Microplastics in Cosmetics: Emerging Risks for Skin Health and the Environment

Abstract

Microplastics, increasingly recognized as environmental pollutants, have raised concerns regarding their potential effects on human health. In cosmetics and personal care products, microplastics may pose a risk through skin absorption. This review explores the presence of microplastics in cosmetics, their potential exposure pathways, and their dermatological implications. Evidence suggests that microplastics can penetrate the skin barrier, induce oxidative stress, promote inflammation, and contribute to premature aging. Despite growing regulatory efforts, global inconsistencies hinder comprehensive policy implementation. Rising environmental and health concerns have also fueled interest in sustainable alternatives such as biodegradable polymers and eco-friendly packaging. Further research is necessary to clarify long-term health effects and guide regulatory strategies.

1. Introduction

Plastics have become ubiquitous since the invention of synthetic polymers in 1907, prized for their versatility, durability, and low cost [1,2]. Over time, they have become indispensable in daily life, with consumption increasing exponentially. Consequently, an estimated 10 to 40 million tonnes of microplastics are released into the environment each year. However, beneath the convenience that plastics provide lies growing concern over their environmental impact and potential risks to human health [3]. As plastic waste undergoes degradation, it fragments into microplastics (<5 mm) and nanoplastics (<1 μm) [3,4]. These microscopic particles have been found in marine environments, soil, air, and even human biological samples such as placental tissue, breast milk, and blood [5].

While the long-term health effects of microplastics remain unclear, emerging evidence suggests that they may impact multiple human systems, including the digestive, respiratory, endocrine, reproductive, and immune systems [6,7]. Although ingestion and inhalation are considered the primary exposure routes, dermal absorption is increasingly recognized as a potential pathway [7].

Microplastics are not only pervasive in the environment but are also intentionally added to personal care and cosmetic products (PCCPs) for exfoliation, texture enhancement, and product stabilization. This widespread use raises concerns about direct dermal exposure, inadvertent inhalation, and environmental contamination [8,9]. This review aims to examine the presence of microplastics in cosmetics, elucidate their potential routes of exposure, and evaluate their effects on skin health.

2. Methods

A search was conducted in the electronic databases PubMed and Cochrane Library, covering all available records from database inception to March 31, 2025, using search terms including “microplastics”, “nanoplastics”, “personal care products”, “microbeads”, “health effect”, “dermatologic effect”, “dermatology”, “moisturizers”, “emollients”, “cosmetics”, “skin absorption”, “cutaneous exposure”, “dermal toxicity”, “skin barrier”, “inflammation”, “oxidative stress”, “skin aging”, “senescence”, “cellular senescence”, and “skin cancer”. We included English-language articles that evaluated the presence, absorption, and dermatologic impact of microplastics and nanoplastics in cosmetic or personal care products. In vitro, in vivo, and clinical studies assessing skin-related outcomes were considered. Non-English articles were excluded unless relevant dermatological findings were reported. Preference was given to high-quality peer-reviewed articles, and reference lists were reviewed to include relevant studies.

This review has a limitation in that we did not perform a formal risk-of-bias or quality assessment of the included studies. Although we aimed to include peer-reviewed and relevant literature, the lack of standardized appraisal may limit the ability to evaluate potential bias and the methodological rigor of the reviewed studies.

3. Microplastics

3.1. Definition of Microplastics

Microplastics are synthetic polymer particles measuring less than 5 mm in diameter and are composed primarily of carbon and hydrogen atoms linked in polymer chains [4,10]. These particles are insoluble in water and have been detected across diverse environments, including marine ecosystems, soil, air, and even in food and drinking water [3,11].

Microplastics are generally classified into two categories based on their origin [3]. Primary microplastics are deliberately manufactured at the microscopic scale for use in commercial and industrial applications, such as cosmetics, medical products, and toothpaste [2,10] Microbeads, commonly used in exfoliating products, are a typical example [8]. In contrast, secondary microplastics originate from the breakdown of larger plastic debris through mechanical abrasion, thermal degradation, photolysis, or biological activity [8,10]. Nanoplastics, typically defined as plastic particles smaller than 1 μm [4,10,11], pose particular concern due to their enhanced ability to penetrate biological tissues and interact with cells. Because of their persistence and potential toxicity, both microplastics and nanoplastics have become major subjects of environmental and biomedical research. Their widespread presence and potential for bioaccumulation underscore the urgent need for effective mitigation and regulatory strategies [12].

