Evidence on microplastic exposure and respiratory health outcomes: a systematic review

Abstract

Background:

Plastic fragmentation leads to widespread microplastic (MP) pollution. Inhalation of airborne MPs is a key human exposure route. Evidence links MPs to respiratory diseases, but causal mechanisms and real-world risks remain unclear.

Objectives:

This review synthesizes evidence on human exposure to airborne MPs and their role in major respiratory diseases. It aims to identify critical knowledge gaps and improve the framework for assessing inhalation health risks.

Design:

This is a systematic review study.

Data sources and methods:

PubMed, Scopus, and Web of Science were searched (up to 15 June 2025) using keywords for MPs and respiratory diseases. Two researchers independently screened articles, extracted data, and assessed the quality of the studies.

Results:

A total of 17 studies were included. MPs are found in human lungs and can induce inflammation. Evidence associates chronic exposure with increased risks of COPD, asthma, and pulmonary fibrosis. A major limitation is that experimental animal studies use MP concentrations vastly exceeding environmental levels, limiting real-world risk extrapolation. Research is also disproportionately focused on polystyrene (PS), while occupational data implicate other polymers.

Conclusion:

Airborne MPs are a respiratory toxicant, but definitive causal evidence is constrained by a critical gap between experimental and environmentally relevant concentrations and a polymer-specific research bias. Future studies must prioritize environmentally relevant exposures, investigate high-risk polymers, and integrate exposomics with advanced toxicology.

Keywords

environmental pollution exposome microplastics nanoplastics respiratory diseases

Introduction

MPs, conventionally defined as synthetic polymer particles < 5 mm, were first conceptualized in a seminal 2004 publication by Thompson’s team.¹ This classification was refined in 2024 to incorporate critical attributes such as morphology, chemical composition, and environmental behavior.² Particles ⩽1 μm are defined as nanoplastics (NPs). These micro- and nanoplastics (MNPs) persist as environmental contaminants, accumulating in ecosystems and posing potential health risks, including to the respiratory system.

MPs vary widely and are usually classified by their polymer type and chemical structure. Upon their origin, MPs are classified as primary MPs, intentionally manufactured for products such as cosmetics, and secondary MPs, resulting from the environmental degradation of larger plastic waste.² These materials exist in diverse physical forms, including fragments, granules, filaments, fibers, spheres, and films. Of the numerous MPs varieties, six polymers—polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC), polyethylene terephthalate (PET), polystyrene (PS), and polyamide (PA)—are most frequently encountered by humans and are of greatest pathological concern.³ Critically, these distinct physicochemical characteristics, namely polymer composition and morphology, are key determinants of their biological behavior in humans, directly influencing their retention time, absorption efficiency, and systemic clearance rates, thereby modulating their potential health impacts.⁴

The current World Health Organization suggests a potential daily inhalation of up to 3000 MPs,⁵ among which larger particles are mainly trapped in the main bronchi, while smaller ones can reach deep alveoli.^6,7 Clinical studies have repeatedly detected MPs in human lung tissues and bronchoalveolar lavage fluid (BALF),^8–10 with levels linked to health status. Experimental models show that MPs trigger respiratory pathogenesis via persistent inflammation, oxidative stress, and cytotoxicity^11,12—common mechanisms underlying COPD, asthma, and pulmonary fibrosis. Yet the precise etiological mechanisms remain poorly defined. Current evidence is largely phenomenological, lacking a systematic synthesis of key molecular pathways. Critical gaps also exist in epidemiological data and environmental relevance, as most toxicological studies use unrealistically high MP concentrations. Several fundamental challenges persist in current MNPs research that necessitate cautious interpretation of the evidence.^13,14 One key concern is that real-world exposure concentrations and accurate measurement of MNPs in human biospecimens are uncertain. Many studies use monodisperse particles that do not reflect the complexity of environmental MNPs, which often leach toxic chemicals.^15,16 In addition, methodological limitations abound because conventional detection techniques such as gas chromatography-mass spectrometry (GC-MS) may produce false positives due to contamination or biological interference (e.g., lipids).^17,18 Moreover, the biological plausibility of reported translocation data is questionable¹⁹ as particles larger than a few microns are difficult to cross barriers; therefore, remote detection of MNPs in real-world studies is frequently inconsistent with basic experimental results. Finally, strong epidemiological evidence linking MNP exposure to respiratory diseases remains scarce. These challenges indicate that the understanding of the relationship between MNP exposure and human health is still evolving and precautionary principles are increasingly required.

