to three groups: normal chow diet group (CON, n = 11), high-fat diet/high-fructose (HFD/HF) group (n = 11), and high-fat diet/high-fructose + endurance exercise (HFD/HF + EXE) group (n = 11). HFD/HF + EXE mice performed treadmill running exercise for 60 min·d, 5 d·wk for 12 wk. RESULTS: Our data showed that EXE ameliorated HFD/HF-induced weight gain, fasting blood glucose levels, and visceral fat gain. More importantly, HFD/HF diet promoted cellular senescence, whereas EXE reversed it, evidenced by a reduction in the levels of p53, p21, p16, beta-galactosidase (SA-ß-gal), and lipofuscin. Furthermore, EXE prevented HFD/HF-induced neuroinflammation (e.g., tumor necrosis factor-α and interleukin-1ß) by inhibiting toll-like receptor 2 downstream signaling cascades (e.g., tumor necrosis factor receptor-associated factor 6, c-Jun N-terminal kinase, and c-Jun) in parallel with reduced reactive glial cells. This anti-inflammatory effect of EXE was associated with the reversion of HFD/HF-induced cellular oxidative stress. CONCLUSION: Our study provides novel evidence that EXE-induced antisenescence against metabolic distress in the hippocampus may be a key neuroprotective mechanism, preventing neuroinflammation and oxidative stress.

Modulation of mitochondrial phenotypes by endurance exercise contributes to neuroprotection against a MPTP-induced animal model of PD.

AIM: Endurance exercise (EE) has been reported to confer neuroprotection against Parkinson's disease (PD); however, underlying molecular mechanisms of the protection remain still unclear. Since mitochondrial impairment is commonly observed in the brain of PD patients and animals, this study investigated whether EE-induced neuroprotection is associated with mitochondrial phenotypes, using a mouse model of PD induced by intraperitoneal administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MAIN METHODS: SH-SY5Y cells were cultured with a neurotoxin MPP+ known to cause PD-like symptoms to examine if modifications of mitochondrial morphology are linked to etiology of PD. For in vivo experiments, C57BL/6 male mice were randomly assigned to four groups: control (CON, n = 12), endurance exercise (EXE, n = 12), MPTP (MPTP, n = 12) and MPTP plus endurance exercise (MPTP + EXE, n = 12). Mice assigned to endurance exercise performed treadmill running at 12 m/min for 60 min/day, 5 days/week for 6 weeks. KEY FINDINGS: SH-SY5Y cells exposed to a neurotoxin MPP+ exhibited mitochondrial fragmentation and diminished mitochondrial proteins, and cell death. Similarly, animals administered with MPTP displayed comparable impairments in the substantia nigra pars compacta (SNpc). In contrast, EE intervention restored motor function to control levels and reduced apoptosis. These propitious effects of EE were associated with mitochondrial phenotypic changes such as upregulated anti-apoptotic proteins (e.g., MCL-1 and BLC-2), reduced a pro-apoptotic protein (e.g., AIF), and improved mitochondrial biogenesis and fusion. SIGNIFICANCE: Our finding that EE-induced mitochondrial phenotypic changes that resist mitochondrial impairment and cell death against PD introduce potential insight into mitochondria as a new therapeutic target for PD.

Endurance Exercise Mediates Neuroprotection Against MPTP-mediated Parkinson's Disease via Enhanced Neurogenesis, Antioxidant Capacity, and Autophagy.

Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction. Growing evidence has demonstrated that endurance exercise (EE) confers neuroprotection against PD. However, the exact molecular mechanisms responsible for exercise-induced protection of dopaminergic neurons in PD remain unclear. Since oxidative stress plays a key role in the degenerative process of PD. We investigated whether EE-induced neuroprotection is associated with enhanced antioxidative capacity and autophagy, using a mouse model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration. C57BL/6 male mice were randomly assigned to four groups: control (CON, n = 12), exercise (EXE, n = 12), MPTP (MPTP, n = 12) and MPTP + exercise (MPTP + EXE, n = 12). Our data demonstrated that while MPTP treatment impaired motor function, EE restored MPTP-induced motor deficits. Our biochemical data showed that EE-induced neuroprotection occurs in combination with multiple synergic neuroprotective pathways: (1) increased neurogenesis shown by an increase in BrdU-positive neurons; (2) diminished loss of dopaminergic neurons evidenced by upregulated tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels; (3) increased antioxidant capacity (e.g., CuZnSOD, CATALASE, GPX1/2, HO-1, DJ1 and PRXIII); and (4) enhanced autophagy (LC3 II, p62, BECLIN1, BNIP3, LAMP2, CATHEPSIN L and TFEB). Our study suggests that EE-induced multiple synergic protective pathways including enhanced neurogenesis, antioxidative capacity, and concordant autophagy promotion contribute to restoration of impaired dopaminergic neuronal function caused by PD. Thus, PD patients should be encouraged to actively participate in regular EE as a potent nonpharmacological therapeutic strategy against PD.

Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats.

Elevation of anabolism and concurrent suppression of catabolism are critical metabolic adaptations for muscular hypertrophy in response to resistance exercise (RE). Here, we investigated if RE-induced muscular hypertrophy is acquired by modulating a critical catabolic process autophagy. Male Wistar Hannover rats (14 weeks old) were randomly assigned to either sedentary control (SC, n = 10) or resistance exercise (RE, n = 10). RE elicited significant hypertrophy of flexor digitorum profundus (FDP) muscles in parallel with enhancement in anabolic signaling pathways (phosphorylation of AKT, mTOR, and p70S6K). Importantly, RE-treated FDP muscle exhibited a significant decline in autophagy evidenced by diminished phosphorylation levels of AMPK, a decrease in LC3-II/LC3-I ratio, an increase in p62 level, and a decline in active form of lysosomal protease CATHEPSIN L in the absence of alterations of key autophagy proteins: ULK1 phosphorylation, BECLIN1, and BNIP3. Our study suggests that RE-induced hypertrophy is achieved by potentiating anabolism and restricting autophagy-induced catabolism.

Correction to: Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection.

The article Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection, written by Youngil Lee.

Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection.

Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury. However, although the body of evidence supporting EICA and EICM is growing, the molecular mechanisms of EICA and EICM and their possible roles in cardioprotection against an I/R injury are poorly understood. Here, we introduce the general mechanisms of autophagy in an attempt to integrate potential molecular pathways of EICA and EICM and also highlight a potential insight into EICA and EICM in cardioprotection against an I/R insult.

Treadmill exercise produces neuroprotective effects in a murine model of Parkinson's disease by regulating the TLR2/MyD88/NF-κB signaling pathway.

Parkinson's disease (PD) is characterized by progressive dopamine depletion and a loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Treadmill exercise is a promising non-pharmacological approach for reducing the risk of PD and other neuroinflammatory disorders, such as Alzheimer's disease. The goal of this study was to investigate the effects of treadmill exercise on α-synuclein-induced neuroinflammation and neuronal cell death in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. Eight weeks of treadmill exercise improved motor deficits and reduced α-synuclein expression, a major causative factor of PD-like symptoms, in MPTP mice. Treadmill exercise also down-regulated the expression of toll-like receptor 2 and its associated downstream signaling molecules, including myeloid differentiation factor-88, tumor necrosis factor receptor-associated factor 6, and transforming growth factor-ß-activated protein kinase 1. These effects were associated with reduced ionized calcium-binding adapter molecule 1 expression, decreased IκBα and nuclear transcription factor-κB phosphorylation, decreased tumor necrosis factor α and interleukin-1ß expression, and decreased NADPH oxidase subunit expression in the SNpc and striatum. Additionally, it promoted the expression of tyrosine hydroxylase and the dopamine transporter, as well as plasma dopamine levels, in MPTP mice; these effects were associated with decreased caspase-3 expression and cleavage, as well as increased Bcl-2 expression in the SNpc. Taken together, our data suggest that treadmill exercise improves MPTP-associated motor deficits by exerting neuroprotective effects in the SNpc and striatum, supporting the notion that treadmill exercise is useful as a non-pharmacological tool for the management of PD.

