Ecotoxicology and Environmental Safety最新文献

Objectives: To systematically evaluate associations between environmental toxicants and periodontitis and to quantify the mediating role of systemic inflammatory biomarkers.

Methods: We extracted data from National Health and Nutrition Examination Survey (NHANES) 2013-2014. The study covers 73 environmental toxicants spanning 12 categories. Exposome-wide association study (ExWAS) was used to identify individual toxicant associations, and adaptive elastic net regularization was employed to develop an environmental risk score (ERS). Mediation analysis quantified the contribution of inflammatory biomarkers to observed associations RESULTS: Among 1210 participants, 49.4 % were male and 50.6 % were female. The ExWAS identified 29 toxicants across 9 categories significantly associated with periodontitis. Notably, detectable monohydroxybutenyl mercapturic acid (MHBMA2) levels were associated with a 2.798-fold higher periodontitis odds (95 % CI: 1.799-4.352) versus undetectable levels. Stratified analyses revealed that associations were stronger among males and younger adults (< 60 years). The ERS, derived from 17 prioritized toxicants via elastic net regression, demonstrated a significant positive dose-response relationship with periodontitis risk, where each IQR increase was associated with a 59.7 % higher disease risk (OR = 1.597). Mediation analysis indicated that white blood cell count (11.5 %), neutrophils (10.2 %), monocytes (5.1 %), systemic immune-inflammation index (6.3 %), neutrophil-to-lymphocyte ratio (5.7 %), and systemic inflammation response index (7.4 %) significantly mediated toxicant-periodontitis associations.

Conclusions: This nationally representative exposome-wide investigation identified significant associations between multiple environmental toxicants and periodontitis, with inflammatory pathways partially mediating these relationships. These findings establish potential environmental etiological factors for periodontitis and highlight specific toxicants as targets for exposure reduction strategies to improve periodontal health at the population level.

The significant ecological risks posed by microbial communities in ballast water and sediments highlight the necessity for accurate species monitoring. However, the complex physicochemical conditions within ballast tanks limit the effectiveness of conventional environmental DNA (eDNA) metabarcoding approaches. This study focuses on two key challenges in monitoring viable microorganisms in ballast tank sediments: interference from relic DNA and PCR inhibition. For eDNA samples from the ballast tanks of three vessels, we paired PMA (propidium monoazide)-treated and untreated samples; each extract was either further processed to remove PCR inhibitors or left untreated. The resulting four sample groups were subjected to qPCR for 16S rRNA gene quantification, 16S rRNA amplicon sequencing, and comparative microbial diversity analyses to assess the impacts of these methodologies. PMA treatment successfully differentiated between intact and relic DNA, reducing total DNA and 16S rRNA gene copies by 9.45 % and 6.93 %, respectively. Subsequent inhibitor removal unmasked the true community abundance, yielding a 16-fold increase in 16S rRNA gene copies and a significant restructuring of the microbial composition. Notably, combining PMA treatment with inhibitor removal decreased 16S rRNA gene copies while increasing ASV richness, suggesting that inhibitors may impair PMA's ability to exclude relic DNA. Our findings emphasize the need to combine PCR inhibitor removal with PMA treatment for quantifying viable microorganisms; however, the optimal protocols for their co-processing require further refinement.

Surfactants and pesticides are frequently co-detected in field environments, but the effects of surfactants on the bioavailability of pesticides remain unclear. In this study, a rice soil culture experiment was conducted to investigate the effect of anionic surfactant sodium dodecyl benzenesulfonic acid (SDBS) on the absorption of metalaxyl in rice plants. It was found that SDBS enhanced the solubility of metalaxyl, leading to a dose-dependent increase in its concentration in soil pore water. The enrichment of metalaxyl in rice plants was proportional to the content of metalaxyl in soil pore water. Besides, the dissipation rates of metalaxyl were accelerated in the 0.5 mg/kg and 5 mg/kg SDBS groups while slowed down in 50 mg/kg SDBS group. The phenomenon may be caused by the biphasic effect on soil enzyme activity, where SDBS exposure produced low-concentration promotion and high-concentration inhibition of dehydrogenase, carboxylesterase and urease in soil. In addition, it was found that the 50 mg/kg SDBS treatment also inhibited root elongation and disrupted rice growth. Furthermore, metabolomics analysis revealed that key metabolic pathways in rice were affected, as SDBS treatment severely impacted amino acid biosynthesis and reduced the contents of secondary metabolites in rice roots. These findings improve the understanding of the environmental co-exposure effects of surfactants and pesticides and help evaluate their safety to crops.