3.2. Routes of Microplastic Exposure

Humans can be exposed to microplastics through multiple sources, including plastic packaging, textiles, degraded plastic materials, fishing gear, and personal hygiene products [7]. The primary exposure pathways are ingestion, inhalation, and dermal contact [12].

Widespread marine contamination has made seafood and the broader food chain significant conduits for microplastic ingestion [13]. Due to their small size, microplastics consumed by marine organisms may bioaccumulate and ultimately be transferred to humans through dietary intake [14,15]. Studies have confirmed the presence of microplastics in aquatic animals, table salt, honey, and sugar [13,16,17]. Alarmingly, drinking water is also a notable source: microplastics have been detected in both bottled and tap water [18]. A global study found microplastic contamination in 81% of 159 tap water samples, primarily consisting of fibers smaller than 5 mm [19]. Other investigations revealed that both glass and plastic bottles contain comparable levels of microplastic particles [20,21]. It is estimated that individuals who exclusively consume bottled water may ingest up to 90,000 microplastic particles annually, compared to approximately 4000 from tap water [22].

Airborne microplastics represent an emerging exposure concern [7,23,24]. Recent studies have identified microplastic particles in the air. Notably, one study involving European participants reported an average of 9.18 ± 2.45 microplastic particles per 100 mL of bronchoalveolar lavage fluid, with a mean particle size of 1.73 ± 0.15 mm [25]. Moreover, research has demonstrated that inhaled microplastics can translocate to the placenta and fetal tissues [26].

Although dermal exposure is generally considered a less significant route, several factors influence skin permeability. Particle size plays a key role—nanoplastics are more likely to penetrate, while larger particles may infiltrate through hair follicles, sweat glands, or abrasions [27,28]. In vitro studies with primary skin cells demonstrate that nano-sized plastics can penetrate and accumulate in skin tissues, with particles up to 6 μm absorbed by keratinocytes [29]. Additional research has shown that nanoplastics smaller than 200 nm can migrate through skin furrows, lipid channels, and hair follicles, reaching the viable epidermis and even being internalized by skin cells [30].

A quantitative study on skin exposure revealed that after 24 h, the highest concentrations of microplastics were detected in scalp hair, followed by facial and hand skin. The accumulation on the scalp may be attributed to its larger surface area and electrostatic properties, which facilitate microplastic retention [31]. Additionally, higher humidity levels were associated with increased microplastic adhesion. It has also been reported that substances such as oleic acid and ethanol can alter the lipid fluidity of the stratum corneum, thereby enhancing the transdermal absorption of microplastics [32].

4. Dermatologic Effects of Microplastics

Microplastics and nanoplastics have been increasingly scrutinized for their potential effects on skin health (Figure 1). Although much of the current evidence stems from in vitro and animal studies, emerging data suggest that these particles may disrupt skin barrier function, provoke inflammatory responses, alter the skin microbiome, accelerate aging processes, and possibly contribute to carcinogenesis (

Table 1. Effect of microplastics on skin.

Skin barrier dysfunction	− Reduce the stability of the stratum corneum lipid monolayer, weakening the skin barrier [33]. − Increase proapoptotic protein expression, activating mitochondrial apoptosis and oxidative stress [34,35,36]. − β-catenin pathway activation reduces cell adhesion proteins (E-cadherin, vinculin), weakening cell junctions and allowing for external substance infiltration [29].
Inflammation	− Activate the NF-κB signaling pathway, increasing pro-inflammatory cytokines (TNF-α, IFN-γ, IL-2, IL-6, IL-8, IL-1β) and decreasing anti-inflammatory cytokines (IL-4, IL-10) [37]. − Activate NLRP3 inflammasome, increasing IL-1β synthesis and immune overactivation, exacerbating tissue damage and inflammatory responses through interaction with NF-κB [37,38].
Microbiome imbalance	− Disrupt the balance between beneficial and harmful bacteria in the gut microbiome [6,39,40,41].
Skin aging	− Induce oxidative stress, cause DNA damage and apoptosis [42]. − Disrupt cellular metabolism via autophagy and ER stress [43,44]. − Induce mitochondrial oxidative stress and AIM2 inflammasome activation [45].
Skin cancer	− Induce cell cycle abnormality [46]. − Induce mitochondrial ROS and pro-inflammatory microenvironment [46]. − Induce DNA damage [47].

