Associations of insulin sensitivity and immune inflammatory responses with child blood lead (Pb) and PM2.5 exposure at an e-waste recycling area during the COVID-19 lockdown.

Fine particular matter (PM2.5) and lead (Pb) exposure can induce insulin resistance, elevating the likelihood of diabetes onset. Nonetheless, the underlying mechanism remains ambiguous. Consequently, we assessed the association of PM2.5 and Pb exposure with insulin resistance and inflammation biomarkers in children. A total of 235 children aged 3-7 years in a kindergarten in e-waste recycling areas were enrolled before and during the Corona Virus Disease 2019 (COVID-19) lockdown. Daily PM2.5 data was collected and used to calculate the individual PM2.5 daily exposure dose (DED-PM2.5). Concentrations of whole blood Pb, fasting blood glucose, serum insulin, and high mobility group box 1 (HMGB1) in serum were measured. Compared with that before COVID-19, the COVID-19 lockdown group had lower DED-PM2.5 and blood Pb, higher serum HMGB1, and lower blood glucose and homeostasis model assessment of insulin resistance (HOMA-IR) index. Decreased DED-PM2.5 and blood Pb levels were linked to decreased levels of fasting blood glucose and increased serum HMGB1 in all children. Increased serum HMGB1 levels were linked to reduced levels of blood glucose and HOMA-IR. Due to the implementation of COVID-19 prevention and control measures, e-waste dismantling activities and exposure levels of PM2.5 and Pb declined, which probably reduced the association of PM2.5 and Pb on insulin sensitivity and diabetes risk, but a high level of risk of chronic low-grade inflammation remained. Our findings add new evidence for the associations among PM2.5 and Pb exposure, systemic inflammation and insulin resistance, which could be a possible explanation for diabetes related to environmental exposure.

Anionic Chemistry Modulation Enabled Environmental Self-Charging Aqueous Zinc Batteries: The Case of Carbonate Ions.

Anionic chemistry modulation represents a promising avenue to enhance the electrochemical performance and unlock versatile applications in cutting-edge energy storage devices. Herein, we propose a methodology that involves anionic chemistry of carbonate anions to tailor the electrochemical oxidation-reduction reactions of bismuth (Bi) electrodes, where the conversion energy barrier for Bi (0) to Bi (III) has been significantly reduced, endowing anionic full batteries with enhanced electrochemical kinetics and chemical self-charging property. The elaborately designed batteries with an air-switch demonstrate rapid self-recharging capabilities, recovering over 80% of the electrochemical full charging capacity within a remarkably short timeframe of 1 hour and achieving a cumulative self-charging capacity of 5 Ah g-1. The aqueous self-charging battery strategy induced by carbonate anion, as proposed in this study, holds the potential for extending to various anionic systems, including seawater-based Cl- ion batteries. This work offers a universal framework for advancing next-generation multi-functional power sources.

Construction of Fully Integrated and Energy Self-Sufficient NO2 Gas Sensors Utilizing Zinc-Air Batteries.

Exploration of novel self-powered gas sensors free of external energy supply restrictions, such as light illumination and mechanical vibration, for flexible and wearable applications is in urgent need. Herein, this work constructs a flexible and self-powered NO2 gas sensor based on zinc-air batteries (ZABs) with the cathode of the ZABs also acting as the gas-sensitive layer. Furthermore, the SiO2 coating film, serving as a hydrophobic layer, increases the three-phase interfaces for the NO2 reduction reaction. The constructed sensors exhibit a high sensing response (0.3 V @ 5 ppm), an ultralow detection limit (61 ppb), a fast sensing process (129 and 103 s), and excellent selectivity. Moreover, the sensors also possess a wide working temperature range and a low working temperature tolerance (0.34 V at -15 °C). Simulations indicate that the hydrophobic surface at the cathode-hydrogel interface will accommodate more NO2 gas molecules at the reaction sites and prevent the influence of inner water evaporation and direct dissolution of NO2 in the electrolyte, which is beneficial to the enhanced gas sensing abilities. Finally, the self-powered sensing device is incorporated into a smart sensing system for practical applications. This work will pave a new insight into the construction of integrated and energy self-sufficient smart gas sensing systems.

