Polybag-mediated microplastics in fruits and vegetables: Emerging global threat to health

Plastics are synthetic polymers composed of smaller monomers and additives that improve their properties. Plastics are ubiquitous across modern food systems. Small plastic particles (commonly defined as <5 mm) are now detected in soils, water, air, and biota. Global demand for plastics has increased significantly since the 1950s due to their low cost, durability, water resistance, and ease of manufacture, which have often overshadowed the severe environmental and health concerns they pose. Global plastic production reached a new record of around 430.9 Mt in 2024. Polyethylene (PE) and polypropylene (PP) accounted for the majority of its shares, at around 26 and 19 percent, respectively [1]. According to a United Nations Environment Program (UNEP) report, each year 19-23 million tons of plastic waste from land-based sources enter aquatic environments and contaminate rivers, lakes, and oceans. The report further shows that approximately three-quarters of all plastic waste is improperly managed, which leads to its accumulation in natural ecosystems as open dumps, mismanaged debris, or dispersed waste in terrestrial and aquatic habitats [2]. Due to inadequate waste management and limited recycling capacity, the accumulation of plastic waste continues to rise, intensifying the burden on both human health and the environment.
MPs are broadly categorized into primary MPs, which are intentionally manufactured for use in various products, and secondary MPs, which form unintentionally through the fragmentation and degradation of larger plastic items. When these particles reach the nanoscale (usually less than 100 nm), they are categorized as nanoplastics (NPs). The most frequently detected MPs in food products include polyethylene (PE), used in shopping bags and packaging films; PP, found in reusable containers, single-use masks, and bottle caps; polystyrene (PS), commonly used in Styrofoam; polyethylene terephthalate (PET), widely used in beverage bottles and textile fibers; and Polyvinyl chloride (PVC), found in pipe, window frame and shoe laces [3]. Emerging studies estimate that individuals may ingest nearly 5 g of plastic particles each week through food [4]. Fruits and vegetables receive plastics both indirectly (from contaminated agricultural inputs such as biosolids, mulches, irrigation water, and airborne deposition) and directly via contact with plastic packaging (PE/PP bags, wraps) used in markets and retail. Several recent reviews and primary studies confirm that produce can carry microplastics (MPs) on surfaces or within tissues [5]. MPs have been detected in human blood [6], breast milk [7], placental tissue [8], and stool [9]. This has raised serious concerns regarding its implications for human health [10]. The physiological effects of MPs exposure differ depending on particle size, polymer composition, and duration of exposure [11]. Experimental evidence shows that MPs can induce oxidative stress in human cells by elevating reactive oxygen species (ROS), which in turn triggers inflammatory pathways and other cytotoxic responses [12], [13].
However, the majority of MPs’ related studies focus on polystyrene microplastics (PS-MPs), so the specific impacts of polyethylene microplastics (PE-MPs) on different organs and cellular systems remain insufficiently understood. This knowledge gap is particularly important given the widespread use of PE-based products, such as polybags, which contribute substantially to environmental MP contamination. Through this review, we aim to bring together current evidence on microplastic contamination in fruits and vegetables, focusing especially on PE-MPs.

Multiple surveys using FTIR/Raman microscopy, pyrolysis-GCMS, and visual microscopy have confirmed the presence of MPs on the surfaces and sometimes within the tissues of fruits and vegetables [14]. The detected particles vary widely in number and size, ranging from 0.1 µm to 1 mm, and polymer types such as PE, PP, and PET [15]. These variations show differences in the methods used for sampling, digestion, and detection. A 2023 study on 72 fruit and vegetable samples observed an average of 2.9 ± 1.6 particles per gram of MPs; the highest levels were found in tomatoes. Consistent MP detection is also confirmed by recent global reviews from 2024 to 2025, which also highlighted significant differences in the approaches used in various studies [16]. Studies on animals and fish provide additional evidence of biological impacts that extend beyond human exposure. MPs have been found in zebrafish studies to induce oxidative stress, disrupt lipid metabolism, and trigger inflammatory responses [17]. Evaluation of fish and mammals indicates gastrointestinal accumulation and potential transfer within the food chain [18]. Research with rodents also shows that smaller MPs can move to the liver, kidney, and brain, suggesting possible systemic toxicity [19]. Together, these findings indicate that eating contaminated fruits and vegetables may lead to long-term microplastic exposure in humans and animals. This reinforces the need for regular monitoring and better control measures [20].

Three plausible and partly overlapping mechanisms explain how polybags increase MP burden on produce, as shown in Figure 1.

