8-OHdG mediates the association of co-exposure to fifty-five typical endocrine-disrupting chemicals with renal function: a cross-section investigation in Southern Chinese adults.

Individual typical endocrine-disrupting chemicals (EDCs), including organophosphate triesters (OPEs), parabens, triclosan (TCS), bisphenols, benzophenones (BPs), phthalates (PAEs), and synthetic phenolic antioxidants (SPAs), are associated with renal dysfunction. However, the combined effects and underlying mechanisms of mixed EDC exposure on renal function remain unclear. Two hundred ninety-nine adult participants were enrolled in the cross-sectional survey conducted in Guangzhou, China. Urinary levels of 7 OPEs, 6 parabens, TCS, 14 bisphenols, 8 BPs, 15 PAEs, 4 SPAs, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were determined, and estimated glomerular filtration rate (eGFR) was served as the outcome index. We found elevated levels of diphenyl phosphate (DPP), bisphenol A (BPA), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono-butyl phthalate (MBP) showed dose-responsive associations with eGFR decline, However, nonlinear associations were observed for bis(2-butoxyethyl) hydrogen phosphate (BBOEP), TCS, 4-hydroxybenzophenone (HBP), mono-n-pentyl phthalate (MnPP), and mono-benzyl phthalate (MBzP). The quantile-based g-computation model demonstrated that a quartile increase in the EDC mixture corresponded to a 0.383-SD decrease (95% CI - 0.658 ~ - 0.108, P = 0.007) in eGFR. Notably, BPA was identified as the primary contributor to this effect. Moreover, 8-OHdG mediated the eGFR decline associated with EDC mixtures with a mediation proportion of 25.49%. A sex-modified effect was also observed (P = 0.004), indicating that exposure to the mixture of EDC was linked to more pronounced renal dysfunction in females. Our novel findings suggest that exposure to a typical mixture of EDCs is associated with renal dysfunction in the general adult population of Southern China. Furthermore, 8-OHdG may play a role in the pathogenesis of EDC mixture-related renal dysfunction.

First-Principles Study on Evolution of Magnetic Domain in Two-Dimensional BaTiO3 Ultrathin Film Doped with Co under Electric Field.

The magnetization mechanism of Co-doped BaTiO3 ultrathin films is a subject of debate, which results in difficulties with the design of new multiferroics based on BaTiO3 matrixes. With the aid of a first-principles approach, it was observed that when the interstitial site and Ti vacancy were filled with Co, the configuration behaved in a nonmagnetic manner, indicating the significance of the Co content. Moreover, in the case of Co substituting two neighboring Ti atoms, when a direct current field was applied in the [100] direction, the magnetic domains excluding those in the [100], [010], and [001] directions were directed away. Further, the magnetoelectric constant was evaluated at ~449.3 mV/cmOe, showing strong magnetoelectric coupling at room temperature. Clearly, our study indicates that strict control of Ba, Ti, O, and Co stoichiometry can induce an electric and magnetic field conversion in two-dimensional BaTiO3 and may provide a new candidate for single-phase multiferroics for application in next-generation multifunctional devices.

Mechanisms of neurocentral-eyestalk-intestinal immunotoxicity in whiteleg shrimp Litopenaeus vannamei under ammonia nitrogen exposure.

Ammonia-N, as the most toxic nitrogenous waste, has high toxicity to marine animals. However, the interplay between ammonia-induced neuroendocrine toxicity and intestinal immune homeostasis has been largely overlooked. Here, a significant concordance of metabolome and transcriptome-based "cholinergic synapse" supports that plasma metabolites acetylcholine (ACh) plays an important role during NH4Cl exposure. After blocking the ACh signal transduction, the release of dopamine (DA) and 5-hydroxytryptamine (5-HT) in the cerebral ganglia increased, while the release of NPF in the thoracic ganglia and NE in the abdominal ganglia, and crustacean hyperglycemic hormone (CHH) and neuropeptide F (NPF) in the eyestalk decreased, finally the intestinal immunity was enhanced. After bilateral eyestalk ablation, the neuroendocrine system of shrimp was disturbed, more neuroendocrine factors, such as corticotropin releasing hormone (CRH), adrenocorticotropic-hormone (ACTH), ACh, DA, 5-HT, and norepinephrine (NE) were released into the plasma, and further decreased intestinal immunity. Subsequently, these neuroendocrine factors reach the intestine through endocrine or neural pathways and bind to their receptors to affect downstream signaling pathway factors to regulate intestinal immune homeostasis. Combined with different doses of ammonia-N exposure experiment, these findings suggest that NH4Cl may exert intestinal toxicity on shrimp by disrupting the cerebral ganglion-eyestalk axis and the cerebral ganglion-thoracic ganglion-abdominal ganglion axis, thereby damaging intestinal barrier function and inducing inflammatory response.

