Emerging Public Health Concerns of Micro- and Nanoplastics in Humans: Detection and Health Impact

Abstract

Microplastics (MPs) and nanoplastics (NPs) have become pervasive environmental contaminants, raising growing concern regarding their potential accumulation within the human body and associated health risks. MP particles can translocate into systemic circulation and multiple organs, necessitating a comprehensive evaluation of current human biomonitoring data. This comprehensive review aimed to synthesize current evidence on the occurrence, distribution, detection technologies, exposure reduction and potential health implications of microplastics in human biological samples. The reviewed literature confirms the presence of microplastics in blood, placenta, amniotic fluid, umbilical cord blood, breast milk, semen, urine, and selected tissues including cardiovascular, renal, and reproductive samples. Detection frequencies in some matrices exceeded 70–90%, with polymer types such as polyethylene, polypropylene, polystyrene, and polyethylene terephthalate most commonly identified. Reported particle sizes ranged from nanometer-scale fragments to particles over 100 µm, indicating both systemic circulation and potential tissue retention. Spectroscopic techniques such as μFTIR and μRaman dominate polymer identification, while thermoanalytical approaches such as Py-GC/MS provide quantitative polymer confirmation. Emerging evidence suggests associations with oxidative stress, inflammatory responses, endothelial dysfunction, and impaired reproductive parameters, although causal relationships remain uncertain due to methodological heterogeneity and limited longitudinal data. This review provides an integrated overview of current human exposure evidence, identifies analytical gaps, and highlights the urgent need for harmonized detection frameworks and longitudinal risk assessment studies to inform public health policy and future biomonitoring strategies.

1. Introduction

Microplastics (MPs, plastic particles < 5 mm) and nanoplastics (NPs, plastic particles < 1 µm) are increasingly recognized as pervasive contaminants capable of entering and accumulating within the human body [1]. Their omnipresence in air, water, food, and consumer products has raised concerns regarding chronic internal exposure [2,3,4]. Over the past decade, rapid advances in analytical chemistry have enabled the detection of plastic particles in human biological matrices, shifting the research focus from environmental contamination to direct human biomonitoring [5,6,7].

Evidence now confirms the presence of MPs in peripheral blood. The first quantitative report identified polyethylene terephthalate (PET), polyethylene (PE), and polystyrene (PS) in 77% of human blood samples using pyrolysis–gas chromatography–mass spectrometry (Py-GC/MS) [5]. Subsequent investigations in Korea and the United Kingdom reported detection frequencies of 88.9% and 90%, respectively, primarily involving PS, polypropylene (PP), and PE [8,9]. In China, laser direct infrared spectroscopy (LD-IR) and scanning electron microscopy (SEM) analyses revealed particles with sizes from 184 μm in perioperative blood and cardiac tissues, confirming systemic distribution [10]. Notably, MPs identified within carotid plaques were associated with a 4.5-fold increased risk of cardiovascular events, suggesting possible pathological relevance [11].

Maternal–fetal exposure has become an area of particular concern. MPs have been identified in placenta, umbilical cord blood, and amniotic fluid, indicating transplacental transfer [12,13,14]. All analyzed umbilical vein and amniotic fluid samples in recent Chinese cohorts contained MPs, with abundance correlated to maternal age and body mass index [13]. Breast milk contamination, first reported in Italy and later confirmed in China and Poland, demonstrates early-life exposure pathways [6,15,16]. Given the vulnerability of neonatal immune and gastrointestinal systems, these findings warrant careful evaluation.

Reproductive tissues represent another emerging research frontier. MPs have been detected in human semen and testicular tissues across multiple countries, with detection rates ranging from 60% to 100% [17,18]. Experimental and observational evidence suggests associations with oxidative stress, blood–testis barrier disruption, and reduced sperm motility [18,19]. Additionally, MPs have been identified in prostate tumors and renal tissues, further expanding the spectrum of organ involvement [20,21].

The diversity of detected polymers including PE, PP, PET, PS, polyvinyl chloride (PVC), polyamide (PA), and polyurethane (PU) reflects widespread industrial usage and environmental persistence [22,23]. However, heterogeneity in particle size, morphology, and associated chemical additives complicates toxicological interpretation [24,25,26]. Methodological differences in digestion, filtration, and analytical detection further limit cross-study comparability [27].

Spectroscopic techniques such as micro-Fourier transform infrared spectroscopy (μFTIR) and micro-Raman spectroscopy (μRaman) dominate polymer identification, each with inherent strengths and size-dependent detection limitations [6,9,15]. Thermoanalytical approaches like Py-GC/MS provide quantitative polymer mass confirmation but lack particle-level morphological information [5,28]. The need for standardized protocols, contamination control strategies, and harmonized reporting frameworks is therefore urgent.

This comprehensive review aimed to (i) synthesize current evidence on the presence and distribution of microplastics in human fluids, tissues, and organs; (ii) critically evaluate detection technologies and methodological challenges; and (iii) discuss emerging biological and public health implications with exposure reduction in MPs to guide future research and biomonitoring frameworks.

2. Literature Search Strategy and Review Methodology

This review was conducted as a comprehensive narrative review to summarize current evidence regarding the occurrence, detection, distribution, and potential health implications of microplastics (MPs) and nanoplastics (NPs) in human biological systems. A structured literature search was performed using multiple electronic databases, including PubMed, Scopus, Web of Science, Google Scholar, and ScienceDirect.

Relevant peer-reviewed articles published primarily between 2018 and 2026 were identified using combinations of the following keywords and Boolean operators: “microplastics”, “nanoplastics”, “human biomonitoring”, “human tissues”, “human blood”, “placenta”, “breast milk”, “semen”, “urine”, “microplastic toxicity”, “detection technologies”, “FTIR”, “Raman spectroscopy”, “Py-GC/MS”, “oxidative stress”, “reproductive toxicity”, and “public health implications”. Additional articles were identified through manual screening of reference lists from relevant publications.

Studies were considered eligible if they reported the detection, characterization, exposure pathways, analytical methodologies, or toxicological implications of MPs/NPs in human biological matrices, tissues, or organ systems. Both observational human biomonitoring studies and relevant mechanistic or experimental studies were included where appropriate to support toxicological interpretation. Conference abstracts, non-English articles without accessible translations, duplicate reports, and studies lacking sufficient methodological details were excluded.

The collected literature was critically evaluated and thematically organized into major sections including exposure routes, biological distribution, detection technologies, analytical challenges, toxicological implications, and public health concerns. Due to substantial heterogeneity in study design, analytical techniques, particle size reporting, polymer identification methods, and outcome measurements, a quantitative meta-analysis was not performed. Therefore, the findings are presented as a qualitative evidence synthesis intended to provide an updated overview of current knowledge and existing research gaps in the field of human microplastic exposure.

3. Cellular and Molecular Mechanisms Underlying Microplastic-Induced Toxicity

Microplastics (MPs) enter the human body primarily through ingestion, inhalation, and, to a lesser extent, dermal contact. Following oral exposure, MPs pass through the gastrointestinal tract, where smaller particles (<150 µm) may penetrate the intestinal epithelium via endocytosis, paracellular transport, or uptake by microfold (M) cells in Peyer’s patches [29] (Figure 1). Although the cellular internalization pathways shown in Figure 1 are largely derived from experimental studies, similar mechanisms are hypothesized to facilitate microplastic translocation across human intestinal, pulmonary, and placental barriers, ultimately contributing to systemic distribution and organ accumulation.

Nanoplastics can translocate across biological barriers more readily, entering systemic circulation and potentially accumulating in secondary organs such as the liver, kidneys, and spleen [3]. Inhaled MPs may deposit in the respiratory tract, inducing local inflammation and oxidative stress [22,30]. At the cellular level, MPs can trigger the generation of reactive oxygen species (ROS), mitochondrial dysfunction, and activation of pro-inflammatory signaling pathways (e.g., NF-κB) [26,31]. Surface-bound additives, plasticizers, and adsorbed environmental contaminants (e.g., heavy metals, persistent organic pollutants) may further enhance toxicity [7]. Chronic exposure has been associated with epithelial barrier disruption, dysbiosis of gut microbiota, immune dysregulation, and low-grade systemic inflammation [28]. Collectively, these mechanisms contribute to tissue damage and may increase the risk of metabolic, respiratory, and inflammatory disorders.

4. Types of Microplastics Clinically Relevant in Humans

Microplastics (MPs) and nanoplastics (NPs) are ubiquitous environmental contaminants with the potential to enter and accumulate within the human body through multiple exposure pathways [2,32]. This discovery has encouraged more research in the last ten years [33,34,35]. An important issue, however, is that these particles are of great variety, with various compositions, shapes, and sizes. Because of such diversity, it is not simple to identify their effects on human health [24,25,26]. When MPs and NPs are extracted from human tissues, the researchers identify particles of a wide variety of origins and different natures. Consequently, it has proved to be very hard to correlate some of the properties of these particles to the effects that they produce in the body [24,25,26]. From the toxicological perspective, such heterogeneity makes it difficult to coherently state what the most damaging particle features are to humans.

4.1. Polymer Types: The Material of Concern

The polymers occurring in the human tissues show a curious pattern. What researchers discover within us is almost what industries create most [31,36,37]. The most common ones are polyethylene, polypropylene, and polyethylene terephthalate. People use these plastics daily in textiles, bottles, and packaging [22,38] (

Table 1. Characteristics of major polymer types identified in human biota.