This review aims to address these deficiencies and consolidate contemporary evidence on pulmonary exposure pathways and pathophysiological sequelae to delineate causal relationships and inform subsequent scientific inquiry.

Methodology

The reporting of this study conforms to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement (PRISMA) 2020 checklist.²⁰ The PRISMA checklist is presented as Supplement 1. The systematic review protocol was registered in the PROSPERO (International Prospective Register of Systematic Reviews) database (No. CRD420261336554). Two authors (C.C and N.W) performed all stages, including the development of inclusion and exclusion criteria and data extraction to prevent bias.

Search strategy

The articles in the English language were searched on 15 June 2025. The chosen databases were PubMed, Scopus, and Web of Science. The core search term related to the pollutant of interest (e.g., “microplastic*” OR “nanoplastic*”) was combined with terms related to the biological system under investigation (e.g., “respiratory diseases,” “COPD,” “asthma,” “ILD,” “lung cancer,” “pulmonary embolism”) using the “AND” operator. The PRISMA flow diagram summarizing the study search and selection process is illustrated in Figure 1.

Figure 1.

Article selection flow diagram.

Inclusion and exclusion criteria

Inclusion criteria were: (1) original research articles published in English; (2) investigation of microplastics (with a focus on particles < 5 mm in size) as a primary exposure; (3) assessment of their impact on the respiratory system, including human observational studies, in vivo experiments using vertebrate animals, and in vitro cellular model studies.

Exclusion criteria were: (1) review articles, commentaries, editorials, and book chapters; (2) studies focusing primarily on plastic additives or other pollutants rather than the plastic particles themselves; (3) studies that did not directly assess respiratory endpoints (e.g., those investigating only gastrointestinal exposure or systemic distribution without pulmonary outcomes). Studies that did not meet all inclusion criteria were excluded.

Data extraction and synthesis

Given the anticipated heterogeneity in study designs, MP types, exposure regimens, and measured outcomes, a meta-analysis was deemed inappropriate. Therefore, a narrative synthesis was conducted. The findings are organized thematically by respiratory disease entity (COPD, asthma, ILD, etc.). Table 1 is used to summarize the characteristics and main findings of the included studies.

Table 1.

Summary of characteristics of included studies.

