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19 November 2025

Microplastics in Humans: A Critical Review of Biomonitoring Evidence and Immune–Metabolic Associations

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1
Poznan University of Medical Sciences, Department of Bromatology, Rokietnicka 3, 60-806 Poznan, Poland
2
Poznan University of Medical Sciences, Doctoral School, Bukowska 70, 60-812 Poznan, Poland
*
Author to whom correspondence should be addressed.
Appl. Sci.2025, 15(22), 12289;https://doi.org/10.3390/app152212289
This article belongs to the Special Issue Advanced Research on Microplastics, Human Exposure and Food Safety
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Abstract

Microplastics in the human body pose a significant health challenge due to their potential impact on the immune system and metabolic processes. This review summarises and critically evaluates current evidence regarding the detection of microplastics in human tissues and biological fluids, as well as their potential biological mechanisms of action. Published studies were examined with particular attention to methodological diversity, analytical techniques, and differences in study design. The review highlights consistent observations of microplastic presence in human organs, including the placenta, blood, and lungs, while also revealing significant variability in detection methods and exposure assessment. Evidence suggests that microplastics may have a potential impact on immune functions, including the modulation of the immune response, the risk of autoimmunity and immunosuppression, and metabolic homeostasis disorders that affect hormone regulation, glucose, and lipid levels. Despite the growing number of studies, major gaps include the lack of standardised analytical protocols, limited long-term human data, and insufficient mechanistic understanding at the molecular level. Addressing these gaps is crucial for enhancing risk assessment and developing effective preventive strategies to minimise human exposure to microplastics and safeguard public health.

1. Introduction

The presence of microplastics (MPs) is an emerging global environmental problem and one of the most serious ecological challenges of the 21st century. Defined as plastic particles smaller than 5 mm, MPs originate either from deliberate industrial production or from the fragmentation of larger plastic waste [1,2]. Their widespread distribution has been documented across oceans, lakes, soils, and the atmosphere, with the potential to enter food chains [3,4].
MPs form a diverse group of materials with varying physicochemical properties and additives. They include thermoplastics—such as polyethylene (PE), polypropylene (PP), polystyrene (PS), and polyvinyl chloride (PVC)—used in packaging and textiles, as well as elastomers found in coatings, rubber products, and synthetic consumer goods. These differences affect their environmental behaviour, degradation, toxicity, and interactions with biological systems [3,5,6]. MPs originate from various sources: primary MPs, like microbeads in cosmetics or microfibres from synthetic clothing, enter the environment directly; secondary MPs result from the breakdown of larger plastic debris under UV radiation, mechanical stress, or chemical processes. They spread via air, wind, and water, facilitating long-distance transport and entry into living organisms [6,7].
Humans are exposed to MPs through ingestion of contaminated food and beverages, inhalation of airborne particles, and skin contact with polluted surfaces [8]. MPs have been detected in food, drinking water, and air, indicating their ability to penetrate the digestive and respiratory systems. Due to their small size and chemical properties, MPs can be absorbed and distributed in tissues, raising health concerns [8,9]. Mechanisms such as endocytosis, paracytosis, and barrier disruption allow MPs to reach deeper tissues, potentially causing oxidative stress, inflammation, DNA damage, and neurotoxicity [10].
Global plastic production exceeds 350 million tonnes annually, much of which becomes short-lived waste that fragments into MPs [11]. MPs can act as carriers for toxic substances, such as heavy metals, PCBs, and PAHs, thereby increasing the risk of bioaccumulation and biomagnification [12,13,14]. They also transport microorganisms, including pathogens, posing microbiological risks. MPs are found not only in marine environments but also in soils, the atmosphere, and food products intended for human consumption [15,16].
Despite growing research, the mechanisms by which MPs affect human health remain poorly understood. Studies show that MPs can accumulate in organs such as the intestines, liver, kidneys, lungs, placenta, and breast milk, crossing biological barriers and disrupting physiological functions. MPs are increasingly recognised as carriers of substances with immunotoxic, carcinogenic, and endocrine-disrupting properties, which may interfere with immune signaling, hormonal regulation, and cellular homeostasis [9,17]. In vitro and in vivo studies suggest links to DNA damage, oxidative stress, inflammation, and metabolic disorders, potentially contributing to chronic diseases including cardiovascular, neurodegenerative, and oncological conditions [9,18]. Of particular concern are the effects of MPs on immune and metabolic functions, where they may modulate immune responses and disrupt physiological homeostasis [19]. Microplastics continue to pose a global environmental threat with largely unexplored consequences for human health (Figure 1). Their complexity, diverse sources, detection challenges, and the absence of standardised risk assessment protocols underscore the urgent need for further research and coordinated international action.
Figure 1. Microplastics: sources, distribution, human exposure and health.
The aim of this review is to analyse the presence of microplastics in the human body and their impact on immune and metabolic systems. This review provides a novel and comprehensive synthesis of the available evidence, identifying potential health risks, evaluating the accuracy of detection methods, and highlighting areas requiring further research to support public health protection and raise awareness of microplastic-related threats.

