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Review

Microplastics as Pervasive Contaminants: Ecosystem Disruption, Human Health Risks, and Detection Approaches

by
Tejaswi Boyapati
1,*,
Sumit Ragho Gawai
2 and
Pradeep Kumar
1,*
1
Department of Agricultural and Biosystems Engineering, South Dakota State University, Brookings, SD 57007, USA
2
Department of Food Technology, Vignan’s Foundation for Science, Technology and Research, Guntur 522213, India
*
Authors to whom correspondence should be addressed.
Pollutants 2026, 6(2), 23; https://doi.org/10.3390/pollutants6020023
Submission received: 23 November 2025 / Revised: 27 February 2026 / Accepted: 3 April 2026 / Published: 14 April 2026
(This article belongs to the Special Issue The Effects of Global Anthropogenic Trends on Ecosystems, 2025)
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Abstract

Microplastic (MP) contamination has become a global environmental and public health concern due to the extensive use of plastics and ineffective waste management. These microscopic particles are now detected in air, water, soil, and food products, raising serious concerns about their persistence, bioaccumulation, and potential risks. Microplastics (MPs) have been shown to disrupt marine biodiversity, affect plant metabolism, and enter food webs, leading to accumulation in human tissues. Chronic exposure is increasingly linked to reproductive toxicity, carcinogenesis, neurotoxicity, and metabolic disorders. This review provides a comprehensive overview of the sources, pathways, and environmental fate of microplastics, with an emphasis on their ecotoxicological effects and human health implications. It also summarises key analytical methods for detecting microplastics in environmental and food matrices, including spectroscopy, microscopy, and emerging sensor-based technologies. Finally, the review highlights the need for improved waste management, stronger policy interventions, and enhanced public awareness to mitigate microplastic pollution and protect ecosystem and human health.

Graphical Abstract

1. Introduction

1.1. Global Plastic Waste and Environmental Dispersion

The pervasive presence of microplastics in the environment has become a growing global concern. Plastics, now an integral part of modern life, are primarily produced from synthetic polymers such as polypropylene (PP), polyethylene (PE), polyethylene terephthalate (PET), polystyrene (PS), polyamide (PA), polycarbonate (PC), and polyvinyl chloride (PVC) [1]. Microplastics, defined as plastic fragments smaller than 5 mm, are broadly classified into primary and secondary types [2,3]. Primary microplastics are intentionally manufactured at small sizes for use in personal care products and other household applications, whereas secondary microplastics result from the degradation of larger plastic items through physical, chemical, and biological processes [3].
These synthetic polymers are valued for their flexibility, light weight, portability, and ease of transport, making them attractive for large-scale use in industries such as food packaging, cosmetics, textiles (microfibers from synthetic fabrics), and automotive manufacturing [2,4]. However, their durability and resistance to biodegradation, combined with inadequate waste management, have led to the widespread and persistent accumulation of microplastics in the environment [4].
Microplastics are now detected in air, water, soil, and various food products, easily dispersed by wind and rain across environmental compartments [2]. According to the OECD’s Global Plastics Outlook (2022) (https://doi.org/10.1787/de747aef-en (accessed on 2 April 2026)), global plastic waste generation more than doubled from 2000 to 2019, reaching 353 million tons. Without intervention, this figure is projected to nearly triple by 2060 [5,6]. The environmental footprint of this waste is profound, with the food and beverage industry alone accounting for more than 61% of beach litter waste [7]. Consequently, significant accumulations of microplastics are now ubiquitous in oceans, seas, and freshwater bodies, acting as persistent stressors in aquatic biomes and altering water quality [7].

1.2. Pathways of Human Exposure

Beyond environmental degradation, microplastic infiltration poses a direct threat to human health. The food supply chain has inadvertently become a conduit for this exposure. Evidence [8] suggests that microplastics enter the human diet not only through seafood but also through processed foods, table salt, fast food products, and food packaging materials [3,7]. Consumption of these contaminated products has been linked to potential cytotoxicity, immune disruption, neurological effects, and metabolic dysfunctions in humans [3], necessitating a shift in how food safety risks are assessed.

1.3. Analytical Challenges and Review Objectives

As microplastics permeate the food supply chain, they become embedded in complex organic matrices ranging from raw agricultural produce to highly processed packaged goods. However, identifying these particles in food poses unique analytical challenges compared to environmental sampling.
A major challenge in studying microplastics in food lies in their typically low concentrations, which require precise pretreatment methods to isolate them from complex food matrices. While relatively simple samples such as table salt can be analyzed with straightforward procedures, complex matrices like seaweed contain natural polymers and oligomers that are difficult to distinguish from synthetic plastics [9]. Standardised detection protocols remain limited, and analytical techniques must be adapted to different food matrices. Sources of microplastics in indoor and outdoor areas are depicted in Figure 1. Outdoor sources are dominated by industrial activities, agricultural runoff (including plastic mulching), and the degradation of macro-plastics in landfills and oceans. In contrast, indoor environments contribute significantly through the shedding of synthetic fibers from textiles and dust accumulation, posing a direct inhalation risk to humans. Understanding these diverse indoor and outdoor source apportionments is critical, as they directly dictate the primary pathways of human exposure.
This review provides a comprehensive overview of the environmental and ecological impacts of microplastics, their accumulation in food chains, associated human health risks, and current analytical methods for their detection. By summarizing current knowledge and research gaps, we emphasize the need for improved waste management strategies, standardized detection protocols, and increased public awareness to address the growing threat of microplastic pollution. Recent comprehensive reviews have significantly advanced the field, focusing on general human health risks [2] and highlighting food chain contamination [3]. Nevertheless, most of the literature continues to examine these compartments in isolation. This review stands out by comprehensively connecting three unique, under-researched pillars: (1) the precise molecular mechanisms of human toxicity, especially nano plastic intracellular biotransformation; (2) the synergistic ‘Trojan horse’ effect of microplastics serving as vectors for co-contaminants such as PFAS and heavy metals; and (3) a rigorous assessment of emerging bio separation technologies, coupled with the suggestion of validated, tiered exposure-risk assessment frameworks for regulatory policy.

