Although cadmium (Cd) is a toxic heavy metal that reportedly causes liver injury, few studies have investigated biomarkers of Cd-induced liver injury. The purpose of this study is to investigate the role of bile acid (BA) in Cd-induced liver injury and determine reliable and sensitive biochemical parameters for the diagnosis of Cd-induced liver injury. In this study, 48 Sprague-Dawley rats were randomly divided into six groups and administered either normal saline or 2.5, 5, 10, 20, and 40 mg/kg/d cadmium chloride for 12 weeks. A total of 403 subjects living in either a control area (n = 135) or Cd polluted area (n = 268) of Dongdagou-Xinglong (DDGXL) cohort were included, a population with long-term low Cd exposure. The BA profiles in rats' liver, serum, caecal contents, faeces, and subjects' serum were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS). Changes in rats' and subjects' liver injury indices, rats' liver pathological degeneration, and rats' liver and subjects’ blood Cd levels were also measured. Cadmium exposure caused cholestasis and an increase in toxic BAs, leading to liver injury in rats. Among them, glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), and taurodeoxycholate acid (TDCA) are expected to be potential biomarkers for the early detect of Cd-induced liver injury. Serum BAs can be used to assess Cd-induced liver injury as a simple, feasible, and suitable method in rats. Serum GUDCA, GLCA, TDCA, and TLCA were verified to be of value to evaluate Cd-induced liver injury and Cd exposure in humans. These findings provided evidence for screening and validation of additional biomarkers for Cd-induced liver injury based on targeted BA metabolomics.

Ambient particles with aerodynamic diameter <0.1 μm (PM₀.₁) have been suggested to have significant health impact. However, studies on the association between long-term PM₀.₁ exposure and human blood lipid metabolism are still limited. This study was aimed to evaluate such association based on multiple lipid biomarkers and dyslipidemia indicators. We matched the 2006–2009 average PM₀.₁ concentration simulated using the neural-network model following the WRF-Chem model with the clinical and questionnaire data of 15,477 adults randomly recruited from 33 communities in Northeast China in 2009. After controlling for social demographic and behavior confounders, we assessed the association of PM₀.₁ concentration with multiple lipid biomarkers and dyslipidemia indicators using generalized linear mixed-effect models. Effect modification by various social demographic and behavior factors was examined. We found that each interquartile range increase in PM₀.₁ concentration was associated with a 5.75 (95% Confidence interval, 3.24–8.25) mg/dl and a 6.05 (2.85–9.25) mg/dl increase in the serum level of total cholesterol and LDL-C, respectively. This increment was also associated with an odds ratio of 1.25 (1.10–1.42) for overall dyslipidemias, 1.41 (1.16, 1.73) for hypercholesterolemia, and 1.90 (1.39, 2.61) for hyperbetalipoproteinemia. Additionally, we found generally greater effect estimates among the younger participants and those with lower income or with certain behaviors such as high-fat diet. The deleterious effect of long-term PM₀.₁ exposure on lipid metabolism may make it an important toxic chemical to be targeted by future preventive strategies.

As drug abuse has become increasingly serious, carbamazepine (CBZ) is discharged into the aquatic environment with municipal sewage, causing potential harm to aquatic organisms. Here, we utilized zebrafish, an aquatic vertebrate model, to comprehensively evaluate the hepatotoxicity of CBZ. The larvae were exposed to 0.07, 0.13, and 0.26 mmol/L CBZ from 72 hpf to 144 hpf, and the adults were exposed to 0.025, 0.05, and 0.1 mmol/L CBZ for 28 days. The substantial changes were observed in the size and histopathology of livers, indicating that CBZ induced severe hepatoxicity in the larvae and adults. Oil red O staining demonstrated CBZ exposure caused severe lipid accumulation in the livers of both larvae and adults. Furthermore, CBZ exposure facilitated hepatocyte apoptosis through TUNEL staining, which was caused by rising ROS content. Subsequently, down-regulation of genes related to the Wnt pathway in exposure groups indicated that CBZ inhibited the development of liver via the Wnt/β-catenin signaling pathway. In conclusion, CBZ induced severe hepatotoxicity by promoting lipid accumulation, generating excessive ROS production, and inhibiting the Wnt/β-catenin signaling pathway in zebrafish. The results reveal the occurrence of CBZ-induced hepatotoxicity in zebrafish and clarify its mechanism of action, which potentially illustrate environmental concerns associated with CBZ exposure.

