Published online Sep 22, 2026. doi: 10.4291/wjgp.122786
Revised: June 3, 2026
Accepted: June 24, 2026
Published online: September 22, 2026
Processing time: 133 Days and 17.1 Hours
Microplastics and nanoplastics (MNPs) are increasingly recognized as ubiquitous environmental contaminants with unavoidable human exposure through inge
Core Tip: Microplastics and nanoplastics are emerging as ubiquitous environmental contaminants of potential relevance in inflammatory bowel disease (IBD). Experimental evidence suggests that intestinal exposure may promote dysbiosis, mucus barrier disruption, epithelial permeability and immune activation, all pathways implicated in IBD pathogenesis. Current evidence supports biological plausibility but is limited to simplified preclinical models and small observational human studies. Prospective human studies are needed to investigate whether micro- and nanoplastics may contribute to IBD onset, activity or progression.
- Citation: Hall R, Colwill M, Patel K, Honap S, Poullis A. Microplastics and nanoplastics in inflammatory bowel disease: Mechanistic plausibility, human evidence and future research priorities. World J Gastrointest Pathophysiol 2026; 17(3): 122786
- URL: https://www.wjgnet.com/2150-5330/full/v17/i3/122786.htm
- DOI: https://dx.doi.org/10.4291/wjgp.122786
Plastics have become indispensable materials in the modern world, with global production increasing from 2 million metric tons annually in 1950 to more than 475 million metric tons in 2022, with production forecast to continue rising[1]. Plastics’ durability, versatility and low cost have enabled widespread use across multiple industries; however, these same properties also make them challenging to dispose of, leading to widespread environmental accumulation and persistence. Over time, larger plastics progressively degrade through ultraviolet radiation, mechanical abrasion and environmental weathering, creating increasingly smaller particles known as microplastics and nanoplastics (MNPs) which are now widely detected across all ecosystems[2].
The term microplastic was first introduced in 2004 and is widely defined as plastic fragments smaller than 5 mm in diameter[3,4]. In contrast, nanoplastics refer to plastics < 1000 nm (1 μm) in size, although definitions can vary[5]. MNPs encompass a broad group of polymers including polyethylene (PE), polypropylene (PP), polystyrene (PS), polyvinyl chloride (PVC) and PE terephthalate (PET) and many also contain additional chemical additives[6]. Owing to their small size and environmental persistence, MNPs have become ubiquitous and are increasingly detected in the human food chain including drinking water[7,8], bottled drinks[9], fish[9,10], seafood[11,12], agricultural products[13] and air[14].
Human exposure to MNPs is increasingly unavoidable and consequently MNPs have been detected in several human biological samples including lungs[15], liver[16], breast milk[17], placenta[18], urine[19], vascular plaques[20], blood[21] and stool[22]. The gastrointestinal tract is of particular interest as it represents a primary interface between MNPs, the gut microbiota, intestinal epithelium and the intestinal immune system. MNPs were previously assumed to have limited biological relevance however experimental studies now suggest that intestinal exposure to MNP may cause dysbiosis, disrupted epithelial integrity and activate the immune system[23,24].
Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC)[25] and Crohn’s disease (CD)[26], is a chronic immune-mediated disorder characterized by relapsing-remitting intestinal inflammation. IBD typically presents in early adulthood and is caused by a complex interplay between genetics, immune dysregulation, dysbiosis and environmental factors[27]. The global burden of IBD has increased substantially over recent decades with prevalence now approaching 1% in some high-income countries[28,29]. At the same time, incidence of IBD is rising in newly industrializing regions, supporting an important role for environmental factors in IBD pathogenesis[30].
Given the widespread human exposure to MNPs, and their potential to interact with immunological pathways implicated in intestinal inflammation, there is growing interest in whether MNPs may contribute to IBD pathogenesis. This narrative review examines the evidence linking MNPs exposure to intestinal inflammation and evaluates the relevance of these findings to IBD. It examines the challenges in studying the health effects of exposure to MNPs and discusses the future directions.
A literature search of MEDLINE via the PubMed platform between January 2026 and March 2026 to identify relevant articles. Search terms included, alone and in combination, “microplastic”, “nanoplastic”, “inflammatory bowel disease”, “IBD”, “ulcerative colitis”, “UC”, “Crohn”, “colitis”, “intestinal inflammation”, “dysbiosis”, “permeability”, “mucus” and “colon”. Reference lists of key papers were manually screened for additional original studies and review articles. ClinicalTrials.gov and ISRCTN.com were searched for planned, ongoing or recently completed studies. Only articles published in English were included.
Studies were selected according to their relevance to the scope of this narrative review with priority given to human studies if available, followed by mechanistic animal and in vitro studies addressing gastrointestinal exposure to MNPs and epithelial barrier function, microbiota, mucosal inflammation and IBD. Studies investigating MNPs in pre-existing or induced colitis models were included. Studies focused solely on detection or non-gastrointestinal outcomes were excluded. Study selection aimed to include key human data, recent systematic reviews, representative mechanistic studies, and relevant negative findings to reduce selective citation.
MNPs arise from both primary and secondary sources. Primary MNPs are intentionally manufactured at small sizes for industrial and personal use, for example, in cosmetics and personal care products. In contrast, secondary MNPs are created through the progressive fragmentation of larger plastics through weathering processes such as ultraviolet radiation, mechanical abrasion and/or chemical degradation. Although fragment size remains a key differentiator between MNPs no universally accepted definition exists. Microplastics are commonly defined as plastics with a diameter of 1 μm to 5 mm in at least one dimension, whereas nanoplastics are often defined as fragments < 1 μm, some using a threshold of < 0.1 μm[5,31].
The term MNPs represents a heterogeneous group of particles that vary in morphology and chemical composition. MNPs can occur as fibers, foams, fragments, microbeads or films, and are derived from a range of polymers including PE, PP, PVC, PET, PA and PS[32]. PE is the most widely manufactured polymer globally accounting for over a third of total plastic production, and is widely used in packaging materials, food containers and water bottles[33]. In addition to the polymer itself, MNPs often contain additional additives such as dyes, stabilisers, flame retardants and plasticisers which can further diversify human exposure[6]. Particle size is highly relevant for human health as smaller particles have greater potential for uptake from the gastrointestinal tract and subsequent migration into the systemic circulation.
Human exposure to MNPs occurs predominantly through ingestion and inhalation[34,35], while dermal contact is considered a less significant exposure route[36]. The main pathways contributing to human exposure are summarised in Figure 1. Ingested particles may derive from contaminated food, drinking water, food and drink packaging, or particles cleared from the respiratory tract following inhalation. MNPs have been detected in human stool samples, providing direct evidence of gastrointestinal exposure, with a wide range of polymers detected[22,37]. Ingestion is likely to represent the principal gastrointestinal exposure pathway for most individuals, although the relative contribution remains uncertain. Dietary exposure to MNPs has been reported across a broad range of foods and beverages including seafood, salt, honey, alcohol, fruit and vegetables, tap water and bottled water[7,38,39]. Additionally, plastic teabags have been shown to release large numbers of MNPs during brewing[40], while heated plastic take-out food containers[41,42] and paper cups with plastic additives have also demonstrated temperature-dependent MNPs release[43,44]. Drinking water has emerged as a potentially important contributor for chronic exposure[45]. A recent United Kingdom study analyzing 177 tap water samples, and 85 branded bottled water samples detected MNPs in all samples tested[7]. Evidence is now emerging that MNPs exposure may also begin in very early life. PP infant feeding bottles have been shown to release large numbers of MNPs during formula preparation[46] and MNPs have also been detected in breast milk[17].
Attempts to quantify daily adult MNPs intake have produced highly variable estimates. Cox et al[47] estimated the annual adult MNP ingestion at 39000 to 52000 particles annually. Mohamed Nor et al[48] estimated mean daily dietary exposure at 883 particles per person per day, while a systematic review of 76 studies estimated adult daily intake ranging from 0.0002 to 1531524 particles per day with the highest values derived from bottled water[38]. This striking range reflects substantial variation in sampling methods, particle size thresholds, contamination control, digestion and extraction techniques, and analytical equipment across the published literature. The lack of standardisation in sampling, extraction, contamination control, polymer identification and exposure estimates make direct comparison between studies challenging.
In addition to dietary intake, inhalation may represent an important and under recognised source of gastrointestinal MNPs exposure. Recent indoor exposure estimates that adults inhale approximately 68000 MNP/day in the 1-10 μm range, and 3200 MNPs/day in the 10-300 μm range. Larger particles tend to be cleared by the mucociliary system and are subsequently swallowed into the gastrointestinal tract therefore contributing to overall intestinal microplastics exposure[14].
Once microplastics enter the gastrointestinal tract they have the potential to interact with the intestinal cells via multiple overlapping mechanisms. These mechanisms include disrupting the gut microbiota, impairment of the mucus and epithelial barrier function, and activation of the immune pathways (Figure 2). Particle size appears central to these interactions. Larger particles, typically considered > 150 μm, are not absorbed by epithelial cells and remain in the intestinal lumen, here they can make direct contact with the apical surface of epithelial cells promoting intestinal inflammation and activating the immune system[49]. In contrast, smaller particles < 150 μm have the potential to cross the mucus barrier and be internalised into epithelial cells[50] via endocytosis, M-cell uptake or paracellular leakage[51]. From here they can be retained in intestinal mucosa or be absorbed into the systemic circulation and accumulate in distant organs[49,52].
The current published evidence base is heavily dependent on animal models and in vitro models, most of which replicate MNPs exposure by using a single polymer type, particle size and morphology (often spherical PS beads), and replicate exposure at doses that are unlikely to reflect typical human exposures. MNPs should not be considered a uniform exposure class, their biological effects are likely to depend on size, polymer composition, surface, shape, concentration and the pre-existing intestinal environment.
The gut microbiota comprises a complex community of microorganisms that inhabit the gastrointestinal tract including bacteria, viruses, fungi and protozoa. It plays an essential role in metabolic homeostasis, mucosal immunity, maintenance of epithelial barrier integrity and xenobiotic handling[53,54]. Dysbiosis, broadly defined as disruption in the composition or function of the gut microbiota, has been strongly associated with IBD pathogenesis[27,55,56].