Associations of co-exposure to polycyclic aromatic hydrocarbons and lead (Pb) with IGF1 methylation in peripheral blood of preschool children from an e-waste recycling area.

BACKGROUND: Childhood exposure to polycyclic aromatic hydrocarbons (PAHs) or lead (Pb) is associated with epigenetic modifications. However, the effects of their co-exposures on IGF1 (Insulin-like growth factor 1) methylation and the potential role in child physical growth are unclear. METHODS: From our previous children study (N = 238, ages of 3-6), 75 children with higher total concentrations of urinary ten hydroxyl PAH metabolites (∑10OH-PAHs) from an e-waste recycling area, Guiyu, and 75 with lower ∑10OH-PAHs from Haojiang (reference area) were included. Pb and IGF1 P2 promoter methylation in peripheral blood were also measured. Multivariable linear regression analyses were performed to estimate individual associations, overall effects and interactions of co-exposure to OH-PAHs and Pb on IGF1 methylation were further explored using Bayesian kernel machine regression. RESULTS: Methylation of IGF1 (CG-232) was lower (38.00 vs. 39.74 %, P < 0.001), but of CG-207 and CG-137 were higher (59.94 vs. 58.41 %; 57.60 vs. 56.28 %, both P < 0.05) in exposed children than the reference. The elevated urinary 2-OHPhe was associated with reduced methylation of CG-232 (B = -0.051, 95 % CI: -0.096, -0.005, P < 0.05), whereas blood Pb was positively associated with methylation of CG-108 (B = 0.106, 95 %CI: 0.013, 0.199, P < 0.05), even after full adjustment. Methylations of CG-224 and 218 significantly decreased when all OH-PAHs and Pb mixtures were set at 35th - 40th and 45th - 55th percentile compared to when all fixed at 50th percentile. There were bivariate interactions of co-exposure to the mixtures on methylations of CG-232, 224, 218, and 108. Methylations correlated with height, weight, were observed in the exposed children. CONCLUSIONS: Childhood co-exposure to high PAHs and Pb from the e-waste may be associated with IGF1 promoter methylation alterations in peripheral blood. This, in turn, may interrupt the physical growth of preschool children.

Alterations of gut microbiota and its metabolomics in children with 6PPDQ, PBDE, PCB, and metal(loid) exposure.

The composition and metabolites of the gut microbiota can be altered by environmental pollutants. However, the effect of co-exposure to multiple pollutants on the human gut microbiota has not been sufficiently studied. In this study, gut microorganisms and their metabolites were compared between 33 children from Guiyu, an e-waste dismantling and recycling area, and 34 children from Haojiang, a healthy environment. The exposure level was assessed by estimating the daily intake (EDI) of polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), 6PPD-quinone (6PPDQ), and metal(loid)s in kindergarten dust. Significant correlations were found between the EDIs of 6PPDQ, BDE28, PCB52, Ni, Cu, and the composition of gut microbiota and specific metabolites. The Bayesian kernel machine regression model showed negative correlations between the EDIs of five pollutants (6PPDQ, BDE28, PCB52, Ni, and Cu) and the composition of gut microbiota. The EDIs of these five pollutants were positively correlated with the levels of the metabolite 2,4-diaminobutyric acid, while negatively correlated with the levels of d-erythro-sphingosine and d-threitol. Our study suggests that exposure to 6PPDQ, BDE28, PCB52, Ni, and Cu in kindergarten dust is associated with alterations in the composition and metabolites of the gut microbiota. These alterations may be associated with children's health.