Study (year)	Study design	MP type	Control	Findings	Relevant disease
Wei et al.²¹ (2025)	Human study + Animal study + In vitro	PS	Human: non-COPD lung tissues Animal: air-exposed mice (no PS) and COPD mice without PS Cell: Untreated pDHBE cells	PS-MPs accumulate in COPD lungs and trigger AECOPD by inducing mito-ROS-mediated autophagy-dependent ferroptosis in bronchial epithelial cells	COPD
Paplińska-Goryca et al.²² (2025)	In vitro	PA	Untreated human nasal epithelial cells	Asthmatic and COPD epithelial cells show altered gene expression and heightened susceptibility to microplastic-induced damage vs. controls; effects linked to Th2 inflammation, stress response modulation, and carcinogenesis	Asthma, COPD
Dong et al.²³ (2020)	In vitro	PS	Untreated human BEAS-2B cells	PS-MPs induce ROS, inflammation, and barrier disruption in lung epithelial cells; decrease α1-antitrypsin, suggesting COPD risk	COPD (risk indicated)
Yang et al.²⁴ (2024)	Animal study	PS	Control mice (no PS)	PS-NPs induce COPD-like lung injury in mice via oxidative stress, inflammation, mitochondrial/ER stress, and ferroptosis	COPD
Chen et al.²⁵ (2023)	Human study	PP, PE, PET, etc.	CAP group (for comparison)	MPs detected in BALF of asthmatic children; levels did not differ significantly from the CAP group	Asthma
Xu et al.²⁶ (2025)	Animal study + In vitro	PS	Animal: saline-treated mice (no MPs) and HDM-only mice Cells: untreated BEAS-2B cells and untreated ASMCs	Microplastics aggravate asthmatic airway remodeling via HSP90α secretion and PI3K-Akt-mTOR pathway activation	Asthma
Hu et al.²⁷ (2025)	Animal study	PE	PBS control; MP alone; HDM alone	Co-exposure with HDM aggravates airway inflammation and epithelial barrier dysfunction via CXCL1 signaling	Asthma
Paplińska-Goryca et al.²² (2025)	In vitro	PA	Untreated human nasal epithelial cells	Asthmatic and COPD epithelial cells show altered gene expression and heightened susceptibility to microplastic-induced damage vs. controls; effects linked to Th2 inflammation, stress response modulation, and carcinogenesis	Asthma, COPD
Lu et al.²⁸ (2021)	Animal study	Fluorescent PS microspheres	Normal + saline; Asthma + saline	MP exposure causes lung inflammation, macrophage aggregation, phagocytosis of MPs, and alters immune/stress-related genes; aggravates mucus production in asthma	Asthma
Özgen Alpaydin et al.²⁹ (2024)	Human study	PA, PET, PVC, PU, PE	Control group (non-ILD patients)	MPs detected in 55% of suspected ILD patients (mostly fibrotic type) in BAL, suggesting potential association with ILD	ILD
Li et al.¹¹ (2022)	Animal study	PS	Deionized water; solvent control (PEG)	PS-MPs induce dose-dependent pulmonary fibrosis via oxidative stress and the Wnt/β-catenin pathway; melatonin alleviates fibrosis	Pulmonary fibrosis (ILD)
Li et al.³⁰ (2022)	Animal study + In vitro	Tire wear microplastics (TWMPs)	Animal: Unexposed mice Cells: Untreated BEAS-2B cells	TWMPs induce pulmonary fibrosis via miR-1a-3p/twinfilin-1-mediated cytoskeletal rearrangement and EMT	Pulmonary fibrosis (ILD)
Cao et al.³¹ (2023)	Animal study + In vitro	PS, carboxyl-modified	Animal: saline-treated mice Cells: untreated A549 or HEK293 cells	PS-MPs induce lung inflammation, oxidative stress, apoptosis and fibrosis via the TLR2/NF-κB pathway; smaller size (1–5 μm) causes more severe damage.	Pulmonary fibrosis (ILD)
Zhang et al.³² (2024)	Animal study + In vitro	PS	Animal: Sham (deionized water) Cells: Untreated A549 cells	PS-MPs induce pulmonary fibrosis via cGAS/STING-mediated alveolar epithelial cell ferroptosis	Pulmonary fibrosis (ILD)
Chen et al.³³ (2022)	Human study	fibers > 20 μm, sub-micron particles	Adjacent normal lung tissue	Microplastics detected in human lung tissues; higher abundance in GGN tumor vs normal tissue (58% vs 46%), suggesting association with GGN formation	Lung ground-glass nodules (GGN)/lung cancer
Gutiérrez-García et al.³⁴ (2025)	In vitro	PET	Passage-matched untreated BEAS-2B cells	30-week PET-NPL exposure induces genotoxicity, anchorage-independent growth, invasiveness, and oncogene upregulation (KRAS, MET, RET)	Lung cancer
Lee et al.³⁵ (2025)	In vitro	Aged PP	Untreated A549, NCI-H1650, RAW 264.7 cells	Aged PP-MPs with increased surface roughness promote lung cancer cell proliferation, M2 macrophage polarization, Notch-1 expression, and ROS generation; effects increase with aging time	Lung cancer
Wang et al.³⁶ (2024)	Human study	PA, PVC, PE, ACR, PP, CPE, PMMA, PU, etc.	Procedural blanks (catheters, containers, instruments) and MP-undetected patients	MPs detected in 80% of thrombi (IS, MI, DVT); median concentrations: IS 61.8, MI 141.8, DVT 69.6 μg/g; MP concentration positively associated with NIHSS score and D-dimer level	Thrombotic diseases

Assessment of quality

Risk of bias was assessed independently by two reviewers using tools appropriate to each study design. For human studies, the Newcastle-Ottawa Scale for cross-sectional studies (NOS-xs) was used to assess the risk of bias, while the SYRCLE tool was applied for animal experiments. Due to the lack of an internationally recognized standard for in vitro studies, a self-developed risk of bias assessment form was used. Disagreements were resolved by discussion or consultation with a third reviewer. The studies were scored as low, moderate, or high risk of bias according to each criterion. Results of bias assessment are presented as Supplement 2.

