Characteristics and potential cytotoxicity of halogenated organic compounds in shale gas wastewater-impacted surface waters in Chongqing area， China.

Recent screening surveys have shown the presence of unknown source halogenated organic compounds (HOCs) in shale gas wastewater. However, their occurrence, profile, transport in surrounding surface water and environmental risk potentials remain unclear. Here, a method for the extraction and quantitative determination of 13 HOCs in water by solid phase extraction combined with gas chromatography-mass spectrometry (GC-MS) was established. All of the targeted HOCs were detected and peaked at the outfall, while these contaminants were generally not detected in samples upstream of the outfall, suggesting that these contaminants originated from the discharge of shale gas wastewater; this was further supported by the fact that these pollutants were generally detected in downstream samples, with a tendency for pollutant concentrations to decrease progressively with increasing distance from the outfall. However，different HOCs had different transport potential in water. In addition, the toxicological effects of typical HOCs were evaluated using HepG2 as a model cell. The results indicated that diiodoalkanes suppressed HepG2 cell proliferation and induced ROS generation in a concentration-dependent manner. Mechanistic studies showed that diiodoalkanes induced apoptosis in HepG2 cells via the ROS-mediated mitochondrial pathway, decreasing mitochondrial membrane potential and increasing intercellular ATP and Ca2+ levels. On the other hand, RT-qPCR and Western blot assays revealed that the SLC7A11/GPX4 signaling pathway and HO-1 regulation of ferritin autophagy-dependent degradation (HO-1/FTL) pathway were involved in the ferroptosis pathway induced by diiodoalkane in HepG2 cells. Our study not only elucidates the contamination profiles and transport of HOCs in surface water of typical shale gas extraction areas in China, but also reveals the toxicity mechanism of typical diiodoalkane.

Endoplasmic reticulum stress participates in apoptosis of HeLa cells exposed to TPHP and OH-TPHP via the eIF2α-ATF4/ATF3-CHOP-DR5/P53 signaling pathway.

Purpose: Triphenyl phosphate (TPHP) is a widely used organophosphate flame retardant, which can be transformed in vivo into diphenyl phosphate (DPHP) and 4-hydroxyphenyl phosphate (diphenyl) ester (OH-TPHP) through biotransformation process. Accumulation of TPHP and its derivatives in biological tissues makes it necessary to investigate their toxicity and molecular mechanism. Methods: The present study evaluated the cellular effects of TPHP, DPHP, and OH-TPHP on cell survival, cell membrane damage, oxidative damage, and cell apoptosis using HeLa cells as in vitro model. RNA sequencing and bioinformatics analysis were conducted to monitor the differently expressed genes, and then RT-qPCR and Western bolt were used to identify potential molecular mechanisms and key hub genes. Results: Results showed that OH-TPHP had the most significant cytotoxic effect in HeLa cells, followed by TPHP; and no significant cytotoxic effects were observed for DPHP exposure within the experimental concentrations. Biological function enrichment analysis suggested that TPHP and OH-TPHP exposure may induce endoplasmic reticulum stress (ERS) and cell apoptosis. The nodes filtering revealed that ERS and apoptosis related genes were involved in biological effects induced by TPHP and OH-TPHP, which may be mediated through the eukaryotic translation initiation factor 2α/activating transcription factor 4 (ATF4)/ATF3- CCAAT/ enhancer-binding protein homologous protein (CHOP) cascade pathway and death receptor 5 (DR5) /P53 signaling axis. Conclusion: Above all, these findings indicated that ERS-mediated apoptosis might be one of potential mechanisms for cytotoxicity of TPHP and OH-TPHP.

Metabolic disturbance and transcriptomic changes induced by methyl triclosan in human hepatocyte L02 cells.

PURPOSE: Methyl triclosan (MTCS) is one of the biomethylated by-products of triclosan (TCS). With the increasing use of TCS, the adverse effects of MTCS have attracted extensive attention in recent years. The purpose of this study was to investigate the cytotoxicity of MTCS and to explore the underlining mechanism using human hepatocyte L02 cells as in vitro model. RESULTS: The cytotoxicity results revealed that MTCS could inhibit cell viability, disturb the ratio of reduced glutathione (GSH) and oxidized glutathione (GSSG), and reduce the mitochondrial membrane potential (MMP) in a dose-dependent manner. In addition, MTCS exposure significantly promoted the cellular metabolic process, including enhanced conversion of glucose to lactic acid, and elevated content of intracellular triglyceride (TG) and total cholesterol (TC). RNA-sequencing and bioinformatics analysis indicated disorder of glucose and lipid metabolism was significantly induced after MTCS exposure. Protein-protein interaction network analysis and node identification suggested that Serine hydroxy methyltransferase 2 (SHMT2), Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2), Asparagine synthetase (ASNS) and Phosphoglycerate dehydrogenase (PHGDH) are potential molecular markers of metabolism imbalance induced by MTCS. CONCLUSION: These results demonstrated that oxidative stress and metabolism dysregulation might be involved in the cytotoxicity of MTCS in L02 cells.

