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Microplastics (MPs) are ubiquitous in the environment and pose substantial threats to the water ecosystem. However, the impact of natural aging of MPs on their toxicity has rarely been considered. This study found that visible light irradiation with hydrogen peroxide at environmentally relevant concentration for 90 days significantly altered the physicochemical properties and mitigated the toxicity of polyamide (PA) fragments to infantile zebrafish. The size of PA particles was reduced from ∼8.13 to ∼6.37 μm, and nanoparticles were produced with a maximum yield of 5.03%. The end amino groups were volatilized, and abundant oxygen-containing groups (e.g., hydroxyl and carboxyl) and carbon-centered free radicals were generated, improving the hydrophilicity and colloidal stability of degraded MPs. Compared with pristine PA, the depuration of degraded MPs mediated by multixenobiotics resistance was much quicker, leading to markedly lower bioaccumulation in fish and weaker inhibition on musculoskeletal development. By integrating transcriptomics and transgenic zebrafish [Tg(lyz:EGFP)] tests, differences in macrophages-triggered proinflammatory effects, apoptosis via IL-17 signaling pathway, and antioxidant damages were identified as the underlying mechanisms for the attenuated toxicity of degraded MPs. This work highlights the importance of natural degradation on the toxicity of MPs, which has great implications for risk assessment of MPs.

The increasing applications of single-layer molybdenum disulfide (SLMoS2) pose great potential risks associated with environmental exposure. This study found that metallic-phase SLMoS2with nanoscale (N-1T-SLMoS2, ∼400 nm) and microscale (M-1T-SLMoS2, ∼3.6 μm) diameters at 10–25 mg/L induced significant algal growth inhibition (maximum 72.7 and 74.6%, respectively), plasmolysis, and oxidative damage, but these alterations were recoverable. Nevertheless, membrane permeability, chloroplast damage, and chlorophyll biosynthesis reduction were persistent. By contrast, the growth inhibition (maximum 55.3%) and adverse effects of nano-sized semiconductive-phase SLMoS2(N-2H-SLMoS2, ∼400 nm) were weak and easily alleviated after 96 h of recovery. N-1T-SLMoS2(0.011 μg/h) and N-2H-SLMoS2(0.008 μg/h) were quickly biodegraded to soluble Mo compared with M-1T-SLMoS2(0.004 μg/h) and excreted by algae. Incomplete biodegradation of SLMoS2(26.8–43.9%) did not significantly mitigate its toxicity. Proteomics and metabolomics indicated that the downregulation of proteins (50.7–99.2%) related to antioxidants and photosynthesis and inhibition of carbon fixation and carbohydrate metabolism contributed to the persistent phytotoxicity. These findings highlight the roles and mechanisms of the size and phase in the persistent phytotoxicity of SLMoS2, which has potential implications for risk assessment and environmental applications of nanomaterials.

To comprehensively clarify human exposure to halogenated flame retardants (HFRs) and polychlorinated biphenyls (PCBs) through dermal uptake and hand-to-mouth intake, skin wipe samples from four typical skin locations from 30 volunteers were collected. The total concentration of the target chemicals (24 HFRs and 16 PCBs) ranged from 203 to 4470 ng/m2. BDE-209 and DBDPE accounted for about 37 and 40% of ∑24HFRs, respectively, and PCB-41 and PCB-110 were the dominant PCB congeners, with proportion of 24 and 10%, respectively. Although exhibiting relatively lower concentrations of contaminants than bared skin locations, clothing-covered skin areas were also detected with considerable levels of HFRs and PCBs, indicating clothing to be a potentially significant exposure source. Significant differences in HFR and PCB levels and profiles were also observed between males and females, with more lower-volatility chemicals in male-bared skin locations and more higher-volatility compounds in clothing-covered skin locations of female participants. The mean estimated whole-body dermal absorption doses of ∑8HFRs and ∑16PCBs (2.9 × 10–4and 6.7 × 10–6mg/kg·d) were 1–2 orders of magnitude higher than ingestion doses via hand-to-mouth contact (6.6 × 10–7and 3.1 × 10–7mg/kg·d). The total noncarcinogenic health risk resulted from whole-body dermal absorption and oral ingestion to ∑7HFRs and ∑16PCBs were 5.2 and 0.35, respectively.