Elevated plasma solMER concentrations link ambient PM2.5 and PAHs to myocardial injury and reduced left ventricular systolic function in children.

Exposure to fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) is known to be associated with the polarization of pro-inflammatory macrophages and the development of various cardiovascular diseases. The pro-inflammatory polarization of resident cardiac macrophages (cMacs) enhances the cleavage of membrane-bound myeloid-epithelial-reproductive receptor tyrosine kinase (MerTK) and promotes the formation of soluble MerTK (solMER). This process influences the involvement of cMacs in cardiac repair, thus leading to an imbalance in cardiac homeostasis, myocardial injury, and reduced cardiac function. However, the relative impacts of PM2.5 and PAHs on human cMacs have yet to be elucidated. In this study, we aimed to investigate the effects of PM2.5 and PAH exposure on solMER in terms of myocardial injury and left ventricular (LV) systolic function in healthy children. A total of 258 children (aged three to six years) were recruited from Guiyu (an area exposed to e-waste) and Haojiang (a reference area). Mean daily PM2.5 concentration data were collected to calculate the individual chronic daily intake (CDI) of PM2.5. We determined concentrations of solMER and creatine kinase MB (CKMB) in plasma, and hydroxylated PAHs (OH-PAHs) in urine. LV systolic function was evaluated by stroke volume (SV). Higher CDI values and OH-PAH concentrations were detected in the exposed group. Plasma solMER and CKMB were higher in the exposed group and were associated with a reduced SV. Elevated CDI and 1-hydroxynaphthalene (1-OHNa) were associated with a higher solMER. Furthermore, increased solMER concentrations were associated with a lower SV and higher CKMB. CDI and 1-OHNa were positively associated with CKMB and mediated by solMER. In conclusion, exposure to PM2.5 and PAHs may lead to the pro-inflammatory polarization of cMacs and increase the risk of myocardial injury and systolic function impairment in children. Furthermore, the pro-inflammatory polarization of cMacs may mediate cardiotoxicity caused by PM2.5 and PAHs.

Cell type-dependent response to benzo(a)pyrene exposure of human placental cell lines under normoxic, hypoxic, and pro-inflammatory conditions.

Benzo(a)pyrene (BaP) can be detected in the human placenta. However, little is known about the effects of BaP exposure on different placental cells under various conditions. In this study, we aimed to investigate the effects of BaP on mitochondrial function, pyrin domain-containing protein 3 (NLRP3) inflammasome, and apoptosis in three human trophoblast cell lines under normoxia, hypoxia, and inflammatory conditions. JEG-3, BeWo, and HTR-8/SVneo cell lines were exposed to BaP under normoxia, hypoxia, or inflammatory conditions for 24 h. After treatment, we evaluated cell viability, apoptosis, aryl hydrocarbon receptor (AhR) protein and cytochrome P450 (CYP) gene expression, mitochondrial function, including mitochondrial DNA copy number (mtDNAcn), mitochondrial membrane potential (ΔΨm), intracellular adenosine triphosphate (iATP), and extracellular ATP (eATP), nitric oxide (NO), NLPR3 inflammasome proteins, and interleukin (IL)-1ß. We found that BaP upregulated the expression of AhR or CYP genes to varying degrees in all three cell lines. Exposure to BaP alone increased ΔΨm in all cell lines but decreased NO in BeWo and HTR-8/SVneo, iATP in HTR-8/SVneo, and cell viability in JEG-3, without affecting apoptosis. Under hypoxic conditions, BaP did not increase the expression of AhR and CYP genes in JEG-3 cells but increased CYP gene expression in two others. Pro-inflammatory conditions did not affect the response of the 3 cell lines to BaP with respect to the expression of CYP genes and changes in the mitochondrial function and NLRP3 inflammasome proteins. In addition, in HTR-8/SVneo cells, BaP increased IL-1ß secretion in the presence of hypoxia and poly(I:C). In conclusion, our results showed that BaP affected mitochondrial function in trophoblast cell lines by increasing ΔΨm. This increased ΔΨm may have rescued the trophoblast cells from activation of the NLRP3 inflammasome and apoptosis after BaP treatment. We also observed that different human trophoblast cell lines had cell type-dependent responses to BaP exposure under normoxia, hypoxia, or pro-inflammatory conditions.