Experimental evidence supports the plausibility that MNPs can alter gut microbiota composition, but the evidence is dominated by animal models and human derived in vitro simulations[57]. A recent systematic review on the impact of MNPs on human gut microbiota only found 12 eligible studies, including 5 observational human studies and 7 in vitro models[58]. The review concluded that MNP is associated with altered microbiota composition and metabolic dys
Across published in vivo studies MNPs have been shown to alter gut microbial communities in multiple species[59], although the direction and magnitude of the change measured can vary depending on the polymer type, particle size, morphology and duration of exposure. In mice, Djouina et al[60] demonstrated that six weeks of oral PE exposure altered microbiota composition, with the greatest effects seen when different particle sizes were combined. Similarly, Jin et al[61] demonstrated that 5 μm PS exposure in mice altered the α and β diversity of the gut microbiota, altered the metabolic pathways and induced barrier dysfunction. Recently, Zhang et al[24] used environmentally relevant concentrations of PS-MNP particles in mice and found that MNPs exposure reduced Firmicutes/Bacteroidetes ratios, reduced the number of beneficial bacterial, increased the number of harmful bacteria and also altered SCFA metabolism. Interestingly in this model microbiota depletion attenuated MNP-induced colonic inflammation, suggesting that microbiota disruption may be more than an epiphenomenon and could mediate downstream host injury. Similar diversity and metabolic changes have been seen in other studies[62-64]. Tu et al[64] reported that mice exposed to 5 μm PS-MNPs demonstrated compositional changes, reduced fecal SCFA’s - acetate, propionate, butyrate and isobutyrate - and altered bile acid related metabolites[64].
Notably the effects of MNPs on microbiota composition are not a universal finding across studies. Harusato et al[65] used irregular shaped low dose PET particles to better mimic environmentally derived particles and found no overt colonic inflammation or mucus disruption, with only modest microbiota changes seen. These findings were despite clear transcriptomic effects on gut immune cells, highlighting a key limitation in current data, outcomes are heavily influenced by the particle characteristics and exposure models used and therefore risk potentially overstating the biological re
Human derived in vitro studies have also been used to assess the impact of MNPs on gut microbiota. In the SIMGI® model, Tamargo et al[66] showed that PET MNPs altered colonic microbial community structure including reduced Bacteroides and Alistipes and increase in pro-inflammatory bacteria Escherichia, Shigella, Bilophila and enrichment of Firmicutes. They also observed bacterial adhesion and biofilm-like structures on PET surfaces, raising the possibility that microplastics may act as novel ecological niches. In an infant gut model Fournier et al[67] demonstrated an increase in α-diversity together with an increase in taxa associated with pathobionts behaviours when exposed to PE polymers. Ren et al[68] used Simulator of the Human Intestinal Microbial Ecosystem to demonstrate microbiota shifts, altering Firmicutes/Bacteroidota ratios, loss of Bifidobacteriaceae and change in SCFA metabolism.
Overall, current evidence suggests that MNP exposure may alter both intestinal microbiota composition and microbial metabolic function. This supports a plausible link between MNP exposure and dysbiosis, but the evidence remains pre-clinical and highly dependent on the exposure model used. It should therefore be interpreted cautiously and does not establish causality or confirm similar effects in humans.
The intestinal mucus layer is an important component of the intestinal immune system functioning not only as a physical barrier but also a biologically active interface containing anti-microbial peptides and immunoglobulins[69-71]. Mucus barrier dysfunction is well described in IBD[72] where goblet cell depletion and reduced mucin 2 secretion led to a thinning of the mucus layer, increased epithelial exposure and increased inflammation[73].
Experimental models have suggested that MNPs may impair the mucus barrier through several mechanisms. In mouse models oral MNP administration has been shown to reduce colonic mucin density and expression[74], reduce goblet cell number and goblet cell morphology[75-77]. Several in vivo studies have also reported reduced mucin 2 expression, the major secreted glycoprotein, consistent with impaired mucus production[74,76,78,79].
Notably, the effect of MNPs on the mucus layer may depend on the underlying intestinal conditions. Zolotova et al[78] demonstrated that MNP exposure altered mucin composition differently in healthy and inflamed mucosa. In healthy mice they observed an increase in highly sulphated mucins, however in dextran sodium sulfate colitis conditions, there was a reduction in neutral mucins leading to more severe inflammation. Furthermore, in vitro models have observed an increase in mucin 2 expression following PS exposure, suggesting an adaptive response to environmental stressors[80]. van Wijngaarden et al[81] also demonstrated that an intact human intestinal mucus layer reduced microplastics uptake, cytotoxicity and reactive oxygen species supporting the protective role of a healthy mucus layer.
Overall, the relationship between MNP exposure and the mucus barrier appears context-dependent. In healthy mucosa, increased or altered mucin production may represent an adaptive protective response, whereas in inflamed mucosa, impaired mucin composition or goblet-cell dysfunction may amplify epithelial exposure and intestinal injury.
The intestinal barrier, consisting of a single layer of epithelial cells held together by complex structures called tight junctions, adherens junctions and desmosomes[82]. Tight junctions play a crucial role in regulating the passage of nutrients and other luminal contents whilst preventing entry of pathogens and toxins[83]. Increased intestinal per
Both in vivo and in vitro models suggest that MNPs can disrupt intestinal barrier function through disruption of tight junctions and oxidative stress-related epithelial damage, therefore potentially allowing translocation of both MNPs and other toxins[61,79,88]. Importantly, changes in tight junction protein expression should be separated from functional assessment of intestinal permeability, both of which have been demonstrated in mice models following MNP exposure. Zeng et al[89] demonstrated that mice exposed to PS-MNP for 28 days resulted in downregulation of tight junction proteins zonula occludens-1, occludin and claudin-1 accompanied by increased epithelial permeability. This effect was attenuated by pre-treatment with the antioxidant N-acetylcysteine implicating a reactive oxygen species dependent mechanism. Li et al[90] demonstrated that following environmentally relevant concentrations of PS-MNPs reduced expression of tight junction proteins occludin, claudin-1 and zonula occludens-1 particularly at higher doses. By contrast, Liang et al[79] demonstrated functional barrier impairment in mice following exposure to PS particle sized 50 nm, 500 nm and 5000 nm assessed using creatinine, 4 kDa dextran and 70 kDa dextran flux assays.
IBD is driven by a dysregulated immune system involving both the innate and adaptive pathways. This is characterised by infiltration of the lamina propria of T cells, B cells, macrophages and neutrophils, together with failure of normal regulatory mechanisms to control the inflammatory response. In IBD, intestinal immune cells produce high levels of pro-inflammatory cytokines including tumour necrosis factor (TNF), interleukin (IL)-1β, interferon-γ and cytokines within the IL-23 pathway[91-93].
Animal models support the plausibility that MNPs can activate overlapping pro-inflammatory pathways[94,95] and impair regulatory pathways such as T-reg cells[96,97]. In mice, chronic oral exposure to PS-MNPs have been shown to increase pro-inflammation cytokines IL-6, TNF-α and IL-1β, increase B cells in mesenteric lymph nodes and reduce intestinal CD8+ T cells supporting disruption to both innate and adaptive immune response[90]. Oral exposure to PS-MNPs have also been shown to increased intestinal nuclear factor kappa B/NOD-Like receptor pyrin domain-containing protein 3 signaling in mice[98], a key mediator of inflammation[99,100]. This upregulation subsequently led to increased expression of IL-1β and IL-18, which in turn can recruit macrophages and neutrophils into the intestinal mucosa. PE-MNPs have been associated with increased serum IL-1α and upregulation of intestinal toll-like receptor 4, activator protein 1 and interferon regulatory factor 5 and reduced Th17 and Treg number. In experimental models, immune effects appear more pronounced in the presence of pre-existing or chemically induced intestinal inflammation, suggesting that MNPs may be more relevant as amplifiers of established inflammation than as primary initiators. PS-MNPs have been shown to exacerbate dextran sodium sulfate colitis in mice[95,101,102] and induce CD-like ileitis with increased expression of Th17 cells and increased expression of IL-1β and TNF-α in the lamina propria[103]. In contrast, in healthy mice chronic exposure to PET-MNPs did not result in an increase in neutrophils, T cells, B cells or macrophages there was also no increase in expression of pro-inflammatory cytokines.
In vitro modelling outcomes are highly dependent on model complexity and inflammatory context. Lehner et al[104] used a model consisting of Caco-2/HT29-MTX-E12, human blood monocyte-derived macrophages and dendritic cells finding no major pro-inflammatory response after exposure to MNPs. In a Caco-2/HT29-MTX-E12/THP-1 model, exposure to PS or PVC caused no clear effect in a healthy intestinal model, whereas PVC exposure in an inflamed model increased IL-1β release[105]. In organoid-derived epithelial models, PS-MNPs demonstrated increased TNF-α, IL-6 and IL-8, particularly in M-cell-containing models[106].
Overall, the available data supports immune-mediated mechanistic plausibility, particularly in experimental models of pre-existing intestinal inflammation, but they do not establish that MNPs directly activate these pathways in human IBD.