Empirical analysis of lead neurotoxicity mode of action and its application in health risk assessment.

The mode of action (MOA) framework is proposed to inform a biological link between chemical exposures and adverse health effects. Despite a significant increase in knowledge and awareness, the application of MOA in human health risk assessment (RA) remains limited. This study aims to discuss the adoption of MOA for health RA within a regulatory context, taking our previously proposed but not yet validated MOA for lead neurotoxicity as an example. We first conducted a quantitative weight of evidence (qWOE) assessment, which revealed that the MOA has a moderate confidence. Then, targeted bioassays were performed within an in vitro blood-brain barrier (BBB) model to quantitatively validate the scientific validity of key events (KEs) in terms of essentiality and concordance of empirical support (dose/temporal concordance), which increases confidence in utilizing the MOA for RA. Building upon the quantitative validation data, we further conducted benchmark dose (BMD) analysis to map dose-response relationships for the critical toxicity pathways, and the lower limit of BMD at a 5% response (BMDL5) was identified as the point of departure (POD) value for adverse health effects. Notably, perturbation of the Aryl Hydrocarbon Receptor (AHR) signaling pathway exhibited the lowest POD value, measured at 0.0062 µM. Considering bioavailability, we further calculated a provisional health-based guidance value (HBGV) for children's lead intake, determining it to be 2.56 µg/day. Finally, the health risk associated with the HBGV was assessed using the hazard quotient (HQ) approach, which indicated that the HBGV established in this study is a relative safe reference value for lead intake. In summary, our study described the procedure for utilizing MOA in health RA and set an example for MOA-based human health risk regulation.

First Insight into Fetal Exposure to Legacy and Emerging Plasticizers Revealed by Infant Hair and Meconium: Occurrence, Biotransformation, and Accumulation.

Epidemiological studies have demonstrated the embryonic and developmental toxicity of plasticizers. Thus, understanding the in utero biotransformation and accumulation of plasticizers is essential to assessing their fate and potential toxicity in early life. In the present study, 311 infant hair samples and 271 paired meconium samples were collected at birth in Guangzhou, China, to characterize fetal exposure to legacy and emerging plasticizers and their metabolites. Results showed that most of the target plasticizers were detected in infant hair, with medians of 9.30, 27.6, and 0.145 ng/g for phthalate esters (PAEs), organic phosphate ester (OPEs), and alternative plasticizers (APs), and 1.44, 0.313, and 0.066 ng/g for the metabolites of PAEs, OPEs, and APs, respectively. Positive correlations between plasticizers and their corresponding primary metabolites, as well as correlations among the oxidative metabolites of bis(2-ethylhexyl) phthalate (DEHP) and 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH), were observed, indicating that infant hair retained the major phase-I metabolism of the target plasticizers. While no positive correlations were found in parent compounds or their primary metabolites between paired infant hair and meconium, significant positive correlations were observed among secondary oxidative metabolites of DEHP and DINCH in hair and meconium, suggesting that the primary metabolites in meconium come from hydrolysis of plasticizers in the fetus but most of the oxidative metabolites come from maternal-fetal transmission. The parent compound/metabolite ratios in infant hair showed a decreasing trend across pregnancy, suggesting in utero accumulation and deposition of plasticizers. To the best of our knowledge, this study is the first to report in utero exposure to both parent compounds and metabolites of plasticizers by using paired infant hair and meconium as noninvasive biomonitoring matrices and provides novel insights into the fetal biotransformation and accumulation of plasticizers across pregnancy.

Metabolomics perspectives into the co-exposure effect of polycyclic aromatic hydrocarbons and metals on renal function: A meet-in-the-middle approach.

