Microplastics and inflammation: what the data shows

Almost every microplastic toxicology paper reports inflammation. That is not, on its own, informative. Inflammation is what mammalian tissue does when it encounters a foreign particle at high dose, whether that particle is silica, titanium dioxide, urate crystals, or polystyrene. The scientific question is not whether microplastics can trigger inflammation. It is which of the inflammatory signals seen in cells and animals correspond to real disease processes in humans, at exposures humans actually receive [1-2]. That distinction (signal vs. relevant signal) is where the literature is most useful and where it is easiest to misread.

The evidence base has three tiers. In vitro exposures at high concentrations reliably produce oxidative stress, cytokine release, macrophage activation, and inflammasome-mediated cell death [3-6]. Rodent studies at doses well above modelled human intake reproduce the same signatures in gut, liver, lung, brain, kidney, heart, spleen, and reproductive tissue [7-8]. Human evidence is sparser but is finally moving from tissue detection to physiological association: fecal microplastic burden correlates with inflammatory bowel disease severity [9]; particles have been recovered from atherosclerotic carotid plaque and linked to elevated cardiovascular event risk in acute coronary syndrome cohorts [10-11]. Each tier answers a different question. Read together, they describe an exposure that plausibly contributes to inflammatory disease at the population level, while leaving the specific dose-response for most endpoints unresolved [12-16].

Why this matters

Chronic low-grade inflammation is a shared feature of the diseases that now dominate mortality in high-income countries — cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease, inflammatory bowel disease, neurodegeneration, several cancers [16-17]. The clinical importance of inflammation is not that it is loud; it is that it is persistent. A modest but sustained elevation in inflammatory tone over decades reshapes the trajectory of vascular, metabolic, and neural aging. That is the register in which chronic environmental exposures matter, and it is the register in which the microplastic literature must be read.

Microplastics are relevant to that register for two reasons. First, exposure is chronic and effectively universal (e.g., through diet, drinking water, indoor air, and household dust) with no lower bound in most human tissues that have been carefully examined [13-15]. Second, the mechanisms by which particles drive inflammation are not novel: reactive oxygen species, pattern-recognition receptor activation, phagocyte engagement, inflammasome assembly, cytokine release [1,4,18]. These pathways are shared with silica, asbestos, urate, cholesterol crystals, and other particulates whose long-term inflammatory effects are well characterised. The question is whether microplastics at real-world doses produce a comparable trajectory. The current answer is that mechanistic plausibility is high, animal evidence is consistent, and human confirmation is early but no longer absent.

Background: what "inflammation" means in the microplastic literature

Inflammation is a coordinated tissue response, not a single molecule. In experimental studies of microplastic exposure it usually refers to some combination of the following: elevated reactive oxygen species and lipid peroxidation products (MDA, 8-OHdG); activation of transcription factors NF-κB, AP-1, and Nrf2; upregulation of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-18; recruitment or activation of macrophages, neutrophils, and dendritic cells; assembly of the NLRP3 inflammasome and downstream caspase-1 activation; expression of tight-junction and mucin genes at epithelial barriers; and, at the tissue level, histological infiltrates, edema, and fibrotic remodelling [3,5,17-20].

None of these markers is specific to microplastics. All of them can be evoked by other particulates and by biological insults that have nothing to do with plastic. What the microplastic literature has established is that these responses can be elicited by micro- and nanoplastic exposure across cell types, animal models, and exposure routes, and that the pattern of activation is consistent enough across independent laboratories to constitute a coherent mechanistic case [18,21-23].

Two design distinctions govern how to read that case. The first is size. Below roughly one micrometre, and especially below a few hundred nanometres, particles cross biological membranes, enter cells, and reach compartments that larger microplastics do not. Nanoplastic inflammation is therefore usually a cell-interior story (mitochondria, ER, autophagy machinery). Microplastic inflammation is usually a barrier and phagocyte story (epithelium, macrophages, tissue infiltrates) [23]. The second is polymer and surface chemistry. Pristine polystyrene beads dominate the experimental literature because they are commercially available and easy to characterise. Environmental exposures are heterogeneous — polyethylene, polypropylene, PET, PVC, and polystyrene fragments with weathered surfaces and adsorbed chemistry. The two need not produce identical inflammatory profiles, and comparisons across polymer types are still fragmentary [15,21].

Oxidative stress: the upstream trigger

Across cell type, tissue, and species, the earliest reproducible response to micro- and nanoplastic exposure is oxidative stress — reactive oxygen species (ROS) generation exceeding what antioxidant defences can neutralise [1,18,24]. It is the input that most of the downstream inflammatory signalling depends on.

In zebrafish liver, polystyrene microplastic exposure at environmentally suggestive concentrations produces measurable ROS accumulation, elevated MDA, and depleted glutathione within days [25]. In mice, tissue accumulation of polystyrene beads is accompanied by biomarker responses (SOD, CAT, GPx) consistent with sustained oxidative demand across multiple organs [26]. In human hepatocyte and HepG2 systems, polystyrene micro- and nanoplastics drive ROS-dependent hepatocyte apoptosis, calcium overload, glycolytic dysregulation, mitochondrial fragmentation, and mitophagy [27-31]. The dose-response is monotonic in most experimental systems and steeper for smaller and more charge-modified particles.

The mechanistic origin of the ROS signal is at least three-fold. First, direct particle-membrane interaction perturbs mitochondrial electron transport, elevating superoxide leak from complexes I and III [27,29-30]. Second, phagocytic engagement of larger microplastics activates NADPH oxidase in macrophages, producing an intended respiratory burst that becomes injurious when the particle is not degradable [32]. Third, cellular uptake of nanoplastics loads the endolysosomal system with material it cannot clear, triggering lysosomal membrane permeabilisation and secondary ROS from cathepsins and Fenton-active iron [32-34]. Environmental weathering (for example UV oxidation, mechanical abrasion) increases surface oxygen chemistry and consistently raises the ROS response per particle in cell-based assays [34-35].

A meta-analysis across bivalve studies concluded that microplastic exposure meets the operational definition of an oxidative stressor: SOD, CAT, and GPx activities and MDA levels move together in the predicted direction across independent studies, with effect sizes that scale with dose and inversely with particle size [24]. Reviews focused on mammals reach the same qualitative conclusion [18].

ROS matters here because it is upstream of nearly everything else. NF-κB activation, NLRP3 assembly, ferroptosis, autophagic cell death, and endothelial dysfunction all depend on redox state [36-39]. That gives oxidative stress two properties: it is the most reproducible finding in the microplastic literature, and it is the least specific. A response present in almost every study is not, on its own, diagnostic of anything. But its consistency is what lets the downstream mechanisms carry weight, because those mechanisms have a plausible upstream trigger that is documented across nearly every experimental system.

Pattern-recognition signalling: NF-κB and the toll-like receptors

Once ROS has been generated, or once a particle has been recognised by innate immune receptors, the transcriptional programme most consistently activated by microplastic exposure is the NF-κB pathway. Toll-like receptors (TLRs), particularly TLR2 and TLR4, sit upstream. NF-κB sits at the centre. The output is the coordinated transcription of pro-inflammatory cytokines, adhesion molecules, and NLRP3 inflammasome components [40-42].

In mice given oral polystyrene or polyethylene microplastics, the sequence documented across independent laboratories is: gut microbiota dysbiosis → increased circulating LPS → TLR2/TLR4 activation in liver and gut → NF-κB nuclear translocation → NLRP3 upregulation → IL-1β and IL-18 secretion → tissue injury [40-41,43]. Inhalation exposure produces the same pathway in lung and, via systemic spillover, in multiple organs [42,44]. Chicken kidney, thymus, and cardiac tissue show TLR/NF-κB-driven inflammation with associated necroptosis or pyroptosis [45-47]. In endothelial and cardiomyocyte systems, NF-κB activation is accompanied by metabolic reprogramming and MAPK signalling [48]. In brain, chronic polystyrene exposure activates a PERK-NF-κB pathway that produces anxiety-like behaviour in mice [49]. The convergent picture is that once inflammation has been initiated, NF-κB is the transcriptional hub through which the signal propagates.

Two properties of this signalling deserve emphasis. The pathway is engaged both by direct particle recognition (TLR-mediated) and by damage-associated signals downstream of ROS. And the same NF-κB module is engaged in cancer, cardiovascular disease, and inflammatory bowel disease, so it is not novel biology — it is a known inflammatory circuit that microplastics can trip [50].

Cytokines: what actually gets released

The cytokine output measured across microplastic studies is dominated by TNF-α, IL-1β, IL-6, IL-8, and IL-18 (the classical NF-κB and inflammasome-dependent pro-inflammatory panel) with variable induction of IL-4, IL-10, and IFN-γ depending on cell type, particle chemistry, and duration [51-53].