) [2]. While this review summarizes the current understanding of microplastic-induced dermatologic effects, it is important to note that most existing studies are based on in vitro experiments. Therefore, caution is warranted when interpreting these findings in the context of actual human health risks. Many of the experimental conditions do not fully reflect the complexity of real-life human exposure, including factors such as dermal absorption rates, skin barrier integrity, and chronic low-dose exposure. To accurately assess the potential health impacts of microplastics on human skin, further studies using in vivo models, human-relevant exposure conditions, and quantitative exposure assessments are needed.

4.1. Skin Barrier Dysfunction

A growing body of evidence indicates that microplastics and nanoplastics may compromise skin barrier integrity through both physical interaction and immune-mediated mechanisms [2]. A recent study demonstrated that the introduction of nanoplastics into a stratum corneum membrane model significantly reduced the stability of the lipid layer. This effect was concentration-dependent, with nanoplastics tested at 0, 5, 10, 50, and 100 mg/L, and greater disruption was observed at higher concentrations, especially at 100 mg/L [33]. Due to their minuscule size, microplastics and nanoplastics can penetrate the skin and interact with cells and structural biomolecules [34,48,49].

Upon contact with the skin, these particles may trigger immune responses via the recognition of pathogen-associated and damage-associated molecular patterns by receptors expressed on keratinocytes, Langerhans cells, dendritic cells, melanocytes, macrophages, and T cells [2]. The subsequent activation cascade results in the release of antimicrobial peptides and pro-inflammatory cytokines—including IL-1, IL-6, IL-10, IL-17, IL-18, IL-22, and TNF—which disrupt skin homeostasis, recruit additional immune cells, and weaken the structural integrity of the epidermis [35,50].

Furthermore, experimental models showed 5 nm sized nanoplastics can disrupt protein structure by inducing misfolding and denaturation and compromise lipid bilayers, thereby undermining cellular membrane integrity [51,52]. Prolonged exposure to nanoparticles (30–300 nm) may activate mitochondrial apoptotic pathways, increasing oxidative stress and inflammation, which in turn weakens the skin barrier and may predispose individuals to conditions such as atopic dermatitis [34,35,36].

In vitro, microplastics and nanoplastics (200 nm to 6 µm) have also been shown to interfere with intercellular adhesion by activating the β-catenin signaling pathway, which reduces the expression of adhesion proteins such as E-cadherin and vinculin. This reduction compromises cell–cell junctions [29], increases skin permeability, and exacerbates inflammatory responses [49].

4.2. Skin Inflammation

Microplastics and nanoplastics have been detected in human blood and various organs, raising significant concern regarding their systemic and cutaneous effects. While much of the existing research has focused on internal organ systems—including the respiratory, digestive, reproductive, endocrine, nervous, and immune systems [7,12,17]—an increasing number of studies are now highlighting their dermatological implications [2]. Although the exact mechanisms by which microplastics and nanoplastics affect the skin remain to be fully elucidated, accumulating evidence suggests that they may trigger or exacerbate inflammatory skin conditions.

Experimental models have demonstrated that the internalization of polyethylene microplastics (8 μm, 1000 ng/L) by gill skin cells activates the NF-κB signaling pathway, a central mediator of inflammation and immune regulation. This activation leads to increased expression of pro-inflammatory cytokines, including TNF-α, IFN-γ, IL-2, IL-6, IL-8, and IL-1β, while concurrently suppressing anti-inflammatory cytokines such as IL-4 and IL-10 [37]. This pro-inflammatory shift also promotes apoptosis via increased caspase-3 expression and activates the NLRP3 inflammasome, resulting in elevated IL-1β synthesis and immune overactivation [37,38]. The crosstalk between NF-κB signaling and the NLRP3 inflammasome appears to synergistically amplify inflammatory responses, contributing to the development or worsening of inflammatory skin conditions [29,53].

