Agricultural plastic mulching films are the main source of plastic pollution in farmlands. Long-term exposure to light radiation may cause their aging and degradation, and precipitation and irrigation further promote the release of additives into the water, posing a potential threat to the ecological environment. This study systematically investigated the changes in the physical and chemical properties of the film during aging and the neurotoxic effects of its leachate. The results showed that light radiation promoted the presence of oxygen-containing functional groups, increasing with the degree of aging, which facilitated the release of plastic additives. The toxicity assessment using the Caenorhabditis elegans model indicated that high concentrations of leachate could significantly inhibit the locomotion ability of the nematode. It is notable that the exudates from the photoaging film had a stronger inhibitory effect on the locomotion behavior of the nematode. Further analysis revealed that the aged film leachate reduced the content of key neurotransmitters in the nematode. Molecular biology studies showed that this neurotoxic effect was closely related to the expression inhibition of neurotransmission-related genes (dop-3, eat-4, mod-1, and unc-47). This study provides important scientific evidence for assessing the environmental risks of agricultural plastic mulching film pollution.
Cellulose biochar was prepared via microwave-assisted pyrolysis at 500 degrees C and subsequently composited with sepiolite through ball milling to fabricate a sepiolite-biochar adsorbent for efficient tetracycline (TC) removal from water. The influence of the sepiolite-to-biochar mass ratio on the structure, composition, porosity, and adsorption performance was systematically investigated. Among biochars prepared at different pyrolysis temperatures, BC500 exhibited the highest TC adsorption capacity and was therefore selected as the precursor for composite preparation. The 1:1 sepiolite-biochar composite achieved 92.8% removal of 20 mg L-1 TC within 65 min at pH 5 using 1 g L-1 adsorbent. Adsorption kinetics followed a pseudo-second-order model, and equilibrium data were well described by the Langmuir isotherm, indicating monolayer chemisorption. Mechanistic analyses suggested that adsorption was dominated by pore filling and pi-pi interactions, supplemented by hydrogen bonding, electrostatic interactions, and cation exchange. The composite demonstrated excellent cyclic stability, retaining over 86% of its initial TC removal efficiency after three adsorption-desorption cycles. These findings highlight the potential of sepiolite-biochar composites as cost-effective, efficient, and reusable adsorbents for antibiotic-contaminated water, providing guidance for the design of mineral-biochar composites with enhanced adsorption performance.
Central air‑conditioning filter (CACF) dust can accumulate persistent organic pollutants, yet its dioxin content remains under characterized. As a stable, long‑term sampler that is minimally influenced by short‑term human activity, CACF dust offers unique insight into indoor dioxin exposure. Here, we quantified PCDD/Fs in CACF dust collected from public spaces near a waste‑to‑energy (WtE) plant in eastern China. Total PCDD/F concentrations ranged from 105.8 to 362.7 ng/kg (ΣTEQ: 2.82-7.98 ng‑TEQ/kg) and were broadly consistent across seasons and wind directions. Hepta‑ and octa‑chlorinated congeners dominated the profiles, with minor shifts associated with CACF heating operations. Source‑fingerprinting and PCA identified WtE emissions and traffic as the primary contributors. Probabilistic risk assessment following USEPA guidance indicated that both carcinogenic and non‑carcinogenic risks were below commonly applied safety thresholds for all age groups. These results demonstrate that CACF dust is a reliable indicator of indoor dioxin exposure and provide an empirical basis for targeted control strategies to mitigate long‑term health risks in WtE‑impacted areas.
