Microplastics: an often-overlooked issue in the transition from chronic inflammation to cancer

Abstract

The presence of microplastics within the human body has raised significant concerns about their potential health implications. Numerous studies have supported the hypothesis that the accumulation of microplastics can trigger inflammatory responses, disrupt the microbiome, and provoke immune reactions due to their physicochemical properties. Chronic inflammation, characterized by tissue damage, angiogenesis, and fibrosis, plays a crucial role in cancer development. It influences cancer progression by altering the tumor microenvironment and impairing immune surveillance, thus promoting tumorigenesis and metastasis. This review explores the fundamental properties and bioaccumulation of microplastics, as well as their potential role in the transition from chronic inflammation to carcinogenesis. Additionally, it provides a comprehensive overview of the associated alterations in signaling pathways, microbiota disturbances, and immune responses. Despite this, the current understanding of the toxicity and biological impacts of microplastics remains limited. To mitigate their harmful effects on human health, there is an urgent need to improve the detection and removal methods for microplastics, necessitating further research and elucidation.

Background

Millions of tons of plastic are produced and utilized globally each year, presenting one of the most challenging and concerning issues worldwide [1, 2]. Due to its high stability and persistence, plastic is difficult to degrade over decades. Eventually, it breaks down into smaller particles, such as microplastics (MPs) [3] and nanoplastics (NPs), through environmental processes [4]. MPs primarily originate from land-based industrial source, including landfill, weathering, sewage and tire abrasion. These particles can eventually accumulate in various species through atmospheric, oceanic and continental circulation, as well as precipitation [5,6,7].

Significantly, numerous studies have detected MPs in human excretion, the colon, and the placenta. MPs can accumulate within the body, increasing the risk of tissue damage, fibrosis, and carcinogenesis. This risk is attributed to the induction of immune responses such as oxidative stress, apoptosis, and necrosis in the liver, intestines, brain, and other organs [8, 9]. Consequently, the widespread presence of MPs in ecosystems and their accumulation in the human body have raised concerns about their potential health threats.

In addition, exposure to MPs has been widely reported to trigger the upregulation of reactive oxygen species (ROS) and inflammatory mediators, resulting in DNA damage, oxidative stress, immune responses and chronic inflammation. Moreover, these effects should not be explored solely at the level of individual organisms; greater attention must be given to the alternations in the population structure of specific species and the potential for these changes to ultimately disrupt the dynamics of entire ecosystems [10]. The secretion of various pro-inflammatory cytokines and chemokines by inflammatory cells creates an environment conducive to cancer cell development. Inflammation can accelerate cancer progression and promote all stages of tumorigenesis [11]. Furthermore, existing research has demonstrated that exposure to MPs and NPs can directly promote the proliferation of tumor cells and influence the onset and progression of tumors by regulating inflammatory responses [12,13,14,15]. Although current studies on the exact mechanisms by which MPs precipitate tumor proliferation are limited, the transition from chronic inflammation to cancer, attributed to immune modulation caused by MP exposure, represents a highly promising research direction.

Therefore, this review synthesized knowledge on the distribution, physical, and chemical properties of MPs, as well as their toxicity and biological immune responses following intake. Additionally, we explored the potential mechanisms on the cancer progression under prolonged MP exposure through cancer-promoting inflammation. It may elucidate conclusive evidence of correlation between microplastic and chronic inflammation to cancer and paved the way for new detection, prevention and treatment strategies. This review could facilitate continued research innovation in the biological impact and mechanistic insights of microplastic, which is crucial for safeguarding public health, particularly in the prevention and treatment of cancer in the future.

Definition of MPs and its physicochemical properties

MPs primarily originate from consumer products and industrial processes exposed to the environment as small particle [16]. Secondary MPs are often degraded from larger plastics or textile fibers due to UV radiation, abrasion, and biological degradation [17]. Notably, prominent microplastic were found in atmospheric fallout, domestic sewage, and industrial wastewater [18]. MPs are any water-insoluble, solid, synthetic particle or polymeric matrix, with diameter ranging from 1 μm to 5 mm which can be either the regular or irregular in shape [19]. The primary types of polymers include polypropylene (PP), polystyrene (PS), polyethylene (PE), polycarbonate (PC), polyvinyl chloride (PVC), polyethylene terephthalate (PET), polymethyl methacrylate (PMMA), and polyurethane (PU) [20]. Among these, PE, PP, and PS are the predominant type of MPs found in China marine systems [21].

