Enhanced removal of 1,2-dichloroethane by nanoscale calcium peroxide activation with Fe(III) coupled with different iron sulfides.

Fe(II) is of great importance in iron-based advanced oxidation processes. However, traditional methods to maintain Fe(II) concentration, such as the addition of chelating agents or reducing agents, may lead to an increase in chemical oxygen demand of secondary pollution. Therefore, in this study, iron sulfides, namely ferrous sulfide (FeS), pyrite (FeS2), and sulfidated nanoscale zero-valent iron (S-nZVI), were applied for not only the regeneration of Fe(II) but also the direct dissolution of Fe(II). Nanoscale calcium peroxide (nCaO2) was synthesized and used as the oxidant. The removal of 1,2-dichloroethane (1,2-DCA) were significantly promoted from 8.8 to 98.2, 79.2, and 80.8% with the aid of FeS, FeS2, and S-nZVI within 180 min, respectively. The dominant reactive oxygen species were demonstrated and their steady-state concentrations were quantified. Besides, the dechlorination of 1,2-DCA reached 90.4, 69.5, and 83.9% in nCaO2/Fe(III) systems coupled with FeS, FeS2, and S-nZVI, respectively. All three systems had high tolerance to the complex water conditions, of which FeS-enhanced nCaO2/Fe(III) system displayed the best performance, which could be recommended to put into practice for the remediation of 1,2-DCA contaminated groundwater.

1,2-Dichloroethane causes anxiety and cognitive dysfunction in mice by disturbing GABA metabolism and inhibiting the cAMP-PKA-CREB signaling pathway.

1,2-Dichloroethane (1,2-DCE) is a powerfully toxic neurotoxin, which is a common environmental pollutant. Studies have indicated that 1,2-DCE long-term exposure can result in adverse effects. Nevertheless, the precise mechanism remains unknown. In this study, behavioral results revealed that 1,2-DCE long-term exposure could cause anxiety and learning and memory ability impairment in mice. The contents of γ-aminobutyric acid (GABA) and glutamine (Gln) in mice's prefrontal cortex decreased, whereas that of glutamate (Glu) increased. With the increase in dose, the activities of glutamate decarboxylase (GAD) decreased and those of GABA transaminase (GABA-T) increased. The protein and mRNA expressions of GABA transporter-3 (GAT-3), vesicular GABA transporter (VGAT), GABA A receptor α2 (GABAARα2), GABAARγ2, K-Cl cotransporter isoform 2 (KCC2), GABA B receptor 1 (GABABR1), GABABR2, protein kinase A (PKA), cAMP-response element binding protein (CREB), p-CREB, brain-derived neurotrophic factor (BDNF), c-fos, c-Jun and the protein of glutamate dehydrogenase (GDH) and PKA-C were decreased, while the expression levels of GABA transporter-1 (GAT-1) and Na-K-2Cl cotransporter isoform 1 (NKCC1) were increased. However, there was no significant change in the protein content of succinic semialdehyde dehydrogenase (SSADH). The expressions of adenylate cyclase (AC) and cyclic adenosine monophosphate (cAMP) contents were also reduced. In conclusion, the results of this study show that exposure to 1,2-DCE could lead to anxiety and cognitive impairment in mice, which may be related to the disturbance of GABA metabolism and its receptors along with the cAMP-PKA-CREB pathway.

Biochar-enhanced anaerobic mixed culture for biodegradation of 1,2-dichloroethane: Microbial community, mechanisms, and techno-economics.

