Microplastics (MPs) pose emerging threats to human health, with growing concerns about liver toxicity and other harmful effects from plastic particles. While aquatic species exhibit hepatic vulnerability to micro/nanoplastics, the role of submicroplastics (100 nm-1 μm) in mammalian non-alcoholic fatty liver disease (NAFLD) progression remains unclear. We investigated the effects of a 12-week exposure to 0.5 μm polystyrene MPs (submicroplastics) in drinking water, administering this to ApoE-deficient mice fed either a chow diet (CD) or a Western diet (WD). Submicroplastics accumulated predominantly in the liver and were excreted in the feces. Histologically, submicroplastics significantly increased NAFLD activity scores, hepatic steatosis (Oil Red O-positive area), and fibrosis (Masson-positive area), with maximal severity in the WD+MPs group. Also, the MPs exposure group had increases in positive areas for F4/80 and inflammatory markers TNF-α, IL-1β and IL-6 expression under both diets. Concurrently, submicroplastics inhibited antioxidant defenses by lowering levels of superoxide dismutase and glutathione, while also increasing the lipid peroxidation marker malondialdehyde. WD-fed mice exhibited pronounced MPs-induced lipid dysregulation, including elevated hepatic triglycerides, total cholesterol, and free fatty acids (FAs). Mechanistically, submicroplastics upregulated FA synthesis regulators (ACC, FASN, SREBP1) while downregulating FA oxidation mediators (CPT1A, ACOX1, PPARα) in the livers under a WD. Our findings demonstrate that chronic submicroplastics-exposure exacerbates the progression of NAFLD in ApoE-deficient mice by disturbing lipid metabolism, enhancing oxidative stress, and amplifying inflammatory responses. This study provides experimental evidence linking environmental plastic pollution to accelerated metabolic liver disease, thereby highlighting the urgent need for plastic exposure control strategies.

The ubiquitous presence of micro-and nanoplastics (MNPs) in the environment and everyday products has attracted global attention for their hazardous risks. However, the effects and underling mechanisms of MNPs chronic exposure on behavioral/visual changes of the adult and offspring remain unclear. The present study investigated the impact of polystyrene (PS) nanoplastics of 80, 200 and 500 nm diameters on zebrafish visual behaviors at an environmentally relevant concentration of 0.1 mg/L. Exposure to PS resulted in zebrafish hyperactivity, enhanced aggression, compacted shoaling and less sociability, and especially suppressed the adult optokinetic response (OKR) and offspring larval phototactic behavior, with the 500 nm PS being the most detrimental. Histopathological analysis showed 500 nm PS caused significant structural damage to the retina's pigment epithelium (RPE), photoreceptor cells (PRC), and crystalline lens. Fluorescence observation found PS accumulation in retinal layers correlated with reduced oligodendrocyte transcription factor 2 (Olig2) in optic nerve. Further transcriptomic analysis of the adult eye tissue revealed that 500 nm PS affected the transforming growth factor β (TGFβ) and phototransduction signaling pathways, dysregulated visual perception and lens development, potentially leading to dysopia in zebrafish. Specifically, TGFβ and its regulated-extracellular matrix/inflammatory factors and crystallin genes were increased, but the visual perception genes were decreased, suggesting the TGFβ-crystallin axis disorders contribute to the eye dysfunction induced by PS exposure. Collectively, our results provide new evidence revealing the molecular mechanisms of PS-induced visual toxicity and neurobehavioral changes highlighting that MNPs may pose a risk to vision health.

The relationship between the environment and diseases is a crucial and complex topic that has garnered significant attention in recent years. In our study, we also follow the thread and explore the correlation between microplastics (MPs) and osteoporosis (OP).

We found that MPs were detected in the blood samples of nearly all participants. Moreover, It was compelling that PVC and PET emerged as the most common MP polymers in our study. A verification process was conducted comparing the clinical data with the results of MPs detection. This analysis revealed a significant exposure risk to MPs from sources such as bottled water, take-out containers. Through molecular biology techniques, we confirmed that MPs have a significant toxic effect on osteoblasts and associated with abnormal gene expression.

MPs may be considered to have a potential correlation with the progression of OP.

The massive use of face masks during and after the COVID-19 pandemic has raised global concerns about environmental issues. Microplastics released from face masks pose great threats to ecosystems and human health. However, the potentially hazardous effects of face mask-derived microplastics (FMMs) on humans remain poorly understood. Using neural organoid models aims to reveal the toxicity of FMMs to human early neural development. Retinal organoids derived from human embryonic stem cells were exposed to FMMs for 21 days during early retinogenesis. FMMs were internalized by retinal organoids. Exposure to FMMs disrupted the growth and development of retinal organoids in dose- and time-dependent manners, as evidenced by abnormal morphologies. Aberrant cell events, such as cell proliferation, apoptosis, and differentiation contributed to the disarrangement of the neural retina. Transcriptome data proved that the neurotoxicity of FMMs was closely related to disordered neurogenesis, anatomical structure morphogenesis, and axon guidance. Co-exposure to triphenyl phosphate (a common organophosphate flame retardant) and FMMs exhibited more pronounced neurotoxicity than FMM exposure alone. These findings are expected to uncover the potential threats of FMMs to human neurodevelopment and emphasize the importance of optimizing the management and safe disposal of used face masks.

Microplastic (1 μm - 5 mm) and nanoplastic (<1 μm) pollution is a heightening global challenge affecting the environment and the health of living creatures within. As primary precursors for plastic manufacturing, microplastics predominantly get into the environment through plastic product degradation and integrate into water, food chain and consumer products leading to potential health consequences. The mammalian system is equipped with several blood-tissue barriers with exclusive tight junctions that selectively regulate material transfer and protect vulnerable and functionally important organs. Nonetheless, emerging evidence indicates microplastics interact, traverse and compromise the integrity of these complex barriers. This review summarises the known and potential impact of microplastics on human health, focusing on specific organ barrier breaches. Evidence of microplastic traversal and deposition in distal mammalian organs are discussed. We further highlight current challenges facing both researchers and clinicians and provide an outlook for expanding our understanding of the impact of microplastic on health.

