Unveiling Small-Sized Plastic Particles Hidden behind Large-Sized Ones in Human Excretion and Their Potential Sources.

Health risks of microplastic exposure have drawn growing global concerns due to the widespread distribution of microplastics in the environment. However, more evidence is needed to understand the exposure characteristics of microplastics owing to the limitation of current spectrum technologies, especially the missing information on small-sized particles. In the present study, laser direct infrared spectroscopy and thermal desorption-gas chromatography-mass spectrometry combined pyrolysis using a tubular furnace (TD-GC/MS) were employed to comprehensively detect the presence of plastic particles down to 0.22 µm in human excreted samples. The results showed that polyethylene (PE), polyvinyl chloride, PE terephthalate (PET), and polypropylene dominated large-sized (>20 µm) and small-sized plastic plastics (0.22-20 µm) in feces and urine. Moreover, fragments accounted for 60.71 and 60.37% in feces and urine, respectively, representing the most pervasive shape in excretion. Surprisingly, the concentration of small-sized particles was significantly higher than that of large-sized microplastics, accounting for 56.54 and 50.07% in feces (345.58 µg/g) and urine (6.49 µg/mL). Significant positive correlations were observed between the level of plastic particles in feces and the use of plastic containers and the consumption of aquatic products (Spearman correlation analysis, p < 0.01), suggesting the potential sources for plastic particles in humans. Furthermore, it is estimated that feces was the primary excretory pathway, consisting of 94.0% of total excreted microplastics daily. This study provides novel evidence regarding small-sized plastic particles, which are predominant fractions in human excretion, increasing the knowledge of the potential hazards of omnipresent microplastics to human exposure.

Optimum Parameters in Ultrasound Coherent Plane Wave Compounding for High LPWV Estimation: Validation on Phantom and Feasibility in 10 Subjects.

OBJECTIVES: The aim of this study is to determine the optimum and fine values of the number and transmission angles of tilted plane waves for coherent plane-wave compounding (CPWC)-based high local pulse wave velocity (LPWV) estimation. METHODS: A Verasonics system incorporating a linear array probe L14-5/38 with 128 elements and a pulsatile pump, CompuFlow1000, were used to acquire radio frequency data of 3, 5, 7, and 9 tilted plane wave sequences with angle intervals from 0° to 12° with a coarse interval increment step of 1°, and the angle intervals from 0° to 2° with a fine interval increment step of 0.25° from a carotid vessel phantom with the LPWV of 13.42 ± 0.90 m/s. The mean value, standard deviation, and coefficients of variation (CV) of the estimated LPWVs were calculated to quantitatively assess the performance of different configurations for CPWC-based LPWV estimation. Ten healthy human subjects of two age groups were recruited to assess the in vivo feasibility of the optimum parameter values. RESULTS: The CPWC technique with three plane waves (PRF of 12 kHz corresponding to a frame rate of 4000 Hz) with an interval of 0.75° had LPWVs of 13.52 ± 0.08 m/s with the lowest CV of 1.84% on the phantom, and 5.49 ± 1.46 m/s with the lowest CV of 12.35% on 10 subjects. CONCLUSIONS: The optimum parameters determined in this study show the best repeatability of the LPWV measurements with a vessel phantom and 10 healthy subjects, which support further studies on larger datasets for potential applications.

Association Analysis of Gene Sequencing by NeoSeq Combined with Tandem Mass Spectrum and Four Neonatal Diseases.

BACKGROUND: NeoSeq is a new method of gene sequencing for newborn screening. The goal is to explore the relationship between gene sequencing by NeoSeq combined with tandem mass spectrum (TMS) and four neonatal diseases. METHODS: A total of 1,989 newborns from August 2010 to December 2021 were enrolled. The case number of congenital hypothyroidism, phenylketonuria, adrenocortical hyperplasia, and glucose-6-phosphate dehydrogenase deficiency was counted, and the results of gene sequencing by NeoSeq and TMS were analyzed. RESULTS: The proportion of male newborns was higher than that of female newborns (51.68% vs. 48.32%). The detection rate of glucose-6-phosphate dehydrogenase deficiency was higher than that of the other three diseases (0.60% vs. 0.05%, 0.05%, 0.15%). A total of 121 newborns were recalled from 1989 newborns by traditional screening technique, and TMS detected phenylketonuria, citrullinemia, glutaric acidemia type I, and 3-methylcro-tonyl-CoA carboxylase deficiency in 1 newborn each. Gene sequencing by NeoSeq of newborns with positive TMS results confirmed the presence of susceptibility genes, and 17 of 1,868 newborns with normal biochemical tests had pathogenic genes. CONCLUSIONS: The incidence of glucose-6-phosphate dehydrogenase deficiency is relatively higher in four neonatal diseases, and the detection rate of gene sequencing by NeoSeq combined with TMS is high.

