Sewage treatment plants (STPs) are considered as “hotspots” for the emergence and proliferation of antibiotic resistance. However, the impact of heavy metals contamination on dispersal of antibiotic resistance in STPs is poorly understood. This study simultaneously investigated the effect of removal of metal and antibiotic resistance as well as mobile elements at different treatment units of STPs in Delhi, India. Results showed that treatment technologies used in STPs were inefficient for the complete removal of metal and antibiotic resistance, posing an ecological risk of co-selection of antibiotic resistance. The strong correlations were observed between heavy metals, metal and antibiotic resistance, and integrons, implying that antibiotic resistance may be exacerbated in the presence of heavy metals via integrons, and that metal and antibiotic resistance share a common or closely associated mechanism. We quantified an MRG rcnA, conferring resistance to Co and Ni, and identified that it was more abundant than all MRGs, ARGs, integrons, and 16S rRNA, suggesting rcnA could be important in antibiotic resistance dissemination in the environment. The associations between heavy metals, metal and antibiotic resistance, and integrons highlight the need for additional research to better understand the mechanism of co-selection as well as to improve the removal efficacy of current treatment systems.

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.

Light at night (LAN) has received increasing attention for its potential health hazards to human and animals. However, to our knowledge, no study has explored the specific effects of bedroom nighttime light exposure on allostatic load (AL). To investigate the association between bedroom individual-level LAN exposure and AL among young adults, an integrative index manifests multiple system dysregulation. Using data from a cohort of 484 Chinese young adults aged 16–22 years. Bedroom light was objectively recorded at 1-min intervals for two nights using a portable illuminance meter. Fasting blood samples were collected at one-year follow-up for the detection of AL parameters. AL score was derived as sum of the top quartile of twelve physiological biomarkers in four systems: metabolic system (BMI, WC, TC, HDL, LDL, TG, HbA1c, INS, GLU); cardiovascular system (SBP, DBP); immune and inflammatory systems (hs-CRP), with HDL was lowest quartile. Univariate and multivariate linear regression models were used to evaluate the association between LAN intensity with AL score and separate AL parameters. The average age of subjects was 18.7 years, 64.3% were female. The mean AL score of LAN group (average LAN intensity ≥ 3lx) was significantly higher than Dim group (3.6 ± 2.6 vs. 2.7 ± 2.1; P = 0.007). For each 1 lx increase of LAN intensity was associated with 0.15-unit increase in AL score (95% CI: 0.06, 0.24; P = 0.001). Moreover, LAN group was associated with increased 1.01-unit in AL score (95% CI: 0.36–1.66; P = 0.003) compared to Dim group. Significant associations between bedroom LAN exposure with allostatic load and separate AL biomarkers were observed in our study. Keeping bedroom darkness at night may be a practicable option to reduce the wear of multiple body systems and improve human cardiometabolic health from early in life.

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.

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.

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.

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.

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.

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.