Regulation of electron density redistribution for efficient alkaline hydrogen evolution reaction and overall water splitting.

The rational design of morphology and heterogeneous interfaces for non-precious metal electrocatalysts is crucial in electrochemical water decomposition. In this paper, a bifunctional electrocatalyst (Ni/NiFe LDH), which coupling nickel with nickel-iron layer double hydroxide (NiFe LDH), is synthesized on carbon cloth. At current density of 10 mA cm-2, the Ni/NiFe LDH exhibits a low hydrogen evolution reaction (HER) overpotential of only 36 mV due to the accelerated electrolyte penetration, which is caused by superhydrophilic interface. Moreover, an alkaline electrolyzer is formed and provide a current density of 10 mA cm-2 with a voltage of only 1.49 V. It is confirmed by the density functional theory (DFT) that electron from the Ni layer is transferred to NiFe LDH layer, redistributing the local electron density around the heterogeneous phase interface. Thus, the Gibbs free energy for hydrogen adsorption is optimized. This work provides a promising strategy for the rational regulation of electrons at heterogeneous interfaces and the synthesis of flexible electrocatalysts.

Activating and Stabilizing a Reversible four Electron Redox Reaction of I-/I+ for Aqueous Zn-Iodine Battery.

Low capacity and poor cycle stability greatly inhibit the development of zinc-iodine batteries. Herein, a high-performance Zn-iodine battery has been reached by designing and optimizing both electrode and electrolyte. The Br- is introduced as the activator to trigger I+, and coupled with I+ forming interhalogen to stabilize I+ to achieve a four-electron reaction, which greatly promotes the capacity. And the Ni-Fe-I LDH nanoflowers serve as the confinement host to enable the reactions of I-/I+ occurring in the layer due to the spacious and stable interlayer spacing of Ni-Fe-I LDH, which effectively suppresses the iodine-species shuttle ensuring high cycling stability. As a result, the electrochemical performance is greatly enhanced, especially in specific capacity (as high as 350 mAh g-1 at 1 A g-1 far higher than two-electron transfer Zn-iodine batteries) and cycling performance (94.6 % capacity retention after 10000 cycles). This strategy provides a new way to realize high capacity and long-term stability of Zn-iodine batteries.

Spatiotemporal variation of 6PPD and 6PPDQ in dust and soil from e-waste recycling areas.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its derivative 6PPDQ have been detected in various environmental media, with harmful consequences for both ecosystems and biological health. However, the distribution of 6PPD and 6PPDQ in areas around e-waste recycling areas is currently unknown. We collected soil and dust samples from areas around a traditional e-waste recycling zone, an emerging recycling park, and a reference area. Higher levels of 6PPD were found in dust from residential areas around the traditional e-waste recycling zone compared to the reference area (median: 108.99 versus 33.57 ng/g, P < 0.01). Lower levels of 6PPDQ were detected in dust samples from around the emerging e-waste recycling parks compared to traditional e-waste recycling zones (median: 15.40 versus 46.37 ng/g, P < 0.05). The median concentrations of 6PPD and 6PPDQ were higher in the dust samples than in the soil samples (P < 0.001). The concentrations of 6PPD and 6PPDQ in the dust and soil varied seasonally, with the highest total concentrations occurring in the winter. Results from a multiple linear regression analysis indicate that 6PPDQ is negatively correlated with temperature and positively correlated with 6PPD, O3, and radiation. This study confirms that e-waste is a potential contributor to 6PPD and 6PPDQ. In residential areas, 6PPD and 6PPDQ are more likely to accumulate in dust than in soil. The emerging e-waste recycling parks have greatly improved the local 6PPDQ pollution situation. Further studies are necessary to understand the distribution of newly found substances in various settings.

