Ecotoxicology and Environmental Safety最新文献

Premature Ovarian Insufficiency refers to the premature decline in ovarian function before the age of 40, resulting in menstrual irregularities or complete cessation of menstruation, and affecting fertility. Widely used bisphenol compounds may have potential health effects, including premature ovarian insufficiency (POI). This study employs computational biology and bioinformatics to investigate the effects of bisphenols (BPs) on POI. Using bioinformatics tools, we identified potential target genes related to both bisphenols and POI, and conducted functional enrichment analysis. Further, we calculated differentially expressed genes for POI, extracted core networks, and explored immune function and screened core genes. Molecular docking and molecular dynamics simulations were used to explore the stable binding between bisphenols and core POI genes. Our results constructed a protein network of 56 potential target genes and extracted core subnetworks. Functional enrichment analysis indicated that estrogen metabolism, estrogen receptor pathways, steroid hormone metabolism, and carbohydrate and lipid metabolism may be involved in the process of BPs-induced POI. The differentially expressed genes obtained through further screening, CYP1A1 and CYP19A1, were subjected to molecular docking and dynamics simulations to reveal the mechanism by which bisphenols participate in estrogen metabolism through their stable binding. Our findings underscore the role of bisphenols in inducing POI and the potential mechanisms involved, providing new directions for further epidemiological and molecular biological research into this regulatory process.

The existing evidence indicating that prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with a range of adverse outcomes, including alterations in anthropometric indices, underscores the need for further investigation into the underlying mechanisms. This study aims to examine the effects of prenatal PAH exposure on anthropometric indices and telomere length (TL), as well as to explore whether changes in TL can serve as a predictor of alterations in anthropometric measures. The study was conducted in Shenyang, China, with 2460 pregnant women participating between 2022 and 2023. Maternal urine samples were analyzed for eleven PAH metabolites, and neonatal outcomes, such as birth weight (BW), birth length (BL), and head circumference (HC), were extracted from medical records as anthropometric indices. We employed multiple linear regression (MLR), generalized quantile g-computation (g-comp), Bayesian Kernel Machine Regression (BKMR), and mediation analysis to comprehensively assess the associations between PAH exposure and umbilical TL and neonatal outcomes. Notably, significant negative associations were found between several PAH metabolites and umbilical telomere length (TL). These metabolites included 2-hydroxy naphthalene (2-OH Nap), 1-hydroxy pyrene (1-OH Pyr), 6-hydroxy chrysene (6-OH Chr), 9-hydroxy benzo(a)pyrene (9-OH Bap), and the sum of hydroxylated PAHs (Σ-OH PAHs). Additionally, negative correlations were identified between specific PAH metabolites and HC, although no significant associations were found for BW. Birth weight showed a significant inverse relationship with metabolites such as 1-hydroxy phenanthrene (1-OH Phe), 9-hydroxy phenanthrene (9-OH Phe), and 1-hydroxy naphthalene(1-OH Nap). Results from g-comp analysis and BKMR indicated significant mixture effects of PAHs on umbilical TL and HC, with more heterogeneous effects on BW and BL. Mediation analysis indicated that alterations in umbilical TL partially mediated the associations between PAH exposure and BW and HC. Notably, metabolites such as 2-OH Nap and the Σ-OH PAHs demonstrated substantial mediation effects. Overall, our findings suggest that changes in umbilical TL partially mediate the associations between prenatal PAH exposure and HC and BW, highlighting the complex pathways through which PAH metabolites may influence neonatal development.

The abrasion of melamine cleaning sponges release microplastic fibers (MPFs) into the environment, yet the potential risks remain unknown. Here, we evaluated the ingestion, elimination, and toxic effects of melamine MPFs on Daphnia magna through acute and chronic exposures. This new type of MPFs displayed different morphology (a combination of linear and branched fibers with a length ranging from 10 to 157 μm) from the widely-studied MPFs released from textiles (longer and thicker linear fibers but no branched fibers). Although the lethality of melamine MPFs to neonates was not observed upon a short-term exposure (24 h), such effect was detected when the animals were exposed for a longer period (21 d) and showed a concentration-dependent manner. The MPFs tended to aggregate in the gut of D. magna, leading to a slow elimination compared to polystyrene microspheres. The MPFs remaining in the gut triggered an elevation in the intracellular reactive oxygen species, which further induced oxidative damage and eventually death. The long-term exposure to MPFs also stimulated D. magna to produce more offspring. Our findings show the chronic toxicity of the sponges-derived MPFs to typical freshwater zooplankton and accentuate the environmental impacts related to the extensive use of the sponges.

