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Plastic pollution and its potential risks have been raising public concerns as a global environmental issue. Global plastic waste may double by 2030, posing a significant challenge to the remediation of environmental plastics. In addition to finding alternative products and managing plastic emission sources, effective removal technologies are crucial to mitigate the negative impact of plastic pollution. However, current remediation strategies, including physical, chemical, and biological measures, are unable to compete with the surging amounts of plastics entering the environment. This perspective lays out recent advances to propel both research and action. In this process, phytoaccumulation, phytostabilization, and phytofiltration can be applied to reduce the concentration of nanoplastics and submicron plastics in terrestrial, aquatic, and atmospheric environments, as well as to prevent the transport of microplastics from sources to sinks. Meanwhile, advocating for a more promising future still requires significant efforts in screening hyperaccumulators, coupling multiple measures, and recycling stabilized plastics from plants. Phytoremediation can be an excellent strategy to alleviate global micro/nanoplastic pollution because of the cost-effectiveness and environmental sustainability of green technologies.

The widespread use of plasticizers like phthalate esters (PAEs) has led to environmental and health concerns. The neurobehavioral toxicity of these compounds in marine environments, particularly regulated by the “brain-gut” axis, remains unclear, especially concerning wild demersal fish of high ecological value. Our investigation into the behavioral effects of three common PAEs, i.e., dimethyl phthalate (DMP), di-n-butyl phthalate (DBP), and di(2-ethylhexyl) phthalate (DEHP), and their molecular mechanisms on juvenile Sebastes schlegelii, revealed alarming results from molecular to population levels. After a 20-day foodborne exposure at a low marine environmental concentration (1.0 μg g−1), we observed that all three PAEs significantly increased the thigmotaxis (behavioral tendency to stay close to physical boundaries) and mobility of juvenile fish by 28.2–59.4 % and 23.3–74.5 %, respectively, indicating anxiety-like behavior of fish. DEHP exhibited the most pronounced effects, followed by DBP and DMP. PAEs accumulated in the juvenile fish in the order of brain > liver > gut > muscle, with DEHP showing the highest brain concentrations (23.2 ± 2.98 μg g−1). This accumulation led to oxidative damage, inflammatory responses, and neurodegenerative changes in the optic tectum, resulting in cholinergic system dysfunction. In the gut, PAEs caused inflammatory lesions, disrupted the gut barrier, and altered the gut microbiome, exacerbating the neurotoxicity via “brain-gut” communication. These findings underscore the significant neurobehavioral toxicity of PAEs, emphasizing their critical impact on fish behavior. We also stress the crucial need for further research on fish and other marine species beyond the laboratory scale to fully understand the broader implications of PAE exposure in marine ecosystems and to guide future conservation efforts.

Hematite, as an extensive natural mineral with multiple crystal facets, profoundly affects the migration and transformation of pollutants in the natural environment. However, little is known about the photochemical behavior of microplastics on different facets of hematite in the aquatic environment. In this work, the photoaging of polystyrene microplastics (PS-MPs) on different crystal planes ({001}, {100}, and {012} facets) and related mechanisms were studied. Two-dimensional correlation spectroscopy analysis illustrated that the reaction pathways of PS-MPs photoaging on hematite tended to preferential chemical oxidization. The stronger performance of PS-MPs photoaging, expressed by particle size reduction and surface oxidation, was observed on the {012} crystal facet. Under irradiation, {012} facet-dominated hematite with a narrower bandgap (1.93 eV) reinforced the photogenerated charge carrier separation, and the lower activation energy barrier (1.41 eV calculated from density functional theory) led to effective •OH formation from water oxidation. These findings elucidate the underlying photoaging mechanism of MPs on hematite with different mineralogical phases.

Exposure to micro- and nanoplastics (MNPs) is inevitable due to their omnipresence in the environment. A growing body of studies has advanced our understanding of the potential toxicity of MNPs but knowledge gaps still exist regarding the adverse effects of MNPs on the cardiovascular system and underlying mechanisms, particularly in humans. Here, we reviewed up-to-date data published in the past 10 years on MNP-driven cardiovascular toxicity and mechanisms. Forty-six articles concerning ADME (absorption, distribution, and aggregation behaviors) and toxicity of MNPs in the circulatory system of animals and human cells were analyzed and summarized. The results showed that MNPs affected cardiac functions and caused toxicity on (micro)vascular sites. Direct cardiac toxicity of MNPs included abnormal heart rate, cardiac function impairment, pericardial edema, and myocardial fibrosis. On (micro)vascular sites, MNPs induced hemolysis, thrombosis, blood coagulation, and vascular endothelial damage. The main mechanisms included oxidative stress, inflammation, apoptosis, pyroptosis, and interaction between MNPs and multiple cellular components. Cardiovascular toxicity was determined by the properties (type, size, surface, and structure) of MNPs, exposure dose and duration, protein presence, the life stage, sex, and species of the tested organisms, as well as the interaction with other environmental contamination. The limited quantitative information on MNPs’ ADME and the lack of guidelines for MNP cardiotoxicity testing makes risk assessment on cardiac health impossible. Furthermore, the future directions of cardiovascular research on MNPs are recommended to enable more realistic health risk assessment.