Exposure routes and transport of microplastics (MPs) from the environment into the human bodies deserve considerable attention. Intravenous injection has been reported as a direct MP-intrusion pathway. However, it is unclear whether or how the infusion fluid composition influences polymer degradation and MP release. Here, we determined that the concentrations of MPs shed from infusion bags ranged from 522 to 5455 particles/L. The storage period, mechanical shaking, and storage temperature all contributed to MP release to some extent; however, the infusion fluid composition affected the formation of MPs more than any other factor. Infusion fluids containing moxifloxacin hydrochloride, etimicin sulfate, and sodium bicarbonate ringer's solution generated more reactive oxygen species than those containing sodium chloride, grape sugar, and glucose and sodium chloride. Specifically, the generation of reactive oxygen species (hydroxyl radicals, carbonate radicals, and single oxygen) facilitated oxygen-containing functional group formation and breaking of carbon chains on the surface of the polypropylene plastic, which increased aging and fragmentation. Overall, this study provides knowledge of the mechanisms underlying MP release from infusion bags during storage and transportation. This offers insight for optimizing the use and handling of infusion bags in medical settings to minimize contamination.

Microplastics are emerging pollutants with a wide range of ecological and biological effects, including the ability to accumulate in organisms and induce toxicity. Although numerous studies have investigated the distribution and toxicity of microplastics in murine models and cell lines, the conclusions are inconsistent owing to variations in experimental designs, particle sizes, exposure methods, and dose quantifications. To address these gaps, we systematically evaluated the size-dependent internalization and toxicity of polystyrene microplastics (PS-MPs) using in vitro and in vivo models. Fluorescently labeled PS-MPs were used to confirm the negligible toxicity of fluorophores on macrophages, demonstrating their suitability for tracking particle accumulation. In vitro experiments using RAW 264.7 cell lines and primary peritoneal macrophages revealed size-dependent phagocytosis and cytotoxicity, with smaller particles (0.5 µm) demonstrating higher internalization and causing greater mitochondrial depolarization, reactive oxygen species generation, and apoptosis compared to that with larger particles (5 µm). Acute in vivo experiments comparing oral administration and tail-vein injection revealed that the absorbed dose and toxicity were significantly influenced by particle size, with smaller PS-MPs showing higher organ retention and alterations in hematological and metabolic parameters. Additionally, a 28-day subacute oral exposure study highlighted systemic toxicity, including weight loss, disrupted food intake, elevated oxidative stress markers, and reduced antioxidant enzyme activity. By integrating multiple exposure routes, macrophage models, and fluorescence toxicity evaluations, this study provided a comprehensive and realistic assessment of microplastic toxicity, offering valuable insights for advancing toxicological evaluations and regulatory frameworks. However, this study did not address the influence of other plastic types, shapes, or environmental factors on toxicity. Future studies are thus needed to explore these variables and the long-term implications of real-world microplastic exposure.

Microplastics (MPs) in soil, groundwater, and human (SGH) present a significant global challenge due to their ecological and human health impacts. However, current protocols for detecting MPs in these environments and humans are limited, inconsistently applied, and vary significantly, particularly during the pretreatment stages of MP analysis. Moreover, no study has investigated the impact of methodological flaws on MP detection. This study conducted a thorough global assessment of the existing soil and groundwater (SG) pretreatment methods, using statistical tests to evaluate their effectiveness. It also reviewed filtration and analytical techniques for MPs in SGH samples. The analysis included research articles from PubMed, Google Scholar, Scopus, and Web of Science published between 2015 and 2024. Findings show that pretreatment using more than 100 g of soil can impact MP quantification, likely due to soil heterogeneity, while groundwater volume did not significantly affect MP quantification, likely due to the homogeneity of groundwater. During SGH pretreatment, various salts (e.g., ZnCl2 and NaCl) can be used for density flotation. Fenton's reagent was found to be a better choice than H2O2 for organic material removal because less heat was released. Post treatment MPs in SGH samples can be analyzed using various instruments and resolutions such as FTIR down to 1-5 µm, ATR-FTIR down to 2 µm, micro-Raman down to 500 nm, and LDIR down to 1 µm. This study lays the foundation for developing an effective MP analysis in SGH.

The contamination of yogurt and buttermilk (doogh), two widely consumed dairy products, with microplastics (MPs) and phthalic acid esters (PAEs), and subsequently the health effects caused by the contamination of these products on humans, is a potential concern. In this study, the abundance and characteristics of MPs as well as the PAEs concentration in different types of yogurts and buttermilk available in the Iranian market were investigated. The average abundance of MPs in different types of yogurts and buttermilk was between 0.63 and 0.76 and 0.52-0.7 items/mL, respectively. Most detected MPs in yogurt and buttermilk samples were in the size range of 1000-5000 μm with the predominant color and shape of transparent and fiber, respectively. Polyethylene terephthalate (PET) and polyamide (PA) were the dominant polymers in yogurt and buttermilk samples, respectively. The average concentrations of PAEs in different types of yogurt and buttermilk samples were between 5.79 and 11.36 and 1.46-6.93 µg/L, respectively. The findings showed that Di(2-ethylhexyl) phthalate (DEHP) levels in yogurt and buttermilk samples may have a carcinogenic risk for adults and adolescents. According to the results of this study, the intake of MPs and PAEs through high consumption of yogurt and buttermilk should be recognized as a significant source of MPs in the human body.

The online version contains supplementary material available at 10.1007/s40201-025-00939-z.

Hirudo nipponica Whitman (HNW) is a traditional Chinese medicine (TCM) processed from leeches, commonly used for treating blood stasis syndrome, particularly in promoting blood circulation and alleviating blood stasis. This study aimed to examine microparticles (MPs) contamination of leeches and whether the production of MPs was related to processing. The results showed that the abundance of MPs in the whole, sectioned and powdery of HNW was 12.39, 13.93, 35.11 items/g, respectively. Fiber-like particles accounted for 90 % total. Transparent particles were the most abundant, followed by blue and black. Particles <1 mm were the most frequent. Notebly, 100 % cotton was the most detected material in the HNW, while rayon, cellulose and polyester accounted for 46 % of the total. The abundance of particles in powdery HNW increased significantly, with a higher percentage of <1 mm, similar type and colour to whole and sectioned HNW. It suggests that the large MPs may have been cut into smaller MPs during processing and bring more risk of MPs. It alerts us to the fact that pharmaceuticals and even commonly touched food products may pose a greater risk of MPs due to processing.