Results

Included studies

Based on the PRISMA flow diagram, 622 records were screened from three databases. After duplicate removal, 539 were screened, 344 excluded, and 195 full texts assessed. Finally, 17 studies were included, covering COPD, asthma, ILD, lung cancer, and thrombotic diseases. PS was the most frequently investigated MP type, followed by PE, PP, PA, PET, and tire-wear particles. Key findings showed that MPs can induce oxidative stress, inflammation, epithelial barrier disruption, ferroptosis, and activation of signaling pathways (e.g., NF-κB, PI3K-Akt-mTOR, and cGAS/STING). Human studies confirmed the presence of MPs in lung tissues, BALF, and thrombi, with concentrations associated with disease severity.

Exposure pathways of MPs

Human MP exposure is unavoidable via ingestion, inhalation, and dermal contact, with iatrogenic routes also emerging as significant (Figure 2).

Figure 2.

Major human exposure pathways to microplastics.

Ingestion

Common dietary MP sources include seafood, dairy products,³⁷ honey, sugar,³⁸ salt,³⁹ and bottled water.⁴⁰ MPs bioaccumulate in marine species,^41,42 with nearly half of 338 fish species containing MPs (3.5 ± 0.8 particles/fish),⁴³ thereby enabling trophic transfer to humans.⁴⁴ Annual adult ingestion is estimated at 488,000–577,000 particles from food, with bottled water contributing far more^45,46—up to 2649 ± 2857 particles/L in PET containers,⁴⁷ potentially reaching 35.7 million particles/year.⁴⁸ MPs also contaminate rice and meat via production/packaging chains.^49,50

Inhalation

Daily adult MP inhalation is ~170 particles, giving an annual intake of 61,928 ± 68,865 particles.⁵¹ MPs have also been detected in deep lung tissues of living humans (11/13 surgical specimens).⁵² Additional estimates suggest that annual inhalation exposure ranges from 9000 to 79,000 particles,⁵³ with indoor air accounting for approximately 90% of exposure and a projected annual intake of 160,000 to 2.3 million particles.⁴⁵

Though indoor airborne MPs are mainly > 20 μm fibers,⁵⁴ particles < 2.5 μm should be prioritized in future studies owing to their deep alveolar penetration.⁵¹

Dermal contact

Dermal contact is a significant but under-studied MP uptake route.⁵⁵ Skin barrier penetration depends on particle size, shape, and surface chemistry,^56,57 with NPs translocating more easily,⁵⁸ mainly from cosmetic exfoliants, textile fibers, and medical device debris.⁵⁹ These particles can enter via hair follicles, sweat glands, or damaged skin.⁶⁰ Dermal MP exposure links to local inflammation, allergy, and possible systemic effects.^56,61 Therefore, standardized methods for tissue MP quantification are needed for risk assessment.

Iatrogenic exposure

Plastic medical devices directly expose patients to MPs.

For example, during intravenous infusion, the initial 12 ml saline solution flowing through the tubing during IV therapy releases as much as 8.4 ± 3.6 µg/L of MPs.⁶² In addition, larger MPs particles (50–213 µm) are exposed into the bloodstream after percutaneous coronary intervention, which was smaller than 50 µm pre-intervention.⁶³ MPs also appear in cardiac tissues after valve replacement.⁶⁴ Although individual procedure exposure is low, cumulative burden requires risk and device safety assessments.

Detection strategies of MPs in human lung specimens

Table 2 summarizes key findings on MP detection in human respiratory samples. Multiple analytical techniques, including Raman spectroscopy, micro-Fourier-transform infrared spectroscopy (μ-FTIR), and laser direct infrared (LDIR), have been employed to detect MPs in human lung tissues. The detection rates vary from 65% to 100%, with predominant polymers including PP, PE, PVC, and PET.^8,52,65 Particle sizes range from submicron to several hundred micrometers, with fragments and fibers being the most common morphologies.^8–10,52 Notably, MP abundance and polymer composition differ between smokers and non-smokers,^10,66 as well as between tumor and adjacent normal tissues.³³ These findings confirm widespread MP presence in the human respiratory system and urgent requirements for systemic investigations.

Table 2.

Characteristics and analytical methods for microplastics in lung specimens.

