Systematic Review: Dietary Exposure to Microplastics and Human Health Outcomes

Abstract

This comprehensive review synthesizes current evidence on dietary exposure to microplastics and associated human health outcomes. Dietary intake represents a primary exposure pathway, with estimated median consumption of 721 microplastic particles per kilogram of body weight per day, though total intake ranges span from 7.7 × 10⁻³ to 3.8 × 10⁸ MPs/kg bw/day [4,58]. Contrary to previous assumptions, vegetables, grains, and meat contribute more significantly to daily microplastic intake than seafood, which has been overrepresented in literature due to methodological biases [5,43,59]. The polymeric composition of microplastics in food closely mirrors global plastic production, dominated by polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP) [6,44,47].

Strong evidence links microplastic exposure to oxidative stress, inflammatory responses, immune dysregulation, and endocrine disruption [2,50]. Recent clinical studies have detected microplastics in human arterial plaques, with their presence correlating with a 4.53-fold increased hazard ratio for major adverse cardiovascular events (MACE) over 34 months [37,91,148]. Nanoplastics (<100 nm) demonstrate heightened toxicity due to their ability to translocate across biological barriers, accumulating in placental tissue, brain tissue, and systemic circulation [9,39,64].

Methodological challenges significantly impede risk quantification. No standardized protocols exist for microplastic detection in food or human tissues, with analytical techniques including FTIR, Raman, and pyrolysis-GC/MS producing inconsistent results [28,29,51]. The formation of biomolecule coronas on particle surfaces represents a critical but poorly characterized modifier of toxicity [18,20,77].

This review identifies cardiovascular outcomes, developmental toxicity, and inflammatory pathways as research priorities requiring standardized detection methods, longitudinal human studies, and dose-response modeling under environmentally relevant conditions [12,17,63]. Regulatory initiatives such as the EU's microplastic restrictions [52,53] and ongoing methodological advancements using AI and biosensors [73,88] offer promising pathways forward.

1. Introduction

The proliferation of plastic pollution since the mid-20th century has generated a pervasive environmental crisis extending to global food systems and human health. Microplastics (MPs), defined as plastic particles smaller than 5 millimeters, along with their smaller counterparts nanoplastics (NPs, <100 nm), have been detected in virtually all environmental compartments, from marine sediments to atmospheric deposition, and consequently in food chains worldwide [3,28]. The ubiquity of these contaminants has prompted urgent scientific investigation into human exposure pathways and potential health consequences.

Human exposure to microplastics occurs predominantly through ingestion via food products, alongside inhalation and dermal contact [1,61]. Dietary intake encompasses consumption of contaminated seafood, agricultural products, processed foods, and beverages, representing a complex exposure scenario influenced by food production, processing, and packaging practices [67]. The emerging evidence that microplastics can translocate across biological barriers, accumulate in human tissues, and interact with cellular structures at the molecular level has raised significant public health concerns [9,39].

This systematic review aims to critically evaluate the current evidence on dietary microplastic exposure and associated human health outcomes. Specifically, it addresses: (1) exposure pathways and quantification in food systems; (2) characterized health effects across organ systems; (3) methodological approaches for detection and analysis; and (4) critical research gaps requiring immediate attention. The review prioritizes research areas with the greatest potential impact on human health and development while acknowledging the methodological limitations that currently hinder precise risk assessment [12].

The current evidence landscape reveals both substantial progress and significant gaps. While animal and in vitro studies demonstrate clear toxicity mechanisms, human epidemiological evidence remains limited by methodological constraints and lack of standardized exposure assessment [63,108]. This review synthesizes findings from recent advances in detection technologies, toxicological studies, and emerging clinical research to provide a comprehensive understanding of the state of the science and future research directions.

2. Exposure Pathways and Quantification

2.1 Dietary Sources and Intake Estimates

Dietary ingestion represents the predominant pathway for human microplastic exposure, accounting for an estimated 39,000–52,000 particles annually [61]. Comprehensive analysis of 193 studies reveals a median estimated daily intake of 721 microplastic particles per kilogram of body weight, though estimates vary substantially from 7.7 × 10⁻³ to 3.8 × 10⁸ MPs/kg bw/day [4,58,175]. This considerable range reflects methodological inconsistencies and actual variation in contamination levels across food items and geographic regions.