While anaerobic digestion (AD) has been employed for the degradation of chlorinated aliphatic hydrocarbons, the associated digester performance might suffer from volatile fatty acids accumulation, insufficient substrate-microbes interaction, and lower biogas yields. To overcome these limitations, this study is the first to augment the hydrocarbon-degrading microbial capacities by adding agricultural waste-based biochar to the digestion medium. 1,2-dichloroethane (1,2-DCA) was selected as the target pollutant because it is discharged in large quantities from oil refining, petrochemical, and chemical industries, causing serious environmental and human health concerns. A multi-chamber anaerobic reactor (MAR) was operated at a 1,2-DCA loading rate of 1.13 g/L/d, glucose dosage (as an electron donor) range of 200-700 mg/L, and hydraulic retention time of 11.2 h, giving dechlorination = 32.2 ± 6.9% and biogas yield = 210 ± 30 mL/g CODremoved. These values increased after biochar supplementation (100 mg/g volatile solids, VS, as an inoculum carrier) up to 60.2 ± 11.5% and 290 ± 40 mL/g CODremoved, respectively, owing to the enhancement of dehydrogenase enzyme activities. Burkholderiales (15.3%), Clostridiales (2.3%), Bacteroidales (3.5%), Xanthomonadales (3.3%), and Rhodobacterales (6.1%) involved in 1,2-DCA degradation were dominant in the reactor supplemented with biochar. It's suggested that biochar played a major role in facilitating the direct interspecies electron transfer (DIET) between syntrophic bacteria and methanogens, where chloride, ethylene glycol, and acetate derived from 1,2-DCA dechlorination could be further used to promote methanogenesis and methane production. The synergetic effect of adsorption and dechlorination towards 1,2-DCA removal was validated at various biochar dosages (50-120 mg/g) and 1,2-DCA concentrations (50-1000 mg/L). The techno-economic results showed that the cost of treating 1,2-DCA-laden discharge (100 m3/d) by the MAR module could be 0.83 USD/m3 with a payback period of 6.24 years (NPV = 2840 USD and IRR = 10%), retrieving profits from pollution reduction (9542 USD/yr), biogas selling (10418 USD/yr), and carbon credit (10294 USD/yr).

Creating an efficient 1,2-dichloroethane-mineralizing bacterium by a combination of pathway engineering and promoter engineering.

Currently, 1,2-dichloroethane (DCA) is frequently detected in groundwater and has been listed as a potential human carcinogen by the U.S. EPA. Owing to its toxicity and recalcitrant nature, inefficient DCA mineralization has become a bottleneck of DCA bioremediation. In this study, the first engineered DCA-mineralizing strain KTU-P8DCA was constructed by functional assembly of DCA degradation pathway and enhancing pathway expression with a strong promoter P8 in the biosafety strain Pseudomonas putida KT2440. Strain KTU-P8DCA can metabolize DCA to produce CO2 and utilize DCA as the sole carbon source for cell growth by quantifying 13C stable isotope ratios in collected CO2 and in lyophilized cells. Strain KTU-P8DCA exhibited superior tolerance to high concentrations of DCA. Excellent genetic stability was also observed in continuous passage culture. Therefore, strain KTU-P8DCA has enormous potential for use in bioremediation of sites heavily contaminated with DCA. In the future, our strategy for pathway construction and optimization is expected to be developed as a standard pipeline for creating a wide variety of new contaminants-mineralizing microorganisms. The present study also highlights the power of synthetic biology in creating novel degraders for environmental remediation.

Adsorption-enforced Fenton-like process using activated carbon-supported iron oxychloride catalyst for wet scrubbing of airborne dichloroethane.

Wet scrubbing is a low-cost process for disposing of air pollutants. Nevertheless, this method is rarely used for the treatment of volatile organic compounds (VOCs) because of their poor water solubility. In this study, we used a unique wet scrubbing system containing H2O2 and activated carbon (AC)-supported iron oxychloride (FeOCl) nanoparticles to remove airborne dichloroethane (DCE). The operating conditions of the wet scrubber were optimized, and the mechanism was explored. The results showed that the adsorption of dissolved DCE onto AC promoted its transfer from air to water, while the accumulation of DCE on AC facilitated its oxidation by •OH generated on FeOCl catalyst. The wet scrubber performed well at pH 3 and low H2O2 concentrations. By pulsed or continuous dosing H2O2, the cooperative adsorption-catalytic oxidation allowed long-term DCE removal from air. Benefiting from satisfactory cost-effectiveness, avoidance of toxic byproduct formation, and less corrosion and catalyst poisoning, wet scrubbers coupled with cooperative adsorption and heterogeneous advanced oxidation processes could have broad application potentials in VOC control.

Using sequential H2O2 addition to sustain 1,2-dichloroethane detoxification by a nanoscale zerovalent iron-induced Fenton's system at a natural pH.