Lipid metabolic disturbance induced by triphenyl phosphate and hydroxy metabolite in HepG2 cells.

Triphenyl phosphate (TPHP) has been widely used as flame retardants and been detected with increasing frequency in environment. TPHP can transform into mono-hydroxylated phosphate (OH-TPHP) and diester diphenyl phosphate (DPHP) through biotransformation. So far, information on the cytotoxicity and molecular regulatory mechanisms of TPHP metabolites are still limit. This study investigated the adverse effects of TPHP, OH-TPHP, and DPHP in HepG2 cells in terms of cell proliferation, lactate dehydrogenase release, reactive oxygen species generation, and mitochondrial membrane potential. The transcriptomic changes were measured using RNA sequencing, and bioinformatics characteristics including biological functions, signal pathways and protein-protein interaction were analyzed to explore the potential molecular mechanisms. Results displayed that the order of cytotoxicity was OH-TPHP> TPHP> DPHP. The prioritized biological functions changes induced by TPHP and OH-TPHP were correlated with lipid metabolism. Significant lipid accumulation was observed as confirmed by increased total cholesterol and triglycerides contents, and enhanced oil red O staining. Enrichment of PPARα/γ and down-stream genes suggested the participation of PPARs signal pathway in lipid metabolism disorder. In addition, TPHP and OH-TPHP induced endoplasmic reticulum stress (ERS), which was further confirmed by the ERS inhibitor experiment. In general, TPHP and OH-TPHP had obvious cytotoxic effects in HepG2 cells. PPARs signal pathway and endoplasmic reticulum stress may be involved in the lipid metabolism disorder induced by TPHP and OH-TPHP.

Atmospheric gaseous aromatic hydrocarbons in eastern China based on mobile measurements: Spatial distribution, secondary formation potential and source apportionment.

Monocyclic aromatic hydrocarbons (MAHs) and polycyclic aromatic hydrocarbons (PAHs) are both well known as hazardous air pollutants and also important anthropogenic precursors of tropospheric ozone (O3) and secondary organic aerosols (SOA). In recent years, there have been intensive studies covering MAHs emission from various sources and their behavior under stimulated photochemical conditions. Yet in-situ measurements of PAHs presence and variations in ambient air are sparse. Herein we conducted large geometrical scale mobile measurements for 16 aromatic hydrocarbons (AHs, including 7 MAHs and 9 PAHs) in eastern China between October 27 and November 8, 2019. This unique dataset has allowed for some insights in terms of AHs concentration variations, accompanying chemical composition, source contributions and spatial distributions in eastern China. In general, AHs showed a clear concentration variability between the south and the north of the Yangtze River Delta (YRD). The concentrations of PAHs were approximately 9% of AHs, but contributed 23% of SOA formation potential. Source apportionment via positive matrix factorization (PMF) model revealed that industrial processes as the largest source (44%) of observed AHs, followed by solvent usage (21%), vehicle exhaust (19%), coal combustion (11%) and coking processes (6%). In the perspective of PAHs sources, coal combustion emissions were identified as the dominating factor of a share of 41%-52% in eastern China. Our findings complemented the simultaneously monitoring information of PAHs and MAHs in eastern China, revealed the importance of PAHs to SOA formation and highlighted the necessity of formulating strategies to reduce emissions from anthropogenic sources and reduce risks to human health.

Short- and medium-chain chlorinated paraffins in urban road dust of Shanghai, China: concentrations, source apportionment and human exposure assessment.