Polymer Type	Common Sources	Detected in Humans	Clinical Concerns	References
Polyethylene (PE)	Food packaging (films, bags), disposable plastics, bottles	Blood, placenta, feces, lung, liver, arterial plaque, colon	Inflammation, oxidative stress, carrier for additives; component of atherosclerotic plaques; potential for tissue accumulation	[15,22,39]
Polypropylene (PP)	Food containers, bottle caps, textiles, furniture	Blood, placenta, feces, lung, arterial plaque, colon	Endocrine disruption (potential), inflammation; high prevalence in the GI tract; component of atherosclerotic plaques	[40,41,42]
Polyethylene Terephthalate (PET)	Beverage bottles, synthetic fibers (clothing), food packaging	Blood, placenta, feces, lung, arterial plaque	Fibrous forms in lungs, potential respiratory irritation; component of atherosclerotic plaques; systemic circulation	[15,22,39]
Polystyrene (PS)	Disposable cutlery, food containers, insulation	Blood, feces, placenta, brain (animal models)	Cytotoxicity, oxidative stress, neurotoxicity (especially NPs); potential for blood–brain barrier crossing	[22,43,44,45,46]
Polyvinyl Chloride (PVC)	Pipes, flooring, cling film, and medical devices	Arterial plaque, feces	Leaching of plasticizers (e.g., phthalates) with endocrine-disrupting effects; component of atherosclerotic plaques	[15,47,48,49]
Polyamide	Synthetic fibers (clothing, carpets), fishing nets	Feces, lung	Fibrous forms, potential for respiratory and gastrointestinal accumulation	[22]
Alkyd Resin	Paints, coatings, varnishes	Human vein tissue	Detected in blood vessels; origin and clinical significance are still emerging	[23,50]

). Additionally, human samples also contain other types of plastics, such as polystyrene, polyvinyl chloride, polyamide, and even less well-known types of plastics, such as alkyd resins [23,38].

This diversity presents a problem to the toxicologists since every polymer contains a unique chemical composition and additives. Therefore, all of them may have varying effects on our bodies. The presence of PE and PET in human blood indicates that they are circulated throughout the body and can reach any organs [22]. This is of increasing concern with polystyrene, which has been demonstrated to accelerate atherosclerotic plaque development in mice and has been detected in human arterial plaques. It implies the existence of cardiovascular risks that cannot be overlooked [11,38]. Notably, it is still not clear why PE and PET are found more in human tissues. This may be because people are exposed to them more, they stay longer in the body, or our current tests cannot detect other types well.

4.2. Physical Form and Biological Interactions

The shape of MPs and NPs is a factor that contributes significantly to their behavior in the body, similar to their chemical composition. In human samples, these particles occur in diverse shapes, including irregular fragments, long and narrow fibers, round smooth spheres, and thin sheets (

Table 2. Morphological features of microplastics and nanoplastics and their observed role in human tissue interaction.

Shape	Typical Origin	Size Range (μm/nm)	Detected in Humans	Biological Interactions/Effects	References
Fragments	Mechanical degradation of larger plastic items (e.g., packaging)	Varied, often irregular (µm to mm)	Blood, feces, lung, liver, arterial plaque, placenta	Physical obstruction, inflammatory responses, carrier for adsorbed chemicals, tissue accumulation	[15,23,39]
Fibers	Abrasion of synthetic textiles (clothing, carpets), fishing gear	Typically elongated (10–100 of µm in length)	Lung, blood, feces, placenta	Respiratory irritation, physical entanglement, transport through airways, potential for inflammatory lung disease	[22,23]
Spherules	Primary microplastics (cosmetics, industrial abrasives) or secondary fragmentation	Generally uniform (µm to sub-µm)	Feces, placenta	Cellular uptake, oxidative stress (especially NPs), and less physical abrasion than irregular shapes	[22]
Films/Sheets	Breakdown of plastic films (e.g., packaging, bags)	Thin, sheet-like (µm thickness, variable area)	Feces	Gastrointestinal irritation, surface area for chemical leaching, is less studied in human tissues directly

). A large percentage of the particles that are present in human samples consist of fragments, which, in general, are the result of the degradation of larger plastic objects [23]. The synthetic fibers that are discharged from clothing and textiles are often located in respiratory tissues and in the lungs. Conversely, spherical microbeads commonly used in cosmetics are less frequently detected in the human body [23]. Such variations in shape and origin largely determine particle interactions with biological systems [51,52]. The prevalence of irregular shapes (e.g., 90% irregular in human vein samples) implies that mechanical fragmentation is one of the main processes leading to human internal microplastic load [23]. The shape of these particles is also likely to influence their adhesion to tissues, their migration in the body, and potentially their harmful nature [53,54]. Nevertheless, the number of studies that compare various shapes of particles in human tissues is very limited.

4.3. Size Distribution: The Nano-Dimension of Concern

The size of the particles is an important factor in MPs and NPs risks [55]. Normally, MPs fall under the size of 5 mm, whereas NPs are significantly smaller and can be <1 µm [56,57]. The significance of this size disparity is that smaller particles, particularly those smaller than 1.5 μm, are more apt to be absorbed by the organism and be able to penetrate biological barriers [58]. Significantly, NPs have the ability to cross the cell membranes, the placental barrier, and even the blood–brain barrier [36,59] (

Table 3. Size-dependent distribution and pathophysiological implications of microplastics and nanoplastics in human systems.

Size Category	Description	Ability to Cross Biological Barriers	Primary Human Accumulation Sites	Hypothesized Pathophysiological Effects	References
Large MPs (>100 µm)	Visible fragments	Limited crossing of intact barriers; primarily confined to the GI/respiratory tract	Gastrointestinal tract, upper respiratory tract, lungs, feces	Physical obstruction, localized inflammation, expulsion	[2,60]
Small MPs (1–100 μm)	Most commonly ingested or inhaled	Limited crossing of intact barriers; some uptake via M-cells or damaged epithelia	Gastrointestinal tract, lung tissue (deeper regions), feces, arterial plaque	Localized inflammation, macrophage uptake, potential for chronic irritation, and early-stage plaque formation	[2,15]
Nanoplastics (<1 μm)	Extremely small MPs	Enhanced crossing of most biological barriers (gut, lung, BBB, placenta, cell membranes)	Blood, liver, spleen, kidney, heart, brain, placenta, fetal tissues, cellular cytoplasm	Systemic inflammation, oxidative stress, cytotoxicity, genotoxicity, neurotoxicity, and developmental toxicity	[36,43,45,61]

).

This can be supported by the experiments that indicate that when small particles, such as 0.293 μm of polystyrene, are ingested, they reach the brain very quickly, but larger ones, such as 1.14 μm or 9.55 μm, do not [45]. Smaller particles appear to be rather perilous as they are able to move more easily within the body and access vulnerable organs. Nevertheless, we have only limited information on their distribution and their impacts on the human body since it is difficult to detect and trace these small particles.

4.4. Common Sources of MPs in Daily Life

Microplastics originating from routine daily activities represent an important and often overlooked source of environmental contamination [2,4]. A wide range of household, personal care, food-related, transportation, and agricultural products contribute to the continuous release of primary and secondary microplastic particles into surrounding ecosystems (Figure 2). Household sources include synthetic textiles that shed microfibers during washing, carpets and upholstery materials, plastic cutting boards, and non-stick cookware coated with polytetrafluoroethylene (PTFE) [36,55]. Indoor dust also serves as a reservoir of accumulated microplastic fibers [36]. Personal care and hygiene products such as exfoliating scrubs, toothpaste, wet wipes, sanitary products, and disposable face masks contribute additional synthetic fibers and polymer particles [5,22].

Food-related sources include plastic packaging, bottled water containers, takeaway boxes, plastic tea bags, and food storage containers, particularly when exposed to elevated temperatures [7]. Transportation-associated inputs arise primarily from vehicle tire wear and abrasion of synthetic shoe soles [24]. Moreover, paint flakes from household surfaces and road markings, cigarette filters composed of cellulose acetate, agricultural plastic films, and detergent pod films represent additional contributors [24,26]. Collectively, these sources facilitate the continuous introduction of microplastics into air, water, and soil through mechanical abrasion, thermal degradation, environmental weathering, and improper waste disposal, underscoring the pervasive nature of microplastic exposure in everyday life [29,36,55].

5. Exposure Routes of Microplastics and Nanoplastics into the Human Body

Plastic pollution surrounds us, and therefore we are subjected to MPs and NPs all the time. The sources and causes of this exposure are numerous. The exposure mode is useful in determining the health effects. However, it is difficult to identify the toxicodynamics (how particles affect the body) and toxic dynamics (how the body handles particles) properly.

5.1. Ingestion: The Pervasive Dietary Pathway

A route of human exposure to MPs and NPs is ingestion, which is highly frequent and common (Figure 3). In the last 10 years, these particles have been identified in various food and drinking water sources in great numbers. The contamination is almost inevitable, and MPs are found in bottled water, tap water, sea salt, seafood, fruits, vegetables, beer, and other drinks [62,63,64,65,66]. Humans are estimated to consume tens of thousands to millions of particles annually, and bottled water is one of the important sources [36,39]. In particular, an adult can consume approximately 5.1 × 10³ particles from table salt and up to 4.1 × 10⁴ particles from drinking water per year [39]. The problem is also not limited to direct contamination because the MPs in the soil and irrigation water can be absorbed by plants and transferred to humans through food [67].

After being swallowed, the gastrointestinal tract is the primary site of interaction of particles with tissues (Figure 3). Larger particles (more than 10 mm) are usually blocked by the gut epithelium [68] but smaller MPs and NPs can more easily get through this barrier. The particles could be taken up by endocytosis via intestinal cells, by tight junction (when very small NPs), or by M-cells in Peyer’s patches [58,68]. This process depends on the size of the particles, their charge on the surface, their hydrophobicity, and protein corona formation [68]. Also, the exposure to NPs may modify the gut microbiome, weaken the gut barrier, and result in dysbiosis, which in turn may result in even greater particle permeation and cause adverse health outcomes [2,69].