The surge in plastic production has spurred a global crisis as plastic pollution intensifies, with microplastics and nanoplastics emerging as notable environmental threats. Due to their miniature size, these particles are ubiquitous across ecosystems and pose severe hazards as they are ingested and bioaccumulate within organisms. Although global plastic production has reached an alarming 400.3 MTs, recycling efforts remain limited, with only 18.5 MTs being recycled. Currently, out of the total plastic waste, 49.6 % is converted into energy, 27 % is recycled, and 23.5 % is recovered as material, indicating a need for better waste management practices to combat the escalating pollution levels. Research studies on micro-nanoplastics have primarily concentrated on their environmental presence and laboratory-based toxicity studies. This review critically examines the sources and detection methods for micro-nanoplastics, emphasising their toxicological effects and ecological impacts. Organisms like zebrafish and rats serve as key models for studying these particle's bioaccumulative potential, showcasing adverse effects that extend to DNA damage, oxidative stress, and cellular apoptosis. Studies reveal that micro-nanoplastics can permeate biological barriers, including the blood-brain barrier, neurological imbalance, cardiac, respiratory, and dermatological disorders. These health risks, particularly relevant for humans, underscore the urgency for broader, real-world studies beyond controlled laboratory conditions. Additionally, the review discusses innovative energy-harvesting technologies as sustainable alternatives for plastic waste utilisation, particularly valuable for energy-deficient regions. These strategies aim to simultaneously address energy demands and mitigate plastic waste. This approach aligns with global sustainability goals, providing a promising avenue for both pollution reduction and energy generation. The review calls for further research to enhance detection techniques, assess long-term environmental impacts, and explore sustainable solutions that integrate energy recovery with pollution mitigation, especially in regions most affected by both energy shortages and increased plastic waste.

Microplastics are recognised as ubiquitous pollutants as they are now found in all terrestrial and marine ecosystems. The interactions between microbiota and microplastics are an issue of fundamental importance in studying and maintaining global health. Microplastics alter the structures and functions of microbial communities, resulting in adverse health effects. A comprehensive understanding of these effects through interdisciplinary research is essential to mitigate pollution and protect the health of ecosystems. The review aims to explore these interactions within a One Health framework. Indeed, a deeper understanding of the processes involved in the interaction between microbiota and microplastics could pave the way for new and promising strategies to mitigate the harmful effects of microplastics on ecosystems and human health.

As an emerging contaminant, nanoplastics have evolved into a global ecological issue. Studies have shown that nanoplastics induce neurotoxicity across species, however, the causal mechanism remains unknown. This study aimed to explore the mechanism underlying the neurotoxicity caused by polystyrene nanoplastics (PS-NPs) via microbiota-gut-brain axis in immature mice, which serve as a model of infants and young children who are at higher exposure risk to NPs. The results indicated that while only a minority of PS-NPs reached the brain after exposure, they still had significant neurotoxic effects, as reflected by abnormalities in behavior, biochemical marker levels and histopathology. Proteomics and quantification analyses revealed that a proteostasis imbalance mediated by lysosomal and proteasome dysfunction in the brain is the key reason for the induced neurotoxicity. Further, we confirmed the indirect role of gut microbiota in the neurotoxicity induced by PS-NPs through 16S rDNA analyses and fecal microbiota transplantation. Crucial bacterial species such as Eubacterium coprostanoligenes potentially act as indicators for gut dysbiosis after PS-NPs exposure. Notably, we first estimated the indirect effect of gut microbiota on neurotoxicity attributed to PS-NPs in immature mice as 39.20% by high-dimensional mediation analysis. Trehalose was identified as a mediator connecting the gut microbiota and the brain, and the crucial role of trehalose supplementation was highlighted in remodeling the brain proteostasis to alleviate the neurotoxicity in immature mice. These findings are expected to contribute to a deeper understanding of the risk assessment and health protection of the nervous system from exposure to PS-NPs early in life.

Micro- and nanoplastics (M/NPs), as ubiquitous global environmental pollutants, have garnered increasing attention due to their pervasive presence. These particles can interact with biological molecules through various mechanisms, subsequently inducing potential toxic effects on living organisms. This review investigates the hazards of M/NPs and their interactions with biological membranes and proteins, focusing on their interaction mechanisms and potential effects on biomolecular structure and function. Specifically, we summarize the exposure pathways and potential harms of M/NPs, which can enter the human body through ingestion, inhalation, and skin contact, potentially causing toxicity, inflammation responses, oxidative stress, and endocrine disruption. Additionally, we highlight the interaction between M/NPs and biological membranes, which can induce structural changes, including membrane thickening, increased fluidity, and pore formation, thereby compromising membrane integrity and affecting cellular health. Besides, we emphasize the interaction between M/NPs and proteins, suggesting that protein structural changes and corona formation can influence oxidative stress responses and cytotoxicity, thereby impacting cellular functions and viability. Ultimately, suggestions and outlooks for further research are proposed. Overall, this review systematically summarizes current research on the interactions between M/NPs and biomolecules, including their mechanisms and biological effects, providing researchers with a comprehensive understanding of the field.

We live in a world increasingly dominated by plastic, leading to the generation of microplastic particles that pose significant global health concerns. Microplastics can enter the body via ingestion, inhalation, and direct contact, accumulating in various tissues and potentially causing harm. Despite this, the specific cellular mechanisms and signaling pathways involved remain poorly understood. Macrophages are essential in absorbing, distributing, and eliminating microplastics, playing a key role in the body's defense mechanisms. Recent evidence highlights oxidative stress signaling as a key pathway in microplastic-induced macrophage dysfunction. The accumulation of microplastics generates reactive oxygen species (ROS), disrupting normal macrophage functions and exacerbating inflammation and organ damage. This review serves as the first comprehensive examination of the interplay between microplastics, macrophages, and oxidative stress. It discusses how oxidative stress mediates macrophage responses to microplastics and explores the interactions with gut microbiota. Additionally, it reviews the organ damage resulting from alterations in macrophage function mediated by microplastics and offers a novel perspective on the defense, assessment, and treatment of microplastic-induced harm from the viewpoint of macrophages.

The release of micro/nanoplastics (MNPs) from biodegradable plastics in gastrointestinal environments due to photoaging, along with their associated mechanisms and potential cytotoxicity, is largely unknown. Here, we show that poly(lactic acid)/poly(butylene adipate-co-terephthalate) (PLA/PBAT) films undergo ultraviolet photoaging, resulting in increased surface roughness and a higher quantity of MNPs on the surface. This aging process involves the generation of carbon- and oxygen-centered free radicals, chain scission, and the formation of oxidation products with hydroxyl and carbonyl groups. These MNPs can be released under water shear force, significantly increasing the normalized mass loss of aged films to approximately 0.128 mg/cm2 (18 times higher than that of unaged films in water). In the gastrointestinal environment, the normalized mass loss further increases to about 0.196 mg/cm2 (28 times higher), likely due to potential enzymatic digestion and ion-swelling effects. These MNPs, primarily composed of PLA, are smaller and carry more negative charges under gastrointestinal conditions. In the THP-1 cell model, these MNPs affect cell viability in a dose-dependent manner. MNPs obtained through ultrafiltration, compared to those collected via centrifugation, display a broader size distribution and induce more pronounced toxicity in THP-1 cells, with an EC50 of 243 mg/L. Preliminary comparative analysis indicates that PLA/PBAT-derived MNPs present toxicity risks comparable to, or greater than, those of conventional plastic MNPs. These findings underscore the potential hazards associated with biodegradable plastics.