The bioavailability of MPs depends on their physical and chemical characteristics, such as size, density, shape, and color, as well as their abundance and other variables like exposure concentrations, surface charge (electrostatic potential), hydrophobicity, functionalization, and the formation of a protein corona [22, 23]. The small size of MPs allows them to pass through biological membranes, posing greater risks to cells and organs [24]. The density of these particles determines the type of plastic ingested by aquatic organisms, with low-density MPs like PE being encountered by surface-dwelling plankton, while high-density MPs like PVC may be found at the bottom of the water column.

Irregular-shape MPs with sharp edge and high curvature can directly damage cell membranes upon contact [25]. The shape of MPs also affects their movement, interactions with other MPs and biological barriers by influencing surface area and charge, thereby causing indirect cell damage and death [26]. Surface charge impacts the uptake and digestion of MPs by modifying their size, surface area, and the electrostatic forces between the particles and cell membranes [27]. Hydrophobicity affects protein adsorption to the particle surface, leading to the formation of a unique protein pattern or corona, which may attract toxins and antigens. Surface functionalization significantly alters the recognition and uptake of MPs.

Due to these properties, MPs have an enhanced ability to spread through circulatory system, traverse cellular barriers, and accumulate within organisms, facilitating their entry into the food web and impacting ecosystem. Consequently, the ecological, social, and economic impacts of MPs are substantial.

Accumulation process of MPs in human body

The toxicity of MPs towards living organism is mainly caused by the characteristics of the plastic and the degradative intermediates produced when MPs was inhaled or ingested. Factors such as size, shape, charge, and the presence of additives, along with their role as vectors for toxic contaminants, contribute to their bioavailability upon ingestion [28, 29].

MPs have been found to accumulate in various organs. (Fig. 1) For example, a pivotal study in 2018 revealed the presence of 15 types of MPs in human stool, with a notable prevalence in patients with inflammatory bowel disease (IBD), predominantly comprising PP (62.8%) and PET (17.0%) [30]. MPs can enter the human body through inhalation and ingestion [31]. For instance, airborne small particles (< 2.5 μm) are capable of crossing cell membranes, inducing oxidative stress and inflammation, which are associated with increased risks of respiratory diseases [32,33,34]. Beyond detection in stool, a 2021 study discovered MPs in the human placenta, where three particles were identified as PP from thermoplastic bottles, and nine others as pigments from daily chemical products like cosmetics and toothpaste [35]. In 2022, quantifiable MPs were detected in the blood samples of 17 participants, with a detection rate of 77%, indicating their ability to enter the human bloodstream [36]. In 2023, MPs were also found in human heart tissue and carotid artery [37, 38]. Besides, their association with Parkinson’s disease was noted due to their capacity to cross the blood-brain barrier and accumulate in the brain [9]. In 2024, MPs were substantiated to damage the self-renewal of hematopoietic stem cells by interfering gut microbiota and signal pathway [39]. In summary, MP can enter almost all organs through the cell membrane, but the exact mechanisms of absorption, distribution, metabolism, and excretion of MPs in the human body, as well as their dose-dependent effects, remain unclear.

Fig. 1

MPs Intake and Accumulation in Vivo. Microplastics (MPs), originating from the degradation of plastic materials in food packaging, bottles, and cosmetics due to solar radiation, mechanical fractionation, and weathering processes, enter the human body predominantly through inhalation, ingestion, and dermal absorption. Upon entry via the trachea and esophagus, MPs accumulate in the lungs and gastrointestinal tract, where they may be internalized into cells through endocytic and phagocytic mechanisms. Furthermore, MPs can penetrate the circulatory system, transported via blood and lymphatic fluids, leading to their accumulation in critical organs such as cardiac tissue and the brain, posing significant health risks. The graphical abstract was created with BioRender.com

As MP pollution levels rise, individuals are increasingly exposed to these particles through inhalation, oral ingestion, and dermal contact in their daily lives [40,41,42]. Inhalation and ingestion are two major routes for MP entry into organisms [43, 44], while dermal exposure occurs when MPs and NPs are absorbed onto the skin, primarily from cosmetic products [45].

Furthermore, MPs inhaled into the bronchus and lungs can translocate through diffusion, direct cellular penetration, or active cellular uptake via endocytic and phagocytic processes [34]. In the gastrointestinal tract, a major entry point for ingested foreign particles, MPs are initially trapped in the mucus layer before crossing epithelial barriers. They must endure the acidic conditions of the stomach and intestinal lumen, with the potential for particles entering the gastrointestinal system to translocate into the circulatory system via cell internalization by macrophages [46].