5.2. Inhalation: An Unavoidable Atmospheric Burden

Another significant and the most common path of exposure to MPs and NPs is inhalation because they are present in the indoor and outdoor air. They are the products of multiple sources, e.g., the destruction of outdoor plastics, the wearing of tires of cars, the shedding of indoor textiles and furniture [70,71]. Indeed, the concentrations of MPs in indoor air are often higher as compared to outdoor air [70]. The destiny of these particles after inhalation is dependent on their size. The larger particles settle in the nose and throat, whereas smaller ones, such as those of the PM2.5 range, can be transported to the deeper areas of the lungs, such as bronchioles and alveoli [23,72]. Ultrafine particles (PM0.1), the ones that are similar to NPs, can even enter directly into the bloodstream across the lungs [2]. The evidence about the presence of MPs in human lung tissue increases, and their inhalation may cause lung inflammation [23,73]. Interestingly, the particles trapped in the upper respiratory tract might be removed by the mucus or sneezing as well as coughing, and may be later swallowed as part of the consumed amount [60]. The problem lies in the fact that it is difficult to distinguish the effect of environmental exposure and internal accumulation and entirely comprehend the long-term impact of chronic inhalation on respiratory and general health.

5.3. Dermal Exposure: An Emerging Frontier

MPs and NPs are also being considered as important to dermal exposure, as they were previously regarded as less significant than ingestion and inhalation. The skin, as the largest organ and a powerful shield, may still be exposed to such particles in such products as cosmetics, fabrics, and contaminated water [74,75]. Although the skin on the outside is typically the protective barrier, the particles still find their way through. MPs and NPs have access to the body through the ducts of sweat, hair follicles, or broken skin [75,76]. It is shown that particles less than 40 nm can pass through the skin barrier, and polystyrene particles up to 200 nm have been detected in the dermis [75,76]. Nonetheless, the extent to which these particles penetrate the body through the skin, and not through other exposures such as ingestion and inhalation, remains unclear, and further studies are required.

5.4. Translocation Mechanisms and Systemic Distribution

After MPs and NPs get into the body, these particles can travel throughout the body and reach different organs and tissues [43,77]. The emigration of these particles through the different barriers of the body depends on several factors, such as size, shape, surface charge, and hydrophobicity [2,68].

Once these particles are absorbed by the gastrointestinal system, they may be absorbed into the lymphatic system or blood. The inhaled exceptionally small particles can also penetrate the alveolar–capillary barrier in the lungs [2]. When they enter the bloodstream, MPs and NPs interact with plasma proteins, forming a protein corona that influences their distribution and cellular uptake [78]. Such particles may be deposited in different organs, including the liver, spleen, kidney, and heart. This widespread distribution poses a potential health hazard that may impact almost any organ system [15,61,79]. They can also pass some selective barriers, mainly the blood–brain barrier and the placental barrier [43,61,80]. When these particles pass the placental barrier, this causes maternal–fetal transfer, which is particularly alarming. But the mechanism of their long-term retention, excretion, and effect is intricate. These processes are still under research in order to know more about them.

6. Current Evidence of Microplastics in Human Body Fluids

Recent biomonitoring studies provide compelling evidence that microplastics (MPs) circulate in multiple human body fluids, indicating systemic exposure (Table 4). The first landmark detection of plastics in human blood was reported by Leslie et al. [5] in the Netherlands, identifying PET, PE, PS, PP, and PMMA in 77% (17/22) of participants using Py–GC/MS, with particle sizes ≥ 700 nm. PET was dominant, suggesting widespread exposure from packaging materials. More recent studies from Korea and the UK reported MPs in 88.9% (32/36) and 90% (18/20) of blood samples, respectively, mainly PS, PP, and PE [8,9]. In China, LD-IR and SEM analyses identified particles ranging from submicron to 184 µm in perioperative blood and cardiac tissues [10], reinforcing bloodstream contamination. Notably, MPs in carotid plaques were associated with a 4.5-fold increased risk of cardiovascular events [11], suggesting clinical relevance.

Breast milk contamination was first reported in Italy, where Ragusa et al. [6] detected PE, PP, PVC, and PS (2–12 µm) in 26/34 samples via μ-Raman spectroscopy. Subsequent Chinese studies identified up to 16 polymer types (>20 µm), including PA and PU [15], indicating maternal transfer likely via dietary ingestion and inhalation followed by systemic circulation. Given infant gut immaturity and developing immunity, early-life exposure may influence microbiota composition and inflammatory programming.

Emerging reproductive evidence shows MPs in semen across China, Italy, Spain, Turkey, and the USA. Detection rates range from 60 to 100%, with PS, PE, PVC, PET, and PP predominant [18,77]. Particle sizes vary from 0.72 to 286 µm. Associations with reduced sperm motility, oxidative stress, and blood–testis barrier disruption are supported by both human observations and animal models. Urine and kidney deposition studies from Italy reported PE and PS (1–29 µm), confirming renal filtration and excretion pathways [81]. Saliva and sputum analyses reveal PE, PET, PU, and PS, indicating inhalational and oral retention routes [82,83]. Collectively, these findings demonstrate multi-route exposure and systemic distribution of MPs in human fluids.

Table 4. Distribution and characteristics of microplastics identified in human body fluids.

Sample Type	Country	Published Year	No. of Positive Samples	MPs Types	Particle Size	Detection Method	References
Blood	Italy	2024	181	PE, PVC	N/A	Py–GC/MS	[11]
Blood	Netherlands	2022	16	PET, PS, PE, PMMA and PP	≥0.7 μm	Py-GC/MS	[5]
Blood	China	2023	15	PET, PU, PS, PA, PVC, PE, PP, PC, PMMA	184 μm	LD-IR and SEM	[10]
Blood	UK	2024	18	PE, EPDM, EVA, EVOH, PA	5 µm–800 µm	μ-FTIR spectroscopy	[9]
Blood	Korea	2024	32	PS, PP	N/A	μ-FTIR	[8]
Umbilical Vein Blood	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Amniotic Fluid	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Fetal Cord Blood	China	2024	9	PP, PE, PS, PVC	100–400 μm	Micro-Raman spectroscopy	[14]
Breast milk	Italy	2022	26	PP, PVC, PE, PS, PES, and PEMA	2~12 μm	μ-Raman	[6]
Breast milk	China	2023	7	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PB, PMMA, PLA, PS	>20 μm	LD-IR	[15]
Breast milk	Poland	2025	N/A	PE, PS	N/A	Raman spectroscopy, FTIR	[16]
Breast milk	Thailand	2024	23	PP, PE, PS, PVC	N/A	Raman micro spectroscopy	[84]
Semen	China	2025, 2023, 2025	11	PVC, PE, PA, PS, PP and PET	21.76–286.71 μm	LD-IR and Py-GC/MS	[17,18,85]
Semen	Italy	2023, 2023, 2025	6	PP, PS, PET, PVS, PC, POM, Acrylic	2–5 μm	Raman microspectroscopy	[3,86,87]
Semen	China	2024	40	PS, PE, PVC, PP, PET, PA, PU, PC	0.72–7.02 μm	Raman microspectroscopy	[77]
Semen	China	2026, 2025	34	PET, BR, CPE	20.3–189.7 μm	LD-IR	[88,89]
Semen	Spain	2025	24	PA, PTFE, PE, PU, PP, PET, PS, PVC, PLA	N/A	LD-IR	[90]
Semen	China	2025	51	PE, PVC	N/A	Py-GC/MS	[91]
Semen	Turkey	2025	82	Fiber-type	≥30 µm	Light microscopy following (KOH) digestion	[92]
Semen	Italy	2021	N/A	BPA, phthalates	0.1 µm to 5 mm	Raman microspectroscopy	[19]
Semen	USA	2024, 2024	23	PVC, PET, PE, PVC, N66, N6, SBR, PU, PP, ABS, PMMA, PET, PC, PS	N/A	Py-GC/MS	[93,94]
Semen	China	2022	N/A	PS, PVC, PA66, PMMA	N/A	Py-GC/MS	[95]
Semen	China	2024	N/A	PS	<5000 μm	N/A	[96]
Urine	Italy	2024	10	PE, PS	3–13 μm	Micro-Raman spectroscopy	[81]
Urine	Italy	2022	4	PVA, PVC, PP, and PE MPs	4~15 μm	μ-Raman	[97]
Sputum	China	2022	22	PU, PES	>500 μm	μ-FTIR	[83]
Saliva	Iran	2025	2000	PE, PET, PS, PVC	100–500 μm	N/A	[82]
Maternal amniotic fluid	China	2025, 2021	25	PE and PP	20–100 μm	LD-IR, spectroscopic analysis	[98,99]
CSF	China	2025, 2024	28	PS, PE, PP, PVC	N/A	Microscopic spectroscopy	[100,101]
CSF	China	2025	32	PP, PVC, PE, PS	0.001–5000 μm	N/A	[102]
BALF	Iran	2025	30	PE, PS, PP, PET	20–500 μm	μ-Raman	[103]
BALF	Turkey	2025, 2024	10	PA, PET, PVC, PU	4.19 μm–792.00 μm	μ-Raman spectroscopy	[104,105]
Plural fluid	Iran	2025	2	PE, PP, PET, N-6 PS, PMMA/acrylic, rubber, polyester, FEP, PFA PPTA/Kevlar, SBS, PVA, PS, PVP, PU, SAN, ABS, cellulose (dyed) cotton, CA	<100 μm	Micro-Raman and SEM/EDS analysis	[106]

Footnotes: x: No. of sample positive, N: No. of sample tested; Bronchoalveolar Lavage Fluid (BALF).