Primary human monocytes and monocyte-derived dendritic cells respond to polydisperse nanoplastics with dose-dependent secretion of IL-6, IL-8, and TNF-α at concentrations that overlap with modelled tissue exposures [51]. Human macrophages, dendritic cells, and T cells all show measurable inflammatory response to micro- and nanoplastics of varied polymer type and size, with polystyrene and PET producing the largest cytokine shifts and negatively charged particles more inflammatory than positively charged in most assays [52]. Human and murine intestinal epithelial lines exposed to polystyrene microplastics upregulate IL-6, IL-8, and CXCL10 while inducing epithelial apoptosis at higher concentrations [53]. Human bronchial and alveolar epithelial cells respond to polystyrene microplastics with elevated IL-6 and IL-8 that scale with particle size and dose, and asthmatic bronchial epithelium responds more strongly than healthy epithelium [54-55].

Systemic effects have been documented in mice. Polystyrene micro- and nanoplastics produce hematopoietic damage tied to a gut-microbiota-metabolite-cytokine axis with elevated pro-inflammatory cytokines in peripheral blood [56]. Human peripheral blood lymphocytes show cytotoxic and inflammatory responses to polyethylene microplastics in ex vivo exposure [57]. Kidney tubular epithelial cell lines respond to polystyrene and polyethylene microplastics with inflammatory and oxidative marker dysregulation [58].

Two limits should be kept in view. First, cytokine responses in vitro often use particle concentrations several orders of magnitude above modelled human tissue exposures, so the size of the response should not be read as a size estimate of the effect in vivo. Second, cytokine profiles are highly context-dependent; the same particle can be pro-inflammatory in one tissue and immunosuppressive in another, particularly at doses that overwhelm phagocyte function [52,59]. The reproducible signal is directional (pro-inflammatory) more than it is quantitative.

Macrophages and the phagocyte response

Macrophages are the cellular interface through which most microplastic contact with tissue is mediated. They ingest particles, attempt to digest them, fail (plastics are not enzymatically degradable), and remain loaded with the particle. That "frustrated phagocytosis" is the mechanism through which durable inflammatory activation occurs; familiar from silica, asbestos, and other biopersistent particulates [60-61].

The direct in vitro data are consistent. Human macrophages exposed to micro- and nanoplastics ingest particles and show altered polarisation, cytokine secretion, and lysosomal function, with responses that depend on polymer identity and particle size [60]. THP-1-derived macrophages exposed to polystyrene microplastics maintain viability at low doses but shift toward pro-inflammatory M1-like activation with elevated TNF-α and IL-6 [61]. Microplastics released from food containers suppress lysosomal activity in mouse macrophages, blunting the antimicrobial response to a subsequent bacterial challenge [59]. Polystyrene nanoplastics dysregulate lipid metabolism in murine and human macrophages, promoting a foamy phenotype relevant to atherosclerotic biology [62-63]. Oxidised particle surfaces amplify these effects: oxidised nano- and microplastics produce larger cytokine and ROS responses in human monocytes and neutrophils than pristine equivalents [35].

Polarisation is dose- and size-dependent. Smaller polystyrene nanoplastics push macrophages toward M1 more effectively than larger ones, and the polarisation is accompanied by an energy-metabolism shift toward glycolysis that mirrors classical inflammatory activation [64-65].

Size also governs internalisation and downstream systemic transport in human macrophage systems, with smaller particles more readily distributed beyond the site of initial phagocytosis [66]. In mouse liver, polystyrene microplastics elicit macrophage extracellular trap formation, a chromatin-based amplification of local inflammation analogous to NETs in neutrophils [67]. Nanoplastics can trigger neutrophil extracellular traps directly in mouse neutrophils [68]. In human peripheral blood exposed ex vivo to nanoplastics, single-cell mass cytometry shows internalisation across myeloid populations and phenotypic shifts consistent with immune activation, with detectable effects at concentrations lower than most in vitro assays report [69].

The macrophage story extends beyond local tissue effects. In mice, oral nanoplastic exposure activates intestinal macrophage IL-1 signalling that alters brain function through a gut-immune-brain circuit [70]. Microglia, the brain's resident macrophages, internalise polystyrene microplastics and undergo altered immune activation with associated neuronal apoptosis [71]. Neither of these findings is confined to the local tissue where the particle was encountered.

The NLRP3 inflammasome: pyroptosis and the signature of durable inflammation

The NLRP3 inflammasome is a multiprotein complex that assembles in response to a two-hit signal: an NF-κB-dependent priming step, and a second activation step triggered by cellular stress. When assembled, NLRP3 activates caspase-1, which cleaves pro-IL-1β and pro-IL-18 to their mature forms and initiates gasdermin D-mediated pyroptotic cell death [72]. The inflammasome is the mechanism through which particulate materials (silica, asbestos, cholesterol crystals, urate) produce durable, IL-1β-driven inflammation. That microplastics engage the same machinery is now well established.

A systematic screen of a large panel of micro- and nanoplastics in THP-1 cells found that NLRP3 activation is a common but not universal response, with signal strength depending on particle size, polymer identity, and surface chemistry [73]. Independent studies have documented NLRP3-caspase-1-driven pyroptosis in ovarian granulosa cells [74], cardiomyocytes and chicken heart [75-76], duodenal epithelium co-stimulated with LPS [77], intestinal epithelium of mice exposed to polyethylene microplastics [78], and airway epithelium of infants exposed to microplastic shed from baby bottles [79]. In lung tissue, endoplasmic reticulum stress is now proposed as a novel upstream trigger for NLRP3 activation by polystyrene microplastics; an alternative to the classical ROS or lysosomal-disruption inputs [80]. In BV2 microglia, nanoplastic-driven inflammation converges with ferroptosis through the JNK/HO-1/FTH1 axis [81]. Co-exposure with DEHP produces synergistic activation of the NF-κB/NLRP3 axis in liver, consistent with the particle-as-delivery-vehicle mechanism [82].

The strength of the inflammasome case rests on three properties. NLRP3 is a canonical particulate-inflammation sensor; the responses to microplastic exposure share the signature of other particulate exposures whose long-term disease consequences are well described. The activation is reproducible across cell type, tissue, and species. And it produces IL-1β and IL-18; cytokines with defined roles in atherosclerosis, type 2 diabetes, inflammatory bowel disease, and neurodegeneration. If a single mechanism explains how a low-dose environmental particulate could contribute to the chronic inflammatory landscape of modern disease, NLRP3 is a strong candidate [72].

The limits are also worth naming. Most NLRP3 studies use polystyrene beads. Whether environmental heterogeneous plastics activate the inflammasome as efficiently, and at what tissue concentrations, remains under characterisation [73]. The inflammasome literature is also biased toward acute high-dose exposures; the chronic low-dose kinetics that would be required to translate to human disease are less well studied.

Neuroinflammation and microglial activation

Microglia are the resident macrophage population of the central nervous system. Their activation by microplastics is the neurological analogue of the macrophage response in periphery, and it is now supported by direct in vivo and in vitro evidence.

In mice, oral polystyrene nanoplastic exposure produces particle accumulation in the brain, blood-brain barrier disruption, microglial activation, and neuronal injury [83]. Independent work with polystyrene nanoplastics has confirmed microglial activation with associated memory and behavioural deficits [84]. In an Alzheimer's disease mouse model, polystyrene microplastic exposure accelerated cognitive decline with a signature of microglia-mediated neuroinflammation [85]. Primary cell cultures from mouse brain (neurons, astrocytes, microglia) show dose-dependent cytotoxicity and inflammatory activation on nanoplastic exposure [86]. Human iPSC-derived neurons exposed to environmentally relevant concentrations of micro- and nanoplastics of varied shape and polymer identity undergo ROS-dependent degeneration [87], and human neural stem cells show molecular signatures of nanoplastic exposure at the transcriptomic and pathway level [88]. In mice, oral polystyrene microplastic exposure impaired hippocampus-dependent learning and memory in association with inflammatory and oxidative markers in hippocampal tissue [89]. Reviews consolidate a coherent picture across models of neurodegenerative risk from micro- and nanoplastic exposure, though most doses used are experimental rather than modelled human [90-91].

The gut-brain axis provides a mechanistic bridge that does not require particles to cross the blood-brain barrier. Oral nanoplastic exposure in mice induces intestinal macrophage IL-1 signalling that alters brain function via peripheral immune-to-brain communication [70]. Oxidised polyethylene microplastics produce neurotoxicity in mice through gut-brain axis disruption [92]. Polystyrene nanoplastics have been shown to worsen Parkinson's-like pathology in a mouse model via a gut-to-brain propagation pathway [93], and single-nucleus brain transcriptomics after chronic nanoplastic exposure show Parkinson's disease-like transcriptional signatures [94]. The gut-brain vector is important because it does not require the particle itself to reach the brain; a peripheral inflammatory signal is sufficient to produce measurable central effects.

The BV2 microglia data extend this to a specific molecular pathway: nanoplastic exposure activates JNK/HO-1/FTH1 signalling that couples inflammation to ferroptosis, providing a mechanism by which chronic exposure could produce cumulative neuronal loss [81]. Interpretation caveat: most of this is animal or cell evidence. Human confirmation is limited to biomonitoring detections of microplastic in olfactory bulb and other brain regions, and to post-mortem tissue work suggesting that blood-brain barrier damage accelerates accumulation of micro- and nanoplastics in the human central nervous system [95], without linked functional measurements.