Chlorinated paraffins (CPs) are ubiquitous anthropogenic contaminants that have been found in various environmental media. The objective of this study was to determine concentrations, spatial distribution, possible sources and potential health risk of SCCPs and MCCPs in urban road dust collected from Shanghai, China. The concentrations ranged from 9.74 to 11,400 ng g-1 for ΣSCCPs, 44.1 to 49,900 ng g-1 for ΣMCCPs and 53.9 to 61,400 ng g-1 for total CPs, respectively. MCCPs were the dominant component in all road dust, averagely accounting for 82.8% of total CPs. The concentrations of CPs in dust collected from traffic and commercial areas were significantly higher than those from campus, industrial, park and residential areas (p < 0.01), which could be attributed to tire wear in heavy traffic. All dust samples were divided into two groups by hierarchical cluster analysis for both SCCPs and MCCPs, and the most abundant homologue groups in most samples were C10Cl7-10 and C13Cl7-9 for SCCPs, and C14Cl7-9 and C15Cl8-9 for MCCPs. Correlation analysis showed that all carbon homologues in road dusts were highly correlated each other, suggesting SCCPs and MCCPs in dust maybe came from similar sources. Three sources for CPs in dust samples were apportioned by the PMF model; their relative contributions to the total CPs burden in dust were 25.6% for factor 1 (commercial CP mixture), 13.7% for factor 2 (long-distance transport) and 60.7% for factor 3 (commercial CP mixture). The median estimated daily intakes of total CPs via road dust were 1.78 × 10-5 for children and 3.0 × 10-6 mg kg-1 day-1 for adults, respectively. Quantitative risk assessment using non-cancer hazard index and total margin of exposure of total CPs indicated that total CPs at the present level in road dust pose no significant risk for both children and adults in Shanghai.

Toxicity Assessment of Octachlorostyrene in Human Liver Carcinoma (HepG2) Cells.

Octachlorostyrene (OCS) is a ubiquitous persistent organic pollutant; however, information regarding the toxicological effects of OCS remains limited. In this study, we studied the toxicity mechanisms of OCS using human liver carcinoma (HepG2) cells. The results showed that OCS reduced cell viability in a time- and dose-dependent manner. Compared with that in the control, the level of reactive oxygen species (ROS) was significantly increased in all treated HepG2 cells. We also found that (1) OCS induced damage in the HepG2 cells via the apoptotic signaling pathway, (2) OCS increased intracellular free Ca2+ concentration (>180%), and (3) following exposure to 80 µM OCS, there was an increase in mitochondrial transmembrane potential (MMP, ~174%), as well as a decrease in ATP levels (<78%). In conclusion, OCS is cytotoxic and can induce apoptosis, in which ROS and mitochondrial dysfunction play important roles; however, the observed increase in MMP appears to indicate that HepG2 is resistant to the toxicity induced by OCS.

New Insights into Human Biotransformation of BDE-209: Unique Occurrence of Metabolites of Ortho-Substituted Hydroxylated Higher Brominated Diphenyl Ethers in the Serum of e-Waste Dismantlers.

Extremely high levels of decabromodiphenyl ether (BDE-209) are frequently found in the serum of occupationally exposed groups, such as e-waste dismantlers and firefighters. However, the metabolism of BDE-209 in the human body is not adequately studied. In this study, 24 serum samples were collected from workers at a typical e-waste recycling workshop in Taizhou, Eastern China, and the occurrence and fate of these higher brominated diphenyl ethers (PBDEs) were investigated. The median concentration of the total PBDEs in the serum was 199 ng/g lipid weight (lw), ranging from 125 to 622 ng/g lw. Higher brominated octa- to deca-BDEs accounted for more than 80% of the total PBDEs. Three ortho-hydroxylated metabolites of PBDEs─6-OH-BDE196, 6-OH-BDE199, and 6'-OH-BDE206─were widely detected with a total concentration (median) of 92.7 ng/g lw. The concentrations of the three OH-PBDEs were significantly higher than their octa- and nona-PBDE homologues, even exceeding those of the total PBDEs in several samples, indicating that the formation of OH-PBDEs was a major metabolic pathway of the higher brominated PBDEs in occupationally exposed workers. An almost linear correlation between 6-OH-BDE196 and 6-OH-BDE199 (R = 0.971, P < 0.001) indicates that they might undergo a similar biotransformation pathway in the human body or may be derived from the same precursor. In addition, the occurrence of a series of penta- to hepta- ortho-substituted OH-PBDEs was preliminarily identified according to their unique "predioxin" mass spectral profiles by GC-ECNI-MS. Taken together, the tentative metabolic pathway for BDE-209 in e-waste dismantlers was proposed. The oxidative metabolism of BDE-209 was mainly observed at the ortho positions to form 6'-OH-BDE-206, which later underwent a consecutive loss of bromine atoms at the meta or para positions to generate other ortho-OH-PBDEs. Further studies are urgently needed to identify the chemical structures of these ortho-OH-PBDE metabolites, and perhaps more importantly to clarify the potentially toxic effects, along with their underlying molecular mechanisms.