Potential role of MPs in cancer promotion (Table 1)

When MPs are ingested and distributed in the body via blood circulation, the immune system initiates process to recognize and eliminate foreign pathogens and stimuli molecules. Innate immunity plays a significant role in neutralizing MPs through tissue barriers, pattern recognition receptors, and phagocytosis [47]. Due to their size and resistance to degradation, MPs may persist inside immune cells, physically interfere with the normal functioning [48]. Additionally, the presence of MPs leads to the release of pro-inflammatory cytokines and chemokines by immune cells, either directly or indirectly. Furthermore, MP-related interactions with the host microbiome can also trigger innate and inflammatory responses. Due to the important role chronic inflammation played in cancer progression, MPs could act as a catalyst for tumor progression.

Given the crucial role that chronic inflammation plays in cancer progression, MPs could act as catalysts for tumor development. MPs may contribute to the transition from chronic inflammation to cancer by activating pro-inflammatory signaling pathways, promoting cytokine release, and affecting immune responses.

Table 1 Potential role of MPs in cancer promotion

Transition from chronic inflammation to cancer

Inflammation, a response to tissue injury and pathogen invasion, leads to the accumulation of fluid and leukocyte. Acute inflammation combats infection through innate and adaptive responses. However, chronic inflammation characterized by tissue damage, angiogenesis, and fibrosis plays a key role in cancer development by promoting tumorigenesis and metastasis. It does so by shaping the tumor microenvironment (TME) and influencing immune surveillance [49]. Cancer progression involves complex interactions between host microenvironment, tumor cells, inflammatory responses, and stromal cells, with inflammatory factors altering the TME and affecting tumor-stromal interactions [50]. Thus, understanding the potential effects of MPs on tumors and their immune microenvironment is crucial for identifying how chronic inflammation induced by MPs may promote cancer.

Immune regulation in chronic inflammation to cancer transition

Innate and adaptive immunity are crucial in tumor initiation, progression, and metastasis. Chronic inflammation induces genetic mutations and alterations in epithelial cells, impacting tumor suppressor and oncogenic pathways. This inflammation can foster tumor progression by recruiting and activating specific immune cells, creating an immunosuppressive TME rich in suppressive cells and cytokines, thus providing an environment conducive to tumor development [51].

Innate immune cells, including macrophages, neutrophils, dendritic cells and innate lymphoid cells, defend against tissue damage and prevent tumor initiation. However, some innate cells like mast cells and myeloid derived suppressor cells in the TME can promote cancer [52]. For example, neutrophils and tumor-associated neutrophils (TANs) facilitate tumor progression through neutrophil extracellular traps (NETs), suppressing adaptive immune responses and enhancing neutrophil-cancer cell interactions [53, 54]. Cancer-associated fibroblasts (CAFs) and eosinophils, driven by inflammatory cytokines, contribute to cancer cell proliferation and angiogenesis [55, 56]. Mast cells release mediators like Interleukin-1 (IL-1β), Interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α), recruiting various cells to the TME [57]. Macrophages and neutrophils produce ROS and reactive nitrogen intermediates (RNI) species, inducing mutations. M2-type tumor-associated macrophages (TAMs) secrete cytokines to maintain TME immunosuppression and inhibit T-cell function, affecting adaptive immunity.

The adaptive immune response, specific to antigens and retaining memory, typically inhibits tumorigenesis. However, certain T cells like T helper 2 cells (Th2 cells), T helper cells 17 (Th17 cells), regulatory T cells (Treg cells), and regulatory B cells promote tumor progression [58]. Specifically, Th2 cells contribute to M2 macrophage function in the inflammatory TME and promote metastasis [59, 60]. Treg cells induce immune suppression in the TME, inhibiting co-stimulatory signals and secreting inhibitory cytokines [61]. And pro-tumoral IL-17⁺ γδT cells induce an immunosuppressive microenvironment and promote angiogenesis by producing various cytokines as regulatory Th17/Treg/Th2-like cells [62]. Regulatory B cells exert immunosuppressive effects through cytokine secretion, such as Interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), or upregulation of programmed cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) [63].

