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Review

The Effects of Microplastics and Nanoplastics in the Nasal Airway and Upper Respiratory Tract

by
Maayan S. Kahan
1,
Benjamin S. Bleier
1,2,
Mansoor M. Amiji
3 and
Alan D. Workman
1,2,*
1
Department of Otolaryngology—Head & Neck Surgery, Massachusetts Eye and Ear, Boston, MA 02114, USA
2
Harvard Medical School, Boston, MA 02115, USA
3
Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, Boston, MA 02115, USA
*
Author to whom correspondence should be addressed.
Sinusitis 2026, 10(1), 1; https://doi.org/10.3390/sinusitis10010001
Submission received: 29 October 2025 / Revised: 10 December 2025 / Accepted: 18 December 2025 / Published: 22 December 2025
Browse Figure
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Abstract

Environmental microplastic pollution is rising, and the recent literature reflects these conditions primarily by focusing on the effects of microplastics in the human lung and gut region. Despite the specific prevalence of airborne microplastics, the bulk of the existing literature neglects the point of initial contact of microplastics with the human body, namely the upper airway, specifically the nasal region. This review aims to highlight recent findings surrounding the effects of microplastics in the nose in both in vitro and clinical models. Areas of particular interest include changes in cell morphology, microplastic permeation, cytotoxicity, and inflammatory effects. Although permeation and toxicity findings vary across studies, the literature collectively indicates hazards to cellular health and potential impacts on patient quality of life.

1. Introduction

The rise in industrialization has been accompanied by an increase in environmental pollutants and contaminants. Plastic production has increased by a factor of 20 in the past 50 years, generating an estimated 9200 million metric tons [1]. As plastic production and use have expanded, so too has the degree of human exposure to these materials. In recent years, the presence of microplastics and nanoplastics in the environment has gained recognition within the broader scientific community. Microplastics range in size from 1 µm to 5 mm [1], while nanoplastics refer to particles less than one micron in size [2]. Collectively, these substances are referred to as micro(nano)plastics, or MNPs. These particles can take many forms, including but not limited to fragments, foam, films, granules, fibers, and beads [3]. Primary MNPs are intentionally manufactured largely for personal care products and cosmetics, while secondary MNPs are the result of both the biotic and abiotic degradation of manufactured materials [3]. MNPs exist in virtually all environments; however, concentration in indoor air is considerably higher than that of the outdoors [4]. Airborne MNPs can be released from a variety of sources, the most common of which include synthetic fibers, tire degradation, and road dust (Figure 1) [5].
MNPs can be internalized in two major ways, namely inhalation and ingestion. While it is becoming increasingly common for individuals to take precautions against the ingestion of MNPs, avoiding the consumption of MNPs entirely is impossible [5]. On average, humans ingest 0–7.3 × 104 plastic items per year via table salt, 0–4.7 × 103 plastic items per year via drinking water, and 0–3.0 × 107 plastic items per year via the air [5]. Past research has demonstrated that MNPs are capable of entering the human body and permeating tissue and cells [6]. However, the vast majority of this research has been focused on the effects of MNPs in the lung and gut region, with minimal investigation being performed on the effects of MNPs in the nose, despite the prevalence of MNP exposure via inhalation and the nose being the site of first contact between the invading MNPs and the body. This review aims to summarize research on the effects of MNPs on human cells with a particular focus on the effects MNPs have in the nasal airway. All primary non-review articles in PubMed through to 1 October 2025 covering the effects of plastic particulates on the upper airway were considered for inclusion in this review; manuscripts were excluded if they lacked objective outcomes or effect measurements. Due to the lack of literature focused solely on the nasal airway, broader sources incorporating the pulmonary airway have been included as well for context. Various types of experimental plastic exposure will be presented, as well as the extent of their permeation and subsequent observed effects in cellular behavior and morphology.