Understanding environmental fate is a prerequisite for the safe application of nanoparticles. However, the fundamental persistence and environmental transformation of single-layer molybdenum disulfide (SLMoS2, a 2D nanosheet attracting substantial attention in various fields) remain largely unknown. The present work found that the dissolution of SLMoS2was pH and dissolved oxygen dependent and that alterations in phase composition significantly occur under visible light irradiation. The 1T phase was preferentially oxidized to yield soluble species (MoO42–and SO42–), and the 2H phase remained as a residual. The transformed SLMoS2exhibited a ribbon-like and multilayered structure and low colloidal stability due to the loss of surface charge. Dissolved oxygen competitively captured the electrons of SLMoS2to generate superoxide radicals and accelerated the dissolution of nanosheets. Compared to pristine 1T–phase SLMoS2, the transformed 2H–phase SLMoS2could not easily enter algal cells and induced a low developmental inhibition, oxidative stress, plasmolysis, photosynthetic toxicity and metabolic perturbation. The downregulation of amino acids and upregulation of unsaturated fatty acids contributed to the higher toxicity of 1T–phase SLMoS2. The dissolved ions did not induce apparent phytotoxicity. The connections between environmental transformation (phase change and ion release) and phytotoxicity provide insights into the safe design and evaluation of 2D nanomaterials.

Thorough investigations of the environmental fate and risks are necessary for the safe application of engineered nanomaterials. Nevertheless, the current understanding of potential transformations of MoS2(an intensively studied two-dimensional nanosheet) upon interactions with ubiquitous environmentally relevant thiols (ERTs) in water is limited. This study revealed that two ERTs, l-cysteine and mercaptoacetic acid, could modify MoS2by covalently grafting thiol groups on S atoms of 1T phases, improving the colloidal persistence and chemical stability of MoS2. Compared with the pristine form, MoS2–thiols with higher dispersity exhibited significantly mitigated envelopment and ultrastructural damage to microalgae. MoS2-triggered growth inhibition, upregulation of reactive oxygen species, photosynthetic injury, and metabolic perturbation in algae were remarkably attenuated by ERTs. The diminished capability for MoS2to generate reactive intermediates and glutathione oxidation driven by ERTs caused the weakness of oxidative stress and negative effects. Additionally, molecular dynamics simulations demonstrated that ERTs altered the extent of the influence of MoS2on the secondary structures and functions of adsorbed intracellular proteins, which also contributed to the lower phytotoxicity of MoS2. Our findings provide evidence for the crucial role of specific organic ligands in the risk of MoS2in aquatic environments.

To gather enough energy to respond to harmful stimuli, most immune cells quickly shift their metabolic profile. This process of immunometabolism plays a critical role in the regulation of immune cell function. Triclosan, a synthetic antibacterial component present in a wide range of consumer items, has been shown to cause immunotoxicity in a number of organisms. However, it is unclear whether and how triclosan impacts immunometabolism. Here, human macrophages were used as model cells to explore the modulatory effect of triclosan on immunometabolism. Untargeted metabolomics using integrated liquid chromatography–mass spectrometry (LC–MS) and gas chromatography–mass spectrometry (GC–MS) revealed that triclosan changed the global metabolic profile of macrophages. Furthermore, Seahorse energy analysis and 13C isotope-based metabolic flux analysis revealed that triclosan decreased mitochondrial respiratory activity and promoted a metabolic transition from oxidative phosphorylation to glycolysis. Triclosan also polarizes macrophages to the proinflammatory M1 phenotype and activates the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing receptor 3 (NLRP3) inflammasome, which is consistent with triclosan-induced metabolic phenotypic modifications. Collectively, these findings showed that triclosan exposure at micromolar concentrations caused metabolic reprogramming in macrophages, which triggered an inflammatory response. These findings are important for understanding the immunotoxicity caused by triclosan, which is necessary for determining the risk posed by triclosan in the environment.