Given the purported effect of immune regulation on the transition from chronic inflammation to cancer, the reshaping of the immunosuppressive microenvironment by microplastics (MPs) may foster cancer progression. MPs can impair the functionality of anti-tumor immune cells by disrupting normal antigen presentation processes or interfering with the cell signaling pathways that are essential for the activation and coordination of immune cells. Concurrently, MPs can induce the release of pro-inflammatory cytokines and chemokines from suppressive immune cells, further modulating the transition from chronic inflammation to cancer. This dual mechanism underscores the complex role of MPs in influencing immune responses and highlights their potential impact on cancer development and progression.

Potential impact of MPs on inflammation and cancer transformation

When inhaled or ingested, MPs can induce various biological effects, including oxidative stress, metabolic disturbances, inflammation, immune reactions. These biological responses are critically implicated in the formation of TME and immunosuppression, potentially leading to tumorigenesis through the transition from chronic inflammation to cancer. These effects are mediated by the upregulation of cytokines and activation of key signaling pathways, contributing to cancer-promoting inflammation and immune responses at the molecular level. (Fig. 2)

Fig. 2

MP Exposure Induces Chronic Inflammation and Potential TME Formation. Exposure to polypropylene microplastics (PP-MPs) or polystyrene microplastics (PS-MPs) has been observed to induce a range of biological responses, including DNA damage, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, inflammation, and apoptosis. Such exposure activates multiple pro-inflammatory signaling pathways, notably the mitogen-activated protein kinase (MAPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and AKT signaling pathways. This activation results in the upregulation of cytokine release, such as interleukin-1 beta (IL-1β) and interleukin-6 (IL-6). Nonetheless, the detailed mechanisms underlying microplastic (MP)-triggered signaling pathways necessitate further elucidation. The secretion of cytokines plays a crucial role in the onset of chronic inflammation, which can alter the ratios of immune cells and potentially further impact the development of the TME. Upon MP stimulation, an elevation in T helper cells (Th2, Th17) and regulatory T cells (Treg) has been observed. Consequently, the pro-inflammatory signaling pathways activated by MP exposure may lead to immune dysfunction and foster the initiation of tumorigenesis. The graphical abstract was created with BioRender.com

Activation of pro-inflammatory signaling pathways related to oxidative stress

After the uptake of MPs, immune cells make effective modulation in transcriptional levels, from enzymatic activities to cytokine release. And MPs can induce cellular injury of innate immune cell in phagocytosis. Mitochondrial injury resulting from exposure to airborne MPs may directly lead to oxidative stress, cytotoxicity, and inflammation through MAPK and NF-κB signaling pathways. The NF-κB family (RelA, RelB, c-Rel, p105/p50, and p100/p52) is a critical regulator of innate and adaptive immunity, crucial for inflammation, cell recruitment, and reshaping the TME [64]. The NF-κB pathway includes canonical and non-canonical pathways, where the canonical pathway induces pro-inflammatory cytokines, leading to inflammatory responses and cancer progression [65]. PS-MPs have been reported to cause intestinal oxidative stress and metabolomic alterations in zebrafish [66], and polypropylene microplastics (PP-MPs) exposure leads to lung inflammation pathogenesis through mitochondrial damage and activation of the p38 phosphorylation-mediated NF-κB pathway [67]. This exposure can cause DNA damage and mutations in epithelial and stromal cells.

PS-MP exposure has been shown to induce mitochondrial damage and endoplasmic reticulum (ER) stress via the alterations in MAPK, AKT/mTOR signaling, leading to increased inflammation and autophagy in kidney cells. Besides, PS-MPs also lead to reproductive toxicity in male mice through the activation of P38 MAPK signaling pathway [68, 69]. MAPK are a family of serine/threonine protein kinases that respond to various stimuli, including oxidative stress and inflammatory cytokines, regulating cellular functions such as proliferation, differentiation, survival, and apoptosis [70]. Mammalian MAPKs include extracellular regulated protein kinase (ERK1/2), c-Jun N-terminal kinase (JNK), and p38, and they can convert external stimuli to cellular responses. ERKs are activated by mitogens and differentiation signals, while JNK and p38 are activated by inflammatory stimuli and stress [71]. ERK promotes cancer-associated inflammation by regulating inflammatory cytokines, thus facilitating tumor development. JNK downstream genes regulate inflammatory mediators and accelerate inflammatory-caused cancer development. P38 proinflammatory activity significantly affects cancer progression in nonmelanoma skin cancer, breast cancer and glioma [72]. However, its role as a tumor suppressor or activator depends on cell type, stimulus duration, quality, intensity, and interactions with other pathways.