Chiral signatures of polychlorinated biphenyls in serum from e-waste workers and their correlation with hydroxylated metabolites.

Elevated concentrations of polychlorinated biphenyls (PCBs) found in environmental media and biota from typical e-waste dismantling sites have raised concerns regarding their human body burden and potential negative health effects. In the present study, the enantiomeric compositions of three typical chiral congeners (PCB-95, PCB-132, and PCB-149) were measured in 24 serum samples from e-waste workers by using gas chromatography coupled to triple quadrupole tandem mass spectrometry. The mean enantiomer fractions (EFs) of chiral congeners in serum from the workers were 0.655 ± 0.103, 0.679 ± 0.164, and 0.548 ± 0.095 for PCB-95, PCB-132, and PCB-149, respectively. The (+) enantiomers of PCB-95, PCB-132, and PCB-149 were enantioselectively enriched in serum. Significant positive correlations were observed between the EF of the chiral congener PCB-95 and the total concentration of OH-PCBs, suggesting that EF values of chiral PCBs could be used to indicate the extent of biological metabolism. In addition, the EF of PCB-95 in serum samples increased with increasing work duration of the e-waste workers, thus demonstrating the usefulness of EF values of chiral PCBs as tracers of human exposure to PCBs. Because of the enantioselective enrichment of (+) enantiomers of PCB-95, PCB-132, and PCB-149, further studies are needed to explore the metabolism and toxicity of chiral contaminants in humans.

Removal of triclosan from water by sepiolite supported bimetallic Fe/Ni nanoparticles.

A simple and low-cost route to fabricate sepiolite-supported bimetallic Fe/Ni (Sep-Fe/Ni) nanoparticles was obtained by synchronous liquid phase reduction method. The as prepared composite was used to remove triclosan (TCS) from aqueous solutions. X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and Brunauer-Emmett-Teller (BET) analysis were used for characterization of the materials. As the supporting material, Sep dispersed Fe/Ni nanoparticles on its surface effectively and reduced the agglomeration phenomenon, providing more reactive sites. Sep-Fe/Ni had a large surface area of 90.5 m2/g, which was considerably higher than that of Fe/Ni (9.2 m2/g). Sep-Fe/Ni exhibited an enhanced TCS removal efficiency, as compared to the Fe/Ni and Sep materials. Operation factors, including the solution pH, initial TCS concentration, and material dosage, were investigated and found to be influential for TCS removal. The kinetic analysis indicated that the depletion of TCS in aqueous solutions conformed to the pseudo-first-order kinetic model under optimized conditions. The transformation pathway of TCS was studied in detail, revealing that the dechlorination of TCS by Sep-Fe/Ni is a stepwise reaction, namely from TCS to di-chlorinated intermediates, with the newly formed intermediate products also degrading into mono-chlorinated products by further reductive dechlorination. This study demonstrated that Sep-Fe/Ni is a promising reductant for TCS removal in water.

Occurrence, source apportionment, and carcinogenic risk assessment of polycyclic aromatic hydrocarbons in urban road dusts in Shanghai.

Polycyclic aromatic hydrocarbons (PAHs), as a class of important environmental pollutants, have received considerable concern due to their widespread existence and biological toxicity. The main purpose of this study was to determine concentrations, spatial distribution, possible sources, and potential health risk of PAHs in urban road dust in Shanghai, China. The concentration of Σ26PAHs ranged from 53.0 to 28,700 ng g-1 in road dust samples from Shanghai, which is at the low to medium level compared with other areas around the world. PAHs with 4-5 rings were predominant components in road dust. The level of PAHs in road dust was significantly higher than those in soil and river sediment in Shanghai. Six possible sources of PAHs were apportioned by PMF model. The contribution of pyrogenic PAHs accounted for 91.3% of the total PAHs in road dusts. The motor vehicular emission, natural gas, and coal combustion were main sources for urban road dust PAHs from Shanghai. Four dibenzopyrene (DBP) isomers were contributed averagely 75% of total TEQBaP concentration. DBalP, BaP, DBaiP, BbF, and DBA were main contributors to total carcinogenic potency, which totally contributed from 69.6 to 91.8% (median 89.1%) to total TEQBaP in urban road dusts of Shanghai. The results of incremental lifetime carcinogenic risk (ILCR) assessment showed that the total risk values exposed to 24 PAHs in road dust were lower than 10-4 at all sampling sites, indicating that exposure to dust-bound PAHs at present level was unlikely to result in high carcinogenic risk for both children and adults in Shanghai.