Sample sources	Analytical method	Concentration/abundance	Type/size /morphology	References
Lung tissue (n = 20)	Raman spectroscopy	Detection rate: 65% (13/20 cases), 33 particles + 4 fibers identified	Polymers: PP (35.1%) and PE (24.3%) most frequent Size: Fragments all < 5.5 µm (mean 3.92 µm); Fibers: 8.12–16.8 µm (mean 11.23 µm) Morphology: Predominantly fragments (87.5%), fibers (12.5%)	[8]
Lung tissue (n = 13)	μ-FTIR (size limitation: 3 μm)	Detection rate: 84.6% (11/13 cases) Mean: 1.42 ± 1.50 MP/g (raw), 0.69 ± 0.84 MP/g (blank-corrected) Highest in lower lobe (3.12 MP/g)	Polymers: 12 types identified, PP (23%), PET (18%), resin (15%) most frequent. Size (mean ± SD): Length: 223.10 ± 436.16 μm; Width: 22.21 ± 20.32 μm Morphology: Fibers (49%), fragments (43%), films (8%)	[52]
BALF from patients with diffuse lung disease (n = 30)	Nile Red staining fluorescence microscopy + Raman spectroscopy	Detection rate: 100% (30/30 cases) Median: 684.7 particles/mL Higher in lung areas with consolidation	Polymers: 8 types identified, PVC (25.5%), PS (19.1%), PET (12.8%) most frequent Size: Median 3.29 µm; 81.5% of particles < 10 µm Morphology: Particles (93.5%), fibers (6.5%)	[65]
Sputum (n = 13) BALF (n = 11) Pleural Fluid (n = 10)	Micro-Raman + SEM	Range (particles/100 mL): Sputum: 156-468; BALF: 28-133; Pleural Fluid: 21-210 Factors (p < 0.05): Sampling type, occupational exposure, smoking, mask-wearing	Polymers: 22 types identified; PET predominant (62%–72%) across all samples Size: Particles < 100 μm most abundant (sputum:75.9%, BALF:50%, pleural fluid:94.4%) Morphology: Fibers dominant in sputum (77%) & BALF (70%); Fragments dominant in pleural fluid (63%)	[9]
BALF from nonsmokers (n = 18)	LDIR+SEM	Total MPs (median [IQR]): 0.91 [6.58] N/g; PE: 0.38 [8.05] N/g	Polymers: 13 types identified; PE most abundant (86.1%), followed by PET (7.5%), PP (1.9%) Size: Median diameter 34.0 μm (IQR 26.0); Majority within 20–80 μm Morphology: Fibers (4.2%), fragments (95.8%)	[10]
BALF from smokers (n = 17) and nonsmokers (n = 15)	LDIR	Smokers: 3.48 to 81.37 particles/g Non-smokers: 2.04 to 57.38 particles/g	Polymers: More types in smokers. Size: Majority 20–100 μm in diameter. Morphology: Predominantly irregular-shaped particles	[66]
Surgical lung tissues from GGN patients: tumor tissues (n = 50) and adjacent normal tissues (n = 50)	μ-FTIR + Raman + LDIR	Tumor: 58% microfiber+ (38 fibers), 16 MPs; Normal: 46% microfiber+ (27 fibers), 8 MPs	Types: cotton, rayon, polyester, acrylic, PET, phenoxy resin, chipboard. Size: fibers > 20 μm (up to 5 mm), sub-micron particles 0.8–3.6 μm. Morphology: fibrous, with high surface roughness in lung tissues	[33]

BALF, bronchoalveolar lavage fluid; IQR, interquartile range; LDIR, laser direct infrared; MP, microplastics; PE, polyethylene; PET, polyethylene terephthalate; PP, polypropylene; PS, polystyrene; PVC, polyvinyl chloride; SD, standard deviation; SEM, scanning electron microscopy; μ-FTIR, micro-Fourier transform infrared spectroscopy.

MPs and respiratory diseases

Direct clinical evidence on MPs’ respiratory effects is limited. Current animal and in vitro studies show MPs induce inflammation, oxidative stress, cell death, and fibrosis. This review illustrates the molecular and cellular mechanisms (Figure 3).

Figure 3.

An overview of the molecular and cellular mechanisms by which microplastics cause respiratory diseases.