Neuroprotective effects of endurance exercise against neuroinflammation in MPTP-induced Parkinson's disease mice.

Parkinson's disease (PD) is one of the main degenerative neurological disorders accompanying death of dopaminergic neurons prevalent in aged population. Endurance exercise (EE) has been suggested to confer neurogenesis and mitigate the degree of seriousness of PD. However, underlying molecular mechanisms responsible for exercise-mediated neuroprotection against PD remain largely unknown. Given the relevant interplay between elevated α-synuclein and neuroinflammation in a poor prognosis and vicious progression of PD and anti-inflammatory effects of EE, we hypothesized that EE would reverse motor dysfunction and cell death caused by PD. To this end, we chose a pharmacological model of PD (e.g., chronic injection of neurotoxin MPTP). Young adult male mice (7 weeks old) were randomly divided into three groups: sedentary control (C, n=10), MPTP (M, n=10), and MPTP + endurance exercise (ME, n=10). Our data showed that EE restored motor function impaired by MPTP in parallel with reduced cell death. Strikingly, EE exhibited a significant reduction in α-synuclein protein along with diminished pro-inflammatory cytokines (i.e., TNF-α and IL-1ß). Supporting this, EE prevented activation of Toll like receptor 2 (TLR2) downstream signaling cascades such as MyD88, TRAF6 and TAK-1 incurred by in MPTP administration in the striatum. Moreover, EE reestablished tyrosine hydroxylase at levels similar to C group. Taken together, our data suggest that an EE-mediated neuroprotective mechanism against PD underlies anti-neuroinflammation conferred by reduced levels of α-synuclein. Our data provides an important insight into developing a non-pharmacological countermeasure against neuronal degeneration caused by PD.

Substance flow analysis and environmental releases of PBDEs in life cycle of automobiles.

Polybrominated diphenyl ethers (PBDEs), a class of brominated flame retardants, have been widely used in many applications in industry such as automobiles, textiles, and electronics. This study focused on a quantitative substance flow analysis (SFA) of PBDEs in automobiles in order to identify their flow by life cycle and treatment pathways of PBDEs-containing materials in end-of-life vehicles (ELVs) in Korea. In addition, this study has estimated environmental releases of PBDEs in automobiles by life cycle in Korea. During this study, PBDEs were analyzed for the samples collected from several ELVs treatment facilities using X-ray fluorescence and gas chromatography/mass spectrometry (GC/MS) methods. The system boundary for SFA of PBDEs ranged from manufacturing/trade to disposal stage of automobiles by life cycle. Based on the result of the SFA, it was found that the amount of PBDEs in automobiles were the highest in use stage (7748ton/year), followed by production stage (1743ton/year) in 2014. In disposal stage, automobile shredded residues (ASR) and seat fabrics were the main components with relatively high levels of PBDEs in ELVs. The major treatment methods of such components included incineration (84%), energy recovery (9%), and landfilling (6%). This research indicates that PBDEs were emitted the highest amount from interior components during the use stage of automobiles, followed by recycling processes such as dismantling and shredding. This study suggests that PBDEs in ASR and seat fabrics should be properly managed to prevent the widespread dispersion in the environment.

Static and dynamic flow analysis of PBDEs in plastics from used and end-of-life TVs and computer monitors by life cycle in Korea.