Gut inflammation, barrier function, and colitis

The gastrointestinal tract is the tissue with the highest cumulative microplastic exposure. Across zebrafish, mice, and rats, oral exposure to polystyrene, polyethylene, or polypropylene microplastics reproducibly produces microbiota dysbiosis, elevated intestinal inflammatory cytokines, mucin gene dysregulation, tight-junction disruption, and histological injury [97-103]. In mouse models of colitis (DSS-induced, TNBS-induced), microplastic co-exposure exacerbates disease severity, extends histological damage, and prolongs the inflammatory response [104-107]. Polystyrene nanoplastics with different surface functionalisations at environmentally relevant concentrations induce Crohn's ileitis-like features in mice [108]. Polystyrene nanoplastics accelerate the development of colitis-associated colorectal cancer through combined lipid metabolism disruption and DNA damage [109]. Chronic nanoplastic exposure disrupts both the mechanical (tight junction) and immune (Paneth cell, IgA) arms of intestinal barrier function [110].The mechanistic picture is layered. The particle itself contributes to oxidative and inflammatory injury in epithelial and immune cells [53,78]. Microbiota disruption — loss of short-chain fatty acid producers, expansion of pro-inflammatory taxa, elevated Enterobacteriaceae — is a consistent feature that amplifies the primary particle effect [98, 99, 101]. Combined polystyrene micro- and nanoplastic co-exposure produces greater barrier dysfunction than either size alone, via ROS-mediated epithelial apoptosis [111]. And co-exposure with LPS, high-fat diet, or other environmental stressors amplifies the inflammatory response beyond additive expectation [77, 106]. Aged polystyrene microplastics carrying adsorbed benzo[a]pyrene produce colonic barrier injury in the human Caco-2 model via oxidative-stress-mediated Notch signalling, illustrating how realistic weathered particles combine with adsorbed environmental chemistry to produce larger effects than either component alone [112].Human relevance for this compartment is stronger than for most others. The human feces study by Yan and colleagues — the first population-level correlation between microplastic burden and inflammatory disease status — found that fecal microplastic concentrations were significantly higher in patients with active IBD than in healthy controls, and that the concentration correlated with disease severity [9]. This does not establish causation, but it is a first alignment between the animal mechanistic literature and human clinical inflammation.Systemic low-grade inflammation and metabolic diseaseThe low-grade inflammation hypothesis for microplastics holds that chronic exposure at ambient doses produces a modest but persistent elevation in systemic inflammatory tone that contributes to the metabolic diseases already accelerating in prevalence — obesity, insulin resistance, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and cardiovascular disease [16-17]. The evidence for this hypothesis, as of 2025, is convergent in animals and mechanistically plausible in humans.In mice, polystyrene microplastic exposure exacerbates high-fat-diet-induced obesity, systemic inflammation, and metabolic disturbance beyond what the diet produces alone [113-115]. Polystyrene microplastic exposure produces insulin resistance in mice through a mechanism combining gut microbiota dysbiosis and pro-inflammatory signalling in liver and adipose tissue [116-117]. Nanoplastic exposure worsens outcomes in a mouse model of type 2 diabetes [118]. Polystyrene nanoplastic exposure accelerates hepatic fibrosis in mice fed a high-fat diet, with liver immune-microenvironment remodelling documented at single-cell resolution [119-120], and independent work has identified cGAS/STING innate-immune activation as a specific fibrotic mechanism in the microplastic-exposed liver [121]. A dedicated review of NAFLD and microplastic exposure concluded that both ingested and inhaled particles are plausible contributors to hepatic lipid dysregulation and inflammatory progression, with mechanistic support from multiple independent models [122].The gut-liver-adipose axis is the connecting infrastructure. Particles alter gut microbiota; microbial metabolites and translocated LPS reach the liver via portal circulation; hepatic Kupffer cells and stellate cells respond with cytokine release and fibrotic remodelling; adipose tissue macrophages contribute a parallel inflammatory tone; and the systemic result is insulin resistance and altered lipid handling [113,115,117]. This is the exact circuit that supports diet-induced metabolic disease in humans, and microplastic exposure appears able to enter it at multiple nodes.Cardiovascular inflammation and the vessel wallCardiovascular tissue is the human system in which the inflammation-microplastic linkage has been most directly documented. Two properties of vascular biology matter here: the atherosclerotic plaque is a chronic macrophage-driven inflammatory lesion, and it can now be sampled directly in surgical cohorts.The 2024 study by Marfella and colleagues documented microplastic particles (polyethylene and PVC) in atherosclerotic carotid plaque removed from 257 patients undergoing endarterectomy, and reported that patients with detectable plaque plastic had a higher subsequent risk of composite cardiovascular events over 34 months than those without — an effect that persisted after adjustment for standard risk factors [10]. A separate 2024 study in acute coronary syndrome patients found microplastics associated with elevated atherosclerotic burden and increased vascular lesion complexity [10]. A 2025 study extended the linkage to major adverse cardiac events after myocardial infarction [11]. None of these are randomised interventions; they are association studies with the acknowledged limits of confounding. They are also the first human clinical data with cardiovascular endpoints, and they align with a substantial animal literature.In experimental systems, long-term polystyrene nanoplastic exposure in ApoE-knockout mice produces atherosclerotic plaque expansion, hepatic lipid metabolism disruption, and elevated systemic inflammatory markers [123]. A mechanistic study identified long-chain acyl carnitines as an accelerant of nanoplastic-induced atherosclerosis, acting through the macrophage receptor MARCO [124]. Polystyrene microplastics produce direct vascular injury and inflammation in mice [125], and low-dose exposure produces cardiotoxicity in both mice and human cardiac organoids [126]. In cardiomyocytes, polystyrene microplastics trigger NLRP3-driven pyroptosis [76]; PET micro/nanoplastics exacerbate post-infarction inflammation and fibrosis via macrophage-driven remodelling [127]; polystyrene nanoplastics drive endothelial senescence in vitro via a defined signalling axis [128]; nanoplastic exposure induces myocardial cell senescence through the cGAS-STING innate immune pathway [129]. Reviews from 2022 and 2025 consolidate the cardiovascular case [130-131].The convergence between the human plaque findings and the animal atherosclerosis mechanism is the strongest such alignment currently available in the microplastic literature. It is important not to overstate it. The human data are association, not intervention, but it is the closest the field has come to demonstrating that particles seen in human tissue are doing biology consistent with what the animal literature predicted.Other tissue-specific inflammatory signalsThe organ-specific inflammatory literature is now sufficiently broad that a full accounting is not practical. Selected findings that establish the breadth of the pattern:Kidney. Polystyrene microplastics at realistic environmental concentrations damage human kidney proximal tubular epithelial cells and induce inflammation in mouse kidney [132-133]. Multiple studies document NF-κB and inflammasome-driven nephrotoxicity in rodents [45,131].Lung. Polystyrene microplastics induce pulmonary fibrosis and NLRP3-driven inflammation in mice; nanoplastic exposure in mouse lung produces COPD-like injury; human airway organoids exposed to microplastic fibers develop persistent inflammatory responses [80,134-135]. Textile microplastic fibers impair airway epithelial differentiation in a human bronchial system [136]. Nasal epithelial cells from asthmatic and COPD donors show impaired response to microplastic stimulation compared with healthy donors [134]. Polystyrene nanoplastics drive oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line [137], and microplastic exposure produces senescence of human lung epithelial cells and of mouse lungs through ROS signalling — connecting acute pulmonary inflammation to the cellular-senescence phenotype