In organisms, long-term nanopolystyrenes (PS-NPs) exposure can cause toxicity, including neurotoxicity. Quercetin, the flavonol with extensive distribution within plants, possesses diverse biological activities. Nevertheless, the possible effect of quercetin to suppress PS-NPs-induced neurotoxicity and its associated mechanism remains unknown. Thus, in the present work, Caenorhabditis elegans was utilized as the model animal to investigate quercetin\'s pharmacological effect on suppressing PS-NPs-induced neurotoxicity and the underlying mechanism. PS-NPs exposure at 1-100 μg/L remarkably reduced locomotion behavior, while only PS-NPs exposure at 100 μg/L significantly decrease sensory perception behavior. Meanwhile, the increase in the number of worms with dopaminergic neurodegeneration was detected in nematodes exposed to 100 μg/L PS-NPs and the decreased dopamine content was observed within nematodes exposed to 10-100 μg/L PS-NPs, demonstrating the function of dopaminergic neurodegeneration and disruption of dopamine metabolism in inducing PS-NPs toxicity on neuron capacity. After 100 μg/L PS-NPs exposure, the 25-100 μM quercetin treatment effectively increased the locomotion behavior and the sensory perception behavior. Developmentally, quercetin treatment (100 μM) remarkably enhanced fluorescence intensity while decreasing worm number with neurodegeneration within BZ555 transgenic strains exposed to 100 μg/L PS-NPs. Physiologically, quercetin treatment (100 μM) significantly enhanced dopamine content within nematodes exposed to 100 μg/L PS-NPs. Molecularly, quercetin treatment (100 μM) notably decreased the expressions of genes governing neurodegeneration (mec-4, deg-3, unc-68, itr-1, clp-1, and asp-3) while significantly increasing the expression of genes governing dopamine metabolism (cat-2, cat-1, dop-1, dop-2, dop-3). As revealed by molecular docking results, quercetin might bind to excitotoxic-like ion channels receptors (MEC-4 and DEG-3) and dopamine secreted protein (CAT-2). Consequently, findings in this work demonstrated that long-term PS-NPs exposure within the μg/L range (1-100 μg/L) was toxic to neuron capacity, which was associated with the enhancement in dopaminergic neurodegeneration and disruption of dopamine metabolism. Notably, PS-NPs-mediated neurotoxicity to nematodes is probably suppressed through subsequent quercetin treatment.

Nanoplastics (NPs) pose great challenges to soil-groundwater systems. This study investigated the transport and retention of self-synthesized 0.5-μm polystyrene NPs with different shapes using column experiments. The regular NPs were with spherical shapes, while the irregular NPs were with toroid-like shapes. The toroid-like shapes were the irregular shapes (with low aspect ratio) which have not been studied yet. The explorations were carried out in both 5-25 mM NaNO3 and 1-10 mM Ca(NO3)2 solutions. Both breakthrough curves (BTCs) and retained profiles (RPs) were monitored. Our findings uncovered a clear disparity in the transport of irregular and regular NPs, with irregular particles exhibiting lower transport ability compared to the regular ones. For example, the average breakthrough plateaus of the regular and irregular NPs were ∼0.9 and ∼0.5, respectively, in 10 mM NaNO3. In-depth theoretical analysis indicated that the lower XDLVO interaction energy barrier between the irregular NPs and quartz sand was one factor, and the greater margination of irregular NPs on quartz sand, as verified by the numerical simulation, was another factor leading to the decreased transport and increased retention of the irregular NPs. The obtained results highlighted the significance of considering particle shape in future modelling and predicting the fate of NPs in real environmental circumstances.

Microplastics (MPs) and nanoplastics (NPs) have increasingly been found in the environment. Until recently, most MPs/NPs toxicological research has been done in aquatic systems resulting in a gap in knowledge regarding terrestrial systems. Plastics have been shown to enter the circulatory system of humans, and can accumulate within organs, little is known about the effect this has on health. Heart disease is the leading cause of death globally, so it\'s critical to understand the possible impacts MPs/NPs have on the heart. The Drosophila model has been growing in popularity within the toxicology field, it allows for affordable and rapid research on the impacts of a variety of toxins, including plastics. Some research has examined toxicological effects of plastics on the fly, evaluating the effects on mortality, fecundity, development, and locomotion. However, no one has studied the effects on the Drosophila heart. We utilize the Drosophila model to identify the potential effects of oral exposure to polystyrene MPs (1 µm in diameter) and NPs (0.05 µm in diameter) particles on heart function. Flies were exposed to 1.4 × 1011 particles/d/kg of larvae for MPs and 1.2 × 1018 particles/d/kg of larvae for NPs from egg to pupal eclosion. Heart function was then analyzed utilizing semi-intact dissections and Semi-automatic Optic Heartbeat Analysis software (SOHA). Following exposure to MPs and NPs we see sexually dimorphic changes to heart size and function. This study highlights the importance of additional Drosophila MPs/NPs research to identify the molecular mechanisms behind these changes.