Table 4. Distribution and characteristics of microplastics identified in human body fluids.

Sample Type	Country	Published Year	No. of Positive Samples	MPs Types	Particle Size	Detection Method	References
Blood	Italy	2024	181	PE, PVC	N/A	Py–GC/MS	[11]
Blood	Netherlands	2022	16	PET, PS, PE, PMMA and PP	≥0.7 μm	Py-GC/MS	[5]
Blood	China	2023	15	PET, PU, PS, PA, PVC, PE, PP, PC, PMMA	184 μm	LD-IR and SEM	[10]
Blood	UK	2024	18	PE, EPDM, EVA, EVOH, PA	5 µm–800 µm	μ-FTIR spectroscopy	[9]
Blood	Korea	2024	32	PS, PP	N/A	μ-FTIR	[8]
Umbilical Vein Blood	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Amniotic Fluid	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Fetal Cord Blood	China	2024	9	PP, PE, PS, PVC	100–400 μm	Micro-Raman spectroscopy	[14]
Breast milk	Italy	2022	26	PP, PVC, PE, PS, PES, and PEMA	2~12 μm	μ-Raman	[6]
Breast milk	China	2023	7	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PB, PMMA, PLA, PS	>20 μm	LD-IR	[15]
Breast milk	Poland	2025	N/A	PE, PS	N/A	Raman spectroscopy, FTIR	[16]
Breast milk	Thailand	2024	23	PP, PE, PS, PVC	N/A	Raman micro spectroscopy	[84]
Semen	China	2025, 2023, 2025	11	PVC, PE, PA, PS, PP and PET	21.76–286.71 μm	LD-IR and Py-GC/MS	[17,18,85]
Semen	Italy	2023, 2023, 2025	6	PP, PS, PET, PVS, PC, POM, Acrylic	2–5 μm	Raman microspectroscopy	[3,86,87]
Semen	China	2024	40	PS, PE, PVC, PP, PET, PA, PU, PC	0.72–7.02 μm	Raman microspectroscopy	[77]
Semen	China	2026, 2025	34	PET, BR, CPE	20.3–189.7 μm	LD-IR	[88,89]
Semen	Spain	2025	24	PA, PTFE, PE, PU, PP, PET, PS, PVC, PLA	N/A	LD-IR	[90]
Semen	China	2025	51	PE, PVC	N/A	Py-GC/MS	[91]
Semen	Turkey	2025	82	Fiber-type	≥30 µm	Light microscopy following (KOH) digestion	[92]
Semen	Italy	2021	N/A	BPA, phthalates	0.1 µm to 5 mm	Raman microspectroscopy	[19]
Semen	USA	2024, 2024	23	PVC, PET, PE, PVC, N66, N6, SBR, PU, PP, ABS, PMMA, PET, PC, PS	N/A	Py-GC/MS	[93,94]
Semen	China	2022	N/A	PS, PVC, PA66, PMMA	N/A	Py-GC/MS	[95]
Semen	China	2024	N/A	PS	<5000 μm	N/A	[96]
Urine	Italy	2024	10	PE, PS	3–13 μm	Micro-Raman spectroscopy	[81]
Urine	Italy	2022	4	PVA, PVC, PP, and PE MPs	4~15 μm	μ-Raman	[97]
Sputum	China	2022	22	PU, PES	>500 μm	μ-FTIR	[83]
Saliva	Iran	2025	2000	PE, PET, PS, PVC	100–500 μm	N/A	[82]
Maternal amniotic fluid	China	2025, 2021	25	PE and PP	20–100 μm	LD-IR, spectroscopic analysis	[98,99]
CSF	China	2025, 2024	28	PS, PE, PP, PVC	N/A	Microscopic spectroscopy	[100,101]
CSF	China	2025	32	PP, PVC, PE, PS	0.001–5000 μm	N/A	[102]
BALF	Iran	2025	30	PE, PS, PP, PET	20–500 μm	μ-Raman	[103]
BALF	Turkey	2025, 2024	10	PA, PET, PVC, PU	4.19 μm–792.00 μm	μ-Raman spectroscopy	[104,105]
Plural fluid	Iran	2025	2	PE, PP, PET, N-6 PS, PMMA/acrylic, rubber, polyester, FEP, PFA PPTA/Kevlar, SBS, PVA, PS, PVP, PU, SAN, ABS, cellulose (dyed) cotton, CA	<100 μm	Micro-Raman and SEM/EDS analysis	[106]

Footnotes: x: No. of sample positive, N: No. of sample tested; Bronchoalveolar Lavage Fluid (BALF).

7. Evidence of Microplastics in Human Tissues and Organs

Accumulating evidence confirms that MPs not only circulate in fluids but also accumulate in vital organs. The first report of placental MPs by Braun et al. [107] and Ragusa et al. [6] demonstrated PE, PP, PS, and PVC (5–10 µm) in maternal and fetal placental sides, indicating transplacental transfer. More recent quantitative analysis in the USA detected MPs in 100% (62/62) of placentas, with concentrations ranging from 6.5 to 685 µg/g (mean 126.8 µg/g), predominantly PE localized at the maternal–fetal interface [28]. Umbilical cord and fetal membrane studies further confirm intrauterine exposure [13]. Potential mechanisms include trophoblastic endocytosis and paracellular diffusion, raising concerns regarding fetal immune and developmental programming (Table 5).

Pulmonary deposition is well documented. MPs were found in 11 lung samples in the UK [108] and 13 in Brazil, with particle sizes as small as 1.6 µm [109]. Ground-glass nodules have been preliminarily associated with MP accumulation [110], supporting inhalational entry and deep airway retention.

Liver and kidney studies reveal selective accumulation. Horvatits et al. [111] detected PS, PVC, and PET (4–30 µm) in cirrhotic but not normal livers, indicating a potential association with cardiovascular pathology that requires validation in larger longitudinal studies. Kidney analyses in Italy and China confirmed PE and PVC deposition, up to 293 particles detected per tissue [81,112] (Table 5).

Gastrointestinal tissues consistently show MP retention. Chinese intestinal studies reported 7.9–9.45 particles/g (PVC-dominant) in both small and large intestines [7]. MPs may disrupt gut microbiota and increase intestinal permeability, potentially contributing to inflammatory bowel disease.

Cardiovascular accumulation has been observed in thrombi and atherosclerotic plaques, with concentrations up to 156.5 µg/g in coronary plaques [113] and associations with HDL-C alterations [114]. MPs may infiltrate vascular walls via endothelial dysfunction or immune-cell transport (Table 6).

Recent studies detected MPs and nanoplastics in human brain tissues, including samples from individuals with dementia; however, the clinical significance of these findings remains uncertain and requires further investigation [78,83]. Olfactory bulb detection supports inhalational translocation [84]. Animal models demonstrate blood–brain barrier penetration, neuro-inflammation, and oxidative stress, highlighting potential neurodegenerative implications [115].

Table 5. Current evidence of microplastics in human organs and tissues.

Sample Type	Country	Published Year	No. of Positive Samples	MPs Types	Particle Size	Detection Method	References
Placenta	Germany	2021	N/A	PE, PP, PS, PE, PET, PVK, PC	5 to 10 μm	Raman microspectroscopy	[106]
Placenta	Italy	2022	4	PP with some other non-identify fragments	5 to 10 μm	μRaman	[6]
Placenta	China	2023	17	PSF. Mainly PVC (43.27%), PP (14.55%), PBS (10.90%)	20–307.29 μm	LD-IR	[12]
Placenta	China	2023	18	PU, PA, PE, PET, PC	20–500 μm	LD-IR	[15]
Placenta	USA	2024	62	PE, PVC, Nylon, Rayon, PS	>1 μm	Py-GC-MS, ATR-FTIR, fluorescence microscopy	[28]
Prostate tissue	China	2021, 2025	22	PA, PET, PVC, PS, PP, PE	20 to 100 μm	Py-GC/MS, LD-IR, SEM	[20,116]
Penile cancerous tissue	China	2025	29	PE, PP, PVC, PA	20–50 µm	LD-IR, spectroscopy	[117]
Penile tissue	USA	2024	4	PET, PP, PMMA	2 μm to 500 μm	LD-IR, SEM	[118]
Lungs	UK	2022	11	PP, PET, resin	N/A	μ-FTIR	[107]
Lung tissue	Brazil	2021	13	PP, PE, cotton, PVC, CA, PA, PS, PU	1.6–16.8 μm	N/A	[108]
Lung granule nodules	China	2022	100	Cotton, PA, PE, denim, phenoxy resin	>20 μm	μ-FTIR	[109]
Liver	Germany	2022	17	PS, PVC, PET, PMMA, POM, and PP	4 to 30 μm	μ-Raman	[110]
Small intestine	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
Large intestine	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
GI tissue	Italy	2025	N/A	PE, PP, PS, PVC	N/A	FTIR, Raman, Py-GC/MS	[119]
Tonsil	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
Thymus	China	2024	24	PS	5 μm	Fluorescence microscopy	[120]
Integumentary system (face skin)	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Integumentary system (hand skin)	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Integumentary system	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Cardiovascular system	China	2023	15	PET, PU, PS, PA, PVC, PE, PP, PC, PMMA	184 μm	LD-IR and SEM	[10]
Cardiovascular system	China	2022	24	LDPE, pigment, chromium oxide, phthalocyanine	2.1–26.0 μm	Raman spectrometer	[39]
Cardiovascular system	United Kingdom	2023	4	AR, PVP, nylon-EVA, nylon-EVA TL	16–1074 μm	μ-FTIR spectroscopy	[23]
Testes	China	2023	4	PS, PVC, PE, and PP	20~100 μm	LD-IR and Py-GC/MS	[18]
Kidney	Italy	2024	10	PE, PS	1 to 29 μm	Micro-Raman spectroscopy	[81]
Kidney	China	2025	28	PE, PVC	20–500 µm	Py-GC/MS, LD-IR, SEM	[111]
Kidney	Brazil	2024	N/A	PE, PP, PS, PVC	0.001–5000 μm	FTIR, Raman, LD-IR, Py-GC/MS, and SEM	[122]
Renal carcinoma tissue	China	2025	N/A	PE, PVC, FKM	N/A	Py-GC/MS, LDIR, SEM	[21]
Brain	USA	2025	20	PE, PP, PVC, SBR, ABS, PET, N-6, N-66, PMMA, PU, PC, PS	Largely 100–200 nm in length and <40 nm in width	Py-GC/MSATR-FTIR spectroscopy; SEM with EDS; TEM; polarization wave microscopy	[79]
Brain	Turkey	2025	N/A	PE, PP, PVC, styrene-butadiene rubber	N/A	Py-GC/MS, ATR-FTIR Spectroscopy, EDS	[113]
Brain (olfactory bulb)	Brazil	2025, 2021	8	Polypropylene	5.5–26 μm	Micro-Fourier transform infrared spectroscopy	[60,108]
Bones	China	2025	8	PP, PET, PCEVA, PS, PU	138.9 ± 105.7 µm	Raman microspectroscopy	[34]
Bone marrow	China	2024	16	PE, PS, PVC, PA66, PP	<100 μm	Py-GC/MS, LD-IR, SEM	[123]
Carotid plaque (tissue)	China	2025	20	PP (23.1%), PE (20.3%), SBR (19.8%), PVC (18.5%), PS (5.7%), ABS, PET, PMMA, PC, PA6, PA66, PU (<5% each)	N/A	Py-GC/MS	[112]
Umbilical cord	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Ovarian and reproductive tissues	Slovakia	2026	N/A	PS, PE, PP	MPs (1 µm–5 mm), NPs (<1 µm)	FTIR, Raman spectroscopy, SEM	[124]
Uterus (endometrium)	China	2025, 2024	22	PA, PU, PET, PP, PS, and PE	2 to 200 μm	Raman microspectroscopy	[4,33]