Developmental toxicity of disinfection by-product monohaloacetamides in embryo-larval stage of zebrafish.

As an emerging class of nitrogenous disinfection by-products (N-DBPs), haloacetamides (HAcAms) have been widely detected in drinking water. Limited toxicity studies have shown an inconsistent toxicity of monoHAcAms, including CAcAm, BAcAm and IAcAm. In this study, the developmental toxicity of monoHAcAms was evaluated in embryo-larval stage of zebrafish. Embryos were exposed to one concentration of 2.50, 5.00, 10.0, 20.0, 40.0 and 80.0 mg/L monoHAcAms from 4 h post-fertilization (hpf) to 120 hpf. Multiple endpoints, including hatching rate, morphological abnormalities, mortality as well as locomotor behavior were assessed at specified stages (24, 48, 72, 96 and 120 hpf). Results showed that 80 mg/L CAcAm and 40 mg/L BAcAm significantly decreased the hatching rate, IAcAm decreased the hatching rate and delayed the hatching process in a concentration-dependent manner with an EC50 of 16.37 mg/L at 72 hpf. The frequency and severity order of morphological abnormalities increased with the raised exposure concentrations and prolonged exposure time, and the corresponding EC50 at 96 hpf were 21.10, 9.77 and 16.60 mg/L for CAcAm, BAcAm and IAcAm, respectively. MonoHAcAms exposure resulted in a time- and dose-dependent response in mortality and the calculated LC50 at 72 hpf were 38.44, 17.74 and 28.82 mg/L for CAcAm, BAcAm and IAcAm, respectively. Based on EC50 for morphological abnormalities and LC50, a toxicity rank order of BAcAm > IAcAm > CAcAm was observed. Different degrees of hyperactivity and hypoactivity were observed from locomotor behavior analysis in larvae from ≤10.0 mg/L monoHAcAms exposure groups. The light-dark periodic change was disappeared in larvae of 10.0 mg/L BAcAm exposure group. In summary, our study showed that monoHAcAms were developmentally toxic to zebrafish even at very low concentrations and BAcAm exerted higher toxicity than IAcAm and CAcAm. These results will further our understanding of the toxicity of HAcAms and its potential toxicological impact on human and ecological environment.

Involvement of the delayed rectifier outward potassium channel Kv2.1 in methamphetamine-induced neuronal apoptosis via the p38 mitogen-activated protein kinase signaling pathway.

Methamphetamine (Meth) is an illicit psychostimulant with high abuse potential and severe neurotoxicity. Recent studies have shown that dysfunctions in learning and memory induced by Meth may partially reveal the mechanisms of neuronal channelopathies. Kv2.1, the primary delayed rectifying potassium channel in neurons, is responsible for mediating apoptotic current surge. However, whether Kv2.1 is involved in Meth-mediated neural injury remains unknown. In the present study, the treatment of primary cultured hippocampal neurons with Meth indicated that Meth induced a time- and dose-dependent augmentation of Kv2.1 protein expression, accompanied by elevated cleaved-caspase 3 and declined bcl-2/bax ratio. The blockage of Kv2.1 with the inhibitor GxTx-1E or the knockdown of the channel noticeably abrogated the pro-apoptotic effects mediated by Meth, demonstrating the specific roles of Kv2.1 in Meth-mediated neural damage. Additionally, the p38 mitogen-activated protein kinase (MAPK) signaling was demonstrated to be involved in Meth-mediated Kv2.1 upregulation and in the subsequent pro-apoptotic effects, as treatment with a p38 MAPK inhibitor significantly attenuated Meth-mediated Kv2.1 upregulation and cell apoptosis. Of note, PRE-084, a sigma-1 receptor agonist, obviously attenuated Meth-induced upregulation of Kv2.1 expression, neural apoptosis and p38 MAPK activation. Taken together, these results reveal a novel mechanism involved in Meth-induced neural death with implications for therapeutic interventions for Meth users.