Notably, a study assessing the impact of fragmented polystyrene (fPS) ≤ 10 µm in size on human skin revealed that exposure of keratinocytes (HaCaT cells) and dermal fibroblasts to fPS resulted in cellular infiltration, increased cytotoxicity, and significant inflammatory responses. In a 3D human skin model, fPS particles penetrated the dermis within one hour, with particles smaller than 2 μm detected at an average maximum concentration of 4.7 μg. RNA sequencing identified marked upregulation of pro-inflammatory genes such as IL-1α, IL-1β, IL-18, IL-6, IL-8, ICAM-1, FOS, and JUN at both the mRNA and protein levels [54].

Complementary findings from a zebrafish model demonstrated that the expression patterns of TNF-α and IL-1β varied depending on microplastic particle size (0.1 μm, 5 μm, and 200 μm). Similarly, primary skin cell studies showed that inflammatory responses were most significantly altered when exposed to nanoplastics and microplastics smaller than 6 μm. These results suggest that particle size is a critical determinant of immune reactivity, with smaller particles exhibiting a greater capacity to interact with and activate skin cells [29].

4.3. Microbiome Imbalance

Microplastics have been implicated in disrupting the microbiome balance in various organ systems, including the skin. While most existing studies focus on the gastrointestinal microbiome, emerging research suggests that microplastics may also alter the composition and function of the skin microbiota.

Although direct studies on the skin microbiome remain limited, parallels can be drawn from evidence on the gut microbiome [55,56]. Ingestion of polyethylene microplastics has been shown to increase the abundance of potentially pathogenic bacterial groups such as Firmicutes and Bacteroidetes [6,40,41] while reducing beneficial bacteria and butyrate production [57]. Previous research using juvenile guppies exposed to polystyrene microplastics (32–40 μm, 100–1000 μg/L for 28 days) demonstrated that microplastics accumulated in the gut, reduced digestive enzyme activity, and triggered inflammatory immune responses. Moreover, gut microbiota diversity and functional capacity were significantly disrupted [39]. Similar microbial imbalances—or dysbioses—are hypothesized to occur on the skin surface upon chronic exposure to microplastics.

Disruptions in the skin microbiome can compromise barrier integrity and immune modulation, potentially exacerbating inflammatory dermatoses such as atopic dermatitis, psoriasis, and acne [58,59,60,61,62]. Moreover, changes in microbial diversity and the relative abundance of commensal vs. pathogenic species may influence cytokine production, sebum composition, and skin pH, further contributing to cutaneous inflammation [58,59,60,61,62]. Cutibacterium acnes is widely recognized as a major contributor to acne development, with RT4 and RT5 strongly associated with acne-prone skin [63,64]. Notably, acne severity appears to be driven more by a loss of strain diversity—particularly the dominance of phylotype IA1—than by an overall increase in bacterial load [61,65]. Recent studies have identified notable differences in the skin microbiome between psoriasis patients and healthy individuals. In psoriasis, microbial diversity tends to be reduced, particularly in lesional skin [66]. Psoriatic plaques often show an increased presence of Staphylococcus aureus, Staphylococcus epidermidis, Bacillus spp., Corynebacterium spp., and Klebsiella pneumoniae, while beneficial microbes like Cutibacterium spp., Actinobacteria spp., and Bacteroides spp. are decreased [67,68].

Emerging research highlights the bidirectional relationship between the gut and skin, known as the gut–skin axis [69,70]. Dysbiosis of the gut microbiome caused by microplastics can result in the systemic release of inflammatory mediators and metabolic byproducts that negatively affect skin health [70]. Hence, microplastic-induced microbial dysregulation may have both local and systemic implications for dermatologic conditions [69].