1.1. Deposition and Impaction in the Nasal Cavity and Epithelium

The unique inhalation patterns of an individual and the characteristics of the inhaled particles are important when analyzing the final site of deposition. By creating a digital model of the respiratory pathway, Shang et al. isolated three primary hotspots of particle deposition, involving the top of the vestibule, the nasopharynx, and the boundary of the middle turbinate and the middle meatus [7]. There are four primary mechanisms of particle deposition within the nasal cavity, these being inertial impaction, sedimentation, diffusion, and interception [8]. For fibrous particles, interception is the most significant, while inertial impaction is of primary importance for particles greater than one micron in diameter [8]. Particles smaller than 50 nm primarily disperse through diffusion, while for particles in the 0.05–1 μm range, diffusion, inertial impaction, and sedimentation are all of relatively equal significance, although their overall effect is lesser [8]. Using a separate computer model, Huang et al. compared the deposition patterns of micro- and nanoparticles of various diameters under different breathing conditions [9]. When the model was run under fast breathing conditions, large microparticles were concentrated in the anterior nasal cavity, with a significantly lesser portion of small microparticles deposited towards the larynx [9]. For nanoparticles under the same conditions, the particles were much more uniformly distributed throughout the entire nasal cavity, with the particles particularly concentrated in the larynx region [9]. In cases of moderate breathing, the microparticles covered more extensive areas within the same region, while nanoparticles exhibited reduced coverage with concentration at the oropharynx [9]. For microparticles, the most extensive coverage was observed under conditions of slow breathing, with approximately half of the surface area covered by microparticles [9]. On the other hand, nanoparticles inhaled via low breathing display a decrease in deposition concentrated in the middle oropharynx and regions above and below the vocal cords [9]. When this data is incorporated with the particle’s respective deposition and escape fractions, the overall trend revealed that both micro- and nanoparticles exhibit longer transport distances and deeper airway deposition with slower breathing patterns [9]. The larger microparticles exhibited reduced transport distances and the deepest airway depositions among all the conditions, while smaller nanoparticles displayed the most extended transport distances and deeper airway depositions under the same conditions [9]. Upon impaction, foreign particulates encounter the nasal epithelium, the body’s first line of nasal defense. Should the integrity of the epithelial barrier be compromised, these particulates can penetrate downwards and induce further immune responses [10]. The epithelial barrier consists of physical, chemical, immunological, and microbiological elements. Particulate matter poses a particular hazard to both the physical and chemical barriers. Particulates have been demonstrated to downregulate claudin-1, zonula occludens-1, and epithelial cadherin expression, as well as decrease transepithelial electrical resistance (TEER) and fluorescein isothiocyanate–dextran 4 kDa permeability on the nasal mucosa, causing harm to the physical barrier [10]. Damage to the chemical barrier can be observed in the downregulation of ciliated cell expression and the induction of several human mucin genes causing abnormal mucus secretion and ciliated cell dysfunction in the nasal epithelium [10].

1.2. In Vitro Experimental Protocols Investigating MNPs

Due to the many types of MNPs in the environment and their various means of entering the body, there are several different methods of study when investigating the effects of MNPs in humans. Polystyrene (PS) is a popular choice due to its known chemical properties and prevalence throughout the environment [11]. Many experiments opt to use beads instead of the more environmentally relevant fiber-shaped fragments. Cells are often exposed to plastics in several different ways, including co-culturing and aerosol treatments. The experimental sizes and concentrations utilized are also highly varied (Table 1). A previous study found that microplastics smaller than 10 µm can cross the cell membrane [12]. The threshold concentrations of MNPs that alter cell behavior are not established, so studies have used a wide range of doses.
The most common form of microplastic utilized is neutrally charged polystyrene particles in an aqueous suspension. Due to the variety of worldwide environmental conditions and particulate matter, size and concentration significantly varied amongst groups. Most solutes were administered in the same form as provided by the manufacturer, but certain groups have made modifications to better mimic real-world conditions or to enhance the experimental conditions. In addition to neutral particles, Huang et al. tested two other forms of polystyrene with different surface functional groups (carboxylic and amino), as well as a form of neutral fluorescent polystyrene. A-PS50 has a positive z-potential, while all other particles had a negative z-potential. Nasal mucus is negatively charged according to ref. [13], suggesting that the potential for MNP adhesion would increase with a positive charge. Bare MNPs without surface adhesions have negative z-potential, although it has been demonstrated that when the MNPs were exposed to culture media, the absolute value of their negatively charged particles decreased [14]. Vailionytė et al. [6] formulated their experimental particles from scratch to replicate the irregular particles found in the actual environment by using standard manufactured pellets of PE3.0*105; they thoroughly washed the particles then artificially aged them via 48 h exposure to UV light and a combined treatment of graphene oxide–TiO2 photocatalyst and H2O2. These aged particles were then crushed to a fine powder to be used to treat the cells. Paplińska-Goryca et al. also created their own sample through a process of cutting 1–2 mm lengths of polyamide thread and a fishing line which were then homogenized and exposed to UV radiation, choosing to specifically focus on MNPs in fibrous form, the most common form of airborne microplastics [15].
Co-incubation was the primary method utilized in the administration of the MNPs into the cells. Cells were cultured independently for time periods ranging between 12 and 24 h before the introduction of the MNPs. The particles were then left to interact with the cells for a minimum of 24 h up to 96 h with no repeated dosing. In addition to a monoculture of HNEpCs, Paplińska-Goryca et al. tested a co-culture of HNEpCs and monocyte-derived macrophages to further investigate the relationship between epithelial cells and immune cells. HNEpCs were primarily grown using air–liquid interface (ALI) cultures to better mimic intranasal conditions via the utilization of the transwell insert. As an alternative to ALI culturing, some groups opted to treat their cells with MNPs by aerosolizing liquid samples of polystyrene beads to recreate the form of MNPs that most come into contact with the nasal epithelium [16].