Biotransformation of Tris(2-chloroethyl) Phosphate (TCEP) in Sediment Microcosms and the Adaptation of Microbial Communities to TCEP.

Tris(2-chloroethyl) phosphate (TCEP), a typical chlorinated organophosphate ester (OPE), is an emerging contaminant of global concern because of its frequent occurrence, potential toxic effects, and persistence in the environment. In this study, we investigated the microbial TCEP biotransformation and the development of microbial communities in sediment microcosms with repeated TCEP amendments. The TCEP degradation fitted pseudo-zero-order kinetics, with reaction rates of 0.068 mg/(L h) after the first spike of 5 mg/L and 1.85 mg/(L h) after the second spike of 50 mg/L. TCEP was mainly degraded via phosphoester bond hydrolysis, evidenced by the production of bis(2-chloroethyl) phosphate (BCEP) and mono-chloroethyl phosphate (MCEP). Bis(2-chloroethyl) 2-hydroxyethyl phosphate (TCEP-OH), phosphoric bis(2-chloroethyl) (2-oxoethyl) ester (TCEP-CHO), phosphoric acid bis(2-chloroethyl)(carboxymethyl) ester (TCEP-COOH), and 2-chloroethyl 2-hydroxyethyl hydrogen phosphate (BCEP-OH) were also identified as microbial TCEP transformation products, indicating that TCEP degradation may follow hydrolytic dechlorination and oxidation pathways. Microbial community compositions in TCEP-amended microcosms shifted away from control microcosms after the second TCEP spike. Burkholderiales and Rhizobiales were two prevalent bacterial guilds enriched in TCEP-amended microcosms and were linked to the higher abundances of alkaline and acid phosphatase genes and genes involved in the metabolism of 2-chloroethanol, a side product of TCEP hydrolysis, indicating their importance in degrading TCEP and its metabolites.

Reaction kinetic study of nonthermal plasma continuous degradation of acetone in a closed-loop reactor.

Nonthermal plasma (NTP) degradation has been shown to be a promising method for volatile organic compounds (VOCs) removal from air. However, there have been few studies on the degradation of indoor VOCs using NTP, and even less on their reaction kinetics. In this study, NTP degradation of acetone, a representative of oxygenated VOCs, in a closed-loop reactor operating in recirculation mode was investigated. Acetone and organic by-products were characterized in real-time by proton transfer reaction time-of-flight mass spectrometry. The results showed that approximately 85.7% of the acetone degraded within 7.5 h with dielectric barrier discharge treatment at 4.3 W. Methanol, acetaldehyde, formic acid, and acetic acid were observed to be the main organic byproducts with concentrations time-dependent on the order of ppb/ppm. The concentrations of the inorganic by-products O3 and NO2 are also time-dependent and can decrease to nearly 0 after a sufficient degradation time. Based on the concentration measurement in real-time, several rate laws were used to fit the concentration variations of acetone and the organic by-products, and it was observed that they strictly followed the simple kinetic reaction rate laws: acetone followed the first-order rate law, and formic acid formation followed the one-half-order rate law, etc. This study provides a good example of characterizing NTP removal of VOCs in airtight spaces and has important theoretical and practical significance in designing a better NTP device, predicting NTP degradation reaction rate, and accelerating the practical application of NTP technology for indoor air treatment.

Polybrominated diphenyl ethers and polychlorinated biphenyls in mangrove sediments of Shantou, China: Occurrence, profiles, depth-distribution, and risk assessment.