Chronic obstructive pulmonary disease

Although tobacco smoking and inhaled irritants are the predominant risk factors of COPD pathogenesis,^67,68 MPs exposure is investigated primarily. Polyurethane (PU) was identified in BALF of smokers, with significantly higher concentrations (4.66 particles/L) versus non-smokers.⁶⁶ Moreover, PS‑MP concentrations are significantly elevated in lung tissues of COPD patients compared to controls.²¹

In COPD, epithelial cells showed a distinct response to PA-MPs, with 22 differentially expressed genes enriched in chemokine/neutrophil pathways and enhanced by macrophage co-culture.²² PS-MPs activate type II alveolar epithelial cells (AT2) and alveolar macrophages (AMs), thereby prompting interleukin-6 (IL-6) and interleukin-8(IL-8) release and initiating inflammation.⁶⁹ Dong et al.²³ further reported that PS-MPs induce reactive oxygen species (ROS) generation, leading to cytotoxicity and inflammation in human lung epithelial cells (BEAS-2B), and downregulate alpha1-antitrypsin (α1-AT) expression—a known risk factor for COPD development.⁷⁰ In addition, PS‑MPs compromise the lung epithelial barrier by downregulating zona occludens protein 1(ZO‑1) and reducing transepithelial electrical resistance (TEER), which elevates airway permeability and raises COPD risk.

Animal studies show that inhaled PS‑NPs cause COPD‑like lung injury in mice.²⁴ Recent studies show that PS‑MPs trigger mitochondrial ROS overproduction, overactivate autophagy, and promote ferroptosis/autophagy-dependent ferroptosis (ADF), amplifying inflammation and tissue damage, thus driving COPD pathogenesis and progression.^21,23,24 Emerging evidence indicates MPs, especially PS-MPs, can worsen COPD progression via oxidative stress, inflammation, and barrier disruption. Even at low concentrations, long-term exposure raises disease risk.

Asthma

Asthma is an airway disorder linked to air pollution and multiple factors, yet the role of MPs in its pathogenesis remains under-investigated.^71,72 MPs can penetrate deeply into the lungs and reach the area of the alveolar gas-blood exchange barrier. Chen et al.²⁵ compared MPs (predominantly PP, PE, polyester) concentrations in BALF from children with community-acquired pneumonia (CAP) and asthma. Children with severe CAP had significantly higher MPs than non-severe cases, whereas no significant difference was found between CAP and asthma groups. Similarly, healthy volunteers had lower MPs in nasal wash than allergic rhinitis patients, a finding relevant given its link to allergic asthma.⁷³

MPs activate PI3K-Akt-mTOR signaling, driving heat shock protein 90 alpha (HSP90α) secretion and airway smooth muscle cells (ASMCs) proliferation, ultimately inducing airway constriction and hyperresponsiveness.²⁶ PE-MPs disrupt the airway epithelial barrier, increasing permeability and facilitating allergen invasion, correlating with elevated interleukin-33 (IL-33) secretion, neutrophil activation, and CXCL1 signaling.²⁷ In asthma models, fibrous MPs in lower airways exacerbate inflammation, mucus production, and fibrosis, and they may also alter the lung microbiota, thereby contributing to asthma development.⁷⁴

Studies suggest that MPs may trigger a Th2 immune response in asthma patients. PS-MPs activate transient receptor potential ankyrin 1(TRPA1) and p38 mitogen-activated protein kinase (p38 MAPK) pathways, eliciting oxidative stress and inflammatory cascades that promote Th2 differentiation, exacerbating airway inflammation.⁷⁵ PE-MPs also aggravate barrier dysfunction and Th2-skewed inflammation via CXCL1 signaling.²⁷ PA-MPs induce Th2 reactivity, evidenced by upregulated CD193+ (CCR3) on basal epithelial cells, which triggers eosinophil-related Th2 inflammation.²² An animal study further confirmed that MPs exclusively upregulate Th2 cytokines in asthmatic mice.²⁸

Interstitial lung diseases

Interstitial lung diseases (ILD) involve persistent inflammation and progressive fibrosis. Emerging evidence suggests MPs exposure likely contributes to pulmonary fibrosis pathogenesis.⁷⁶ Özgen Alpaydin and colleagues²⁹ detected MPs in BALF from 55% of suspected ILD patients, particularly those with a fibrotic phenotype. PA, PET, PVC, and PU (size range 4.19–792.00 μm) were mainly detected in BALF, whereas PA and PE(13.14–20.29 μm) were dominated in blood.