2. Scope and Approach

This review was prepared per the PRISMA 2020 (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines [20]. Systematic and detailed searches of the scientific literature were conducted using selected keywords such as: “microplastics”, “presence of microplastics in the human body”, “immune system functions”, “metabolic functions”, “long-term exposure to microplastics”, “microplastic toxicology”, “microplastic biomarkers”, “molecular toxicity of microplastics”, “microplastic accumulation in tissues” and “impact of microplastics on human health”. The searches used PubMed, Google Scholar, Web of Science, Embase, and Cochrane Library databases.

2.1. Inclusion Criteria

The review included articles that met the following criteria: they concerned the presence of microplastics in humans, contained data on microplastic levels in various tissues or body fluids (e.g., blood, lymph), and assessed the impact of microplastics on the functioning of the immune or metabolic systems (e.g., through analysis of the immune response or metabolic parameters). Only studies published within the last decade (since 2015) and available in full in English were included to ensure the review was up to date and relevant.
Studies written in languages other than English, studies conducted exclusively on animal models or cell lines without direct reference to humans, and so-called low-quality publications that do not present data on microplastics in the body or contain limited information on this subject were excluded.

2.2. Selection Process

The search for relevant publications was conducted systematically. At the initial stage, duplicates were removed, followed by an analysis of titles and abstracts to assess their compliance with the established inclusion criteria. Selected articles were then subjected to a detailed analysis of the complete texts to confirm that they met the methodological and thematic requirements. To ensure the objectivity and reliability of the review, recognised quality assessment criteria based on Cochrane guidelines were applied. The studies were assessed for methodological soundness, including the presence of randomisation, the use of control groups, and the implementation of blinding procedures. The description of the methods used, the statistical analysis method, and the study sample size were also analysed in detail. The results presented had to be transparent and reproducible. Only those studies that met high methodological standards were included for further analysis, which enabled the formulation of robust and reliable conclusions.
A total of 216 relevant publications were identified. After removing 44 duplicate articles, the remaining studies underwent a detailed analysis of titles and abstracts, resulting in the selection of 40 articles. Their eligibility and methodological quality were then assessed, resulting in the final inclusion of 10 publications in the review (Figure 2). The final selection of ten publications was based on their thematic alignment with the objectives of the review, the availability of original data on the presence of microplastics in human tissues or body fluids, and the fulfilment of rigorous methodological criteria, including clarity of study design, robustness of statistical analysis, and reproducibility of results, in accordance with the evaluation criteria described above.
Figure 2. PRISMA diagram.
The main topic of the analysed articles was assessing microplastics’ impact on human health, particularly their toxicity, bioaccumulation in human organs, and related health risks. The studies focused on the mechanisms of microplastic translocation in the body and its potential contribution to developing respiratory and digestive diseases and endocrine disorders. Particular attention was paid to the bioaccumulation of microplastics in organs such as the liver, kidneys and lungs, and their impact on the immune and endocrine systems. Prenatal exposure was also analysed, including the possibility of microplastics crossing the placenta, suggesting potential long-term health effects for offspring. The studies considered different fractions of microplastics, such as microspheres and fibres, and their ability to migrate within the human body. Microplastic penetration was mainly assessed in the context of migration pathways from the digestive and respiratory systems to other tissues. In addition, studies indicated possible links between exposure and the development of cancer, metabolic diseases, hormonal disorders, and abnormalities in brain and nervous system development.