Microplastics (MPs) are solid plastic particles less than or equal to 5 mm in size that are insoluble in water, and when the diameter is further reduced to <1 micrometer (μm), we call them nanoplastics (NPs). MPs and NPs are widely present in the atmosphere, and plastic particles have also been detected in the sputum of patients with respiratory diseases. This warns us that these tiny plastic particles are a potential threat to human respiratory health. The lungs, as the main organs of the respiratory system, are more likely to be adversely affected by inhaled NPs. However, the mechanism of transport and transformation of NPs in the lung is not clear, so our review mainly focuses on a series of effects and mechanisms of NPs on lung cells through absorption, distribution, metabolism, excretion (ADME) after inhalation into the human body. The most commonly used models in these experimental studies we focus on are A549 and BEAS-2B cells, which are used to model the lung cell response to plastic particles. In addition, we also summarize some shortcomings of these experiments and prospects for future studies, hoping to provide further clues for future studies and contribute to the prevention of related hazards and diseases.

Nanoplastics could cause toxic effects on organism and their offsprings; however, how this transgenerational toxicity is formed remains largely unclear. We here examined potential involvement of germline histone acetylation regulation in modulating transgenerational toxicity of polyetyrene nanoparticle (PS-NP) in Caenorhabditis elegans. At parental generation (P0-G), PS-NP (1-100 μg/L) decreased expressions of germline cbp-1 and taf-1 encoding histone acetyltransferases, as well as germline expressions of sir-2.1 and hda-3 encoding histone deacetylase. Decrease in these 4 germline genes were also observed in the offspring of PS-NP (1-100 μg/L) exposed nematodes. Germline RNAi of cbp-1, taf-1, sir-2.1 and hda-3 resulted in more severe transgenerational PS-NP toxicity on locomotion and brood size. Meanwhile, in PS-NP exposed nematodes, germline RNAi of cbp-1, taf-1, sir-2.1 and hda-3 increased expression of genes encoding insulin, FGF, Wnt, and/or Notch ligands and expressions of their receptor genes in the offspring. Susceptibility to transgenerational PS-NP toxicity in cbp-1(RNAi), taf-1(RNAi), sir-2.1(RNAi), and hda-3 (RNAi) was inhibited by RNAi of these germline ligands genes. Moreover, histone deacetylase inhibition served as molecular initiating event (MIE) leading to transgenerational toxicity in epigenetic adverse outcome pathway (AOP) for nanoplastics. Our data provided evidence that germline histone acetylation regulation functioned as an important mechanism for transgenerational toxicity of nanoplastics at predicted environmental doses (PEDs) by affecting secreted ligands in organisms.

BACKGROUND: In 2019 the World Health Organisation published a report which concluded microplastics in drinking water did not present a threat to human health. Since this time a plethora of research has emerged demonstrating the presence of plastic in various organ systems and their deleterious pathophysiological effects.
METHODS: A scoping review was undertaken in line with recommendations from the Johanna Briggs Institute. Five databases (PubMed, SCOPUS, CINAHL, Web of Science and EMBASE) were systematically searched in addition to a further grey literature search.
RESULTS: Eighteen articles were identified, six of which investigated and characterised the presence of microplastics and nanoplastics (MNPs) in the human urinary tract. Microplastics were found to be present in kidney, urine and bladder cancer samples. Twelve articles investigated the effect of MNPs on human cell lines associated with the human urinary tract. These articles suggest MNPs have a cytotoxic effect, increase inflammation, decrease cell viability and alter mitogen-activated protein kinases (MAPK) signalling pathways.
CONCLUSIONS: Given the reported presence MNPs in human tissues and organs, these plastics may have potential health implications in bladder disease and dysfunction. As a result, institutions such as the World Health Organisation need to urgently re-evaluate their position on the threat of microplastics to public health.
UNASSIGNED: This scoping review highlights the rapidly emerging threat of microplastic contamination within the human urinary tract, challenging the World Health Organisation\'s assertion that microplastics pose no risk to public health. The documented cytotoxic effects of microplastics, alongside their ability to induce inflammation, reduce cell viability and disrupt signalling pathways, raise significant public health concerns relating to bladder cancer, chronic kidney disease, chronic urinary tract infections and incontinence. As a result, this study emphasises the pressing need for further research and policy development to address the challenges surrounding microplastic contamination.

