Microplastics and Nanoplastics in Human Health: Toxicological Mechanisms Involving Oxidative Stress, Endocrine Interference, and Inflammatory Responses

Abstract

The increasing prevalence of microplastics (MPs) and nanoplastics (NPs) in various environments has raised significant public health concerns worldwide. Defined as plastic particles smaller than 5 mm (MPs) and under 1 ?m (NPs), they arise from both industrial manufacturing processes and the breakdown of larger plastic items. MPs and NPs are found in air, water, soil, and food systems, representing an unavoidable source of human exposure. This review synthesizes scientific research on the toxicological effects of MPs and NPs, focusing on three main biological mechanisms: oxidative stress, endocrine disruption, and inflammation. Experimental studies reveal that these plastic particles lead to increased production of reactive oxygen species, resulting in mitochondrial damage, lipid peroxidation, protein oxidation, and DNA injury. Such oxidative effects disrupt critical signaling pathways, including Nrf2, MAPKs, and toll-like receptor-associated pathways. Additionally, MPs and NPs can transport endocrine-disrupting chemicals like bisphenols and phthalates, which interfere with hormone synthesis and neuroendocrine regulation. The particles also trigger innate immune responses by enhancing inflammation through inflammasome activation and prolonged release of inflammatory mediators. The combination of oxidative stress, endocrine disruption, and chronic inflammation has been linked to continuous damage across multiple organ systems, including reproductive, gastrointestinal, hepatic, cardiovascular, and nervous systems. Despite accumulating experimental evidence, there are still considerable knowledge gaps regarding exposure levels, dose-response relationships, and the clinical impacts on humans, which are essential to address for effective risk assessment and regulatory policy development.

Keywords

Introduction

Mechanisms of Endocrine Disruption

Chemical Additives as Endocrine Disruptors

The critical issue of MP/NP toxicity is primarily originating from their function as vectors for endocrine-disrupting chemicals (EDCs) [1], [7], [8]. Plastics contain many additives—plasticizers, flame retardants, stabilizers, antioxidants, etc.—that can leach into biological systems [8]. Among these compounds, bisphenol-A (BPA) and phthalates are the most extensive studies on the link between plastic exposure and EDCs [1], [7], [14]. In polycarbonate plastics and epoxy resins, BPA binds to estrogen receptors (ERs) and mimics endogenous estrogen signaling, showing estrogenic activity [1], [14]. Phthalates, used as plasticizers found in flexible PVC products, exert anti-androgenic activities by inhibiting testosterone production and androgen receptor recruitment [1], [7]. These chemicals may be emitted from MPs/NPs during ambient weathering and/or post-ingestion, resulting in both particles and dissolved EDCs exposure [1], [8]. The endocrine-disrupting effects of MPs/NPs in the endocrine-disruptive properties cannot even be restricted to BPA and phthalates alone, but it can also extend to other heterogeneous agents with hormonal activity [8], [12]. Such chemical complexity complicates elucidation of the separation of the effects of particles from those of the associated chemicals per se, but there is evidence for synergistic toxicity [1], [8].

Interactions between hormones and receptors of hormones

EDCs derived from MPs/NPs cause endocrine disruption via several mechanisms including hormone receptor interactions as one of the major pathway [7], [14]. BPA and structurally similar bisphenol derivatives bind to estrogen receptors (ERα and ERβ), triggering, or inhibiting estrogen signalling pathways [14]. This interaction can modulate gene transcription, cellular proliferation and differentiation pathways in estrogen-responsive tissues such as reproductive organs, breast tissue and bone [14]. Phthalates and their metabolites act to inhibit androgen receptor (AR) signaling, which results in suppressed androgen-dependent gene expression and perturbation of male reproductive development [2], [7]. Some phthalates also activate peroxisome proliferator-activated receptors (PPARs), nuclear receptors that regulate lipid metabolism and adipogenesis [7]. This PPAR activation leads to metabolic dysregulation and explains the obesogenic characteristics of some plastic additives [7]. Disruption of thyroid hormone is also a significant endocrine consequence of MP/NP exposure [7]. Certain plastic additives affect thyroid hormone synthesis, transport and metabolism modifying the thyroid hormone levels [7]. Thyroid hormones play a crucial role in metabolism and growth, as well as neurodevelopment, hence their disruption has major health consequences especially in unborn fetuses and children [7], [9].