Tire wear particles (TWP) are a prevalent form of microplastics (MPs) extensively distributed in the environment, raising concerns about their environmental behaviors and risks. However, knowledge regarding the properties and toxicity of these particles at environmentally relevant concentrations, specifically regarding the role of environmentally persistent free radicals (EPFRs) generated during TWP photoaging, remains limited. In this study, the evolution of EPFRs on TWP under different photoaging times and their adverse effects on Caenorhabditis elegans were systematically investigated. The photoaging process primarily resulted in the formation of EPFRs and reactive oxygen species (O2•−, ⋅OH, and 1O2), altering the physicochemical properties of TWP. The exposure of nematodes to 100 μg/L of TWP-50 (TWP with a photoaging time of 50 d) led to a significant decrease in locomotory behaviors (e.g., head thrashes, body bends, and wavelength) and neurotransmitter contents (e.g., dopamine, glutamate, and serotonin). Similarly, the expression of neurotransmission-related genes was reduced in nematodes exposed to TWP-50. Furthermore, the addition of free-radical inhibitors significantly suppressed TWP-induced neurotoxicity. Notably, correlation analysis revealed a significantly negative correlation between EPFRs levels and the locomotory behaviors and neurotransmitter contents of nematodes. Thus, it was concluded that EPFRs on photoaged TWP induce neurotoxicity by affecting neurotransmission. These findings elucidate the toxicity effects and mechanisms of EPFRs, emphasizing the importance of considering their contributions when evaluating the environmental risks associated with TWP.
Microplastics (MPs) are ubiquitous environmental contaminants that exert multiple toxicological effects. Current studies have mainly focused on modeled or unaged MPs, which lack environmental relevance. The generation and toxicity of environmentally persistent free radicals (EPFRs) on photoaging polystyrene (PS) have not been well studied, and the role of EPFRs on the toxic effects of photoaged PS is easily ignored. Photoaging primarily produces EPFRs, followed by an increase in reactive oxygen species (ROS) content and oxidative potential, which alter the physicochemical properties of photoaged PS. The mean lifespan and lipofuscin content were significantly altered after acute exposure to photoaged PS for 45 d (PS-45) and 60 d (PS-60) in Caenorhabditis elegans. Intestinal ROS and gst-4::GFP expression were enhanced, concomitant with the upregulation of associated genes. Treatment with N-acetyl-L-cysteine by radical quenching test significantly decreased EPFRs levels on the aged PS and inhibited the acceleration of the aging and oxidative stress response in nematodes. Pearson’s correlation analysis also indicated that the EPFRs levels were significantly associated with these factors. Thus, the EPFRs generated on photoaged PS contribute to the acceleration of aging by oxidative stress. This study provides new insights into the potential toxicity and highlights the need to consider the role of EPFRs in the toxicity assessment of photoaged PS.
Microplastics, recognized as emerging contaminants, are commonly observed to be charged in the environment, potentially exerting toxic effects on various organisms. However, the transgenerational reproductive toxicity and underlying mechanisms of polystyrene (PS), particularly carboxyl-modified PS (PS-COOH) and amino-modified PS (PS-NH2), remain largely unexplored. In this study, the parental generation (P0) of Caenorhabditis elegans was subjected to environmental concentrations (0.1-100 mu g/L) of PS, PS-COOH, and PS-NH2, with subsequent generations (F1-F4) cultured under normal conditions. Exposure to PS-NH2 at concentrations of 10-100 mu g/L exhibited more pronounced reproductive toxicity compared to PS or PS-COOH, resulting in decreased brood size, egg ejection rate, number of fertilized eggs, and cell corpses per gonad. Similarly, maternal exposure to 100 mu g/L of PS-NH2 induced more severe transgenerational reproductive effects in C. elegans. Significant increases in H3 on lysine 4 dimethylation (H3K4me2) and H3 on lysine 9 trimethylation (H3K9me3) levels were observed in the subsequent generation, concurrent with the transgenerational upregulation of set-30 and met-2 following parental exposure to PS, PS-COOH, and PS-NH2. Correlation analyses revealed significant associations between the expression of these genes with the reproductive ability. Molecular docking studies suggested that PS-NH2 exhibited higher affinity for SET-30 and MET-2. Further analysis demonstrated that transgenerational effects on reproduction were absent in set-30(gk315) and met-2(n4256) mutants, highlighting the pivotal role of set-30 and met-2 in mediating the transgenerational effect. This study provides novel insights into the environmental risks associated with negatively and positively charged microplastics.
Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that are ubiquitously detected in various environments and have toxic effects on various organisms. Nevertheless, the transgenerational reproductive toxicity and underlying mechanisms of PS-NPs remain largely unknown, especially for photoaged PS-NPs under ultraviolet irradiation. In this study, only the parental generation (P0) was exposed to virgin and aged PS-NPs at environmentally relevant concentrations (0.1-100 μg/L), and subsequent generations (F1-F4) were cultured under normal conditions. Ultraviolet irradiation induced the generation of environmentally persistent free radicals and reactive oxygen species, which altered the physical and chemical characteristics of PS-NPs. The results of toxicity testing suggested that exposure to aged PS-NPs caused a more severe decrease in brood size, egg ejection rate, number of fertilized eggs, and hatchability than did the virgin PS-NPs in the P0, F1, and F2 generations. Additionally, a single maternal exposure to aged PS-NPs resulted in transgenerational effects on fertility in the F1 and F2 generations. Increased levels of H3K4 and H3K9 methylation were observed in the F1 and F2 generations, which were concomitant with the transgenerational downregulation of the expression of associated genes, such as spr-5, set-17, and met-2. On the basis of correlation analyses, the levels of histone methylation and the expression of these genes were significantly correlated to transgenerational reproductive effects. Further research showed that transgenerational effects on fertility were not observed in spr-5(by134), met-2(n4256), and set-17(n5017) mutants. Overall, maternal exposure to aged PS-NPs induced transgenerational reproductive effects via H3K4 and H3K9 methylation, and the spr-5, met-2, and set-17 genes were involved in the regulation of transgenerational toxicity. This study provides new insights into the potential risks of photoaging PS-NPs in the environment.
Microplastics (MPs) are emerging environmental contaminants that often co-exist with tetrabromobisphenol A (TBBPA) in the environment. However, the joint effect of TBBPA and photoaged MPs at ambient concentrations remains unknown largely. In this study, the combined toxicity of ultraviolet-aged polystyrene (UV-PS) and TBBPA was investigated in Caenorhabditis elegans. UV irradiation could change the physical and chemical characteristics of polystyrene (PS), and UV-PS (90.218 μg/g) showed a stronger adsorption capacity than PS of 79.424 μg/g. Toxicity testing showed that 1 μg/L UV-PS enhanced the toxic effect of 1 μg/L TBBPA by reducing body length, locomotion behavior, and brood size in nematodes. Using ROS production, lipofuscin accumulation, and expression of gst-4::GFP as endpoints, the combined exposure of UV-PS and TBBPA induced stronger oxidative stress than TBBPA alone. Joint exposure to UV-PS and TBBPA significantly increased of Nile red and blue food dye in its intestinal tract compared to that in the TBBPA exposure group, indicating that co-exposure enhanced intestinal permeability. After co-exposure to UV-PS and TBBPA, the expression of the associated genes detected increased significantly. Therefore, UV-PS enhances the adverse effects of TBBPA through intestinal damage and oxidative stress in nematodes. These findings suggest that the co-presence of photoaged PS and TBBPA results in high environmental risks.
Ambient exposure to polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) is suspected to cause adverse human health outcomes. Herein, serum samples from 40 residents in the neighborhood of a municipal solid waste incinerator (MSWI) in the metropolitan area were measured for PCDD/Fs. The mean toxic equivalent (TEQ) concentration of total PCDD/Fs in human serum samples was 16.8 pg TEQ/g lipid. Serum PCDD/F levels were significantly higher in residents adjacent to the MSWI than in those from areas far from the emission source (p < 0.01). In addition, there were no significant associations between serum PCDD/Fs levels and factors, such as gender, age, and BMI in donors. For non-occupationally exposed populations, OCDD and 1,2,3,7,8-PeCDD in serum are available as indicators of total PCDD/Fs and total TEQ, respectively. The atmospheric PCDD/Fs levels were within a relatively low range in areas upwind and downwind of the MSWI. The results of the principal component analysis showed a distinct difference in PCDD/F congener patterns between air and serum samples, suggesting inhalation exposure could have a limited influence on the human body burden. Our findings will deepen the current knowledge of endogenous PCDD/F exposure in urban populations, and also facilitate public health protection strategies near MSWIs.