The inflammatory microenvironment within tumors increases mutation rates, leading to abnormal cellular proliferation, inflammation and the formation of the TME [73]. In mice, exposure to synthetic polymer MPs results in immune alternation, which characterizes by gene upregulation, Th2-related cytokines and immunoglobulins release [74]. Studies also indicate that ROS generation mediated by PS-MPs influences immune defense mechanism by altering the expression profile of antioxidant genes and the apoptosis process via activating the p53 signaling pathway [75, 76]. Additionally, polyethylene microplastics (PE-MPs) can increase mitochondrial ROS and cause skin cancer cell proliferation via NLRP3 inflammasome-mediated inflammation [14].

Formation of pro-inflammatory TME based on cytokine release

Cytokines, primarily secreted by inflammatory cells such as macrophages, monocytes, and lymphocytes, are categorized into pro-inflammatory (IL-1, IL-6, IL-15, IL-17, IL-23, TNF-α, IFN-γ) and anti-inflammatory (IL-4, IL-10, IL-13, TGF-β) types. These cytokines either facilitate or inhibit inflammation, respectively. In the context of cancer-promoting inflammation, cytokines contribute to cellular malignancy, transformation, and the formation of the TME. Some cytokines have been identified as key players in cancer-promoting inflammation [77]. For instance, tumor-promoting cytokines such as IL-6, TGF-β, and TNF-α activate signal transducer and activator of transcription (STAT) proteins, inhibit apoptosis, and promote epithelial-mesenchymal transition (EMT) [78]. The IL-6 and IL-10 families, common in chronic inflammation and the TME, are key STAT3 activators [79]. STAT3 interacts directly and indirectly with NF-κB and ReLA, aiding NF-κB activation in cancer. Studies have shown increased expression of IL-6, TNF-α, IL-8, and IL-1β in lung tissues of Sprague Dawley rats, carp and zebrafish exposed to PS-MPs [80, 81]. MPs released from PP infant feeding bottles have been linked to the release of ROS and elevated levels of pro-inflammatory cytokines such as IL-6 and TNFα, leading to intestinal inflammation [82]. Additionally, PS-MPs were found to alter microglial differentiation and apoptosis markers in the brain, alongside activating pro-inflammatory cytokines [83].

The suppression of adaptive anticancer immunity also contributes to formation of TME. PS-NPs and PE-NPs induce Treg and Th17 cell differentiation associated with T cell exhaustion, and they upregulate cytokines and immune checkpoint proteins, including IL-1β, IL-17a, CTLA-4, and PD-1, in the colon. This process leads to the development of an inflamed and immunosuppressive TME, thereby promoting colon tumorigenesis [13].

Given the prolonged accumulation of MPs in the human body, inflammatory cytokines are likely to foster a cancer-promoting inflammatory state.

Alteration of microbiota to impact immune function

The intestine is a vital organ that interacts extensively with the external environment. The gut microbiome plays a pivotal role in shaping the intestinal microenvironment by protecting against harmful microorganisms and pathogens and modulating host immune responses [84]. It contributes to host health through four primary functions: metabolism maintenance, development of gut-associated lymphoid tissues (GALTs), vitamin production, and defense against pathogenic invasion [85]. Consequently, the gut microbiota is crucial for maintaining intestinal homeostasis and overall human health.

Exposure to MPs can lead to an imbalance in specific microorganisms, causing microbiota dysbiosis, which in turn may induce metabolic disorders, inflammation, and damage to gut immunity. Recent studies have shown that exposure to varying sizes of MPs leads to gut microbiota dysbiosis, significantly altering key microbiomes at the genus and phyla levels and causing gastrointestinal system damage. Disruption in the abundance of Firmicutes and Bacteroides has been observed in zebrafish and mice treated with PE-MPs and PS-MPs [86,87,88]. PS-NPs exposure in zebrafish cause a Firmicutes and Bacteroides imbalance, leading to further dysregulation of the brain-intestine-microbiota axis [89].

Among the human intestinal microbiota bacteria, the phyla Firmicutes and Bacteroidetes are the most dominant. Firmicutes in the cecum are known to enhance nutrient absorption, and an altered Firmicutes/Bacteroidetes ratio is associated with obesity [90]. In a balanced state, Bacteroides contribute to carbohydrate fermentation and production of volatile fatty acids, providing a significant energy source [91].