Figure 1. Figure 1. Contamination pathways. Low-density polyethylene (LDPE), high-density polyethylene (HDPE), and polypropylene (PP).

Mechanical abrasion and shedding

Repeated friction between produce and low-density polyethylene (LDPE) or other bags can shear off micro- and nano-scale fragments from the bag itself, especially if bags are old, printed, or exposed to sunlight and heat. Experimental work on other food packaging (e.g., tea bags) demonstrates that common food-grade plastics can release huge quantities of micro/nanoplastics under realistic use conditions, implying that physical contact between polybags and produce is a plausible source [21].

Migration of additives and formation of secondary particles

Plastic additives (plasticizers, stabilizers, slip agents) can leach and, under environmental conditions, contribute to polymer degradation and fragmentation. Additive-rich films under UV, heat, or microbial action fragment faster. Several reviews of food-packaging sources summarize these pathways and note that packaging can act not only as a particle source but as a vector for sorbed contaminants [22].

Surface transfer and airborne re-deposition during handling

Produce handled while inside or wrapped by bags may pick up MPs already present on the bag surface (from manufacturing, previous contacts, or ambient dust). Market handling, transport vibration, and compression can dislodge particles and redistribute them onto produce surfaces. Field studies that sampled market produce (even when original packaging was not retained) suggest that handling and retail conditions contribute to variability in MP presence [23].

Dietary ingestion is a major human exposure route for MPs. Evidence from food, beverage, and human tissue studies shows MPs in the human body (reports of MPs in blood, placenta, breast milk, and various organs have raised alarms). Toxicological studies (in vitro and in vivo) suggest a potential impact of MPs on disease pathophysiologies, including inflammation, oxidative stress, endocrine disruption, and translocation (Figure 2). Regulatory bodies (e.g., FDA) currently state there is not yet sufficient evidence to conclude that packaging-to-food migration is a major source in all contexts, but they acknowledge the presence of MPs in food and the need for standardized methods and more safety data [24].

Figure 2. Figure 2. Mechanism of Polybag-mediated MPs’ health complications. Polybag-mediated MPs induce oxidative stress either through excessive ROS or by inhibiting antioxidants such as glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), which can lead to toxic and diseased conditions, including neurotoxicity, immunotoxicity, and cancers. Polybag-mediated MPs also elevated the inflammatory biomarkers, including IL-6, IL-8, and IL-1β, leading to inflammation. Polybag-mediated MPs also exhibited lipid and energy metabolism dysregulation, gut microbiota imbalance, genotoxicity, and reproductive toxicity that ultimately resulted in severe health complications.

Oxidative stress
Oxidative stress plays a critical role in the progression of various diseases [25, 26]. ROS are natural byproducts produced during mitochondrial energy production. However, excessive amounts of ROS cause oxidative stress, which damages essential biomolecules such as DNA, proteins, and membrane lipids, and eventually leads to cell death. Both in vivo and in vitro studies have revealed that the presence of MPs disrupts the mitochondrial structure and function, which in turn promotes elevated ROS accumulation [27]. MPs trigger oxidative stress in the body by either elevating ROS levels or altering the function of antioxidants such as glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) [28]. And this MPs-mediated oxidative stress has been observed in the majority of human organs, including the brain, lungs, liver, kidney, spleen, and placenta. 
PE-MPs can cross the blood-brain barrier (BBB) and have been shown to induce neurotoxicity through the generation of oxidative stress in various kinds of animal models, including rats and zebrafish [29-32]. Sprague-Dawley rats exhibited increased lipid peroxidation and reduced antioxidant enzymes, leading to oxidative stress when treated with PE-MPs [33]. A recent study by Zhao et al. observed a significant elevation of intracellular ROS as well as Caspase-9 mRNA expression when the AML12 hepatic cell line was treated with 0.5 mg/ml polystyrene MPs for 48 hours, suggesting that oxidative stress triggered apoptotic priming  [34]. Similarly, according to Chen et al. MPs disrupt mitochondrial membrane potential and suppress the antioxidant enzyme heme oxygenase-1, causing oxidative stress-mediated cytotoxicity in human embryonic kidney 293 (HEK293) cells [35]. Another alarming study revealed that pregnant mice given MPs orally for 14 days had a significant rise in oxidative stress markers along with a reduction in placental and fetal weights, as well as fetus numbers  [36]. High PE content in the follicular fluid of 44 infertile women, whereas female mice treated with PE-MPs exhibited high ROS production as well as poor quality oocytes [37]. Human term Placenta also exhibited a significant rise in ROS after being exposed to 100µg/ml polystyrene MPs, indicating their impact on our future generations [38].