2. Cellular Alterations Seen with MNP Exposure

Many of the protocols surveyed incorporated some form of cellular imaging to determine the localization and permeation of MNPs. The necessary fluorescence was achieved by either staining existing MNP-treated cells and MNPs or using specially dyed MNPs and conducting a separate round of exposure at a specific concentration. Protocols often utilized different concentrations for imaging purposes compared to cells that were assayed. However, the extent of the permeation of the microplastics into the interior of the cell is insufficient to address the effects that MNPs have. There have been reports of plastics having adverse effects in several different cell types on cellular behavior such as inducing inflammatory cytokine responses and degrading the quality of the tissue, although the relative danger of these conditions remains a matter of debate.

2.1. Plastic Localization

Results regarding the localization of MNPs within the cell varied greatly, ranging from the adherence of MNPs to the exterior of the cell to nucleic permeation. Using a combination of confocal microscopy, atomic microscopy, and flow cytometry, MNPs were detected in the cytosol by different groups at initial concentrations, ranging from as low as 5 ug/mL in A549 cells [17] up to 250 ug/mL in HNEpCs [18]. Some further observed that larger particles which were unable to permeate the cell fixated themselves to the exterior of the cell membrane [6,17]. The degree of MNP permeation was found to be inversely related to the size of the particles. Those that assayed their cells multiple times with increasing time points found that the number of cells involved and the degree of particle uptake increased with duration of exposure [17,18].
Huang et al. found in HNEpCs that the most significant increase in the rate of cellular uptake occurred between the 2 h and 6 h mark [18]. Whether MNPs enter the nucleus remains uncertain. With a negatively charged nucleic shell, ref. [19] had positively charged MNPs that were theorized to be more effective in nucleic permeation. Ref. [18] showed that no positively charged MNPs were imaged in any of the aforementioned experiments. Some studies observed MNP permeation that extended only through the cytosol, such as in ref. [6], while others noted significant clustering surrounding the periphery of the nucleus, with no particles crossing the nuclear membrane [14,17]. Conversely, Huang et al. observed MNPs in the nucleus beginning only 2 h post-exposure and theorizes that this phenomenon is due to MNPs being phagocytosed by HNEpCs and entering the nucleus [18]. This unique observation could possibly be attributed to the significant increase in concentration and smaller diameter of MNPs compared to other similar experiments. The specific mechanism of both inter- and intracellular translocation necessitates further investigation. Studies have indicated the potential role the lymphatic and circulatory systems in the translocation of MNPs, such as ref. [3], while research in nanomedicine suggests the innervated features of the nose allow for potential modes of neuronal transport, although both of these pathways come with their own unique limitations and parameters that are beyond the scope of this paper [20].

2.2. Particle Uptake

The progressive increase in the cellular uptake of MNPs suggests that endocytosis plays an important role in how cells interact with these particles [18,21]. Particles can enter the cell through either phagocytosis or pinocytosis, the latter of which can be further differentiated into macropinocytosis, clathrin-mediated, caveolae-mediated, and clathrin/caveolae-independent endocytosis [21]. Phagocytosis internalizes foreign bodies via specialized cells known as phagocytes, while pinocytosis takes up matter by forming an invagination to accept molecules [22]. Current research indicates that particle size is the primary factor determining the mechanism of endocytosis; phagocytosis is typically utilized for long, thin fibers along with particles larger than 0.5 μm, while smaller particles are moved through pinocytosis [21]. Clathrin-mediated endocytosis is limited to approximately 100 nm, while the typical size of an endosome in caveolae-mediated endocytosis is 50–80 nm [21]. The capacity of macropinocytosis is much broader, with vesicles ranging in size from 0.2 to 5 μm [21]. In addition to affecting the degree of permeation, surface modifications also play a role in determining the uptake mechanism, with one study determining that while amino-functionalized MNPs were absorbed via clathrin-mediated endocytosis, particles lacking that modification were internalized via clathrin-independent endocytosis [21]. Recent findings by Zhang et al. suggest that temperature affects the uptake kinetics of MNPs by observing that while the cellular concentration of microplastics remained relatively constant after 30 min exposure at 4 °C, the concentration continuously increased in the same cell line at 37 °C, well past the 30 min mark [21].
While many attribute microplastic presence in the cell to phagocytosis, others have pointed to phagocytosis in conjunction with mucociliary movement as a principal method of microplastic clearance [3]. Following initial uptake, particles encounter early endosomes which transport the particles to their respective locations, with a portion of the contents being repurposed to the plasma membrane by recycling endosomes [22]. The early endosomes continue to develop into late endosomes which then merge with lysosomes to create endolysososmal vesicles, while hydrolytic enzymes degrade the contents [22]. With regard to mucociliary movement, ciliary beat frequency in lung cells demonstrates a dose-dependent increase with MNP exposure, which results in a higher rate of mucociliary clearance, indicating the departure of MNPs [16].

