Ecotoxicology and Environmental Safety最新文献

Selective attention is essential for cognitive and behavioral self-regulation. However, the association between lead exposure and selective attention remains unclear. We examined the association between blood lead levels and selective attention, and evaluated whether this association is influenced by sleep duration. We used data from a prospective cohort of 377 Korean children. Blood lead concentrations and Stroop Color and Word Test (SCWT) scores were repeatedly measured at 6, 8, and 10 years of age. Generalized propensity scores (GPSs) were generated using linear regression models predicting lead levels. Associations between lead levels and SCWT scores were assessed using causal inference approaches, such as linear mixed models adjusted for both GPS and potential confounders, as well as doubly robust estimation models. In models adjusted for both GPS and potential confounders, a doubling of lead levels was associated with lower color [β = -1.46, 95 % confidence interval (CI): -2.63, -0.30] and color-word (β = -1.52, 95 % CI: -3.00, -0.04) test scores. In doubly robust models, these associations persisted for the color (β = -1.35, 95 % CI: -2.36, -0.34) and color-word (β = -1.33, 95 % CI: -2.61, -0.04) test scores. The associations varied by sleep duration, with stronger effects observed among children sleeping ≤ 8 h compared with those sleeping longer. By applying multiple causal inference approaches, this study provides robust evidence that lead exposure impairs selective attention in school-age children. The detrimental associations were amplified among those sleeping ≤ 8 h, suggesting that sufficient sleep may mitigate the neurotoxic effects of lead exposure.

Groundwater is a vital freshwater resource but is increasingly threatened by both conventional pollutants and contaminants of emerging concern (CECs). This review synthesizes the evolution of groundwater contamination research using a bibliometric analysis of 38,759 publications from 1991 to 2024. Scientific production rose sharply after 2004, driven by China and India, while Africa and parts of South Asia remain underrepresented despite facing serious groundwater challenges. Thematic mapping shows a transition from conventional contaminants (e.g., MTBE, TCE) to CECs (e.g., PPCPs, PFAS, microplastics). Regulatory frameworks are well established for conventional contaminants, but most CECs remain unregulated due to analytical limitations, scarce toxicological data, and slow policy processes. Remediation still relies on pump & treat, in situ chemical oxidation, permeable reactive barriers, and bioremediation, although heterogeneity and rebound effects limit success. Advanced methods (e.g., high-performance adsorbents, advanced oxidation processes, membrane filtration) show promise but face challenges of by-product formation, cost, and limited validation. Treatment-train strategies, such as combining membrane filtration with advanced oxidation, offer pathways to overcome current limitations. Future progress will require shifting from rigid concentration-based standards toward performance-based metrics such as mass discharge reduction coupled with SMART goals, providing more realistic benchmarks for persistent contaminants. Sustainable progress will also depend on integrating renewable energy, while low-cost designs are essential to improve applicability in developing regions. Expanding data sharing and supporting underrepresented regions remain critical to strengthen global equity. Overall, this review synthesizes past and present research and highlights directions for advancing monitoring, regulation, and remediation under growing environmental pressures.

Recent epidemiological studies have indicated that exposure to arsenic (As), particularly during key phases of central nervous system development, may be an environmental risk factor for autism spectrum disorder (ASD). While nicotinamide mononucleotide (NMN) confers neuroprotection by elevating tissue nicotinamide adenine dinucleotide (NAD+), its efficacy against ASD pathophysiology remains unexplored. Here, a mouse model of perinatal As exposure (1.2 mg/kg/d) and NMN intervention (500 mg/L) was employed, and NMN was found to rescue As-induced NAD+ depletion in offspring brain tissues. This restoration coincided with increased synaptic density in the cortex and significant attenuation of autism-like behavioural phenotypes. Additionally, NMN restored As-induced intestinal dysbiosis and enriched beneficial genera including Lactobacillus and Akkermansia, restoring the Firmicutes/Bacteroidetes ratio. Consistently, As exposure exacerbated inflammatory damage in colonic tissues, elevated pro-inflammatory cytokine levels in serum, and activated cortical microglia and astrocytes. In contrast, NMN supplementation markedly alleviated these inflammatory and neuroimmune disturbances. Notably, NMN also increased Clostridium species, which synthesise vitamin B3 (VB3), a precursor of NAD+ . Moreover, the intervention alleviated the As-induced disruption of colonic epithelial tight junctions and polarity, while concomitantly upregulating NAD+ synthase and NAD+ precursor transporter proteins that were inhibited by As. Collectively, these actions restored perinatal As-induced NAD+ deficits in offspring, providing novel mechanistic insights into the therapeutic potential of NMN against As-driven autism-like phenotypes. These findings offer a foundation for dietary supplementation with NMN as a strategy for clinical translation.