1,2-dichloroethane (1,2-DCA) is a chlorinated hydrocarbon used for polyvinyl chloride plastic production. As such, 1,2-DCA is a common persistent contaminant in saturated zones. While nanoscale zerovalent iron (NZVI) is considered an effective reductant for removing a wide range of chlorinated hydrocarbons, 1,2-DCA is resistant to reduction by NZVI as well as by modified forms of NZVI (e.g., sulfidated-NZVI). Hydroxyl radicals produced in Fenton's reaction can effectively degrade 1,2-DCA, but Fenton's reaction requires the acidification of saturated zones to achieve a groundwater pH of 3 to facilitate the catalytic reaction. To overcome this problem, this study has developed a sequential treatment process using an NZVI-induced Fenton-like reaction that can effectively degrade 1,2-DCA at an initially neutral pH range. The experiments were conducted using a high 1,2-DCA concentration (2000 mg/L) to evaluate the feasibility of using the treatment process at source zones. The process degraded 99% of 1,2-DCA with a pseudo-first-order rate constant of 0.49 h-1. Unlike the single-stage treatment process, the sequential treatment can control the used H2O2 concentration in the system, thus sustaining the reaction and resulting in more efficient 1,2-DCA degradation. To mimic subsurface conditions, batch experiments were conducted to remove 1,2-DCA sorbed in contaminated soil. The results show that 99% removal of 1,2-DCA was obtained within 16 h. Additionally, this study suggests that the NZVI can be used for at least three consecutive 1,2-DCA degradation cycles while maintaining high removal efficiency.

[Analysis on incidence of occupational diseases in Guangzhou from 2010 to 2020].

Objective: To analyze the incidence characteristics of occupational diseases in Guangzhou from 2010 to 2020, provide scientific basis for formulating occupational disease prevention and control policies. Methods: In January 2021, based on the data of occupational diseases in Guangzhou reported in the Information Monitoring System of Occupational Diseases and Occupational Health, descriptive epidemiological method was used to analyze the types and characteristics of occupational diseases in Guangzhou from 2010 to 2020. Results: A total of 1341 cases of 38 kinds of occupational diseases in 9 categories were reported in the past 11 years. The incidence of occupational pneumoconiosis, occupational otolaryngology and oral diseases and occupational chemical poisoning ranked the top three, accounting for 38.1% (511/1341) , 30.5% (409/1341) and 16.2% (217/1341) of the total cases respectively. The cases of pneumoconiosis in welders and silicosis accounted for 47.7% (244/511) and 34.4% (176/511) of the cases of occupational pneumoconiosis respectively. The cases of noise deafness accounted for 99.8% (408/409) of occupational otorhinolaryngology oral diseases. Acute occupational chemical poisoning cases accounted for 26.7% (58/217) of the occupational chemical poisoning cases, in which dichloroethane poisoning cases ranked the first, accounting for 79.3% (46/58) . Chronic occupational chemical poisoning cases accounted for 73.3% (159/217) of the occupational poisoning cases, in which benzene and lead poisoning cases ranked the top two, accounting for 79.2% (126/159) and 17.6% (28/159) respectively. Conclusion: Pneumoconiosis, silicosis, noise deafness, benzene poisoning, lead poisoning, dichloroethane poisoning should be supervised and managed as key occupational diseases in Guangzhou.

Removal of 1,2-dichloroethane in groundwater using Fenton oxidation.

Among the chlorinated aliphatic hydrocarbons, 1,2-dichloroethane (1,2-DCA) is widely used for the synthesis of vinyl chloride monomers. Despite the high demand for 1,2-DCA, it poses a risk to the environment because it is persistent and carcinogenic. Therefore, in this study, several reagents (dithionite, hydrosulfide, sulfite, persulfate, sulfate radicals, and hydroxyl radicals) were evaluated for the degradation of 1,2-DCA. Among these, the hydroxyl radicals generated by the Fenton reaction were the most suitable oxidant, decomposing 92% of 1,2-DCA. Chloride, one of the final oxidized products, was observed, which supported the oxidation reaction. Moreover, with an increasing concentration of hydroxyl radicals, the degradation of 1,2-DCA increased. Furthermore, sufficient amounts of hydrogen peroxide were more important than Fe(II) in the decomposition of 1,2-DCA. The radical reaction can generate larger molecules via the degradation of 1,2-DCA, which are degraded over time. The applicability of Fenton oxidation was evaluated using real 1,2-DCA-contaminated groundwater. Although the degradation of target contaminant was lowered due to the alkaline pH and the presence of chloride and bicarbonate ions in groundwater, the Fenton reaction was still efficient to oxidize 1,2-DCA. These results indicate that Fenton oxidation is an effective technique for the treatment of 1,2-DCA in contaminated groundwater.