4.4. Skin Aging

Microplastics and nanoplastics have been shown to induce oxidative stress, contributing to tissue toxicity. In a mouse model, oral administration of microplastics and nanoplastics of various sizes (50 nm, 500 nm, and 5000 nm) led to increased particle distribution across multiple organs and elevated reactive oxygen species (ROS) production [42]. Similarly, a study using primary gill epidermal cells demonstrated that these polyethylene microplastics (8 μm, 1000 ng/L) generate ROS and suppressed antioxidant enzyme activity, resulting in DNA damage and apoptosis [37].

In in vitro studies using BEAS-2B bronchial epithelial cells, nanopolystyrene particles (~50 nm, 10 and 50 μg/mL) were internalized by cells, leading to increased ROS production, mitochondrial membrane depolarization, and early apoptosis. These exposures also induced autophagy and endoplasmic reticulum stress, accompanied by elevated levels of amino acids and TCA cycle intermediates, as well as upregulated expression of stress markers such as LC3-II, ATF6, DDIT3, and ERN1 [43,44]. When the body’s antioxidant defense mechanisms are overwhelmed and unable to effectively neutralize ROS, oxidative stress can accelerate skin cell aging [71,72]. An in vitro study using two skin cell lines showed that nano-sized microplastics were internalized in a time- and dose-dependent manner, leading to increased inflammation and cellular senescence via upregulation of p16 and p21. Mitochondrial oxidative stress and AIM2 inflammasome activation were identified as key mechanisms [45].

These findings collectively suggest that microplastic exposure may contribute to oxidative stress-induced skin damage and premature aging.

4.5. Skin Cancer

Emerging evidence suggests that microplastics can infiltrate cells, disrupt key biological processes, and create a carcinogenic microenvironment [5,73]. These particles contribute to cancer development through multiple mechanisms, including the induction of DNA damage, oxidative stress, inflammation, and interference with cellular signaling pathways.

In vitro research has shown that microplastics (1 μm, 0.25 to 1.0 mg/mL) penetrate squamous cell carcinoma cell lines (SCL-1, A431), enhancing cell proliferation and accelerating cell cycle progression, as indicated by increased expression of Cyclin D1, c-Myc, Bcl-2, and Ki-67. This is associated with the induction of mitochondrial ROS, disruption of mitochondrial membrane potential, and opening of the mitochondrial permeability transition pore, which leads to the release of mitochondrial DNA into the cytoplasm. The cytosolic mitochondrial DNA subsequently activates the NLRP3 inflammasome, contributing to the formation of a pro-inflammatory microenvironment and further enhancing tumor cell proliferation [46]. In addition, a previous report indicated that microplastics activate signaling pathways such as ERK, JNK/SAPK, p38, and MAPK, which are associated with tumorigenesis and uncontrolled cell proliferation [73].

Moreover, microplastics trigger inflammatory responses by activating the NLRP3 inflammasome and upregulating pro-inflammatory mediators such as TNF-α, IFN-γ, TLR4, AP-1, IRFs, Th17, IL-6, and IL-1β [37,46,74]. These inflammatory cascades promote tumor initiation, angiogenesis, invasion, and metastasis. Concurrently, microplastics impair immune surveillance by disrupting the immune system’s capacity to recognize and eliminate malignant cells, thereby facilitating immune evasion and cancer progression [73,75]

Additionally, microplastics may contribute to tumorigenesis through endocrine disruption and genetic and epigenetic alterations, including DNA methylation, histone modification, and microRNA dysregulation. In a study using fathead minnows (Pimephales promelas), researchers examined DNA methylation changes induced by polyethylene microplastics (150–500 μm) at concentrations of 100 and 2000 particles/L. Persistent methylation changes were also observed in the F1 generation, indicating a transgenerational epigenetic effect. The differentially methylated genes were associated with hormone signaling, metabolism, inflammation, and tRNA function [47]. Acting as vectors, microplastics can also carry and concentrate carcinogenic substances such as persistent organic pollutants and heavy metals, further amplifying their toxic effects. Notably, even at environmentally relevant concentrations, microplastics have been shown to induce cytotoxicity, compromise skin barrier integrity, and alter gene expression profiles [73].