3. Results and Discussion

The review covers more than a dozen studies on the presence of microplastics in human organisms and their potential impact on health, with particular emphasis on foetal tissues and the circulatory system. The studies came from various regions, including Europe (Italy, Germany, The Netherlands, Poland), Asia (China) and the Middle East (Iran), covering diverse population groups, including healthy pregnant women, newborns, adults and patients with autoimmune and cancerous diseases.
The identification and quantitative analysis of polymers were possible thanks to the use of advanced analytical techniques, such as Raman spectroscopy, FTIR-ATR (Fourier Transform Infrared Attenuated Total Reflectance), and pyrolytic gas chromatography coupled with mass spectrometry (Py-GC/MS). These methods allowed the detection of microplastics in samples from the placentas of healthy pregnant women, the placentas and meconium of newborns, women with IUGR-complicated pregnancies, the blood of healthy donors, and the amniotic fluid and placentas of patients with PPROM (Preterm Premature Rupture of Membranes). The most common polymers identified were PE, PP, PET, PS, and PVC [21,22,23,24,25,26].
Most clinical and observational studies involved relatively small groups, e.g., six healthy pregnant women in Italy [21], thirteen women in labour and their newborns [22], thirteen patients with IUGR pregnancy [24], twenty-two healthy blood donors in the Netherlands [25] and ten patients with preterm birth in China [26]. Despite the limited size of the study populations, microplastics were detected in more than half of the placenta samples and in most of the blood and amniotic fluid samples, confirming their ability to penetrate and accumulate in the human body [21,22,23,24,25,26].
Table 1 summarises key data on the prevalence of microplastics in human tissues and body fluids, with particular emphasis on their impact on reproductive health and fetal development.
Table 1. Summary of key studies on the impact of microplastics on human health.

3.1. Accumulation of Microplastics in Human Tissues

In most of the studies analysed, the presence of microplastics was confirmed in various human tissues and body fluids, including the placenta, amniotic fluid, meconium, blood, and organs such as the lungs, intestines and tonsils. Particular attention was paid to the ability of microplastics to penetrate the prenatal environment and their potential bioaccumulation. Studies involving pregnant women have shown the presence of microplastics in both amniotic fluid and placenta samples [21,23]. Similar results were also obtained in a group of healthy blood donors, in whom microplastics were detected in blood and plasma, confirming their bioavailability and ability to penetrate the body [25,26].
Studies conducted on samples from healthy pregnant women showed the presence of PE, PP and PET microplastics in both the placenta and amniotic fluid [21]. Similar results were obtained in other studies involving pregnant women, in whose amniotic fluid samples PE, PP, PET, PS and PVC were identified, confirming the wide range of polymers that can penetrate the prenatal environment [23]. Higher concentrations of microplastics were found in a group of pregnant women with IUGR complications, with PE and CPE being the dominant polymers, and their presence correlated with adverse developmental parameters in newborns [24]. Studies involving healthy blood donors also confirmed the presence of microplastics in plasma, with a predominance of PE, PP and PET, indicating that exposure to microplastics is not limited to patients with pregnancy pathologies, but also affects healthy individuals [25]. Microplastics with a diverse polymer structure were confirmed in amniotic fluid and placenta samples from women with preterm labour and PPROM [26].
Higher concentrations of microplastics were found in pregnancies complicated by IUGR [24] and in cases of preterm premature rupture of membranes (PPROM) [26]. In the group of pregnancies with IUGR, a significant correlation was found between the presence of microplastics and reduced birth weight, shorter body length of newborns and lower Apgar scores [24].
Other studies involving patients with autoimmune and cancerous diseases, compared to healthy volunteers, showed significantly higher concentrations of microplastics in patients’ blood. A correlation was also found between microplastic levels and the occurrence of chronic diseases, suggesting a potential link between exposure to these particles and the development of pathological processes [27].