that underlies chronic lung disease [138]. Airborne microplastic exposure produces inflammatory injury across multiple murine organs via TLR-driven signalling [44].Reproductive tract. Rat granulosa cell pyroptosis via NLRP3/caspase-1 has been documented for polystyrene microplastic exposure [74]. Human ovarian granulosa cells respond to polystyrene nanoplastics with cellular stress in vitro, with matched effects in female mice [139]. Polyethylene microplastic exposure adversely affects oocyte quality in both human and mouse systems [140]. Microplastics have now been detected directly in human ovarian follicular fluid, the first female-reproductive biomonitoring point in humans [141]. Male reproductive systems show consistent inflammatory injury with ROS and inflammasome involvement across multiple mouse studies; polystyrene nanoplastics suppress steroidogenic StAR expression in Leydig cells via HIF-1α activation, providing a specific molecular mechanism for the endocrine-disrupting component of the phenotype [142].Oral cavity and airway. Human gingival fibroblasts respond to microplastics with inflammation-pathway activation [143]. Microplastics have been detected in nasal lavage from patients with allergic rhinitis [144].The pattern across these tissues is that the same core mechanism — oxidative stress → NF-κB → cytokines and NLRP3 → tissue injury — is reproducible in essentially every mammalian tissue that has been examined. What varies is the histological outcome, the dominant cell type, and the downstream disease relevance.Human evidenceHuman evidence for microplastic-driven inflammation now spans three types of study: tissue detection, correlational health outcome data, and ex vivo exposure of primary human cells and organoids. Each contributes something different.Tissue detection with disease correlation. The fecal microplastic study by Yan and colleagues found that patients with inflammatory bowel disease had significantly higher fecal microplastic concentrations than healthy controls, with a monotonic association between concentration and disease severity across mild, moderate, and severe categories [9]. This is the first human population-level linkage of microplastic burden to a clinical inflammatory disease endpoint. The 2024 study by Marfella and colleagues extended the linkage to cardiovascular events: patients with polyethylene and PVC particles in atherosclerotic carotid plaque had elevated composite cardiovascular event risk over 34 months of follow-up, after adjustment for traditional risk factors [10]. The 2024 acute coronary syndrome study reported association between microplastic detection and both plaque burden and vascular lesion complexity [10]. The 2025 myocardial infarction study reported association with major adverse cardiac events [11]. Detection of microplastics in patients with allergic rhinitis provides a smaller but consistent nasal-airway signal [144]. First-of-kind human biomonitoring points continue to accumulate in tissues with direct implications for chronic inflammatory disease: intracellular microplastics in human placenta [145], particles in human ovarian follicular fluid [141] and human semen [146], microplastics in human skeletal tissue [147], and microplastics in human blood — with polymer identification by μFTIR [148] and, in a separate cohort, association with clinically interpretable changes in the coagulation panel [149].Ex vivo primary human cell data. Primary human monocytes and dendritic cells respond to environmentally realistic nanoplastic concentrations with pro-inflammatory cytokine secretion [51]. Human macrophage, dendritic cell, and T cell populations show inflammatory responses to nanoplastics of varied polymer type in ex vivo exposure [52]. Single-cell mass cytometry after ex vivo exposure of human whole blood shows nanoplastic internalisation across myeloid populations and immune phenotype shifts at concentrations lower than most in vitro assays report [69]. Human peripheral blood lymphocytes show genotoxic and cytotoxic responses to polyethylene microplastics [57]. Human bronchial and airway organoids exposed to microplastic fibers develop inflammatory responses, with responses larger in tissue from patients with airway disease than in healthy tissue [134, 135]. Human liver and lung cell lines show mitochondrial damage and metabolic reprogramming after nanoplastic exposure [29]. Human kidney proximal tubular cells show inflammation-consistent injury on polystyrene microplastic exposure [132].Biomonitoring context. The broader human biomonitoring literature — microplastics in blood, stool, breast milk, lung, semen, placenta, testis, liver, kidney, and brain — has established that exposure is universal and that particles reach essentially every tissue that has been carefully examined [13-15]. This does not prove disease. It defines the exposure at the point where the inflammation biology applies. A rapid systematic review of microplastic effects on human digestive, reproductive, and respiratory health concluded that the human evidence base is still limited but converging with the animal literature on directionally consistent findings [12,150].The interpretation that best fits the current human evidence is that the exposure and the mechanistic tissue response are documented; the causal linkage between exposure and clinical disease is supported at the plaque-cardiovascular event and IBD-fecal burden endpoints; and the wider inflammatory implications for metabolic and neurological disease remain plausible but not yet demonstrated at population scale.Methodological limitationsThe inflammation literature carries the same characteristic limitations as most emerging environmental toxicology. They are worth naming so that the evidence tiers are read correctly.Particle type. The dominant particle in the experimental literature is pristine polystyrene, in monodisperse spherical form, at sizes chosen for tractability. Environmental particles are heterogeneous mixtures of polyethylene, polypropylene, PET, PVC, polystyrene, and polyurethane, in irregular shapes and sizes, with weathered surfaces carrying oxidised chemistry and adsorbed environmental compounds. Direct comparisons show that oxidised particles produce larger inflammatory responses than pristine ones [34,35], and that environmental exposure enhances internalisation compared with laboratory particles [34]. Extrapolating from polystyrene beads to environmental exposure probably underestimates the additive-driven component of the inflammation and overestimates the pure-particle component [15,21].Dose. Many in vivo mouse studies use doses one to several orders of magnitude above modelled human intake, chosen for statistical power in short protocols. This is not disqualifying but means the observed effect at the observed dose cannot be directly translated to human population risk without an exposure-response model [22]. A few studies have used environmentally relevant doses [108,133,151] and find qualitatively similar inflammation at smaller amplitude — a pattern consistent with a low-grade inflammatory contribution rather than acute injury.Cell system. In vitro dosing is often expressed in mass or number per volume of medium without correction for what fraction of that dose actually contacts the cell layer. Comparisons across in vitro studies are therefore weaker than they appear. A rapid review and meta-regression of microplastic toxicological effects in human cells found the strongest and most reproducible effects at high doses, with substantial heterogeneity at lower doses that overlap plausible tissue exposure [21].Measurement. Detection of microplastic in tissue is technically demanding. Blank contamination is a persistent risk; particle-counting methods vary; some techniques (pyrolysis-GC/MS) quantify polymer mass while others (μ-FTIR, μ-Raman) count individual particles down to a size-dependent detection limit. Quantitative comparisons across studies must be made cautiously [14].Co-exposure. Almost every environmental plastic exposure is co-exposure with plastic additives (bisphenols, phthalates, brominated flame retardants), adsorbed heavy metals, and other environmental contaminants. Studies with pristine polystyrene alone underrepresent the additive contribution [82,112]. A distinct and mechanistically informative case is polylactic acid, where gut-enzyme-catalysed release of oligomer nanoparticles triggers acute inflammation independent of the parent particle — a reminder that "the particle" is not always the primary insult [152]. Co-exposure studies consistently show inflammatory synergy — the particle amplifies the additive effect and vice versa — which is directionally important for real-world exposure assessment [77,111].Species translation. Mouse, rat, chicken, zebrafish, and