Nanoplastics (NPs) can accumulate in animal brain, but their kinetics and potential adverse impacts on the brain are not yet understood. This study compared the impacts of 200 nm (L-NPs) and 50 nm (S-NPs) NPs on the zebrafish (Danio rerio) brain at environmentally relevant concentration (500 μg L-1), exploring how these nanoparticles were accumulated and removed, as well as their subsequent adverse effects at various biological levels. The bioconcentration factor and biological half-time in brain of L-NPs were 11.8 L kg-1 and 1.54 d, while those for S-NPs were 18.9 L kg-1 and 2.48 d, respectively. S-NPs displayed a higher tendency to accumulate and a slower elimination with a higher potential for long-term brain accumulation. Proteomic analysis of fish brain revealed that S-NPs exposure exhibited a higher level of differential expression of vesicle transport proteins. Transcriptomic analysis suggested that both NPs exposure significantly impacted pathways linked to inflammation and locomotion, while S-NPs additionally leading to increased enrichment of pathways associated with photoreceptor and phototransduction disorders. Both L-NPs and S-NPs caused damages in brain regions and even led to heightened oxidative stress across the whole brain regions. At the behavioral level, NPs induced abnormal patterns and feeding responses, and S-NPs further heightened the zebrafish sensitivity to light stimulation. Our study provides strong evidence of the risk of neurological diseases stemming from the prolonged accumulation of NPs in the brain, especially for the smaller-sized NPs.

Biodegradable polylactic acid (PLA) plastics have been praised as an effective solution to the global pollution caused by petroleum-based plastics, and their widespread use in food packaging and disposable tableware has resulted in increased oral exposure to PLA microplastics (PLA-MPs). Despite their eco-friendly and biodegradable reputation, the in vivo behaviors of PLA-MPs concerning fermentation, carbon cycle, and adverse effects remain unknown. Here, we showed that gut microbiota from the colon can effectively degrade the PLA-MPs by secreting esterase FrsA, whereas esterase FrsA-producing bacteria were identified to dominate this behavior in male C57BL/6 mice. Using isotope tracing and multiomics techniques, we uncovered that 13C-labeled PLA-MPs were incorporated into the carbon cycle of gut microbiota as a carbon source. Meanwhile, these degraded PLA-MPs fragments entered the succinate pathway of the tricarboxylic acid cycle within gut epithelial cells. These processes altered the metabolic phenotype of the gut, resulting in the decreased linear short-chain fatty acids that are primary energy sources of the gut epithelium. Furthermore, we found that exposure of PLA-MPs significantly reduced the appetite and body weight of mice. Our findings present an overall process of biodegradable plastics within hosts, with the focus on the entire double carbon cycle of PLA-MPs in the gut, which offers indispensable insights into the potential impact of exposure to PLA-MPs.

Acrylamide (AA) and nanoplastics (NPs) are common food toxicants. However, their combined toxicity and health risks call for further studies. This study aimed to investigate the combined toxicity of AA and polystyrene NPs (PS-NPs) in mice through drinking water exposure. Co-exposure to AA and PS-NPs aggravated colon and liver damage, including more severe inflammatory infiltration, higher levels of colonic and hepatic pro-inflammatory cytokines, and elevated serum content of lipopolysaccharide and activities of diamine oxidase, alanine aminotransferase, and aspartate aminotransferase compared to single exposures. Co-exposure also significantly downregulated the expression of colonic tight-junction genes ZO-1 and Claudin-5. Metabolomics revealed that co-exposure induced more profound metabolic disorders in the liver, particularly affecting amino acid and carbohydrate metabolism. 16S amplicon sequencing showed that co-exposure caused more drastic gut microbiota dysbiosis, characterized by a decrease in beneficial bacteria (unclassified_f__Oscillospiraceae, Roseburia, UCG-005, Ruminiclostridium, unclassified_o__Clostridia_UCG-014, Fournierella, and Acetatifactor) and an increase in pathogenic bacteria (Eubacterium_xylanophilum_group and Eubacterium_nodatum_group). Correlation analysis indicated a negative correlation between beneficial bacteria and intestinal-liver toxicity indicators and a positive correlation between pathogenic bacteria and these indicators. Overall, our findings showed that AA and PS-NPs exerted synergistic toxicity to the gut-liver axis in mammals, highlighting the higher health risks of their combined ingestion.

The widespread occurrence of microplastics (MPs) in the environment has raised significant concerns regarding their potential health impacts, particularly in relation to carcinogenesis. This study aimed to identify and analyze microplastics present in peritumoral and tumor tissues of patients diagnosed with colorectal cancer (CRC). Utilizing advanced scanning electron microscopy (SEM) and laser direct infrared (LDIR) imaging systems, we systematically examined tissue samples to detect and characterize the microplastics. Our findings revealed a diverse array of microplastic types, notably polyvinyl chloride (PVC) and polyethylene (PE), within both peritumoral and tumor regions. Compared to adjacent non-cancerous tissues, tumor tissues exhibited a greater variety and distribution of microplastics. Furthermore, Clathrin-a key protein involved in endocytosis-was found to be highly expressed in colorectal cancer specimens, facilitating the substantial uptake of microplastics. These results suggest a potential association between exposure to microplastics and the pathogenesis of colorectal cancer. This study highlights the urgent need for increased awareness and regulatory measures aimed at mitigating microplastic pollution along with its associated health risks.

Understanding the distribution and drivers of microplastics (MPs) in remote and sensitive environments is essential for assessing their ecological impacts and devising mitigation strategies. This study investigates the distribution and characteristics of MPs in streams and sediments of the Mt. Everest region. Results show that microplastic (MP) abundance during the non-monsoon season was 2-4 times higher than in the monsoon season. MPs were predominantly fragments, composed of specific polymer types (PA, PET), and fell within the 10-30 µm size range. An ecological risk assessment was conducted to better evaluate MP pollution in the Mt. Everest region. The study found that recharge sources of streams influenced MP distribution, with streams receiving non-glacial recharge exhibiting higher MP concentrations during the monsoon season, likely due to the dilution effect of glacier meltwater. Principal component analysis highlighted correlations between MP abundance and environmental factors such as wind speed, dissolved oxygen, stream order, and elevation. These findings advance our understanding of MP pollution dynamics in high-altitude streams, establish a foundation for evaluating their ecological impacts, and offer valuable insights for developing mitigation strategies. This study provides a critical reference for further exploring MP contamination in high-elevation ecosystems and addressing its challenges.