Meta-analysis of genome-wide association data identifies novel susceptibility loci for obesity.

Obesity is a major public health problem with strong genetic determination. Multiple genetic variants have been implicated for obesity by conducting genome-wide association (GWA) studies, primarily focused on body mass index (BMI). Fat body mass (FBM) is phenotypically more homogeneous than BMI and is more appropriate for obesity research; however, relatively few studies have been conducted on FBM. Aiming to identify variants associated with obesity, we carried out meta-analyses of seven GWA studies for BMI-related traits including FBM, and followed these analyses by de novo replication. The discovery cohorts consisted of 21 969 individuals from diverse ethnic populations and a total of over 4 million genotyped or imputed SNPs. The de novo replication cohorts consisted of 6663 subjects from two independent samples. To complement individual SNP-based association analyses, we also carried out gene-based GWA analyses in which all variations within a gene were considered jointly. Individual SNP-based association analyses identified a novel locus 1q21 [rs2230061, CTSS (Cathepsin S)] that was associated with FBM after the adjustment of lean body mass (LBM) (P = 3.57 × 10(-8)) at the genome-wide significance level. Gene-based association analyses identified a novel gene NLK (nemo-like kinase) in 17q11 that was significantly associated with FBM adjusted by LBM. In addition, we confirmed three previously reported obesity susceptibility loci: 16q12 [rs62033400, P = 1.97 × 10(-14), FTO (fat mass and obesity associated)], 18q22 [rs6567160, P = 8.09 × 10(-19), MC4R (melanocortin 4 receptor)] and 2p25 [rs939583, P = 1.07 × 10(-7), TMEM18 (transmembrane protein 18)]. We also found that rs6567160 may exert pleiotropic effects to both FBM and LBM. Our results provide additional insights into the molecular genetic basis of obesity and may provide future targets for effective prevention and therapeutic intervention.

How ABA block polymers activate cytochrome c in toluene: molecular dynamics simulation and experimental observation.

While the conjugation of enzymes with ABA copolymers has resulted in increased enzymatic activities in organic solvents, by several orders of magnitude, the underpinning mechanism has not been fully uncovered, particularly at the molecular level. In the present work, a coarse-grained molecular dynamics simulation of cytochrome c (Cyt c) conjugated with a PEO-PPO-PEO block copolymer (ABA) in toluene was simulated with Cyt c as a control. It is shown that the hydrophilic segments (PEO) of the conjugated block copolymer molecules tend to entangle around the hydrophilic patch of Cyt c, while the hydrophobic segments (PPO) extend into the toluene. At a lower temperature, the PEO tails tend to form a hairpin structure outside the conjugated protein, whereas the Cyt c-ABA conjugates tend to form larger aggregates. At a higher temperature, however, the PEO tails tend to adsorb onto the hydrophilic protein surface, thus improving the suspension of the Cyt c-ABA conjugates and, consequently, the contact with the substrate. Moreover, the temperature increase drives the conformational transition of the active site of Cyt c-ABA from an "inactive state" to an "activated state" and thus results in an enhanced activity. To validate the above simulations, Cyt c was conjugated to F127, an extensively used ABA copolymer. By elevating the temperature, a decrease in the average size of the Cyt c-F127 conjugates along with a great increase in the apparent activity in toluene was observed, as can be predicted from the molecular dynamics simulation. The above mentioned molecular simulations offer a molecular insight into the temperature-responsive behaviour of protein-ABA copolymers, which is helpful for the design and application of enzyme-polymer conjugates for industrial biocatalysis.

Intraarticular gene transfer of SPRY2 suppresses adjuvant-induced arthritis in rats.

