Ecotoxicology and Environmental Safety最新文献

Cardiovascular-kidney-metabolic (CKM) syndrome links metabolic dysfunction, kidney injury, and cardiovascular disease; however, how real-world toxic exposures and social disadvantage accelerate CKM progression is not well defined. We followed a pollution-exposed rural cohort in Northeast China from 2016 to 2021 (n = 472; 2360 person-visits). Urinary chromium (Cr), cadmium (Cd), manganese (Mn), and lead (Pb) were measured by inductively coupled plasma mass spectrometry, and CKM stage was assigned using the current American Heart Association framework. We modeled advanced CKM (stages 3-4) versus non-advanced CKM (0-2) using generalized linear mixed-effects models (LME) with participant-level random intercepts, and evaluated nonlinearity, mixture effects, and metal-metal interactions using random-intercept Bayesian kernel machine regression (BKMR). Higher urinary Cd [odds ratio (OR) 1.43, confidence interval (CI) 1.01-2.03], Pb (1.38, 1.05-1.80), and Mn (1.35, 1.02-1.80) were associated with advanced CKM, whereas Cr showed an inverse association (0.79, 0.60-0.97). The metal mixture as a whole increased advanced CKM risk and displayed nonlinear, interacting behavior (notably Cd- and Mn-driven effects and Cr×Cd, Cr×Mn, Pb×Cd, Pb×Mn interactions). Although single social determinants of health (education, income, employment, insurance) did not independently predict advanced CKM, cumulative disadvantage (≥2 adverse factors) amplified the Cd-CKM association (interaction OR 2.12, 1.00-4.54), indicating that inequity modifies biological susceptibility. Network and pathway analysis highlighted STAT3 as a central inflammatory-metabolic hub linking metal-responsive signaling to cardio-renal-metabolic injury, and molecular docking suggested direct coordination of Cd²⁺, Mn²⁺, and Pb²⁺ to STAT3. Notably, this study leverages a longitudinal repeated-measures design and mixture modeling framework to assess combined metal exposures in relation to CKM progression, and integrates epidemiological inference with systems-level analyses to generate mechanistic hypotheses. These findings outline an exposure-inequity-inflammation axis and nominate mixture reduction and social protection as dual prevention targets.

Copper (Cu) is extensively used in agriculture, yet its environmental accumulation raises significant ecotoxicological concerns. Nano-formulations have been developed as alternatives allowing to decrease Cu application rates, but their effects on non-target species remain poorly understood, particularly in aquatic ecosystems. This study evaluated the ecotoxic potential of the commercial copper-based nanopesticide, Kocide 3000® in comparison with the conventional formulation Kocide 2000®, using the freshwater gastropod Planorbarius corneus as a model species. A copper salt was also included as a control to specifically assess copper- related toxicity. Juvenile snails were submitted to a 48-hour acute toxicity test. Egg masses (embryos) were exposed to a range of copper concentrations (10-500 µg Cu/L) for 12 days until hatching. Growth, developmental progression, heart rate, and shell size were assessed as multiple endpoints. A recovery assay was conducted to investigate whether the impact of an early exposure was reversible. All three formulations induced measurable adverse developmental effects with increasing copper concentrations. Across all endpoints, nano and conventional formulations induced comparable effects, suggesting minimal nanomaterial-specific impacts and indicating that copper load, primarily drives toxicity under these exposure conditions. Interestingly, recovery potential differed between the copper salt and the commercial formulations since only CuSO₄-exposed embryos showed a return to a developmental state comparable to unexposed individuals after transfer to clean water. This finding highlights the influence of product composition in persistence and recovery dynamics. These results emphasize the importance of evaluating complete pesticide formulations, not just active ingredients in the hazard assessment of agrochemicals.

Prostate cancer (PCa) remains one of the most common malignancies in men, with rising global incidence and mortality rates. Recently, the impact of environmental pollutants on PCa initiation and progression has garnered significant attention. Benzophenone-3 (BP3), a ubiquitous ultraviolet filter in personal care products, possesses potential endocrine-disrupting and pro-carcinogenic properties; however, its specific role in PCa remains poorly defined. In this study, we demonstrated that BP3 significantly promoted PCa cell proliferation and migration. A BP3-derived nomogram was developed, which not only predicted PCa prognosis but also revealed an associated immunosuppressive microenvironment characterized by increased Treg and M2 macrophage infiltration alongside decreased CD8⁺ T cell populations. Mechanistic investigations identified acyl-CoA dehydrogenase 9 (ACAD9) as a pivotal mediator of these effects, as ACAD9 knockdown effectively reversed BP3-induced oncogenic phenotypes. Functional assays further elucidated that BP3 accelerates the fatty acid oxidation (FAO) rate while suppressing reactive oxygen species (ROS) production, a metabolic shift abrogated by ACAD9 silencing. Finally, in vivo xenograft models validated that BP3 monotherapy markedly promotes PCa progression, whereas ACAD9 deficiency neutralizes this effect. In summary, our findings characterized BP3 as an environmental pro-carcinogen that drives PCa malignancy via the BP3/ACAD9 axis, offering new insights into environmental risk factors and potential therapeutic targets for PCa.