Roles of Crosstalk between Astrocytes and Microglia in Triggering Neuroinflammation and Brain Edema Formation in 1,2-Dichloroethane-Intoxicated Mice.

We have previously reported that the activation of astrocytes and microglia may lead to the overproduction of proinflammatory mediators, which could induce neuroinflammation and cause brain edema in 1,2-dichloroethane (1,2-DCE)-intoxicated mice. In this research, we further hypothesized that astrocyte-microglia crosstalk might trigger neuroinflammation and contribute to brain edema in 1,2-DCE-intoxicated mice. The present research revealed, for the first time, that subacute intoxication with 1,2-DCE might provoke the proinflammatory polarization of microglia, and pretreatment with minocycline, a specific inhibitor of microglial activation, may attenuate the enhanced protein levels of ionized calcium-binding adapter molecule1 (Iba-1), cluster of differentiation 11b (CD11b), glial fibrillary acidic protein (GFAP), soluble calcium-binding protein 100B (S100B), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), Toll-like receptor 4 (TLR4), MyD88, and p-p65, and ameliorate the suppressed protein expression levels of occludin and claudin 5; we also observed changes in water content and made pathological observations on edema in the brains of 1,2-DCE-intoxicated mice. Moreover, pretreatment with fluorocitrate, an inhibitor of reactive astrocytes, could also reverse the alteration in protein expression levels of GFAP, S100B, Iba-1, CD11b, TNF-α, IL-6, iNOS, VCAM-1, ICAM-1, MMP-9, occludin, and claudin 5 in the brain of 1,2-DCE intoxicated mice. Furthermore, pretreatment with melatonin, a well-known anti-inflammatory drug, could also attenuate the above-mentioned changes in the brains of 1,2-DCE-intoxicated mice. Altogether, the findings from this research indicated that microglial activation might play an important role in triggering neuroinflammation, and hence may contribute to brain edema formation; additionally, the findings suggested that molecular crosstalk between reactive astrocytes and activated microglia may amplify the neuroinflammatory reaction, which could induce secondary brain injury in 1,2-DCE-intoxicated mice.

Investigation of potential early key events and mode of action for 1,2-dichloroethane-induced mammary tumors in female rats.

1,2-dichloroethane (DCE or EDC) is a chlorinated hydrocarbon used as a chemical intermediate, including in the synthesis of polyvinyl chloride. Although DCE has induced tumors in both rats and mice, the overall weight-of-evidence suggests a lack of in vivo mutagenicity. The present study was conducted to explore a potential mode of action further for tumor formation in rat mammary tissue. Fischer 344 rats were exposed to target concentrations of 0 or 200 ppm of DCE vapors (6 hours/day, 7 days/week) for at least 28 days; 200 ppm represents a concentration of ~20% higher than that reported to induce mammary tumors. Endpoints examined included DNA damage (via Comet assay), glutathione (reduced, oxidized and conjugated), tissue DNA adducts, cell proliferation and serum prolactin levels. Exposure to DCE did not alter serum prolactin levels with consistent estrous stage, did not cause cell proliferation in mammary epithelial cells, nor result in histopathological alterations in the mammary gland. DNA adducts were identified, including the N7 -guanylethyl glutathione adduct, with higher adduct levels measured in liver (nontumorigenic target) compared with mammary tissue isolated from the same rats; no known mutagenic adducts were identified. DCE did not increase the Comet assay response in mammary epithelial cells, whereas DNA damage in the positive control (N-nitroso-N-methylurea) was significantly increased. Although the result of this study did not identify a specific mode of action for DCE-induced mammary tumors in rats, the lack of any exposure-related genotoxic responses further contributes to the weight-of-evidence suggesting that DCE is a nongenotoxic carcinogen.

Liver fibrosis associated with potential vinyl chloride and ethylene dichloride exposure from the petrochemical industry.