carp inform mechanism, but immune system architecture, gut microbiota composition, and metabolic physiology differ across species. The animal-to-human bridge for microplastic inflammation is best supported for pathways that are evolutionarily conserved (NLRP3, NF-κB, macrophage polarisation) and weakest for outcomes that depend on species-specific physiology.SynthesisThe clearest single sentence is this: microplastics engage a set of inflammatory pathways that are shared with other biopersistent particulate exposures whose long-term disease consequences are well characterised, and human exposure to microplastics is chronic and universal, but the population-level dose-response for most inflammatory endpoints is not yet established.The mechanistic case is mature. Micro- and nanoplastics reproducibly generate oxidative stress in the cells and tissues they reach [18,24]. That stress activates pattern-recognition and NF-κB signalling with production of the canonical pro-inflammatory cytokine panel [40,42,51]. Macrophages and other phagocytes engage the particle, fail to degrade it, and shift toward inflammatory activation with disrupted lipid handling and lysosomal function [60,62]. The NLRP3 inflammasome, the specific sensor for particulate materials in innate immunity, is engaged across cell types and produces IL-1β and IL-18, cytokines with defined roles in atherosclerosis, metabolic disease, and inflammatory bowel disease [72-73]. In animal models, this circuit reproduces gut, liver, lung, cardiovascular, renal, reproductive, and neurological injury with an inflammatory signature [45-46,80,102,117,123]. In human systems, the same molecular responses are observed in primary immune cells, organoids, and biomonitoring cohorts [51-52,69,134-135].The specific new human data (fecal microplastic burden correlating with IBD severity [9], microplastic particles in atherosclerotic carotid plaque predicting cardiovascular events [10], microplastics associated with post-MI adverse cardiac outcomes [11]) are the first alignment of the animal mechanistic literature with clinical disease endpoints. They do not establish causation. They do establish that microplastics reach human tissue compartments where the mechanistic story predicts they would drive inflammation, and that presence in those compartments is prognostic.The low-grade inflammation hypothesis is best evaluated as a chronic-exposure argument, not an acute-toxicity argument. The strongest reading of the current evidence is that microplastics probably contribute a small but persistent elevation in inflammatory tone to tissues in which they accumulate; with the largest expected effects in gut (highest exposure), cardiovascular (documented plaque involvement), liver (portal delivery and Kupffer cell response), and brain (via gut-brain and, for the smallest particles, direct entry). Whether this contribution is quantitatively meaningful against the background of diet, exercise, sleep, and other lifestyle-driven inflammation is not yet established in humans. The mechanistic plausibility is strong; the population attributable fraction is unknown.ConclusionInflammation is the biological theme through which nearly all microplastic toxicology can be organised. The mechanisms are known, such as oxidative stress, NF-κB signalling, macrophage engagement, NLRP3 inflammasome assembly, cytokine release. The animal evidence for these mechanisms is now extensive and reproducible across laboratories, tissues, and polymer types. The human evidence has moved in the last three years from tissue detection alone to detection linked to clinical inflammatory disease at two important endpoints (e.g., cardiovascular events and inflammatory bowel disease severity) with more expected as the biomonitoring infrastructure matures.The most accurate framing is that microplastic exposure is a plausible contributor to the chronic low-grade inflammatory tone that underlies much of modern non-communicable disease, that the mechanistic plausibility is well supported, and that the population-scale magnitude of the contribution remains to be quantified. The exposure is universal. The mechanistic pathways are conserved. The clinical alignment is beginning. What is not yet in hand is the intervention data that would allow attribution.Winnow works upstream of most of this. Our probiotic strains have been shown in laboratory testing to bind micro- and nanoplastics, before absorption and before the particle-driven inflammatory pathways that this article describes can be engaged. It is a narrow intervention at a specific point in the exposure chain. It does not resolve the exposure question at the population or regulatory level. But at the level of one meal, one exposure event, one person, it reduces the load that the downstream inflammation biology has to work with.References[1] Das, A. The emerging role of microplastics in systemic toxicity: Involvement of reactive oxygen species (ROS). Sci. Total Environ. 895, 165076 (2023). https://pubmed.ncbi.nlm.nih.gov/37391150/[2] Winiarska, E., Jutel, M. & Zemelka-Wiacek, M. The potential impact of nano- and microplastics on human health: Understanding human health risks. Environ. Res. 251, 118535 (2024). https://pubmed.ncbi.nlm.nih.gov/38460665/[3] Prata, J. C., Costa, J. P. da, Lopes, I., Duarte, A. C. & Rocha-Santos, T. Environmental exposure to microplastics: An overview on possible human health effects. Sci. Total Environ. 702, 134455 (2020). https://pubmed.ncbi.nlm.nih.gov/31733547/[4] Wright, S. L. & Kelly, F. J. Plastic and Human Health: A Micro Issue? Environ. Sci. Technol. 51, 6634–6647 (2017). https://pubmed.ncbi.nlm.nih.gov/28531345/[5] Blackburn, K. & Green, D. The potential effects of microplastics on human health: What is known and what is unknown. Ambio 51, 518–530 (2022). https://pubmed.ncbi.nlm.nih.gov/34185251/[6] Li, Y. et al. Potential Health Impact of Microplastics: A Review of Environmental Distribution, Human Exposure, and Toxic Effects. Environ. Heal. 1, 249–257 (2023). https://pubmed.ncbi.nlm.nih.gov/39474495/[7] Rahman, A., Sarkar, A., Yadav, O. P., Achari, G. & Slobodnik, J. Potential human health risks due to environmental exposure to nano- and microplastics and knowledge gaps: A scoping review. Sci. Total Environ. 757, 143872 (2021). https://pubmed.ncbi.nlm.nih.gov/33310568/[8] Zhang, Z. et al. Polystyrene microplastics induce size-dependent multi-organ damage in mice: Insights into gut microbiota and fecal metabolites. J. Hazard. Mater. 461, 132503 (2024). https://pubmed.ncbi.nlm.nih.gov/37717443/[9] Yan, Z. et al. Analysis of Microplastics in Human Feces Reveals a Correlation between Fecal Microplastics and Inflammatory Bowel Disease Status. Environ. Sci. Technol. 56, 414–421 (2022). https://pubmed.ncbi.nlm.nih.gov/34935363/[10] Yang, Y. et al. Microplastics are associated with elevated atherosclerotic risk and increased vascular complexity in acute coronary syndrome patients. Part. Fibre Toxicol. 21, 34 (2024). https://pubmed.ncbi.nlm.nih.gov/39164741/[11] Zhang, Y. et al. Microplastics and nanoplastics increase major adverse cardiac events in patients with myocardial infarction. J. Hazard. Mater. 489, 137624 (2025). https://pubmed.ncbi.nlm.nih.gov/40007360/[12] Chartres, N. et al. Effects of Microplastic Exposure on Human Digestive, Reproductive, and Respiratory Health: A Rapid Systematic Review. Environ. Sci. Technol. 58, 22843–22864 (2024). https://pubmed.ncbi.nlm.nih.gov/39692326/[13] Feng, Y. et al. A systematic review of the impacts of exposure to micro- and nano-plastics on human tissue accumulation and health. Eco-Environ. Heal. 2, 195–207 (2023). https://pubmed.ncbi.nlm.nih.gov/38435355/[14] Zuri, G., Karanasiou, A. & Lacorte, S. Human biomonitoring of microplastics and health implications: A review. Environ. Res. 237, 116966 (2023). https://pubmed.ncbi.nlm.nih.gov/37634692/[15] Dzierżyński, E. et al. Microplastics in the Human Body: Exposure, Detection, and Risk of Carcinogenesis: A State-of-the-Art Review. Cancers 16, 3703 (2024). https://pubmed.ncbi.nlm.nih.gov/39518141/[16] Krause, S. et al. The potential of micro- and nanoplastics to exacerbate the health impacts and global burden of non-communicable diseases. Cell Rep. Med. 5, 101581 (2024). https://pubmed.ncbi.nlm.nih.gov/38781963/[17] Sandys, O. & Velde, A. te. Raising the Alarm: Environmental Factors in the Onset and Maintenance of Chronic (Low-Grade) Inflammation in the Gastrointestinal Tract. Dig. Dis. Sci. 67, 4355–4368 (2022). https://pubmed.ncbi.nlm.nih.gov/34981314/[18] Kadac-Czapska, K., Ośko, J., Knez, E. & Grembecka, M. Microplastics and Oxidative Stress—Current Problems and Prospects. Antioxidants 13, 579 (2024). https://pubmed.ncbi.nlm.nih.gov/38790684/[19] Hirt, N. & Body-Malapel, M. Immunotoxicity and intestinal effects of nano- and microplastics: a review of the literature. Part. Fibre Toxicol. 