Industrialization has accelerated plastic production and emissions, resulting in pervasive environmental plastic pollution. Plastic debris can fragment into microplastics (<5 mm) and nanoplastics, collectively referred to as microplastics and nanoplastics (MNPs). Beyond their ubiquity in ecosystems, MNPs have also been detected in human-relevant matrices (e.g., placenta and breast milk), intensifying concerns about potential organ-specific health risks. Although particle size is increasingly recognized as a critical determinant of MNP toxicity, a cross-system synthesis of size-dependent effects and their implications for risk assessment remains incomplete. This review integrates current evidence on size-associated toxicological outcomes across major organ systems, including the digestive, reproductive, urinary, cardiovascular, respiratory, and nervous systems. Across many experimental settings, a broadly consistent pattern emerges in which smaller MNPs, particularly sub-10 μm particles and nanoscale plastics, more often elicit stronger adverse responses than larger particles. This tendency is generally consistent with size-related internal fate and tissue delivery that enhance barrier crossing and cellular interactions, thereby promoting oxidative stress and immune or inflammatory activation and ultimately contributing to organ-level impairment and functional disruption. Future studies should adopt harmonized size classification and reporting, appropriate exposure metrics, environmentally relevant test materials, and long-term or low-dose designs, complemented by human-relevant biomonitoring, to strengthen size-resolved risk assessment while prioritizing monitoring and mitigation of the difficult-to-capture sub-10 μm fraction.

Cadmium (Cd) pollution adversely affects plant growth and development, leading to reductions in crop yields and posing a threat to human health. Selenium (Se) is an essential micronutrient for both humans and animals. Wheat, an important cereal crop, is particularly prone to accumulating Cd in polluted environments. However, there is a paucity of studies examining the mitigation mechanisms of Se on the photosynthetic systems of wheat leaves under Cd stress. In this study, the alleviating effect of Se on Cd toxicity in wheat was investigated. The results showed Se increased wheat biomass by 20 %-50 %, photosynthetic parameters by 26 %-55 %, chlorophyll content by 17 %-29 % and help to keep normal leaf structure under Cd stress. Se upregulated key starch anabolism genes TaAGPS1, TaSUT2, and TaSWEET15 expression level, and thus complemented soluble sugar content by 16 %-21 %, starch content by 15 %-59 % disturbed by Cd stress. Under Cd stress, Se decreased wheat shoot Cd content by 6 %-19 %, and increased shoot Fe, Mn, Zn content by 5-28 %, 23-58 %, 8-32 %, respectively. These results suggest that Se mitigates Cd stress in wheat by limiting Cd translocation to shoots and regulating the expression of key carbon metabolism genes.

Benzo(a)pyrene (B(a)P), a prominent environmental carcinogen, is known to promote lung cancer progression; however, its underlying mechanistic pathways remain poorly defined. Here, we identify the EP300-H2BK5ac epigenetic axis as a key regulator of membrane surface tension and epithelial-mesenchymal transition (EMT) in lung cancer cells under B(a)P exposure. Using A549 and SW900 cells, we demonstrate that B(a)P treatment induces a dose-dependent reduction in membrane tension and promotes EMT, migration, and invasion. Mechanistically, B(a)P downregulates EP300 expression, leading to decreased H2BK5ac acetylation and impaired binding of H2BK5ac to the promoter of the endocytosis-related gene HSPA1A, as revealed by co-immunoprecipitation and ChIP-qPCR. EP300 knockdown mimics these effects, enhancing malignant behaviors, whereas EP300 overexpression restores H2BK5ac levels, increases HSPA1A expression, and suppresses B(a)P-induced phenotypes. Notably, HSPA1A overexpression in EP300-deficient cells partially rescues membrane tension and reverses EMT progression. These findings uncover a previously unrecognized EP300-H2BK5ac-HSPA1A regulatory pathway that links environmental exposure to biomechanical and epigenetic remodeling in lung cancer. Targeting this axis may offer new strategies to mitigate B(a)P-driven metastasis.