2.3. Tissue and Cellular Integrity

Treated bronchial epithelial cells developed exterior roughness due to the adherence of MNPs to the cell membrane [6]. Broader morphological changes were also observed, with an increase in cell height in the range of 3–6 um [6]. In their observation of A549 cells, Goodman et al. found that while unexposed cells grew as puffy shapes in close contact with one another, MNP-exposed cells ceased close contact with one another almost entirely and grew in much smaller clusters, if at all [17]. Furthermore, the observed cells were exposed to both 10 µm and 1 µm MNPs, but no major changes in cell shape were observed as a result of varied particle sizes [17]. Filipodia were observed on exposed cells, while they were rare in unexposed cells [17]. Exposed cells were found to have many nonretractile spots theorized to be developing focal adhesions of a distancing cell [17]. Nonretractile spots were more common in cells with 1 µm MNP exposure, while lamellipodia extensions grown over filipodia were more common in cells exposed to 10 µm MNPs [17]. Tissue integrity is commonly measured via a TEER assay, in which the degree of electrical resistance detected correlates with the strength of the tissue. In a TEER assay of the lower airway epithelium, cells were shown to exhibit increased resistance when exposed to even the smallest dose of MNPs and did not show significant dependence on the strength of the dose [16]. When the same test was administered to HNEpCs, cells dosed with microplastics exhibited little significant change in resistance [23]. In addition to the tissue, MNPs have adverse effects on cell membrane integrity, inducing lower density, fluidity changes, and a thickening of the dipalmitoyl phosphatidylcholine bilayer [24].

2.4. Immune Response

Both bronchial and nasal epithelial cells exposed to MNPs showed a range of inflammatory and immune responses. In the lower airway models, the most widely reported inflammatory cytokine secretions consist of IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP-1)α, and IL-1β. Transforming grow factor (TGF)-β, a family of inflammatory proteins associated with leaky membrane barriers, has been the subject of some discourse between various publications, with several reporting increased TGF-β expression in A549 cells [17,23,25], with the notable exception of Breidenbach et al.’s finding of a TGF-β reduction in airway epithelial cells; nevertheless, they concede that these findings indicate immunomodulatory effects. Vailionytė et al. observed an increase in pro-inflammatory soluble adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), E-selectin, and CDR2P [6]. In addition to the lower TGF-β levels reported, several other factors were noted to be downregulated in association with MNP exposure, such as cytokines IL-21, IL-2, IL-15, and IP-10 [16].

3. Toxicity

One of the most contested topics in this area of study is the degree of cytotoxicity microplastics have on cells. Significant contributing factors to this phenomenon include the cell line observed, concentration of MNPs, type of MNP used, method of co-incubation, and length of exposure.

3.1. Cell Viability

Only certain plastics such as PS20, aerosolized PS50, and PS500 were observed to exhibit dose-dependent cytotoxic effects, as seen in ref. [18], while others found no correlation between cytotoxicity and particle concentration or size. Bare MNPs are more likely to induce apoptosis, while amine-modified MNPs appear to lead to cell necrosis in HNEpCs [18]. However, amongst all potential surface variations, amine-modified MNPs induce the most toxicity [18]. Certain variations in polystyrene microparticles were observed to significantly reduce cell viability in HNEpCs at concentrations as low as 10 μg/mL, while others did not have any obvious effect on cell viability in concentrations as high as 1250 μg/mL, with all effects being observed within 48 h [18]. In an experiment that utilized microfibers as opposed to microparticles, no cytotoxic effects were observed on HNEpCs during the same time window [23]. In a different study which utilized a less extensive selection of microplastic particles consisting solely of A-PS50 and A-PS500, no cytotoxic effects on HNEpCs were observed in 24 h with doses ranging from 0.5 μg/mL to 100 μg/mL [14]. Bronchial epithelial cells were found to only express decreased cell viability at concentrations exceeding 1000 μg/mL [6]. In a similar experiment with A549 cells exposed to PS1000 and PS10000 at 0.05–100 ug/mL for up to 96 h [17] and human airway epithelial cells for 72 h of aerosolized polystyrene in concentrations of up to 2500 μg/mL, cytotoxic affects were exhibited under all conditions [16].