Micro(nano)plastics (MNPs), a ubiquitous environmental pollutant, have received increasing attention for their impacts on human health. We conducted an in-depth study on the role of polyethylene terephthalate (PET) MNPs in myocardial infarction (MI). Blood from the coronary circulation of MI patients was collected to detect microplastics (MPs). Peripheral monocytes (PBMCs) and AC16 cells were used to assess inflammation, cell proliferation and apoptosis after PET nanoplastics (NPs) stimulation. The mouse MI model was established after PET NPs respiratory or oral exposure. The results showed that various types of MPs, including high levels of PET MPs, were detected in the coronary circulation. PET NPs promoted inflammatory factors secretion by PBMCs, inhibited AC16 cell proliferation and promoted hypoxia-induced AC16 cell apoptosis. PET NPs exacerbated post-MI inflammation and fibrosis through activating the NLRP3 inflammasome pathway. Through macrogenetic sequencing and metabolomics analyses, we observed that PET NPs reprogrammed the intestinal and lung microbiota and metabolome in MI mice, leading to chronic inflammation. In conclusion, PET MPs were widely present in the coronary circulation of MI patients. PET MNPs can activate the NLRP3 inflammasome pathway to exacerbate post-MI ventricular remodelling, which may be related to the reprogramming of the gut and lung microbiota and metabolome.

Polystyrene microplastics (PS-MPs) are common microplastics that pose significant health hazards to humans. Due to multifunctionality in the gut system, MP-associated damage and mechanisms require further exploration. This study was undertaken with the objective of elucidating the impact of PS-MP exposure on colonic inflammation in rats, and to explore its potential mechanisms. Forty-eight specific-pathogen-free Wistar male rats were administered 0, 0.5, 5, and 50 mg/kg/d of PS-MPs for 90 days, after which intestinal flora distribution, inflammatory factor levels in the colon, and TLR4/NF-κB/COX-2 gene levels were examined. To clarify whether PS-MPs directly infiltrate intestinal epithelial cells and induce cytotoxicity, human intestinal epithelial cells (HIECs) were exposed to a range of PS-MP concentrations (0 ∼ 100 μg/mL) for 48 h, and CCK-8 assays were conducted to assess the cell survival rates. In the colon tissue of rats exposed to PS-MP, goblet cells decreased, muscular layer arrangements were disordered, and disrupted and discontinuous crypt structures appeared in colon tissue, while high numbers of inflammatory cells infiltrated the colonic mucosa and submucosa. PS-MPs could accumulate in HIECs, and cell survival rates were decreased. In the colons of rats exposed to PS-MPs, the levels of Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were found to be elevated. Additionally, the mRNA and protein levels of TLR4/MyD88 in the colons of PS-MP-exposed rats exhibited a significant increase. Furthermore, the TLR4/NF-κB/COX-2 signaling pathway in rat colons was activated after MP exposure. When the TLR4/NF-κB/COX-2 signaling pathway was inhibited, the significant increases in IL-6 and TNF-α levels caused by PS-MPs were significantly reversed. PS-MP exposure also altered intestinal flora abundance in rats. Compared with the control group, the proportion of Firmicutes, Proteobacteria and Actinobacteria in PS-MPs exposed group was increased. In contrast, the proportion of Bacteroidetes and Verrucomicrobia decreased. Taken together, our results suggest that PS-MP could exert adverse effects on the gastrointestinal health of rats. Pro-inflammatory cytokine (IL-6, IL-1β and TNF-α) levels increased, and the TLR4/NF-κB/COX-2 signaling pathway was triggered. Thus, flora changes and increased intestinal inflammation may interact with each other.

Microplastic ubiquity has been demonstrated in several studies. They are polluting the environment, as well as food and water for human consumption, where the most significant concern has arisen over the ingestion of microplastics. However, there are very few studies on the potential health risks associated with nanoparticles, including those related to polyethylene terephthalate (PET). In this work, PET nanoparticles (253 ± 16 d nm) with irregular shape obtained under controlled conditions, were used for ex vivo analysis of rat intestinal tissue (n = 3 each condition) and their effects on the muscle tone related to peristalsis were determined. Twenty-minute treatment with increasing concentrations of PET-NPs from 0.1 to 100 μg/mL (low concentrations) and from 250 to 750 μg/mL (high concentrations) were assayed. The results showed the rapid capability of PET nanoparticles to cross the intestinal barrier, assessed by fluorescence microscopy and corroborated by RAMAN micro-spectroscopy. Furthermore physiological analysis in isolated rat intestinal segments have demonstrated the effects of PET, especially at 10 μg/mL, on tissue contraction. These results evidenced the potential health risk related to nano-plastic ingestion, due to PET nanoparticles tissue accumulation and the effects on contraction and relaxation tissue functions.

This paper examines microplastic hotspots and their drastic effects on human health and the environment pointing out microplastic pollution as one of the biggest global issues. Besides, it analyses the key sources including industrial effluent discharge, littered plastic wastes, and deterioration of synthetic products together with pathways and routes of exposure. The review also focuses on microplastic contamination in food systems such as meat, plant-based products, dairy, and seafood, detailing their entry into the food chain via soil, water, and air. On the other hand, this work also focuses on human health issues including cellular absorption, and bioaccumulation, which results in tissue oxidative stress, inflammation, hormonal imbalance and adverse long-term effects, including carcinogenicity and organ toxicity. The ultimate effects of microplastic pollution on the condition of the soil, water, and fauna and flora of the ecosystem, highlighting on the need for the prevention measures, were also addressed. This paper seeks to critically ascertain the problems posed by microplastics, including their slow biodegradation limit, the absence of proper regulations, and lack of a universally accepted standard. It also highlights that microplastic pollution requires interdisciplinary analyses, future studies, and high standards-compliant policies and regulations. This work raises the alarm for a collective international effort to protect the public health, food, and the earth.

The ubiquitous presence of microplastic particles encompasses the human tissues and secreta. Unfortunately, the complex biological matrix hampers the proper polymer identification, and harsh purification protocols damage the microplastic particles (MPs), change the specimens frequently used and needed for additional diagnostics, and bias the final result. Moreover, purification of human milk samples is sometimes impossible, as the samples can not be subjected to any chemical pretreatment. Thus, this paper aims to check the feasibility of complementary spectral approaches, namely FTIR (Fourier-transform infrared) and Raman spectroscopy, to the fast scanning of selected MPs presence, in particular polyethylene (PE), and polystyrene (PS), in human milk samples without any previous purification to prevent the change of matrix. Although the proposed approach cannot be used for the quantitative measurement of MPs concentration or the detection of low-size fractions, it is a valuable tool for the preliminary screening of numerous population samples, and some preliminary conclusions can be drawn. One may easily detect the most common MPs and observe their eco-corona. Mapping mode is beneficial for scanning large areas. Furthermore, the spectral methods turned out to be efficient in the milk itself diagnosis, for instance, the monitoring of the fat content. The results were placed in the context of the ongoing broad discussion about MPs interaction with the human body and several possible impact mechanisms.