Disruption of HPG and HPT

Axis MP/NP exposure disrupts neuroendocrine regulation by modulating physiological response at the levels of the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-thyroid (HPT) axes [2], [16]. When MPs/NPs alter normal functioning of the hypothalamic-pituitary-ovarian axis, they disrupt equilibrium with ovarian androgens and endocrine regulation in female reproductive systems [2]. This disruption reduces gonadal proliferation, compromises ovarian operation and decreases ovarian reserve size [2]. Animal studies have shown that MP/NP exposure affects release of gonadotropin-releasing hormone (GnRH) from hypothalamus, luteinizing hormone (LH) and follicle stimulating hormone (FSH) from pituitary and sex steroids from gonads [2], [16]. These hormonal levels in turn cascade over the reproductive system disrupting folliculogenesis, ovulation and fertility [2]. In males, MP/NP exposure disturbs hypothalamic-pituitary-testicular axis, which leads to abnormal testosterone synthesis and lack of success in spermatogenesis [5], [16]. Plastic particles in mice bioaccumulate in the testes, disrupting spermatozoa morphology and reducing sperm vitality [5], [16]. The endocrine disruption extends beyond reproductive hormones to affect both metabolic and stress hormone systems [7], [10].

Reproductive and Developmental Toxicity

The reproductive system is one of the major targets of endocrine disruption due to MP/NP [2], [5], [16]. Continuous exposure to MPs/NPs induced ovarian toxicity in the female host with smaller follicle numbers and granulosa cell apoptosis and poor oocyte quality. These effects impair fertility and could promote reproductive aging [2]. Human follicular fluid has been detected with MPs/NPs, which suggests potential direct impact on oocyte growth [1]. MPs/NPs accumulate in the placental environment and can have deleterious effects on fetal development [5], [9]. Placenta has poor detoxifying ability and is immunely regulated, which renders it an essential site of such a possible site of foreign particles [5]. MPs/NPs may cross the placental barrier, which exposes the developing fetus to particles and a variety of associated EDCs with critical stages during development [5], [9]. This exposure may cause metabolic changes, interfere with fetal development, and program long-term health outcomes [2], [5]. The transfer of MPs/NPs through maternal channels via breast milk creates postnatal exposures to nursing infants [2], [7]. Maternal MP/NP exposure has been documented by animal studies to alter energy and lipid metabolism in offspring, raising the possibility of continuing developmental programming effects beyond the exposure period [7]. These transgenerational effects invite worry about intergenerational cumulative effects [16]. Reproductive toxicity of MPs/NPs affects both sexes and extends across the lifespan, spanning endocrine disturbance and physiological response through reproductive maturity [16]. Endocrine disruption, oxidative stress and inflammation combine to form a multi-hit mechanism affecting reproductive health on numerous levels [2], [16]. 

Mechanisms of Inflammatory Response.

Activation of Inflammasome of NLRP3 NLRP3 (NOD-like receptor family pyrin domain containing 3)

Inflammasome appears a key monitor for MP/NP immunotoxicity and a key mediator for pro-inflammatory responses [3], [17], [30]. Inflammasomes are multi-protein complexes that sense pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), and therefore activate innate immunity [30]. Among subtypes of inflammasomes, particulate matter, such as MPs/NPs is specific to NLRP3 [30]. The following pathways are reported to be activated by MP/NP activation of the NLRP3 inflammasome [3], [17], [30]. The lysosomal deconstruction resulting from particle ingestion also leads to an accumulation of cathepsins in the cytoplasm which act as a danger signal triggering the assembly of inflammasome [30]. Moreover, MP/NP induced mitochondrial defects and ROS production are also strong NLRP3 activators [3], [17]. The mitochondrial ROS spike induced by MP stimulation is essential for triggering the inflammatory cascade [3]. It can activate the NLRP3 inflammasome to recruit the adaptor protein ASC (apoptosis associated speck-like protein containing a CARD), as well as pro-caspase-1 and generates a large multiprotein complex [3], [30]. The assembly promotes caspase-1 activation that cleaves pro-IL-1β and pro-IL-18 to their mature, bioactive functional forms [3], [30]. The ROS/NLRP3/Caspase-1/IL-1β signaling cascade is one of the major pathways linking oxidative stress and inflammatory-driven responses in MP/NP toxicity [3]. Microplastics from infant feeding bottles induced by human intestinal cells exhibit clearly mediated activation of this pathway, with increased activity of caspase-1 and secretion of IL-1β [3]. Consequently, the NLRP3 inflammasome acts as a molecular pipeline linking particle recognition, oxidative stress, and the production of inflammatory cytokines [17], [30].