Surface and columnar sediments were collected from four mangrove Wetlands in Shantou coastal areas of South China to investigate the level, distribution, possible sources and ecotoxicological risks of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs). Total concentration of 14 PBDEs (∑14PBDEs) and 41 PCBs (∑41PCBs) varied from 0.61 to 180 ng/g and 42-636 pg/g dry weight (dw) in surface sediments, respectively. The concentration of PBDEs was much higher than that of PCBs. Compared with other mangrove Wetlands around the world, PCBs levels in the studied area were relatively low, while the concentrations of PBDE were at higher level. Decabromodiphenyl ether (BDE-209) was the predominant PBDEs homologue in all sediment samples, indicating the extensive use of deca-BDE in this area. Penta-CBs and hexa-CBs were the main homologues of PCBs. Spatial variations showed that the concentration of PBDEs might be mainly affected by anthropogenic activities in specific sites of this region, whereas dry and wet deposition might be an important input source of PCBs in this area. Although accurate sediment chronology was not available, higher concentrations of PBDEs and PCBs were still found in some deeper sediment layers, suggesting that new input quantity tends to decrease with the increase of control. Risk assessment showed that penta-BDEs and deca-BDE may have potential negative ecological effects on the ecological of Shantou mangrove sediments, while the effects of PCBs can be neglected.

Organophosphate esters in the water, sediments, surface soils, and tree bark surrounding a manufacturing plant in north China.

Emission from manufacturing facilities to the surrounding environment is one of the important input source of pollutants. However, no information on the levels of organophosphate esters (OPEs) contamination in the environmental media around the manufacturing facility is available to date. In this study, samples from various environmental media, including sediments, water, surface soils, and tree bark, were obtained near an OPE manufacturing plant in Hengshui, Hebei Province, North China. The three main congeners, detected were tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) phosphate (TCIPP), and triphenyl phosphate (TPHP), with the summed OPE concentrations (∑OPEs) ranging from 340 to 270,000 µg kg-1 dry weight (d.w.), 7100 to 33,000 ng L-1, not detected (N.D.) to 14,000 ng kg-1 d.w., and 5300 to 19,000 ng g-1 lipid weight in the sediments, water, soils, and tree bark, respectively. These findings suggest that point sources of OPEs could have widespread effects on its surrounding environments. Sediment and water concentrations of TCEP and TCIPP measured in this study were among the highest concentrations yet reported in the world. Meanwhile, the concentration ranges of TCEP and TCIPP in surface soils were significantly lower than those in the sediment and water, and among the lowest concentrations yet reported in soil data worldwide. This suggests that the manufacturing facility influenced the OPE distribution in different environmental media in different ways. Furthermore, TCEP and TCIPP might have been transported within the water stream from roots into the aboveground plants and then accumulated in tree barks.

Assessment of exposure to polybrominated diphenyl ethers associated with consumption of market hens in Guangzhou.

To evaluate contamination by polybrominated diphenyl ethers (PBDEs) in market hens and human PBDE exposure via hen consumption in Guangzhou, hens were collected and their muscle, liver, fat, blood, yolk, and ingluvies tissues were analyzed for 13 PBDE congeners. The median highest concentration of ∑PBDEs was found in the ingluvies (5.30 ng/g lw), followed by the muscle (2.53 ng/g lw), with the lowest located in the yolk (0.09 ng/g lw). The concentrations of PBDEs in the muscle tissue of market hens in Guangzhou were at medium levels compared to others reported around the world. BDE-47, -153, -99, and -183 were the predominant congeners. The daily intake concentrations of PBDEs from hen muscle were estimated to range from 0.08 to 0.31 ng/kg/day in this study, with a Hazard Quotient (HQ) below 1.0. These results suggest that the health risk of PBDEs for the general population, through the consumption of market hens in Guangzhou, was generally low. However, the intake of PBDEs via food consumption may be one major exposure pathway for the general population of Guangzhou.

Polychlorinated biphenyls and their hydroxylated metabolites in the serum of e-waste dismantling workers from eastern China.

A number of studies have reported on the exposure of e-waste dismantling workers to significantly high concentrations of halogenated organic pollutants such as polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers. Such exposure can have adverse health effects. However, little information on the metabolites of these contaminants exists. In this study, we investigated PCBs levels and their hydroxylated metabolites (OH-PCB) in the serum of e-waste workers in Taizhou in eastern China. Our results indicate elevated PCB and OH-PCB levels in the serum of the workers, with medians of 443.7 and 133.9 ng/g lw, respectively. Tri- to hexachlorinated PCB congeners were the dominant homologue groups in all of the samples. 4-OH-CB107 was the predominant homologue among the hydroxylated metabolites, accounting for 88.9% of the total OH-PCB concentrations. While dietary sources (e.g., fish) appear to be an important route for PCB accumulation in non-occupational exposure groups, exposure via ingestion of house dust and inhalation of pollutants derived from the recycling of PCB-containing e-wastes may primarily contribute to the high body burden observed in the occupational groups. Since we found concentrations of metabolites higher than those of their parent compounds, further studies need to pay more attention to their bioaccumulation and toxicity.

Tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) induced apoptosis and cell cycle arrest in HepG2 cells.

The purpose of this study was to investigate the cytotoxic effects of tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) and to explore the underlying molecular mechanism focusing on oxidative stress, apoptosis, and cell cycle arrest. The results showed that TBP and TBEP could inhibit cell proliferation, induce cellular reactive oxidative stress, and suppress the mitochondrial membrane potential in HepG2 cells. TBP and TBEP could induce both mitochondrial and p53 mediated apoptosis through different mitogen-activated protein kinase (MAPK) signal pathways. TBP activated the c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK1/2) pathways, while TBEP activated the JNK pathway. Furthermore, TBP and TBEP caused a concentration-dependent decrease of cyclin D1 expression and an increase of cyclin-dependent kinase (CDK) inhibitor proteins such as p21 and p27, resulting in significant cell cycle arrest in the G0/G1 phase. Taken together, the toxicity of TBP and TBEP on the HepG2 cells was associated with apoptosis and cell cycle arrest induced by oxidative stress.

Organophosphate esters in total suspended particulates of an urban city in East China.

Organophosphate esters (OPEs) are ubiquitous contaminants in the environment, but little is known on the occurrence and distribution of OPEs in the background atmosphere of urban environments. In this study, air samples were collected from two sites in the city of Shanghai, a typical fast developing metropolitan of East China, for investigating the concentration levels, composition profiles, potential sources and human health risk to OPEs. The annual average (median) values of total suspended particulates ΣOPEs concentrations were 19.4 (16.6) and 6.6 (4.4) ng/m3 for the sub-urban (BS) and urban (XJH) sampling sites, respectively. The ΣOPEs concentrations at BS were significantly higher than those at XJH (P < 0.01), suggesting that more local sources of these compounds in the sub-urban area. The composition profile for ΣOPEs concentrations was different between the two sites, possibly because they originated from different sources. At BS, the dominated OPEs profile was TPhP followed by TCPP and TCEP > TDCPP > TBP > TCP, accounting for 37.0%, 19.6%, 15.8%, 11.8%, 11.0% and 4.2% of the ΣOPEs, respectively. Comparatively, chlorinated OPEs (TCEP, TCPP, and TDCPP) were major contributors to ΣOPEs concentrations at XJH, with the sum of all three chlorinated OPEs concentrations comprising 69.0% of the ΣOPEs. Based on the measured data in the present study human daily intake of each OPEs through particulate inhalation were estimated using a Monte Carlo simulation and the preliminary exposure assessments suggested a low risk of OPEs via inhalation in Shanghai.

In vitro study on the biotransformation and cytotoxicity of three hexabromocyclododecane diastereoisomers in liver cells.

In order to clarify the cytotoxicity of hexabromocyclododecane (HBCD) diastereoisomers, and to investigate the correlation of cytotoxicity and biotransformation of HBCDs, the immortalized human liver cells L02 and human hepatoma cells HepG2 were exposed to individual HBCD diastereoisomer (α-, ß- and γ-HBCD). Cytotoxicity was assayed in terms of cell viability, reactive oxygen species (ROS) level and DNA damage. Metabolic rate, bioisomerization and enantiomer fractions were analyzed using the liquid chromatograph coupled to triple quadrupole mass spectrometer (LC-MS/MS). The α-, ß- and γ-HBCD all had cytotoxicity in L02 and HepG2 cells with the toxicity order ß-HBCD ≥ Î³-HBCD > α-HBCD according to the results of proliferation assay. The cytotoxicity mechanism between the two cells seemed different: a) the stability of intracellular redox state plays an important role in inducing cell toxicity in HepG2 cells. b) DNA damage status is central to inhibit proliferation in L02 cells. The metabolic capability of HepG2 was superior to L02 for HBCD diastereoisomers, which may explain the greater toxicity of HBCDs in HepG2 cells. The bioisomerization and enantiomer enrichment were also detected in this study, although the results were inconsistent with other reports, which might result from species-specific differences in HBCDs metabolism or experimental conditions. The cytotoxicity and metabolic mechanism of individual enantiomers must be further investigated to evaluate the health risks of HBCDs.