Microplastics (MPs) are readily ingested by organisms and tend to accumulate in intestinal tissues, posing potential health risks. However, most existing MP extraction methods are designed for aquatic organisms and are unsuitable for terrestrial organisms with high lipid content. In this study, we developed an efficient Fenton oxidation-based method for extracting MPs from mouse intestinal tissues. Optimal conditions for iron precipitate removal were established at pH 0.8, with incubation at 50 °C for 2 h. Key digestion parameters (H2O2 dosage, FeSO4 dosage, maximum reaction temperature, and secondary incubation time) were optimized using response surface analysis. The optimal conditions were: 37 mL of 18.5 % H₂O₂, 20 mL of 0.024 mol/L FeSO₄, a maximum reaction temperature of 60 °C, and a secondary incubation time of 35 h. Under these conditions, a digestion rate of 95 % was achieved, with minimal MP degradation. Specifically, mass loss was 2.5 %, size reduction was 2.78 %, the carbonyl index increased by 12.9 %, and infrared spectral similarity remained at 95 %. The method was also successfully applied to intestinal tissues from chickens, ducks, cows, and pigs, achieving digestion rates between 93 % and 95 %. These results demonstrate the method's effectiveness for extracting MPs from terrestrial organisms while minimal degradation, offering a valuable tool for MP research and health risk assessment.

There is a growing consensus on addressing the global plastic pollution problem by advocating for bioplastics. While starch-based plastics are prevalent, the potential health implications of starch-based microplastics (SMPs) remain largely unexplored. This is particularly concerning given their potential for accidental ingestion and subsequent interference with blood glucose metabolism. Our research provides the first investigation into the distribution and adverse effects of long-term exposure to environmentally relevant doses of SMPs in female mice, approximately 14-81 particles per mouse per day. After three months of exposure, SMPs were found to infiltrate the liver, intestine, and ovarian tissues, causing microstructural lesions. Exposure to SMPs also resulted in elevated blood glucose levels, increased hepatic oxidative stress, and disrupted lipid metabolism. A multiomics analysis further uncovered abnormalities in gene expression and microbiota, as well as enriched pathways related to insulin regulation and circadian rhythms in the exposed mice. Our results indicate that prolonged exposure to environmentally relevant doses of SMPs can have widespread health effects in mice, potentially disrupting circadian rhythms by inducing insulin resistance. This suggests that the safety of bioplastics requires further evaluation before their large-scale application in food packages.

Microplastics (MPs) are emerging environmental pollutants that pose a significant threat to wildlife within forest ecosystems. However, the quantity and types of MPs in wildlife forest habitats remain unclear. This study is the first to assess the distribution of MPs in the Amur tiger habitat of northeast China. Our results showed that MPs were detected in soil, water, atmosphere, forage plants, and ungulate and top predator feces within the forest ecosystem, respectively. The average diameter of all detected MPs was 44.99 ± 34.80μm. The predominant polymers found in the samples were polyamide, polyvinyl chloride, and polyurethane. Certain sample types shared similar MP polymer type distributions, indicating potential links in their sources and transfer pathways. Consequently, these findings provide some new insights on the new pollution problem in Amur tiger forest habitats and prompt us to consider how to control and manage the MPs pollution sources in the tiger conservation.

Numerous studies have demonstrated that micro- and nanoplastics can induce adverse effects in both zebrafish and mice, primarily targeting the intestine in oral exposure scenarios. Organisms under disease conditions are suggested to exhibit increased susceptibility to environmental pollutants, with inflammatory bowel disease (IBD) serving as a relevant model for understanding toxicity initiated in a diseased intestine. Here, we compared the adverse outcomes of polystyrene micro- (PSMPs) and nanoplastics (PSNPs) in both normal and IBD-like zebrafish and mouse models. We found that in zebrafish, no significant difference in mortality was elicited by the two particles, while IBD-like fish exhibited greater susceptibility to exposure. Conversely, transcriptomic analysis of surviving fish revealed that PSNPs disrupted metabolic pathways, particularly galactose metabolism, and induced more pronounced apoptosis in intestinal epithelial cells compared to PSMPs in IBD-like fish. These effects were further associated with an increase in the genus Flavobacterium. Similarly, in IBD-like mice, PSNPs induced a more significant increase in crypt length than control mice and more severe histological injury and greater disruptions in gut microbial diversity compared to PSMPs, mirroring the findings in zebrafish. Notably, two shared pathways, glycosphingolipid synthesis (globo and isoglobo series) and NOD-like receptor signaling, were identified in response to PSNP and PSMP exposure in two models, respectively, along with a consistent decline in Firmicutes abundance. These findings suggest that smaller-sized PSNPs may pose higher environmental and health risks compared to larger-sized PSMPs, providing key insights into the interactions between polystyrene particles and compromised biological systems and their resulting adverse outcomes.

Crohn's disease (CD) patients exhibit heightened vulnerability to environmental triggers. However, the impact of microplastics (MPs) on CD remains unexplored. This study investigates MPs in ileal segments and mesenteric adipose tissue from CD patients. We recruited paired involved and adjacent uninvolved ileal segments, along with attached creeping fat (CF) and adjacent uninvolved mesenteric adipose tissue (CD-MAT) samples to assess MPs exposure of CD patients. Using laser infrared imaging spectrometer, we identified 12 types of MPs, including Chlorinated polyethylene (CPE), Acrylate copolymer (ACR), Fluororubber, and Polyethylene (PE). MP concentrations were correlated positively with the severity of intestinal fibrosis. Laser Direct Infrared spectroscopy revealed that 31.96% of MPs were 20-50 μm in size. Our findings underscored that the high-risk practices, such as frequent invasive gastrointestinal tract examinations, exacerbated of MPs accumulation in fibrotic intestines. We detected a parallel change in the concentrations of MPs at the lesion sites, with a significant increase observed compared to the surrounding tissues. When compared to CD-MAT and uninvolved ileum, the concentration ratios of PU and AUR were higher in the more fibrotic regions of CF and involved ileum, whereas CPE and Fluororubber exhibited a concurrent decrease. This suggests that MPs can penetrate the epithelial barrier and enter both fibrotic intestines and CF. This study provided the first evidence of widespread MP contamination in the fibrotic intestine and adjacent mesenteric adipose tissue of CD patients, correlating with fibrosis severity and might function as an exacerbating factor in the development of CF and fibrotic intestines.