As outlined in Table 1, human studies directly investigating the role of MNPs in IBD remain limited and are currently restricted to small observational datasets. Yan et al[107] measured fecal MNPs concentration in 52 patients with IBD and compared this to 50 healthy controls. IBD patients had a significantly higher levels of MNPs compared to controls (41.8 items/g vs 28.0 items/g), with MNP concentration correlated positively with IBD activity. In a pilot analysis of the ongoing PLANET study, available as a conference abstract, MNPs were detected in all third trimester stool samples and MNPs count positively correlated with fecal calprotectin, a marker of bowel inflammation[108]. Huang et al[109] measured serum levels of MNPs in 241 CD patients and 43 healthy controls and found that serum MNPs were higher in CD patients than healthy controls. Furthermore, higher serum MNPs were associated with more severe endoscopic inflammation, a structuring or penetrating phenotype and was an independent risk factor for disease progression (hazard ratio = 2.95, 95% confidence interval: 1.57-5.57). Finally, Wu et al[110] reported MNP accumulation in fibrotic intestinal tissues and adjacent mesenteric adipose tissue from six ileal resections from patients with CD, with concentrations correlating with fibrosis severity.
| Ref. | Publication status | Number | Population | Study design | Biospecimen | Analytical method | Main findings |
| Yan et al[107], 2022 | Full article | 52 IBD; 50 healthy controls | Adults with IBD and healthy controls | Cross sectional case-controlled study | Feces | Raman spectrometry | Fecal MNP concentration was higher in IBD than controls (41.8 items/g dry matter vs 28.0 items/g dry matter). Fecal MP burden correlated with IBD severity |
| Lykkemark et al[108], 2025 | Abstract | 4 CD; 7 non-IBD | Pregnant patients in third trimester with and without CD | Prospective pilot study | Feces | μFTIR | MNPs > 10 μm were detected in all stool samples, with counts ranging 34 particles/g to 410 particles/g dry weight. MNPs count correlated positively with fecal calprotectin, after adjusting for IBD status (Spearman r = 0.65, P = 0.04) |
| Wu et al[110], 2025 | Full article | 10 CD patients (32 tissue samples) | CD patients undergoing intestinal resection for CD complication | Cross sectional paired tissue study | Surgical specimens: Paired involved ileum, uninvolved ileum, creeping fat and mesenteric adipose | Laser infrared spectroscopy | MNPs were detected in fibrotic intestine and adjacent mesenteric adipose tissue. MNPs concentrations correlated positively with fibrosis severity, and fibrotic sites showed significantly greater accumulation than surrounding tissue. Approximately 31.96% of detected particles were 20-50 μm in size |
| Huang et al[109], 2026 | Abstract | 241 CD patients; 43 healthy controls | Adults with CD and healthy controls | Two centers, prospective; cross sectional baseline analysis with longitudinal follow up | Serum | Py-GC-MS | Serum total MNPs were higher in CD than controls (90.7 ± 33.7 μg/g vs 32.8 ± 12.5 μg/g; P < 0.001). MNPs burden associated with more severe endoscopic or MRE inflammation, and with structuring or penetrating phenotype (OR = 2.65, 95%CI: 1.41-5.11). High MNPs baseline concentration associated with disease progression (45.7% vs 25.8%) and independently increased progression risk (HR = 2.95, 95%CI: 1.57-5.57) |
The human evidence base remains small, with some data only available as conference abstracts. These abstracts are included because relevant human studies are limited, but should be interpreted cautiously and given less weight than full peer reviewed articles. Taken together, the available studies suggest a potential association between increased MNP burden and IBD disease activity. However, the evidence remains observational and vulnerable to confounding, reverse causation and uncertainly around exposure chronology. These studies demonstrate associations only, they do not establish that MNPs can cause increased disease activity or directly drive intestinal fibrosis. It remains unknown whether the associations seen reflect a causal role in disease activity, increased retention because of increased disease activity or an unrelated correlator. Robust prospective human studies examining whether MNPs exposure may precede onset or alter disease course are currently lacking.
There are currently a number of ongoing studies, outlined in Table 2, that are currently investigating the link between MNPs and IBD. MAP-IBD (NCT07141238)[111] is recruiting paediatric patients with IBD undergoing planned colo
| Study title | Ref. | Trial acronym | Registry ID | Study design | Key population | Planned biospecimen | Outcomes | Target enrollment |
| Microplastic Analysis in Pediatric Inflammatory Bowel Disease | Marszk[111] | MAP-IBD | NCT07141238 | Observational case-controlled study; single center | Children < 18 years undergoing clinically indicated colonoscopy, with and without a previous diagnosis of UC or CD | Intestinal mucosal biopsies, stool, urine and blood | Detect and quantify MNPs in intestinal biopsies | 40 (20 IBD + 20 controls) |
| The Presence of Microplastics and Nanoplastics in the Humans Ileum, Colon, and Rectum and Their Relation With Inflammatory Bowel Disease | Sileri[112] | MATISSE | NCT06525558 | Cross sections observational case controlled | Adults undergoing planned surgical resection involving ileum, colon or rectum with and without IBD | Resected bowel specimens | Determine presence and characterization of MNPs in bowel tissue and assess correlation with IBD; exploratory metabolomics/proteomics and plastic-exposure assessment | 102 (25 UC + 26 CD + 51 healthy controls) |
| Pregnant Women With and Without Crohn’s Disease to Explore the Role of Plastics and Toxins in Intestinal Inflammation | Agrawal[113] | PLANET | NCT06001450 | Prospective observational maternal-infant cohort | Women > 18 years old who are pregnant or planning pregnancy with and without a diagnosis of CD | Maternal stool & saliva; placenta; cord blood; breast milk; infant stool | Measuring the concentration, size and shape distributions of MNPs in stool samples of women with CD, healthy controls and any relatives. Microbiome characterization and fecal calprotectin | 46 |
Although direct human evidence linking MNPs to IBD is limited, studies in other diseases provide indirect support for biological plausibility. A 2026 systematic review identified 25 in vivo human studies examining MNPs and health outcomes across several other organ systems. Overall, the evidence was largely observational and heterogeneous, however in one notable study, Marfella et al[20] identified MNPs in 58.4% of carotid artery plaques from 257 patients undergoing carotid endarterectomy. The presence of MNPs in plaques was associated with higher inflammatory markers and an increased risk of myocardial infarction, stroke or death (adjust hazard ratio = 4.5; 95% confidence interval: 2.0-10.3). These findings support the concept that MNPs can accumulate in human tissues, contribute to inflammation and lead to adverse clinical outcomes, although causation remains unproven.
The changing global epidemiology of IBD[115,116] strongly supports an important role for environmental factors in disease pathogenesis[30,117]. Incidence has been rising in newly industrialised regions[116] and prospective cohort studies have demonstrated that favourable lifestyle factors are associated with lower IBD risk, even in individuals considered at high genetic risk[118]. Plastic and MNPs production have increased exponentially over the past 70 years and may represent a relevant environmental exposure. However, any link remains hypothetical with many confounding factors including diet, antibiotics, pollution and emulsifiers and therefore should be interpreted cautiously[119].
Studies investigating MNPs in IBD are limited by major methodological challenges. These include non-standardised analytical protocols for sample collection, digestion, identification and reporting, high contamination risk, uncertainty regarding the most biologically relevant exposure metric, and the predominance of observational study designs that are vulnerable to confounding and reverse causation[120].
Contamination: Contamination of biological samples is a major concern throughout the analytical process. Contamination could occur at all stages of samples collection, storage, preparation and analysis. Common sources of contamination include consumables, filters, airborne fibers and synthetic clothing. Rigorous quality assurance is essential, including the use of non-plastic equipment and contamination-controlled workspaces alongside analysis of blank samples[121].
Sample preparation: Isolating MNPs from biological matrices such as blood, stool and biopsies require the removal of organic tissue without altering or degrading the MNPs. Current studies have used a range of protocols including enzymatic degradation, acidic digestion, alkaline digestion, oxidation and density separation, however there is currently no universally accepted standard[122].
Detection and characterisation: Once MNPs have been isolated from the biological matrix the next step is detection and characterisation of the MNPs. Several techniques can be used, each with their own limitations[123]. Optical microscopy allows visualisation of MNPs down to a minimum size of 100 μm, however using this technique means that smaller particles will not be detected. Optical microscopy also cannot determine polymer composition[124]. When optical microscopy is combined with dye staining, commonly Nile Red dye[125], this does improve detection rates however it remains heavily dependent on the operator and remains non-specific.
Polymer identification is more commonly performed using vibrational spectroscopic techniques, principally Fourier transform Infrared spectroscopy and Raman spectroscopy[126]. These techniques are non-destructive and allow accurate determination of polymer type, quantities, shapes and sizes. Fourier transform Infrared spectroscopy generally allows analysis of particles down to 10 μm in size whereas Raman spectroscopy can detect particles down to 1 μm in size.
Thermal analytical methods, such as pyrolysis with chromatography-mass spectrometry (Py-GC-MS) offer mass-based polymer quantification, however this technique is destructive and based on thermal degradation of products at specific temperatures in oxygen free conditions. The main advantage of Py-GC-MS is its mass-based quantification of specific polymers however it provides no information on the number, size or morphology of the polymer and therefore is often done in conjunction with vibrational spectroscopy. Recent validation on human blood samples have suggested that Py-GC-MS may not reliably quantify some common polymers including PE and PVC[127].
A limitation in MNP research is inconsistent reporting of quality-control procedures. Future studies should report minimum methodological standards, including field and procedural blanks, recovery rates from spiked samples, limits of detection and quantification, spectral matching thresholds, reference libraries, and contamination-control measures[128-130]. These details are essential to determine whether reported MNP concentrations reflect true sample burden, rather than background contamination, incomplete recovery, or differences in analytical classification. This would improve comparability between studies and strengthen interpretation of exposure relationships.
There are several obstacles that make studying environmental triggers challenging in IBD and these are particularly relevant to research in MNPs[119].
Firstly, whilst stool samples are attractive biospecimens as they are non-invasive, spot stool samples reflect recent MNPs excretion burden and potentially ingestion rather than chronic exposure or mucosal bioavailability. Stool based measurements therefore cannot be assumed to represent the quantity or polymer relevant to disease pathogenesis. Interpretation is further complicated by the fact that little is known about how the gastrointestinal tract alters the particles during transit. These limitations are important when interpreting the currently available cross-sectional evidence in IBD studies. Associations between higher stool MNPs level and disease activity may suggest a causative role however they may equally reflect reverse causation. Active inflammation could alter transit, increase particle retention and increase epithelial permeability therefore altering fecal MNPs concentrations. Additionally, active IBD may lead to dietary and behavioural changes introducing further confounding factors.
Many experimental studies have used simplistic models that do not reflect real world human exposures. Both in vivo and in vitro studies commonly use a single polymer, single particle size, single particle shape and doses that exceed normal human exposures. This contrasts with weathered, irregular and mixed polymers that humans are chronically exposed to in the real world[131]. Furthermore, real world exposure to MNPs often contain chemical additives, plasticisers, stabilisers, and environmental contaminants which further diversify human exposures. This limits the external validity of the models, as complex exposures may result in different biological effects. Differing polymer size[79] and shape[132] have been demonstrated to alter the effects observed. It also remains unclear whether MNPs are able to initiate intestinal inflammation in the presence of healthy mucosa, and/or exacerbate inflammation in the presence of pre-existing inflammation[78].