17, 57 (2020). https://pubmed.ncbi.nlm.nih.gov/33183327/[20] Mahmud, F., Sarker, D. B., Jocelyn, J. A. & Sang, Q.-X. A. Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence. Cells 13, 1788 (2024). https://pubmed.ncbi.nlm.nih.gov/39513895/[21] Danopoulos, E., Twiddy, M., West, R. & Rotchell, J. M. A rapid review and meta-regression analyses of the toxicological impacts of microplastic exposure in human cells. J. Hazard. Mater. 427, 127861 (2022). https://pubmed.ncbi.nlm.nih.gov/34863566/[22] Brito, W. A. da S. et al. Consequences of nano and microplastic exposure in rodent models: the known and unknown. Part. Fibre Toxicol. 19, 28 (2022). https://pubmed.ncbi.nlm.nih.gov/35449034/[23] Khan, A. & Jia, Z. Recent insights into uptake, toxicity, and molecular targets of microplastics and nanoplastics relevant to human health impacts. iScience 26, 106061 (2023). https://pubmed.ncbi.nlm.nih.gov/36818296/[24] Li, Z. et al. Is microplastic an oxidative stressor? Evidence from a meta-analysis on bivalves. J. Hazard. Mater. 423, 127211 (2022). https://pubmed.ncbi.nlm.nih.gov/34844346/[25] Lu, Y. et al. Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver. Environ. Sci. Technol. 50, 4054–4060 (2016). https://pubmed.ncbi.nlm.nih.gov/26950772/[26] Deng, Y., Zhang, Y., Lemos, B. & Ren, H. Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure. Sci. Rep. 7, 46687 (2017). https://pubmed.ncbi.nlm.nih.gov/28436478/[27] Li, S. et al. Polystyrene microplastics trigger hepatocyte apoptosis and abnormal glycolytic flux via ROS-driven calcium overload. J. Hazard. Mater. 417, 126025 (2021). https://pubmed.ncbi.nlm.nih.gov/34229379/[28] Cheng, W. et al. Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids. Sci. Total Environ. 806, 150328 (2022). https://pubmed.ncbi.nlm.nih.gov/34571217/[29] Lin, S. et al. Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells. Environ. Sci. Technol. 56, 12483–12493 (2022). https://pubmed.ncbi.nlm.nih.gov/36005547/[30] Li, Y. et al. ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells. Chem.-Biol. Interact. 379, 110502 (2023). https://pubmed.ncbi.nlm.nih.gov/37084995/[31] He, Y. et al. Cytotoxic effects of polystyrene nanoplastics with different surface functionalization on human HepG2 cells. Sci. Total Environ. 723, 138180 (2020). https://pubmed.ncbi.nlm.nih.gov/32224412/[32] Jeon, S. et al. The reactive oxygen species as pathogenic factors of fragmented microplastics to macrophages. Environ. Pollut. 281, 117006 (2021). https://pubmed.ncbi.nlm.nih.gov/33812130/[33] Rubio, L., Barguilla, I., Domenech, J., Marcos, R. & Hernández, A. Biological effects, including oxidative stress and genotoxic damage, of polystyrene nanoparticles in different human hematopoietic cell lines. J. Hazard. Mater. 398, 122900 (2020). https://pubmed.ncbi.nlm.nih.gov/32464564/[34] Ramsperger, A. F. R. M. et al. Environmental exposure enhances the internalization of microplastic particles into cells. Sci. Adv. 6, eabd1211 (2020). https://pubmed.ncbi.nlm.nih.gov/33298447/[35] Visalli, G. et al. Enhancement of biological effects of oxidised nano- and microplastics in human professional phagocytes. Environ. Toxicol. Pharmacol. 99, 104086 (2023). https://pubmed.ncbi.nlm.nih.gov/36842547/[36] Shengchen, W., Jing, L., Yujie, Y., Yue, W. & Shiwen, X. Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes. J. Hazard. Mater. 417, 125962 (2021). https://pubmed.ncbi.nlm.nih.gov/33979708/[37] Wu, Q. et al. Polystyrene nanoplastics-induced lung apoptosis and ferroptosis via ROS-dependent endoplasmic reticulum stress. Sci. Total Environ. 912, 169260 (2024). https://pubmed.ncbi.nlm.nih.gov/38086481/[38] Mu, Y. et al. Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice. Chemosphere 291, 132944 (2022). https://pubmed.ncbi.nlm.nih.gov/34793849/[39] Wei, Y. Y. et al. Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease. Autophagy 21, 1717–1743 (2025). https://pubmed.ncbi.nlm.nih.gov/40114310/[40] Xu, R., Cao, J., Lv, H., Geng, Y. & Guo, M. Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice. Sci. Total Environ. 917, 170518 (2024). https://pubmed.ncbi.nlm.nih.gov/38286276/[41] Chen, X. et al. Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice. Sci. Total Environ. 935, 173458 (2024). https://pubmed.ncbi.nlm.nih.gov/38796000/[42] Cao, J., Xu, R., Geng, Y., Xu, S. & Guo, M. Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice. Environ. Pollut. 320, 121068 (2023). https://pubmed.ncbi.nlm.nih.gov/36641069/[43] Zeng, G. et al. Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway. Environ. Pollut. 345, 123473 (2024). https://pubmed.ncbi.nlm.nih.gov/38301820/[44] Xia, Q. et al. Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway. Environ. Sci. Technol. 58, 18603–18618 (2024). https://pubmed.ncbi.nlm.nih.gov/39389766/[45] Meng, X. et al. Polystyrene microplastics induced oxidative stress, inflammation and necroptosis via NF-κB and RIP1/RIP3/MLKL pathway in chicken kidney. Toxicology 478, 153296 (2022). https://pubmed.ncbi.nlm.nih.gov/36029908/[46] Zhang, Q. et al. Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp. Fish Shellfish Immunol. 135, 108690 (2023). https://pubmed.ncbi.nlm.nih.gov/36944415/[47] Li, J. et al. Polystyrene microplastics mediate inflammatory responses in the chicken thymus by Nrf2/NF-κB pathway and trigger autophagy and apoptosis. Environ. Toxicol. Pharmacol. 100, 104136 (2023). https://pubmed.ncbi.nlm.nih.gov/37127111/[48] Fan, X. et al. Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice. J. Environ. Sci. 137, 553–566 (2024). https://pubmed.ncbi.nlm.nih.gov/37980039/[49] Li, G. et al. Polystyrene microplastics induce anxiety via HRAS derived PERK-NF-κB pathway. Environ. Int. 185, 108543 (2024). https://pubmed.ncbi.nlm.nih.gov/38452464/[50] Xu, T., Cui, J., Xu, R., Cao, J. & Guo, M. Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp. Aquat. Toxicol. 262, 106659 (2023). https://pubmed.ncbi.nlm.nih.gov/37586228/[51] Weber, A. et al. Nanoplastics affect the inflammatory cytokine release by primary human monocytes and dendritic cells. Environ. Int. 163, 107173 (2022). https://pubmed.ncbi.nlm.nih.gov/35303527/[52] Wolff, C. M., Singer, D., Schmidt, A. & Bekeschus, S. Immune and inflammatory responses of human macrophages, dendritic cells, and T-cells in presence of micro- and nanoplastic of different types and sizes. J. Hazard. Mater. 459, 132194 (2023). https://pubmed.ncbi.nlm.nih.gov/37572607/[53] Mattioda, V. et al. Pro-Inflammatory and Cytotoxic Effects of Polystyrene Microplastics on Human and Murine Intestinal Cell Lines. Biomolecules 13, 140 (2023). https://pubmed.ncbi.nlm.nih.gov/36671525/[54] Hwang, J. et al. Potential toxicity of polystyrene microplastic particles. Sci. Rep. 10, 7391 (2020). https://pubmed.ncbi.nlm.nih.gov/32355311/[55] Lu, K. et al. Detrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology. J. Hazard. Mater. 416, 126069 (2021). https://pubmed.ncbi.nlm.nih.gov/34492895/[56] Jing, J. et al. Polystyrene micro-/nanoplastics induced hematopoietic damages via the crosstalk of gut microbiota, metabolites, and cytokines. Environ. Int. 161, 107131 (2022). https://pubmed.ncbi.nlm.nih.gov/35149446/[57] Çobanoğlu, H., Belivermiş, M., Sıkdokur, E., Kılıç, Ö. & Çayır, A. Genotoxic and cytotoxic effects of polyethylene microplastics on human peripheral blood lymphocytes. Chemosphere 272, 129805 (2021). https://pubmed.ncbi.nlm.nih.gov/35534956/[58] Palaniappan, S., Sadacharan, C. M. & Rostama, B. Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro. Expo. Heal. 14, 75–85 (2022). https://pubmed.ncbi.nlm.nih.gov/34337190/[59] Deng, J. et al. Microplastics released from food containers can suppress lysosomal activity in mouse macrophages. J. Hazard. Mater. 435, 128980 (2022). https://pubmed.ncbi.nlm.nih.gov/35523089/[60] Adler, M. Y. et al. Effect of micro- and nanoplastic particles on human macrophages. J. Hazard. Mater. 471, 134253 (2024). https://pubmed.ncbi.nlm.nih.gov/38642497/[61] Koner, S., Florance, I., Mukherjee, A. & Chandrasekaran, N. Cellular response of THP-1 macrophages to polystyrene microplastics exposure. Toxicology 483, 153385 (2023). https://pubmed.ncbi.nlm.nih.gov/36464069/[62] Florance, I., Ramasubbu, S., Mukherjee, A. & Chandrasekaran, N. Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro. Toxicology 458, 152850 (2021). https://pubmed.ncbi.nlm.nih.gov/34217793/[63] Florance, I., Chandrasekaran, N., Gopinath, P. M. & Mukherjee, A. Exposure to polystyrene nanoplastics impairs lipid metabolism in human and murine macrophages in vitro. Ecotoxicol. Environ. Saf. 238, 113612 (2022). https://pubmed.ncbi.nlm.nih.gov/35561548/[64] Jiang, W. et al. Polystyrene nanoplastics of different particle sizes regulate the polarization of pro-inflammatory macrophages. Sci. Rep. 14, 16329 (2024). https://pubmed.ncbi.nlm.nih.gov/39009713/[65] Li, S. et al. The crosstalk between M1 macrophage polarization and energy metabolism disorder contributes to polystyrene nanoplastics-triggered testicular inflammation. Food Chem. Toxicol. 