BACKGROUND: The understanding of the relationship between exposure to carcinogenic vinyl chloride (VCM) and ethylene dichloride (EDC) and liver fibrosis is limited. OBJECTIVE: This study aimed to investigate the associations between the urinary metabolite levels of VCM and EDC and the risk of liver fibrosis in residents living near a petrochemical complex. METHODS: Our study comprised 447 adult residents of two townships with questionnaire survey and health examination near the largest petrochemical complex in central Taiwan. The urinary levels of thiodiglycolic acid (TdGA), the metabolite of VCM and EDC, were detected in study subjects. We utilized fibrosis-4 (FIB-4) as the noninvasive liver fibrosis index. Adjusted linear model was applied to evaluate the associations between the distance from the complex and the urinary TdGA levels. Adjusted logistic regression model was applied to evaluate the associations between the urinary TdGA levels and the risk of liver fibrosis. RESULTS: The study subjects living in the closer township had significant higher urinary TdGA levels than those living in the more distant township (269.6 ± 200.7 vs. 199.2 ± 164.7 µg/g creatinine) (p < 0.001). It showed that urinary TdGA levels were decreased 0.53-fold when the distances from the complex were increased 1-fold after adjusting for confounding factors. It demonstrated that the study subjects with the highest TdGA levels (>343.3 µg/g creatinine) had a higher risk of FIB-4>1.29 (OR = 2.09; 95% CI: 1.17, 3.78), and those with higher TdGA levels (232.7 to 343.3 µg/g creatinine) had a marginally higher risk of FIB-4>1.29 (OR = 1.65; 95% CI: 0.94, 2.90). CONCLUSION: The residents living closer to the VCM/PVC plant in the petrochemical complex had higher urinary TdGA levels, which were associated with an increased risk of fibrosis. This confirmed that the EDC and VCM potentially emitted from the petrochemical industry may have an impact on the liver health of nearby residents.

Distribution characteristics and health risk assessment of volatile organic compounds in the groundwater of Lanzhou City, China.

Volatile organic compounds (VOCs) typically exist in the aqueous environment due to global anthropogenic activities. The distribution and contaminated profile (or characteristics) of VOCs in the groundwater of Lanzhou, China, were investigated in this study. Groundwater samples were collected from 30 sampling points in December 2015, and a total of 17 VOCs were analyzed by purge and trap gas chromatography-mass spectrometry. Thirteen types of VOCs were detected at 29 sampling points in the study area. Of these, dichloromethane and toluene, which were found at 22 sampling points, had the highest detection frequency (73.3%), followed by benzene (66.7%), 1,2-dichloroethane (50%), and xylenes (50%). The highest average concentration among the detected VOCs was found for chloroform (5151.5 µg/L). The spatial distribution of VOC contamination in four major urban areas of Lanzhou and the variation in VOC concentration caused by land use transitions were also analyzed. The results showed that Xigu district was the most polluted area in Lanzhou, mainly due to land use for industrial proposes. On the contrary, the samples for Anning district showed lower VOC concentrations because of better groundwater quality, which is associated with the absence of manufacturing industries in this region. The health risk assessment model developed by the United States Environmental Protection Agency was employed in this study to evaluate safety for drinking water use. This study found that despite considering the volatilization of VOCs from water due to heating, six sampling points (G05 in Qilihe district; G07 and G09 in Xigu district; G16, G17, and G15 in Chengguan district) showed non-carcinogenic risks, ranging from 1.63 to 14.2, while three points (G16 in Chengguan district, and G10 and G07 in Xigu district) exhibited high carcinogenic risks for human health, ranging from 2.94 × 10-4 to 6.85 × 10-4. Trichloroethylene, tetrachloroethylene, and 1,2-dichloroethylene were identified as the dominant VOCs, presenting high non-carcinogenic risk. 1,2-dichloroethane and vinyl chloride were the primary factors for high carcinogenic risk. The high-risk areas were concentrated in Xigu and Chengguan districts, suggesting the need to alert the relevant local government departments.

1,2-Dichloroethane induces cerebellum granular cell apoptosis via mitochondrial pathway in vitro and in vivo.