GIMAP5 deficiency reveals a mammalian ceramide-driven longevity assurance pathway.

Preserving cells in a functional, non-senescent state is a major goal for extending human healthspans. Model organisms reveal that longevity and senescence are genetically controlled, but how genes control longevity in different mammalian tissues is unknown. Here, we report a new human genetic disease that causes cell senescence, liver and immune dysfunction, and early mortality that results from deficiency of GIMAP5, an evolutionarily conserved GTPase selectively expressed in lymphocytes and endothelial cells. We show that GIMAP5 restricts the pathological accumulation of long-chain ceramides (CERs), thereby regulating longevity. GIMAP5 controls CER abundance by interacting with protein kinase CK2 (CK2), attenuating its ability to activate CER synthases. Inhibition of CK2 and CER synthase rescues GIMAP5-deficient T cells by preventing CER overaccumulation and cell deterioration. Thus, GIMAP5 controls longevity assurance pathways crucial for immune function and healthspan in mammals.

Association between 6PPD-quinone exposure and BMI, influenza, and diarrhea in children.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-quinone) has received extensive attention due to its ubiquitous distribution and potential toxicity. However, the distribution characteristics of 6PPD-quinone in dust from e-waste recycling areas and the consequential health risks to children are unclear. A total of 183 dust samples were collected from roads (n = 40), homes (n = 91), and kindergartens (n = 52) in Guiyu (the e-waste-exposed group) and Haojiang (the reference group) from 2019 to 2021. The results show that the concentrations of 6PPD-quinone in kindergarten and house dust from the exposed group were significantly higher than those from the reference group (P < 0.001). These findings show that e-waste may be another potential source of 6PPD-quinone, in addition to rubber tires. The exposure risk of 6PPD-quinone in children was assessed using their daily intake. The daily intake of 925 kindergarten children was calculated using the concentration of 6PPD-quinone in kindergarten dust. The daily intake of 6PPD-quinone via ingestion was approximately five orders of magnitude higher than via inhalation. Children in the exposed group had a higher exposure risk to 6PPD-quinone than the reference group. A higher daily intake of 6PPD-quinone from kindergarten dust was associated with a lower BMI and a higher frequency of influenza and diarrhea in children. This study reports the distribution of 6PPD-quinone in an e-waste recycling town and explores the associated health risks to children.

Effects of endocrine disrupting chemicals and their interactions with genetic risk scores on cardiometabolic traits.

Ubiquitous non-persistent endocrine disrupting chemicals (EDCs) have inconsistent associations with cardiometabolic traits. Additionally, large-scale genome-wide association studies (GWASs) have yielded many genetic risk variants for cardiometabolic traits and diseases. This study aimed to investigate the associations between a wide range of EDC exposures (parabens, bisphenols, and phthalates) and 14 cardiometabolic traits and whether these are moderated by their respective genetic risk scores (GRSs). Data were from 1074 participants aged 18 years or older of the Lifelines Cohort Study, a large population-based biobank. GRSs for 14 cardiometabolic traits were calculated based on genome-wide significant common variants from recent GWASs. The concentrations of 15 EDCs in 24-hour urine were measured by isotope dilution liquid chromatography tandem mass spectrometry technology. The main effects of trait-specific GRSs and each of the EDC exposures and their interaction effects on the 14 cardiometabolic traits were examined in multiple linear regression. The present study confirmed significant main effects for all GRSs on their corresponding cardiometabolic trait. Regarding the main effects of EDC exposures, 26 out of 280 EDC-trait tests were significant with explained variances ranging from 0.43 % (MMP- estimated glomerular filtration rate (eGFR)) to 2.37 % (PrP-waist-hip ratio adjusted body mass index (WHRadjBMI)). We confirmed the association of MiBP and MBzP with WHRadjBMI and body mass index (BMI), and showed that parabens, bisphenol F, and many other phthalate metabolites significantly contributed to the variance of WHRadjBMI, BMI, high-density lipoprotein (HDL), eGFR, fasting glucose (FG), and diastolic blood pressure (DBP). Only one association between BMI and bisphenol F was nominally significantly moderated by the GRS explaining 0.36 % of the variance. However, it did not survive multiple testing correction. We showed that non-persistent EDC exposures exerted effects on BMI, WHRadjBMI, HDL, eGFR, FG, and DBP. However no evidence for a modulating role of GRSs was found.