Contrary to initial assumptions that marine sources dominate dietary exposure, recent evidence demonstrates that vegetables, grains, and meat contribute more significantly to daily microplastic intake than seafood [5,43,109]. The overrepresentation of seafood in existing literature results from methodological bias toward filter-feeding marine organisms rather than actual exposure magnitude [59,70]. Seafood consumption still contributes relevant exposure, with South Korean studies reporting average concentrations of 0.47 pieces/g across commonly consumed marine products, while sea salt reaches 2.22 pieces/g [7]. Crustacean consumption alone contributes an estimated 521 pieces/person/year in that population [7].

Infants and children face disproportionately higher exposure relative to body weight. Bottle-fed infants may ingest up to 1.5 million microplastic particles annually from polypropylene formula bottles, representing exposure levels two orders of magnitude higher than adults [161]. Similarly, infants exhibit the highest calculated inhalation exposure dose of microplastics and nanoplastics across all indoor and outdoor environments, with passive sampling-derived exposures reaching up to 549.8 MPs/kg-BW/day in indoor combined settings [124]. This elevated early-life exposure raises particular concerns for developmental toxicity given the vulnerability of developing physiological systems [122,123].

2.2 Polymeric Composition and Contamination Patterns

The polymeric composition of microplastics in food closely mirrors global plastic production patterns, with polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP) consistently identified as the most prevalent contaminants across food categories [6,44,47,111]. This correspondence suggests that contamination pathways relate more directly to packaging materials and agricultural inputs than to environmental degradation alone [46]. In seafood, polypropylene (PP), polyethylene (PE), and polystyrene (PS) fragments of 20–200 μm dominate the polymeric profile [7].

Analytical protocols significantly influence quantification outcomes, particularly in fruits, vegetables, and bottled water [45,48]. Studies demonstrate that different methodologies can produce unpredictable variations in reported particle concentrations without consistent directional bias [72]. This methodological dependency severely undermines cross-study comparability and necessitates standardized detection protocols for reliable exposure assessment [110,144].

The specific mechanisms of contamination vary across food categories. For produce, microplastics likely originate from agricultural plastics, irrigation water, and atmospheric deposition [68]. For meat animals, transmission occurs through feed and water contamination, while seafood acquires microplastics through direct environmental ingestion [67]. Processed foods and beverages face additional contamination from food processing equipment and packaging materials, particularly with products in direct contact with plastic containers or tubing [60].

2.3 Environmental and Occupational Exposure Vectors

Beyond dietary intake, inhalation represents a significant exposure route, particularly in indoor environments where concentrations exceed outdoor levels by approximately 1.5-fold [8]. Indoor air contains approximately 4% of organic particulate matter as micro- and nanoplastics, primarily synthetic fibers such as polyester and polyamide [38]. These airborne particles, particularly those ≤2.5 μm in diameter, can penetrate alveolar regions and potentially enter systemic circulation [200].

Occupational exposure scenarios substantially exceed general population estimates. Workers in plastic recycling facilities during grinding processes face exposure levels reaching 22,531 MPs/kg-BW/day, surpassing environmental exposure benchmarks by orders of magnitude [126]. These elevated exposures highlight the importance of protective measures in industrial settings and suggest that current environmental sampling significantly underestimates peak human exposure scenarios [126].

The environmental sources of dietary microplastic contamination are diverse and interconnected. Agricultural soils receive microplastic inputs through mulch films, compost amendments, and irrigation using contaminated water sources [68]. These terrestrial environments subsequently transfer contamination to crops and livestock, creating a complex web of exposure pathways that extends beyond marine systems to encompass the entire food production continuum [67].

3. Human Health Outcomes

3.1 Cardiovascular Effects

The most compelling evidence for human health impacts comes from cardiovascular studies. A landmark 2024 study involving 257 patients undergoing carotid endarterectomy demonstrated that microplastics detected in atherosclerotic plaques correlated with a 4.53-fold increased hazard ratio (95% CI: 2.00–10.27; P < 0.001) for major adverse cardiovascular events (MACE), including nonfatal stroke, nonfatal myocardial infarction, or all-cause mortality, over a 34-month follow-up period [37,91,148]. Microplastics, primarily polyethylene terephthalate (PET), polyamide-66 (PA-66), polyvinyl chloride (PVC), and polyethylene (PE), were detected in arterial tissues at a mean concentration of 118.66 ± 53.87 μg/g of tissue [92].