2. Impact of Microplastics on Ecosystems

Microplastics are a significant source of both terrestrial and marine pollution due to their ease of transport across environmental compartments. Their movement is influenced by physical properties such as size and density, as well as dynamic processes including sedimentation, surface drifting, and water currents in both marine and freshwater systems. Consequently, microplastic toxicity poses risks to marine organisms, terrestrial ecosystems, and, ultimately, human health through bioaccumulation and trophic transfer [10].
Rising seafood consumption has increased human exposure to microplastics, making it a direct pathway for plastic toxicity to enter the human diet. Documented toxic effects in various organisms, including fish, plants, animals, and plankton, include growth inhibition, DNA and tissue damage, inflammation, oxidative stress, and neurotoxicity [10]. In humans, exposure via the food chain is linked to altered metabolism, immune system disruption, carcinogenicity, cytotoxicity, and neurotoxicity [11].

2.1. Mechanisms of Ecotoxicity: Dysbiosis, Oxidative Stress, and Endocrine Interference

Rather than isolated instances of species-specific harm, cross-taxa synthesis reveals conserved mechanisms of microplastic ecotoxicity. Across both aquatic and terrestrial models, microplastic exposure consistently triggers severe oxidative stress, disruption of energy metabolism, and microbiome dysbiosis, which cascade into systemic physiological failures [12,13].

2.1.1. Gut Microbiota Dysbiosis and Metabolic Disruption

Exposure to microplastics systematically alters the gut microbiome in diverse aquatic species, fundamentally disrupting energy metabolism. Experimental models involving juvenile guppies and adult zebrafish exposed to polystyrene and polyethene particles consistently demonstrate reductions in beneficial microbial populations (e.g., Firmicutes, Verrucomicrobia) and a pathogenic proliferation of Proteobacteria [14,15]. This microbial shift directly compromises repair pathways and immune defence, resulting in goblet cell inflammation and liver necrosis [2]. Furthermore, transcriptomic profiling reveals that microplastic ingestion systematically downregulates the expression of critical antioxidant enzymes, such as catalase (CAT) and superoxide dismutase (SOD), leading to unabated accumulation of reactive oxygen species (ROS) and metabolic pathway alterations across diverse marine species [16,17].

2.1.2. Terrestrial Phytotoxicity and Systemic Oxidative Stress

The induction of severe oxidative stress is not limited to aquatic models; it represents a shared toxicological mechanism in terrestrial ecosystems. In agricultural environments, microplastics accumulate in the rhizosphere, physically obstructing water and nutrient uptake through plant roots [18,19]. While particles larger than 1.2 µm are largely excluded from root pores, smaller nano plastics can translocate through the xylem and phloem [20]. Once internalized, these particles induce direct cytotoxicity, inhibit photosynthetic efficiency, and compromise intrinsic plant defence mechanisms [2,19]. Studies on terrestrial crops demonstrate that exposure to polymers such as PVC triggers aggressive oxidative stress responses, significantly reducing seed germination and biomass [21]. This suggests that polymer accumulation systematically disrupts fundamental cellular energy pathways across host species [10].

2.1.3. Endocrine Interference and Reproductive Toxicity

Beyond metabolic disruption, microplastics act as potent endocrine-disrupting chemicals (EDCs), severely interfering with the hypothalamic-pituitary-gonadal axis across mammalian models [22]. In male models, exposure to polystyrene microplastics induces germ cell apoptosis mediated by the p53 signalling pathway, significantly increasing oxidative stress and downregulating spermatogenesis [23,24]. Microplastic exposure has been shown to induce oxidative stress and inflammatory responses in reproductive tissues, leading to impaired spermatogenesis, reduced sperm viability, and increased sperm deformities in mammalian models [25]. The recent analytical detection of microplastics in human semen, testes, and placental tissues [26,27] unequivocally confirms that these persistent particles are successfully crossing reproductive barriers. This raises profound public health concerns regarding their capacity for intergenerational endocrine interference and long-term epigenetic programming [26,28].

2.2. Systemic Human Health Risks: Barrier Translocation and Synergistic Toxicity

To fully understand the threat of microplastics, it is essential to trace their translocation from environmental vectors into systemic human circulation [3]. While ecological models demonstrate baseline metabolic disruption, human exposure pathways trigger highly specific mechanisms of intracellular toxicity, barrier translocation, and synergistic contamination.

2.2.1. Nano Plastic Biotransformation and Cellular Infiltration

A major thematic shift in recent toxicology is the critical distinction between microplastics (>1 µm) and nano plastics (<100 nm) [29]. Due to their minute size and large surface-area-to-volume ratio, nano plastics exhibit unique biokinetic profiles. Upon entering human biological fluids, they rapidly acquire a biomolecular “protein corona”—a dynamic layer of adsorbed proteins that masks the polymer’s synthetic identity, facilitating immune evasion and cellular internalization via endocytosis [30]. Unlike larger microplastics, which largely induce physical luminal blockages, nano plastics can successfully cross stringent biological barriers, including the intestinal epithelium, the blood-brain barrier (BBB), and the human placenta [31]. In vitro models using human trophoblasts demonstrate that, once internalised, nano plastics interact directly with organelles, triggering elevated production of reactive oxygen species (ROS), cell cycle arrest, and compromised placental viability [30].