5. Microplastics and Cosmetics

5.1. Microplastics in Cosmetics

Microplastics in cosmetics are broadly categorized into primary microplastics, which are intentionally added as ingredients, and secondary microplastics, which originate from the degradation or abrasion of cosmetic packaging materials (Figure 2) [8]. Primary microplastics are incorporated into cosmetic formulations to fulfill various functional roles, e.g., exfoliation, cleansing, opacity modulation, imparting a smooth or silky texture, and achieving an illuminating effect on the skin. They can be used in lipstick, loose or pressed powders, and liquid or thick emulsions with a powdery feel and may also be used as a carrier for other ingredients.

Among environmental plastic pollutants, those derived from personal care and cosmetic products (PCCPs) constitute a significant share, particularly due to their high particle count and widespread usage [76,77].

Microbeads, a common type of primary microplastic, are small plastic particles found in various PCCPs such as shampoos, toothpaste, exfoliants, nail art products, and glitter [76,78]. These particles vary in size and composition, often exhibiting irregular shapes and the ability to aggregate into larger masses [78]. Microbeads used in facial scrubs or body exfoliants typically have rough, uneven surfaces, which confer a high surface-area-to-volume ratio, enhancing their capacity to adsorb and transport harmful substances [79,80].

Once used, rinse-off products containing microbeads enter household drainage systems and are not completely removed by conventional wastewater treatment facilities. As a result, these particles can be released into natural water systems and eventually accumulate in marine environments [80,81].

Beyond direct cosmetic ingredients, recent studies have revealed that microplastics can also originate from cosmetic packaging. For instance, microplastic fragments are generated during routine actions such as opening, cutting, or tearing plastic containers [82]. This highlights packaging as an underrecognized source of microplastic pollution. While primary microplastics used in toxicology studies often have standardized shapes and sizes, secondary microplastics are highly variable, making risk assessment more complex [40]. These particles can be cubic, spherical, rod-shaped, or even jagged, with sharp-edged microplastics posing a particular concern due to their potential to cause physical irritation or injury within biological tissues [7].

5.2. Regulations and Efforts to Address Microplastics in Cosmetics and Personal Care Products

As awareness has grown regarding the environmental and health hazards associated with microplastics in personal care and cosmetic products (PCCPs), coordinated efforts by governments, industries, and environmental organizations have accelerated. Non-governmental organizations have played a pivotal role in raising public awareness and prompting regulatory action. One of the most influential campaigns, “Beat the Microbead”, was launched in 2012 by the Plastic Soup Foundation. This initiative identifies microplastic-containing products, provides consumers with an ingredient-scanning app, and advocates for global bans on microplastics in cosmetics (https://www.beatthemicrobead.org/about-us/ (accessed on 1 June 2025)). In response to such advocacy and mounting scientific evidence, several countries have implemented regulatory measures (

Table 2. Regulation of the use of microbeads and microplastics in cosmetics.

Country	Year Enacted	Regulations
USA	2015	The Microbead-Free Waters Act was signed into law in 2015, banning the manufacture of rinse-off cosmetics containing microbeads.
Australia	2015	Ban on microbeads in personal care, cosmetic, and cleaning products.
Canada	2016	Ban on microbeads in personal care products used to exfoliate or cleanse.
Taiwan	2016	Ban on solid microplastic particles used for exfoliation or body cleansing.
Brazil	2016	Ban on microbeads in cosmetics.
Republic of Korea	2017	Ban on sale of microbeads in cosmetics.
New Zealand	2018	Ban on import, manufacture, and sale of microbeads in rinse-off cosmetics.
UK	2018	Ban on microbeads in rinse-off cosmetics and personal care products in England and Scotland.
Sweden	2018	Ban on sale of microbeads in rinse-off cosmetics, following an earlier ban on import and manufacture.
Italy	2020	Ban on microbeads in rinse-off cosmetics.
China	2020	Ban on microbeads in rinse-off cosmetics, toothpaste, and toothpowder.
Thailand	2020	Ban on microbeads in cosmetics.
Argentina	2020	Ban on microbeads in cosmetics and oral hygiene products.
EU	2023	Restrictions on synthetic polymer microparticles on their own or intentionally added to mixtures in everyday products.