Between 2014 and 2024, unhatched eggs from several wild bird species were analyzed at the Center for Analysis and Diagnosis of Wildlife (CAD, Spain), including eggs from threatened species such as the bearded vulture (Gypaetus barbatus) and the Spanish imperial eagle (Aquila adalberti). The aim of this study was to characterize exposure of wild birds to environmental contaminants and discuss their potential implications for reproduction. To this end, eggs were subjected to detailed examination, including biometric measurements, evaluation of embryonic development, and investigation of possible causes of reproductive failure. In addition, chemical analyses were performed on eggshells and egg contents to detect residues of different groups of xenobiotics, including metals, pesticides, pharmaceutical compounds and polychlorinated biphenyls (PCBs). Several contaminants were detected in the analyzed samples, mainly persistent organochlorine compounds such as DDT degradation products (o,p'-DDE and p,p'-DDE) and PCBs. Residues of currently used pesticides, including pyrethroids and fipronil, were also identified in some samples, whereas pharmaceutical residues were not detected during the study period. Although most contaminant concentrations were relatively low, their persistence, potential sublethal effects, and the simultaneous presence of multiple compounds in the same sample suggest that chemical exposure could represent a potential risk factor for avian reproduction. The results highlight the value of wild bird eggs as bioindicators of environmental contamination and emphasize the importance of long-term toxicological monitoring, particularly for species of conservation concern characterized by long lifespans and low reproductive rates.

Genetic diversity within plant populations is a key determinant of ecosystem functioning, especially, in shaping plant productivity. However, existing research examining how genetic diversity influences productivity has primarily focused on genotypic richness (number of genotypes), leaving the role of genotypic evenness (relative abundance of genotypes) understudied. Moreover, while microplastics has become a widespread contaminant, it is unknown whether microplastics could influence the impact of genetic diversity on plant growth performance. To address these gaps, we conducted an experiment using the clonal plant Hydrocotyle verticillata, manipulating both genotypic richness (1, 3, 6) and genotypic evenness (low, medium, high), crossing treatments with three types of soil microplastics (polylactic acid (PLA), poly-3-hydroxybutyrate (PHB) and polybutylene succinate (PBS)) and a control group without microplastics. All three microplastics significantly decreased biomass of H. verticillata. Genotypic richness had no effects on biomass, however, its effect on ramet numbers was altered by microplastics. The effect of genotypic evenness on both biomass and ramets were regulated by microplastics. With PBS, H. verticillata with high genotypic evenness produced significantly lower biomass and ramet numbers than those with low or medium evenness. However, this pattern was not observed under the PHB or PLA treatments. The study concludes that microplastics can modulate the effects of genotypic richness and evenness on the population performance of H. verticillata, but the effects vary depending on the type of microplastics. Our findings highlight the role of microplastics in regulating biodiversity-productivity relationships.

Environmental plasticizers are increasingly implicated in asthma susceptibility, yet the mechanisms linking chemical exposure to airway inflammation remain poorly defined. Here we show that the plasticizer di(2-ethylhexyl) phthalate (DEHP) directly drives a neutrophil-dominant asthma phenotype through activation of IL-17-centered immune pathways. Integrative network toxicology identified IL-6 and IL-1β as central inflammatory nodes connecting DEHP exposure with Th17 differentiation and IL-17 signaling. Consistent with these predictions, inhalational DEHP exposure in mice induced airway hyperresponsiveness, mixed granulocytic airway inflammation, mucus hypersecretion, and elevated pulmonary IL-6, IL-1β, and IL-17A expression. Immune profiling revealed expansion of IL-17A-producing lymphocytes, including Th17 cells and type 3 innate lymphoid cells (ILC3s). Genetic ablation of IL-17A markedly attenuated airway hyperresponsiveness and neutrophilic inflammation following DEHP exposure. Together, these findings identify an IL-6/IL-1β-Linked Th17/ILC3 axis as a mechanistic link between environmental plasticizer exposure and non-type 2 asthma, providing a conceptual framework for pollutant-driven airway disease.