Table 5. Current evidence of microplastics in human organs and tissues.

Sample Type	Country	Published Year	No. of Positive Samples	MPs Types	Particle Size	Detection Method	References
Placenta	Germany	2021	N/A	PE, PP, PS, PE, PET, PVK, PC	5 to 10 μm	Raman microspectroscopy	[106]
Placenta	Italy	2022	4	PP with some other non-identify fragments	5 to 10 μm	μRaman	[6]
Placenta	China	2023	17	PSF. Mainly PVC (43.27%), PP (14.55%), PBS (10.90%)	20–307.29 μm	LD-IR	[12]
Placenta	China	2023	18	PU, PA, PE, PET, PC	20–500 μm	LD-IR	[15]
Placenta	USA	2024	62	PE, PVC, Nylon, Rayon, PS	>1 μm	Py-GC-MS, ATR-FTIR, fluorescence microscopy	[28]
Prostate tissue	China	2021, 2025	22	PA, PET, PVC, PS, PP, PE	20 to 100 μm	Py-GC/MS, LD-IR, SEM	[20,116]
Penile cancerous tissue	China	2025	29	PE, PP, PVC, PA	20–50 µm	LD-IR, spectroscopy	[117]
Penile tissue	USA	2024	4	PET, PP, PMMA	2 μm to 500 μm	LD-IR, SEM	[118]
Lungs	UK	2022	11	PP, PET, resin	N/A	μ-FTIR	[107]
Lung tissue	Brazil	2021	13	PP, PE, cotton, PVC, CA, PA, PS, PU	1.6–16.8 μm	N/A	[108]
Lung granule nodules	China	2022	100	Cotton, PA, PE, denim, phenoxy resin	>20 μm	μ-FTIR	[109]
Liver	Germany	2022	17	PS, PVC, PET, PMMA, POM, and PP	4 to 30 μm	μ-Raman	[110]
Small intestine	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
Large intestine	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
GI tissue	Italy	2025	N/A	PE, PP, PS, PVC	N/A	FTIR, Raman, Py-GC/MS	[119]
Tonsil	China	2024	6	PVC-dominant; also identified: PE, PP, PS, PET, PA	20–100 μm	LD-IR spectroscopy	[7]
Thymus	China	2024	24	PS	5 μm	Fluorescence microscopy	[120]
Integumentary system (face skin)	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Integumentary system (hand skin)	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Integumentary system	Iran	2021	2000	PE, PET, PS, PVC	100–500 μm	N/A	[121]
Cardiovascular system	China	2023	15	PET, PU, PS, PA, PVC, PE, PP, PC, PMMA	184 μm	LD-IR and SEM	[10]
Cardiovascular system	China	2022	24	LDPE, pigment, chromium oxide, phthalocyanine	2.1–26.0 μm	Raman spectrometer	[39]
Cardiovascular system	United Kingdom	2023	4	AR, PVP, nylon-EVA, nylon-EVA TL	16–1074 μm	μ-FTIR spectroscopy	[23]
Testes	China	2023	4	PS, PVC, PE, and PP	20~100 μm	LD-IR and Py-GC/MS	[18]
Kidney	Italy	2024	10	PE, PS	1 to 29 μm	Micro-Raman spectroscopy	[81]
Kidney	China	2025	28	PE, PVC	20–500 µm	Py-GC/MS, LD-IR, SEM	[111]
Kidney	Brazil	2024	N/A	PE, PP, PS, PVC	0.001–5000 μm	FTIR, Raman, LD-IR, Py-GC/MS, and SEM	[122]
Renal carcinoma tissue	China	2025	N/A	PE, PVC, FKM	N/A	Py-GC/MS, LDIR, SEM	[21]
Brain	USA	2025	20	PE, PP, PVC, SBR, ABS, PET, N-6, N-66, PMMA, PU, PC, PS	Largely 100–200 nm in length and <40 nm in width	Py-GC/MSATR-FTIR spectroscopy; SEM with EDS; TEM; polarization wave microscopy	[79]
Brain	Turkey	2025	N/A	PE, PP, PVC, styrene-butadiene rubber	N/A	Py-GC/MS, ATR-FTIR Spectroscopy, EDS	[113]
Brain (olfactory bulb)	Brazil	2025, 2021	8	Polypropylene	5.5–26 μm	Micro-Fourier transform infrared spectroscopy	[60,108]
Bones	China	2025	8	PP, PET, PCEVA, PS, PU	138.9 ± 105.7 µm	Raman microspectroscopy	[34]
Bone marrow	China	2024	16	PE, PS, PVC, PA66, PP	<100 μm	Py-GC/MS, LD-IR, SEM	[123]
Carotid plaque (tissue)	China	2025	20	PP (23.1%), PE (20.3%), SBR (19.8%), PVC (18.5%), PS (5.7%), ABS, PET, PMMA, PC, PA6, PA66, PU (<5% each)	N/A	Py-GC/MS	[112]
Umbilical cord	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]
Ovarian and reproductive tissues	Slovakia	2026	N/A	PS, PE, PP	MPs (1 µm–5 mm), NPs (<1 µm)	FTIR, Raman spectroscopy, SEM	[124]
Uterus (endometrium)	China	2025, 2024	22	PA, PU, PET, PP, PS, and PE	2 to 200 μm	Raman microspectroscopy	[4,33]

Table 6. Current evidence of microplastics in human biological samples.

Sample Type	Country	Published Year	No. of Positive	MPs Types	Particle Size	Detection Method	References
Meconium	Germany	2024	2	PE, PP, PS	>50 μm	FTIR	[73,107]
Meconium	China	2021	3	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PS, PMMA, PLA, PS	>20 μm	LD-IR	[15]
Meconium	China	2024	9	PP, PE, PS, PVC, PET	100–400 μm	Micro-Raman spectroscopy	[14]
Infant feces	China	2023	12	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PS, PMMA, PLA, PS, PB	>20 μm	LD-IR	[15]
Feces	Austria	2023, 2019	8	PP, PET, PS, PE, POM, PC, PA, PVC, PU	50–500 μm	FTIR	[86,125]
Feces	Hong Kong, China	2022	8	PS, PP, PE, PET, PVC	40.2–4812.9 μm	FTIR	[126]
Feces	China	2021	27	PET, PA, PP, PE, PC, PVC, POM, PTFE, EVA, PS, PMMA, PBT, AS, PET, TPU	4.4–333.2 μm	Raman spectroscopy	[127]
Feces	China	2021	25	PET, PA, PP, PE, PC, PVC, POM, PTFE, EVA, PS, PMMA, PBT, AS, PET, TPU	1.7–393.8 μm	Raman spectroscopy	[127]
Feces	Indonesia	2021	11	HDPE, LDPE, LLDPE, PP, PS, PET	<5000 μm	Raman spectroscopy	[128]
Feces	Indonesia	2021	11	PET, PS, PP, PE, HDPE, LDPE	<5000 μm	Raman spectroscopy	[99]
Fetal membrane	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]

Table 6. Current evidence of microplastics in human biological samples.