3.2. Rates of Proliferation

As opposed to outright cell death, MNPs appear to have the capacity to reduce the rates of cellular proliferation, which inhibits the growth of the cells and the broader capacity of the functionality of the organism. Vailionyte et al. found that after 48 h in bronchial epithelial cells which exhibited a lower rate of proliferation, cell cycle analysis indicated an accumulation of cells in between G0/G1, suggesting a transition towards cell cycle arrest [6]. Exposed A549 cells were observed to have initial decreases in proliferation as early as 24 h, culminating at the 96 h mark at which point cultures exposed to both 1 μm or 10 μm plastics exhibited a four- to five-fold reduction in Ki-67 protein expression, a known marker of cell cycling [17]. Goodman et al. assayed both metabolic activity and cellular proliferation in A549 cells and found that despite an initially greater rate of suppressed metabolic activity compared to cell proliferation, after 24 h, all the decreased metabolic activity could be attributed to the aforementioned reduction in proliferation as opposed to outright cell death [17].

3.3. Reactive Oxygen Species Generation

While reactive oxygen species (ROS) are critical as cell signaling molecules, excessive amounts signal oxidative stress and can induce apoptosis [26]. Increased levels of ROSs were consistently reported across multiple studies of MP exposure [3]. The overproduction of mitochondrial ROS has been identified as a significantly contributing factor to mitochondrial damage, particularly the integrity of the mitochondrial membrane [27]. About 5% or more of all inhaled O2 is reduced into ROSs O−2, H2O2, and OH, reactive intermediaries that disrupt homeostasis between ROSs and antioxidants and induce oxidative stress [28]. Antioxidant enzymes and free radical scavengers are the body’s primary defense mechanisms against ROSs, but these systems can be overwhelmed in the face of excessive ROS generation [28]. High ROS levels have been shown to induce both nuclear and mitochondrial DNA damage, the oxidative damage of proteins, and lipid peroxidation, all of which can lead to cell death with sufficient severity [28]. Additionally, ROSs and oxidative stress have been shown to be linked with many age-related degenerative diseases including arthritis, cardiovascular disease, inflammation, diabetes, cancer, Alzheimer’s disease, and Parkinson’s disease [29]. ROS accumulation as a result of MNP exposure has been theorized to lead to ferroptosis, necroptosis, and apoptosis [30]. Interestingly, in conjunction with being a target for ROS damage, the mitochondria additionally serve as a source for the generation of ROSs [29]. ROS exposure induces damage in the mitochondria via the oxidation of membrane proteins, particularly cysteine and methionine residues, as well as the peroxidation of mitochondrial membrane lipids [31]. When ROS levels were measured in HNEpCs exposed to 100 μg/mL of PS-50 and PS-500, both exhibited notably higher ROS levels, with PS-50 having a slightly more significant effect than PS-500 [14]. When mitochondrial membrane potential was measured under the same conditions, HNEpCs exposed to PS-500 exhibited a slight decrease in membrane potential, while those exposed to PS-50 displayed a much more significant loss in membrane potential, indicating the size-dependent effects of MNP on the mitochondrial membrane potential [14]. A seahorse metabolic analysis conducted on BEAS-2B cells showed disturbances in mitochondrial bioenergetics, as well as decreased mitochondrial function, ATP production, and respiratory capacity as measured by oxygen consumption and extracellular acidification rates at exposure concentrations of 1000 μg/cm2 [6]. While the positive relationship between MNP exposure and ROS generation has become more significantly established in recent years, the specific mechanism by which MNP generates ROS requires further elucidation.