2.2.2. Gastrointestinal Pathogenesis and Neurotoxicity

The gastrointestinal tract is the primary interface for human exposure to microplastics. Clinical analyses have established a direct, quantitative correlation between fecal microplastic concentrations and Inflammatory Bowel Disease (IBD), with significantly higher particle burdens observed in patients exhibiting severe mucosal ulcerations [32]. Once translocated across the damaged gut epithelium, circulating particles can induce systemic neurotoxicity. Epidemiological evidence indicates that chronic environmental exposure to polymer derivatives, such as styrene, strongly correlates with neurotoxic symptoms, including cognitive fatigue, impaired vision, and dizziness [29,33]. Furthermore, targeted analyses of mother-infant pairs have detected high concentrations of PET and PVC particles in infant faeces and meconium, directly linking early-life exposure to the degradation of feeding bottles and plastic toys [31].

2.2.3. The “Trojan Horse” Effect and Co-Contaminants

Crucially, microplastics rarely exert toxicity in isolation. Due to their highly hydrophobic surfaces and charged functional groups, they act as potent sorbents for environmental co-contaminants—a phenomenon defined as the “Trojan horse” effect [3]. Microplastics systematically adsorb heavy metals, pharmaceuticals, and per- and polyfluoroalkyl substances (PFAS) from surrounding aquatic environments [34]. Upon ingestion, the polymer matrix acts as a vector, delivering concentrated doses of these adsorbed toxins directly to the intestinal epithelium [3]. This vector dynamic significantly amplifies the baseline oxidative stress and cytotoxicity of the polymer itself, dictating that modern human health assessments must evaluate the synergistic toxicity of the plastic particle alongside its leachable additives and acquired environmental pollutants [34].

3. Impact of Microplastic Toxicity on Human Health

Micro- and nano plastics can enter the human body via ingestion, inhalation, and dermal contact. Studies have detected microplastics in human semen, testes, breast milk, placenta, liver, and blood, with particle sizes ranging from ≥800 nm to 5 mm. Interestingly, microplastics have not yet been detected in fetal lung or kidney samples [29].
The toxicological effects of microplastics in humans remain insufficiently characterized, with most evidence derived from animal models. Experimental studies on aquatic organisms and higher mammals indicate potential impacts on human health, including inflammation, oxidative stress, immune modulation, metabolic disruption, and possible genotoxic effects. However, epidemiological studies and research using human cell lines are urgently needed to clarify these risks [2]. Table 1 presents an overview of findings from experimental models evaluating the effects of microplastic exposure, highlighting key physiological and biochemical pathways affected. An overview of the health effects of microplastic exposure in humans is presented in Figure 2. It is important to acknowledge that most current toxicological data are derived from animal models, such as murine and zebrafish systems (Table 1). While these models provide essential insights into potential biological mechanisms, such as oxidative stress and inflammation, direct extrapolation to human health remains complex due to interspecies differences in metabolism and the varying dosage levels used in laboratory settings versus real-world environmental exposure. Consequently, there is a critical need for long-term epidemiological studies to validate these risks in human populations.

3.1. Impact of Microplastics on the Gastrointestinal Tract and Nervous System

A significant limitation of early plastic toxicology was the failure to differentiate between microplastics (>1 µm) and nanoplastics (<100 nm) [29]. Due to their minute size and massive surface-area-to-volume ratio, NPs exhibit entirely distinct biokinetic profiles [42]. Upon entering biological fluids (such as gastric acid or blood plasma), NPs rapidly acquire a “protein corona”—a dynamic layer of adsorbed biomolecules [22]. This corona alters the particle’s thermodynamic identity, often allowing it to bypass immune recognition and facilitate cellular uptake via endocytosis or passive diffusion [30]. Unlike larger MPs, which largely induce physical blockages or localised inflammation in the gut lumen, NPs have been shown to translocate across stringent biological barriers, including the intestinal epithelium, the blood-brain barrier (BBB), and the human placenta [26,29,31]. Intracellularly, NPs accumulate in lysosomes and mitochondria, triggering excessive production of reactive oxygen species (ROS), lipid peroxidation, and ultimately cellular apoptosis [30,43]. Researchers [32] reported a clear association between microplastic concentration in faecal samples and inflammatory bowel disease (IBD). Their findings revealed that stool from IBD patients, particularly those with ulcerative lesions in the rectal mucosa, contained significantly higher concentrations of microplastics than that of healthy individuals. Additionally, trace amounts of nanoplastics were detected on mucosal surfaces, suggesting the potential for targeted drug delivery to treat infected intestinal mucosa [44].
Several studies have also established a correlation between plastic exposure and carcinogenesis. Epidemiological evidence and meta-analyses indicate that workers in the rubber and plastic manufacturing industries have an increased risk of colorectal cancer, as well as a notable rise in pancreatic cancer incidence [29].
A large-scale investigation conducted in 2011 assessed the potential neurological impacts of styrene exposure among more than 21,000 residents in the U.S. Gulf Coast region. Researchers quantified environmental styrene concentrations and evaluated blood samples from 874 participants to assess body burden. Approximately one-third of the exposed individuals experienced neurological symptoms such as impaired vision, headache, dizziness, fatigue, numbness, and nausea. These findings strongly suggest that chronic styrene exposure can result in neurotoxic effects [29,33].
In order to further investigate the effects of microplastics on eighteen mother-infant pairs, a researcher collected samples of the infant’s feces, placenta, meconium, and formula over the first six months of life [31]. The study identified plastic toys and feeding bottles as major microplastic sources for infants, while toothpaste and cleaning products were potential sources for mothers. PVC and PET particles were detected in infant faeces, and higher microplastic release was correlated with increased bottle usage and breast milk ingestion.