Nitrate (NO₃^-) pollution in groundwater is a worldwide environmental issue, particularly in developed planting-breeding areas where there is a substantial presence of nitrogen-related sources. Here, we explored the key sources and potential health risks of NO₃^- in a typical planting-breeding area in the North China Plain based on dual stable isotopes and Monte Carlo simulations. The analysis results revealed that the NO₃^- concentration ranged from 0.02 to 44.6 mg/L, with a mean value of 7.54 mg/L, along with a significant spatial variability. Analysis by combining stable isotopes (δ¹⁵N-NO₃^- and δ¹⁸O-NO₃^-) with the Bayesian isotope mixing model (MixSIAR) revealed that soil N (60.3 %) and manure and sewage (35.9 %) contributed the most NO₃^- in groundwater, followed by chemical N fertilizer (2.9 %) and atmospheric N deposition (0.8 %). However, the contribution of N fertilizer may be underestimated because it has undergone a long-term applied history and have progressively accumulated in the soil, and then promoted the entry of groundwater under frequent rainfall and irrigation practices. From the probabilistic health risk assessment, a relatively low probability of exceeding the threshold (HI=1) was observed (0.2 % for adults and 2.59 % for children); nevertheless, children still face some nonnegligible risk, particularly for the oral ingestion of drinking water at high-pollution sites. Therefore, we highlight the importance of effective management of manure and sewage from breeding plants and reduction of chemical N fertilizer usage are suggested in developed agricultural areas.

Soil nitrogen (N) transformations control N availability and plant production and pose environmental concerns when N is lost, raising issues such as soil acidification, water contamination, and climate change. Former studies suggested that soil N cycling is chiefly regulated by microbial activity; however, emerging evidence indicates that this regulation is disrupted by heavy metal (HM) contamination, which alters microbial communities and enzyme functions critical to N transformations. Environmental factors like soil organic carbon, soil texture, water content, temperature, soil pH, N fertilization, and redox status play significant roles in modulating the response of soil N cycling to HM contamination. This review examines how different HMs affect soil N processes, including N fixation, mineralization, nitrification, denitrification, dissimilatory nitrate reduction to ammonium (DNRA), and immobilization, as well as microbial activities and functional genes related to soil N transformations. The review additionally outlines the impact of HMs on environmental degradation, including the risk of soil N losses (e.g., leaching, runoff, and gaseous emissions) and depletion of soil fertility, thus threatening the sustainability of the ecosystem. The effect of edaphic factors and fertilization on soil N cycling response to HM contamination was also examined. The effect of phytoremediation, a sustainable approach to remediate HM polluted soils, on N cycling was also reviewed. Thus, this review underscores the importance of increasing research and innovative strategies to combat HM pollution's effects to enhance soil health, boost crop yields, and protect soil stability and productivity.

The existing studies on the association between multi-metal mixture exposure and cognitive function in the older adults are limited and controversial, with no studies considering the mediating effect of thyroid hormones on the connection between them. This study of 441 urban older adults assessed 21 urinary metal levels and cognitive function using the Mini-Mental State Examination (MMSE). Urinary metal levels were measured via inductively coupled plasma mass spectrometry (ICP-MS), and thyroid hormones levels were obtained from medical records. Mediation analysis evaluated the role of thyroid hormones in the link between metals exposure and cognitive function. The General Linear Model (GLM) showed negative correlations between MMSE scores and titanium (Ti), copper (Cu), rubidium (Rb), and molybdenum (Mo), and positive correlations with selenium (Se) and barium (Ba). Nonlinear inverse U-shaped associations between Mo, Rb, and MMSE scores were identified using Restricted Cubic Splines (RCS) and Bayesian Kernel Machine Regression (BKMR). Mediation analysis revealed that Free Thyroxine (FT4) mediated the relationship between Rb and MMSE scores by 29.10 % and between Zinc (Zn) and language performance by 35.00 %. Total thyroxine (TT4) mediated the link between Cu and orientation score by 24.69 %, and Thyroid Stimulating Hormone (TSH) mediated the association between Cu and attention score by 38.96 %. Ti, Se, Rb, Mo, Ba and Cu were significantly associated with cognitive impairment risk. Mixed exposure to Mo and Rb was linked to an increased risk of cognitive impairment. Additionally, levels of TSH, FT4 and TT4 were associated with cognitive function, mediating the effects of Rb, Zn and Cu on cognitive function.

Glyphosate, a widely used herbicide globally, has prompted concerns regarding its potential health impacts. This study aimed to explore the link between glyphosate exposure and renal function by combining NHANES, a zebrafish model, and metabolomics. A cross-sectional analysis of 2013-2014 NHANES data investigated the relationship between glyphosate exposure and renal function [albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR)]. A subsequent zebrafish experiment was conducted to verify this association. Embryos (0.75 hpf-96 hpf) were exposed to different glyphosate concentrations dissolved in water (0, 30, 60, 90, 120 μg/mL). The underlying mechanism of the association between glyphosate and renal function was explored by the real-time quantitative polymerase chain reaction (RT-qPCR) and non-targeted metabolomics analysis [embryos (0.75 hpf-96 hpf) were exposed to 90 μg/mL glyphosate]. 1170 participants were enrolled in the NHANES study. The NHANES-based study found a positive association between glyphosate and ACR [0.07 (0.01, 0.13)]. Higher urinary glyphosate levels, particularly in the third quartile group, were negatively linked to eGFR [-3.72 (-5.98, -1.46)]. Further zebrafish experiments indicated that zebrafish exposed to 90 μg/mL glyphosate exhibited increased mortality rates, higher fluorescence intensity, up-regulated the havcr1 expression level, and cystic dilatation of the kidney. Non-targeted metabolomics analysis identified differential metabolites (e.g., 5-Hydroxyindole acetic acid) and pathways (e.g., ABC transporters) influenced by glyphosate. Glyphosate exposure is negatively associated with renal function in community adults. The damage to the kidneys caused by glyphosate may be mediated through the regulation of metabolic pathways, and the specific mechanisms require further experimental investigation.