3.4. Autophagy

Autophagy is triggered under cellular stress to recycle damaged organelles and proteins, helping to maintain cell survival [14]. A specific group of autophagy-related (ATG) proteins assemble into functional complexes which are then activated and recruited to initiate autophagy [32]. Relevant proteins include the unc-51-like autophagy activating kinase (ULK) complex, the class III lipid kinase complex, WD-repeat protein interacting with phosphoinositide (WIPI), ubiquitin-like conjugation complex, and the transmembrane protein ATG9 [32]. These proteins collectively form autophagosomes which then fuse with lysosomes where the autophagosome contents can empty into the lysosome to be fully degraded [32]. Although autophagy is a mechanism of cell death, it is currently primarily regarded as a defense mechanism with the goal of maintaining homeostasis [30]. Elevated ROS levels are frequently related to the induction of autophagy [30]. Conflicting reports have shown both the enhancement and impairment of autophagic processes in cells upon MNP exposure and elevated ROS levels [30]. Annangi et al. [14] analyzed the autophagic markers of microtubule-associated protein 1 light chain 3-II (LC3-II) and the ubiquitin p62 in HNEpCs and found that both PS-50 and PS-500 can block the autophagy pathway once they are internalized within the cell. In typical autophagy, LC3-II levels increase as an indication of autophagosome accumulation, while p62, a substrate of autophagy, decreases. However, when PS-50 and PS-500 were introduced in the presence of chloroquine, a lysosomal and autophagosome inhibitor, LC3-II levels were elevated. Even without the presence of chloroquine, p62 levels were found to be significantly higher than the untreated control, suggesting a blockage of the autophagy pathway. Similarly, in BEAS-2B cells, Vailionytė et al. found elevated ROS levels and the activation of the NRF2/ARE pathway, a key component in cellular defense against oxidative stress [6]. However, autophagy-related protein levels of p62, phospho-p62, and autophagy marker light chain 3 (LC3A/B) likewise increased, a result which the authors theorize to indicate impaired autophagic flux in which autophagosomes are formed but not properly degraded [6]. Human neuroblastoma cells exposed to polystyrene MNPs exhibited a noted increase in several autophagy-related proteins as well as a decrease in p62, indicating functional autophagy as a result of PS-NP induction [33]. Functional autophagic pathways were additionally observed in human umbilical vein endothelial, gastric epithelial, and kidney proximal tubule epithelial cells following microplastic exposure [30]. Exposure to environmental contaminants such as MNPs could lead to the induction of autophagy as a means of protection [14].

3.5. Genotoxicity

Recent findings indicate that microplastic exposure generates adverse chromosomal effects, with effects ranging from structural damage to genetic dysregulation [34]. Multiple studies have identified several forms of nucleic dysregulation in aquatic animals as a result of both direct and indirect microplastic consumption [34]. Deformations included micronucleation, constricted nuclei, notched nuclei, and nuclear buds [34]. Jakubowska et al. investigated the genotoxic effects of various microplastics and found that the degree of genotoxicity in fish larvae increased substantially in the sequence of polystyrene > polyethylene terephthalate > polyethylene [35]. Some theorize that the nucleic deformation can be attributed to the generation of reactive oxidative species, with one study finding expression reduction in several antioxidant-related genes [34]. Other studies noted the decreased expression of protein kinase B and MAPK/ERK kinase, which further indicates oxidative stress [34]. Revel et al. found no changes in the antioxidant enzyme levels of blue mussels but did find that structural DNA damage increased between 30% and 54% in groups exposed to 10 μg/L and 100 μg/L of plastics, respectively [36]. Sussarellu et al. analyzed differentially expressed genes in gonadal and oocyte samples from adult oysters following polystyrene exposure [37]. They found 46 differentially expressed transcripts in gonadal tissues with enriched processes including glutamine synthesis, the stimulation of insulin secretion, epithelial cell proliferation, and adhesion between ovarian follicle cells [37]. In oocyte cells, 81 transcripts were differentially expressed involving proteolysis, embryotic development, and ion bonding [37]. Between the two, the most significantly enriched gene ontology (GO) biological processes consisted of a response to glucocorticoid stimulus, fatty acid catabolic processes, respiratory burst, and the cellular response to mechanical stimulus [37]. Terrestrial organisms exhibited similar responses to aquatic organisms with the additional discoveries of enhanced occurrences of nucleoplasmic bridges and decreases in the mitotic index accompanied by increases in the chromosomal abnormality index and nuclear abnormality index [34]. The most notable difference is the contrasting findings pertaining to p53 gene expression, with gene suppression noted in Mediterranean mussels, while a p53-responsive luciferase reporter gene assay of human osteosarcoma cells exhibited positive p53 expression, suggesting genotoxic stress [34]. Potential mechanisms of DNA damage resulting from p53 activation include physical disruption to the cell membrane, endocytosis, and/or the transformation of microplastics in various cellular compartments that could lead to the release of toxic chemicals [38].