1,2-Dichloroethane (1,2-DCE) is a widely used chlorinated organic toxicant, but little is known about the cerebellar dysfunction induced by excessive exposure to it. To uncover 1,2-DCE-induced neurotoxicity in cerebellar granular cells (CGCs), and to investigate the underlying mechanisms, we explored this, both in vitro and in vivo. Our findings showed significant cell viability inhibition in human CGCs (HCGCs) treated with 1,2-DCE. Flow cytometry and mitochondrial membrane potential analyses discovered an increase in apoptotic-mediated cell death in HCGCs after 1,2-DCE treatment. This HCGC apoptosis was involved in the increases of protein expression in Cytochrome c, Caspase-3, Bad, Bim, transformation related protein 53, Caspase-8, tumor necrosis factor-α, and Survivin. Quantitative real-time PCR (qPCR) and western blot confirmed the increases in Cytochrome c, Caspase-3, cleaved Caspase-3, and Bad in HCGCs after 1,2-DCE treatment. Bax inhibitor peptide V5 rescued 1,2-DCE-induced HCGC apoptosis. Furthermore, 80 CD-1 male mice were exposed to 1,2-DCE by inhalation at 0, 100, 350, and 700 mg/m3 for 6 h/day for 4 weeks. An open field test found abnormal neurobehavioral changes in the mice exposed to 1,2-DCE. Histopathological examination showed significantly shrunken and hypereosinophilic cytoplasm with nuclear pyknosis in mouse CGCs from the 700 mg/m3 1,2-DCE group. TdT-mediated dUTP nick-end labeling assay verified significant increases in apoptotic positive cells in the mouse CGCs after 1,2-DCE exposure. We confirmed the increases in the expressions of Cytochrome c, Caspase-3, cleaved Caspase-3 and Bad in the mice exposed to 1,2-DCE. These findings suggest that 1,2-DCE exposure can induce CGC apoptosis and cerebellar dysfunction, at least in part, through mitochondrial pathway.

N-doped porous carbon supported Ni catalysts derived from modified Ni-MOF-74 for highly effective and selective catalytic hydrodechlorination of 1,2-dichloroethane to ethylene.

Metal-organic frameworks (MOFs) have received significant attention as promising precursors or sacrificial templates in the preparation of porous carbon supported catalysts. In this study, N-doped porous carbon supported Ni catalysts (denoted as Ni/NC) were prepared using furfuryl alcohol (FA) loaded Ni-MOF-74 as the precursor followed by NH4OH treatment and pyrolysis under N2 atmosphere. For comparison purpose, Ni catalysts supported on porous carbon (denoted as Ni/C) were also prepared by direct pyrolysis of Ni-MOF-74. The selective gas phase catalytic hydrodechlorination of 1,2-dichloroethane to ethylene was carried out to evaluate the catalytic performances of the catalysts. It was found that for Ni catalysts prepared at the same pyrolysis temperature, Ni particle sizes in Ni/NC catalysts were significantly smaller (20-40% smaller) than that of Ni/C. This reflected that pre-modification of Ni-MOF-74 using FA and NH4OH could effectively increase Ni dispersion in Ni catalysts derived from Ni-MOF-74. Moreover, Ni/NC had a markedly stronger ability to form spillover H2 owing to the enhanced metal-support interactions by N-doping. Accordingly, Ni/NC catalysts exhibited much higher catalytic activities than Ni/C catalysts. The turnover frequencies of Ni/NC catalysts were found to be 1.22-1.65 times higher than Ni/C catalysts. Increasing pyrolysis temperature led to decreased catalytic activities of both Ni/C and Ni/NC catalysts, due to the aggregation of Ni particles at higher treatment temperature. The findings from this study demonstrate that the MOF-mediated synthesis method offers a promising way to prepare Ni-based catalysts for catalytic hydrodechlorination of chlorinated hydrocarbons.

Exploring adsorption behavior of ethylene dichloride and dibromide vapors on blue phosphorene nanosheets: A first-principles acumens.