Human observational studies investigating associations between MNP exposure and IBD are susceptible to con
The impact of MNPs on human health, and specifically IBD, remains unknown. The field is in an early stage and studies exploring the impact on human health have significant challenges, including contamination risk, ethical constraints, cost, technical complexity and substantial confounding from diet, lifestyle, occupation and geography. Standardisation of analytical techniques, experimental protocols and reporting are crucial if results are to be comparable across studies[134]. Experimental studies should move away from single homogeneous polymers towards environmentally relevant particles that reflect human exposures, although the generation of these particles has its own challenges[131,135].
Direct human exposure experiments are ethically challenging and therefore prospective observational cohorts with exposure reduction may be feasible alternatives. Longitudinal epidemiological studies examining whether estimated or measured MNPs exposure precedes IBD onset, influences disease phenotype, predicts relapse or alters treatment response will also provide valuable evidence. Planned biopsy-based studies comparing inflamed and non-inflamed mucosa will help understand if particle burden is linked to disease activity. Exposure questionnaires may also have a role as scalable epidemiological tools that can be used, but further work is required to validate these in IBD[136].
MNPs are now unavoidable environmental exposures and there is plausible mechanistic evidence that oral ingestion can contribute to inflammatory pathways implicated in IBD. Current evidence is dominated by preclinical models that use simplified particle types and exposure conditions that do not reflect real-world human exposure. Human data in IBD is still sparse and limited to small observational studies that are highly vulnerable to confounding and reverse causation. Consequently, current evidence is insufficient to determine if MNPs may cause or exacerbate existing IBD or have a future clinical use. Further studies are required to understand the impact that MNPs may have on IBD disease course.
| 1. | Landrigan PJ, Dunlop S, Treskova M, Raps H, Symeonides C, Muncke J, Spring M, Stegeman J, Almroth BC, Chiles TC, Cropper M, Deeney M, Fuller L, Geyer R, Karasik R, Mafira T, Mangwiro A, Matias DM, Mulders Y, Park Y, Velis CA, Vermeulen R, Wagner M, Wang Z, Whitman EM, Woodruff TJ, Rocklöv J. The Lancet Countdown on health and plastics. Lancet. 2025;406:1044-1062. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 3] [Cited by in RCA: 61] [Article Influence: 61.0] [Reference Citation Analysis (0)] |
| 2. | Kumar M, Chaudhary V, Kumar R, Chaudhary V, Srivastav AL. Microplastics, their effects on ecosystems, and general strategies for mitigation of microplastics: A review of recent developments, challenges, and future prospects. Environ Pollut Manag. 2025;2:87-105. [DOI] [Full Text] |
| 3. | Thompson RC, Olsen Y, Mitchell RP, Davis A, Rowland SJ, John AW, McGonigle D, Russell AE. Lost at sea: where is all the plastic? Science. 2004;304:838. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 2946] [Cited by in RCA: 4013] [Article Influence: 182.4] [Reference Citation Analysis (2)] |
| 4. | Frias JPGL, Nash R. Microplastics: Finding a consensus on the definition. Mar Pollut Bull. 2019;138:145-147. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 693] [Cited by in RCA: 1004] [Article Influence: 143.4] [Reference Citation Analysis (0)] |
| 5. | Gigault J, Halle AT, Baudrimont M, Pascal PY, Gauffre F, Phi TL, El Hadri H, Grassl B, Reynaud S. Current opinion: What is a nanoplastic? Environ Pollut. 2018;235:1030-1034. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 735] [Cited by in RCA: 1104] [Article Influence: 138.0] [Reference Citation Analysis (5)] |
| 6. | Chen Y, Chen Q, Zhang Q, Zuo C, Shi H. An Overview of Chemical Additives on (Micro)Plastic Fibers: Occurrence, Release, and Health Risks. Reviews Env Contamination (formerly:Residue Reviews). 2022;260:22. [RCA] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 12] [Article Influence: 3.0] [Reference Citation Analysis (0)] |
| 7. | Al-Mansoori M, Stephenson M, Harrad S, Abdallah MA. Synthetic Microplastics in UK tap and bottled water; Implications for human exposure. Emerg Contam. 2025;11:100417. [DOI] [Full Text] |
| 8. | Mintenig SM, Löder MGJ, Primpke S, Gerdts G. Low numbers of microplastics detected in drinking water from ground water sources. Sci Total Environ. 2019;648:631-635. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 440] [Cited by in RCA: 485] [Article Influence: 69.3] [Reference Citation Analysis (0)] |
| 9. | Sajedi S, An C, Chen Z. Unveiling the hidden chronic health risks of nano- and microplastics in single-use plastic water bottles: A review. J Hazard Mater. 2025;495:138948. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 24] [Cited by in RCA: 7] [Article Influence: 7.0] [Reference Citation Analysis (0)] |
| 10. | Ghosh T. Microplastics bioaccumulation in fish: Its potential toxic effects on hematology, immune response, neurotoxicity, oxidative stress, growth, and reproductive dysfunction. Toxicol Rep. 2025;14:101854. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 50] [Cited by in RCA: 24] [Article Influence: 24.0] [Reference Citation Analysis (0)] |
| 11. | Kadac-Czapska K, Knez E, Grembecka M. Food and human safety: the impact of microplastics. Crit Rev Food Sci Nutr. 2024;64:3502-3521. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 67] [Cited by in RCA: 71] [Article Influence: 17.8] [Reference Citation Analysis (0)] |
| 12. | Süssmann J, Krause T, Fischer EK, Walz E, Greiner R, Rohn S, Fritsche J. Microplastics in fresh and processed seafood – A survey of products sold in Germany. Food Control. 2026;179:111565. [DOI] [Full Text] |
| 13. | Masciarelli E, Casorri L, Di Luigi M, Beni C, Valentini M, Costantini E, Aielli L, Reale M. Microplastics in Agricultural Crops and Their Possible Impact on Farmers' Health: A Review. Int J Environ Res Public Health. 2024;22:45. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 29] [Cited by in RCA: 11] [Article Influence: 5.5] [Reference Citation Analysis (0)] |
| 14. | Yakovenko N, Pérez-Serrano L, Segur T, Hagelskjaer O, Margenat H, Le Roux G, Sonke JE. Human exposure to PM10 microplastics in indoor air. PLoS One. 2025;20:e0328011. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 21] [Reference Citation Analysis (0)] |
| 15. | Jenner LC, Rotchell JM, Bennett RT, Cowen M, Tentzeris V, Sadofsky LR. Detection of microplastics in human lung tissue using μFTIR spectroscopy. Sci Total Environ. 2022;831:154907. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 173] [Cited by in RCA: 800] [Article Influence: 200.0] [Reference Citation Analysis (0)] |
| 16. | Horvatits T, Tamminga M, Liu B, Sebode M, Carambia A, Fischer L, Püschel K, Huber S, Fischer EK. Microplastics detected in cirrhotic liver tissue. EBioMedicine. 2022;82:104147. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 2] [Cited by in RCA: 471] [Article Influence: 117.8] [Reference Citation Analysis (1)] |
| 17. | Saraluck A, Techarang T, Bunyapipat P, Boonchuwong K, Pullaput Y, Mordmuang A. Detection of Microplastics in Human Breast Milk and Its Association with Changes in Human Milk Bacterial Microbiota. J Clin Med. 2024;13:4029. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 40] [Reference Citation Analysis (0)] |
| 18. | Zurub RE, Bainbridge S, Rahman L, Halappanavar S, El-Chaâr D, Wade MG. Particulate contamination of human placenta: Plastic and non-plastic. Environ Adv. 2024;17:100555. [DOI] [Full Text] |
| 19. | Pironti C, Notarstefano V, Ricciardi M, Motta O, Giorgini E, Montano L. First Evidence of Microplastics in Human Urine, a Preliminary Study of Intake in the Human Body. Toxics. 2022;11:40. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 3] [Cited by in RCA: 184] [Article Influence: 46.0] [Reference Citation Analysis (0)] |
| 20. | Marfella R, Prattichizzo F, Sardu C, Fulgenzi G, Graciotti L, Spadoni T, D'Onofrio N, Scisciola L, La Grotta R, Frigé C, Pellegrini V, Municinò M, Siniscalchi M, Spinetti F, Vigliotti G, Vecchione C, Carrizzo A, Accarino G, Squillante A, Spaziano G, Mirra D, Esposito R, Altieri S, Falco G, Fenti A, Galoppo S, Canzano S, Sasso FC, Matacchione G, Olivieri F, Ferraraccio F, Panarese I, Paolisso P, Barbato E, Lubritto C, Balestrieri ML, Mauro C, Caballero AE, Rajagopalan S, Ceriello A, D'Agostino B, Iovino P, Paolisso G. Microplastics and Nanoplastics in Atheromas and Cardiovascular Events. N Engl J Med. 2024;390:900-910. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 871] [Cited by in RCA: 698] [Article Influence: 349.0] [Reference Citation Analysis (0)] |
| 21. | Leslie HA, van Velzen MJM, Brandsma SH, Vethaak AD, Garcia-Vallejo JJ, Lamoree MH. Discovery and quantification of plastic particle pollution in human blood. Environ Int. 2022;163:107199. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 503] [Cited by in RCA: 1942] [Article Influence: 485.5] [Reference Citation Analysis (1)] |
| 22. | Schwabl P, Köppel S, Königshofer P, Bucsics T, Trauner M, Reiberger T, Liebmann B. Detection of Various Microplastics in Human Stool: A Prospective Case Series. Ann Intern Med. 2019;171:453-457. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 586] [Cited by in RCA: 1120] [Article Influence: 160.0] [Reference Citation Analysis (0)] |
| 23. | Lu T, Liu H, Yuan X, Li D, Zhang G, Wang Y, Xie Q, Wang X, Chi J, Wang Z, Wang S, Gao Y, Zhou L, Xu M. Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice. Ecotoxicol Environ Saf. 2025;298:118330. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 12] [Reference Citation Analysis (0)] |