Studies on the dose effects of kidney impairment and metabolomes in co-exposure to polycyclic aromatic hydrocarbons (PAHs) and metals are limited. We aimed to identify overall associations and metabolic perturbations in 130 participants (53 petrochemical workers and 77 controls) exposed to a PAHs-metals mixture in Southern China. The urinary 7 hydroxylated PAHs and 15 metal(loid)s were determined, and serum creatinine, beta-2 microglobulin, and estimated glomerular filtration rate were health outcomes. The liquid chromatography-mass spectrometry-based method was applied to serum metabolomics. Generalized weighted quantile sum (gWQS) regressions were used to estimate the overall dose-response relationships, and pathway analysis, "meet-in-the-middle" approach, and mediation effect analyses were conducted to identify potential metabolites and biological mechanisms linking exposure with nephrotoxic effects. Our results indicated that renal function reduction was associated with a PAHs-metals mixture in a dose-dependent manner, and 1-hydroxynaphthalene and copper were the most predominant contributors among the two families of pollutants. Furthermore, the metabolic disruptions associated with the early onset of kidney impairment induced by the combination of PAHs and metals encompassed pathways such as phenylalanine-tyrosine-tryptophan biosynthesis, phenylalanine metabolism, and alpha-linolenic acid metabolism. In addition, the specifically identified metabolites demonstrated excellent potential as bridging biomarkers connecting the reduction in renal function with the mixture of PAHs and metals. These findings shed light on understanding the overall associations and metabolic mechanism of nephrotoxic effects of co-exposure to PAHs and metals.

Mechanisms of ammonotelism, epithelium damage, cellular apoptosis, and proliferation in gill of Litopenaeus vannamei under NH4Cl exposure.

Excessive ammonia-N in coastal environment and aquaculture threatens the health of marine organisms. To explore the mechanism of gill damage induced by ammonia-N, transcriptome of Litopenaeus vannamei 's gill was carried out under 20 mg/L NH4Cl for 0, 6, and 48 h. K-means clustering analysis suggested that ammonia excretion and metabolism-related genes were elevated. GO and KEGG enrichment analysis suggested that glycosyltransferase activity and amino acid metabolism were affected by ammonia. Moreover, histological observation via three staining methods gave clues on the changes of gill after ammonia-N exposure. Increased mucus, hemocyte infiltration, and lifting of the lamellar epithelium suggested that gill epithelium was suffering damage under ammonia-N stress. Meanwhile, the composition of extracellular matrix (ECM) in connective tissue changed. Based on the findings of transcriptomic and histological analysis, we further investigated the molecular mechanism of gill damage under multiple concentrations of NH4Cl (0, 2, 10, 20 mg/L) for multiple timepoints (0, 3, 6, 12, 24, 48, 72 h). First, ammonia excretion was elevated via ion channel, transporter, and exocytosis pathways, but hemolymph ammonia still kept at a high level under 20 mg/L NH4Cl exposure. Second, we focused on glycosaminoglycan metabolism which was related to the dynamics of ECM. It turned out that the degradation and biosynthesis of chondroitin sulfate (CS) were elevated, suggesting that the structure of CS might be destructed under ammonia-N stress and CS played an important role in maintaining gill structure. It was enlightening that the destructions occurred in extracellular regions were vital to gill damage. Third, ammonia-N stress induced a series of cellular responses including enhanced apoptosis, active inflammation, and inhibited proliferation which were closely linked and jointly led to the impairment of gill. Our results provided some insights into the physiological changes induced by ammonia-N and enriched the understandings of gill damage under environmental stress.

The immunotoxicity mechanism of hemocytes in Chlamys farreri incubated with noradrenaline and benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide alone or in combination.

Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) is the active intermediate metabolite of benzo[a]pyrene (B[a]P) and is considered the ultimate immunotoxicant. The neuroendocrine immunoregulatory network of bivalves is affected under pollutant stress. Besides, bivalves are frequently affected by pollutants in marine environments, yet the combined effects of neuroendocrine factors and detoxification metabolites on bivalves under pollutant stress and the signal pathways that mediate this immunoregulation are not well understood. Therefore, we incubated the hemocytes of Chlamys farreri with the neuroendocrine factor noradrenaline (NA) and the B[a]P detoxification metabolite BPDE, alone or in combination, to examine the immunotoxic effects of NA and BPDE on the hemocytes in C. farreri. Furthermore, the effects of NA and BPDE on the hemocyte signal transduction pathway were investigated by assessing potential downstream targets. The results revealed that NA and BPDE, alone or in combination, resulted in a significant decrease in phagocytic activity, bacteriolytic activity and the total hemocyte count. In addition, the immunotoxicity induced by BPDE was further exacerbated by co-treatment with NA, and the two showed synergistic effects. Analysis of signaling pathway factors showed that NA activated G proteins by binding to α-AR, which transmitted information to the Ca2+-NF-κB signaling pathway to regulate the expression of phagocytosis-associated proteins and regulated cytokinesis through the cAMP signaling pathway. BPDE could activate PTK and affect phagocytosis and cytotoxicity proteins through Ca2+-NF-κB signal pathway, also affect the regulation of phagocytosis and cytotoxicity by inhibiting the AC-cAMP-PKA pathway to down-regulate the expression of NF-κB and CREB. In addition, BPDE and NA may affect the immunity of hemocytes by down-regulating phagocytosis-related proteins through inhibition of the lectin pathway, while regulating the expression of cytotoxicity-related proteins through the C-type lectin. In summary, immune parameters were suppressed through Ca2+ and cAMP dependent pathways exposed to BPDE and the immunosuppressive effects were enhanced by the neuroendocrine factor NA.

Study on Corrosion Behavior of Porous Pure Copper Based on Electrochemistry and Scanning Kelvin Probe.

Porous metals are widely used in filtration and separation, flame retardant explosion-proof, biomedical application, etc. Compared with its corresponding dense metal, the presence of porous structures also leads to different corrosive performances in porous metal. Some studies have utilized the weight loss method, electrochemical impedance to evaluate porous metal corrosion behavior; however, the influence of pore structure on metal corrosion is still ambiguous, and present methods used for analyses of porous metal corrosion are statistical averages of the corrosion behavior of the entire porous material, which cannot accurately reflect the corrosion behavior inside the pores. Herein, we prepare the porous copper samples with 0, 24, 72, and 96 pores using a mechanical process, and employ scanning Kelvin probe combined with electrochemical polarization and impedance spectroscopy to test the corrosion performance of the porous copper in static and dynamic NaCl solutions. The relevant results indicate that in the static solution, the corrosion resistance of the samples gradually increases with the rise in the number of pores. By contrast, in the dynamic solution, the 24-pore sample is more susceptible to corrosion than the sample without the pore.

The immunotoxicity mechanism of NH4Cl exposure to Litopenaeus vannamei based on the cerebral ganglion-eyestalk-haemocytes axis.

Ammonia nitrogen, as a water environmental toxin, poses a potential threat to aquatic animals. Although NH4Cl stress is known to cause immunotoxicity, mechanistic pathways linking stress networks in the neuroendocrine system to immunotoxicity remain poorly understood. In this study, firstly, using transcriptome analysis of cerebral ganglion and eyestalk in shrimp, we identified significant changes in genes related to biogenic amines, acetylcholine, crustacean hyperglycemic hormones, and neuropeptide F. Additionally, expression patterns of neuroendocrine factors in different tissues of shrimp were evaluated to explore the sources of these factors. Here, we showed that NH4Cl exposure activates acetylcholine (ACh) neurons in cerebral ganglion of shrimp and dramatically upregulates high affinity choline transporter 1 (ChT1) gene expression. The knockdown of ChT1 gene enhanced the immunity of haemocytes in shrimp compared with saline and GFP dsRNA groups. And after eyestalk ablation, the levels of neuroendocrine factors in the cerebral ganglion and thoracic ganglion were disturbed, and haemocytes parameters induced by NH4Cl were significantly decreased. Combined with different doses of NH4Cl exposure experiments, we demonstrated that: (1) In a short period of NH4Cl exposure, the neuroendocrine factors CRH-ACTH-cortisol and 5-HT-DA in the cerebral ganglion-eyestalk axis of shrimp play a major role in regulating haemocytes immunity; (2) With the prolongation of exposure, the immunotoxicity induced by NH4Cl was mainly due to the release of more ACh in the cerebral ganglion, which promoted the release of NPF in the thoracic ganglion, and CHH and NPF in the eyestalk, as well as weakened the effect of biogenic amines. Subsequently, these neuroendocrine factors regulate immunity through intracellular signaling pathways. Collectively, these results established a new mechanism that NH4Cl might directly regulate haemocytes immunotoxicity through the cerebral ganglion and thoracic ganglion; or through the cerebral ganglion-eyestalk axis or cerebral ganglion-thoracic ganglion axis cause haemocytes immunotoxicity.