Inflammation
Inflammation is associated with the progression of a variety of diseases [39-41]. MPs, characterized as particulate xenobiotics, have emerged as notable immunomodulatory contaminants capable of activating inflammatory pathways and interacting directly with immune components [42]. A substantial amount of evidence suggests that MP-induced inflammation is triggered by oxidative stress, which acts as an initiating factor for multiple inflammatory cascades [43], [44]. MPs mediated inflammation involves the direct activation of the innate immune system. Macrophages and natural killer cells respond to MP exposure by releasing pro-inflammatory mediators such as IL-6, IL-1β, and IL-8, findings that have been consistently reported across several cell-line models [44-48]. Animal studies provide additional confirmation for these observations [49], [50]. A study by Djouina et al. reported that exposure to PE-MPs also induced colonic inflammation in mice, as evidenced by increased levels of pro-inflammatory cytokines IL-1β, IL-6, TNF, and IFN-γ, when the mice were given different-sized PE-MPs orally [51]. Beyond innate immunity, emerging data suggest that MPs also imbalance the T cell component of adaptive immune functions; however, the direct impact on B cell function has yet to be thoroughly researched [52]. 

Cancer
The prevalence of cancers is a global problem [53-55]. MP particles (PS, PE, PVC) have been detected on several carcinoma cells, including lung, gastric, colorectal, and pancreatic cancer [56]. Growing evidence indicates that MPs are linked to carcinogenesis and may act as both genotoxic carcinogens (through DNA damage) and non-genotoxic carcinogens (through inflammation) [11]. As genotoxic carcinogens, MPs induce an excessive production of ROS and oxidative stress, which can lead to DNA damage, cell-cycle arrest, and necrosis. And as non-genotoxic carcinogens, MPs promote cancer progression by sustaining chronic inflammation, altering the tumor microenvironment, and impairing immune surveillance [57]. 
Significant MP accumulation has been found in human cancer tissues, including 80% positivity in lung cancer samples, 70% in pancreatic cancer samples, and 50% in colorectal cancer samples. These findings suggest that MPs may serve as an environmental factor that contributes to the development and progression of tumors [11, 56]. Additionally, several studies have suggested an association between PE-MPs and cancer. In human gastric adenocarcinoma (AGS) cells, a 72-hour exposure to PE-MPs and PP-MPs significantly increased cancer cell proliferation [58]. Similarly, a study demonstrated that acute PE-MP exposure enhanced proliferation in U87 glioblastoma cells after 72 hours. These glioblastoma cells exhibited marked increases in proliferation and migration, as well as morphological changes such as spheroid formation, after being exposed to chronic 0.005 g PE-MP for 26 days [59]. 

Dysregulation of lipid and energy metabolism
Metabolism is the sum of all chemical reactions in cells that convert food into energy, build new cellular components, and remove waste, enabling life functions. Dysregulation of lipid and energy metabolism may lead to various diseases [60, 61]. MPs released from polybags can enter the human body through the ingestion of food stored, transported, or sold in polybags, thereby entering the human gastrointestinal tract. It eventually reaches our metabolic organs, such as the liver. Once inside the cells, these particles interfere with basic energy processes by disrupting mitochondrial function. The micro- and nanoplastics do this by weakening the mitochondrial membrane potential, which reduces ATP production, which limits the liver’s ability to perform energy-intensive processes such as β-oxidation. As mitochondrial dysfunction and oxidative stress accumulate, enzymes responsible for fat breakdown are suppressed, and hepatocytes shift toward lipid storage. So, now instead of utilizing the lipids, they store more lipids, which results in abnormal lipid buildup and metabolic imbalance. This metabolic disturbance does not occur in isolation. Plastic-derived endocrine-disrupting chemicals, such as phthalates and bisphenols, are also released by polybags, which further disturb human lipid regulation. These compounds interact with hormonal pathways such as PPAR, estrogen, and thyroid hormone signaling, leading to increased lipid synthesis, altered cholesterol handling, and an increased risk of metabolic imbalance [62]. Long-term exposure to nanoplastics has also been shown to alter human genes related to lipid transport and inflammatory pathways, patterns associated with dyslipidemia and early atherosclerosis risk [63]. These mechanisms show that MPs from polybag interaction may impact human lipid metabolism and induce long-term metabolic disorders.