| 24. | Zhang Z, Xu M, Wang L, Gu W, Li X, Han Z, Fu X, Wang X, Li X, Su Z. Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice. Environ Int. 2023;182:108353. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 76] [Cited by in RCA: 115] [Article Influence: 38.3] [Reference Citation Analysis (0)] |
| 25. | Le Berre C, Honap S, Peyrin-Biroulet L. Ulcerative colitis. Lancet. 2023;402:571-584. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 1251] [Cited by in RCA: 1228] [Article Influence: 409.3] [Reference Citation Analysis (5)] |
| 26. | Dolinger M, Torres J, Vermeire S. Crohn's disease. Lancet. 2024;403:1177-1191. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 405] [Cited by in RCA: 432] [Article Influence: 216.0] [Reference Citation Analysis (1)] |
| 27. | Calvez V, Puca P, Di Vincenzo F, Del Gaudio A, Bartocci B, Murgiano M, Iaccarino J, Parand E, Napolitano D, Pugliese D, Gasbarrini A, Scaldaferri F. Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases. Biomedicines. 2025;13:305. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 63] [Cited by in RCA: 72] [Article Influence: 72.0] [Reference Citation Analysis (0)] |
| 28. | Kaplan GG. The global burden of inflammatory bowel disease: from 2025 to 2045. Nat Rev Gastroenterol Hepatol. 2025;22:708-720. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 49] [Cited by in RCA: 72] [Article Influence: 72.0] [Reference Citation Analysis (0)] |
| 29. | Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2021;18:56-66. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1095] [Cited by in RCA: 1048] [Article Influence: 209.6] [Reference Citation Analysis (8)] |
| 30. | Estevinho MM, Midya V, Cohen-Mekelburg S, Allin KH, Fumery M, Pinho SS, Colombel JF, Agrawal M. Emerging role of environmental pollutants in inflammatory bowel disease risk, outcomes and underlying mechanisms. Gut. 2025;74:477-486. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 52] [Cited by in RCA: 51] [Article Influence: 51.0] [Reference Citation Analysis (0)] |
| 31. | Hartmann NB, Hüffer T, Thompson RC, Hassellöv M, Verschoor A, Daugaard AE, Rist S, Karlsson T, Brennholt N, Cole M, Herrling MP, Hess MC, Ivleva NP, Lusher AL, Wagner M. Are We Speaking the Same Language? Recommendations for a Definition and Categorization Framework for Plastic Debris. Environ Sci Technol. 2019;53:1039-1047. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 958] [Cited by in RCA: 1433] [Article Influence: 204.7] [Reference Citation Analysis (0)] |
| 32. | Nawab A, Ahmad M, Khan MT, Nafees M, Khan I, Ihsanullah I. Human exposure to microplastics: A review on exposure routes and public health impacts. J Hazard Mater Adv. 2024;16:100487. [DOI] [Full Text] |
| 33. | Geyer R, Jambeck JR, Law KL. Production, use, and fate of all plastics ever made. Sci Adv. 2017;3:e1700782. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 6592] [Cited by in RCA: 7129] [Article Influence: 792.1] [Reference Citation Analysis (1)] |
| 34. | Lombardi G, Di Russo M, Zjalic D, Lanza T, Simmons M, Moscato U, Ricciardi W, Chiara C. Microplastics inhalation and their effects on human health: a systematic review. Eur J Public Health. 2022;32:ckac131.152. [DOI] [Full Text] |
| 35. | Vianello A, Jensen RL, Liu L, Vollertsen J. Simulating human exposure to indoor airborne microplastics using a Breathing Thermal Manikin. Sci Rep. 2019;9:8670. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 335] [Cited by in RCA: 394] [Article Influence: 56.3] [Reference Citation Analysis (0)] |
| 36. | Akpojevwe Abafe O, Harrad S, Abou-Elwafa Abdallah M. Assessment of human dermal absorption of flame retardant additives in polyethylene and polypropylene microplastics using 3D human skin equivalent models. Environ Int. 2024;186:108635. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 44] [Cited by in RCA: 23] [Article Influence: 11.5] [Reference Citation Analysis (0)] |
| 37. | Ghasemi FF, Dehghani M, Dobaradaran S, Hoseini M, KalantarHormozi MR, Samaei MR. Detection and characterization of MPs in the human stool: an observational study in Bushehr, Iran. Sci Rep. 2026;16:9609. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Reference Citation Analysis (0)] |
| 38. | Heo SJ, Moon N, Kim JH. A systematic review and quality assessment of estimated daily intake of microplastics through food. Rev Environ Health. 2025;40:371-392. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 1] [Cited by in RCA: 24] [Article Influence: 24.0] [Reference Citation Analysis (0)] |
| 39. | Al-Mansoori M, Harrad S, Abdallah MA. Synthetic microplastics in hot and cold beverages from the UK market: Comprehensive assessment of human exposure via total beverage intake. Sci Total Environ. 2025;996:180188. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 1] [Cited by in RCA: 9] [Article Influence: 9.0] [Reference Citation Analysis (0)] |
| 40. | Hernandez LM, Xu EG, Larsson HCE, Tahara R, Maisuria VB, Tufenkji N. Plastic Teabags Release Billions of Microparticles and Nanoparticles into Tea. Environ Sci Technol. 2019;53:12300-12310. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 425] [Cited by in RCA: 644] [Article Influence: 92.0] [Reference Citation Analysis (0)] |
| 41. | Bai CL, Liu LY, Guo JL, Zeng LX, Guo Y. Microplastics in take-out food: Are we over taking it? Environ Res. 2022;215:114390. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 2] [Cited by in RCA: 47] [Article Influence: 11.8] [Reference Citation Analysis (0)] |
| 42. | Du F, Cai H, Zhang Q, Chen Q, Shi H. Microplastics in take-out food containers. J Hazard Mater. 2020;399:122969. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 117] [Cited by in RCA: 237] [Article Influence: 39.5] [Reference Citation Analysis (0)] |
| 43. | Ranjan VP, Joseph A, Goel S. Microplastics and other harmful substances released from disposable paper cups into hot water. J Hazard Mater. 2021;404:124118. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 73] [Cited by in RCA: 134] [Article Influence: 26.8] [Reference Citation Analysis (0)] |
| 44. | Liu G, Wang J, Wang M, Ying R, Li X, Hu Z, Zhang Y. Disposable plastic materials release microplastics and harmful substances in hot water. Sci Total Environ. 2022;818:151685. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 16] [Cited by in RCA: 66] [Article Influence: 16.5] [Reference Citation Analysis (0)] |
| 45. | Gambino I, Bagordo F, Grassi T, Panico A, De Donno A. Occurrence of Microplastics in Tap and Bottled Water: Current Knowledge. Int J Environ Res Public Health. 2022;19:5283. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 28] [Cited by in RCA: 86] [Article Influence: 21.5] [Reference Citation Analysis (0)] |
| 46. | Li D, Shi Y, Yang L, Xiao L, Kehoe DK, Gun'ko YK, Boland JJ, Wang JJ. Microplastic release from the degradation of polypropylene feeding bottles during infant formula preparation. Nat Food. 2020;1:746-754. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 111] [Cited by in RCA: 347] [Article Influence: 57.8] [Reference Citation Analysis (0)] |
| 47. | Cox KD, Covernton GA, Davies HL, Dower JF, Juanes F, Dudas SE. Human Consumption of Microplastics. Environ Sci Technol. 2019;53:7068-7074. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 883] [Cited by in RCA: 1383] [Article Influence: 197.6] [Reference Citation Analysis (1)] |
| 48. | Mohamed Nor NH, Kooi M, Diepens NJ, Koelmans AA. Lifetime Accumulation of Microplastic in Children and Adults. Environ Sci Technol. 2021;55:5084-5096. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 153] [Cited by in RCA: 357] [Article Influence: 71.4] [Reference Citation Analysis (3)] |
| 49. | Bruno A, Dovizio M, Milillo C, Aruffo E, Pesce M, Gatta M, Chiacchiaretta P, Di Carlo P, Ballerini P. Orally Ingested Micro- and Nano-Plastics: A Hidden Driver of Inflammatory Bowel Disease and Colorectal Cancer. Cancers (Basel). 2024;16:3079. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 43] [Cited by in RCA: 35] [Article Influence: 17.5] [Reference Citation Analysis (0)] |
| 50. | Liu L, Xu K, Zhang B, Ye Y, Zhang Q, Jiang W. Cellular internalization and release of polystyrene microplastics and nanoplastics. Sci Total Environ. 2021;779:146523. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 73] [Cited by in RCA: 310] [Article Influence: 62.0] [Reference Citation Analysis (0)] |
| 51. | Hernández AF, Lacasaña M, Tsatsakis AM, Docea AO. Cellular and Molecular Mechanisms of Micro- and Nanoplastics Driving Adverse Human Health Effects. Toxics. 2025;13:921. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 15] [Article Influence: 15.0] [Reference Citation Analysis (0)] |
| 52. | Schwarzfischer M, Niechcial A, Lee SS, Sinnet B, Wawrzyniak M, Laimbacher A, Atrott K, Manzini R, Morsy Y, Häfliger J, Lang S, Rogler G, Kaegi R, Scharl M, Spalinger MR. Ingested nano- and microsized polystyrene particles surpass the intestinal barrier and accumulate in the body. NanoImpact. 2022;25:100374. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 14] [Cited by in RCA: 46] [Article Influence: 11.5] [Reference Citation Analysis (0)] |
| 53. | Maynard CL, Elson CO, Hatton RD, Weaver CT. Reciprocal interactions of the intestinal microbiota and immune system. Nature. 2012;489:231-241. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 952] [Cited by in RCA: 1140] [Article Influence: 81.4] [Reference Citation Analysis (5)] |
| 54. | Jandhyala SM, Talukdar R, Subramanyam C, Vuyyuru H, Sasikala M, Nageshwar Reddy D. Role of the normal gut microbiota. World J Gastroenterol. 2015;21:8787-8803. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in CrossRef: 2550] [Cited by in RCA: 2038] [Article Influence: 185.3] [Reference Citation Analysis (8)] |