Chronic fluoride exposure causes skeletal fluorosis (SF), a debilitating bone disease, but the lack of a comprehensive understanding of its pathogenesis has hindered the development of effective therapies. Although fluoride is known to stimulate osteoblasts, the role of gut-bone crosstalk in SF remains uninvestigated. In this study, using a rat SF model and in vitro osteoblast studies, we found that fluoride disrupted gut microbial tryptophan metabolism, resulting in decreased serum levels of indole-3-acetic acid (3-IAA) in both SF model rats and human SF patients. This deficiency in 3-IAA impaired the activation of aryl hydrocarbon receptor (AHR), leading to Wnt/β-Catenin pathway hyperactivation, excessive osteoblast differentiation/mineralization, and pathological bone formation. Restoring 3-IAA levels, either through direct supplementation or an intermittent high-tryptophan diet-reactivated AHR, suppressed Wnt/β-Catenin signaling, and alleviated bone damage in vivo. Crucially, knockdown or inhibition of AHR abolished the protective effect of 3-IAA, confirming that the 3-IAA-AHR axis is essential for mitigating SF. In conclusion, we identify a gut microbiota-3-IAA-AHR-Wnt/β-Catenin axis that drives the pathogenesis of SF, and our findings suggest that intermittent tryptophan supplementation could serve as a novel therapeutic strategy to reduce fluoride-induced bone damage by restoring microbial metabolite signaling.

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants commonly involved in multiple health risks. Epidemiological studies have confirmed a direct connection between PFAS exposure(including PFOA and PFOS) with the prevalence of osteoarthritis(OA), but the underlying mechanisms and key targets remain unclear. This study integrates network toxicology, transcriptomic analysis, machine learning, and experimental validation to systematically investigate the role of PFOA/PFOS in OA pathogenesis. We identified 38 common targets shared between PFOA/PFOS exposure and OA, enriched in oxidative stress, endocrine metabolism, and senescence pathways. We further screened seven diagnostic biomarkers using machine learning to construct a nomogram for predicting the early onset of OA. Among these, ESR1 emerged as the core target associated with PFOA/PFOS exposure-related OA through multi-algorithm integration. Moreover, molecular docking and molecular dynamics simulations established that PFOA and PFOS could directly bind to ESR1 in a stable manner. In vitro experiments and single-cell transcriptomic analysis indicated that PFOA and PFOS exacerbate oxidative stress and senescence by downregulating ESR1 expression on chondrocytes, resulting in cartilage matrix degradation. Importantly, the ESR1 agonist raloxifene effectively reversed these detrimental effects to maintain cartilage homeostasis. Overall, these findings revealed ESR1 dysfunction as a critical molecular event in PFAS exposure-related OA, providing novel insights into environmental etiologies of OA and potential therapeutic strategies.