3.2. Effects on Immune Regulation

In recent years, there has been growing interest in the impact of microplastics and nanoplastics on the immune systems of living organisms, including humans. One of the key areas of research is the potential ability of these particles to modulate the immune response, which can lead to both immunosuppression and excessive activation, resulting in autoimmunity. In vitro studies and animal model experiments have shown that microplastic particles, particularly nanoplastics (MNPs), interact with immune system cells, disrupting their functions and homeostasis. MNPs can stimulate the production of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-α), and exacerbate oxidative stress by inducing ROS [31]. As a result, chronic inflammation is activated, leading to damage to immune cells and an imbalance between pro- and anti-inflammatory mechanisms. This dysregulation can result in two different but equally adverse conditions: chronic inflammation (characteristic of autoimmune diseases) or immunosuppression (weakening of the body’s defence mechanisms). An essential element of this mechanism is the disruption of the Th17 and Treg lymphocytes ratio, which is key in controlling inflammation and immune tolerance [31].
Furthermore, it has been shown that microplastics can penetrate lymph nodes and the spleen and accumulate in the lymphatic system, increasing the risk of developing local and systemic autoimmune reactions [31]. Microplastics also affect antigen-presenting cells—macrophages and dendritic cells—which are major in initiating the immune response. The internalisation of particles by macrophages is associated with the activation of signalling pathways (e.g., MAPK, NF-κB), leading to increased production of ROS, nitric oxide (NO) and pro-inflammatory cytokines [32,33]. Despite the observed activation of these cells, no evident polarisation of macrophages towards a pro- or anti-inflammatory phenotype has been observed, suggesting that microplastics may act as an unstable modulator of the immune response, potentially enhancing or inhibiting the response depending on the biological context and duration of exposure [32,33,34].
Microplastic exposure also affects T and B lymphocytes, leading to their activation, differentiation and proliferation disturbances. The result can be either immunosuppression, weakened immune responses, or excessive activation, increasing the risk of autoimmunity. In the long term, this can lead to permanent changes in the immune system’s functioning, especially if exposure is chronic [35,36,37]. Studies on human macrophages have shown that microplastics can induce lysosomal destabilisation, activate key signalling pathways associated with the inflammatory response (including MAPK and NF-κB), and increase pro-inflammatory cytokine production [38,39]. At the same time, it has been observed that microplastics can also inhibit T and B cell functions, indicating their immunosuppressive potential [34,38]. This dual mechanism points to the possibility of modulating the immune system in an ambiguous and potentially unpredictable manner.
The intestinal immune system is susceptible to the effects of microplastics. Exposure can lead to microbiota dysbiosis, increased intestinal barrier permeability (also known as “leaky gut”), and reduced production of anti-inflammatory metabolites, such as short-chain fatty acids (SCFAs) [40,41]. Loss of intestinal barrier integrity allows the translocation of both microplastic particles and other pathogens into the bloodstream, which activates the immune response and may initiate or sustain chronic inflammation [40,41].

3.3. Impact on Metabolic Functions

Microplastics are ubiquitous in the environment and can enter the body by consuming contaminated food and water, raising legitimate concerns about long-term health effects. In recent years, a growing body of research has pointed to its involvement in metabolic dysfunction in living organisms, particularly in regulating hormonal homeostasis and lipid and glucose metabolism [42,43].
Microplastic particles, together with additives used in the plastics manufacturing process and contaminants adsorbed on their surface, can act as endocrine-disrupting chemicals (EDCs). The interaction of these substances with hormone receptors leads to the dysregulation of mechanisms controlling glucose and lipid metabolism. As a result, this may contribute to the development of metabolic disorders such as insulin resistance, type 2 diabetes and dyslipidaemia [42,44]. Microplastics also affect the gut microbiota, providing a substrate for forming biofilms (plastiflora), promoting changes in local biochemical processes and intensifying the inflammatory response [43,45]. An increase in the production of pro-inflammatory cytokines and hormonal signalling disorders has also been observed [42]. Research results also indicate its role in the transport of compounds with oestrogenic properties, such as bisphenol A and phthalates, which can enter the circulatory system, disrupting the functioning of the endocrine system and glucose and lipid metabolism [42]. Another important molecular mechanism is the induction of oxidative stress and mitochondrial dysfunction in metabolically active tissues such as the liver and adipose tissue. The result is a disturbed redox balance, intensification of inflammatory processes and the development of non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome [42].