| 55. | Pittayanon R, Lau JT, Leontiadis GI, Tse F, Yuan Y, Surette M, Moayyedi P. Differences in Gut Microbiota in Patients With vs Without Inflammatory Bowel Diseases: A Systematic Review. Gastroenterology. 2020;158:930-946.e1. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 528] [Cited by in RCA: 478] [Article Influence: 79.7] [Reference Citation Analysis (6)] |
| 56. | Joossens M, Huys G, Cnockaert M, De Preter V, Verbeke K, Rutgeerts P, Vandamme P, Vermeire S. Dysbiosis of the faecal microbiota in patients with Crohn's disease and their unaffected relatives. Gut. 2011;60:631-637. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 935] [Cited by in RCA: 824] [Article Influence: 54.9] [Reference Citation Analysis (5)] |
| 57. | Yang XY, Zhang ZW, Chen GD, Yuan S. Gut microbiome remodeling induced by microplastic exposure in humans. Gut Microbes. 2026;18:2617696. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 13] [Cited by in RCA: 6] [Article Influence: 6.0] [Reference Citation Analysis (0)] |
| 58. | Thin ZS, Chew J, Ong TYY, Raja Ali RA, Gew LT. Impact of microplastics on the human gut microbiome: a systematic review of microbial composition, diversity, and metabolic disruptions. BMC Gastroenterol. 2025;25:583. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 23] [Reference Citation Analysis (0)] |
| 59. | Ghosal S, Bag S, Rao SR, Bhowmik S. Exposure to polyethylene microplastics exacerbate inflammatory bowel disease tightly associated with intestinal gut microflora. RSC Adv. 2024;14:25130-25148. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 9] [Reference Citation Analysis (0)] |
| 60. | Djouina M, Vignal C, Dehaut A, Caboche S, Hirt N, Waxin C, Himber C, Beury D, Hot D, Dubuquoy L, Launay D, Duflos G, Body-Malapel M. Oral exposure to polyethylene microplastics alters gut morphology, immune response, and microbiota composition in mice. Environ Res. 2022;212:113230. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 15] [Cited by in RCA: 70] [Article Influence: 17.5] [Reference Citation Analysis (0)] |
| 61. | Jin Y, Lu L, Tu W, Luo T, Fu Z. Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice. Sci Total Environ. 2019;649:308-317. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 431] [Cited by in RCA: 743] [Article Influence: 106.1] [Reference Citation Analysis (4)] |
| 62. | Souza-Silva TG, Oliveira IA, Silva GGD, Giusti FCV, Novaes RD, Paula HAA. Impact of microplastics on the intestinal microbiota: A systematic review of preclinical evidence. Life Sci. 2022;294:120366. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 65] [Cited by in RCA: 48] [Article Influence: 12.0] [Reference Citation Analysis (0)] |
| 63. | Bora SS, Gogoi R, Sharma MR, Anshu, Borah MP, Deka P, Bora J, Naorem RS, Das J, Teli AB. Microplastics and human health: unveiling the gut microbiome disruption and chronic disease risks. Front Cell Infect Microbiol. 2024;14:1492759. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 67] [Reference Citation Analysis (0)] |
| 64. | Tu P, Xue J, Niu H, Tang Q, Mo Z, Zheng X, Wu L, Chen Z, Cai Y, Wang X. Deciphering Gut Microbiome Responses upon Microplastic Exposure via Integrating Metagenomics and Activity-Based Metabolomics. Metabolites. 2023;13:530. [RCA] [DOI] [Full Text] [Cited by in RCA: 25] [Reference Citation Analysis (0)] |
| 65. | Harusato A, Seo W, Abo H, Nakanishi Y, Nishikawa H, Itoh Y. Impact of particulate microplastics generated from polyethylene terephthalate on gut pathology and immune microenvironments. iScience. 2023;26:106474. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 24] [Reference Citation Analysis (0)] |
| 66. | Tamargo A, Molinero N, Reinosa JJ, Alcolea-Rodriguez V, Portela R, Bañares MA, Fernández JF, Moreno-Arribas MV. PET microplastics affect human gut microbiota communities during simulated gastrointestinal digestion, first evidence of plausible polymer biodegradation during human digestion. Sci Rep. 2022;12:528. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 106] [Cited by in RCA: 185] [Article Influence: 46.3] [Reference Citation Analysis (0)] |
| 67. | Fournier E, Ratel J, Denis S, Leveque M, Ruiz P, Mazal C, Amiard F, Edely M, Bezirard V, Gaultier E, Lamas B, Houdeau E, Engel E, Lagarde F, Etienne-Mesmin L, Mercier-Bonin M, Blanquet-Diot S. Exposure to polyethylene microplastics alters immature gut microbiome in an infant in vitro gut model. J Hazard Mater. 2023;443:130383. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 2] [Cited by in RCA: 43] [Article Influence: 14.3] [Reference Citation Analysis (0)] |
| 68. | Ren X, Su C, Zhu Y, Fang JK, Woh PY. Microplastic Toxicity on Gut Microbiota and Intestinal Cells: Evidence from the Simulator of the Human Intestinal Microbial Ecosystem (SHIME). Toxics. 2025;13:1045. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 4] [Reference Citation Analysis (0)] |
| 69. | Johansson ME, Hansson GC. Immunological aspects of intestinal mucus and mucins. Nat Rev Immunol. 2016;16:639-649. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 399] [Cited by in RCA: 753] [Article Influence: 75.3] [Reference Citation Analysis (3)] |
| 70. | Johansson ME, Sjövall H, Hansson GC. The gastrointestinal mucus system in health and disease. Nat Rev Gastroenterol Hepatol. 2013;10:352-361. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1241] [Cited by in RCA: 1077] [Article Influence: 82.8] [Reference Citation Analysis (4)] |
| 71. | Dupont A, Heinbockel L, Brandenburg K, Hornef MW. Antimicrobial peptides and the enteric mucus layer act in concert to protect the intestinal mucosa. Gut Microbes. 2014;5:761-765. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 69] [Cited by in RCA: 106] [Article Influence: 8.8] [Reference Citation Analysis (0)] |
| 72. | Qiao Y, He C, Xia Y, Ocansey DKW, Mao F. Intestinal mucus barrier: A potential therapeutic target for IBD. Autoimmun Rev. 2025;24:103717. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 46] [Cited by in RCA: 47] [Article Influence: 47.0] [Reference Citation Analysis (0)] |
| 73. | van der Post S, Jabbar KS, Birchenough G, Arike L, Akhtar N, Sjovall H, Johansson MEV, Hansson GC. Structural weakening of the colonic mucus barrier is an early event in ulcerative colitis pathogenesis. Gut. 2019;68:2142-2151. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 467] [Cited by in RCA: 414] [Article Influence: 59.1] [Reference Citation Analysis (1)] |
| 74. | Sun H, Chen N, Yang X, Xia Y, Wu D. Effects induced by polyethylene microplastics oral exposure on colon mucin release, inflammation, gut microflora composition and metabolism in mice. Ecotoxicol Environ Saf. 2021;220:112340. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 166] [Cited by in RCA: 185] [Article Influence: 37.0] [Reference Citation Analysis (0)] |
| 75. | Choi YJ, Kim JE, Lee SJ, Gong JE, Jin YJ, Seo S, Lee JH, Hwang DY. Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks. Lab Anim Res. 2021;37:31. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 35] [Article Influence: 7.0] [Reference Citation Analysis (0)] |
| 76. | Xie L, Chen T, Liu J, Hou Y, Tan Q, Zhang X, Li Z, Farooq TH, Yan W, Li Y. Intestinal flora variation reflects the short-term damage of microplastic to the intestinal tract in mice. Ecotoxicol Environ Saf. 2022;246:114194. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 3] [Cited by in RCA: 58] [Article Influence: 14.5] [Reference Citation Analysis (0)] |
| 77. | Huang J, Sun X, Wang Y, Su J, Li G, Wang X, Yang Y, Zhang Y, Li B, Zhang G, Li J, Du J, Nanjundappa RH, Umeshappa CS, Shao K. Biological interactions of polystyrene nanoplastics: Their cytotoxic and immunotoxic effects on the hepatic and enteric systems. Ecotoxicol Environ Saf. 2023;264:115447. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 39] [Reference Citation Analysis (0)] |
| 78. | Zolotova N, Dzhalilova D, Tsvetkov I, Makarova O. Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis. Toxics. 2023;11:730. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 29] [Cited by in RCA: 21] [Article Influence: 7.0] [Reference Citation Analysis (0)] |
| 79. | Liang B, Zhong Y, Huang Y, Lin X, Liu J, Lin L, Hu M, Jiang J, Dai M, Wang B, Zhang B, Meng H, Lelaka JJJ, Sui H, Yang X, Huang Z. Underestimated health risks: polystyrene micro- and nanoplastics jointly induce intestinal barrier dysfunction by ROS-mediated epithelial cell apoptosis. Part Fibre Toxicol. 2021;18:20. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 43] [Cited by in RCA: 356] [Article Influence: 71.2] [Reference Citation Analysis (1)] |
| 80. | Cui M, He Q, Wang Z, Yu Y, Gao H, Liu Z, Peng H, Wang H, Zhang X, Li D, Chen L, Xing X, Xiao Y, Chen W, Wang Q. Mucin2 regulated by Ho1/p38/IL-10 axis plays a protective role in polystyrene nanoplastics-mediated intestinal toxicity. Environ Pollut. 2023;330:121808. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 18] [Reference Citation Analysis (0)] |
| 81. | van Wijngaarden EW, Arias SL, Rhee M, Silberstein MN, Brito IL. The role of human intestinal mucus in the prevention of microplastic uptake and cell damage. Biomater Sci. 2025;13:1010-1020. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 8] [Reference Citation Analysis (0)] |
| 82. | Neurath MF, Artis D, Becker C. The intestinal barrier: a pivotal role in health, inflammation, and cancer. Lancet Gastroenterol Hepatol. 2025;10:573-592. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 8] [Cited by in RCA: 306] [Article Influence: 306.0] [Reference Citation Analysis (0)] |
| 83. | Michielan A, D'Incà R. Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut. Mediators Inflamm. 2015;2015:628157. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 583] [Cited by in RCA: 538] [Article Influence: 48.9] [Reference Citation Analysis (4)] |