AKT and ERK pathways have been implicated as therapeutic targets for human rheumatoid arthritis (RA), fibroblast-like synoviocytes (FLS) inhibition, and thus RA treatment. Sprouty2 (SPRY2) has been known as a tumor suppressor by blocking both ERK and AKT signaling cascades. Whether SPRY2 can function as a suppressor of tumor-like inflammatory FLS and RA through negatively regulating AKT and ERK activation has not been reported. The purpose of this study was to determine whether SPRY2 might have antiarthritic effects in experimental animal model of RA. We first determined that expression of SPRY2 mRNA was decreased in FLS from patients with RA compared with patients with osteoarthritis (OA). Further studies demonstrated that intraarticular gene transfer with AdSPRY2, the recombinant adenovirus containing SPRY2 complementary DNA, resulted in a significant suppression of rat adjuvant-induced arthritis (AIA) compared with the control AdGFP, the adenoviral vector encoding green fluorescent protein, as reflected in both clinical and histological observations. AdSPRY2 suppressed the production of proinflammatory cytokines and matrix metalloproteinases (MMPs), and the activation of ERK and AKT signals in AIA ankle joints. These results suggest that using SPRY2 to block the AKT and ERK pathways effectively reduces the inflammatory responses and arthritic progression in AIA. Thus, the development of an immunoregulatory strategy based on SPRY2 may therefore have therapeutic potential in the treatment of RA.

Involvement of mitogen-activated protein kinase and NF-κB signaling pathways in perfluorooctane sulfonic acid-induced inflammatory reaction in BV2 microglial cells.

Microglial activation is closely related to the pathogenesis of neurodegenerative diseases by producing proinflammatory cytokines. Perfluorooctane sulfonic acid (PFOS), known as an emerging persistent organic pollutant, is reported to disturb human immune homeostasis; however, whether it affects cytokine production or the immune response in the central nervous system remains unclear. The present study was aimed to explore whether PFOS contributed to inflammatory action and to investigate the corresponding mechanisms in BV2 microglia. PFOS-mediated morphologic changes, cytokine responses and signaling events were examined by light microscopy, real-time polymerase chain reaction, enzyme-linked immunosorbent assay and Western blot assays. Our results indicated that PFOS increased BV2 cells activation and simultaneously increased tumor necrosis factor alpha and interleukin-6 expression. In addition, the c-Jun N-terminal protein kinase inhibitor (SP600125), as well as ERK1/2 blocker (PD98059), transcriptionally at least, displayed anti-inflammatory properties on PFOS-elicited cytokine responses. Moreover, the inflammatory transcription factor NF-κB was specifically activated by PFOS as well. These results, taken together, suggested that PFOS exerts its functional effects on the response of microglial cell activation via, in part, the c-Jun N-terminal protein kinase, ERK and NF-κB signaling pathways with its subsequent influence on proinflammatory action.

The toxic effects of Bisphenol A on the mouse spermatocyte GC-2 cell line: the role of the Ca2+-calmodulin-Ca2+/calmodulin-dependent protein kinase II axis.

Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is known to induce male reproductive toxicity in rodents. However, its toxic effects on the germ cells are still poorly understood. It has been proposed that Ca(2+) homeostasis and Ca(2+) sensors, including calmodulin (CaM) and calmodulin-dependent protein kinase II (CaMKII), play critical roles in spermatogenesis. Therefore, in the present study, we aimed to investigate whether a perturbation in Ca(2+)-CaM-CaMKII signaling was involved in the BPA-induced injury to mouse spermatocyte GC-2spd (ts) (GC-2) cells. Our results showed that BPA (range from 0.2 to 20 µM) induced obvious GC-2 cell injury, including decreased cell viability, the release of mitochondrial cytochrome c and the activation of caspase-3. However, these processes could be partially abrogated by pretreatment with a Ca(2+) chelator (BAPTA/AM), a CaM antagonist (W7) or a CaMKII inhibitor (KN93). These results, taken together, indicate that BPA exposure contributes to male germ cell injury, which may be partially mediated through a perturbation in Ca(2+)/CaM/CaMKII signaling and the mitochondrial apoptotic process.

[Trends and forecast of hepatocellular carcinoma in Nantong, China: mortality rates from 1999 to 2011].