Mechanistic insights from experimental models reveal several pathways through which microplastics may promote cardiovascular pathology. Polystyrene microplastics induce cardiac fibrosis via activation of the Wnt/β-catenin pathway, elevate cardiac troponin I and creatine kinase-MB levels, and promote mitochondrial dysfunction in cardiomyocytes [93,195]. Nanoplastics accelerate vascular aging through ROS-mediated CDK5 signaling and enhance thrombosis by promoting platelet aggregation [165,201]. In macrophages and endothelial cells, microplastics activate the NLRP3 inflammasome via TLR2/4 signaling, triggering pyroptosis through Gasdermin D and amplifying vascular inflammation through IL-1β, IL-6, and TNF-α release [194].

Human blood contains an average of 1.6 μg/mL microplastics, with levels correlating with altered coagulation parameters including prolonged aPTT and elevated fibrinogen and CRP [117]. A pilot intervention study demonstrated that healthy adults switching from plastic to glass beverage containers experienced reduced systolic and diastolic blood pressure, suggesting potential reversibility of some cardiovascular effects with reduced exposure [117].

3.2 Developmental and Reproductive Toxicity

The placenta serves as both a barrier and target for micro- and nanoplastic translocation. Studies have confirmed microplastic presence in human placental tissue at concentrations of 149 particles per sample (20.34–307.24 μm), with polymer types including polyethylene, polypropylene, and polystyrene [64]. Nanoplastics (20-100 nm) demonstrate even higher translocation potential, with in vitro studies showing rapid internalization in human placental trophoblasts [40,82].

Experimental evidence demonstrates that nanoplastics disrupt critical placental functions. Polystyrene nanoplastics (20 nm) induce cytotoxicity at environmental concentrations (≥1 µg mL⁻¹), reduce cell viability, cause lysosomal accumulation, and trigger mitochondrial dysfunction [40,84]. These particles directly disrupt endocrine function by significantly reducing β-hCG secretion at concentrations similar to those detected in human blood (~1.6 µg mL⁻¹), representing the first documented evidence of nanoplastics impairing human placental hormone production [42,83,180]. Additionally, exposure induces a pro-inflammatory response with IL-1β upregulation at all tested concentrations and IL-6 and TNF-α elevation at higher concentrations (100 µg mL⁻¹) for smaller particles [41,179].

Reproductive effects extend beyond placental function. Microplastics have been detected in human semen (0.23 ± 0.45 particles/mL) [196], while animal studies demonstrate that micro- and nanoplastics can disrupt gut microbiota crucial for metabolic health and reproductive function [95,101]. The Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy applied to placental reproductive toxicity from micro/nanoplastics assigned a composite evidence score of 5.63, indicating moderate-to-low risk with smaller particle sizes correlating with increased toxicity due to enhanced cellular internalization and mitochondrial dysfunction [121].

3.3 Neurological and Cognitive Impacts

Nanoplastics' ability to cross the blood-brain barrier raises significant concerns for neurological health. Polystyrene nanoplastics (30–50 nm) ingested by rodents cross the intestinal barrier and blood-brain barrier via endocytosis and protein corona-mediated transcytosis, inducing oxidative stress, microglial activation, and α-synuclein aggregation—mechanisms directly linked to Parkinson's disease pathology [113]. Human brain autopsies have detected polypropylene fragments in 8 of 15 olfactory bulbs, suggesting potential nasal-to-brain transmission pathways [113].

Human cerebrospinal fluid (CSF) from Alzheimer's disease patients contains significantly elevated levels of polyethylene and PVC microplastics, which correlate with lower CSF Aβ42, reduced Mini-Mental State Examination (MMSE) scores, and faster cognitive decline over one year [114]. This correlation suggests CSF plastic burden as a potential biomarker for neurodegenerative progression, though causality remains unestablished [114].