3.2. Impact of Microplastics on the Reproductive and Fertility System

Both male and female reproductive systems are susceptible to microplastic-induced toxicity. Experimental studies using mouse and rat models exposed to polystyrene microplastics have shown reductions in ovarian weight, decreased follicle counts, altered cytoskeletal protein responses, and increases in cystic and atretic follicles. Furthermore, levels of key reproductive hormones, including testosterone, estradiol, anti-Müllerian hormone, and follicle-stimulating hormone, were disrupted [22,45,46]. Accumulation of microplastics in female reproductive organs also induced oxidative stress, increased fibrosis, promoted fibroblast proliferation, and triggered pro-inflammatory signalling [22,46,47].
Researchers [27] investigated microplastic accumulation in male reproductive tissues, analysing six testicular and thirty semen samples using laser direct infrared spectroscopy and pyrolysis–gas chromatography/mass spectrometry. Microplastics were detected in all samples, with mean concentrations of 11.60 ± 15.52 particles/g in testis and 0.23 ± 0.45 particles/mL in semen. Polystyrene fragments accounted for over 60% of microplastics in testes, while PVC and PE predominated in semen. These findings provide crucial baseline data on the reproductive risks of microplastics in humans. Molecular mechanisms of male reproductive toxicity of microplastics are depicted in Figure 3.
Experimental data from murine models indicate that spermatogenesis is susceptible to disruption by plastic-associated toxicants, suggesting a theoretical risk to human fertility that requires longitudinal epidemiological validation. Although no studies have directly linked microplastics to sperm quality or epigenetic alterations in mammals, the potential risk remains significant [22,28,49].
Recent studies have also detected microplastic accumulation in placental tissue from both vaginal and C-section deliveries, with concentrations ranging from 0.28 to 9.55 particles/g tissue [22]. Commonly identified polymers include PA, PE, PS, PU, and PVC. Microplastics were localized in both maternal and fetal compartments, as well as in the chorioamniotic membranes [22,26].
In vitro experiments using the immortalised HTR-8/SVneo extravillous cytotrophoblast cell line demonstrated that exposure to micro- and nanoplastics leads to cytoplasmic accumulation, elevated reactive oxygen species (ROS) production, increased pro-inflammatory cytokine secretion, cell cycle arrest, and reduced cell viability [22,30].

4. The “Trojan Horse” Effect: Co-Contaminants and Vector Dynamics

Microplastics rarely exert toxicity in isolation [2,10]. Their highly hydrophobic surfaces and charged functional groups make them potent sorbents for organic and inorganic pollutants, fundamentally altering their environmental fate and toxicity [34]. This phenomenon, known as the “Trojan horse” effect, occurs when plastics act as vectors, delivering concentrated doses of co-contaminants directly into an organism’s digestive system [10]. For instance, microplastics readily adsorb heavy metals such as cadmium (Cd) and lead (Pb); co-exposure has been shown to significantly increase toxicity by increasing gut permeability and exacerbating intestinal and hepatic damage compared to isolated metal exposure [50]. Furthermore, the interaction between microplastics and per- and polyfluoroalkyl substances (PFAS) leads to synergistic toxicity, disrupting lipid metabolism and neurogenesis [51]. A robust risk assessment must therefore evaluate the combined synergistic toxicity of the polymer, its leachates, and its adsorbed environmental co-contaminants [2,34].

5. Analytical Methods for Microplastics Detection

The detection of microplastics in food generally involves sample separation or extraction, digestion, identification, quantification, and characterisation. Pretreatment is a critical step for spectroscopic analysis, as it enhances extraction efficiency, improves yield, and minimises polymer damage. The choice of pretreatment depends on the food matrix and the characteristics of the target microplastics. Due to the complex nature of food matrices, separating and detecting microplastics can be challenging [3]. Detection techniques used in the food chain are summarised in Table 2.

5.1. Separation Methods for Microplastics

5.1.1. Membrane Pretreatment

Membrane-based pretreatment is a promising approach for recovering microplastics from food matrices. Compared with traditional separation methods that require high energy and complex maintenance, membrane separation offers a simpler, energy-efficient alternative. Depending on particle size, membranes are categorised into microfiltration, ultrafiltration, nanofiltration, and reverse osmosis [3,4]. Studies have reported microplastic contamination in milk from both local and imported brands using membrane technology [69]. A study conducted in Korea demonstrated the use of membrane disk filters combined with ozone treatment and sand filtration for isolation. A few researchers applied filtration to separate microplastics from tap water, achieving 75–91.9% removal efficiency [70,71]. Similarly, another study [72] used microfiltration and chemical techniques to detect microplastics in wastewater, with particle counts ranging from 50,000 to 15 million particles/L. These findings highlight the potential of membrane-based techniques in effective microplastic removal.

5.1.2. Flotation

Flotation is a quick and simple method widely used to recover microplastics. Samples are pre-digested with H2O2 before being mixed with a flotation medium, chosen based on the plastic density. Zinc chloride (1.5–1.7 g/cm3) is used to isolate high-density polymers (e.g., PVC, PET), while saturated sodium chloride (~1.2 g/cm3) is an eco-friendly and cost-effective alternative for targeting lower-density plastics like polyethylene [3]. Advantages include high recovery efficiency (~99%), low cost, and easy regulation. However, flotation can be less effective for complex food matrices.

