Ecotoxicology and Environmental Safety最新文献

The accumulation of polyethylene microplastics (PE-MPs) in marine and coastal environments, particularly mangrove ecosystems, poses significant environmental challenges. To address this, we investigated the bioremediation potential of two bacterial strains, Lysobacter sp. (MAS-1) and Nitratireductor kimnyeongensis (MAS-2), isolated from biofilm-coated PE-film in a Thailand mangrove area. Microbial community analysis revealed a shift toward Proteobacteria (47-92 %) and Actinomycetota (5-41 %) in PE-MP-enriched consortia, indicating niche specialization. Both strains exhibited significant degradation, with MAS-1 achieving 35.4 ± 1.2 % and MAS-2 achieving 23.04 ± 0.8 % weight loss of PE-MPs within 30-days. Biofilm assays confirmed substantial microbial adhesion on PE-MPs, and SEM imaging revealed surface pitting and cracking, indicative of microbial colonization and polymer breakdown. While FT-IR analyses showed oxidative modifications including carbonyl (CO), hydroxyl (-OH), and ether (C-O) groups, enhancing PE surface hydrophilicity. LC-MS/MS identified organic acids and nitrogen- and sulfur-rich compounds in a liquid medium, with in silico BioTransformer 3.0 analysis predicting strain-specific pathways like sulfur oxidation for MAS-1 and dehalogenation of MAS-2. These findings establish the bioremediation potential of mangrove-derived microbes and highlight the strains' distinct metabolic roles in PE-MP degradation.

Based on toxicological evidence, human exposure to phthalates (PHs) and diisononylcyclohexane-1,2-dicarboxylate (DINCH) may contribute to adverse health effects, especially during vulnerable developmental stages. To support the exposure assessment for this group of endocrine disruptors, we developed and validated a method for the analysis of 14 PH and 3 DINCH metabolites in human urine and maternal milk, applied the method in a pilot study, and identified crucial obstacles in the path of establishing maternal milk as a routine matrix in human biomonitoring. Urine and milk samples were extracted with solid-phase extraction (SPE) and QuEChERS salts, respectively, and analysed by liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method accuracy was confirmed for urine samples via a certified standard reference material and the G-EQUAS intercomparison programme. We identified a need for sampling protocols, reference materials, and external method verification schemes in order to establish maternal milk as a routine matrix. Finally, the method was tested for its applicability in a pilot biomonitoring study on 30 paired urine and milk samples from lactating mothers, with medians ranging from

A growing body of evidence highlights the health benefits of green space, but underlying mechanisms remain unclear. We hypothesized that the benefits of greenness on children's visual acuity may be mediated through reduced air pollution exposure. This study examined the mediating role of air pollutants in the association between greenness and visual acuity in 3-year-old children. We used data from the Korean Children's Environmental Health Study. Of 5458 cohort participants, 794 children were included. Residential greenness during pregnancy was measured using the Normalized Difference Vegetation Index (NDVI), and PM_2.5, PM₁₀, and NO₂ were estimated with kriging interpolation for the first year after birth. Visual acuity was assessed with Jin's chart and averaged for both eyes. Associations between NDVI, pollutants, and visual acuity were analyzed using generalized additive models, multivariable regression, and causal mediation analysis. A 1 % increase in z-score- standardized NDVI at 200 m was associated with decreases of 0.25 μg/m³ (95 % CI: -0.31, -0.18), 0.24 μg/m³ (95 % CI: -0.35, -0.22), and 0.55 ppm (95 % CI: -0.61, -0.50) in PM₁₀, PM_2.5, and NO₂. A 1 % NDVI increase at 200 m was also associated with a 0.023-point (95 % CI: 0.013, 0.032) increase in visual acuity score (1.0 equals 40/40 on Snellen chart). Smaller buffers showed stronger associations. At 200 m, decreases in PM₁₀, PM_2.5, and NO₂ mediated the NDVI-visual acuity relationship, with mediation proportions of 11.6 %, 9.8 %, and 55 %. In two-pollutant models, mediation by both PM₁₀ and PM_2.5 was no longer significant after adjustment for NO2. These findings suggest that nearby residential greenness may protect visual function in early childhood primarily through reduced exposure to NO₂.