Potential molecular mechanism underlying the harmed haemopoiesis upon Benzo[a]pyrene exposure in Chlamys farreri.

Benzo[a]pyrene (B[a]P), a ubiquitous contamination in the marine environments, has the potential to impact the immune response of bivalves by affecting the hemocyte parameters, especially total hemocyte count (THC). THC is mainly determined by haematopoietic mechanisms and apoptosis of hemocytes. Many studies have found that B[a]P can influence the proliferation and differentiation of hemocytes. However, the link between the toxic mechanisms of haematopoietic and environmental pollutants is not explicitly stated. This study is to investigate the toxic effects of B[a]P on haematopoietic mechanisms in C. farreri. Through the tissue expression distribution experiment and EDU assay, gill is identified as a potential haematopoietic tissue in C. farreri. Subsequently, the scallops were exposed to B[a]P (0.05, 0.5, 5 µg/L) for 1d, 3d, 6d, 10d and 15d. Then BPDE content, DNA damage, gene expression of haematopoietic factors and haematopoietic related pathways were determined in gill and hemocytes. The results showed that the expression of CDK2 was significantly decreased under B[a]P exposure through three pathways: RYR/IP3-calcium, BPDE-CHK1 and Notch pathway, resulting in cell cycle arrest. In addition, B[a]P also significantly reduced the number of proliferating hemocytes by affecting the Wnt pathway. Meanwhile, B[a]P can significantly increase the content of ROS, causing a downregulation of FOXO gene expression. The gene expression of Notch pathway and ERK pathway was also detected. The present study suggested that B[a]P disturbed differentiation by multiple pathways. Furthermore, the expression of SOX11 and CD9 were significantly decreased, which directly indicated that differentiation of hemocytes was disturbed. In addition, phagocytosis, phenoloxidase activity and THC were also significant decreased. In summary, the impairment of haematopoietic activity in C. farreri further causes immunotoxicity under B[a]P exposure. This study will improve our understanding of the immunotoxicity mechanism of bivalve under B[a]P exposure.

Effects of coexposure to noise and mixture of toluene, ethylbenzene, xylene, and styrene (TEXS) on hearing loss in petrochemical workers of southern China.

Many harmful factors existing simultaneously with noise are reported to induce hearing impairment, such as organic solvents. However, the existing hearing safety limits and current risk assessment for hearing loss rely on single noise exposure. It is urgent to clarify the combined effect of noise and other harmful factors on hearing loss. Petrochemical workers are always exposed to noise and organic solvents, mainly benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS), while the combined effect of their coexposure on hearing remains unclear. Herein we conducted a cross-sectional survey, measuring pure-tone audiometry of 1496 petrochemical workers in southern China. Participants exposed to BTEXS were 569, 524, 156, 452, and 177 respectively. Individual cumulative noise exposure (CNE) levels and BTEXS exposure were assessed. The average CNE was 93.27 ± 4.92 dB(A)·years, and the concentrations of BTEXS were far below the occupational exposure limits of China. Logistic regression analyses showed that CNE was consistently positively associated with hearing loss (HL) and high-frequency hearing loss (HFHL) but not related to speech-frequency hearing loss (SFHL). Compared with participants in the lowest quartile of CNE, those in the highest quartile showed an OR of 5.229 (95% CI: 3.179, 8.598) for HFHL. Two-pollutant model analysis indicated that TEXS exposure was positively associated with HL (OR 1.679, 95%CI 1.086, 2.597), SFHL (OR 2.440, 95%CI 1.255, 4.744), and HFHL (OR 1.475, 95%CI 1.077, 2.020). However, no interactions were observed between CNE and TEXS coexposure on hearing loss. In our study, covariates including smoking and drinking status, body mass index (BMI), ear protection and personal protective equipment, and use of earphone/headphone were adjusted. In conclusion, coexposure to noise and low-level TEXS could induce more severe damage on hearing function than exposure to each alone, especially SFHL. Therefore, petrochemical workers simultaneously exposed to noise and TEXS, even at low-level, should be included in hearing protection programs.