People are continually and simultaneously exposed to various non-persistent pesticides as these chemicals are ubiquitously distributed in the environment. Toxicological studies have indicated the associations between non-persistent pesticides and liver fibrosis in vitro and in vivo. However, epidemical study on the deleterious effect of non-persistent pesticides on the risk of liver fibrosis is rather limited. To examine the relationship between mixed non-persistent pesticides exposure and liver fibrosis, and to identify the potential pesticides of significant importance, this study enrolled the representative individuals from the NHANES 2013-2016 survey cycles, in which urinary non-persistent pesticides were measured. Liver fibrosis was determined based on the alternative noninvasive tests Fibrosis-4 index (FIB-4) and Hepamet Fibrosis Score (HFS). Survey-weighted linear/logistic regression and Bayesian kernel machine regression (BKMR) were used to detected the independent and combined associations between non-persistent pesticides and liver fibrosis, respectively. In single exposure analysis, significant and persistent associations were identified for 3,5,6-trichloropyridinol (TCPY), para-nitrophenol (PNP), glyphosate (GLYP) and 2,4-dichlorophenoxyacetic acid (2,4-D) exposure with both continuous and dichotomous liver fibrosis outcomes. Of them, TCPY and GLYP had the highest effect estimates, with the corresponding FIB-4 coefficient (β) being 0.09 (0.05-0.13, model 3) and 0.09 (0.06-0.12, model 3), respectively. In BKMR analysis, positive associations between pesticides mixture and FIB-4 and HFS liver fibrosis were identified. The results of Posterior Inclusion Probability (PIP) further showed that GLYP, TCPY, and PNP were the main contributors to the overall effects of pesticides mixture, and the corresponding PIPs were 1.000 (1.000), 1.000 (0.914) and 0.972 (0.819) for FIB-4 (HFS) liver fibrosis, respectively. This study indicates that exposure to non-persistent pesticides mixture is associated with increased risk of liver fibrosis in humans, and provide new insight into the hepatotoxic potential of non-persistent pesticides.

Long-term fine particulate matter (PM_2.5) exposure was associated with childhood obesity. However, the key PM_2.5 components and whether PM_2.5 effect may vary by obesity type, growth stage, sex, and individual/family characteristics have yet been examined. In this study, we investigated 213,907 Chinese children and adolescents aged 3-18 years in 2017-2019. Three-year average concentrations of PM_2.5 and five major components were assigned to each participant's address. Multivariable mixed-effects model and weighted quantile sum regression were used to estimate the effect sizes of each component. Stratified analyses were performed by age and sex groups, with the interactive effects of a series of individual/family features evaluated. The odds ratio of childhood obesity was 1.28 (95 %CI: 1.15-1.43) for per interquartile range increase in PM_2.5, with organic matter identified as the key contributor. General central obesity and mixed obesity were more sensitive to PM_2.5 exposure than peripheral obesity. As children aged, the effect size of PM_2.5 attenuated for general central obesity, remained unchanged for mixed obesity and increased for peripheral obesity. Females, children with obese parents, and those with lower levels of physical activity were more vulnerable than others. Other adverse effect modifiers for certain children included family with one child, low family income, and less sleep duration. Our findings emphasize that the influence of exposure to PM_2.5 and its components on risk of obesity in children and adolescents should be considered comprehensively in developing adequate obesity prevention strategies.

Bisphenol A (BPA) is used extensively in producing industrial chemicals such as plastic products, resin, and paper coatings. Concerns have been expressed regarding its possible detrimental consequences, especially on the reproductive system of mammals. Despite extensive study in this domain, there has been no targeted examination of the impact of BPA on F1 generation rabbits. BPA exposure model was developed in pregnant female rabbits to examine the effects of BPA on reproductive hormones, cellular apoptosis, oxidative stress, inflammatory response, and tissue integrity in weaning rabbits. The results indicated that BPA exposure triggered an inflammatory response and oxidative stress, consequently impacting the reproductive system of weaned rabbits and altering reproductive hormone levels. By modulation of the Nrf2 and NF-κB axes, BPA could influence the expression of antioxidant enzymes and inflammatory mediators in the rabbit reproductive system, leading to cell apoptosis and tissue damage. These results underscore the importance of monitoring BPA exposure during pregnancy and emphasize the necessity of implementing measures to mitigate its potential effects on the reproductive health of offspring.