Sample Type	Country	Published Year	No. of Positive	MPs Types	Particle Size	Detection Method	References
Meconium	Germany	2024	2	PE, PP, PS	>50 μm	FTIR	[73,107]
Meconium	China	2021	3	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PS, PMMA, PLA, PS	>20 μm	LD-IR	[15]
Meconium	China	2024	9	PP, PE, PS, PVC, PET	100–400 μm	Micro-Raman spectroscopy	[14]
Infant feces	China	2023	12	PA, PU, PE, PET, PP, PVC, POM, EVA, PTFE, CPE, PS, PMMA, PLA, PS, PB	>20 μm	LD-IR	[15]
Feces	Austria	2023, 2019	8	PP, PET, PS, PE, POM, PC, PA, PVC, PU	50–500 μm	FTIR	[86,125]
Feces	Hong Kong, China	2022	8	PS, PP, PE, PET, PVC	40.2–4812.9 μm	FTIR	[126]
Feces	China	2021	27	PET, PA, PP, PE, PC, PVC, POM, PTFE, EVA, PS, PMMA, PBT, AS, PET, TPU	4.4–333.2 μm	Raman spectroscopy	[127]
Feces	China	2021	25	PET, PA, PP, PE, PC, PVC, POM, PTFE, EVA, PS, PMMA, PBT, AS, PET, TPU	1.7–393.8 μm	Raman spectroscopy	[127]
Feces	Indonesia	2021	11	HDPE, LDPE, LLDPE, PP, PS, PET	<5000 μm	Raman spectroscopy	[128]
Feces	Indonesia	2021	11	PET, PS, PP, PE, HDPE, LDPE	<5000 μm	Raman spectroscopy	[99]
Fetal membrane	China	2024	12	PA, PU	>20–100 μm	LD-IR	[13]

8. Detection Technologies for Microplastics in Human

Accurate detection of microplastics (MPs) in human biological matrices requires rigorous pre-analytical control to prevent contamination from airborne fibers and laboratory plastics, as emphasized in blood and placental studies [5,28] (

Table 7. Overview of analytical approaches for the detection of microplastics in human biological matrices.

Method	Principle (Very Short)	Time for Detection	Success Rate in Human Samples	Types of MPs Detected	References
Enzymatic Digestion	Protein/lipid degradation using enzymes (Proteinase-K, lipase)	24–72 h	High preservation of polymer integrity	All polymers (minimal damage)	[5,6,111]
Oxidative Digestion (H2O2/Fenton)	Organic matrix oxidation	12–48 h	Moderate–High; may damage some polymers	PE, PP, PS, PET	[7,108]
Alkaline Digestion (KOH/NaOH)	Tissue dissolution via base hydrolysis	24–48 h	High for soft tissues; may affect PET/PA	Fibers, fragments	[92,97]
Filtration and Density Separation (ZnCl2/NaCl)	Separation based on density differences	4–12 h	High recovery (>70–90%)	Low/high-density polymers	[2,119]
FTIR/μFTIR	Infrared spectral fingerprinting	Minutes/ sample	70–95%; size limit 10–20 µm	PE, PP, PET, PVC, PS	[15,108]
Raman/μRaman	Inelastic light scattering	Minutes/ sample	High; detects particles down to 1 µm	Wide polymer range; nanoplastics possible	[6,7,86]
Pyrolysis–GC/MS	Thermal degradation polymer-specific fragments	1–2 h/sample	Quantitative mass detection (no particle count)	All polymers incl. PET, PMMA	[5,28]
SEM/TEM	Electron imaging of morphology	2–6 h	High morphological resolution	Fibers, fragments, nanoplastics	[10,109]
AFM	Surface topography at nanoscale	1–3 h	High for nanoplastics	<100 nm particles	[36]
Fluorescence (Nile Red)	Hydrophobic dye binding	<2 h	Rapid screening; false positives possible	PE, PP, PS	[2]
AFM-IR	Combines AFM imaging and IR spectroscopy	Experimental	Ultra-high resolution	Nano-sized MPs	[25]
Hyperspectral Imaging	Spectral pixel mapping	Rapid screening	Emerging; high-throughput	Mixed polymer matrices	[26]
NanoSIMS	Isotopic surface mass analysis	Experimental	Ultra-sensitive	Nanoplastics	[61]
Lab-on-chip Sensors	Microfluidic detection platforms	Minutes	Emerging rapid detection	Small MPs/NPs	[25,30]

Foot notes: FTIR, Fourier transform infrared spectroscopy; μFTIR, micro-FTIR; Raman, Raman spectroscopy; Py–GC/MS, Pyrolysis–gas chromatography–mass spectrometry; SEM, scanning electron microscopy; TEM, transmission electron microscopy; AFM, atomic force microscopy; LD-IR, laser direct infrared spectroscopy.

). Sample digestion remains critical for matrix removal, with enzymatic protocols preserving polymer integrity better than oxidative or alkaline treatments, though hydrogen peroxide and KOH digestion are widely used due to efficiency [31,32]. Filtration and density separation further enhance recovery, especially for low-density polymers such as PE and PP [2].

Spectroscopic techniques dominate polymer identification. μFTIR is robust and reproducible but generally limited to particles >10–20 µm [9,15]. In contrast, μRaman offers higher spatial resolution and can detect particles approaching the submicron range, although fluorescence interference remains a technical challenge [5,33]. Thermoanalytical Py–GC/MS provides quantitative polymer mass confirmation and was pivotal in the first blood and placental quantifications, yet it cannot determine particle number or morphology [5,28].

Electron microscopy (SEM/TEM) and AFM allow nanoscale visualization but lack intrinsic polymer specificity unless coupled with spectroscopic methods [10]. Emerging technologies such as AFM-IR, hyperspectral imaging, NanoSIMS, and microfluidic lab-on-chip systems promise improved sensitivity and standardization, which are urgently needed for harmonized human biomonitoring [25,26]. FTIR, Raman spectroscopy, and Py-GC/MS each provide complementary information. FTIR is widely used for polymer identification but is limited by particle size detection thresholds; Raman spectroscopy offers higher spatial resolution but may be affected by fluorescence interference; Py-GC/MS enables quantitative polymer mass determination but cannot provide particle counts or morphology.

9. Analytical Challenges and Standardization Issues

9.1. Lack of Standardized Protocols

The absence of standardized analytical protocols for analyzing bio-samples is one such challenge in the research of microplastics. This is due to varied digestion, filtering, and methodologies, which are making it difficult to compare data. Although ISO 24187:2023 sets a framework, it does not provide protocols for complicated materials such as blood or tissue, which reduces reproducibility [129,130]. Moreover, identification and quantification reliability are also influenced by some inconsistent criteria in the digestion and extraction stage [27].

9.2. Risk of Contamination During Analysis

Microplastics are everywhere in the air, laboratories, and equipment, meaning contamination control is a challenge. Because of their small size, MPs fibers in the air could lead to contamination of samples and false positives in the analysis of human tissue samples when controls are not properly in place [131]. Strict cleaning protocols, such as plastic-free equipment in laboratories and filtered air, and blanks, are still not in place.

9.3. Distinguishing Nanoplastics from Background Noise

Nanoplastics (NPs) have low size measurements of less than 1 µm, allowing interaction with biological molecules; this hinders detection. False negatives will arise from methods such as vibrational spectroscopy having low sensitivity to distinguish NPs from natural particles [130,132]. In addition, plastic spectra are imitated by proteins or lipids; this makes NPs harder to detect. NPs form aggregates with natural substances; hence, separating NPs from natural signals demands modern equipment, yet this is not common [133].

9.4. Limitations of Current Quantification Approaches

There are no polymer types and sizes of micro- and nanoparticles present in a living matrix that can be detected by one method. It is possible to distinguish polymers using FTIR/Raman spectroscopy but then these are limited by size and matrix effects [134]. Meanwhile, pyrolysis GC/MS measures mass but not number and might give false-positive results because sometimes tissue decomposes [135]. However, microscopy is a means where direct evidence is obtained but there is no chemical confirmation and results might be false until validated using combined methods and also there are different units involved [130,132].

9.5. Need for QA/QC and Inter-Laboratory Validation

To ensure reliability in their findings, it has become imperative for the scientific community to enhance QA/QC methods and inter-laboratory validation. Benchmarking is limited by the lack of approved reference materials, particularly for nanoplastics, even though procedural blanks and calibration standards increase accuracy [136]. An innovative ISO and EU effort exists to enhance evidence-based public health policies by developing standardized methods for comparability globally [130,137].

9.6. Biomonitoring Limitations and Toxicological Uncertainty

Despite increasing reports of microplastics (MPs) in human tissues and biological fluids, several methodological limitations remain. Environmental and laboratory contamination during sample collection and processing may contribute to false-positive findings, particularly for small particles. In addition, differences in digestion protocols, analytical techniques, particle-size thresholds, and reporting units limit comparability among studies. Current detection methods, including FTIR, Raman spectroscopy, and Py-GC/MS, also have important limitations regarding sensitivity, polymer identification, and quantification, especially for nanoplastics. Furthermore, internationally standardized protocols for human biomonitoring of MPs are still lacking, which affects reproducibility and inter-study consistency.

Importantly, the detection of MPs in human samples should not be directly interpreted as evidence of pathological harm. Most available human studies are observational and cannot establish causality. Although experimental findings suggest potential toxicological effects, the long-term clinical significance, exposure thresholds, and health risks of MPs in humans remain uncertain. Therefore, standardized methodologies and longitudinal human studies are urgently needed to better understand the true biological relevance of microplastic exposure.

10. Toxicological and Clinical Implications of Microplastics in the Human Body

10.1. Local vs. Systemic Toxicity

Toxicity caused by microplastics (MPs) is exerted both locally where it is deposited and systemically after translocation which after inhalation can reside in alveolar tissue that triggers inflammatory responses and causes oxidative stress [138] (Figure 4). Experimental investigation verifies that MPs trigger damage to the epithelium and fibrosis in lung biopsies [34]. Systemically, after piercing the biological barrier MPs enter into the circulation and interact with the immune cells which leads to the imbalance of the cytokine [139]. Because of the small size of the nanoplastics, they can cross the cellular membrane and accumulate in organs which intensifies the systemic oxidative damage [140]. MPs serve as vectors for pathogens and heavy metals which further worsen the toxicity [141]. A significant confirmation is that systemic distribution has been found in human blood samples which emphasizes the widespread exposure [142] (Table 8).