| 84. | Yu S, Sun Y, Shao X, Zhou Y, Yu Y, Kuai X, Zhou C. Leaky Gut in IBD: Intestinal Barrier-Gut Microbiota Interaction. J Microbiol Biotechnol. 2022;32:825-834. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 83] [Article Influence: 20.8] [Reference Citation Analysis (1)] |
| 85. | Lee SH. Intestinal permeability regulation by tight junction: implication on inflammatory bowel diseases. Intest Res. 2015;13:11-18. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 684] [Cited by in RCA: 616] [Article Influence: 56.0] [Reference Citation Analysis (3)] |
| 86. | Zeissig S, Bürgel N, Günzel D, Richter J, Mankertz J, Wahnschaffe U, Kroesen AJ, Zeitz M, Fromm M, Schulzke JD. Changes in expression and distribution of claudin 2, 5 and 8 lead to discontinuous tight junctions and barrier dysfunction in active Crohn's disease. Gut. 2007;56:61-72. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1048] [Cited by in RCA: 980] [Article Influence: 51.6] [Reference Citation Analysis (4)] |
| 87. | Chatterjee I, Zhang Y, Zhang J, Lu R, Xia Y, Sun J. Overexpression of Vitamin D Receptor in Intestinal Epithelia Protects Against Colitis via Upregulating Tight Junction Protein Claudin 15. J Crohns Colitis. 2021;15:1720-1736. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 60] [Cited by in RCA: 55] [Article Influence: 11.0] [Reference Citation Analysis (0)] |
| 88. | Stock V, Böhmert L, Lisicki E, Block R, Cara-Carmona J, Pack LK, Selb R, Lichtenstein D, Voss L, Henderson CJ, Zabinsky E, Sieg H, Braeuning A, Lampen A. Uptake and effects of orally ingested polystyrene microplastic particles in vitro and in vivo. Arch Toxicol. 2019;93:1817-1833. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 177] [Cited by in RCA: 393] [Article Influence: 56.1] [Reference Citation Analysis (0)] |
| 89. | Zeng G, Li J, Wang Y, Su J, Lu Z, Zhang F, Ding W. Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway. Environ Pollut. 2024;345:123473. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 105] [Reference Citation Analysis (0)] |
| 90. | Li L, Lv X, He J, Zhang L, Li B, Zhang X, Liu S, Zhang Y. Chronic exposure to polystyrene nanoplastics induces intestinal mechanical and immune barrier dysfunction in mice. Ecotoxicol Environ Saf. 2024;269:115749. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 53] [Reference Citation Analysis (0)] |
| 91. | Neurath MF. Strategies for targeting cytokines in inflammatory bowel disease. Nat Rev Immunol. 2024;24:559-576. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 277] [Cited by in RCA: 279] [Article Influence: 139.5] [Reference Citation Analysis (3)] |
| 92. | Choy MC, Visvanathan K, De Cruz P. An Overview of the Innate and Adaptive Immune System in Inflammatory Bowel Disease. Inflamm Bowel Dis. 2017;23:2-13. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 130] [Cited by in RCA: 116] [Article Influence: 12.9] [Reference Citation Analysis (3)] |
| 93. | Guan Q. A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease. J Immunol Res. 2019;2019:7247238. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 866] [Cited by in RCA: 770] [Article Influence: 110.0] [Reference Citation Analysis (6)] |
| 94. | Zhuang J, Chen Q, Xu L, Chen X. Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice. Ecotoxicol Environ Saf. 2023;267:115637. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 28] [Reference Citation Analysis (0)] |
| 95. | Ma J, Wan Y, Song L, Wang L, Wang H, Li Y, Huang D. Polystyrene nanobeads exacerbate chronic colitis in mice involving in oxidative stress and hepatic lipid metabolism. Part Fibre Toxicol. 2023;20:49. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 6] [Cited by in RCA: 27] [Article Influence: 9.0] [Reference Citation Analysis (0)] |
| 96. | Li B, Ding Y, Cheng X, Sheng D, Xu Z, Rong Q, Wu Y, Zhao H, Ji X, Zhang Y. Polyethylene microplastics affect the distribution of gut microbiota and inflammation development in mice. Chemosphere. 2020;244:125492. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 208] [Cited by in RCA: 467] [Article Influence: 77.8] [Reference Citation Analysis (3)] |
| 97. | Hasegawa Y, Okamura T, Ono Y, Ichikawa T, Saijo Y, Nakanishi N, Sasano R, Hamaguchi M, Takano H, Fukui M. Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice. Front Immunol. 2024;15:1407936. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 29] [Cited by in RCA: 16] [Article Influence: 8.0] [Reference Citation Analysis (0)] |
| 98. | Chen X, Xuan Y, Chen Y, Yang F, Zhu M, Xu J, Chen J. Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice. Sci Total Environ. 2024;935:173458. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 77] [Reference Citation Analysis (0)] |
| 99. | Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther. 2017;2:17023-17023. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 7358] [Cited by in RCA: 6582] [Article Influence: 731.3] [Reference Citation Analysis (5)] |
| 100. | Zhen Y, Zhang H. NLRP3 Inflammasome and Inflammatory Bowel Disease. Front Immunol. 2019;10:276. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 574] [Cited by in RCA: 552] [Article Influence: 78.9] [Reference Citation Analysis (5)] |
| 101. | Djouina M, Pichavant M, Waxin C, Dehaut A, Loison S, Driencourt E, Deborgher A, Balesdent C, Launay D, Dubuquoy L, Duflos G, Body-Malapel M. Ingestion of a human-relevant mixture of environmentally sourced microplastics promotes inflammation and tumorigenesis in the mouse colon. Environ Pollut. 2026;395:127794. [RCA] [PubMed] [DOI] [Full Text] [Reference Citation Analysis (0)] |
| 102. | Liu S, Li H, Wang J, Wu B, Guo X. Polystyrene microplastics aggravate inflammatory damage in mice with intestinal immune imbalance. Sci Total Environ. 2022;833:155198. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 15] [Cited by in RCA: 110] [Article Influence: 27.5] [Reference Citation Analysis (0)] |
| 103. | Xu D, Ma Y, Peng C, Gan Y, Wang Y, Chen Z, Han X, Chen Y. Differently surface-labeled polystyrene nanoplastics at an environmentally relevant concentration induced Crohn's ileitis-like features via triggering intestinal epithelial cell necroptosis. Environ Int. 2023;176:107968. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 66] [Cited by in RCA: 67] [Article Influence: 22.3] [Reference Citation Analysis (1)] |
| 104. | Lehner R, Wohlleben W, Septiadi D, Landsiedel R, Petri-Fink A, Rothen-Rutishauser B. A novel 3D intestine barrier model to study the immune response upon exposure to microplastics. Arch Toxicol. 2020;94:2463-2479. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 31] [Cited by in RCA: 76] [Article Influence: 12.7] [Reference Citation Analysis (0)] |
| 105. | Busch M, Bredeck G, Kämpfer AAM, Schins RPF. Investigations of acute effects of polystyrene and polyvinyl chloride micro- and nanoplastics in an advanced in vitro triple culture model of the healthy and inflamed intestine. Environ Res. 2021;193:110536. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 48] [Cited by in RCA: 108] [Article Influence: 21.6] [Reference Citation Analysis (0)] |
| 106. | Chen Y, Williams AM, Gordon EB, Rudolph SE, Longo BN, Li G, Kaplan DL. Biological effects of polystyrene micro- and nano-plastics on human intestinal organoid-derived epithelial tissue models without and with M cells. Nanomedicine. 2023;50:102680. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 9] [Cited by in RCA: 29] [Article Influence: 9.7] [Reference Citation Analysis (0)] |
| 107. | Yan Z, Liu Y, Zhang T, Zhang F, Ren H, Zhang Y. Analysis of Microplastics in Human Feces Reveals a Correlation between Fecal Microplastics and Inflammatory Bowel Disease Status. Environ Sci Technol. 2022;56:414-421. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 721] [Cited by in RCA: 484] [Article Influence: 121.0] [Reference Citation Analysis (1)] |
| 108. | Lykkemark J, Picker M, Kim T, Nguyen I, Weinstein K, Chen R, Simon-sánchez L, Lordachescu L, Torres J, Stone J, Bianco A, Shaw L, Tavella N, Jess T, Allin K, Peter I, Colombel JF, Vianello A, Vollertsen J, Agrawal M. P1239 Microplastics are associated with biomarker of intestinal inflammation in a pilot analysis of the PLANET Study. J Crohns Colitis. 2025;19:i2242-i2243. [DOI] [Full Text] |
| 109. | Huang L, Zheng W, Wang Y, Feng ST, Li X. DOP020 Serum micro- and nano-plastic burden as a risk marker for Crohn’s disease progression: a multi-omics discovery of gut microbiome–metabolite perturbations. J Crohns Colitis. 2026;20:jjaf231.057. [DOI] [Full Text] |
| 110. | Wu F, Wu F, Liu X, Xie W, Liang Y, Ye Y, Xiao X, Sun K, Bai L, Liu S, Liu Z. Microplastic accumulation in fibrotic intestinal tissue and mesenteric adipose tissue in Crohn's disease patients. Environ Res. 2025;271:121077. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 9] [Reference Citation Analysis (0)] |
| 111. | Marszk D. Microplastic Analysis in Pediatric Inflammatory Bowel Disease. [accessed 2026 Mar 18]. In: ClinicalTrials.gov [Internet]. Bethesda (MD): United States National Library of Medicine. Available from: https://clinicaltrials.gov/study/NCT07141238. |
| 112. | Sileri P. The Presence of Microplastics and Nanoplastics in the Humans Ileum, Colon, and Rectum and Their Relation With Inflammatory Bowel Disease. [accessed 2026 Mar 18]. In: ClinicalTrials.gov [Internet]. Bethesda (MD): United States National Library of Medicine. Available from: https://clinicaltrials.gov/study/NCT06525558?cond=NCT06525558&viewType=Card&rank=1. |
| 113. | Picker M. Pregnant Women With and Without Crohns Disease to Explore the Role of Plastics and Toxins in Intestinal Inflammation. [accessed 2026 Mar 18]. In: ClinicalTrials.gov [Internet]. Bethesda (MD): United States National Library of Medicine. Available from: https://clinicaltrials.gov/study/NCT06001450?cond=NCT06001450&viewType=Card&rank=1&tab=researcher. |