Heavy metal (HM) toxicity is a major constraint for plants, soils, and the environment. Thus, eco-friendly and cost-effective strategies are needed to mitigate HM stress. The bacterial strain Pseudomonas qingdaonensis BD1 and the clay mineral Illite have been identified as promising agents for alleviating lead (Pb), arsenic (As), and cadmium (Cd) stress in soybean. However, their synergistic effects on soybean under combined metal stress (Pb+As+Cd) remain underexplored. In this study, soybean plants grown under controlled conditions were treated with BD1 isolates and 3 % Illite to counter the phytotoxic effects of Pb, As, and Cd (1.5 mM each). HM stress impaired soybean growth by increasing oxidative damage and disrupting photosynthetic functioning, whereas the co-administration of BD1 +Illite restored morpho-physiological performance, including improved chlorophyll (Chl a and Chl b) content, enhanced maximum quantum efficiency of PSII (Fv/Fm), and increased net photosynthetic rate (Pn), indicating effective protection of the photosynthetic apparatus under stress conditions. These physiological improvements were accompanied by enhanced key enzymatic antioxidant activities, including SOD (218.3 %), CAT (84.5 %), POD (57.5 %), and APX (60.9 %), as well as the non-enzymatic antioxidant GSH (108.2 %). These improvements led to reduced malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels. BD1 +Illite also increased the accumulation of sugars and free amino acids, improved the uptake of Ca, K, and Si, and simultaneously reduced Cd, As, and Pb accumulation. Moreover, the treatment modulated phytohormone levels by decreasing abscisic acid (40.3 %) and salicylic acid (13.8 %) while increasing jasmonic acid (44.3 %). BD1 +Illite downregulated GmNCED3 and GmPAL1, but upregulated GmCYP707A2, GmLAX1, and GmCDPK5. Metal ion homeostasis and detoxification-related genes (GmNRAMP5A, GmMT1, GmMT2, GmPCS1, and GmWRKY142) were also differentially expressed, indicating coordinated responses that enhance HM tolerance in soybean. Overall, these findings highlight plant-microbe interaction-based, eco-friendly, and cost-effective strategies to reduce HM toxicity in soybean and other legumes.

Background: Organophosphate esters (OPEs), a class of synthetic flame retardants, have been suggested to alter glucose metabolism. However, their effects among women in early postnatal period have not yet been explored, let alone its joint association with gestational diabetes mellitus (GDM) history.

Methods: Five urinary OPE metabolites from 454 women were determined at 42 days postpartum, of which 354 women and 228 women had fasting plasma glucose (FPG) measured at 42 days and 1 year postpartum, respectively. The levels of OPE metabolites were measured using ultra-performance liquid chromatography-tandem mass spectrometry (LC-MS) and natural log (ln)-transformed, and linear regression was used to assess the association between OPEs metabolites concentration and blood glucose indicators. The joint association of it with a GDM history was also assessed.

Results: In the fully adjusted model, exposure to DoCP was positively associated with FPG at 42 days postpartum (β: 0.12, 95 % CI: 0.05, 0.20). And a joint association was observed, compared with women with low level of DoCP and DBzP and without a history of GDM, women had higher level of DoCP and DBzP and a history of GDM had the highest level of FPG at 42 days postpartum (β=0.20, 95 %CI: 0.01, 0.39 for DoCP; β=0.24, 95 %CI: 0.06, 0.42 for DBzP). No association was found between OPEs exposure at 42 days postpartum and FPG at 1 year postpartum.

Conclusion: Our findings suggest that exposure to OPEs could disturb short-term postpartum glucose metabolism, especially among women who had a GDM history.