Prolonged exposure to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) can pose several adverse outcomes on human health. However, there is limited information on public health associated with indoor PCDD/F exposure in residential environments. Here, we examined PCDD/F concentrations in indoor air and indoor dust samples obtained from households near a municipal solid waste incineration (MSWI) plant. Our measurements revealed that the toxic equivalent (TEQ) concentrations of PCDD/Fs in indoor air ranged from 0.01 to 0.05 pg TEQ/m3, which were below intervention thresholds (0.6 pg TEQ/m3). Additionally, the TEQ concentrations of PCDD/Fs in indoor dust ranged from 0.30 to 11.56 ng TEQ/kg. Higher PCDD/F levels were found in household dust in the town of Taopu compared to those in the town of Changzheng. Principal component analysis (PCA) of PCDD/Fs suggested that waste incineration was the primary source of PCDD/Fs in indoor air, whereas PCDD/Fs in indoor dust came from multiple sources. The results of the health risk assessment showed the carcinogenic risk due to indoor PCDD/F exposure was higher for adults than for nursery children and primary school children. The carcinogenic risks of PCDD/Fs for age groups residing near the MSWI plant were all less than the risk threshold (10-5). Our findings will help to better understand the levels of PCDD/F exposure among urban populations living in residential communities around the MSWI plant and to formulate corresponding control measures to reduce probabilistic risk implications.
Tris(1,3-dichloro-2-propyl)phosphate (TDCPP) is a halogen-containing organophosphorus chemical that is widely employed in various consumer products with a high production volume. As an additive flame retardant (FR), TDCPP tends to be released into the environment through multiple routes. It is ubiquitous in environmental media, biotic matrixes, and humans, and thus is deemed to be an emerging environmental contaminant. To date, significant levels of TDCPP and its primary diester metabolite, bis(1,3-dichloro-2-propyl)phosphate, have been detected in human samples of seminal plasma, breast milk, blood plasma, placenta, and urine, thereby causing wide concern about the potential human health effects resulting from exposure to this chemical. Despite the progress in research on TDCPP over the past few years, we are still far from fully understanding the environmental behavior and health risks of this emerging contaminant. Thus, this paper critically reviews the environmental occurrence, exposure, and risks posed by TDCPP to organisms and human health among the literature published in the last decade. It has been demonstrated that TDCPP induces acute-, nerve-, developmental-, reproductive-, hepatic-, nephron-, and endocrine-disrupting toxicity in animals, which has caused increasing concern worldwide. Simultaneously, TDCPP induces cytotoxicity by increasing the formation of reactive oxygen species and inducing endoplasmic reticulum stress in multiple human cell lines in vitro, and also causes endocrine-disrupting effects, including reproductive dysfunction and adverse pregnancy outcomes, according to human epidemiology studies. This review not only provides a better understanding of the behavior of this emerging contaminant in the environment, but also enhances the comprehension of the health risks posed by TDCPP exposure to ecosystems and humans.
Tetrabromobisphenol A (TBBPA) is a commonly used brominated flame retardant, which has a wide range of toxic effects on organisms. This study investigated the cytotoxic effects on human hepatocytes (L02 cells) after treated with 0, 5, 10, 20, and 40 μM of TBBPA. Results showed that TBBPA significantly increased intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and the ratio of oxidized/reduced glutathione (GSSG/GSH) dose-dependently. TBBPA also decreased the cell mitochondrial membrane potential (MMP), caused the release of cytochrome C (Cyt C) to cytoplasm and promoted the expression of caspase-9 and caspase-3, and finally increased the level of apoptosis. The ROS inhibitor N-acetyl-L-cysteine (NAC) relieved the oxidative stress responses, and prevented the decrease of MMP and increase of apoptosis. In addition, TBBPA promoted the expression of antioxidant genes related to Nrf2, such as quinone oxidoreductase 1 (NQO1), catalase (CAT), and heme oxygenase 1 (HO-1). Oxidative stress initiated by TBBPA, activated mitochondrial apoptosis and Nrf2 pathway, and increased the degree of apoptosis in L02 cells.