OBJECTIVE: To investigate the mortality rates of hepatocellular carcinoma (HCC) in Nantong,China from 1999 to 2011, in order to uncover dynamic trends and provide reasoned advice on intervention strategies to decrease HCC incidence and mortality in Nantong in the future. METHODS: Versions 10 and 9 of the WHO International Classification of Diseases (ICD-10 and ICD-9) were used to determine the number of HCC deaths in Nantong,China for the study's range of years. Thex2 test was applied to compare the HCC mortality rates according to sex and age. The Grey system GM(1,1) model was used to predict the next-5-year HCC mortality for Nantong. RESULTS: Analysis of the standardized mortality in Nantong showed a slight decreasing trend from 1999 to 2011 (x2=57 545.98, P less than 0.001),with males showing a steeper decrease than females. The total mortality of HCC during these years was 53.41 per 100,000 people,with mortality among males being significantly higher than that among females (80.81 per 100,000 people vs. 26.94 per 100,000 people; x2=13 625.42, P less than 0.001). In general, HCC mortality increased with increase in age (general trend:x2=57 545.98, P less than 0.001; male trend: x2=39 878.8, P less than 0.001; female trend: x2=20 105.3, P less than 0.001). However,HCC mortality increased significantly in women after the age of 40 and in men after the age of 35. The GM(1,1) equation was: Yt=-1265.28e(-0.0375t)+1315.5, which predicted that the HCC mortality will decrease to 25.56 per 100,000 people in 2016. CONCLUSION: Although HCC mortality generally decreased from 1999 to 2011, the rate remained high. Public health intervention strategies may be more effective if they focus on males over the age of 35 and females over the age of 40.

Molecular evolution and sequence divergence of plant chalcone synthase and chalcone synthase-Like genes.

Plant chalcone synthase (CHS) and CHS-Like (CHSL) proteins are polyketide synthases. In this study, we evaluated the molecular evolution of this gene family using representative types of CHSL genes, including stilbene synthase (STS), 2-pyrone synthase (2-PS), bibenzyl synthase (BBS), acridone synthase (ACS), biphenyl synthase (BIS), benzalacetone synthase, coumaroyl triacetic acid synthase (CTAS), and benzophenone synthase (BPS), along with their CHS homologs from the same species of both angiosperms and gymnosperms. A cDNA-based phylogeny indicated that CHSLs had diverse evolutionary patterns. STS, ACS, and 2-PS clustered with CHSs from the same species (late diverged pattern), while CTAS, BBS, BPS, and BIS were distant from their CHS homologs (early diverged pattern). The amino-acid phylogeny suggested that CHS and CHSL proteins formed clades according to enzyme function. The CHSs and CHSLs from Polygonaceae and Arachis had unique evolutionary histories. Synonymous mutation rates were lower in late diverged CHSLs than in early diverged ones, indicating that gene duplications occurred more recently in late diverged CHSLs than in early diverged ones. Relative rate tests proved that late diverged CHSLs had unequal rates to CHSs from the same species when using fatty acid synthase, which evolved from the common ancestor with the CHS superfamily, as the outgroup, while the early diverged lineages had equal rates. This indicated that late diverged CHSLs experienced more frequent mutation than early diverged CHSLs after gene duplication, allowing obtaining new functions in relatively short period of time.

Tissue accumulation of microplastics and potential health risks in human.

Microplastics have become ubiquitous throughout the environment. Humans constantly ingest and inhale microplastics, increasing concerns about the health risks of microplastic exposure. However, limited data impedes a full understanding of the internal exposure to microplastics. Herein, to evaluate microplastic exposure via the respiratory and digestive systems, we used laser direct infrared spectroscopy to identify microplastics >20 µm in size in different human tissues. Consequently, 20-100 µm microplastics were concentrated in all tissues, with polyvinyl chloride (PVC) being the dominant polymer. The highest abundance of microplastics was detected in lung tissue with an average of 14.19 ± 14.57 particles/g, followed by that in the small intestine, large intestine, and tonsil (9.45 ± 13.13, 7.91 ± 7.00, and 6.03 ± 7.37 particles/g, respectively). The abundance of microplastics was also significantly greater in females than in males (p < 0.05). Despite significant diversity, our estimation showed that the lungs accumulated the highest amounts of microplastic. Moreover, PVC particles may cause potential health risks because of their high polymer hazard index and maximal risk level. This study provides evidence regarding the occurrence of microplastics in humans and empirical data to support assessments of the health risks posed by microplastics.

Nanoparticle-stabilized liposomes for pH-responsive gastric drug delivery.