Cytokine Profiles and NF-κB Signaling

MP/NP exposure results in a typical pro-inflammatory cytokine profile with prominent activity in interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) [3], [12], [17]. These cytokines mediate local and systemic inflammatory reactions, recruiting immune responses, activate endothelial cells, and initiate acute phase protein production [17]. IL-1β, generated through inflammasome-mediated caspase-1 cleavage, is a powerful proinflammatory mediator that enhances inflammation [3], [30]. IL-6 is pleiotropic and its action can elicit pro-inflammatory and anti-inflammatory activity according to the context [3], [12]. TNF-α, derived from activated macrophages, induces endothelial activation, reinforces leukocyte adhesion, and can also initiate apoptosis pathways [3], [12]. Experimental findings show increased concentrations of these cytokines in response to MP/NP treatment. In response to exposure to microplastics from baby bottles in intestinal cells, elevated IL-6 and TNF-α levels indicated an ongoing inflammatory cascade [3]. Nanoplastics enhance inflammatory cytokines in keratinocytes and macrophages such as macrophages causing fibrosis through fibroblast stimulation [12]. This cytokine-mediated inflammation causes tissue damage and remodeling [12]. Nuclear factor-κB (NF-κB) is a master transcriptional modulator of inflammation elicited by MP/NP exposure [17]. Under basal conditions, NF-κB is kept in the cytoplasm by inhibitory IκB proteins. MP/NP-mediated signaling such as the ROS, cytokines and the activation of pattern recognition receptors induce the phosphorylation and degradation of IκB, which contributes to NF-κB translocation to the nucleus and the transcription of pro-inflammatory genes [17]. The NF-κB pathway in combination with MAPK and NLRP3 inflammasome pathways activate an integrated inflammatory response network. Thus, the downstream activation of the following pathways results in chronic production of inflammatory mediators, maintaining the state of chronic inflammation by inducing the cytokines inflammatory mediators [17].

Immune Cell Responses.

MPs/NPs bind to various immune cell populations, modifying their function which promotes immune-pathogen interactions and contributes to immunotoxicity [14], [17], [30]. As professional phagocytes, macrophages tend to internalize MPs/NPs preferentially, resulting in compromised phagocytic capacity and dysregulated cytokine production [17]. MP/NP exposure adversely affects macrophage phagocytosis, which may undermine host defense to pathogens [17]. Dendritic cells (DCs), essential for the initialization of a response against microbes and viruses, are not properly matured after MP/NP induction [17]. These altered DC function may have detrimental effects, including through disruption to T cell priming and polarization, compromising cellular and humoral immunity [17]. Neutrophils express neutrophil extracellular traps (NETs), web architectures of DNA and antimicrobial proteins, to react with MPs/NPs and the neutrophils and to bind to these NETs will trap pathogens, but they likewise act upon the host cell to damage the tissue [17]. MP/NP exposure affects T and B lymphocyte responses, as seen in various studies where T cell subset distribution and antibody production were altered on different subjects [17]. These detrimental effects in adaptive immunity indicate that they may result in a higher susceptibility to infection by increasing vulnerability with the potential for autoimmune phenomena [17]. Indeed, MP/NP exposure has been shown in preclinical models to aggravate autoimmune diseases such as systemic lupus erythematosus, inflammatory bowel disease, and rheumatoid arthritis [17]. The skin immune cells such as keratinocytes, Langerhans cells, dendritic cells, melanocytes; macrophages; and T cells respond to MP/NP contact, potentially disrupting the integrity of the skin barrier [12]. This multi-cellular immune reaction leads to inflammation of the skin and can induce inflammatory skin conditions [12].

Organ-Specific Toxicity of Microplastics and Nanoplastics

Reproductive System

Microplastic and nanoplastic toxicities have a particularly severe impact upon the reproductive system. As plastic particles accumulate in gonadal tissues, they can provoke oxidative damage, inflammation, and disorders in the endocrine system. In males, it has been linked to low sperm count, reduced sperm motility, testicular lesions, and a dysregulation of the endocrine system. Ovarian failure, altered follicular development, and irregular estrous cycles have been described in females. Microplastics can travel through the placenta during pregnancy, and there are fears of fetal exposure. Placental tissue oxidative stress and inflammation have been shown to impair placental function and may affect fetal development and growth.[2,5,16]

Gastrointestinal System.

The gastrointestinal tract is a primary entry route of ingested microplastics and nanoplastics. Interactions with intestinal epithelial cells may lead to disruption of the tight junctions and increase permeability. It allows plastic particles and their associated contaminants into the bloodstream. Microbiome changes in the gut have also been noted post-plastic particle exposure. Such changes can potentiate inflammation and metabolic derangement as well as further contribute to extra-intestinal health consequences.[3,11,29]

Hepatic System.