Assessment of health risk and dose-effect of DNA oxidative damage for the thirty chemicals mixture of parabens, triclosan, benzophenones, and phthalate esters.

Humans are constantly exposed to parabens (PBs), triclosan (TCS), benzophenones (BPs), and phthalate esters (PAEs) due to the widespread existence of these chemicals in personal care products (PCPs), and the high frequency of usage for humans. Previous studies indicated each class of the above-mentioned chemicals can exhibit potential adverse effects on humans, in particular DNA oxidative damage. However, the health risk assessment of combined exposures to multiple PCPs is limited, especially the overall dose-effect of mixtures of these chemicals on DNA oxidative damage. In this study, we measured the urinary levels of 6 PBs, TCS, 8 BPs, 15 metabolites of PAEs (mono-PAEs), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) from 299 adults simultaneously. PBs, TCS, BPs, and mono-PAEs were frequently detected in urinary samples with median concentrations of 52.888, 0.737, 1.305, and 141.381 ng/ml, suggesting a broad, low-level exposure among participants. Risk assessments indicated approximately 22% and 15% of participants suffered health risks (Hazard index >1) from exposure to TCS and PAEs. The relationship between 8-OHdG levels and chemical exposure was estimated by Bayesian kernel machine regression (BKMR) models. It indicated an overall positive correlation between the mixture of these chemicals and 8-OHdG, with methylparaben and mono-benzyl phthalate contributing the most to this association. Of note, sex-related differences were observed, in which exposure to PCPs led to higher health risks and more pronounced dose-effect on DNA damage in the female population. Our novel findings reveal the health risks of exposure to low-level PCPs mixtures and further point out the overall dose-response relationship between DNA oxidative damage and PCP mixtures.

Benzene Exposure Leads to Lipodystrophy and Alters Endocrine Activity In Vivo and In Vitro.

Benzene is a ubiquitous pollutant and mainly accumulates in adipose tissue which has important roles in metabolic diseases. The latest studies reported that benzene exposure was associated with many metabolic disorders, while the effect of benzene exposure on adipose tissue remains unclear. We sought to investigate the effect using in vivo and in vitro experiments. Male adult C57BL/6J mice were exposed to benzene at 0, 1, 10 and 100 mg/kg body weight by intragastric gavage for 4 weeks. Mature adipocytes from 3T3-L1 cells were exposed to hydroquinone (HQ) at 0, 1, 5 and 25 µM for 24 hours. Besides the routine hematotoxicity, animal experiments also displayed significant body fat content decrease from 1 mg/kg. Interestingly, the circulating non-esterified fatty acid (NEFA) level increased from the lowest dose (ptrend < 0.05). Subsequent analysis indicated that body fat content decrease may be due to atrophy of white adipose tissue (WAT) upon benzene exposure. The average adipocyte area of WAT decreased significantly even from 1 mg/kg with no significant changes in total number of adipocytes. The percentages of small and large adipocytes in WAT began to significantly increase or decrease from 1 mg/kg (all p < 0.05), respectively. Critical genes involved in lipogenesis and lipolysis were dysregulated, which may account for the disruption of lipid homeostasis. The endocrine function of WAT was also disordered, manifested as significant decrease in adipokine levels, especially the leptin. In vitro cell experiments displayed similar findings in decreased fat content, dysregulated critical lipid metabolism genes, and disturbed endocrine function of adipocytes after HQ treatment. Pearson correlation analysis showed positive correlations between white blood cell (WBC) count with WAT fat content and plasma leptin level (r = 0.330, 0.344, both p < 0.05). This study shed light on the novel aspect that benzene exposure could induce lipodystrophy and disturb endocrine function of WAT, and the altered physiology of WAT might in turn affect benzene-induced hematotoxicity and metabolic disorders. The study provided new insight into understanding benzene-induced toxicity and the relationship between benzene and adipose tissue.

Risk assessment and dose-effect of co-exposure to benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS) on pulmonary function: A cross-sectional study.