Arsenic (As) behavior in paddy soils is tightly linked to the redox cycling of electron acceptors such as iron (Fe), nitrate (NO₃^-), and sulfate (SO₄^2-), but the role of counterions (NO₃^- vs. SO₄^2-) in ferric salt-mediated As immobilization remains poorly understood. This study compared ferric nitrate (Fe(NO₃)₃) and ferric sulfate (Fe₂(SO₄)₃) through complementary incubation experiments: paddy flooding simulations and controlled redox gradient tests. Supported by sequential extraction, XRD, and XPS analyses, both ferric salts enhanced soil oxidizing conditions and reduced extractable As concentrations. The reductions ranged from 33.6 to 62.1 % for Fe(NO₃)₃ and 2.1 to 90.3 % for Fe₂(SO₄)₃ with As sequestered into less bioavailable, highly crystalline fractions. Critical differences emerged under controlled redox gradient: Fe(NO₃)₃ stably maintained low porewater As across all redox regimes, whereas Fe₂(SO₄)₃ posed an early As release risk, with concentrations exceeding the control treatment. At equal application rates, Fe(NO₃)₃ outperformed Fe₂(SO₄)₃ by lowering soluble As by 81.9-92.5 % and extractable As by 13.2-69.9 %. Novel mechanistic insights reveal that NO₃^- and SO₄^2- differentially regulate redox status, dissolved Fe dynamics, and mineral-As interactions, which are key drivers of As immobilization efficacy. This work clarifies the overlooked counterion effect, providing a scientific basis for selecting optimal iron-based amendments to mitigate As contamination in paddy ecosystems.

Karst water systems, vital to global freshwater security, are susceptible to trace elements (<1 mg/L) and major anion contamination, particularly in regions with high geological metal backgrounds and dynamic water recharge. Yet the influence of externally sourced (allogenic) water on mitigating such contamination in karst water systems is poorly understood. This study investigates the geochemical behaviour and health risks of trace elements in allogenic water (Aw), surface water recharged by Aw (ASw), groundwater recharged by Aw (AGw), and karst groundwater (Kw) in Guangxi, China. While most trace metal levels met Chinese drinking water standards (GB 5749-2022), Fe exceeded 0.3 mg/L in 34.5 % of samples, and Al and Mn surpassed permissible limits in 13.8 %. Monte Carlo simulations revealed Mn as the dominant non-carcinogenic risk via dermal exposure, with As and Cd posing ingestion risks, especially for children. Multivariate analysis revealed that redox and oxide/clay weathering primarily drive Al, Fe, Mn, Pb, Cd, and As mobility, while carbonate weathering influences Ca, Cr, Ni, and Cd. Agricultural runoff and dilution further shape water chemistry. Allogenic recharge mitigates contamination in AGw through dilution, redox shifts, and adsorption. These findings underscore the need to manage redox-sensitive processes and prioritize Mn, As, and Cd for long-term health protection in karst areas.

Background: Atrazine (ATZ), a widely used herbicide, is implicated in neurodegenerative risks, yet its neurotoxic mechanisms remain unclear. This study investigates how environmentally relevant ATZ exposure disrupts neuron-microglia interactions to drive Parkinson's disease (PD)-like pathology.

Methods: C57BL/6 mice received 28-day oral ATZ (10 mg/kg/day). Behavioral phenotyping (open field, pole climb, wire hanging tests) assessed motor deficits. Midbrain tissues underwent histopathology and single-cell RNA sequencing (scRNA-seq). Intercellular communication networks were reconstructed using the CellChat algorithm, with a focus on neuron-microglia signaling pathways. Quantitative real-time PCR (qPCR) was employed to validate the transcriptomic accuracy of scRNA-seq (n = 6/group).

Result: ATZ induced PD-like motor dysfunction (e.g., mean speed in OFT, P < 0.0001) and neuronal damage. scRNA-seq identified dysregulated calcium homeostasis genes (Atp2b1, Camk2a, Gabbr2) and neurotoxic markers (Mapt, St18) in neurons, alongside M1 microglia polarization via TLR/TNF/IL-17 signaling. Microglial-derived CX3CL1 was found to competitively disrupt neuronal CX3CL1-CX3CR1 signaling, exacerbating neuroinflammation. qPCR indicated high accuracy of the scRNA-seq data.

Conclusion: Environmental ATZ exposure triggers PD-like neurodegeneration through dual mechanisms: (1) neuronal calcium dysregulation inducing oxidative stress and (2) microglia-driven neuroimmune dysfunction via CX3CL1 signaling. This study provides the novel mechanistic evidence linking ATZ to PD-like pathology via neuron-microglia crosstalk, highlighting the need for re-evaluating global ATZ exposure guidelines.