A genome-wide association study of 24-hour urinary excretion of endocrine disrupting chemicals.

Ubiquitous exposure to environmental endocrine disrupting chemicals (EDCs) instigates a major public health problem, but much remains unknown on the inter-individual differences in metabolism and excretion of EDCs. To examine this we performed a two-stage genome-wide association study (GWAS) for 24-hour urinary excretions of four parabens, two bisphenols, and nine phthalate metabolites. Results showed five genome-wide significant (p-value < 5x10-8) and replicated single nucleotide polymorphisms (SNPs) representing four independent signals that associated with mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) and mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP). Three of the four signals were located on chromosome 10 in a locus harboring the cytochrome P450 (CYP) genes CYP2C9, CYP2C58P, and CYP2C19 (rs117529685, pMECPP = 5.38x10-25; rs117033379, pMECPP = 1.96x10-19; rs4918798, pMECPP = 4.01x10-71; rs7895726, pMEHHP = 1.37x10-15, r2 with rs4918798 = 0.93). The other signal was on chromosome 6 close to the solute carrier (SLC) genes SLC17A1, SLC17A3, SLC17A4, and SCGN (rs1359232, pMECPP = 7.6x10-16). These four SNPs explained a substantial part (8.3 % - 9.2 %) of the variance in MECPP in the replication cohort. Bioinformatics analyses supported a likely causal role of CYP2C9 and SLC17A1 in metabolism and excretion of MECPP and MEHHP. Our results provide biological insights into mechanisms of phthalate metabolism and excretion with a likely causal role for CYP2C9 and SLC17A1.

Engineering Fluorine-rich Double Protective Layer on Zn Anode for Highly Reversible Aqueous Zinc-ion Batteries.

The high thermodynamic instability and side reactions of Zn-metal anode (ZMA), especially at high current densities, greatly impede the commercialization of aqueous zinc-ion batteries (AZIBs). Herein, a fluorine-rich double protective layer strategy is proposed to obtain the high reversibility of AZIBs through the introduction of a versatile tetradecafluorononane-1,9-diol (TDFND) additive in aqueous electrolyte. TDFND molecule with large adsorption energy (-1.51 eV) preferentially absorbs on the Zn anode surface to form a Zn(OR)2 - (R=-CH2 -(CF2 )7 -CH2 -) cross-linking complex network, which balances space electric field and controls the Zn2+ ion flux, thus enabling the uniform and compact deposition of Zn (002) crystal planes. Meanwhile, TDFND with low Lowest unoccupied molecular orbital (LUMO, 0.10 eV) energy level is priorly decomposed to regulate the interfacial chemistry of ZMA by building a ZnF2 -rich solid electrode/electrolyte interface (SEI) layer. It is found that a 14 nm-thick SEI layer delivers excellent structural integrity to suppress parasitic reactions by blocking the direct contact of active water and ZMA. Consequently, the Zn electrode exhibits a superior cycling life over 430 h at 10 mA cm-2 and a high average Coulombic efficiency of 99.8 % at 5 mA cm-2 . Furthermore, a 68 mAh pouch cell delivers 80.3 % capacity retention for 1000 cycles.

General Synthesis of Single-Crystal Spinel Cathodes with the Tailored Orientation of Exposed Crystal Planes for Advanced Lithium-Ion Batteries.