10.2. Impact on Reproductive Health

Reproductive toxicity is another growing concern as MPs have been identified in human semen along with lowered motility and change in the morphology of sperm [90]. The impact on female reproductive systems is the same because MPs interrupt the functions of ovary and hormone signaling pathways [143]. Research conducted on the placenta verifies maternal to fetal transfer which raises concerns regarding potential developmental effects, although direct evidence of adverse outcomes in humans remains limited [107]. Animal models showcase endocrine interruption along with alterations in the estrogen caused by MPs and testosterone regulation [144]. Preliminary evidence suggests that MP exposure may be associated with alterations in reproductive parameters; however, causal relationships and population-level effects remain uncertain [141].

10.3. Cardiopulmonary Implications

Cardiopulmonary systems are especially at risk as MPs inhaled via surrounding air assemble in alveolar tissue which weaken the exchange of gas and promote fibrosis [145]. Cardiovascular research shows that MPs are lodged in arterial plaques which indicates vascular infiltration [146]. Laboratory models indicate that MPs provoke the dysfunction of the endothelium, escalating the risk of hypertension and atherosclerosis [147]. In the study on animals, it is found that nanoplastics are linked to the damage of mitochondria and vascular inflammation [148]. Findings from the autopsy of the human body verify the presence of MPs in coronary arteries which supports continued investigation into possible cardiovascular implications, although causality has not yet been established [149].

10.4. Gastrointestinal and Metabolic Effects

Consumption of MPs orally interrupts the gastrointestinal homeostasis and presence of this in the fecal sample verifies the widespread ingestion [125]. Research suggests that MPs alter the composition of gut microbiota which leads to dysbiosis as well as intestinal permeability [150]. Chronic exposure to MPs has been linked to something called “leaky gut” and systemic inflammation [151]. MPs also tamper with the nutrient absorption process which facilitates metabolic syndrome like characteristics in animal models [144]. Population-based human health information suggests a possible association between MP exposure and metabolic outcomes, which requires confirmation in well-designed epidemiological studies [34].

10.5. Transfer to Fetus and Developmental Risks

MPs identified in the tissue of placenta indicate the risks for the development of the fetus [107]. Systemic reviews verify that MPs move across the placental barriers which expose the fetus to potential toxicity [152]. Weakened neonatal immunity and neurodevelopmental pathways may also be caused by nanoplastics [3]. Animal-based research illustrates that MPs interrupt the growth of the fetus and brain development [153]. MPs may contribute to prolonged health risks due to early life exposure which is considered a critical window [154].

10.6. Risk Associated with Associated Chemicals and Additives

MPs dissolve harmful chemicals other than physical particles with Bisphenol A (BPA), phthalates and PFAS being commonly associated with MPs and acting as endocrine disruptors [155,156]. These chemicals worsen the risk of metabolic and reproductive health as they are connected to cancers and neurodevelopmental disorders [157]. Umbrella reviews emphasize the collective risks from plastics-related chemicals which prioritize the necessity for stricter regulation [158].

Table 8. Biological and clinical implications of microplastic accumulation in the human body.

Mechanism/Effect of MPs	Toxicological and Clinical Implications	Affected Body System/Site	Immune Response (Antigen/Antibody)	Cancer Carrier Potential	References
Local deposition in lungs	MPs inhaled into the lungs can trigger inflammation, oxidative stress, epithelial injury, and fibrosis.	Respiratory tract (alveoli, bronchi)	Recognized as foreign particles, MPs stimulate macrophages and cytokine release.	Chronic inflammation may increase susceptibility to lung cancer.	[71,159,160]
Systemic circulation	Once translocated, MPs cause cytokine imbalance, oxidative damage, and accumulate in organs.	Blood, immune system, liver, kidneys	MPs mimic antigens, leading to antibody production and immune dysregulation.	Persistent systemic inflammation is linked to tumor development.	[161,162]
Male reproductive toxicity	Reduced sperm motility and abnormal morphology have been observed with MP exposure.	Testes, semen	Oxidative stress disrupts spermatogenesis.	DNA damage may raise the risk of testicular cancer.	[163,164]
Female reproductive toxicity	MPs interfere with ovarian function, hormone signaling, and can cross the placenta.	Ovaries, placenta	Act as endocrine disruptors, altering estrogen and progesterone pathways.	Endocrine disruption is associated with ovarian and breast cancers.	[165,166,167]
Cardiovascular infiltration	MPs have been found in arterial plaques, contributing to endothelial dysfunction, hypertension, and atherosclerosis.	Arteries, myocardium	Immune cell infiltration promotes vascular inflammation.	Embedded MPs may accelerate cardiovascular cancers.	[146,147,168]
Gastrointestinal dysbiosis	MPs disrupt gut microbiota and cause leaky gut, malabsorption, and systemic inflammation.	Intestines, gut microbiome	MPs act as antigens, disturbing gut immune balance.	Chronic gut inflammation is linked to colorectal cancer.	[150,151]
Fetal transfer and developmental risks	MPs cross the placental barrier, affecting fetal growth, immunity, and neurodevelopment.	Placenta, fetus, neonatal brain	Fetal immune priming occurs as MPs are transferred.	Early-life exposure may predispose to pediatric cancers.	[152,153,167]
Chemical leaching (BPA, PFAS, phthalates)	MPs release harmful additives that disrupt endocrine and neurological functions.	Multiple organs (liver, brain, reproductive system)	Chemicals act as haptens, sensitizing the immune system.	BPA and PFAS are linked to breast, prostate, and liver cancers.	[158,169,170]
Heavy metal adsorption	MPs can carry heavy metals, intensifying systemic toxicity and oxidative stress.	Liver, kidneys, circulatory system	Metal-loaded MPs activate immune responses and generate ROS.	Heavy metal-associated MPs are implicated in carcinogenesis.	[12,171,172]

Table 8. Biological and clinical implications of microplastic accumulation in the human body.

Mechanism/Effect of MPs	Toxicological and Clinical Implications	Affected Body System/Site	Immune Response (Antigen/Antibody)	Cancer Carrier Potential	References
Local deposition in lungs	MPs inhaled into the lungs can trigger inflammation, oxidative stress, epithelial injury, and fibrosis.	Respiratory tract (alveoli, bronchi)	Recognized as foreign particles, MPs stimulate macrophages and cytokine release.	Chronic inflammation may increase susceptibility to lung cancer.	[71,159,160]
Systemic circulation	Once translocated, MPs cause cytokine imbalance, oxidative damage, and accumulate in organs.	Blood, immune system, liver, kidneys	MPs mimic antigens, leading to antibody production and immune dysregulation.	Persistent systemic inflammation is linked to tumor development.	[161,162]
Male reproductive toxicity	Reduced sperm motility and abnormal morphology have been observed with MP exposure.	Testes, semen	Oxidative stress disrupts spermatogenesis.	DNA damage may raise the risk of testicular cancer.	[163,164]
Female reproductive toxicity	MPs interfere with ovarian function, hormone signaling, and can cross the placenta.	Ovaries, placenta	Act as endocrine disruptors, altering estrogen and progesterone pathways.	Endocrine disruption is associated with ovarian and breast cancers.	[165,166,167]
Cardiovascular infiltration	MPs have been found in arterial plaques, contributing to endothelial dysfunction, hypertension, and atherosclerosis.	Arteries, myocardium	Immune cell infiltration promotes vascular inflammation.	Embedded MPs may accelerate cardiovascular cancers.	[146,147,168]
Gastrointestinal dysbiosis	MPs disrupt gut microbiota and cause leaky gut, malabsorption, and systemic inflammation.	Intestines, gut microbiome	MPs act as antigens, disturbing gut immune balance.	Chronic gut inflammation is linked to colorectal cancer.	[150,151]
Fetal transfer and developmental risks	MPs cross the placental barrier, affecting fetal growth, immunity, and neurodevelopment.	Placenta, fetus, neonatal brain	Fetal immune priming occurs as MPs are transferred.	Early-life exposure may predispose to pediatric cancers.	[152,153,167]
Chemical leaching (BPA, PFAS, phthalates)	MPs release harmful additives that disrupt endocrine and neurological functions.	Multiple organs (liver, brain, reproductive system)	Chemicals act as haptens, sensitizing the immune system.	BPA and PFAS are linked to breast, prostate, and liver cancers.	[158,169,170]
Heavy metal adsorption	MPs can carry heavy metals, intensifying systemic toxicity and oxidative stress.	Liver, kidneys, circulatory system	Metal-loaded MPs activate immune responses and generate ROS.	Heavy metal-associated MPs are implicated in carcinogenesis.	[12,171,172]

11. Public Health Implications of Microplastics

11.1. Population-Level Exposure and Burden

Microplastics (MPs) are acknowledged as a widespread contaminant now because exposure occurs through ingestion, inhalation and dermal contact and according to international aspect adults consume approximately 5 g of MPs in a week which is equivalent to the weight of a credit card [173]. The concentration of MPs in a bottle water surpasses the amount contained in tap water which is a major contributor [174]. Geography plays a crucial role in dietary intake with seafood, salt and vegetables functioning as important sources [175]. Encounter via inhalation is of equal concern due to the detection of MPs in indoor and outdoor air samples especially in metropolitan environments [176]. What makes the interaction situation worse is poor management of waste in low- and middle-income countries where MPs gets released into the air and soil by open dumping and burning [177]. The latest bio-monitoring research verifies the presence of MPs in human blood, feces and breast milk which highlights the systemic exposure among populations [5].