Four most concerned heavy metal pollutants, arsenic, cadmium, lead, and mercury may share common mechanisms to induce metabolic syndrome (MetS). However, recent studies exploring the relationships between MetS and metal exposure presented inconsistent findings. We aimed to clarify the relationship between heavy metal exposure biomarkers and MetS using a meta-analysis and systematic review approach. Literature search was conducted in international and the Chinese national databases up to June 2020. Of selected studies, we extracted the relevant data and evaluated the quality of each study’s methodology. We then calculated the pooled effect sizes (ESs), standardized mean differences (SMDs), and their 95% confidence intervals (CIs) using a random-effect meta-analysis approach followed by stratification analyses for control of potential confounders. Involving 55,536 participants, the included 22 articles covered 52 observational studies reporting ESs and/or metal concentrations on specific metal and gender. Our results show that participants with MetS had significantly higher levels of heavy metal exposure [pooled ES = 1.16, 95% CI: 1.09, 1.23; n = 42, heterogeneity I² = 75.6%; and SMD = 0.22, 95% CI: 0.15, 0.29; n = 32, I² = 94.2%] than those without MetS. Pooled ESs in the subgroups stratified by arsenic, cadmium, lead, and mercury were 1.04 (95% CI: 0.97, 1.10; n = 8, I² = 61.0%), 1.10 (0.95, 1.27; 11, 45.0%), 1.21 (1.00, 1.48; 12, 82.9%), and 1.26 (1.06, 1.48; 11, 67.7%), respectively. Pooled ESs in the subgroups stratified by blood, urine, and the other specimen were 1.22 (95% CI: 1.08, 1.38; n = 26, I² = 75.8%), 1.06 (1.00, 1.13; 14, 58.1%), and 2.41 (1.30, 4.43; 2, 0.0%), respectively. In conclusion, heavy metal exposure was positively associated with MetS. Further studies are warranted to examine the effects of individual metals and their interaction on the relationship between MetS and heavy metals.

Previous in vitro studies have indicated that 2,3,3′,4,4′,5-hexachlorobiphenyl (PCB 156) may be a new contributor to metabolic disruption and may further cause the occurrence of nonalcoholic fatty liver disease (NAFLD). However, no study has clarified the specific contributions of PCB 156 to NAFLD progression by constructing an in vivo model. Herein, we evaluated the effects of PCB 156 treatment (55 mg/kg, i.p.) on the livers of C57BL/6 mice fed a control diet (CD) or a high-fat diet (HFD). The results showed that PCB 156 administration increased intra-abdominal fat mass, hepatic lipid levels and dyslipidemia in the CD-fed group and aggravated NAFLD in HFD-fed group. By using transcriptomics studies and biological methods, we found that the genes expression involved in lipid metabolism pathways, such as lipogenesis, lipid accumulation and lipid β-oxidation, was greatly altered in liver tissues exposed to PCB 156. In addition, the cytochrome P450 pathway, peroxisome proliferator-activated receptors (PPARs) and the glutathione metabolism pathway were significantly activated following exposure to PCB 156. Furthermore, PCB 156 exposure increased serum transaminase levels and lipid peroxidation, and the redox-related genes were significantly dysregulated in liver tissue. In conclusion, our data suggested that PCB 156 could promote NAFLD development by altering the expression of genes related to lipid metabolism and inducing oxidative stress.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

Phosphorus (P) is an essential element in the ecosystem and the cause of the eutrophication of rivers and lakes. The river-lake ecotone is the ecological buffer zone between rivers and lakes, which can transfer energy and material between terrestrial and aquatic ecosystems. Vegetation restoration of degraded river-lake ecotone can improve the interception capacity of P pollution. However, the effects of different vegetation restoration types on sediment P cycling and its mechanism remain unclear. Therefore, we seasonally measured the P fractions and physicochemical properties of sediments from different restored vegetation (three native species and one invasive species). The results found that vegetation restoration significantly increased the sediment total P and bioavailable P content, which increased the sediment tolerance to P pollution in river-lake ecotone. In addition, the total P content in sediments was highest in summer and autumn, but lower in spring and winter. The total P and bioavailable P contents in surface sediments were the highest. They decreased with increasing depth, suggesting that sediment P assimilation by vegetation restoration and the resulting litter leads to redistribution of P in different seasons and sediment depths. Microbial biomass-P (MBP), total nitrogen (TN), and sediment organic matter (SOM) are the main factors affecting the change of sediment phosphorus fractions. All four plants’ maximum biomass and P storage appeared in the autumn. Although the biomass and P storage of the invasive species Alternanthera philoxeroides were lower, the higher bioavailable P content and MBP values of the surface sediments indicated the utilization efficiency of sediment resources. These results suggest that vegetation restoration affects the distribution and circulation of P in river and lake ecosystems, which further enhances the ecological function of the river-lake ecotone and prevents the eutrophication and erosion of water and sediment in the river-lake ecotone.