Experimental models demonstrate that nanoplastics trigger neuroinflammation and cognitive dysfunction through microglial activation and blood-brain barrier penetration [9]. In vitro studies reveal that nanoplastics can alter gene expression in human vascular endothelial cells, potentially contributing to cerebrovascular pathology [141]. The developing brain appears particularly vulnerable, with early-life exposure potentially disrupting critical developmental processes through oxidative stress, inflammation, and endocrine disruption pathways [112].

3.4 Metabolic and Endocrine Disruption

Mounting evidence links microplastic exposure to metabolic dysfunction through multiple mechanisms. Microplastics disrupt gut microbiome composition by reducing SCFA-producing bacteria (Lactobacillus, Ruminococcus) and enriching pro-inflammatory taxa (Escherichia-Shigella), leading to intestinal barrier breakdown, endotoxemia, and systemic metabolic dysregulation [95]. Fecal microbiota transplantation from microplastic-exposed mice recapitulates weight gain and lipid dysregulation in germ-free recipients, establishing a causal role for dysbiosis in metabolic toxicity [95].

Endocrine disruption occurs both directly through nanoplastic interactions with endocrine tissues and indirectly through leached additives. Plastic additives like bisphenol A (BPA) and phthalates (e.g., DEHP, BBP) leach from nanoplastics and act as endocrine disruptors at concentrations as low as 0.2–20 ng/mL, directly linking chronic exposure to obesity, cardiovascular disease, and fetal neurodevelopmental damage [186]. The adsorption of endocrine-disrupting chemicals onto microplastic surfaces enhances their bioavailability and persistence in biological systems [97,103].

Despite these mechanisms, clinical endpoints such as altered serum hormone levels (e.g., testosterone, estradiol, TSH), reproductive outcomes, or metabolic dysfunction with statistically significant effect sizes have not been robustly established in human populations [36]. This disconnect between widespread environmental exposure and demonstrated pathophysiological outcomes represents a critical knowledge gap requiring carefully designed human epidemiological studies [36].

3.5 Immunological Effects

The immunomodulatory effects of micro- and nanoplastics present a complex picture with highly context-dependent outcomes. Evidence indicates that nanoplastics can accumulate in immune organs such as the spleen and intestines, disrupting hematopoiesis, immune cell activation, and inflammatory cytokine production [55,56]. In vitro studies reveal significant differences in immune responses between human and murine cells exposed to microplastics, indicating that animal models may not accurately predict human immunotoxicity [146].

Microplastics alter Treg/Th17 balance in colon cancer microenvironments and upregulate cancer markers (N-cadherin, CD44, PD-L1) in gastric cancer cells, suggesting potential interactions between immune dysregulation and carcinogenic pathways [62,107]. The pro-inflammatory effects of nanoplastics are well-documented across multiple cell types, though environmental concentrations often yield minimal or no observable effects in vivo, suggesting that current high-dose laboratory exposures may overestimate real-world risk [147].

Probiotic mitigation strategies show promise for certain aspects of microplastic toxicity. Strains such as Lacticaseibacillus paracasei DT66 and Lactiplantibacillus plantarum DT88 significantly enhance fecal excretion of polystyrene microplastics and reduce intestinal PS residue while mitigating inflammation [100]. However, probiotic effects are strain-specific and dose-dependent, with certain Bacillus strains potentially exacerbating oxidative stress under microplastic exposure [102].

4. Methodological Approaches

4.1 Detection and Quantification Techniques

The detection and quantification of micro- and nanoplastics in food and biological samples present formidable analytical challenges. Current methodologies include visual identification using microscopy, chemical characterization through Fourier-transform infrared (FTIR) spectroscopy, Raman spectroscopy, scanning electron microscopy with energy-dispersive X-ray spectroscopy (SEM-EDX), and pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) [28,29]. Each technique possesses distinct advantages and limitations regarding particle size detection limits, polymer identification capabilities, and throughput capacity.

Raman and FTIR spectroscopy have emerged as complementary techniques for polymer identification. FTIR uniquely enables detection of the microplastic eco-corona in complex matrices like human milk, providing insights into polymer-biological matrix interactions that Raman spectroscopy may not resolve with equal sensitivity [23,128]. Mapping mode in both Raman and FTIR spectroscopy improves efficiency in scanning large sample areas and enables large-scale preliminary screening despite inability to quantify low-size fractions (<10 µm) or exact concentrations [24,129].