). In 2015, the United States enacted the Microbead-Free Waters Act, banning the use of plastic microbeads in rinse-off cosmetics [8]. Canada followed with a ban in 2016 targeting exfoliating and cleansing products, while South Korea introduced a similar ban in 2017 [7]. Other countries, including Italy, Sweden, the United Kingdom, and New Zealand, have also enforced national prohibitions on the use of microplastics in certain cosmetic formulations. More recently, the European Union adopted Commission Regulation (EU) 2023/2055, which restricts the intentional addition of microplastics in a broad range of products.

However, regulatory coverage remains incomplete and inconsistently applied across product categories. While rinse-off products such as facial cleansers and scrubs are frequently targeted by legislation, microplastics are still commonly found in leave-on products, particularly color cosmetics like lipsticks and eye makeup. A 2022 analysis by the Plastic Soup Foundation reported that 87% of products from major European cosmetic brands contained microplastic ingredients, highlighting the limited scope of current regulations. Furthermore, definitions of what constitutes a microplastic vary across jurisdictions. The European Chemicals Agency [83], for instance, does not currently classify engineered nanoplastics, water-soluble polymers, liquid and semi-solid polymers, or biodegradable polymers as microplastics, despite growing concerns about their similar ecological and toxicological impacts. Environmental groups and scientists have criticized this limited definition, warning that it may allow potentially harmful substances to evade regulation. The Plastic Soup Foundation has called for a more comprehensive and inclusive definition of microplastics within EU policy frameworks. In addition, current analytical techniques for microplastic identification and quantification are not yet sufficiently standardized or optimized for regulatory enforcement. While methods such as micro-FTIR and Raman spectroscopy, Py-GCMS, optical microscopy, scanning electron microscopy, and thermogravimetric analysis offer potential, they remain time-consuming and technically demanding, particularly when applied to complex formulations such as leave-on cosmetic products [8,84]. These products often contain emulsifiers, oils, and silicones, which complicate the separation and analysis of microplastic particles and may even degrade them during sample preparation [85,86]. As a result, establishing a rapid, reproducible, and robust testing framework across diverse product categories remains a significant challenge for regulatory bodies. In parallel with regulatory initiatives, the cosmetics industry has increasingly acknowledged the need to reduce its environmental footprint and has taken proactive steps to eliminate microplastics. Unilever, for example, phased out plastic scrub beads from its products as early as 2014. In South Korea, companies such as Amorepacific and LG Household & Health Care began reformulating exfoliating products in 2009, substituting microplastics with biodegradable natural alternatives like cellulose, walnut shell powder, perlite (volcanic ash), and silica. Similarly, Korean cosmetic manufacturers Cosmax and Kolmar Korea have explored innovative plant-based alternatives, such as pear cell-derived ingredients, to minimize microplastic content. In 2022, Kolmar Korea further advanced its sustainability efforts by developing a technology that replaces microplastics in color cosmetics with environmentally friendly silica particles.

Together, these regulatory actions and industry-led innovations represent meaningful progress toward reducing microplastic pollution from the cosmetic sector. However, significant challenges remain, particularly in harmonizing definitions, expanding regulatory scope, and ensuring the safety and efficacy of alternative materials.

6. Future Perspectives

6.1. Alternatives to Conventional Synthetic Polymers

In response to the environmental and health concerns associated with microplastics, there is a growing emphasis on developing biopolymers as sustainable alternatives to conventional synthetic polymers, such as polyethylene, in cosmetic packaging. Biopolymers are derived from natural sources, including plant biomass, cellulose, and microbial metabolites, and are gaining traction due to their biodegradability, biocompatibility, and lower ecological impact [83].

Among these, poly (lactic acid) [74]—a biodegradable aliphatic polyester synthesized through the fermentation of sugars—is widely recognized for its non-toxicity, high mechanical strength, and biocompatibility. PLA is already utilized in food packaging, tissue engineering, pharmaceuticals, and cosmetic packaging [87]. Under natural conditions, particularly sunlight exposure, PLA can biodegrade completely within six months to one year, making it a viable alternative for single-use plastic applications [83,88].