Nanoplastics (NPs) cause serious contamination of drinking water and potential damage to human health. This study aimed to investigate the effects of NPs with different particle sizes and concentrations on the reproductive function of male mice. In this study, free drinking water exposure was used to expose male BALB/C mice to PS-NPs (20 nm, 200 nm, and 1000 nm) at 0.1 mg/L, 1 mg/L, and 5 mg/L for 4 months. The male reproductive function of the mice was assessed after NPs exposure, and fecal and blood samples were collected for macrogenomics and metabolomics. The results showed that PS-NPs resulted in mice with reduced testicular organ coefficients, decreased sperm quality, altered testicular tissue structure, disturbed sex hormone levels, and abnormal levels of inflammatory factors and oxidative stress. Furthermore, this study found that NP exposure affected the alteration of gut communities and metabolic pathways related to male reproduction, such as Clostridium and glutathione metabolism. Importantly, we found an effect of NP particle size on reproductive function. In the future, more attention should be paid to the smaller particle sizes of NPs.

BACKGROUND: The increasing presence of plastics in the human diet is raising public concern about the potential risks posed by nanoplastic (NP) particles, which can emerge from the degradation of plastic debris. NP ingestion poses particular risks to individuals with inflammatory bowel disease (IBD), as compromised epithelial barriers may facilitate NP translocation.
METHODS: In vitro, bone-marrow-derived macrophages (BMDMs) were exposed to 25 nm polymethacrylate (PMMA) or 50 nm polystyrene (PS) particles to assess morphological changes and alterations in pro- and anti-inflammatory gene expression. In vivo, mice received PMMA NP particles for 6 months before acute dextran sodium sulfate (DSS) colitis was induced to investigate NP impacts on intestinal health and inflammation.
RESULTS: PMMA and PS NP exposure in BMDMs induced morphological changes indicative of a proinflammatory phenotype characterized by enlarged amoeboid cell shapes. It also triggered an inflammatory response, indicated by increased expression of proinflammatory cytokines such as Tnfa and Il6. Unexpectedly, long-term PMMA NP administration did not affect the intestinal epithelial barrier or exacerbate acute DSS-induced colitis in mice. Colonoscopy and histological analysis revealed no NP-related changes, suggesting adverse effects on intestinal health or inflammation.
CONCLUSIONS: Our findings from animal models offer some reassurance to IBD patients regarding the effects of NP ingestion. However, variations in lifestyle and dietary habits may lead to significantly higher plastic intake in certain individuals, raising concerns about potential long-term gastrointestinal effects of lifelong plastic consumption.

Micro-nanoplastic particulates (MNPs) have been identified in both indoor and outdoor environments. From these real-world exposures, MNPs have been identified in human fluids and organ tissues, including the placenta and breastmilk. Laboratory studies have identified MNPs are capable of crossing the placental barrier and depositing in fetal tissues; however, it remained unclear if MNPs persist in offspring tissues after birth. Six pregnant Sprague-Dawley rats were divided equally into two groups: control and exposed to polyamide-12 (PA-12) MNP aerosols (11.46 ± 3.78 mg/m3) over an average of 4.35 h ± 0.39 for 10 non-consecutive days between gestational day (GD) 6 - GD 19, in our custom rodent exposure chamber, allowing for whole-body inhalation. Two-weeks after delivery in-house, offspring tissues (i.e. lung, liver, kidney, heart, brain) from 1 male and 1 female pup per litter were fixed in 4 % paraformaldehyde, sectioned, stained with hematoxylin and eosin, and assessed using hyperspectral dark-field microscopy. PA-12 MNPs were identified in all offspring tissues of the exposed dams. No MNPs were visualized in control tissues. These findings have important implications for human MNPs translocation, deposition, maternal/fetal health, and the developmental origins of health and disease. Further research is warranted to quantify MNPs mass deposition, biological accumulation, and systemic toxicity.

Estuaries can behave as plastic pollution hotspots, although the dynamics of accumulation in these unique habitats are not understood. We quantified the current levels of meso-, micro-, and nanoplastic pollution in four Los Angeles County estuaries for the first time, as a function of distance from the water outlet and local population density. Fourier-transform infrared spectroscopy (FTIR) and microscope imaging revealed the presence of six types of plastic; polyethylene or polypropylene dominated the meso- and microplastic, and nanoplastics were identified as mainly polyolefin fibers. The distribution was heterogeneous throughout, although the sand between the river mouth and ocean generally contained more plastic than inland control samples. Population density did not appear to affect the abundance of plastic estuarine pollution. Other factors, such as waste treatment effluent, recreation, and river geography, may contribute to plastic deposition. A positive correlation between meso- and microplastic abundance provides insight into such mechanisms for accumulation.