5.1.3. Chemical Treatment

Chemical pretreatment enables faster sampling and efficient detection. Both alkaline and acid digestion can separate microplastics from tissues, organic matter, and food samples without major polymer degradation [3,73]. Reported efficiencies are 9–40% for HCl, KOH, and NaOH; 64–70% for H2O2; and up to 97% for ethanol extraction [74]. However, strong acids like HNO3 may damage polymers such as polystyrene. Thus, chemical digestion is most suitable for organ or tissue samples but requires careful optimisation to preserve polymer integrity.

5.1.4. Enzymatic Treatment

Enzymatic digestion uses biologically active enzymes to degrade target materials while preserving polymer structure. Although it is less harmful than chemical treatment, it is more time-consuming and often less efficient [3,75]. Common enzymes include chitinase, lipase, cellulase, and protease. A study [76] applied enzymatic treatment with H2O2 to polypropylene in fish and marine invertebrates, achieving 97% recovery with no degradation. While enzymatic methods are suitable for various biological matrices and cause minimal polymer damage, they can be costly, and their efficiency depends heavily on the sample matrix.

5.1.5. Extraction Techniques

Other reported extraction techniques include ultrasound-assisted extraction, solid-phase microextraction (SPME), and magnetic extraction.
  • Ultrasound extraction (using probe or bath sonicators) enhances solvent penetration and reduces sample loss, proving effective for separating microplastics from marine organisms and other samples [3].
  • SPME integrates sampling, extraction, and concentration, with applications in isolating polymers like polystyrene from packaging and complex soil mixtures.
  • Magnetic extraction employs nanoparticles to bind microplastics for high-recovery magnetic separation and can be combined with other methods to boost efficiency.

5.2. Detection Techniques

Various analytical techniques have been employed to detect and characterise microplastics, each with specific strengths and limitations.
  • Optical detection involves visual inspection, often aided by microscopy, and is suitable for particles >500 μm. While simple and low-cost, it is prone to error and unsuitable for routine analysis [3,77].
  • Scanning Electron Microscopy (SEM) provides high-resolution images of microplastic morphology and size by focusing an electron beam on the surface. SEM has been used to detect microplastics in aquatic ecosystems and foods such as canned sardines, sprats, Malaysian fish, and milk. When combined with infrared spectroscopy, X-ray tomography, or energy-dispersive X-ray analysis, it can reveal detailed surface and compositional features. However, SEM requires careful sample preparation and is less suited for large-scale quantitative assessment [3,77].

5.2.1. Fourier Transform Infrared Spectroscopy (FTIR)

Fourier Transform Infrared Spectroscopy (FTIR) is a widely used analytical method for characterising the surface properties of microplastics. In FTIR, samples absorb infrared light at specific wavelengths, producing molecular vibrations that reveal their chemical composition. FTIR can operate in three modes: transmission, reflection, and attenuated total reflectance (ATR). ATR-FTIR is suitable for larger plastic particles, while micro-FTIR enables chemical mapping and imaging of smaller particles [3,78,79].
FTIR has been successfully applied to detect microplastics in drinking water, food samples such as honey, soft drinks, milk, and beer, and in studies combining FTIR with Nile Red staining for enhanced identification in bottled water. However, residual water in samples can interfere with spectral quality, limiting FTIR effectiveness for certain applications [3].

5.2.2. Thermal Analysis Techniques

Thermal analysis methods identify polymers and associated components by thermally degrading samples without the need for solvents. These techniques are often coupled with gas chromatography–mass spectrometry (GC–MS) for high precision [80]. Thermal analysis has been used to detect microplastics in pet food, mussel tissues, and soils, providing detailed information on polymer composition and coexisting organic matter.
Studies indicate that thermal analysis is a sensitive and reliable approach capable of detecting a broad range of microplastic sizes and types. It minimises background contamination and offers accurate, cost-effective analysis, making it a valuable complement to spectroscopic methods.

5.2.3. Critical Comparison and Methodological Limitations

Even though the techniques offer robust detection capabilities, their practical applicability is significantly influenced by the complexity of the sample matrix and the necessary resolution limits. The most cost-effective method for rapid preliminary screening is optical microscopy; however, it is insufficient for definitive analysis due to its high rate of false positives and inability to identify polymer varieties. Although SEM and EDS provide exceptional morphological resolution, the time-consuming nature of the exhaustive sample preparation required (e.g., gold/carbon sputtering) renders them unsuitable for high-throughput food screening.
Raman spectroscopy and FTIR are the current gold standards for chemical identification; however, they have distinct operational limitations. The FTIR is highly susceptible to spectral interference from residual organic matter or water, which means that polymer peaks will be obscured by incomplete digestion of complex dietary matrices (such as mussel tissues or seaweed). In contrast, Raman spectroscopy is significantly limited by inherent background fluorescence in numerous biological samples, even though it provides superior spatial resolution and can detect nano plastics as small as 1 µm. As a result, selecting an appropriate detection method requires a strategic compromise among the scope of available sample pretreatment, the complexity of the matrix, and the size of the target particle.

6. Validated Exposure-Risk Assessment Frameworks

To transition from hazard identification to formalised risk management, regulatory bodies must adopt validated exposure-risk assessment frameworks. A lack of standardisation hampers current assessments in quantifying particle mass versus particle number across the soil-plant-human continuum [3]. A tiered risk assessment model is urgently required: (1) Probabilistic dietary exposure modelling utilizing baseline occurrence data in staple foods and drinking water; (2) In vitro/in vivo dose-response mapping focusing on biologically relevant concentrations; and (3) The establishment of Tolerable Daily Intake (TDI) limits based on the most sensitive mechanistic biomarkers, utilizing health effect sensitivity distribution methods.