Relative abundances of adsorption sites increase with the specific surface area of soil particles and aggregates. In turn, larger sorbed-phase distributions may attenuate pesticide biodegradation rates and ecotoxicological effects. Thus, soil aggregate size may be an important determinant of the fate and ecotoxicological effects of glyphosate and its metabolite aminomethylphosphonic acid (AMPA). We investigate the dynamics of glyphosate degradation, AMPA formation, AMPA degradation, and soil biogeochemical properties over 30 days, in soils composed of aggregates of various sizes: bulk soil (<10 mm), and five distinct size classes (2-10, 1-2, 0.25-1, 0.05-0.25, <0.05 mm). Results show that glyphosate and AMPA degradation rates decreased with decreasing aggregate size, but was statistically significantly different from other sizes only for glyphosate in < 0.05 mm aggregates. Soil biogeochemical properties (organic carbon, total nitrogen, total phosphorous, pH, available phosphorous (AP)), enzyme activities (β-glucosidase, N-acetylamino-β-glucosidase, alkaline phosphatase), and their dynamics significantly differed across different aggregate sizes. The biogeochemical effects of glyphosate, and their sensitivities to aggregate size, were relatively large for enzyme activities and AP. This reveals significant effects on soil microbial activity, particularly activity associated with phosphorus cycling. Crucially, the soil biogeochemical response appears faster, larger and longer lasting in small aggregates. Overall, the biodegradation rates of glyphosate and AMPA are substantially less sensitive to aggregate size than their biogeochemical effects are. Therefore, glyphosate and AMPA persistence, which are straightforward to observe and quantify under field conditions, may not be reliable indicators of the durations or effect sizes of various underlying aspects of their environmental ecotoxicities.

Understanding how metal-oxide-enriched carbon aerosols deposit in the respiratory tract is essential for assessing their indoor health impacts, yet their inhalation behavior and age-dependent risks remain insufficiently quantified. In this study, we combined controlled chamber experiments, detailed particle characterization, and in silico dosimetry to quantify respiratory exposure to three representative metal-oxide-enriched carbon aerosols containing titanium dioxide (TiO₂), zinc oxide (ZnO), and copper oxide (CuO). The aerosols consisted of carbonaceous cores coated with oxidized metal species (Ti⁴⁺, Zn²⁺, Cu²⁺), designed to mimic aged soot typically encountered in indoor environments. Aerosols with diameters between 30 and 250 nm were generated in a 100-L mixing chamber, and their age-specific deposition was estimated using the Multiple-Path Particle Dosimetry (MPPD) model with ICRP morphometric parameters for 3- and 21-year-old subjects under light-activity breathing. Deposition profiles were similar between age groups up to the 15th airway generation but diverged in the deeper lung: adults showed higher deposition between generations 16 and 22, whereas children received greater deposition beyond generation 22. Despite a tenfold difference in exposure concentration between the two modeled episodes, the deposited mass per alveolus remained of similar magnitude, indicating that modest indoor concentrations can still result in appreciable alveolar doses. Modeled deposition patterns were consistent with previously reported experimental data in both magnitude and spatial distribution. Overall, children under seven years of age experienced approximately 35 % higher deep-lung deposition efficiency than adults, largely due to smaller airway dimensions and higher breathing rates. These results show that inhalation risk is governed jointly by particle physicochemical properties and age-specific respiratory physiology and underscore the need to incorporate both into future exposure and health-risk assessment frameworks for metal-oxide-enriched carbon aerosols in indoor environments.

Microplastics have been detected in vitreous samples, providing evidence of ocular health risks associated with direct exposure to micro-nanoplastics (MNPs). However, the primary sources, abundance, morphology and size distribution of these particles remain unclear. Here, we employed pyrolysis-gas chromatography-mass spectroscopy (Pyr-GC/MS) to verify the release of synthetic polymers from commercial disposable eye-drop containers. Due to small sample volumes, this conventional mass-based analytical method struggled to quantify the MNPs concentration effectively. In contrast, the single particle-based analytical techniques, including surface-enhanced Raman spectroscopy (SERS) and scanning electron microscopy, reveal thousands of MNPs released upon opening the container, with 88 % of particles measuring less than 5 μm. Another release mechanism is attributed to pre-existing particles within the container. The detection of oxygenated MNPs further suggests an increased potential for ocular toxicity. This research highlights the feasibility of particle-based methods when it comes for targeting the nanoscale of plastic particles. Furthermore, integration of SERS and SEM identifies a previously uncharacterized direct exposure route of nanoplastics to the human eye via commercial eye drops and emphasizes the importance of single-particle characterization in accurately assessing their implications for ocular health.