| 114. | Agrawal M, Vianello A, Picker M, Simon-Sánchez L, Chen R, Estevinho MM, Weinstein K, Lykkemark J, Jess T, Peter I, Colombel JF, Allin KH, Vollertsen J. Micro- and nano-plastics, intestinal inflammation, and inflammatory bowel disease: A review of the literature. Sci Total Environ. 2024;953:176228. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 20] [Cited by in RCA: 26] [Article Influence: 13.0] [Reference Citation Analysis (0)] |
| 115. | Kaplan GG. The global burden of IBD: from 2015 to 2025. Nat Rev Gastroenterol Hepatol. 2015;12:720-727. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 2331] [Cited by in RCA: 2129] [Article Influence: 193.5] [Reference Citation Analysis (8)] |
| 116. | Hracs L, Windsor JW, Gorospe J, Cummings M, Coward S, Buie MJ, Quan J, Goddard Q, Caplan L, Markovinović A, Williamson T, Abbey Y, Abdullah M, Abreu MT, Ahuja V, Raja Ali RA, Altuwaijri M, Balderramo D, Banerjee R, Benchimol EI, Bernstein CN, Brunet-Mas E, Burisch J, Chong VH, Dotan I, Dutta U, El Ouali S, Forbes A, Forss A, Gearry R, Dao VH, Hartono JL, Hilmi I, Hodges P, Jones GR, Juliao-Baños F, Kaibullayeva J, Kelly P, Kobayashi T, Kotze PG, Lakatos PL, Lees CW, Limsrivilai J, Lo B, Loftus EV Jr, Ludvigsson JF, Mak JWY, Miao Y, Ng KK, Okabayashi S, Olén O, Panaccione R, Paudel MS, Quaresma AB, Rubin DT, Simadibrata M, Sun Y, Suzuki H, Toro M, Turner D, Iade B, Wei SC, Yamamoto-Furusho JK, Yang SK, Ng SC, Kaplan GG; Global IBD Visualization of Epidemiology Studies in the 21st Century (GIVES-21) Research Group. Global evolution of inflammatory bowel disease across epidemiologic stages. Nature. 2025;642:458-466. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 216] [Cited by in RCA: 297] [Article Influence: 297.0] [Reference Citation Analysis (2)] |
| 117. | Ananthakrishnan AN, Kaplan GG, Bernstein CN, Burke KE, Lochhead PJ, Sasson AN, Agrawal M, Tiong JHT, Steinberg J, Kruis W, Steinwurz F, Ahuja V, Ng SC, Rubin DT, Colombel JF, Gearry R; International Organization for Study of Inflammatory Bowel Diseases. Lifestyle, behaviour, and environmental modification for the management of patients with inflammatory bowel diseases: an International Organization for Study of Inflammatory Bowel Diseases consensus. Lancet Gastroenterol Hepatol. 2022;7:666-678. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 123] [Cited by in RCA: 118] [Article Influence: 29.5] [Reference Citation Analysis (2)] |
| 118. | Sun Y, Yuan S, Chen X, Sun J, Kalla R, Yu L, Wang L, Zhou X, Kong X, Hesketh T, Ho GT, Ding K, Dunlop M, Larsson SC, Satsangi J, Chen J, Wang X, Li X, Theodoratou E, Giovannucci EL. The Contribution of Genetic Risk and Lifestyle Factors in the Development of Adult-Onset Inflammatory Bowel Disease: A Prospective Cohort Study. Am J Gastroenterol. 2023;118:511-522. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 93] [Cited by in RCA: 98] [Article Influence: 32.7] [Reference Citation Analysis (0)] |
| 119. | Ananthakrishnan AN, Gerasimidis K, Ho SM, Mayer E, Pollock J, Soni S, Wu GD, Benyacoub J, Ali B, Favreau A, Smith DE, Oh JE, Heller C, Hurtado-Lorenzo A, Moss A, Croitoru K. Challenges in IBD Research 2024: Environmental Triggers. Inflamm Bowel Dis. 2024;30:S19-S29. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 19] [Cited by in RCA: 18] [Article Influence: 9.0] [Reference Citation Analysis (1)] |
| 120. | Deng BD, Sinha SR, Lear G, Tropini C. Microplastics and nanoplastics in the human gut: from signals to standards. Nat Rev Gastroenterol Hepatol. 2026;23:374-375. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 1] [Reference Citation Analysis (0)] |
| 121. | Munno K, Lusher AL, Minor EC, Gray A, Ho K, Hankett J, T Lee CF, Primpke S, McNeish RE, Wong CS, Rochman C. Patterns of microparticles in blank samples: A study to inform best practices for microplastic analysis. Chemosphere. 2023;333:138883. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 13] [Cited by in RCA: 53] [Article Influence: 17.7] [Reference Citation Analysis (0)] |
| 122. | Di Fiore C, Ishikawa Y, Wright SL. A review on methods for extracting and quantifying microplastic in biological tissues. J Hazard Mater. 2024;464:132991. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 37] [Reference Citation Analysis (0)] |
| 123. | Morgan SE, Romanick SS, DeLouise L, McGrath J, Elder A. Understanding Human Health Impacts Following Microplastic Exposure Necessitates Standardized Protocols. Curr Protoc. 2024;4:e1104. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 5] [Reference Citation Analysis (0)] |
| 124. | Primpke S, Christiansen SH, Cowger W, De Frond H, Deshpande A, Fischer M, Holland EB, Meyns M, O'Donnell BA, Ossmann BE, Pittroff M, Sarau G, Scholz-Böttcher BM, Wiggin KJ. Critical Assessment of Analytical Methods for the Harmonized and Cost-Efficient Analysis of Microplastics. Appl Spectrosc. 2020;74:1012-1047. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 167] [Cited by in RCA: 221] [Article Influence: 36.8] [Reference Citation Analysis (0)] |
| 125. | Erni-Cassola G, Gibson MI, Thompson RC, Christie-Oleza JA. Lost, but Found with Nile Red: A Novel Method for Detecting and Quantifying Small Microplastics (1 mm to 20 μm) in Environmental Samples. Environ Sci Technol. 2017;51:13641-13648. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 411] [Cited by in RCA: 459] [Article Influence: 51.0] [Reference Citation Analysis (0)] |
| 126. | Xu JL, Thomas KV, Luo Z, Gowen AA. FTIR and Raman imaging for microplastics analysis: State of the art, challenges and prospects. TrAC Trends Anal Chem. 2019;119:115629. [RCA] [DOI] [Full Text] [Cited by in Crossref: 146] [Cited by in RCA: 301] [Article Influence: 43.0] [Reference Citation Analysis (0)] |
| 127. | Rauert C, Charlton N, Bagley A, Dunlop SA, Symeonides C, Thomas KV. Assessing the Efficacy of Pyrolysis-Gas Chromatography-Mass Spectrometry for Nanoplastic and Microplastic Analysis in Human Blood. Environ Sci Technol. 2025;59:1984-1994. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 80] [Article Influence: 80.0] [Reference Citation Analysis (0)] |
| 128. | Cowger W, Booth AM, Hamilton BM, Thaysen C, Primpke S, Munno K, Lusher AL, Dehaut A, Vaz VP, Liboiron M, Devriese LI, Hermabessiere L, Rochman C, Athey SN, Lynch JM, De Frond H, Gray A, Jones OAH, Brander S, Steele C, Moore S, Sanchez A, Nel H. Reporting Guidelines to Increase the Reproducibility and Comparability of Research on Microplastics. Appl Spectrosc. 2020;74:1066-1077. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 403] [Cited by in RCA: 213] [Article Influence: 35.5] [Reference Citation Analysis (0)] |
| 129. | Brander SM, Renick VC, Foley MM, Steele C, Woo M, Lusher A, Carr S, Helm P, Box C, Cherniak S, Andrews RC, Rochman CM. Sampling and Quality Assurance and Quality Control: A Guide for Scientists Investigating the Occurrence of Microplastics Across Matrices. Appl Spectrosc. 2020;74:1099-1125. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 127] [Cited by in RCA: 168] [Article Influence: 28.0] [Reference Citation Analysis (0)] |
| 130. | Schymanski D, Oßmann BE, Benismail N, Boukerma K, Dallmann G, von der Esch E, Fischer D, Fischer F, Gilliland D, Glas K, Hofmann T, Käppler A, Lacorte S, Marco J, Rakwe ME, Weisser J, Witzig C, Zumbülte N, Ivleva NP. Analysis of microplastics in drinking water and other clean water samples with micro-Raman and micro-infrared spectroscopy: minimum requirements and best practice guidelines. Anal Bioanal Chem. 2021;413:5969-5994. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 19] [Cited by in RCA: 111] [Article Influence: 22.2] [Reference Citation Analysis (0)] |
| 131. | Gouin T, Ellis-Hutchings R, Pemberton M, Wilhelmus B. Addressing the relevance of polystyrene nano- and microplastic particles used to support exposure, toxicity and risk assessment: implications and recommendations. Part Fibre Toxicol. 2024;21:39. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 49] [Cited by in RCA: 41] [Article Influence: 20.5] [Reference Citation Analysis (0)] |
| 132. | Qiao R, Deng Y, Zhang S, Wolosker MB, Zhu Q, Ren H, Zhang Y. Accumulation of different shapes of microplastics initiates intestinal injury and gut microbiota dysbiosis in the gut of zebrafish. Chemosphere. 2019;236:124334. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 339] [Cited by in RCA: 619] [Article Influence: 88.4] [Reference Citation Analysis (20)] |
| 133. | Whelan K, Bancil AS, Lindsay JO, Chassaing B. Ultra-processed foods and food additives in gut health and disease. Nat Rev Gastroenterol Hepatol. 2024;21:406-427. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 210] [Cited by in RCA: 174] [Article Influence: 87.0] [Reference Citation Analysis (2)] |
| 134. | Zielli SO, Pascali JP, Mazzotti A, Fais P, Fini M, Faldini C, Pelotti S. Microplastics and Nanoplastics in human tissues: Systematic review of evidence, analytical protocols, and methodological challenges. Talanta Open. 2026;13:100615. [DOI] [Full Text] |
| 135. | Das M, Calderon L, Singh D, Majumder S, Bazina L, Vaze N, Trivanovic U, DeLoid G, Zuverza-Mena N, Kaur M, Konkol J, Tittikpina NK, Tsilomelekis G, Sadik O, White JC, Demokritou P. Development and characterization of reference environmentally relevant micro-nano-plastics for risk assessment studies. NanoImpact. 2025;38:100567. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 8] [Cited by in RCA: 11] [Article Influence: 11.0] [Reference Citation Analysis (0)] |
| 136. | Wang Y, Zhu Y, Capapelo JJ, Wu Y, Shi L, Yang Y, Chen P, He S, Li J. Exploring alternatives for detecting microplastics in the human body: questionnaire survey. Sci Rep. 2024;14:23458. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 3] [Reference Citation Analysis (0)] |