4. Clinical Implications

Microplastics have been consistently observed within individual tissues regardless of environmental or health status [39]. However, recent evidence suggests a positive relationship between microplastics in the nose and conditions such as allergic rhinitis, chronic rhinitis, and chronic rhinosinusitis (Table 2). It is thus far unknown whether this relationship indicates a potential attribution of MNPs to the exacerbation or induction of nasal conditions. Studies utilized nasal lavages to obtain samples accompanied by patient surveys to determine symptoms and overall quality of life.
In a comparison of patients with acute versus chronic rhinitis, patients with acute rhinitis were found to have more microplastic fibers in the nasal cavity but did not report significantly different symptoms or levels of discomfort [40]. However, when patients with chronic rhinosinusitis were compared with healthy individuals, those with chronic rhinosinusitis had higher plastic levels and worse survey results [44]. Similar findings were reported when comparing healthy individuals to those with allergic rhinitis [41,42]. Xue et al. found that large and small particles were evenly distributed, with granular particles being the most prevalent shape amongst small particles, while linear shapes were most common in large particles [42]. In a separate study, microplastic density was not found to be correlated with quality of life in all patients with rhinitis, but when symptomatic patients were compared to asymptomatic ones, microplastic density was significantly higher in the symptomatic group [43].

5. Limitations

The exploration of the effects of MNPs in the nasal airway is limited to a few empirical/experimental publications that are detailed above, and all findings discussed are heavily weighted towards these specific experimental results due to a lack of replication studies and broader experimentation. Methodology varies widely among the discussed experiments due to a lack of standardization in this burgeoning field. It is important to note that this link between MNP exposure and rhinitis remains hypothetical and that clinical studies of any links are burdened by numerous confounding factors, including air pollution, allergens, and dust exposure. Further experimental and clinical studies are necessary to establish causal deleterious effects of MNPs on nasal tissue.

6. Conclusions and Recommendations

It is increasingly clear that MNPs are prevalent in our environment and interact with human biology in a meaningful way. Even the most conservative findings reveal the presence of MNPs in the airway and identify them as sources of inflammation. Beyond this, microplastics may impede upon cellular growth and functions vital to the survival of the organism. Studies have observed plastics to permeate HNEpCs following MNP exposure in varying sizes and concentrations, in some instances going so far as to encounter the nucleus of the cell. More broadly, particles at much larger sizes and lower concentrations have been shown to induce cytokine secretions and potentially inhibit rates of cellular proliferation. Furthermore, various studies have indicated a rise in ROS levels in MNP-exposed cells, which has been linked to both genotoxicity and autophagy. Recent clinical research presents the possible correlation between MNP concentration and various upper respiratory conditions, although future research is required to properly establish the relationship between MNPs and nasal conditions.
There is a considerable knowledge gap regarding the microplastic specifications including form, size, shape, and charge and their different effects on the human nasal epithelium. Additionally, the movement of MNPs from the airborne environment into the nose and their specific pathway into cells and various cellular compartments needs to be more fully elucidated. Another area of interest is the specific mechanism by which MNPs induce the generation of ROSs and the effects that this has on the cell and broader organism. An additional obstacle in this endeavor is the lack of consistency between studies regarding units and measurements, which increases the difficulty of comparing relevant studies. Thus far, most research conducted has solely consisted of in vitro experimentation. In vivo experimentation proves to be the logical next step in providing a more accurate model to observe the broader effects of microplastic exposure. Furthermore, little is known about both the long- and short-term effects of microplastic exposure, research that will become increasingly relevant as plastic consumption and production continues to spread across the globe.

Author Contributions

Conceptualization, A.D.W., B.S.B., M.M.A. and M.S.K.; Original Draft Preparation, A.D.W. and M.S.K., Writing—Review and Editing, M.M.A. and B.S.B. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No original data was generated for this manuscript.

Conflicts of Interest

The authors declare no conflict of interest.