The liver is a major detoxification organ, and one of the most important sites for microplastic accumulation following systemic distribution. Oxidative stress, inflammation, and lipid metabolism changes have been observed with liver exposure. Experimental models depict hepatocellular degeneration and inflammation as histopathological changes.[1,7,19]

Cardiovascular and Nervous Systems.

Microplastics and nanoplastics are increasingly known to have an influence on cardiovascular function via oxidative stress, endothelial dysfunction, and inflammatory processes. The ability of nanoplastics to cross the blood-brain barrier may lead to neuroinflammation, increased oxidative stress, and potential impact on neurobehavior in the nervous system. [26,29]

Vulnerable Populations and Life-Stage Susceptibility.

In the case of microplastics and nanoplastic toxicity, however, it is not the same for each individual and at all stages of life. There are some who are more susceptible as a result of increased exposure, distinctive physiology, and decrease in the detoxification capacity. Pregnant women, fetuses, infants, and toddlers are in particular of concern. The presence of environmental pollutants in pregnant women can be affected by the physiological and hormonal alterations. The possible passage of microplastics and/or nanoplastics through the placenta is very worrying in terms of fetal exposure to microplastics and/or nanoplastics in critical developmental milestones. Oxidative injury and inflammation in the placenta may hinder transport of nutrients and hormones, contributing to fetal development and future health issues. Microplastic exposure in infants and toddlers can occur via a range of micro-trajectories—including those via baby bottles, toys, clothing, and indoor air. They are unique, through developing organs, underdeveloped antioxidant pathways, and developing brains, in both vulnerability to oxidative stress and dysfunction of hormone function. Such early-life exposures could have lasting consequences, increasing their likelihood of metabolic disorders and reproductive or neurological consequences later in life. The elderly are already at a higher risk, because aging can cause a reduction in the capacity of antioxidant defenses and immune defenses. Other diseases (both chronic and non-chronic) can also increase the toxicity of plastic particles, especially those that act in inflammation and oxidative stress-related pathways.[3,5,16,19]

Factors Influencing the Toxicity of Microplastics and Nanoplastics.

The biological response of microplastic and nanoplastics is characterized by an interaction between a multitude of physical, chemical, and environmental factors. Size is a decisive factor for toxicity, and nanoplastics are bioavailable, and move over the cell-wall membrane better than larger particles of microplastics. The specific surface area/volume ratio of lower-size particles increases cross-site surface interaction with cell membranes and internal structures. Shape is also important. Asymmetric or fibrous particles are likely to be more physically irritating and inflammatory than smooth spherical particles. Protein adsorption and cellular uptake, which are influenced by the charge and functional group chemistry of a particle, can reflect on immune recognition and intracellular signal transporters. Polymer identity and additives complicate biological responses even more. Various plastics degrade at various rates and emit chemicals at various periods. Additives, including plasticizers and stabilizers, leach out, acting independently to drive hormonal and oxidative stress responses. Environmental aging (UV radiation/ grinding/ chemical exposure) changes the chemistry of particles’ surface so that it becomes more biochemically reactive. Older plastics have better affinity to target toxic pollutants and microorganisms from the environment resulting in a unique interaction of particle, chemical, and biological factors that can add upon each other, to produce increased toxicity.

Environmental Interactions and Co-Exposure Effects.

In practice, microplastics and nanoplastics don’t exist independently in the real world. Those co-occur within a list of chemicals and organisms: heavy metals, persistent organic pollutants, pesticides, and microorganisms. Such mixtures may modify the toxicity of plastic particles by promoting the mobility of co-contaminants into tissues. Adsorption of metals and organic pollutants to plastic surfaces may enhance their bioavailability to living organisms, which is likely to enhance oxidative stress and inflammation after exposure. It is also, of course, that plastics may accumulate microorganisms on the polymer on its surface, such that they may develop the form of biofilm that can harbour germs and antibiotic resistance genes. Which is to say that plastics have been shown to function as vectors for microorganisms and present further health hazards. Risk estimation becomes more complicated, especially when such plastic is contaminated with and co-exposed to plastics and the potential contaminants associated with it when they are co-exposed to the other contaminants. Synergistic or antagonistic effects can occur, distorting the total risk. These interactions need to be understood for making informed assessments of real-world health risks.[10,18]

Epigenetic and Transgenerational Factors 

Increased evidence indicates that epigenetic regulation, which may influence gene expression without altering the underlying DNA sequence, may be mediated by microplastic exposure and exposure to nanoplastics. Plastic particle-induced oxidative stress and inflammation might change DNA methylation, histone modifications, and function of non-coding RNA. Even more importantly, epigenetics that occur in critical periods in development can have long-lasting effects on a person’s health and vulnerability to diseases. There is also worry that these changes may be passed down from one generation to the next, leading to cumulative effects of plastic pollution over time. This is still not well understood.[1,7,8] 