The accumulation of plastic waste in the environment has raised widespread concern about the impact of microplastics (MPs) on human and environmental health, particularly regarding aged MPs. This study investigated the effects of subchronic dietary intake on pristine and aged polyethylene microplastics (PE-MPs) in C57BL/6J mice. Results revealed that both pristine and aged PE-MPs, at doses of 0.01 and 1 mg/day, induced plasma metabolic changes primarily associated with lipid metabolism and digestive processes. These alterations were reflected in the expression changes of proteins involved in unsaturated fatty acid pathways in the liver as well as a reduction in beneficial gut microbiota. Key contributors in the toxicity of aged PE-MPs included ATP-binding cassette transporters, gut bacteria alterations (notably Lactobacillus, Akkermansia, Parasutterella, and Turicibacter), and significantly altered proteins related to fatty acid elongation, such as acyl-CoA thioesterase enzyme family and elongation of very long chain fatty acid protein 5. These disruptions exacerbated lipid metabolism disorders, potentially contributing to metabolic diseases. Additionally, decreased levels of glutathione S-transferase A proteins, along with reduced hepatic glutathione and increased reactive oxygen species in both the small intestine and liver, suggested that aged PE-MPs aggravated hepatic and intestinal damage through oxidative stress. These findings indicated that aged PE-MPs caused more severe hepatic dysfunction and gut microbiota disruption. This effect was likely mediated by the transfer of fatty acids and signaling molecules through the gut-liver axis, ultimately leading to hepatic lipid metabolism disorders and oxidative stress.

Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic inflammation of the gastrointestinal tract with unknown etiology. The cause of IBD is widely considered multifactorial, with prevailing hypotheses suggesting that the microbiome and various environmental factors contribute to inappropriate activation of the mucosal immune system in genetically susceptible individuals. Although the incidence of IBD has stabilized in Western countries, it is rapidly increasing in newly industrialized countries, particularly China, making IBD a global disease. Significant changes in multiple biomarkers before IBD diagnosis during the preclinical phase provide opportunities for earlier diagnosis and intervention. Advances in technology have driven the development of telemonitoring tools, such as home-testing kits for fecal calprotectin, serum cytokines, and therapeutic drug concentrations, as well as wearable devices for testing sweat cytokines and heart rate variability. These tools enable real-time disease activity assessment and timely treatment strategy adjustments. A wide range of novel drugs for IBD, including interleukin-23 inhibitors (mirikizumab, risankizumab, and guselkumab) and small-molecule drugs (etrasimod and upadacitinib), have been introduced in the past few years. Despite these advancements, approximately one-third of patients remain primary non-responders to the initial treatment, and half eventually lose response over time. Precision medicine integrating multi-omics data, advanced combination therapy, and complementary approaches, including stem cell transplantation, psychological therapies, neuromodulation, and gut microbiome modulation therapy, may offer solutions to break through the therapeutic ceiling.

Plastics are everywhere. It is widely recognized that they represent a global problem, the extent of which is yet to be defined. Humans are broadly exposed to plastics, whose effects and consequences are poorly characterized so far. The main route of exposure is via alimentary and respiratory intake. Plastics pollutions may come from both: water and food contamination itself, and their packaging. The smaller sizes (i.e. microplastics <150 µm - MPs) are considered to be the most pervasive of living organisms and, therefore, potentially the most harmful. As humans occupy one of the apex positions of the food chain, we are exposed to bioaccumulation and biomagnification effects of MPs. In fact, MPs are commonly found in human stools and blood. However, there are no data available yet on their ability to accumulate and to produce detrimental consequences on biological systems. Even though the effects of plastics pollution are poorly studied in mammals, including humans, they appear to have inflammatory effects, which is rather concerning as many etiologies of disease are based on a pro-inflammatory status.

Plastic is used extensively worldwide. However, plastic particles that are less than 1000 nm (i.e. nanoplastics) may be hazardous to human cells. Nanoplastics might be manufactured intentionally or be formed in the environment by degradation of larger plastic items. Ingestion and inhalation are the two most common routes of human exposure to nanoplastics, indicating that epithelial cells have direct exposure. However, immune cells will also interact with particles during tissue inflammation. An assessment of published studies suggests that polystyrene (PS) particles generate higher levels of DNA damage in immune cells compared to epithelial cells, although it has not been formally studied under the same experimental condition. To investigate this, we assessed cytotoxicity, oxidative stress and DNA strand breaks in lung epithelial (A549) cells, intestinal epithelial (Caco-2) cells, and two monocytes (THP-1 and U937) after exposure to amine-functionalized polystyrene particles (PS-NH2) with declared particle size of 240 nm. No cytotoxicity or intracellular reactive oxygen species production were found at concentrations up to 200 µg/mL. Exposure to PS-NH2 was associated with glutathione depletion in A549 cells. However, there was no increase in the level of DNA strand breaks, measured by the comet assay, in any of the cell lines under standard assay conditions. Diethyl maleate treatment was used to render cells susceptible to oxidative stress. By itself, diethyl maleate treatment led to approximately 50 % glutathione depletion and increased DNA strand breaks, but additional DNA damage was not observed in cells by PS-NH2 exposure in A549, Caco-2, THP-1 and U937 cells.

Marine pollution by micro/nanoplastics (M/NPs) has emerged as a critical global issue, with widespread ecological and economic consequences. Numerous studies have investigated M/NPs pollution in marine environments, but there remains a need to assess progress, identify challenges, and propose future strategies. This review provides updated insights into marine M/NPs, including their sources, detection methods, global data from diverse marine ecosystems, and the challenges in mitigating pollution. The review reveals that the ocean harbors approximately 5.25 trillion plastic debris pieces, with a total of 50-75 trillion plastic and microplastic particles, with deep-sea regions containing up to 4 billion plastic microfibers per square kilometer. Human activities, including industrial practices and aquaculture, are major contributors to M/NPs pollution, which threatens 17% of marine species and incurs an economic loss of 6-9 billion USD. M/NPs are found across various marine habitats, including shorelines, sea floors, water columns, biota, and floating debris. Analyzing nanoplastics is particularly challenging due to their heterogeneous aggregation with other contaminants and their much lower concentrations than natural particles. Key drawbacks in addressing M/NPs pollution include inadequate funding, insufficient regulations, and a lack of policy frameworks on the prevalence, distribution, and sources of M/NPs. There is an increasing focus on utilizing innovative technologies such as artificial intelligence (AI) to monitor, assess risks, and predict the spread of M/NPs. Therefore, urgent global cooperation, involving all stakeholders and the general public, is essential. Additionally, integrating scientific and engineering methods, along with AI technologies, is crucial for monitoring and controlling M/NPs pollution and developing sustainable solutions.