Inhalation is the most frequent route and the lung is the primary damaged organ for human exposure to benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS). However, there is limited information on the risk and dose-effect of the BTEXS mixture on pulmonary function, particularly the overall effect. We conducted a cross-sectional study in a petrochemical plant in southern China. Spirometry and cumulative exposure dose (CED) of BTEXS were used to measure lung function and exposure levels for 635 workers in 2020, respectively. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were tested and interpreted as percentages to predicted values [FVC or FEV1% predicted], and FEV1 to FVC ratio [FEV1/FVC (%)]. We found the reduction in FVC% predicted and the risk of lung ventilation dysfunction (LVD) and its two subtypes (mixed and restrictive ventilation dysfunction, MVD, and MVD) were significantly associated with BTEXS individuals. In addition, pulmonary function damage associated with BTEXS was modified by the smoking status and age. Generalized weighted quantile sum (gWQS) regressions were used to estimate the overall dose-effect on lung function damage induced by the BTEXS mixture. Our results show wqs, an index of weighted quartiles for BTEXS, was potentially associated with the reduction in FVC and FEV1% predicted with the coefficients [95% confidence intervals (CI)] between -1.136 (-2.202, -0.070) and -1.230 (-2.265, -0.195). Odds ratios (ORs) and 95% CIs for the wqs index of LVD, MVD, and RVD were 1.362 (1.129, 1.594), 1.323 (1.084, 1.562), and 1.394 (1.096, 1.692), respectively. Furthermore, xylene, benzene, and toluene in the BTEXS mixture potentially contribute to the development of lung function impairment. Our novel findings demonstrated the dose-response relationships between pulmonary function impairment and the BTEXS mixture and disclosed the potential key pollutants in the BTEXS mixture.

Association between exposure to a mixture of benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS) and small airways function: A cross-sectional study.

BACKGROUND: Lung is one of the primary target organs of benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS). Small airways dysfunction (SAD) might be a sensitive indicator of early chronic respiratory disease. Here, we explored the relationships between exposure to BTEXS and small airways function, and identified the priority control pollutants in BTEXS mixtures. METHODS: 635 petrochemical workers were recruited. Standard spirometry testing was conducted by physicians. The cumulative exposure dose (CED) of BTEXS for each worker was estimated. The peak expiratory flow (PEF), forced expiratory flow between 25 and 75% of forced vital capacity (FEF25∼75%), and the expiratory flow rate found at 25%, 50%, and 75% of the remaining exhaled vital capacity (MEF25%, MEF50%, and MEF75%) were measured. SAD was also evaluated based on measured parameters. The associations between exposure to BTEXS individuals or mixtures and small airways function were evaluated using generalized linear regression models (GLMs) and quantile g-computation models (qgcomp). Meanwhile, the weights of each homolog in the association were estimated. RESULTS: The median CED of BTEXS are 9.624, 19.306, 24.479, 28.210, and 46.781 mg/m3·years, respectively. A unit increase in ln-transformed styrene CED was associated with a decrease in FEF25∼75% and MEF50% based on GLMs. One quartile increased in BTEXS mixtures (ln-transformed) was significantly associated with a 0.325-standard deviation (SD) [95% confidence interval (CI): -0.464, -0.185] decline in FEF25∼75%, a 0.529-SD (95%CI: -0.691, -0.366) decline in MEF25%, a 0.176-SD (95%CI: -0.335, -0.017) decline in MEF75%, and increase in the risk of abnormal of SAD [risk ratios (95%CI): 1.520 (95%CI: 1.143, 2.020)]. Benzene and styrene were the major chemicals in BTEXS for predicting the overall risk of SAD. CONCLUSION: Our novel findings demonstrate the significant association between exposure to BTEXS mixture and small airways function decline and the potential roles of key homologs (benzene and styrene) in SAD.

MiR-486-5p-directed MAGI1/Rap1/RASSF5 signaling pathway contributes to hydroquinone-induced inhibition of erythroid differentiation in K562 cells.