3.4. Analytical Challenges and Perspectives

Although most studies confirm the presence of MPs in human tissues, discrepancies exist in particle concentrations, polymer types, and associated health outcomes [24,25,26,27,28,29,30,31]. For example, pregnancies complicated by IUGR or PPROM often show higher MP concentrations compared to healthy controls [27,29], but MPs are also detected in plasma of healthy individuals [28]. Differences in analytical methods, particle size ranges investigated, sample sizes, and geographic regions contribute to these inconsistencies [42,43,46]. Despite variability, all studies consistently indicate that MPs are bioavailable and capable of accumulating in human tissues.
Recent studies also highlight that particle size and chemical additives critically influence microplastic toxicity. The toxicity of microplastics (MPs) is affected not only by polymer type but also by particle size and chemical additives, including plasticisers, stabilisers, and adsorbed pollutants [42,45,47]. Nanoplastics (<100 nm) can penetrate cellular membranes and organelles, inducing oxidative stress, mitochondrial dysfunction, and inflammation more efficiently than larger particles [42,46]. Additives and adsorbed chemicals can act as endocrine-disrupting compounds (EDCs) and intensify pro-inflammatory responses, thereby exacerbating tissue damage and metabolic disturbances [42,47,48]. Human cell studies demonstrate that particle size and chemical composition significantly modulate cytokine release, ROS generation, and cell viability, highlighting their critical role in determining toxicity [32,38,42,45].
Despite the growing number of studies, current knowledge is still limited. Most studies have been short-term, and the lack of standardisation in micro- and nanoplastics detection methods makes it difficult to compare results and draw consistent conclusions. Therefore, it is necessary to develop and implement standardised analytical procedures covering sampling, material preparation, identification and quantification of microplastics in the environment and in organism tissues [42]. Spectroscopic techniques (FTIR, Raman), electron microscopy and chromatography are of key importance, particularly in the context of nanoplastics (<100 nm), whose potential toxicity may be greater due to their ability to penetrate cells and organelles [42,43,46]. Standardisation of these techniques will allow for comparing research results from different laboratories and regions, which is crucial for drawing reliable conclusions about health risks. It is also necessary to conduct long-term epidemiological studies to assess whether chronic exposure to microplastics causes permanent changes in human metabolic functions and hormonal homeostasis. The lack of standardised and reliable methods for detecting microplastics in organisms makes it difficult to accurately assess exposure levels and identify potential health effects [42,46].
Future studies should prioritise the standardisation of sampling, detection, and quantification methods for micro- and nanoplastics to ensure comparability of results across different laboratories and regions [42,46]. Long-term epidemiological studies are needed to evaluate the effects of chronic exposure to microplastics on human health [42]. Mechanistic research should investigate the influence of particle size and chemical additives on the toxicity of microplastics, particularly regarding immune, metabolic, and reproductive systems [38,42,45]. It is also important to examine the combined effects of microplastics with other environmental pollutants to identify potential synergistic or antagonistic interactions [47,48]. Finally, interdisciplinary approaches integrating environmental, toxicological, and clinical research are essential to inform evidence-based public health policies [49,50].

3.5. Microplastic Pollution of Aquatic Environments: Ecological Implications and Human Exposure Pathways

Pollution of the aquatic environment with microplastics and microfibers, including semi-synthetic materials, is currently one of the most serious ecological and health challenges. Research indicates that these particles not only disrupt the functioning of all trophic levels in aquatic ecosystems but also pose a potential threat to humans [49].
Microplastics, nanoplastics, and semi-synthetic microfibers, resulting from the degradation of larger plastic waste, significantly increase the likelihood of bioaccumulation in aquatic organisms and transmission to humans through the consumption of contaminated water, food, or fish and shellfish products [47]. These particles are characterised by high chemical stability and the ability to adsorb toxic organic and inorganic pollutants, such as heavy metals and polychlorinated biphenyls (PCBs), which translate into potential biological toxicity to aquatic organisms and humans [47]. It is estimated that up to 99% of microfibers are deposited in sewage sludge, which can be used as fertiliser, leading to secondary contamination of groundwater and soil [48]. Microfibers act as carriers of toxic substances for aquatic organisms, accumulate in their tissues, and can cross biological barriers. Consequently, human consumption of such organisms can lead to exposure to microplastics and related chemicals. This can promote oxidative stress, mitochondrial dysfunction, gut dysbiosis, and modulation of the immune response [48].
Exposure of aquatic microorganisms to microplastics and microfibers results in their dysbiosis, which limits the ability of ecosystems to self-clean and recycle organic matter. These disruptions can negatively impact biogeochemical cycles, including nitrogen and phosphorus cycles, and promote eutrophication and algal blooms [47]. Furthermore, there is a decline in the population of sensitive species, changes in the social structure of populations, and a reduction in biodiversity, which impairs nutrient flow and water filtration [48]. In this context, it is necessary to develop modern wastewater treatment technologies that effectively eliminate microfibers, as well as introduce legislative solutions that limit pollutant emissions and support the production of biodegradable materials [48].
After entering the gastrointestinal tract and tissues, microplastics and microfibers bioaccumulate, and their concentration increases higher up the food chain, leading to biomagnification [49]. Biological effects include reproductive disorders, reduced immunity, cellular stress, and increased mortality in fish, crustaceans, and benthic invertebrates.
The presence of microplastics and microfibers in aquatic ecosystems threatens individual organisms and can lead to the destabilisation of entire ecological systems. Due to their persistence, ability to transport toxins, and participation in biomagnification, microplastics contribute to the deterioration of the status of water reservoirs. An effective response to this threat requires coordinated action encompassing scientific research, the implementation of innovative technologies, and the development and enforcement of environmental policies. Only a holistic approach can ensure the protection of biodiversity and the long-term sustainability of aquatic ecosystems [47,49,50].