Disruption of gut microbiota
Gut microbiota is profoundly associated with nearly all aspects of health [64, 65]. Just as MPs derived from polybags interfere with hepatic fat metabolism, they also significantly affect the gut microbiota—one of the body’s central regulators of metabolic and immune stability. After entering the gastrointestinal tract, MPs interact with the intestinal surface and resident microbes, producing physical and chemical stress that disrupts microbial homeostasis. MPs make the intestinal wall weaker by reducing the proteins that keep the gut barrier “tight,” which normally stops harmful substances from leaking through. When this barrier becomes weaker, the mix of bacteria in the gut changes. Useful, healthy bacteria decrease, while stress-related or harmful species become more common [66]. Human stool analyses further demonstrate that individuals exposed to higher microplastic levels exhibit measurable microbial shifts. In some cases, their gut microbes even develop genes that allow them to break down plastic, which shows that the bacteria are directly reacting to MPs [67]. These disturbances can amplify the metabolic consequences described previously. These changes in the gut bacteria increase intestinal permeability, allowing inflammatory molecules to enter the bloodstream, which worsens metabolic inflammation. At the same time, reductions in beneficial bacteria impair short-chain fatty acid production, a key regulator of lipid and glucose metabolism [68]. These findings collectively suggest that polybag-derived MPs disrupt not only the liver but also the gut bacteria. The body’s metabolism becomes even more unbalanced when both the liver and the gut are affected at the same time.

Immunotoxicity and genotoxicity
Nano and MPs cause immunotoxicity in a number of ways, including up to threefold greater levels of pro-inflammatory cytokines, up to 1.8 times more oxidative stress, and up to 70% lymphocyte depletion. In both vertebrate and invertebrate models, all of these actions weaken the immune system  [69].
Repeated exposure to polyamide-12 MPs elevated IL-8 and CXCL-8 secretion in human macrophages (p < 0.01), while leaving IL-1β, IL-18, and IL-10 levels unaffected. Targeted metabolomics increased kynurenine, FAD, and NAD levels by 30% (p < 0.01). Elevated levels of polyamide particles markedly enhanced p53 activation, signifying genotoxic stress (p < 0.01). MPs modify metabolism, induce genotoxicity, and affect cell structure without eliciting inflammation [70]. 
Recent studies on Oreochromis niloticus observe the presence of micronuclei (MN) and binucleated (BN) cells in their erythrocytes, which suggests that MPs and recycled plastics (GPs) may be genotoxic to aquatic animals. Fish exposed to MP dosages of 1, 10, and 25 mg/L for 96 hours exhibited a significant rise in micronuclei and a decrease in red blood cells (RBCs) from 1.9 million/mm³ to 1.3 million/mm³ (p < 0.05). These findings suggest that MPs and recycled plastics in water environments can be harmful to human health, particularly if they accumulate in the food chain and are consumed by humans [71].

Reproductive toxicity
Primary and secondary MPs' long-term exposure significantly disturbed reproduction in three cladoceran species: Daphnia Magana, Daphnia pulex, and Ceriodaphnia dubia, which led to brood size reductions up to 42% at 10 particles/mL. Ceriodaphnia dubia, a smaller species, was more vulnerable to reproductive toxicity. This study suggests that MPs, particularly primary particles, offer an ecological risk to freshwater zooplankton reproduction, which may have devastating impacts on aquatic food webs [72].
A 90-day study in mice demonstrated that administration with PS-MPs (0.125–2 mg/day) led to decreased live births, altered sex ratios, and reduced pup body weight. In addition, a 180-day exposure to 100–1,000 μg/L of PS-MPs resulted in decreased steroidogenic enzyme activity and the induction of sperm abnormalities. Fish exposed to 20–200 mg/L PS-MPs had delayed gonadal maturation, reduced hatching rates, and shorter offspring, with effects lasting generations. Human studies show MPs in blood and lungs, with changed hormone levels and lower sperm quality in exposed workers, although direct evidence is scarce. These findings show dose-dependent, multi-species reproductive concerns from MPs [73].

Neurotoxicity
Studies show that MPs can get through that MPs can cross the blood-brain barrier, potentially leading to neuroinflammation and cognitive deficits by increasing oxidative stress levels by up to 40% and decreasing acetylcholine levels by up to 30%. These actions promote Alzheimer's-related conditions, including the aggregation of amyloid-beta [74]. 
MPs accumulate in seafood, with fish from contaminated regions exhibiting 5.5 ± 1.6 particles/g (500–1000 μm). In mice, exposure to 5.0–5.9 μm polystyrene MPs (0.01–1 mg/day) led to the disorganisation of hippocampal neurones, oxidative stress, and cognitive impairments. Microglia infiltrate human brain tissues, leading to lysosomal overflow, microvascular obstruction, neuroinflammation, and astrogliosis, conditions linked to an elevated risk of dementia [75, 76]. 
MPs enhance neuronal demise and neuroinflammation subsequent to global cerebral ischaemia (GCI). MPs penetrate the blood-brain barrier, resulting in significant increases in inflammatory markers (Iba-1, CD68; p = 0.001) and cytokines (IL-6, TNF-α; p < 0.05). MPs additionally facilitate demyelination, the depletion of synaptic proteins, and tau phosphorylation (p = 0.031). This exacerbates motor and cognitive deficits, as evidenced by elevated mNSS and Morris water maze scores (p < 0.05) [77].