The interrelation of toxic vapors ethylene dichloride (EDC) and ethylene dibromide (EDB) with the sensory base material blue phosphorene nanosheet (BLPNS) is studied using ab-initio method. The formational stability of BLPNS is ensured by the negative value of formation energy. Prior to the adsorption studies, we calculated the formation energy of BLPNS to ensure its stability, which is calculated to be -5.194eV/atom and found stable. The main motive behind the present work is to detect these toxic vapors using BLPNS. The intercommunication between the targeted vapors and the base material has been analyzed using the aid of adsorption energy, Bader charge transfer, energy band gap, and variation of band gap along with energy bands and DOS spectrum. The energy gap of isolated BLPNS is observed to be 1.621eV. However, the adsorption of EDC and EDB modulates the energy gap of BLPNS. The nature of assimilation is noticed to be of physisorption, which facilitates desorption of EDC and EDB molecules much easier. The successful outcome of the present research validates that BLPNS can be deployed as a prominent sensor for detection of EDC and EDB effectively.

LncRNA-241 inhibits 1,2-Dichloroethane-induced hepatic apoptosis.

Chlorinated organic chemical 1,2-dichloroethane (1,2-DCE) is used widely in industrial production processes, and excessive exposure may lead to liver damage. The mechanisms underlying 1,2-DCE-induced hepatotoxicity are not fully understood. Numerous studies have demonstrated that long-non-coding RNAs (lncRNAs) play a pivotal role in the chemical-induced toxicity. To explore whether aberrant lncRNA expression is involved in hepatotoxicity mediated by 1,2-DCE exposure, we detected alterations of lncRNA expression profiling in a mouse model of 1,2-DCE-induced hepatotoxicity by microarray chip. Bioinformatic analysis indicated that a down-regulated lncRNA (lncRNA241) after 1,2-DCE exposure might be involved in 1,2-DCE-induced hepatotoxicity. We treated AML12 cells with 1,2-DCE and its metabolite 2-chloroacetic acid (2-CA) for 48 h, and the results revealed that it was 2-CA rather than primary form (1,2-DCE) that resulted in the decline of lncRNA241 expression in hepatocytes. In vitro intervention studies revealed that the repression of lncRNA241 expression after 2-CA exposure led to the down-regulation of anti-apoptosis-associated factor insulin growth factor-1 (Igf1) at mRNA and protein levels through modulation of their common target mmu-miR-451a, which promoted hepatic apoptosis. This study provides valuable insight into the role of lncRNAs in response to hepatocyte apoptosis induced by 1,2-DCE.

Degradation of 1,2-dichloroethane by photocatalysis using immobilized PAni-TiO2 nano-photocatalyst.

1,2-Dichloroethane is one of the most hazardous environmental pollutants in wastewaters. It is mainly used to produce vinyl chloride monomer, the major precursor for PVC production. It is determined to be a probable human carcinogen and has been listed as a priority pollutant by the United States Environmental Protection Agency. Due to high chemical stability and low biodegradability of 1,2-dichloroethane, heterogeneous photocatalysis was used for degradation of this chlorinated hydrocarbon. PAni-TiO2 nanocomposite was synthesized by in situ deposition oxidative polymerization method and immobilized on glass beads by a modified dip coating and heat attachment method. The characteristics of synthesized PAni-TiO2 nanoparticles were confirmed using the results of morphology tests including Fourier-transform infrared spectra, X-ray diffraction patterns, particle size analysis, UV-Visible spectrophotometer, scanning electron microscope, and energy-dispersive X-ray spectroscopy. The performance of photocatalytic degradation of 1,2-dichloroethane using synthesized PAni-TiO2 nanocomposite in a designed and constructed pilot scale packed bed recirculating photocatalytic reactor under xenon light irradiation was investigated. The response surface methodology based on the central composite design was used to evaluate and optimize the effect of 1,2-dichloroethane concentration, residence time, pH, and coating mass as independent variables on the photocatalytic degradation of 1,2-dichloroethane as the response function. Results showed that actual and predicted results were well fitted with R2 of 0.9870, adjusted R2 of 0.9718, and predicted R2 of 0.9422. The optimum conditions for 1,2-dichloroethane photocatalytic degradation were the 1,2-dichloroethane concentration of 250 mg/L, the residence time of 240 min, pH of 5, and coating mass of 0.5 mg/cm2, which resulted in 88.84% photocatalytic degradation. Kinetic of the photocatalytic degradation at optimal condition follows the Langmuir-Hinshelwood first-order reaction with k = 0.0095 min-1 with R2 = 0.9455. Complete photocatalytic degradation of 1,2-DCE was achieved after 360 min.