Starch-based polymers represent another promising group of bioplastics. Composed primarily of amylose and amylopectin, starch is sourced from potatoes, corn, rice, and wheat [89]. These polymers are low in toxicity, biocompatible, and highly biodegradable. Their functional properties can be enhanced through the incorporation of plasticizers such as citric acid, sorbitol, or glycerol, improving their flexibility and applicability in cosmetic packaging [83,90].

Polybutylene succinate (PBS), which is primarily used in packaging applications, is synthesized via the polycondensation of succinic acid and butanediol. It exhibits excellent thermal stability and mechanical performance. However, high production costs currently hinder its widespread commercial adoption [91].

In parallel, innovative approaches are being explored to develop biomaterials from renewable and waste-derived sources, including seafood waste (e.g., shrimp and shellfish shells), fruit and agricultural byproducts, and marine plastic debris [92,93,94]. Furthermore, bio-composite materials incorporating coconut fibers, jute fibers, and other lignocellulosic materials are under active investigation for cosmetic and packaging applications due to their enhanced sustainability and mechanical performance [95,96].

Within cosmetic formulations, carbohydrate-based biopolymers—such as cellulose beads and starch-based granules—as well as natural exfoliating agents, including salt, sugar, coffee grounds, bamboo powder, almond and apricot seed powders, walnut shell powder, and pumice (volcanic rock), offer effective and biodegradable alternatives to synthetic microbeads, supporting a shift toward eco-conscious product development.

However, most existing studies have evaluated the degradation kinetics of biodegradable polymers and microplastic additives under idealized laboratory or industrial composting conditions, which may not accurately reflect real-world environments such as wastewater systems or marine ecosystems where cosmetic products are ultimately discharged. This study has a limitation in that it does not provide comparative half-life data under realistic environmental conditions. However, future research should aim to generate such data and also address the potential for biodegradable alternatives to fragment into secondary nanoplastics during their use and degradation processes.

6.2. Approaches to Microplastic Removal

Several promising strategies have emerged for mitigating microplastic pollution through biological means. Studies have demonstrated the potential of microorganisms—including bacteria (e.g., Pseudomonas, Bacillus, Rhodococcus), fungi (e.g., Aspergillus, Penicillium), and microalgae (e.g., Chlamydomonas reinhardtii)—to biodegrade microplastics, offering cost-effective and eco-friendly alternatives to conventional physical or chemical degradation processes [97,98,99,100,101,102,103]. These microbial strategies harness specific enzymes, such as hydrolases and oxidases, to break down plastic polymers into smaller, non-toxic byproducts [99,104,105]. Although the practical application of microplastic biodegradation remains limited, recent studies have reported the use of genetic engineering to enhance the microplastic degradation of microbial strains such as Ideonella sakaiensis [106].

In parallel, novel biomedical approaches are being explored to address internal microplastic accumulation. For instance, specific probiotic strains such as Lactiplantibacillus plantarum DT88 and Lacticaseibacillus paracasei DT66 have shown the ability to adsorb polystyrene particles within the gastrointestinal tract, promoting excretion and alleviating intestinal inflammation in mice [107]. These findings suggest that strain-specific probiotics may serve as a future therapeutic option to reduce the health risks associated with microplastic ingestion.

7. Conclusions

Microplastics in cosmetics have emerged as a pressing concern for both human health and environmental sustainability. Although regulatory actions have been implemented in several countries—including the United States, South Korea, and the European Union—microplastics continue to be introduced into the environment through both direct use and packaging-related sources, indicating that current measures are insufficient. Evidence suggests that microplastic exposure may disrupt skin barrier integrity, trigger inflammation, induce oxidative stress, and accelerate skin aging, underscoring the need for safer alternatives.

To address these challenges, recent advancements in biopolymer technologies, sustainable packaging, and the use of natural exfoliants provide promising avenues for reducing microplastic pollution. However, further multidisciplinary research is essential to better understand the long-term health effects of microplastics and to guide the establishment of a comprehensive, globally harmonized regulatory framework.

As public concern and scientific evidence continue to mount, the cosmetics industry must take proactive steps to phase out microplastic ingredients, invest in eco-friendly innovations, and transition toward sustainable product development. Such efforts will not only help mitigate environmental damage but also safeguard consumer health and align with global sustainability goals.