Pollution poses serious threats to marine organisms and ecosystem health, highlighting the need for effective methods of ecological risk assessment. Biomarkers offer valuable tools for evaluating the ecotoxicological effects of pollutants on marine organisms. Over the past decades, the application of biomarkers, particularly at molecular levels, in marine pollution monitoring has attracted growing attention. Here, bibliometric analysis of biomarker-based research is conducted to identify the progress in their application for marine pollution monitoring. The advancement of omics technologies provides new tools to identify specific biomarkers to indicate marine pollution through high-throughput approaches. However, the identification of biomarkers that exhibit both high sensitivity and monotonic response from high-throughput data remains a challenge. Dose-response modeling on omics data facilitates the identification of target biomarkers. Moreover, multivariate biomarker indices provide a more comprehensive assessment of biological responses on marine organisms and the comparison of ecosystem health across time and space. This paper systematically examines methodologies for identifying specific, sensitive and monotonic molecular biomarkers, discusses the characteristics of various multivariate biomarker indices, and highlights the current gaps and perspectives of molecular biomarkers in marine pollution monitoring. The aim of this paper is to inspire further research on biomarker-based approaches strategies for advancing marine ecological risk assessment.

Microplastics (MPs), emerging airborne pollutants detected in human lungs, are increasingly recognized as potential drivers of respiratory disease, yet their roles and pathogenic mechanisms in allergic airway inflammation remain poorly understood. Here we show that MPs exacerbate allergic airway inflammation in house dust mite (HDM)-sensitized mice by promoting epithelial barrier disruption and type 2 immune activation. MPs exposure elevated IL-33 release and expanded IL-5⁺IL-13⁺ ILC2s. Mechanistically, the Peroxisome proliferator-activated receptor gamma (PPARγ) was markedly expressed in MPs+HDM mice and is highly expressed in ILC2s. In epithelial-ILC2s coculture system, MPs selectively enhanced PPARγ expression in ILC2s, triggering metabolic reprogramming characterized by increased fatty acid uptake and lipid droplet accumulation. This metabolic shift fueled ILC2s activation, cytokine production and downstream ST2 activation, while pharmacological inhibition of PPARγ effectively attenuated these effects. Our findings identify a previously unrecognized epithelial-PPARγ-ILC2s axis through which MPs aggravate allergic airway inflammation, revealing a potential immunometabolic mechanism of MPs-induced lung impairment.

Organophosphate flame retardants (OPFRs) are used in many consumer products, and their presence in our environment raises concerns about potential health dangers. In humans, exposure to OPFRs, such as tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is associated with metabolic disorders such as obesity, hyperglycemia, and insulin resistance. Our current study seeks to determine how TDCPP exposure affects body composition, glucose homeostasis, and energy balance in a rodent model. C57Bl/6 J mice were divided into two weight-matched groups and fed purified low phytoestrogen diets containing either 0.1 % DMSO (control) or TDCPP 415 mg/kg resulting in an approximate exposure of 50 mg/kg/day. Both male and female mice were used. Promethion metabolic cages were used to measure the rates of oxygen consumption and CO₂ generation, food intake, and locomotion. Body composition was measured using nuclear magnetic resonance relaxometry. Mice underwent a glucose tolerance test, and hyperinsulinemic euglycemic clamp was used to assess insulin sensitivity. Male TDCPP-treated mice showed higher food intake and energy expenditure without changes in locomotion or energy balance. TDCPP tended to differentially affect respiratory exchange ratio, which was increased in males and decreased in females. Male mice showed impaired glucose tolerance, whereas female mice did not. Hyperinsulinemic clamp revealed no significant decrease in the glucose infusion rate of TDCPP-exposed animals. However, hepatic glucose production during hyperinsulinemia was increased compared to controls signifying liver-specific insulin resistance. This study supports the cause for concern related to detrimental metabolic health effects of TDCPP exposure.