Background: Environmental regulations may yield substantial health benefits, yet their impact on cognitive health remains inadequately understood. This study exaimed the cognitive health benefits of China's Air Pollution Prevention and Control Action Plan (APPCAP) and explored the potential contribution of reduction in air pollution underlying this relationship.

Methods: Data were derived from four waves (2011-2018) of the China Health and Retirement Longitudinal Study (CHARLS). The intervention and control groups were designated based on provincial-level mandated air pollution reduction targets under APPCAP (>5 % vs. ≤ 5 %). Cognitive function was assessed using standardized questionnaires measuring episodic memory and mental status at each wave. Ambient fine particulate matter (PM_2.5) and self-reported household solid fuel use for cooking were evaluated as indicators of outdoor and indoor air pollution, respectively. A difference-in-difference (DID) approach was employed to assess APPCAP's impact on cognitive function, with changes in outdoor and indoor air pollution investigated as potential mechanisms. Heterogeneity in policy effects across sociodemographic groups was also analysed.

Results: Implementation of the APPCAP was associated with significant improvements in cognitive function (β coefficient = 0.72, 95 % CI: 0.50, 0.94). Significant reductions in ambient PM_2.5 concentrations and household solid fuel use contributed to 9.49 % and 6.47 % of the cognitive health improvements associated with the APPCAP, respectively. Subgroup analyses revealed stronger protective effects among middle-aged adults, rural residents, and individuals with lower educational attainment.

Conclusions: This study provides evidence that environmental regulations could effectively protect cognitive health through reductions in air pollution exposure.

Atrazine, a widely used chlorotriazine herbicide, persists in aquatic environments and poses potential carcinogenic risks. While epidemiological studies link atrazine exposure to malignancies, its intrinsic molecular mechanisms across organ systems remain incompletely understood. This study employed integrated network toxicology and transcriptomic analyses to clarify atrazine-associated oncogenic pathways in liver hepatocellular carcinoma (LIHC), kidney renal clear cell carcinoma (KIRC), lung adenocarcinoma (LUAD), and sarcoma (SARC). Transcriptomic data from The Cancer Genome Atlas (TCGA) for these cancers were analyzed to identify atrazine-related genes. Protein-protein interaction networks were constructed and analyzed to identify hub genes. Functional enrichment, immune microenvironment analyses, and survival analysis were performed. Molecular docking validated atrazine-target binding, and independent datasets were used for hub gene expression and pan-cancer relevance validation. We identified 92 (LUAD), 136 (LIHC), 137 (KIRC), and 161 (SARC) atrazine-associated targets. Hub genes including CDC6, MCM5/7, UBE2C, FEN1, CDCA8, and VIM were differentially expressed across these cancers. Enrichment analyses revealed atrazine disruption of core pathways, including cell cycle progression and chromosomal instability, epithelial-mesenchymal transition, metabolic reprogramming, and senescence-associated secretory pathways. Molecular docking confirmed high-affinity binding between atrazine and key targets. Pan-cancer validation implicated these hub genes in multiple additional malignancies. Transcription factor analysis nominated HSD17B8 as a key regulatory node. This study demonstrates that atrazine promotes carcinogenesis by dysregulating conserved networks governing genomic stability, cell proliferation, metabolic adaptation, and immune microenvironment remodeling, providing a mechanistic framework linking aquatic atrazine exposure to multi-organ carcinogenesis and nominating HSD17B8-associated pathways for therapeutic intervention. These findings underscore the imperative for enhanced environmental monitoring of atrazine contamination.