We report a novel pH-responsive gold nanoparticle-stabilized liposome system for gastric antimicrobial delivery. By adsorbing small chitosan-modified gold nanoparticles (diameter ~10 nm) onto the outer surface of negatively charged phospholipid liposomes (diameter ~75 nm), we show that at gastric pH the liposomes have excellent stability with limited fusion ability and negligible cargo releases. However, when the stabilized liposomes are present in an environment with neutral pH, the gold stabilizers detach from the liposomes, resulting in free liposomes that can actively fuse with bacterial membranes. Using Helicobacter pylori as a model bacterium and doxycycline as a model antibiotic, we demonstrate such pH-responsive fusion activity and drug release profile of the nanoparticle-stabilized liposomes. Particularly, at neutral pH the gold nanoparticles detach, and thus the doxycycline-loaded liposomes rapidly fuse with bacteria and cause superior bactericidal efficacy as compared to the free doxycycline counterpart. Our results suggest that the reported liposome system holds a substantial potential for gastric drug delivery; it remains inactive (stable) in the stomach lumen but actively interacts with bacteria once it reaches the mucus layer of the stomach where the bacteria may reside.

Identification of microplastics in human placenta using laser direct infrared spectroscopy.

Microplastics are ubiquitous in the environment, including in food and drinking water. Consequently, there is growing concern about the human health risks associated with microplastic exposure through diet. However, the occurrence of microplastics in the human body, particularly in mothers and fetuses, is incompletely understood because of the limited amount of data on their presence in the body and the human placenta. This study evaluated the presence and characteristics of microplastics in 17 placentas using laser direct infrared (LD-IR) spectroscopy. Microplastics were detected in all placenta samples, with an average abundance of 2.70 ± 2.65 particles/g and a range of 0.28 to 9.55 particles/g. Among these microplastics, 11 polymer types were identified. The microplastics were mainly composed of polyvinyl chloride (PVC, 43.27 %), polypropylene (PP, 14.55 %), and polybutylene succinate (PBS, 10.90 %). The sizes of these microplastics ranged from 20.34 to 307.29 µm, and most (80.29 %) were smaller than 100 µm. Most of the smaller microplastics were fragments, but fibers dominated the larger microplastics (200-307.29 µm). Interestingly, the majority of PVC and PP were smaller than 200 µm. This study provides a clearer understanding of the shape, size, and nature of microplastics in the human placenta. Importantly, these data also provide crucial information for performing risk assessments of the exposure of fetuses to microplastics in the future.

Occurrence and multi-pathway health risk assessment of trihalomethanes in drinking water of Wuxi, China.

Chlorination is widely used to disinfect drinking water to keep humans safe from microorganisms. During chlorination, chlorine and its compounds react with contaminants to form disinfection by-products (DBPs). Toxicological and epidemiological studies have demonstrated that trihalomethanes (THMs) are the most widely investigated DBPs in drinking water, and their exposure has been associated with some adverse health effects. However, studies about risk characteristics in this field are limited. We estimated the health risks of THMs exposure in drinking water through multi-pathways, and systematically analyzed the factors influencing health risks of THMs in Wuxi, China. A total of 488 drinking water samples were collected and analyzed for THMs from four water treatment utilities from 2008 to 2016 in Wuxi. And water exposure parameters were obtained from 602 participants by structured questionnaires. The median concentration of THMs ranged from 6.71 µg/L to 9.18 µg/L. The cumulative cancer risk of THMs exposure through multi-pathways was 1.26 × 10-4, and CHBr2Cl made the largest contribution to the total cancer risk (48.25%). The non-cancer risk of THMs exposure was 2.02 × 10-1. Health risks of the exposure to THMs in drinking water in summer were significantly higher than that in winter (P = 0.0003 for cancer risk, and P = 5.95 × 10-7 for non-cancer risk). In our study, the average individual disability-adjusted life years (DALYs) lost was 1.27 × 10-4 per person-year (ppy). This study attempted to use DALYs for risk assessment of THMs, which will provide useful information for risk comparison and prioritization of hazards in drinking water. This suggested that potential higher risk might exist, and possible measures could be considered to decrease the health risks.

Quantitative determination of bromochloroacetamide in mice urine by gas chromatography combined with salting-out assisted dispersive liquid-liquid microextraction.