Bone marrow failure is a characteristic effect of benzene exposure. Our previous study has shown that miR-486-5p is involved in benzene induced-suppression of erythroid differentiation. However, the mechanism of miR-486-5p to initiate the above process remains unclear. In this study, we used miRTar software to predict putative miRNA targets and pathway. We found that miR-486-5p may target Ras-associated protein-1 (Rap1) signaling pathway-associated genes. Our in vitro study further showed significant dose-dependent upregulation of MAGI1 and RASSF5 expressions in hydroquinone (HQ)-induced suppression of erythroid differentiation of K562 cells. Over-expression or down-regulation of miR-486-5p altered MAGI1 and RASSF5 expression and modified erythroid differentiation. Dual-luciferase reporter assay and fluorescence-based RNA electrophoresis mobility assay (FREMSA) further confirmed that miR-486-5p directly bound to the 3'-untranslated region (3'-UTR) of MAGI1 and RASSF5. In addition, the expressions of RAPGEF2 and RAP1A, which are downstream genes of MAGI1, were also significantly increased when HQ inhibited erythroid differentiation. Knockdown of MAGI1 reversed HQ-induced inhibition of erythroid differentiation via downregulation of RAPGEF2, RAP1A and RASSF5. Together, these data indicate that miR-486-5p directly targets MAGI1 and RASSF5 and integrates with Rap1 signaling to modify HQ-induced inhibition of erythroid differentiation in K562 cells.

Assessment of waste hardened cement mortar utilization as an alternative sorbent to remove SO2 in flue gas.

Developing efficient low-cost absorbents has been recognized as a prerequisite for industrial application of wet flue gas desulfurization (WFGD). Herein, hardened cement mortar (HCM) particles developed from waste concrete blocks were used as an innovative absorbent for SO2. The results show that the SO2 in flue gas can be completely absorbed by the highly alkaline HCM slurry. Under optimum operating conditions, 0.8 g of SO2 was retained by per gram of HCM. Under acid conditions produced upon dissolving SO2 in water, the Ca-rich compounds in HCM particles can continuously release Ca2+ and OH- into the HCM slurry. The Ca2+ ions released can effectively combine with SO32-, resulting in the absorption of SO2 dissolved in water. The dissolution process of HCM particles is well described by the pseudo-second-order model. The desulphurization byproduct was characterized by X-Ray diffraction (XRD) analysis, scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy and energy dispersive spectrometry (EDS). The results show that the desulphurization product mainly consists of gypsum. The technology developed provides a type of new material for removing SO2 in waste flue gas. It also offers an innovative solution for the disposal of waste concrete which is also a global environmental concern.

Fines isolated from waste concrete as a new material for the treatment of phosphorus wastewater.

Waste concrete is a key component of construction and demolition (C&D) waste produced in billions of tons. Exploring new technology for recycling waste concrete has become a global concern. Meanwhile, phosphorus (P) removal from wastewater consumes lots of natural minerals, leading to a heavy burden on the environment. In this study, the cement paste powder (HCPP) was used to remove phosphorus from wastewater. The results indicate that both HCPP and thermally modified HCPP (MHCPP) are effective phosphorus removal materials, with a maximum P-binding capacity of 3.9-mg P/g HCPP and 31.2-mg P/g MHCPP, respectively. The phosphorus removal mechanism of HCPP and MHCPP was also proposed: (1) Ca2+ and OH- can release from the surface of the HCPP or MHCPP to wastewater, forming a high-alkaline and Ca-rich solution; (2) hydrolysis of phosphorus species in the high-alkaline solution environment creates HPO42- species; (3) the HPO42- combines with Ca2+ and H2O, resulting in the formation of brushite; (4) the brushite precipitated from wastewater and adhered on the surface of the HCPP or the MHCPP particles. The study provides a new and low-cost material for treatment of phosphorus wastewater. Further, the study also offers a new approach for reusing of waste concrete fines.

The crystallization and structure features of barium-iron phosphate glasses.

The crystallization and structure features of xBaO·(90-x)(60P2O5-40Fe2O3)·10CaF2 glasses, where x=0, 5, 10, 15 and 20 mol%, are investigated in details by using X-ray diffraction analysis, Fourier transform infrared spectroscopy, Raman spectroscopy and differential thermal analysis. It is found that the major crystalline phase of barium iron phosphate glasses annealed between 650 °C and 850 °C is FePO4, and the crystallization is restrained by barium. The predominant infrared absorption band is attributed to the antisymmetric stretching vibrations of (PO3)(2-) in Q(1) units. Raman and Fourier transform infrared spectra reveal that the glasses' main structural networks are Q(1) and Q(0) tetrahedrons connected by P-O-P linkages. Moreover, the glass transition temperature increases with BaO content, which suggests that barium can strengthen the thermal stability of the iron phosphate glass.