Recent advances demonstrate that spectroscopic methods can directly detect polyethylene (PE) and polystyrene (PS) microplastics in human milk without purification, overcoming limitations of harsh chemical pretreatments that alter sample integrity [127,151]. These non-destructive approaches enable simultaneous monitoring of other sample components like fat content, adding multiparametric value beyond microplastic detection [24,153].

4.2 Standardization Challenges

A fundamental challenge across all analytical methods is the absence of standardized protocols. No fully validated method exists for microplastic and nanoplastic analysis in food and beverages as of 2022, despite numerous techniques being employed [28]. Studies rely on non-uniform definitions of size (1–5 mm for MPs; <100 nm for nanoplastics), polymer types, and analytical approaches, hindering risk quantification and regulatory guideline development [3].

Studies demonstrate that analytical protocols significantly influence quantification outcomes, particularly in fruits, vegetables, tap water, and bottled water, introducing high variability that undermines cross-study comparability [45,48,72]. The choice of detection method can produce unpredictable differences in reported concentrations without consistent directional bias, necessitating standardized methodological frameworks for reliable exposure assessment [110,144].

Inter-laboratory comparison studies, proficiency tests, and ISO-standardized procedures remain virtually absent despite the established use of metrics like LOD, LOQ, and CV in method development [30]. This harmonization gap extends to quality control measures, with inadequate blank controls reported in 20-30% of published protocols due to pervasive atmospheric contamination risks [197].

4.3 Emerging Technologies and Innovations

Artificial intelligence and advanced spectroscopy represent promising frontiers for addressing methodological limitations. AI-driven spectroscopic methods (Raman, FTIR) outperform conventional optical and thermo-analytical techniques in identifying sub-10 µm microplastics in food, achieving >92% classification accuracy through deep learning models trained on polymer-specific spectral signatures [73]. These systems uniquely distinguish synthetic textile fibers (dominant in food samples at 68%) from biological fibers using texture and spectral heterogeneity features, reducing false positives by 41% compared to manual microscopy [74].

Ensemble machine learning approaches combining algorithms like Support Vector Machines, K-Nearest Neighbours, and Random Forests with a neural network fusion layer significantly improve microplastic identification accuracy on imbalanced and fouled datasets, outperforming single-model approaches [25]. These architectures address critical real-world challenges such as functional group overlap and spectral noise from contamination without requiring additional preprocessing or physical sample cleanup [27].

Biosensor-based approaches offer potential for field-deployable detection of microplastics in beverages, with demonstrated capability to detect sub-micron particles and correlate their presence with co-contaminant bioaccumulation of heavy metals like lead and cadmium in aquatic food chains [90]. These real-time monitoring tools could revolutionize exposure assessment by enabling high-frequency data collection across diverse environmental and food processing settings.

5. Critical Research Gaps and Future Directions

5.1 Methodological Standardization

The most urgent research priority remains the development of standardized detection protocols for micro- and nanoplastics across food matrices and biological samples [12,63]. Current methodological fragmentation severely impedes cross-study comparability and regulatory action, with no single technique capable of achieving complete characterization of particles' polymer identity, size quantification, and morphology analysis [29,171].

Specific methodological gaps requiring immediate attention include:

Consensus on size-based classification (1–100 nm for NPs, <5 mm for MPs)
Standardized protocols for particle characterization including surface chemistry and weathering state
Harmonized procedures for sample collection, processing, and contamination control
Certified reference materials for instrument calibration and method validation [63,89]

Efforts such as the EU-funded PlasticTrace project have developed water-soluble PET microplastics reference material tablets with precisely defined particle counts and sizes, representing progress toward methodological standardization [172]. However, comparable reference materials for complex food matrices and biological samples remain critically needed [158,159].