MPs in Dental Materials and Dentistry

Evidence suggests that dental and oral care materials are major contributors to MPs and NPs. The potential sources may include resin-based composite materials, acrylic prosthodontic appliances, aligners, impression materials, toothbrushes, dental floss, and even toothpaste formulations, which can release microscopic polymer particles during wear, polishing, degradation, and clinical use [178,179]. Grinding and polishing of composite restorations generate microparticles of 5–10 µm, while removal of old restorations may produce plastic dust particles of 20–100 µm diameter [180,181]. Airborne microplastics have also been detected in dental healthcare units, suggesting occupational exposure through inhalation of contaminated aerosols and dust [182]. Further studies carried out through biomonitoring also show that MPs/NPs can trigger oxidative stress, inflammation, and intracellular uptake orally, but there is a lack of direct evidence involving humans [179]. Therefore, dentistry may also be responsible for human exposure to MPs/NPs, emphasizing the need for safer biomaterials and improved waste management [181].

11.2. Vulnerable Populations

Certain groups are unfairly affected by MP exposure, and particularly pregnant women and newborns are susceptible due to transplacental transfer and identification of MPs in breast milk [6]. Interaction in the neonatal phage surges concerns about toxicity during development and dysregulation of immune system [107]. People belonging to certain job sectors such as textile workers, waste handlers and industrial laborers are at high risks due to inhalation of fibrous MPs [183]. Further, socioeconomic differences are directly linked to exposure of neglected populations to MPs because they normally consume foods and beverages which are contaminated or contaminated with a high level of probability [184].

11.3. Potential Long-Term Health Outcomes

Despite proof still being found, prolonged exposure of MPs is connected to long-term health complications as it provokes systemic inflammation which may lead to the development of cardiovascular disease [146]. Plastic additives including bisphenol A and phthalates that interrupt the endocrine, which increases concerns about reproductive health and fertility regression [185,186,187]. Gastrointestinal dysbiosis that is related to MPs may increase susceptibility to metabolic disorders of individuals, for example, obesity and diabetes [150]. Another probable consequence is neurotoxicity because nanoplastics can pass over the blood–brain barrier as studies conducted on animals illustrate cognitive deterioration and modified neurotransmission [45,188]. Despite limited epidemiological research, the integration of toxicological and clinical evidence demonstrates the widespread chronic disease burdens [144].

11.4. Risk Assessment and Uncertainties

Information about human biological surveillance is limited because small sample sizes restrict generalizability [5]. Moreover, MPs serve as carriers for other pollutants which further complicates the attribution of health effects [189]. The establishment of exposure thresholds is hampered due to these unpredictabilities which complicate regulatory decision making [184].

11.5. Regulatory and Policy Considerations

International regulatory foundations are still advancing launching efforts to normalize the characterization of microplastics and documenting through ISO guidelines under development [190,191,192]. According to the WHO, there is no decisive limit of exposure that has been established but they support the use of precautionary activities [184]. However, in the USA, the FDA has not officially established specific limits on exposure levels where the current review of MPs in food packaging continues [193,194,195]. The policy challenges are the diversity of polymer types, variable exposure pathways and socioeconomic variations that are at risk [196]. Successful management requires synchronized methodologies and worldwide collaboration [197].

11.6. Public Health Strategies and Preventive Measures

Preventative strategies emphasize minimizing exposure and mitigating risks which are critical to improve waste management and reduce single-use plastics at the population level [198]. Certain dietary actions can reduce ingestions which are minimizing bottled water consumption and promoting safer food packaging [174]. It is necessary for textile and waste workers to provide occupational safety measures including protective equipment [183]. Public awareness campaigns have the ability to enable people to make deliberate decisions; on the other hand, health education programs indicate risks for vulnerable communities [184]. Finally, in order for MPs to be addressed as a worldwide public health hazard, combining environmental and health policies will be required [199].

12. Surveillance, Innovation, and Policy Integration

Effective reduction in human exposure to micro- and nanoplastics requires coordinated integration of environmental surveillance, technological innovation, and regulatory frameworks. Establishing national and regional monitoring systems for micro- and nanoplastics in drinking water, food products, and atmospheric particulates is essential for generating reliable exposure data and conducting evidence-based risk assessments [200]. Continuous surveillance would support early identification of contamination hotspots and inform targeted mitigation strategies [201]. In parallel, investment in sustainable material science, particularly the development of biodegradable polymers, eco-friendly packaging materials, and advanced recycling technologies, can substantially reduce the environmental burden of plastic waste and the subsequent formation of secondary MPs [202]. Regulatory interventions also play a crucial role in minimizing exposure by restricting the use of intentionally added MPs in consumer products and promoting extended producer responsibility (EPR) [203]. Additionally, increasing public awareness about the health and environmental risks of plastics and encouraging people to reduce the use of daily plastic materials such as single-use packaging, plastic containers, and bottled water can significantly contribute to lowering overall micro- and nanoplastics exposure.

13. Knowledge Gaps and Future Research Directions

13.1. Harmonized Detection Methods

Lack of synchronized identification procedures is one of the most urgent gaps in the research of microplastics (MPs) because recent research implements diverse digestion, filtration and spectroscopic methods which make cross comparison challenging [204,205]. What further complicates the data analysis is fluctuation in the size of particle thresholds and detection of polymers [206]. International action plans such as projects of the ISO and EU are working toward standardized workflows yet mutual agreement remains concealed [191]. Epidemiological and toxicological research are at risk of inconsistency without coordination which limits their utility for public health policy [197].

13.2. Exploration of Nanoplastics

Detection of MPs remains tough because most spectroscopic procedures lack appropriate resolution [206,207]. Even though some arising technologies including atomic force microscopy–infrared (AFM-IR) and NanoSIMS demonstrate hope, they still require confirmation [208]. The lack of information related to human biomonitoring highlights the necessity for aimed research [98,209]. In order to assess the unique toxicological profiles of nanoplastics in the future, detection of them must be a top priority [189,210].

13.3. Longitudinal Human Studies

Most of the proof of the presence of microplastics in the human body derives from cross-sectional or small-scale research which underscores the immediate necessity for prolonged cohort research in order to set up causal connections between exposure and disease outcomes [5]. These responses have the capability to enable dose–response modeling and explain chronic effects which include cardiovascular, reproductive and metabolic disorders [211]. Cohorts should include not only biominitoring of blood, feces and breast milk but also information linked to lifestyle and occupation [98,209]. Combining with omnics technologies could unveil molecular pathways of toxicity [212,213]. Evaluation of risk remains assumptive due to the lack of longitudinal data which limits action [214].

13.4. Standardized Reporting of MP Concentration

Another deficiency relies in irregular reporting units because research indicates the concentration of microplastics (MPs) as particles per gram, per liter or per individual sample in different ways which obstruct comparability [215]. Certain standardized metrics including particles per unit mass or volume are crucial for epidemiological synthesis [216]. In addition, documentation should include polymer type, morphology and size distribution in order to contextualize the risks associated with health [5]. In order to establish consensus guidelines worldwide collaboration is required which is similar to those that are used in chemical toxicology [191,217].

13.5. Mechanistic Studies Linking MPs to Diseases

Microplastics are linked to inflammation, oxidative stress and endocrine interruption resulting in limited mechanistic information but their usual pathways are poorly defined [32,212,218]. Moreover, stronger proof is required in order to translate to human disease mechanisms [144,150]. To facilitate the contribution of MPs to chronic conditions including diabetes, infertility and cardiovascular disease, a combination of toxicology with clinical medicine is required [146,214].

13.6. Improving Contamination-Free Workflows

Airborne fibers and plastic labware repeatedly confuse results because the laboratory contamination remains a major challenge, and as a result instances of false positives raise concerns [219]. Strict QA/QC guidelines such as clean air facilities and non-plastic consumables are required [215]. To enhance reproducibility and credibility, inter-laboratory confirmation research is required [216]. Biomonitoring information is at risk of misinterpretation and undermining public trust due to a lack of contamination-free workflows [184].

13.7. Epidemiological Studies Linking Burden to Lifestyle/Exposure

Ultimately, epidemiological research must combine lifestyle and occupational factors as habits linked to diets like seafood and bottled water consumption intensely affect the burden of microplastics [220]. Occupational exposure among textile and waste workers produces inhalation risks [177,183]. Socioeconomic variations shape exposure as well, where ignored populations experience elevated risks because of poor management of waste [221,222]. In order to enable aimed interventions and inform public health approaches, connecting MP burden to lifestyle and exposure patterns is mandatory [189,220].

This review provides a qualitative synthesis of the available literature and does not include meta-analysis, pooled prevalence estimates, risk-of-bias assessment, or formal heterogeneity assessments. Therefore, conclusions are interpreted as a qualitative synthesis of the currently available evidence.

14. Conclusions

The detection of microplastics in human blood, reproductive fluids, maternal–fetal matrices, renal tissues, and tumor samples demonstrates that plastic exposure is not merely environmental but systemic. Evidence of transplacental transfer and early-life exposure underscores potential developmental implications. Associations with cardiovascular pathology and reproductive dysfunction further suggest that MPs may exert clinically relevant biological effects, although causality remains to be firmly established. Despite rapid progress in spectroscopic and thermoanalytical detection methods, methodological heterogeneity limits quantitative comparability across studies. Standardization of sampling, digestion, and analytical protocols is essential for reliable human biomonitoring. Future research must prioritize longitudinal cohort studies, mechanistic toxicology, and harmonized detection strategies to clarify exposure–response relationships. Addressing these gaps will be critical for translating emerging evidence into risk assessment policies and public health interventions.