DISCUSSION 

New emerging evidence suggests that both microplastics and nanoplastics pose an actual and multifaceted risk to human health. Unlike traditional chemicals, microplastics and nanoplastics interact with biological systems in a unique combination of physical, chemical, and biological mechanisms. This multi-modal interaction greatly complicates the task of toxicology and calls for combined, mechanistic analysis. Oxidative stress represents the major mechanism of toxic effects of microplastics and nanoplastics. Overloading cells with reactive oxygen species leads to redox imbalance and leads to macromolecular damage and mitochondrial dysfunction. These redox dysfunctions disrupt the homeostasis of cells and also cause downstream inflammation, immune responses, and a host of related disorders to go into motion. Because plastic particles remain in tissues, this oxidative insult can extend over a long enough duration to enhance the toxicity. And, inflammation is a major downstream result of this redox disturbance. As a result, pro-inflammatory mediators are continuously released via activation of innate immune responses, such as NF-κB signaling, and inflammasome activation. This chronic, low-grade inflammation may promote tissue remodeling, fibrosis, and dysfunction, leading to widespread non-communicable diseases. Disturbance of the endocrine system is a second leading mechanism of plastic toxicity. Microplastics and their additives affect endocrine function in multiple ways (directly and indirectly) via oxidative and inflammatory pathways. Endocrine dysfunction is one of the most common pathophysiologic factors that impact reproductive function, metabolism, and neurodevelopment and is particularly well-known when this dysfunction is present at critical periods of life. Importantly, these mechanisms do not appear to be mutually exclusive. Oxidative stress, inflammation, and endocrine disruption are interconnected pathways, contributing to a network of mechanisms that may play a role in systemic toxicity. Key to identifying areas of prevention and controlling adverse health effects are insights into these relationships. 

Limitations of Present Evidence 

In short, though we have advanced the understanding of the mechanisms of damage caused by microplastics and nanoplastics, there are several gaps with limited information remaining in our knowledge that are vague and difficult to interpret. Much of what we have learned comes from in vitro measurements and from animal studies with exposure levels that might not reflect what will actually occur in humans. This is further complicated by variations in particle size, polymer, surface chemistry, and in the design of the studies. Very limited human epidemiological data is available, and there is no standardized way to measure exposure. It is challenging to assess and quantify nanoplastics in biological specimens, making efforts to understand how internal dose influences health effects more challenging. Likewise, the long-term health effects of low-level chronic exposure have not been well understood. [4,6,20]

Future Research Directions 

Future studies should develop standardized methods in order to analyze microplastics and nanoplastics in environmental and biological samples.[5,6,] Exposure models that simulate natural settings, including realistic concentrations, particle properties, and co-exposure, should be applied to maximize translational impact. Longer-term human studies are needed to validate associations between exposure to plastic particles and their health impact over the life span. Sensitive populations, such as pregnant women, infants, children, and occupational groups with increased exposure, should be given special attention. Recent mechanistic research studies on the linkages between oxidative stress, inflammation, endocrine disruption, and epigenetic factors will provide much-needed insight into cumulative and transgenerational impact. [1,11,17]

Regulatory and Public Health Impact 

Microplastics and nanoplastics are abundant components in the environment and thus they must be actively regulated for public health. That is to say, regulatory frameworks are poorly attuned to addressing particle-based pollutants and the chemical cocktails that pollutants entail. Inclusion of mechanistic information in risk assessments will lead to superior outcomes. Public health options to decrease exposure include waste management solutions, reduction of single-use plastics, development of safer alternatives, and public awareness programs. Sensitive populations need targeted interventions, and the consideration of plastic exposure in maternal and child health programs should be carefully analyzed. [26,27,5,11,17,19] 

CONCLUSION

Microplastics and nanoplastics are ubiquitous environmental pollutants that can negatively contribute towards human health through a vicious circle of oxidative stress, inflammation, and hormone disruption. Previous studies have discovered that these microplastics and nanoplastics can interfere with cellular processes, throw off body hormonal balance, and lead to chronic inflammation in various organs. It is inevitable for humans to come into contact with these particles. Because both microplastics and nanoplastics are very enduring in living organisms and the environment at large, it is only prudent to take a precautionary approach to minimize their exposure. Only future studies are hoped to carry out that combine knowledge of mechanisms with exposure information in order to devise effective policies to protect human health as more and more plastic pollution is released.

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