The spinel Mn-based cathodes with 3D Li+ diffusion channels, high voltage, and low-cost show promise for developing high-power lithium-ion batteries (LIBs). But the disproportionation and Jahn-Teller distortion lead to structural degeneration and capacity decay, especially at high working temperatures. Herein, considering the merits of single crystals and orientation of exposed crystal planes, single-crystal truncated octahedral LiMn2 O4 (TO-LMO) with exposed {111}, {100} and {110} facets is rationally designed, in which the mainly exposed {111} facets are truncated by a small portion of {100} and {110} facets. The Li-deficient intermediate phase is innovatively proposed to prepare the single-crystal TO-LMO. The synergistic effects of single crystals and the orientation of exposed crystal planes significantly reduce the disproportionation of Mn3+ ions and thereby improve their structural stability. Consequently, the cycling stability of the single-crystal TO-LMO is remarkably enhanced, obtaining outstanding capacity retention of 84.3% after 2000 cycles, much better than that of 61.2% for octahedral LiMn2 O4 . The feasibility of preparing single-crystal truncated octahedral LiNi0.5 Mn1.5 O4 with exposed {111}, {100}, and {110} facets via the Li-deficient intermediate phase is further demonstrated. These findings offer new insight into regulating the orientation of exposed crystal planes and improving the reversibility of Mn-based redox couples in LIBs.

An Ultrathin Inorganic Molecular Crystal Interfacial Layer for Stable Zn Anode.

Zn metal anode suffers from dendrite growth and side reactions during cycling, significantly deteriorating the lifespan of aqueous Zn metal batteries. Herein, we introduced an ultrathin and ultra-flat Sb2 O3 molecular crystal layer to stabilize Zn anode. The in situ optical and atomic force microscopes observations show that such a 10 nm Sb2 O3 thin layer could ensure uniform under-layer Zn deposition with suppressed tip growth effect, while the traditional WO3 layer undergoes an uncontrolled up-layer Zn deposition. The superior regulation capability is attributed to the good electronic-blocking ability and low Zn affinity of the molecular crystal layer, free of dangling bonds. Electrochemical tests exhibit Sb2 O3 layer can significantly improve the cycle life of Zn anode from 72 h to 2800 h, in contrast to the 900 h of much thicker WO3 even in 100 nm. This research opens up the application of inorganic molecular crystals as the interfacial layer of Zn anode.

Effects of polycyclic aromatic hydrocarbons (PAHs) on pregnancy, placenta, and placental trophoblasts.

Polycyclic aromatic hydrocarbons (PAHs) are a group of persistent organic pollutants that are carcinogenic, mutagenic, endocrine-toxic, and immunotoxic. PAHs can be found in maternal and fetal blood and in the placenta during pregnancy. They may thus affect placental and fetal development. Therefore, the exposure levels and toxic effects of PAHs in the placenta deserve further study and discussion. This review aims to summarize current knowledge on the effects of PAHs and their metabolites on pregnancy and birth outcomes and on placental trophoblast cells. A growing number of epidemiological studies detected PAH-DNA adducts as well as the 16 high-priority PAHs in the human placenta and showed that placental PAH exposure is associated with adverse fetal outcomes. Trophoblasts are important cells in the placenta and are involved in placental development and function. In vitro studies have shown that exposure to either PAH mixtures, benzo(a)pyrene (BaP) or BaP metabolite benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) affected trophoblast cell viability, differentiation, migration, and invasion through various signaling pathways. Furthermore, similar effects of BPDE on trophoblast cells could also be observed in BaP-treated mouse models and were related to miscarriage. Although the current data show that PAHs may affect placental trophoblast cells and pregnancy outcomes, further studies (population studies, in vitro studies, and animal studies) are necessary to show the specific effects of different PAHs on placental trophoblasts and pregnancy outcomes.