180, 114002 (2023). https://pubmed.ncbi.nlm.nih.gov/37634612/[66] Luo, W.-Q. et al. Size-dependent internalization of polystyrene microplastics as a key factor in macrophages and systemic toxicity. J. Hazard. Mater. 490, 137701 (2025). https://pubmed.ncbi.nlm.nih.gov/40020305/[67] Yin, K. et al. Polystyrene microplastics promote liver inflammation by inducing the formation of macrophages extracellular traps. J. Hazard. Mater. 452, 131236 (2023). https://pubmed.ncbi.nlm.nih.gov/36958159/[68] Zhu, X., Peng, L., Song, E. & Song, Y. Polystyrene Nanoplastics Induce Neutrophil Extracellular Traps in Mice Neutrophils. Chem. Res. Toxicol. 35, 378–382 (2022). https://pubmed.ncbi.nlm.nih.gov/35060696/[69] Fusco, L. et al. Nanoplastics: Immune Impact, Detection, and Internalization after Human Blood Exposure by Single-Cell Mass Cytometry. Adv. Mater. 37, e2413413 (2025). https://pubmed.ncbi.nlm.nih.gov/39449193/[70] Yang, Q. et al. Oral feeding of nanoplastics affects brain function of mice by inducing macrophage IL-1 signal in the intestine. Cell Rep. 42, 112346 (2023). https://pubmed.ncbi.nlm.nih.gov/37022934/[71] Kwon, W. et al. Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo. Sci. Total Environ. 807, 150817 (2022). https://pubmed.ncbi.nlm.nih.gov/34627918/[72] Alijagic, A. et al. NLRP3 inflammasome as a sensor of micro- and nanoplastics immunotoxicity. Front. Immunol. 14, 1178434 (2023). https://pubmed.ncbi.nlm.nih.gov/37143682/[73] Busch, M. et al. Assessing the NLRP3 Inflammasome Activating Potential of a Large Panel of Micro- and Nanoplastics in THP-1 Cells. Biomolecules 12, 1095 (2022). https://pubmed.ncbi.nlm.nih.gov/36008988/[74] Hou, J. et al. Polystyrene microplastics lead to pyroptosis and apoptosis of ovarian granulosa cells via NLRP3/Caspase-1 signaling pathway in rats. Ecotoxicol. Environ. Saf. 212, 112012 (2021). https://pubmed.ncbi.nlm.nih.gov/33550074/[75] Zhang, Y. et al. Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes. Sci. Total Environ. 840, 156727 (2022). https://pubmed.ncbi.nlm.nih.gov/35714743/[76] Wei, J. et al. The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase-1 signaling pathway and oxidative stress in Wistar rats. Environ. Toxicol. 36, 935–944 (2021). https://pubmed.ncbi.nlm.nih.gov/33404188/[77] He, Y. et al. Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway. Chemosphere 307, 135662 (2022). https://pubmed.ncbi.nlm.nih.gov/35830933/[78] Cao, J. et al. Polyethylene microplastics trigger cell apoptosis and inflammation via inducing oxidative stress and activation of the NLRP3 inflammasome in carp gills. Fish Shellfish Immunol. 132, 108470 (2023). https://pubmed.ncbi.nlm.nih.gov/36470402/[79] Xu, Z. et al. Exposure to irregular microplastic shed from baby bottles activates the ROS/NLRP3/Caspase-1 signaling pathway, causing intestinal inflammation. Environ. Int. 181, 108296 (2023). https://pubmed.ncbi.nlm.nih.gov/37924603/[80] Lu, H. et al. Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens. J. Zhejiang Univ.-Sci. B 25, 233–243 (2024). https://pubmed.ncbi.nlm.nih.gov/38453637/[81] Sun, J. et al. Involvement of the JNK/HO-1/FTH1 signaling pathway in nanoplastic-induced inflammation and ferroptosis of BV2 microglia cells. Int. J. Mol. Med. 52, 61 (2023). https://pubmed.ncbi.nlm.nih.gov/37264973/[82] Li, S., Gu, X., Zhang, M., Jiang, Q. & Xu, T. Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused oxidative stress to activate NF-κB/NLRP3 pathway aggravated pyroptosis and inflammation in mouse kidney. Sci. Total Environ. 926, 171817 (2024). https://pubmed.ncbi.nlm.nih.gov/38513858/[83] Shan, S., Zhang, Y., Zhao, H., Zeng, T. & Zhao, X. Polystyrene nanoplastics penetrate across the blood-brain barrier and induce activation of microglia in the brain of mice. Chemosphere 298, 134261 (2022). https://pubmed.ncbi.nlm.nih.gov/35302003/[84] Paing, Y. M. M. et al. Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies. Sci. Total Environ. 924, 171681 (2024). https://pubmed.ncbi.nlm.nih.gov/38490422/[85] Wang, G., Lin, Y. & Shen, H. Exposure to Polystyrene Microplastics Promotes the Progression of Cognitive Impairment in Alzheimer’s Disease: Association with Induction of Microglial Pyroptosis. Mol. Neurobiol. 61, 900–907 (2024). https://pubmed.ncbi.nlm.nih.gov/37670159/[86] Jung, B.-K. et al. Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain. NeuroToxicology 81, 189–196 (2020). https://pubmed.ncbi.nlm.nih.gov/33132133/[87] Vojnits, K. et al. ROS-dependent degeneration of human neurons induced by environmentally relevant levels of micro- and nanoplastics of diverse shapes and forms. J. Hazard. Mater. 469, 134017 (2024). https://pubmed.ncbi.nlm.nih.gov/38518696/[88] Martin-Folgar, R. et al. Molecular effects of polystyrene nanoplastics on human neural stem cells. PLOS ONE 19, e0295816 (2024). https://pubmed.ncbi.nlm.nih.gov/38170698/[89] Lee, C.-W. et al. Exposure to polystyrene microplastics impairs hippocampus-dependent learning and memory in mice. J. Hazard. Mater. 430, 128431 (2022). https://pubmed.ncbi.nlm.nih.gov/35150991/[90] Liu, S. et al. Neurotoxicities induced by micro/nanoplastics: A review focusing on the risks of neurological diseases. J. Hazard. Mater. 469, 134054 (2024). https://pubmed.ncbi.nlm.nih.gov/38503214/[91] Kaushik, A., Singh, A., Gupta, V. K. & Mishra, Y. K. Nano/micro-plastic, an invisible threat getting into the brain. Chemosphere 361, 142380 (2024). https://pubmed.ncbi.nlm.nih.gov/38763401/[92] Wang, J. et al. Oxidized/unmodified-polyethylene microplastics neurotoxicity in mice: Perspective from microbiota-gut-brain axis. Environ. Int. 185, 108523 (2024). https://pubmed.ncbi.nlm.nih.gov/38484610/[93] Liang, X. et al. Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology. ACS Nano 19, 5475–5492 (2025). https://pubmed.ncbi.nlm.nih.gov/39883073/[94] Liang, B. et al. Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice. J. Hazard. Mater. 430, 128459 (2022). https://pubmed.ncbi.nlm.nih.gov/35739658/[95] Xie, J. et al. Blood-brain barrier damage accelerates the accumulation of micro- and nanoplastics in the human central nervous system. J. Hazard. Mater. 480, 136028 (2024). https://pubmed.ncbi.nlm.nih.gov/39366047/[96] Zhao, Y., Liu, S. & Xu, H. Effects of microplastic and engineered nanomaterials on inflammatory bowel disease: A review. Chemosphere 326, 138486 (2023). https://pubmed.ncbi.nlm.nih.gov/36963581/[97] Jin, Y. et al. Polystyrene microplastics induce microbiota dysbiosis and inflammation in the gut of adult zebrafish. Environ. Pollut. 235, 322–329 (2018). https://pubmed.ncbi.nlm.nih.gov/29304465/[98] Qiao, R. et al. Microplastics induce intestinal inflammation, oxidative stress, and disorders of metabolome and microbiome in zebrafish. Sci. Total Environ. 662, 246–253 (2019). https://pubmed.ncbi.nlm.nih.gov/30690359/[99] Li, B. et al. Polyethylene microplastics affect the distribution of gut microbiota and inflammation development in mice. Chemosphere 244, 125492 (2020). https://pubmed.ncbi.nlm.nih.gov/31809927/[100] 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. 220, 112340 (2021). https://pubmed.ncbi.nlm.nih.gov/34015635/[101] Qiao, J. et al. Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction. Nanoscale 13, 8806–8816 (2021). https://pubmed.ncbi.nlm.nih.gov/33904557/[102] Djouina, M. et al. Oral exposure to polyethylene microplastics alters gut morphology, immune response, and microbiota composition in mice. Environ. Res. 212, 113230 (2022). https://pubmed.ncbi.nlm.nih.gov/35398082/[103] Jia, R. et al. Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice. Toxics 11, 127 (2023). https://pubmed.ncbi.nlm.nih.gov/36851002/[104] Xie, S. et al. Microplastics perturb colonic epithelial homeostasis associated with intestinal overproliferation, exacerbating the severity of colitis. Environ. Res. 217, 114861 (2023). https://pubmed.ncbi.nlm.nih.gov/36410465/[105] Zheng, H., Wang, J., Wei, X., Chang, L. & Liu, S. Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis. Sci. Total Environ. 750, 143085 (2021). https://pubmed.ncbi.nlm.nih.gov/33182181/[106] Luo, T. et al. Polystyrene microplastics exacerbate experimental colitis in mice tightly associated with the occurrence of hepatic inflammation. Sci. Total Environ. 844, 156884 (2022). https://pubmed.ncbi.nlm.nih.gov/35752249/[107] Zolotova, N., Dzhalilova, D., Tsvetkov, I. & Makarova, O. Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis. Toxics 11, 730 (2023). https://pubmed.ncbi.nlm.nih.gov/37755741/[108] Xu, D. et al. Differently surface-labeled polystyrene nanoplastics at an environmentally relevant concentration induced Crohn’s ileitis-like features via triggering intestinal epithelial cell necroptosis. Environ. Int. 176, 107968 (2023). https://pubmed.ncbi.nlm.nih.gov/37201399/[109] Tian, S., Li, R., Li, J. & Zou, J. Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage. Environ. Int. 195, 109258 (2025). https://pubmed.ncbi.nlm.nih.gov/39805171/[110] Li, L. et al. Chronic exposure to polystyrene nanoplastics induces intestinal mechanical and immune barrier dysfunction in mice. Ecotoxicol. Environ. Saf. 269, 115749 (2024). https://pubmed.ncbi.nlm.nih.gov/38039854/[111] Liang, B. et al. Underestimated health risks: polystyrene micro- and nanoplastics jointly induce intestinal barrier dysfunction by ROS-mediated epithelial cell apoptosis. Part. Fibre Toxicol. 18, 20 (2021). https://pubmed.ncbi.nlm.nih.gov/34098985/[112] Shaoyong, W. et al. Benzo [a] pyrene-loaded aged polystyrene microplastics promote colonic barrier injury via oxidative stress-mediated notch signalling. J. Hazard. Mater. 457, 131820 (2023). https://pubmed.ncbi.nlm.nih.gov/37320903/[113] Lee, A. G. et al. Polystyrene Microplastics Exacerbate Systemic Inflammation in High-Fat Diet-Induced Obesity. Int. J. Mol. Sci. 24, 12421 (2023). https://pubmed.ncbi.nlm.nih.gov/37569796/[114] Zhao, J. et al. Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice. Ecotoxicol. Environ. Saf. 232, 113239 (2022). https://pubmed.ncbi.nlm.nih.gov/35093814/[115] Zhao, J. et al. Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis. Toxicol. Sci. 198, 210–220 (2024). https://pubmed.ncbi.nlm.nih.gov/38291899/[116] Huang, D. et al. Polystyrene microplastic exposure induces insulin resistance in mice via dysbacteriosis and pro-inflammation. Sci. Total Environ. 838, 155937 (2022). https://pubmed.ncbi.nlm.nih.gov/35588841/[117] Shi, C. et al. Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance. Environ. Int. 164, 107273 (2022). https://pubmed.ncbi.nlm.nih.gov/35526298/[118] Wang, Y. et al. The effect and a mechanistic evaluation of polystyrene nanoplastics on a mouse model of type 2 diabetes. Food Chem. Toxicol. 173, 113642 (2023). https://pubmed.ncbi.nlm.nih.gov/36736609/[119] Li, L., Xu, M., He, C., Wang, H. & Hu, Q. Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice. Environ. Toxicol. 37, 362–372 (2022). https://pubmed.ncbi.nlm.nih.gov/34755918/[120] Liu, W. et al. Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver. Sci. Total Environ. 912, 168308 (2024). https://pubmed.ncbi.nlm.nih.gov/37977403/[121] Shen, R. et al. Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway. Environ. Pollut. 300, 118986 (2022). https://pubmed.ncbi.nlm.nih.gov/35167931/[122] Auguet, T. et al. Are Ingested or Inhaled Microplastics Involved in Nonalcoholic Fatty Liver Disease? Int. J. Environ. Res. Public Heal. 19, 13495 (2022). https://pubmed.ncbi.nlm.nih.gov/36294076/[123] Wen, J., Sun, H., Yang, B., Song, E. & Song, Y. Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice. J. Hazard. Mater. 466, 133583 (2024). https://pubmed.ncbi.nlm.nih.gov/38306833/[124] Wang, B. et al. Long-Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics-Induced Atherosclerosis by Upregulating MARCO. Adv. Sci. 10, 2205876 (2023). https://pubmed.ncbi.nlm.nih.gov/37144527/[125] Yan, J. et al. Toxic vascular effects of polystyrene microplastic exposure. Sci. Total Environ. 905, 167215 (2023). https://pubmed.ncbi.nlm.nih.gov/37734602/[126] Zhou, Y. et al. Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids. Environ. Int. 179, 108171 (2023). https://pubmed.ncbi.nlm.nih.gov/37669592/[127] Gu, X. et al. Exposure to polyethylene terephthalate micro(nano)plastics exacerbates inflammation and fibrosis after myocardial infarction by reprogramming the gut and lung microbiota and metabolome. J. Hazard. Mater. 488, 137410 (2025). https://pubmed.ncbi.nlm.nih.gov/39919626/[128] Shiwakoti, S. et al. Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism. Environ. Int. 164, 107248 (2022). https://pubmed.ncbi.nlm.nih.gov/35461096/[129] Wang, K. et al. Nanoplastics causes heart aging/myocardial cell senescence through the Ca2+/mtDNA/cGAS-STING signaling cascade. J. Nanobiotechnology 22, 96 (2024). https://pubmed.ncbi.nlm.nih.gov/38448951/[130] Zhu, X. et al. Micro- and nanoplastics: A new cardiovascular risk factor? Environ. Int. 171, 107662 (2023). https://pubmed.ncbi.nlm.nih.gov/36473237/[131] Lee, Y.-H., Zheng, C.-M., Wang, Y.-J., Wang, Y.-L. & Chiu, H.-W. Effects of microplastics and nanoplastics on the kidney and cardiovascular system. Nat. Rev. Nephrol. 21, 585–596 (2025). https://pubmed.ncbi.nlm.nih.gov/40537559/[132] Wang, Y.-L. et al. The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice. Environ. Heal. Perspect. 129, 057003 (2021). https://pubmed.ncbi.nlm.nih.gov/33956507/[133] Chen, Y.-C. et al. The nephrotoxic potential of polystyrene microplastics at realistic environmental concentrations. J. Hazard. Mater. 427, 127871 (2022). https://pubmed.ncbi.nlm.nih.gov/34862106/[134] Paplińska-Goryca, M. et al. The impaired response of nasal epithelial cells to microplastic stimulation in asthma and COPD. Sci. Rep. 15, 4242 (2025). https://pubmed.ncbi.nlm.nih.gov/39905077/[135] Winkler, A. S. et al. Human airway organoids and microplastic fibers: A new exposure model for emerging contaminants. Environ. Int. 163, 107200 (2022). https://pubmed.ncbi.nlm.nih.gov/35349910/[136] Song, S. et al. Inhalable Textile Microplastic Fibers Impair Airway Epithelial Differentiation. Am. J. Respir. Crit. Care Med. 209, 427–443 (2024). https://pubmed.ncbi.nlm.nih.gov/37971785/[137] Milillo, C. et al. Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line. Front. Public Heal. 12, 1385387 (2024). https://pubmed.ncbi.nlm.nih.gov/38799687/[138] Jin, W. et al. Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling. Environ. Int. 185, 108489 (2024). https://pubmed.ncbi.nlm.nih.gov/38367553/[139] Zeng, L. et al. The ovarian-related effects of polystyrene nanoplastics on human ovarian granulosa cells and female mice. Ecotoxicol. Environ. Saf. 257, 114941 (2023). https://pubmed.ncbi.nlm.nih.gov/37087970/[140] Wang, Q. et al. Polyethylene microplastic exposure adversely affects oocyte quality in human and mouse. Environ. Int. 195, 109236 (2025). https://pubmed.ncbi.nlm.nih.gov/39729868/[141] Montano, L. et al. First evidence of microplastics in human ovarian follicular fluid: An emerging threat to female fertility. Ecotoxicol. Environ. Saf. 291, 117868 (2025). https://pubmed.ncbi.nlm.nih.gov/39947063/[142] Sui, A. et al. Polystyrene nanoplastics inhibit StAR expression by activating HIF-1α via ERK1/2 MAPK and AKT pathways in TM3 Leydig cells and testicular tissues of mice. Food Chem. Toxicol. 173, 113634 (2023). https://pubmed.ncbi.nlm.nih.gov/36709824/) [143] Caputi, S. et al. Microplastics Affect the Inflammation Pathway in Human Gingival Fibroblasts: A Study in the Adriatic Sea. Int. J. Environ. Res. Public Heal. 19, 7782 (2022). https://pubmed.ncbi.nlm.nih.gov/35805437/[144] Tuna, A. et al. Detection of microplastics in patients with allergic rhinitis. Eur. Arch. Oto-Rhino-Laryngol. 280, 5363–5367 (2023). https://pubmed.ncbi.nlm.nih.gov/37410148/[145] Ragusa, A. et al. Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas. Int. J. Environ. Res. Public Heal. 19, 11593 (2022). https://pubmed.ncbi.nlm.nih.gov/36141864/[146] Montano, L. et al. Raman Microspectroscopy evidence of microplastics in human semen. Sci. Total Environ. 901, 165922 (2023). https://pubmed.ncbi.nlm.nih.gov/37532047/[147] Yang, Q. et al. Microplastics in human skeletal tissues: Presence, distribution and health implications. Environ. Int. 196, 109316 (2025). https://pubmed.ncbi.nlm.nih.gov/39946929/[148] Leonard, S. V. L. et al. Microplastics in human blood: Polymer types, concentrations and characterisation using μFTIR. Environ. Int. 188, 108751 (2024). https://pubmed.ncbi.nlm.nih.gov/38761430/[149] Lee, D.-W. et al. Microplastic particles in human blood and their association with coagulation markers. Sci. Rep. 14, 30419 (2024). https://pubmed.ncbi.nlm.nih.gov/39638849/[150] Xu, J.-L., Lin, X., Wang, J. J. & Gowen, A. A. A review of potential human health impacts of micro- and nanoplastics exposure. Sci. Total Environ. 851, 158111 (2022). https://pubmed.ncbi.nlm.nih.gov/35987230/[151] Deng, Y. et al. Long-Term Exposure to Environmentally Relevant Doses of Large Polystyrene Microplastics Disturbs Lipid Homeostasis via Bowel Function Interference. Environ. Sci. Technol. 56, 15805–15817 (2022). https://pubmed.ncbi.nlm.nih.gov/36282942/[152] Wang, M. et al. Oligomer nanoparticle release from polylactic acid plastics catalysed by gut enzymes triggers acute inflammation. Nat. Nanotechnol. 18, 403–411 (2023). https://pubmed.ncbi.nlm.nih.gov/36864128/