5.2 Longitudinal Human Health Studies

Despite ubiquitous environmental exposure, current toxicological assessments suffer from a critical absence of longitudinal human data correlating micro- and nanoplastic exposure with clinical endpoints [33,78]. Specifically needed are:

Prospective cohort studies tracking cumulative exposure biomarkers and health outcomes
Dose-response modeling under physiologically relevant exposure conditions
Studies examining vulnerable populations including pregnant women, infants, and occupational workers
Research establishing connections between environmental concentrations and clinical endpoints such as inflammation, oxidative stress, or barrier dysfunction [78,120]

The discovery that microplastics in arterial plaques predict cardiovascular events represents a paradigm shift in human health research [139]. Similar studies are needed across other organ systems to establish causality and characterize exposure-response relationships. The prospective multicenter trial currently enrolling patients undergoing cardiac surgery to evaluate micro- and nanoplastic contamination in myocardial tissue and blood represents an important model for future research [150].

5.3 Characterization of Bio-Nano Interactions

The formation of biomolecule coronas—adsorbed layers of proteins, lipids, and other biomolecules on microplastic and nanoplastic surfaces—emerges as a critical but poorly characterized modifier of toxicity [18,20,77]. This dynamic layer may significantly alter cellular interactions and toxicological profiles but remains underexplored in human health risk assessments [32,137].

Key research questions regarding corona formation include:

How do environmental aging and biological conditioning alter nanoplastic bioavailability?
What specific biomolecules comprise coronas in various physiological fluids?
How do coronas influence particle uptake, translocation, and tissue distribution?
Can corona characteristics predict toxicity profiles across polymer types and sizes [138]?

Current evidence suggests that aged or irregular microplastics elicit 2–9× stronger inflammatory and genotoxic responses than pristine particles, highlighting the importance of accounting for environmental transformation in toxicity testing [96]. Co-exposure with endocrine-disrupting chemicals like TBBPA or DEHP further exacerbates DNA damage and ferroptosis, though most mechanistic studies use doses 10³–10⁶× higher than estimated environmental exposure [96].

5.4 Nanoplastic-Specific Research

Nanoplastics (<100 nm) present particular research challenges due to their enhanced bioavailability and ability to cross biological barriers [39,130]. Oral bioavailability for nanoplastics under 50 nm approaches 0.3%—10–100× greater than microplastics—with efficient absorption via Peyer’s patches and lymphatic transport [165,184]. Yet validated detection protocols for nanoplastics in food and biological samples remain virtually nonexistent [28].

Specific nanoplastic research priorities include:

Development of sensitive detection methods for sub-100 nm particles in complex matrices
Characterization of tissue distribution and clearance mechanisms
Toxicity profiling at environmentally relevant concentrations
Investigation of synergistic effects with chemical additives and adsorbed contaminants [32,89]

The finding that a liter of bottled water contains up to 240,000 plastic particles—90% nanoplastics—suggests ingestion is a primary systemic exposure route driving cardiovascular toxicity through mitochondrial dysfunction and Wnt/β-catenin-mediated cardiac fibrosis [39]. This high exposure potential underscores the urgency of nanoplastic-specific research.

6. Regulatory and Public Health Implications

6.1 Current Regulatory Landscape

Regulatory responses to microplastic contamination remain fragmented and limited in scope. The EU enacted Regulation (EU) 2023/2055 on October 17, 2023, banning synthetic polymer microparticles (≤5 mm, organic, insoluble, non-degradable) intentionally added to products, with phased implementation dates ranging from 2027 for rinse-off cosmetics to 2035 for lip, nail, and makeup products [52,80]. The regulation uniquely targets granular infill in synthetic sports surfaces and treated seeds/plant protection products with a 2031 compliance deadline [53].

Transitional periods under Annex XVII of REACH differentiate product categories by exposure duration, application context, and end-use, creating a granular regulatory framework focused primarily on intentionally added microplastics [54,79]. Only non-biodegradable, insoluble plastic glitter falls within scope for immediate restriction, with biodegradable, soluble, inorganic, or natural alternatives exempt [81].

In contrast, the FDA states that while microplastics and nanoplastics are detected in foods and beverages—including bottled water, seafood, honey, and tea—current scientific evidence does not demonstrate they pose a risk to human health, and no FDA regulations currently limit their presence unless a health concern is established [166]. The agency identifies critical research gaps in standardized detection protocols and is actively participating in interagency initiatives to develop standardized methodologies [167,168].