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Sinusitis 10 00001 g001
Figure 1. Nasal microplastic exposure and reviewed hazardous effects (Created In Biorender, M. Kahan, 2005).
Figure 1. Nasal microplastic exposure and reviewed hazardous effects (Created In Biorender, M. Kahan, 2005).
Sinusitis 10 00001 g001
Table 1. Summary of experimental conditions (plastic type given in plastic diameter (nm) format) for relevant studies.
Table 1. Summary of experimental conditions (plastic type given in plastic diameter (nm) format) for relevant studies.
Vailionytė (2025)Goodman (2021)Huang (2022)Breidenbach (2025) Paplińska-Goryca (2025) Annangi (2023)
Cell LineBronchial epithelial cells
(BEAS-2B)		Human adenocarcinoma lung epithelial cells
(A549)		Human nasal epithelial cells (HNEpCs) Donor-provided airway epithelial cells Human nasal epithelial cells (HNEpCs) from control, asthmatic, and COPD patients cultured independently or with monocyte-derived macrophagesHNEpCs
Microplastic TypeArtificially aged and crushed polyethylene PEPS1000 and PS10000 microspheresPS20-2000 F-, C-, and A- microspheresAerosolized PS50Homemade polyamide (PA) fibersPS50, PS500 particles
Microplastic Treatment 24 h or 48 h exposure to MNPs concentrated at 10, 100, or 1000 μg/mL Co-incubation of MNPs concentrated from
0.05 to 100 ug/mL with assay points from 24 h up to 96 h 		48 h co-incubation of MNPs
concentrated at 10, 50, 125, 500, and 1250 μg/mL 		3 min/3x/day exposure for 3 days
at approximately 0.43 μL/insert of solution per exposure		48 h exposure to MNPs at 5 µg/µL 24 h exposure to MNPs ranging from 0.50 to 100 μg/mL
Table 2. Summary of clinical studies detailing sample size and condition, methodology, MNP concentration in patients, and patient self-reporting.
Table 2. Summary of clinical studies detailing sample size and condition, methodology, MNP concentration in patients, and patient self-reporting.
ArticleTuna (2025) [40]Tuna (2023) [41]Xue (2025) [42]Itmec (2025) [43]Tas (2024) [44]
Patient Condition and Sample Size30 chronic rhinitis/30 acute rhinitis36 allergic rhinitis/30 healthy33 allergic rhinitis/22 healthy30 allergic rhinitis/30 nonallergic rhinitis/30 control 50 chronic rhinosinusitis without nasal polyps/30 healthy
Method of MNP IdentificationCollected sample via saline flush, MNPs were found with Nile red staining/fluorescent microscopy.Collected samples via saline nasal lavages. MNPs were found via filtration and fluorescent microscopy with Nile red staining. Collected samples from indoor workers via saline nasal lavage. MNPs were found via filtration. Collected samples via nasal lavage. MNPs were found via filtration and fluorescent microscopy with Nile red staining.Collected samples via saline nasal lavages. MNPs were found via filtration and fluorescent microscopy with Nile red staining.
Concentrations in Patients (particles/mL)Acute: 3.46 ± 1.82 Allergic: 3.10 ± 1.85 Allergic: 9.96Allergic: 3.23 ± 1.30 Chronic: 3.88 ± 2.14
Chronic: 2.50 ± 0.48 Control: 2.38 ± 1.85 Control: 7.72 ± 2.63 Nonallergic: 2.97 ± 0.57 Control:2.34 ± 1.89
Control: 1.18 ± 0.52
Survey MethodTotal Nasal Symptom Score (TNSS)Score For Allergic Rhinitis (SFAR)TNSS TNSS Nasal Obstruction Symptom Evaluation (NOSE)
Patient ScoresAcute:2.17 ± 0.59Allergic: 11.03 ± 3.03Allergic: 8 ± 3.81Allergic: 8.9 ± 3.67Chronic: 10.50 ± 3.28
Chronic: 2.2 ± 0.66Control: 6.83 ± 3.28Control: 0.4 ± 0.94Nonallergic: 9.46 ± 3.38Control: 7.50 ± 3.91
Control: Not surveyed
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Kahan, M.S.; Bleier, B.S.; Amiji, M.M.; Workman, A.D. The Effects of Microplastics and Nanoplastics in the Nasal Airway and Upper Respiratory Tract. Sinusitis 2026, 10, 1. https://doi.org/10.3390/sinusitis10010001

AMA Style

Kahan MS, Bleier BS, Amiji MM, Workman AD. The Effects of Microplastics and Nanoplastics in the Nasal Airway and Upper Respiratory Tract. Sinusitis. 2026; 10(1):1. https://doi.org/10.3390/sinusitis10010001

Chicago/Turabian Style

Kahan, Maayan S., Benjamin S. Bleier, Mansoor M. Amiji, and Alan D. Workman. 2026. "The Effects of Microplastics and Nanoplastics in the Nasal Airway and Upper Respiratory Tract" Sinusitis 10, no. 1: 1. https://doi.org/10.3390/sinusitis10010001

APA Style

Kahan, M. S., Bleier, B. S., Amiji, M. M., & Workman, A. D. (2026). The Effects of Microplastics and Nanoplastics in the Nasal Airway and Upper Respiratory Tract. Sinusitis, 10(1), 1. https://doi.org/10.3390/sinusitis10010001

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