3.6. Limitations

This review faces several significant limitations. The available studies are highly heterogeneous in terms of detection methods, study populations, and experimental designs, which complicates direct comparison and synthesis of results. Moreover, the lack of long-term human studies and standardised analytical procedures limits the ability to fully assess the chronic effects of microplastic exposure on immune and metabolic functions. Methodological constraints, such as varying detection sensitivity and sample representativeness, may also influence data reliability. These issues highlight the urgent need for harmonised research protocols and consistent evaluation criteria in future studies.

4. Conclusions

The presence of microplastics in the human body has been confirmed in numerous scientific studies, a crucial step in understanding the scope and scale of this phenomenon. Despite evidence of microplastic accumulation in tissues and organs, there is still a lack of precise data on its direct impact on the functioning of the immune system and metabolic processes. Preliminary studies suggest that microplastics may trigger inflammatory responses, oxidative stress, and disruptions in hormonal homeostasis disorders, indicating potential risks to public health.
Due to current limitations, including the heterogeneity of research methods, insufficient long-term studies and gaps in molecular data, further detailed analysis is necessary. Long-term and mechanistic studies are critical for understanding microplastic action mechanisms better and assessing the risks associated with their chronic accumulation. Future studies should focus on accurately determining exposure levels, bioaccumulation mechanisms, and long-term health effects to mitigate risks posed by MPs to public health and ecosystems. As part of preventive measures, it is necessary to develop and implement consistent methodological standards for detecting and analysing microplastics in the body and raise public awareness of the potential health effects of exposure. Advancements in these areas will facilitate the development of more effective protective strategies to ensure public health safety in the face of increasing exposure to microplastics, thereby improving our understanding of microplastic action mechanisms.
In light of these findings, future research should address the following questions to advance understanding of microplastic-related health risks:
  • How does chronic exposure to microplastics affect immune system regulation and inflammatory responses?
  • What are the long-term metabolic consequences of microplastic accumulation in humans?
  • Which molecular pathways are disrupted by MPs and their associated chemical additives?
  • How can exposure levels to microplastics be accurately quantified in different populations and environments?
Answering these questions will help clarify the biological mechanisms involved and support the development of effective monitoring and prevention strategies.

Author Contributions

Conceptualization, D.K. and I.G.; writing—original draft preparation, D.K., I.G. and M.K.; writing—review and editing, D.K., I.G., M.K., M.B., K.J. and S.D.-C.; visualization, D.K. and I.G.; Supervision, S.D.-C. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

Not applicable.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
ABSacrylonitrile butadiene styrene
CRPc-reactive protein
EDCsendocrine-disrupting chemicals
EPSexpanded polystyrene
FTIR-ATRFourier transform infrared attenuated total reflectance
IL-6interleukin-6
IUGRintrauterine growth restriction
LOQlimit of quantification
MAPKmitogen-activated protein kinases
NAFLDnon-alcoholic fatty liver disease
NF-κBnuclear factor-kappa b
NOnitric oxide
PAHspolycyclic aromatic hydrocarbons
PCBspolychlorinated biphenyls
PEpolyethene
PETpolyethene terephthalate
PMMApolymethyl methacrylate
PPpolypropylene
PPROMpreterm premature rupture of membranes
PRISMApreferred reporting items for systematic reviews and meta-analyses
PSpolystyrene
PTprothrombin time
PVCpolyvinyl chloride
Py-GC/MSpyrolytic gas chromatography coupled with mass spectrometry
ROSreactive oxygen species
SCFAshort-chain fatty acids
TNF- αtumor necrosis factor alpha

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