7. Current Knowledge Gaps and Mitigation Strategies

Although the widespread presence of microplastics is well documented, translating environmental occurrence data into actionable public health guidelines is hindered by considerable knowledge gaps, notably the absence of systematic, long-term toxicological data on environmentally weathered plastics at relevant concentrations within complex food systems. To tackle this issue, forthcoming research must emphasise realistic exposure scenarios, particularly the synergistic toxicity of adsorbed co-contaminants, while also establishing globally harmonised analytical protocols to facilitate precise cross-comparison of microplastic burdens in global food supplies. To stop this threat, we need to do more than just make progress in the lab. We need to take immediate, coordinated action in the real world, such as upgrading wastewater treatment facilities with advanced tertiary filtration to capture nano plastics before they enter the environment. In addition, these engineering fixes need to be combined with stronger government policies, like Extended Producer Responsibility (EPR) frameworks and strict bans on intentionally adding microplastics. Additionally, it is imperative to implement public awareness campaigns to encourage individuals to stop releasing plastic at the consumer level.

8. Conclusions and Actionable Policy Interface

8.1. Scientific Synthesis and Evidence-Based Conclusions

Micro- and nano plastics (MNPs) are pervasive environmental contaminants that can accumulate across a variety of trophic levels, as evidenced by current toxicological research. The experimental evidence from murine and zebrafish models demonstrates that several conserved mechanisms of toxicity, such as endocrine disruption, oxidative stress, and gut microbiota dysbiosis, are present. Additionally, the “Trojan horse” effect suggests that MNPs act as major vectors for co-contaminants such as PFAS and heavy metals, which could potentially increase systemic toxicity.
Nevertheless, it is imperative to recognise that a significant portion of the current data on human health hazards, particularly in the context of carcinogenesis and reproductive toxicity, is derived from in vitro and animal studies. The direct clinical consequences for human health are still a subject of scientific uncertainty, despite the confirmation of barrier translocation by the detection of MNPs in human tissues (e.g., blood, placenta, and semen). To reconcile the discrepancy between animal observations and human clinical reality, future research must prioritise long-term, low-dose epidemiological investigations.

8.2. Policy Recommendations and Risk Management Strategies

A precautionary approach to risk management is needed, given the potential hazards and the enduring nature of plastic pollution. The subsequent policy and engineering measures are advised to reduce exposure:
Enhanced Wastewater Treatment: Municipal facilities must be modernised with advanced tertiary filtration technologies, such as membrane bioreactors, specifically engineered to capture sub-micron nano plastics before they enter aquatic environments.
Extended Producer Responsibility (EPR): Legislative mandates must establish EPR frameworks that obligate manufacturers to assume financial and operational accountability for the end-of-life management of plastic packaging.
Standardised Regulatory Limits: Regulatory authorities must implement standardised analytical techniques to detect MNPs in the food supply and determine Acceptable Daily Intake (ADI) values.
Global Harmonisation: An immediate necessity is a comprehensive international treaty prohibiting the intentional inclusion of microplastics in personal care products and promoting the development of genuinely biodegradable alternatives. Public Awareness Initiatives: Augmented public education is essential to reduce consumer-level plastic discharge and facilitate a shift towards a Circular Economy.

Author Contributions

Conceptualization, T.B.; methodology, T.B.; validation, T.B. and P.K.; formal analysis, P.K.; S.R.G. and T.B.; investigation, T.B.; resources, T.B.; data curation, T.B. and P.K.; writing—T.B.; writing—review and editing, P.K. and S.R.G.; visualization, P.K. and T.B.; supervision T.B.; project administration, T.B. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Acknowledgments