Polyethylene terephthalate microplastics (PET-MPs) have been detected in the environment and human metabolites or tissues; however, their potential effects on humans under actual exposure doses remain unclear. Herein, male adult mice were exposed to 10 µm PET-MPs at concentrations of 10, 50, and 250 mg/kg per body weight consecutively for 28 days. Changes in blood biochemistry, inflammatory factors, colonic histopathology, colonic mucus gene mRNA levels, and the gut microflora were monitored to study PET-MPs toxicity. The results showed that PET-MPs exposure increased relative serum alanine aminotransferase (ALT) and glucose (GLU) levels in 50 mg/kg bw PET-MPs exposure group, and altered relative levels of inflammatory factors, thereby inducing the inflammatory response. Moreover, PET-MPs exposure increased mRNA expression levels of colonic mucus secretion related and barrier function related genes, indicating intestinal mucus secretion and barrier integrity dysfunction, which was consistent with the results of histopathological results. In addition, gut microbiota analysis revealed that the diversity and community composition were altered after PET-MPs exposure, suggesting a metabolic disorder. Therefore, our results demonstrated that exposure to PET-MPs led to intestinal injury and changes in the gut microbiome composition in mice. Overall, the study findings provided basic data about the health risks of PET-MPs to humans, highlighting that MPs-induced toxicity warrants more concern in the future.

Plastic cutting boards are commonly used in food preparation, increasing human exposure to microplastics (MPs). However, the health implications are still not well understood.

The objective of this study was to assess the impacts of long-term exposure to MPs released from cutting boards on intestinal inflammation and gut microbiota.

MPs were incorporated into mouse diets by cutting the food on polypropylene (PP), polyethylene (PE), and willow wooden (WB) cutting boards, and the diets were fed to mice over periods of 4 and 12 wk. Serum levels of C-reactive protein (CRP), tumor necrosis factor-α (TNF-α ), interleukin-10 (IL-10), lipopolysaccharide (LPS, an endotoxin), and carcinoembryonic antigen (CEA), along with ileum and colon levels of interleukin-1β (IL-1 β ), TNF-α , malondialdehyde (MDA), superoxide dismutase (SOD), secretory immunoglobulin A (sIgA), and myosin light chain kinase (MLCK), were measured using mouse enzyme-linked immunosorbent assay (ELISA) kits. The mRNA expression of mucin 2 and intestinal tight junction proteins in mouse ileum and colon tissues was quantified using real-time quantitative reverse transcription polymerase chain reaction. Fecal microbiota, fecal metabolomics, and liver metabolomics were characterized.

PP and PE cutting boards released MPs, with concentrations reaching 1,088 ± 95.0 and 1,211 ± 322 μ g / g in diets, respectively, and displaying mean particle sizes of 10.4 ± 0.96 vs. 27.4 ± 1.45 μ m . Mice fed diets prepared on PP cutting boards for 12 wk exhibited significantly higher serum levels of LPS, CRP, TNF-α , IL-10, and CEA, as well as higher levels of IL-1β , TNF-α , MDA, SOD, and MLCK in the ileum and colon compared with mice fed diets prepared on WB cutting boards. These mice also showed lower relative expression of Occludin and Zonula occludens-1 in the ileum and colon. In contrast, mice exposed to diets prepared on PE cutting boards for 12 wk did not show evident inflammation; however, there was a significant decrease in the relative abundance of Firmicutes and an increase in Desulfobacterota compared with those fed diets prepared on WB cutting boards, and exposure to diets prepared on PE cutting boards over 12 wk also altered mouse fecal and liver metabolites compared with those fed diets prepared on WB cutting boards.

The findings suggest that MPs from PP cutting boards impair intestinal barrier function and induce inflammation, whereas those from PE cutting boards affect the gut microbiota, gut metabolism, and liver metabolism in the mouse model. These findings offer crucial insights into the safe use of plastic cutting boards. https://doi.org/10.1289/EHP15472.

The presence of micro- and nano-plastics (MNPLs) in the environment has increased significantly in the past decades. However, the direct impact of MNPL particles on human health remains unclear.

In this study, we utilized a modified extraction method with a previously reported staining technique to develop a novel approach for identifying individual plastics in mixtures of MNPLs of commercial and environmental origins to be able to investigate their impacts on human cell inflammation and cell death. Polypropylene (PP), polyethylene (PE), polystyrene (PS), and polyethylene terephthalate (PET) were the plastics analyzed. The plastic composition of the environmental MNPLs was characterized using multiple analytical techniques, including Fourier transform infrared spectroscopy, confocal imaging, scanning electron microscopy, and X-ray diffraction.

We found that both commercial and environmental MNPLs, especially PET, impose a strong inflammatory response on various human cells and tissues. At 1 mg/mL, they robustly stimulate inflammatory IL-1β and IL-6 secretion in a time-dependent manner. Importantly, we observed that the MNPLs induced variable inflammatory responses in cells depending on their plastic composition. Environmental samples rich in PET showed a strong dose-dependent response and induced IL-1β secretion at doses as low as 100 ng/mL. In addition, MNPLs can induce human cell death with or without obviously altering the cell morphology.

These findings are significant because they represent the first instance of authentic MNPLs being collected from ecological water samples for characterization and the first time the direct influences of commercial and environmental MNPLs have been compared in human cell studies. The methods developed in this study provide a foundation for future research to isolate MNPLs from the environment and explore their potential impacts on human health and disease development.

Agricultural land has long been regarded as a resource for food production, but over time, the effects of climate change have reduced the ability of soil to produce food efficiently. Nowadays, farmers have moved from traditional to modern techniques of farming. Across the globe, plastic mulching has become widely used on farmlands. According to a few studies, the breakdown of plastic mulches releases microplastics (MPs) into the soil. Despite studies reporting the presence of MPs in soils, there are limited studies on the sources and impacts on soil organisms, plant growth, fruits, and human health. This study evaluated research articles collected from the Web of Science to assess the origin of MP in soil and crops and its effects on soil organisms, plants, and humans. It was observed that MPs come from different sources such as waste water, organic fertilizer, irrigation water, sewage, and sludge. Plastic mulching, which can spread across agricultural fields at varying depths, is the dominant source. Furthermore, it was observed that MPs alter crop quality, reduce the leaf count of wheat, and decrease the root length of crops such as maize, water spinach, black gram, and garden cress. MP can decrease the abundance of soil microarthropods and nematodes, damage the intestinal walls of earthworms, and reduce the feeding and excretion of snails. MP causes liver damage, inflammation, respiratory irritation, and immunological issues. Ultimately, these contaminants (MPs) can transfer and have been detected in fruits and vegetables, which pose adverse effects on human health.