Ecotoxicology and Environmental Safety最新文献

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.

Mushroom poisoning, predominantly caused by α-amanitin, is a critical food safety concern in worldwide, with severe cases leading to hepatotoxicity and fatalities. This study delves into the hepatotoxic effects of α-amanitin, focusing on the NLRP3 inflammasome and PPAR-γ's regulatory role in inflammation. In vitro studies with L-02 cells showed that α-amanitin reduces cell viability and triggers NLRP3 inflammasome activation, increasing NF-κB phosphorylation and pro-inflammatory cytokines IL-18 and IL-1β. The NLRP3 inhibitor MCC950 mitigated these effects without impacting NF-κB. Conversely, PPAR-γ knockdown intensified the inflammatory response. In vivo, α-amanitin induced dose-dependent liver injury in mice, evident by elevated serum ALT and AST, and histological liver damage. MCC950 pretreatment offered protection against hepatotoxicity, while PPAR-γ inhibition with GW9662 worsened the condition. The study highlights the interplay between α-amanitin, NLRP3, and PPAR-γ in hepatotoxicity, proposing potential therapeutic targets for mushroom poisoning-induced liver diseases.

In order to investigate the causes of population degradation and resource decline, this thesis investigated the ecotoxicological effects of heavy metal Cu(Ⅱ) on the embryonic development of Sepiella maindroni. Results indicate significant effects of Cu(Ⅱ) concentrations on the developmental toxicity, teratogenicity, and lethality of S. maindroni embryos. Different concentrations of Cu(Ⅱ) caused varying degrees of malformations in embryos, altered developmental rates, reduced hatchability and hatchling quality, and increased malformation and mortality of hatchlings. At the same time, Cu(Ⅱ) exposure led to an increase in the content of the lipid peroxidation product malondialdehyde (MDA) and a significant decrease in the activity of antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT]), energy-metabolizing enzymes (adenylate kinase [AK]), and cholinergic-related enzymes (acetylcholinesterase [AChE], choline acetyltransferase [ChAT]). In conclusion, when the concentration of Cu(Ⅱ) in the environment is ≥ 0.01 mg/L, it causes significant lethality toxicity, developmental toxicity and teratogenicity in S. maindroni embryos. These effects are likely related to Cu(Ⅱ)-induced stress impacting the antioxidant capacity, energy metabolism, and cholinergic system. Ultimately, these toxic effects may lead to population degradation and resource decline in fishery organisms by affecting the early replenishment process of fisheries.

Oxytetracycline (OTC), a crop-absorbable antibiotic, poses a health risk to humans through the food chain. Conversely, 24-epibrassinolide (EBL), a plant growth hormone, mitigates the toxic effects of various pollutants on plants. However, the mechanism by which exogenous EBL affects the growth of rape seedlings exposed to OTC remains largely unknown. In this study, we found that environmental OTC concentrations significantly inhibited plant growth and metabolism, whereas exogenous EBL could restore plant growth characteristics. Exogenous EBL significantly decreased reactive oxygen species (ROS) accumulation, alleviating OTC-induced cell membrane lipid peroxidation. This was achieved by increasing the antioxidant capacity and secondary metabolism levels. Notably, our findings suggested that EBL stimulated glutathione S-transferase (GST) and glutathione reductase (GR) activities, enhancing reduced glutathione synthesis and participating in plant OTC detoxification. OTC residues in EBL + OTC-treated seedlings at 21 d were significantly reduced by 29 % compared with OTC alone. Further transcriptomic and metabolomic analyses revealed that the differentially expressed genes and metabolites in the EBL and OTC alone or combined treatment groups were primarily involved in the regulation of phenylpropanoid biosynthesis, glutathione metabolism, and lant hormone signal transduction pathways in response to phytotoxic effects and detoxification mechanisms, as compared to the control group.

In 2023, European Food Safety Authority (EFSA) published a re-evaluation of the safety of bisphenol A (BPA), establishing the new tolerable daily intake (TDI) as 0.2 ng/kg·bw/day with a 20,000-fold reduction compared to 2015, which regained public concern about the impact of bisphenols (BPs) on human health. In order to explore the health risk to thyroid function of BPs, in this study, we assessed the internal exposure levels of BPs and the relationships between urinary BPs and thyroid function in general adults. We carried out a cross-sectional study in Chengdu, China, recruiting 1486 adults without special indentities and diseases (aged 18-68), and measured 6 BPs in urine. We found BPA was the predominant compound in urinary samples of this population, and the estimated daily intake (EDI) of BPA was 0.027 μg/kg·bw/day (geometric mean), exceeding the TDI value by two orders of magnitude. Using multivariable regression model, we observed a negative association between BPA and T3 and T3/T4 in males. Trend tests indicated that higher BPA levels were correlated with higher rates of subclinical hypothyroidism (SCH) in males (OR=1.383, 95 % CI [1.024, 1.867]). We also observed that bisphenol F (BPF) contributed to the occurrence of thyroid globulin antibody positivity (TGAb.P) in both males and females. Although the use of BPs has been restricted, the adverse health effects still deserve public attention.