During the preparation of this work, the authors used ChatGPT 4o and Gemini 3 and 3.1 Pro to improve the readability and language of the manuscript. After using this tool/service, the authors reviewed and edited the content as needed and took full responsibility for the publication’s content.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Sources of indoor and outdoor airborne microplastics.
Figure 1. Sources of indoor and outdoor airborne microplastics.
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Figure 2. Overview of the sources and health effects of microplastics.
Figure 2. Overview of the sources and health effects of microplastics.
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Figure 3. Molecular mechanisms of male reproductive toxicity of MPs. T-bars indicate inhibitory effects; Upward arrows indicate an increase or upregulation; Downward arrows indicate a decrease or downregulation. AKT: Protein Kinase B; BTB: Blood-testis barrier; cAMP: Cyclic adenosine monophosphate; LHR: Luteinizing hormone receptor; MAPK: Mitogen-activated protein kinase; mTOR: Mammalian target of rapamycin; PKA: Protein kinase A; StAR: Steroidogenic acute regulatory protein; TSC1, Tuberous sclerosis complex 1; PIP2, Phosphatidylinositol 4,5-bisphosphate; PI3K, Phosphoinositide 3-kinase; S6K, Ribosomal protein S6 kinase; 4E-BP1, Eukaryotic translation initiation factor 4E-binding protein 1 [34,48].
Figure 3. Molecular mechanisms of male reproductive toxicity of MPs. T-bars indicate inhibitory effects; Upward arrows indicate an increase or upregulation; Downward arrows indicate a decrease or downregulation. AKT: Protein Kinase B; BTB: Blood-testis barrier; cAMP: Cyclic adenosine monophosphate; LHR: Luteinizing hormone receptor; MAPK: Mitogen-activated protein kinase; mTOR: Mammalian target of rapamycin; PKA: Protein kinase A; StAR: Steroidogenic acute regulatory protein; TSC1, Tuberous sclerosis complex 1; PIP2, Phosphatidylinositol 4,5-bisphosphate; PI3K, Phosphoinositide 3-kinase; S6K, Ribosomal protein S6 kinase; 4E-BP1, Eukaryotic translation initiation factor 4E-binding protein 1 [34,48].
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Table 1. Mechanistic Biomarkers and Toxicological Endpoints of Micro/Nano plastic Exposure [2].
Table 1. Mechanistic Biomarkers and Toxicological Endpoints of Micro/Nano plastic Exposure [2].
Sr. No.Experimental ModelsPolymer DetectedExposure Route & DurationExposure ConcentrationDurationRisk AssessmentMechanistic Biomarker AlteredSystemic Health EndpointReferences
1MicePolystyreneOral10 and 40 mg/kg/day60 DaysMicroplastic exposure induces oxidative stress and disrupts energy and lipid metabolism. The study also observed microplastic accumulation in the gut, liver, and kidney tissuesActivation of the p53 signaling pathwayGerm cell apoptosis; testicular vacuolization; male reproductive toxicity[29,35]
2DamsPolystyreneAqueous100 µg/L, 1 mg/L, 10 mg/LGestation to LactationExposure to microplastics led to dysbiosis of the gut microbiota and damage to the gut barrier, resulting in altered metabolism. The study found hepatic lipid accumulation in adult offspring, altering intergenerational metabolism.Gut microbiota dysbiosis (increased Proteobacteria); AChE inhibitionNeurotoxicity: induced organ-dependent oxidative damage to gills and intestine[36]
3Adult Wistar male ratsPolystyreneCellular Incubation1, 3, 6, 10 mg/kg/day5 Weeks (35 Days)Exposure to microplastics for 5 weeks didn’t show any significant impact on the neurological system.Elevated reactive oxygen species (ROS) production; increased pro-inflammatory cytokinesCytoplasmic accumulation; cell cycle arrest; compromised placental viability; and reduced cell viability[27]
4MicePolyethyleneOral6,606,000 µg/day5 WeeksExposure to microplastics results in dysbacteriosis and inflammation observed in the colon and duodenum.Reduced superoxide dismutase (SOD) and catalase (CAT) enzyme activity; activated hepatic stellate cellsHepatic fibrosis; lipid metabolism disruption; ovarian toxicity and granulosa cell apoptosis[27,37,38]
5ICR male micePolystyrene
microplastics (5 µm)		Drinking water100 µg/L, 1000 µg/L, 10 mg/L35 daysOral exposure to polystyrene microplastics induces reproductive toxicity in mammalsIncreased inflammatory markers (IL-1β, IL-6, TNF-α); activation of NF-κB signaling; decreased antioxidant pathway markers (Nrf2, HO-1); increased apoptosis markers (Bax/Bcl-2 ratio)Testicular tissue damage, reduced sperm viability, increased sperm deformities, impaired spermatogenesis[25]
6Swiss micePolystyreneGestational/Lactational Oral12.5 mg/kg30 DaysMicroplastic exposure results in oxidative stress, which damages cognitive function and decreases acetylcholinesterase activity but does not alter locomotor and behavioural modifications.Gut microbiota dysbiosis; severe gut barrier damageAltered intergenerational metabolism; hepatic lipid accumulation in F1 and F2 offspring[39]
7Sprague–Dawley ratsPolystyreneOral0.0125 to 1.25 mg/day7 to 35 DaysExposure to microplastics caused inflammation in the lungsDecreased acetylcholinesterase (AChE) activity; elevated oxidative stress markersDamaged cognitive function; neurological impairment[40]
8C57BL/6 male micePolystyreneAqueous (Parental exposure)100 ppb (mixed sizes)35 DaysExposure to microplastics resulted in germ cell apoptosis triggered by the p53 pathway, raised epididymis weight, and vacuolization of the spermatogenic cell layerAltered gene expression related to circadian rhythmTransgenerational toxicity; reduced hatching rates and immune suppression in F1 offspring[23]
9Wistar ratsPolystyreneOralE2.5, 5, and 10 mg/kg/day45 DaysPolystyrene microplastic exposure reduced antioxidant enzyme activity, disrupted lipid metabolism, and altered reproductive hormone levels in adult female Wistar ratsDecreased SOD and catalase (CAT) activity in liver and ovary; increased total cholesterol, triglycerides, and LDL; elevated FSH, estradiol, and testosterone; increased IL-6 and NF-κB levelsOvarian toxicity; hepatic fibrosis; lipid metabolism disruption; activated hepatic stellate cells; reproductive hormone disruption[41]