6.2 Risk Assessment Challenges

Regulatory action is significantly constrained by methodological limitations and knowledge gaps. No standardized methods exist for detecting and quantifying microplastics in human tissues, leading to non-comparable data across research efforts and hindering robust epidemiological studies linking exposure to long-term health outcomes [51,63,108]. This absence of validated detection protocols particularly affects nanoplastics, for which virtually no standardized analytical methods exist for food and biological matrices [28,158].

Risk assessment faces additional challenges from:

Disparate definitions of micro- and nanoplastics across studies
Inadequate understanding of exposure-response relationships at real-world concentrations
Limited characterization of chemical additives and degradation products
Uncertainty regarding chronic low-dose effects and vulnerable populations [89,159]

The Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy applied to placental reproductive toxicity from micro/nanoplastics assigned a composite evidence score of 5.63 (moderate-to-low risk), highlighting the current uncertainty characterizing risk assessments [121].

6.3 Public Health Interventions

Despite regulatory limitations, several public health interventions show promise for reducing exposure. Switching from plastic to glass beverage containers demonstrated measurable reductions in blood pressure in healthy adults, suggesting potential benefits from simple substitution strategies [117]. Probiotic interventions with specific strains (e.g., Lactiplantibacillus plantarum DT88) enhanced fecal excretion of polystyrene microplastics and reduced intestinal residue by 67% in mouse models [100].

Source reduction through sustainable alternatives to plastic packaging represents the most promising long-term intervention [12,98]. Public awareness campaigns can accelerate behavioral change, particularly regarding single-use plastics and food storage practices [12]. Occupational protections for workers in plastic facilities are urgently needed given their dramatically elevated exposures [126].

Emerging technologies like AI-powered imaging and biosensors offer potential for real-time monitoring of food contamination, enabling more precise risk assessment and targeted interventions [73,88]. The development of reference materials and standardized protocols will facilitate better understanding of exposure pathways and ultimately inform evidence-based regulatory action [172].

7. Conclusion

This comprehensive review demonstrates that dietary exposure to micro- and nanoplastics represents an increasingly well-characterized but incompletely understood risk to human health. The ubiquity of these contaminants in food systems—with median estimated daily intake of 721 microplastic particles per kilogram of body weight—ensures near universal human exposure [4,58]. Vegetables, grains, and meat contribute more significantly to daily intake than previously assumed, challenging the historical focus on seafood as the primary dietary source [5,43].

Strong evidence links microplastic exposure to oxidative stress, inflammatory responses, immune dysregulation, and endocrine disruption [2,50]. The most compelling clinical evidence comes from cardiovascular studies, where microplastics detected in atherosclerotic plaques correlate with a 4.53-fold increased risk of major adverse cardiovascular events [37,91,148]. Nanoplastics present particular concern due to their ability to translocate across biological barriers, including the placenta and blood-brain barrier, potentially exposing developing tissues and the central nervous system to direct toxicity [9,39,64].

Methodological limitations significantly constrain risk assessment. No standardized protocols exist for microplastic detection in food or human tissues, producing inconsistent results across studies and hindering cross-study comparability [28,29,51]. The formation of biomolecule coronas on particle surfaces represents a critical but poorly characterized modifier of toxicity, potentially altering cellular interactions and bioavailability in ways that current assessment frameworks fail to capture [18,20].

Future research must prioritize the development of standardized detection methods, longitudinal human health studies, and characterization of bio-nano interactions under environmentally relevant conditions [12,17,63]. Regulatory initiatives such as the EU's microplastic restrictions [52,53] and technological innovations using AI and biosensors [73,88] offer promising pathways forward, but significant gaps in knowledge remain before comprehensive risk assessment can be achieved.

As evidence mounts regarding microplastic contamination's potential health impacts, a precautionary approach toward exposure reduction appears warranted, particularly for vulnerable populations including pregnant women, infants, and those with pre-existing cardiovascular conditions. The integration of emerging detection technologies with carefully designed epidemiological studies represents the most promising avenue for resolving current uncertainties and informing evidence-based public health interventions.

Sources

Systematically review the evidence on microplastics exposure and human health outcomes: what is s...

Research Report