Additionally, exposure to varying sizes of polystyrene MPs has been linked to disorders in hepatic lipid metabolism in mice [92]. Moreover, PS-MPs have been shown to cause hematopoietic damage via disrupting gut microbiota homeostasis, cytokines, and inflammation, potentially affecting metastasis and hematopoietic malignancy [93].Furthermore, Numerous studies have demonstrated that PE-MPs and PP-MPs can induce small intestinal inflammation by elevating various mediators and altering the gut microbiota [82, 87]. And patients with IBD have an increased risk of developing colorectal cancer [94]. MPs have been observed to significantly impair mouse immune function by reducing spleen weight, decreasing the number of CD8⁺ T cells, and increasing the CD4⁺ to CD8⁺ T cell ratio [95]. PE-MPs exposure has been found to resist immune therapy in gastric cancer by enhancing the expression level of asialoglycoprotein receptor 2 (ASGR2) gene. Upregulation of ASGR2 induces typical cancer hallmarks such as proliferation, N-cadherin, CD44, PD-L1, and increased tumor growth and migration are also observed [12].

In all, MPs can directly cause oxidative stress and cellular changes when innate immune cells engulf them. This process releases many pro-inflammatory cytokines and biological modulators, upregulating signal pathways related to tumor initiation, and forming a pro-inflammatory TME that promotes cancer cell proliferation. Additionally, MP exposure can affect the immune system by altering gut microbiota and the function of immune organs. By inhibiting immune surveillance and shaping pro-inflammatory TME, MPs are likely to impact inflammation and cancer transformation.

Conclusion and prospection

Microplastics (MPs) are increasingly recognized as a significant societal hazard. Although awareness is growing regarding the potential impacts of MPs on individual organisms and even on the structure of entire human populations, there remains limited knowledge about the severity of these effects. Due to their abundance and diminutive size, MPs can infiltrate the human body. Their unique physical and chemical properties lead to a range of biological effects, such as disruption of gut microbiota, immune responses, metabolic disorders, and inflammation, mediated through signaling pathways or changes in cytokines. Existing studies have largely focused on the impacts of MPs on cancer, metabolic disorders, attention-deficit/hyperactivity disorder, and fertility issues. Although some preliminary studies have confirmed the correlation between MPs and tumor development, most current research has primarily focused on the discovery that MPs can induce the upregulation and proliferation of typical cancer biomarkers, oxidative stress, mitochondrial damage, and other cancer-related changes. However, there is still limited exploration of how MPs induce tumorigenesis through microenvironmental changes, and there is a lack of studies investigating the differential regulation of the tumor immune microenvironment by different types of MPs. Moreover, research on specific immune cells in this context is also lacking. In addition, MPs can act as carriers, mediating the transmission of other compounds, including metabolites, and this phagocytic process may trigger specific recognition within tumors and their microenvironment, leading to varied responses in different cells. Based on this, more detailed research on MPs in tumors and their microenvironment is still needed, which will enhance our understanding of the role of MPs in cancer prevention and treatment.

Currently, the detection of MPs primarily relies on visual analysis using stereoscopes or a combination of spectroscopic techniques, includingFourier transform infrared spectroscopy (FT-IR) and Raman spectroscopy, fluorescent staining methods (e.g. Nile Red), thermal analysis, and chromatographic analysis [96,97,98]. However, these methods have limitations and drawbacks. For instance, the use of Nile Red fluorescent staining may complicate the identification of specific polymeric materials [99]. Some methods are subjective, time-consuming, and prone to errors due to the varying appearances and properties of MPs. Therefore, more objective criteria and the assistance of AI or data analysis are needed to help scientists accurately identify the morphological features of MPs. There is an urgent need for scientists to develop more time-efficient and precise methods for detecting MPs in the environment and human bodies, to address the challenges faced in MP detection. With advancements in MP detection technology, especially in the exploration of methods for detecting MPs within the human body, it is anticipated that more direct evidence of the correlation between MPs and human health will be uncovered in the future.

Considering the potential carcinogenic impact of MPs, scientists urgently need to develop more time-efficient and precise methods for detecting MPs in the environment and human bodies. Meanwhile, due to the persistence and widespread distribution of MPs, reducing their formation and enhancing degradation abilities in ecosystems and the human body are critical concerns. However, challenges remain, such as the generation of toxic intermediate products and volatile organic compounds during the degradation process, leading to secondary environmental pollution [100]. Additionally, the biodegradation substances, including microbes and enzymes, have yet to be effectively separated, purified, and characterized. The interactions among diverse microorganisms and numerous enzymes continue to be poorly understood. And the effects exerted by microbial communities on the degradation and utilization of microplastics warrant further research. In summary, there is still a significant journey ahead in researching the hazardous biological effects and mechanisms of MPs.