This study focused on a quantitative substance flow analysis (SFA) of polybrominated diphenyl ethers (PBDEs) in plastics from obsolete TVs and computer monitors that often contain large amounts of the flame retardants. According to the results of the static SFA study, 1.87 tons and 0.28 tons of PBDEs from newly manufactured TVs and computer monitors were introduced into households in 2011 in Korea, respectively. There were approximately 924 tons and 90.3 tons of PBDEs present in TVs and computer monitors in households during product use, respectively. The results of the dynamic SFA study indicated that in 2017 the amount of PBDEs from TVs and computer monitors in the recycling stage is expected to be 2.63 tons and 0.1 tons, respectively. Large fractions of PBDEs from used TVs are present in recycled plastics, while PBDE-containing computer monitors are exported to Southeast Asian countries. This research indicates that PBDEs were emitted the most from recycled plastic pellet processes upon recycling. Further study may be warranted to focus the flow of PBDEs in recycled plastic products in order to determine the final destination and disposal of these chemicals in the environment.

Application of Delphi-AHP methods to select the priorities of WEEE for recycling in a waste management decision-making tool.

The management of waste electrical and electronic equipment (WEEE) or electronic waste (e-waste) has become a major issue of concern for solid waste communities due to the large volumes of waste being generated from the consumption of modern electrical and electronic products. In 2003, Korea introduced the extended producer responsibility (EPR) system to reduce the amount of electronic products to be disposed and to promote resource recovery from WEEE. The EPR currently regulates a total of 10 electrical and electronic products. This paper presents the results of the application of the Delphi method and analytical hierarchy process (AHP) modeling to the WEEE management tool in the policy-making process. Specifically, this paper focuses on the application of the Delphi-AHP technique to determine the WEEE priority to be included in the EPR system. Appropriate evaluation criteria were derived using the Delphi method to assess the potential selection and priority among electrical and electronic products that will be regulated by the EPR system. Quantitative weightings from the AHP model were calculated to identify the priorities of electrical and electronic products to be potentially regulated. After applying all the criteria using the AHP model, the results indicate that the top 10 target recycling products for the expansion of the WEEE list were found to be vacuum cleaners, electric fans, rice cookers, large freezers, microwave ovens, water purifiers, air purifiers, humidifiers, dryers, and telephones in order from the first to last. The proposed Delphi-AHP method can offer a more efficient means of selecting WEEE than subjective assessment methods that are often based on professional judgment or limited available data. By providing WEEE items to be regulated, the proposed Delphi-AHP method can eliminate uncertainty and subjective assessment and enable WEEE management policy-makers to identify the priority of potential WEEE. More generally, the work performed in this study is an example of how Delphi-AHP modeling can be used as a decision-making process tool in WEEE management.

The behavior and long-term fate of metals in simulated landfill bioreactors under aerobic and anaerobic conditions.

The long-term behavior and fate of metals in leachate from four simulated bioreactor landfills were explored using lysimeters under both aerobic and anaerobic conditions for a maximum of 1650 days. Metal concentrations varied with time and stage of landfill activity. The behavior of selected metals (Al, As, Cr, Cu, Fe, Pb, and Zn) significantly differed between aerobic and anaerobic conditions. Leachate from the aerobic lysimeters contained greater concentrations of Al, Cu, and Pb compared to leachate derived from the anaerobic lysimeters (average concentrations of Al, Cu and Pb in the aerobic/anaerobic lysimeters were 8.47/0.78 mg/L, 1.61/0.04 mg/L and 0.10/0.03 mg/L, respectively). In the anaerobic lysimeters, As, Fe and Zn leached at greater concentrations (average concentrations of As, Fe and Zn in the aerobic/anaerobic lysimeters were 0.40/1.14 mg/L, 13.5/136 mg/L and 15.3/168 mg/L, respectively). Though no significant difference in overall Cr concentrations was observed in leachate samples from aerobic and anaerobic lysimeters, during the alkali and methane phases approximately 45% of Cr was presented as Cr(VI) under aerobic conditions, whereas no Cr(VI) was detected under anaerobic conditions.