Studies differ in sampling, blank controls, particle size limits, and polymer identification, making cross-study comparisons difficult. Standardization of sampling, processing, and reporting is urgently required [78]. It is often difficult to attribute MPs on produce to polybags specifically versus environmental sources (soil, irrigation, air). Controlled experiments that simulate real-world bag-produce interactions are relatively few [5]. Most toxicology uses high-dose exposures or spherical/synthetic model particles; relevance to chronic, low-dose dietary exposures to heterogeneous environmental MPs (with sorbed chemicals/microbes) is uncertain. Longitudinal human studies and realistic animal models are missing [79]. MPs are detected by this method, excluding MPs particles ≤ 500 µm and reducing the accuracy of the results, impeding exact quantification and size range assessment of MPs in fruits and vegetables [20].
Established methods for detecting and measuring MPs in fruits and vegetables are required. The long-term health effects of dietary exposure to MPs are not adequately documented [14]. Studies found that MPs' intake is affected by food habits, food types, and geographic locations. An integrated approach of multiple analytical techniques to advance observation accuracy is needed [80].

Give priority to standardized protocols, including sample handling, size cutoffs, and polymer ID, as well as interlaboratory ring trials [78]. Design experiments (such as controlled abrasion studies, package age/UV exposure simulations, and real-world storage trials) that isolate the polybag contribution [21]. Invest in safer packaging materials and design (minimized shedding, additive transparency), and require migration/release testing under realistic use conditions [22]. Develop labeling and guidance for packaging reuse/ageing and for cold chain/retail handling practices that minimize abrasion. Simple mitigation — washing produce (rinsing and gentle scrubbing) and peeling where appropriate can reduce surface MPs (though not necessarily internalized particles). Minimize leaving produce in plastic bags for long periods in sunlight or heat. Prefer loose produce when feasible and support retailers’ reduced-plastic initiatives.
To strengthen research quality, priority should be given to protocols across studies, including standardized sample-handling methods, consistent size cut-offs, and reliable polymer-identification techniques, and conducting interlaboratory ring trials to validate these approaches [78]. Future research should also include experiments that specifically isolate the contribution of polybags, such as controlled abrasion setups, tests comparing different packaging ages and UV-exposure levels, and real-world storage simulations.
From a prevention standpoint, investment is needed in safer packaging materials and designs that shed fewer particles, use transparent additives, and undergo migration/release testing under realistic use conditions [81]. Clear labeling and handling guidelines should be provided to reduce abrasion, particularly through information such as how long packaging can be reused, how aging affects shedding, and suggested practices for cold-chain and retail handling.
Consumers can reduce surface MPs through simple mitigation strategies, such as rinsing produce, gentle scrubbing, or peeling when appropriate, even if internalized particles may remain. Produce should not be left in plastic bags in the heat or direct sunlight for an extended period of time. When possible, choosing to bring reusable bags to shop and supporting retail protocols that reduce the use of plastic can further minimize exposure.

Evidence shows fruits and vegetables can carry MPs, and polybags are a credible though variably quantified contributor via abrasion, additive migration, and handling transfer. The potential health consequences of chronic, low-dose dietary exposure through produce remain an area of active research: compelling signals of biological effect exist from laboratory and human tissue studies, but the real-world risk magnitude is still uncertain. Immediate steps should focus on harmonizing measurement methods, directly testing polybag–produce transfer under realistic conditions, improving packaging design/regulation, and applying pragmatic consumer-level mitigation. 

None.

MJU designed outlines and drafted the manuscript. MK, SA, STH, AIH, AM, and MJU wrote the initial draft of the manuscript. MJU and AM reviewed the scientific contents described in the manuscript. All authors have read and agreed to the published version of the manuscript.

There is no conflict of interest among the authors.

During the preparation of this manuscript, the authors used artificial intelligence (AI) tools (such as Consensus and ChatGPT) to improve readability and language quality. Following the use of technological supports, the author(s) reviewed and edited the text as required and take full responsibility for the text of the publication.