Indoor light environment has altered dramatically and exposure to light at night (LAN) potential leads to the progression of cardiometabolic conditions. However, few studies have investigated the effect of bedroom LAN exposure on cardiometabolic risk. To estimate the associations between multi-period bedroom LAN exposure with cardiometabolic risk among Chinese young adults. We objectively measured multi-period bedroom LAN intensity using portable illuminance meter in an ongoing prospective cohort (n = 484). At one-year follow-up, 230 young adults provided fasting blood samples for quantification of cardiometabolic parameters. Cardiometabolic (CM)-risk score was derived as the sum of standardized sex-specific z-scores for waist circumference (WC), mean arterial pressure (MAP), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG) and homeostasis model assessment for insulin resistance (HOMA-IR), with HDL-C multiplied by – 1. Multivariate and univariable linear regression models were used to examine associations of multi-period bedroom LAN exposure with cardiometabolic risk. Exposure to higher bedroom LAN intensity is associated with 1.47-unit increase in CM-risk score (95% CI: 0.69–2.25; P < 0.001). Besides, post-bedtime light exposure was associated with elevated fasting insulin (PBL-1h: β = 0.06, 95% CI: 0.01–0.10; PBL-4h: β = 0.33, 95% CI: 0.19–0.47) and HOMA-IR (PBL-1h: β = 0.013, 95% CI: 0–0.03; PBL-4h: β = 0.07, 95% CI: 0.04–0.11) while pre-awake light exposure was associated with elevated total cholesterol (PAL-1h: β = 0.03, 95% CI: 0.02–0.04; PAL-2h: β = 0.02, 95% CI: 0.01–0.03), triglyceride (PAL-1h: β = 0.015, 95% CI: 0.01–0.02; PAL-2h: β = 0.01, 95% CI: 0–0.02) and low-density lipoprotein cholesterol (PAL-1h: β = 0.02, 95% CI: 0.01–0.03; PAL-2h: β = 0.02, 95% CI: 0.01–0.03). Among young adults, bedroom LAN exposure was significantly associated with higher cardiometabolic risk. Furthermore, different periods of bedroom light exposure have time-dependent effect on cardiometabolic risk. Further research is needed to confirm our findings and to elucidate potential mechanisms.

This review aims to gather and summarize information about the occurrence of emerging contaminants and antibiotic resistance genes in environmental matrices in Latin America. We aim to contribute to future research by compiling a list of priority pollutants adjusted to the needs and characteristics of Latin America, according to the data presented in this study. In order to perform a comprehensive research and secure a representative and unbiased amount of quality data concerning emerging contaminants in Latin America, the research was performed within the Scopus® database in a time frame from 2000 to July 2019. The countries with higher numbers of published articles were Brazil and México, while most studies were performed in the surroundings of Mexico City and in Southern and Southeastern Brazil. The main investigated environmental matrices were drinking water and surface water. The presence of antibiotic resistance was frequently reported, mainly in Brazil. Monitoring efforts should be performed in other countries in Latin America, as well as in other regions of Brazil and México. The suggested priority list for monitoring of emerging contaminants in Latin America covers: di(2-ethylhexyl) phthalate (DEHP), bisphenol-A (BP-A), 4-nonylphenol (4-NP), triclosan (TCS), estrone (E1), estradiol (E2), ethinylestradiol (EE2), tetracycline (TC), amoxicillin (AMOX), norfloxacin (NOR), ampicillin (AMP) and imipenem (IMP). We hope this list serves as a basis for the orientation of the future research and monitoring projects to better understand the distribution and concentration of the listed emerging substances.

With the development of society and the economy, many Chinese cities are shrouded in pollution haze for much of the year. Scientific studies have identified various adverse effects of air pollutants on human beings. However, the relationships between air pollution and blood lipid levels are still unclear. The objective of this study is to explore the short and long-term effects of air pollution on eight blood lipid markers among elderly hypertension inpatients complicated with or without type 2 diabetes (T2D). Blood lipid markers which met the pre-established inclusion criteria were exported from the medical record system. Air pollution data were acquired from the official environmental protection website. Associations between the air quality index and the blood lipid indexes were analyzed by one-way ANOVA and further Bonferroni correction. In an exposure time of 7 days or longer, blood lipid markers were somewhat affected by poor air quality. However, the results could not predict whether atherosclerosis would be promoted or inhibited by poorer air condition. Changes of blood lipid markers of hypertension inpatients with or without T2D were not completely the same, but no blood lipid markers had an opposite trend between the two populations. The air quality index was associated with changes to blood lipid markers to some extent in a population of hypertension inpatients with or without T2D. Further studies are needed to investigate the potential mechanism by which air pollutants induce blood lipids changes.