10MicePolystyreneOral10 and 40 mg/kg/day60 DaysExposure to microplastics resulted in metabolic disorder, altering the intestinal barrier function, microbiota dysbiosis and decreased intestinal mucus secretion [24]
Note: AChE: Acetylcholinesterase; CAT: Catalase; F1/F2: First/Second filial generation; FSH: follicle stimulating hormone; HO-1: Heme oxygenase-1; IL-1β/IL-6: Interleukin-1 beta/6; LDL: low-density lipoproteins; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf2: Nuclear factor erythroid 2-related factor 2; ROS: Reactive Oxygen Species; SOD: Superoxide Dismutase; TNF-α: Tumor Necrosis Factor-alpha.
Table 2. Detection technique for microplastics in the food chain [3].
Table 2. Detection technique for microplastics in the food chain [3].
Sr. NoSamplesPolymer DetectedDetection MethodReferences
1Cultivated fishPolyethene terephthalate, polystyrene, and polypropyleneOptical microscope, binocular microscope, Raman spectroscopy and high vacuum scanning electron microscope with energy dispersive X-ray microanalyzer [52]
2Commercial migratory fishesPolyethene, rayon, polypropylene, nylon, and other polymer typesStereomicroscope, Fourier transform infrared spectroscopy[53]
3InvertebratesPolyacrylonitrile, Cellophane, polypropylene, polyamide, polyethene, polyethene terephthalateStereomicroscope, micro–Fourier Transform Infrared Microscope[54]
4Beverage containers, glass bottles and returnable & single-use plastic bottlesPolyester, polystyreneMicro-Raman spectroscopy[55]
5Bottled waterPolyethene, polypropylene and Polyethylene terephthalateFourier-transform infrared spectroscopy and Raman stereoscopy[56]
6Public potable water Polypropylene and Polyethene Micro-Raman spectroscopy[57]
7Infant feeding bottlePolypropyleneMicroscope, Raman spectroscopy[38]
8RicePolyethene, polypropylene, Polyethylene terephthalateFourier transform infrared spectroscopy; Pressurized liquid extraction combined with double-shot pyrolysis gas chromatography/mass spectrometry[58]
9Refreshing beverage, skimmed milk, industrial honey, industrial beer and craft beerHigh-density polyethylene, low-density polyethylene, Polypropylene, and polyacrylamideFourier transform infrared spectroscopy, Inverted microscope[59]
10Take-out food containerPolyethene, polypropylene, polystyrene, polyethene terephthalate, x cotton, acrylic, and nylonscanning electron microscope, Carl Zeiss Discovery microscope, μ-Fourier transform infrared spectroscopy[60]
11ChickenPolyetheneDifferential Scanning Calorimetry, Fourier-Transform Infrared Spectroscopy, and Stereoscope[61]
12FishPolyetheneDifferential Scanning Calorimetry, Fourier-Transform Infrared spectroscopy and stereoscope[61]
13Zebrafish (Danio rerio)Polyethene (PE) Micro- and Nano plasticsInduced organ-dependent oxidative damage (gills, intestine); significant gut microbiota dysbiosis (increased Proteobacteria); inhibition of Acetylcholinesterase (AChE) indicating neurotoxicity[62]
14Crucian Carp (Carassius auratus)Polystyrene (PS) 50–500 µmDose-dependent liver cell necrosis and inflammation; downregulation of antioxidant enzymes (CAT, SOD, GST); upregulation of immune-response genes (IL-8, IL-1β).[63]
15Thick-shell Mussel (Mytilus coruscus)Polystyrene (PS) MicrobeadsImmunotoxicity is evidenced by impaired hemocyte viability and phagocytosis, as well as increased vulnerability to harmful algal blooms (HABs) due to compromised immune defense[64]
16Water Flea (Daphnia magna)Mixed Polymers (Meta-analysis)Meta-analysis of 64 studies (369 data points) confirms a 20.8% reduction in offspring production; smaller particles (<1 µm) elicited stronger reproductive toxicity than larger ones[65,66]
17Microalgae (Microglena sp.)Polylactic Acid (PLA) Bio-based plasticInhibition of photosynthesis and chlorophyll biosynthesis; downregulation of flagella-related genes, reducing motility; proof that “biodegradable” plastics still pose physical risks[66]
18Marine Medaka (Oryzias melastigma)Polystyrene (PS) 10 µmTransgenerational toxicity: parental exposure led to reduced hatching rates and immune suppression in F1 offspring; altered gene expression related to circadian rhythm[67]
19Pacific Oyster (Crassostrea gigas)Tire Wear Particles (TWP)Leachates from tire particles caused acute toxicity to larvae; disrupted development and shell formation; high zinc concentrations in leachate were identified as a key stressor[68]
20Marine Algae (Global Analysis)Global Dataset (Meta-analysis)Quantified global decline in photosynthesis due to MPs (7–12% reduction); estimated significant losses in net primary productivity (NPP) and carbon sequestration capacity[65]
Note: PET: Polyethylene terephthalate; PS: Polystyrene; PP: Polypropylene; PE: Polyethylene; PLA: Polylactic Acid; FTIR: Fourier-transform infrared spectroscopy; SEM-EDX: Scanning electron microscope with energy dispersive X-ray microanalyzer; DSC: Differential Scanning Calorimetry; Py-GC/MS: Pyrolysis gas chromatography/mass spectrometry; HABs: Harmful algal blooms.
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Boyapati, T.; Gawai, S.R.; Kumar, P. Microplastics as Pervasive Contaminants: Ecosystem Disruption, Human Health Risks, and Detection Approaches. Pollutants 2026, 6, 23. https://doi.org/10.3390/pollutants6020023

AMA Style

Boyapati T, Gawai SR, Kumar P. Microplastics as Pervasive Contaminants: Ecosystem Disruption, Human Health Risks, and Detection Approaches. Pollutants. 2026; 6(2):23. https://doi.org/10.3390/pollutants6020023

Chicago/Turabian Style

Boyapati, Tejaswi, Sumit Ragho Gawai, and Pradeep Kumar. 2026. "Microplastics as Pervasive Contaminants: Ecosystem Disruption, Human Health Risks, and Detection Approaches" Pollutants 6, no. 2: 23. https://doi.org/10.3390/pollutants6020023

APA Style

Boyapati, T., Gawai, S. R., & Kumar, P. (2026). Microplastics as Pervasive Contaminants: Ecosystem Disruption, Human Health Risks, and Detection Approaches. Pollutants, 6(2), 23. https://doi.org/10.3390/pollutants6020023

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