The clinical and pathological features of toxic encephalopathy caused by occupational 1,2-dichloroethane exposure.

To understand the clinical and pathological features of 1,2-dichloroethane (DCE) toxic encephalopathy.The cases of 4 patients who were admitted to Xiangya hospital between January 8, 2008 and November 8, 2012 with diagnoses of DCE toxic encephalopathy were examined. We recorded data on gender, age of onset, exposure time to DCE, symptom onset to admission interval, symptom onset to worst symptom experience interval, and clinical manifestations, as well as cranial magnetic resonance imaging (MRI) and brain biopsy pathology results.All 4 patients had a history of DCE exposure and presented with symptoms of intracranial hypertension. Cranial MRI revealed extensive brain edema throughout the subcortical white matter, the bilateral globus pallidus, and the cerebellar dentate nuclei. The brain biopsy confirmed severe cerebral edema, including peripherovascular edema, with swelling of various cell types, with extensive glial cell necrosis. After treatment with steroids and mannitol (3-10 weeks), all 4 patients recovered, partially or completely.Severe brain edema and extensive glial cell necrosis were the main pathological features observed in the present cases, with a likely etiology of DCE toxicity. Early, prompt, and long-term treatment with dehydrating agents and glucocorticoids was an effective treatment for this condition.

Toxic effects of combined treatment of 1,2-dichloroethane and ethanol on mouse brain and the related mechanisms.

The aim of this study was to explore the mechanisms of brain damage induced by the combined treatment of mice with 1,2-dichloroethane (1,2-DCE) and ethanol. Mice were divided into control group; 1,2-DCE-intoxicated group; ethanol-treated group; and low-, medium-, and high-dose combined treatment groups. Histological observations along with brain organ coefficients and water content were used to measure the brain damage directly and indirectly. The levels of nonprotein sulfhydryls, malondialdehyde (MDA), and superoxide dismutase activity were used as parameters to evaluate oxidative stress in the brain. Protein and messenger RNA (mRNA) levels of cytochrome P450 2E1 (CYP2E1), zonula occludens-1 (occludin and zo-1), aquaporin-4 (AQP4), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase (HO)-1, and the γ-glutamyl cysteine synthetase catalytic and modulatory subunits (γ-GCSc, GR, and γ-GCSm) in the brain were examined by Western blot analysis and quantitative polymerase chain reaction analysis, respectively. Effects of the combined treatment of 1,2-DCE and ethanol were evaluated by analysis of variance with a factorial design. The results suggested that combined exposure to ethanol and 1,2-DCE synergistically increased CYP2E1 protein and mRNA levels, accelerated the metabolism of ethanol and 1,2-DCE in the brain tissue, induced high production of reactive oxygen species (ROS), and increased MDA levels, thereby damaging the blood-brain barrier and causing obvious pathological changes in brain tissue. However, the increased level of ROS activated the Nrf2 signal transduction pathway, promoting the expression of HO-1 and glutathione-related antioxidant enzymes in the brain to protect the cells from oxidative damage.

1,2-Dichloroethane-induced hepatotoxicity and apoptosis by inhibition of ERK 1/2 pathways.

1,2-Dichloroethane (DCE) is a ubiquitous occupational environmental contaminant. Subacute exposure to DCE can cause severe toxic encephalopathy and has obvious toxic effects on the liver. However, the toxicity of DCE on the liver and its molecular mechanism remain elusive. In the present study, we established a DCE-exposed animal model by inhalation in SD rats and used HepG2 cells in in vitro tests. The DCE-exposed groups showed hepatic dysfunction relative to the control group. Moreover, apoptotic cells and decreased phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) were found in liver tissue of rats in 3 DCE-exposed groups. In vitro tests showed that short-term exposure to DCE induced apoptosis in HepG2 cells. Furthermore, the incubation of cells with DCE significantly decreased the phosphorylation of ERK1/2 in a concentration-dependent manner. Additionally, incubating HepG2 cells with epidermal growth factor, an ERK1/2 activator, significantly increased apoptosis in HepG2 cells. In conclusion, our results suggest that DCE induces apoptosis in HepG2 cells by inhibiting ERK1/2 pathways.