Bromochloroacetamide (BCAcAm) is the main haloacetamide (HAcAm) detected in drinking water in different regions and exhibits strong cytotoxicity and genotoxicity. However, there is no appropriate method for detecting BCAcAm in urine or other biological samples, and thus, the internal exposure level in the population cannot be accurately assessed. In this study, a gas chromatography-electron capture detector (GC-ECD) was combined with salting-out assisted dispersive liquid-liquid microextraction (SA-DLLME) to develop a rapid and robust method for BCAcAm detection in urine of mice continuously exposed to BCAcAm. The factors influencing the pre-treatment procedure, including the type and volume of extraction and disperser solvents, extraction and standing time, and the amount of salt, were evaluated systematically. Under the optimised conditions, the analyte achieved good linearity in the spiked concentration range of 1.00-400.00 µg L-1, and the correlation coefficient was higher than 0.999. The limit of detection (LOD) and the limit of quantification (LOQ) were 0.17 µg L-1 and 0.50 µg L-1, respectively. The recoveries ranged from 84.20% to 92.17%. The detection of BCAcAm at three different calibration levels using this method afforded an intra-day precision of 1.95-4.29%, while the inter-day precision range was 5.54-9.82% (n = 6). This method has been successfully applied to monitor the concentration of BCAcAm in mouse urine in toxicity experiments and can provide technical support for assessing human internal exposure levels and health risks in later studies.

Urinary trihalomethane concentrations and liver function indicators: a cross-sectional study in China.

While it is known that exposure to disinfection by-products (DBPs), including trihalomethanes (THMs), impairs liver function, few epidemiological studies have explored this association. Here, we determined the concentrations of four urinary trihalomethanes (chloroform [TCM], and three Br-THMs, bromodichloromethane [BDCM], dibromochloromethane [DBCM], and bromoform [TBM]), and nine serum liver function indicators in 182 adults ≥ 18 years of age, examined at a medical examination center in Wuxi, China, in 2020 and 2021. Generalized linear model analysis revealed positive associations between urinary DBCM and alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), total protein (TP), and albumin (ALB). Urinary Br-THMs and total THMs (TTHMs) were positively associated with ALT, AST, TBIL, indirect bilirubin (IBIL), TP, and ALB (all P < 0.05). Urinary THMs were not associated with alkaline phosphatase (ALP) or glutamine transaminase (GGT) (all P > 0.05). Generalized additive model-based penalized regression splines were used to confirm these associations. In conclusion, THM exposure was associated with altered serum biomarkers of liver function.

Unveiling the traits of dry and wet pre-magnetized zero-valent iron-activated peroxymonosulfate: Degradation of oxytetracycline.

It has been previously reported that pre-magnetization could enhance the efficacy of zero-valent iron (ZVI) in removing contaminants. However, little is known about the effects and persistence of different magnetization methods on pre-magnetized ZVI (Pre-ZVI) when used in advanced oxidation processes (AOPs). Gaining a comprehensive understanding of the durability of various pre-magnetization methods in enhancing the removal efficiency of different pollutants will significantly impact the widespread utilization of Pre-ZVI in practical engineering. Herein, we investigated the efficiency of dry and wet Pre-ZVI-activated peroxymonosulfate (PMS) in eliminating oxytetracycline (OTC) and evaluated the durability of Pre-ZVI. Additionally, we examined several factors that influence the degradation process's efficiency. Our results found that the reaction constant k values corresponding to the dry Pre-ZVI/PMS system at the pH values of 3, 7, and 9 varied from approximately 0.0384, 0.0331, and 0.0349 (day 1) to roughly 0.0297, 0.0278, and 0.0314 (day 30), respectively. Meanwhile, the wet Pre-ZVI/PMS system exhibited k values ranging from approximately 0.0392, 0.0349, and 0.0374 (day 1) to roughly 0.0380, 0.0291, and 0.0322 (day 30), respectively. Moreover, we proposed four OTC degradation pathways using LC-MS/MS and density functional theory calculations. The toxicity of the degradation products was assessed using the ecological structure activity relationship and the toxicity estimation software tool. Overall, this study provides insights into the application of Pre-ZVI/PMS that can be selectively used to eliminate tetracycline antibiotics from water.