Similarly, MPs were detected in 100% of BALF samples from patients with diffuse lung disease, with PVC, PS, and PET being the most common polymer types.⁶⁶ These findings confirm that MPs frequently inhabit the lower respiratory tract of patients with fibrotic lung diseases. In a 28-day inhalation study, 0.10 μm PS-MPs increased fibrotic factors transforming growth factor-β(TGF-β) and tumor necrosis factor-α(TNF-α) in rat lungs in a concentration-dependent manner.⁷⁷ In mice, 5μm PS-MPs persisted in the lungs and induced pulmonary fibrosis by activating oxidative stress and the Wnt/β-catenin signaling pathway,¹¹ as indicated by decreased superoxide dismutase (SOD) and glutathione (GSH) levels. Additionally, tire wear MPs (TWMPs) also induced pulmonary fibrosis via miR-1a-3p/twinfilin-1-mediated cytoskeletal rearrangement and epithelial-mesenchymal transition (EMT).³⁰ MPs can promote fibrotic processes by inducing pulmonary inflammation, oxidative stress, and apoptosis, as exemplified by PS-MPs triggering severe inflammation and collagen buildup in mouse models.³¹ Furthermore, PS-MPs induce alveolar epithelial cell senescence and enhance senescence-associated secretory phenotype (SASP) secretion, thereby exacerbating inflammatory and fibrotic responses.⁷⁸

Collectively, existing evidence indicates that PS-MPs promote ILD through three pathways: Toll-like receptor (TLR) signaling-mediated inflammation/fibrosis, cGAS/STING-initiated ferroptosis leading to fibrotic changes, and Wnt/β-catenin-induced fibrotic progression.^11,31,32

Other diseases

Lung cancer is linked to tobacco, radon, and occupational carcinogens, but MPs may be an additional risk factor that contributes to pulmonary tumor formation.⁷⁹ Pauly et al.⁸⁰ found higher levels of plastic fibers in cancerous lung tissues than in non-cancerous specimens. A 2022 study detected more MPs in ground-glass nodules (GGN) tumors than in normal tissue (58% vs 46%), suggesting a potential association with GGN formation.³³ In experimental models, female mice exposed to 160 ppm PS-MPs showed increased lung carcinoma incidence.⁸¹ MPs may promote lung cancer via DNA damage, oxidative stress, and inflammation.^82,83 Chronic exposure to PET-MPs induces genotoxic damage and upregulates lung cancer-related oncogenes,³⁴ while aged PP-MPs may accelerate cancer cell growth and trigger immune cells to support tumor progression.³⁵ Although these mechanisms suggest a pro-tumorigenic microenvironment, direct causal evidence remains limited, highlighting the need for further studies.

Thrombotic disorders have established risk factors such as genetics and surgery, with MPs now investigated as a potential novel contributor. MPs enter the circulatory system via inhalation, ingestion, or dermal contact, inducing thrombogenesis and coagulation abnormalities.^84–86 The main mechanisms include facilitating erythrocyte and platelet aggregation, enhancing endothelial adhesiveness, and suppressing erythropoiesis.⁸⁵ One study found that MPs’ presence in thrombi may correlate with the severity of thrombotic diseases such as deep vein thrombosis.³⁶ Chronic pulmonary MPs accumulation may theoretically induce a prothrombotic state, thereby elevating thrombosis risk, which is the principal cause of pulmonary embolism.

Pathophysiological mechanisms of MPs-associated diseases

MPs cause respiratory pathology via physical, chemical, and biological mechanisms, inducing cytotoxicity in AMs, airway epithelium, and endothelium through oxidative stress and impaired repair, modulated by particle properties and exposure (Figure 3).

Macrophages

AMs can phagocytose MPs, activating inflammation, which includes increased IL-6, IL-8,⁶⁹ TNF-α, and altered gene clusters for immunity, stress, and cell death.²⁸ Additionally, macrophages show that high MP uptake causes cytotoxicity.⁸⁷ Smaller particles (0.5 μm) internalize more than larger ones (5 μm), leading to greater mitochondrial damage, ROS, and apoptosis^88,89 Animal studies indicate that MP size critically affects phagocytic efficiency. NR8383 cells show peak uptake for 2–3 μm PE-MPs,⁹⁰ whereas MH-S cells process 1 μm PS-MPs faster than 20 nm particles.⁹¹ Furthermore, MP exposure induces morphological changes and suppresses proliferation in AMs.⁹²

Epithelial cells

MPs compromise airway epithelial cells, the primary physicochemical barrier of the respiratory system, by disrupting barrier integrity (TEER and tight junctions such as ZO-1) and initiating respiratory pathology.^23,27 In BEAS-2B cells, MPs induce oxidative stress, inflammation, and mucus hypersecretion via the PI3K-Akt-mTOR pathway, thereby promoting ASMC proliferation and hyperresponsiveness.²⁶ Environmentally relevant aged low-density polyethylene (LDPE) induces EMT and activates oxidative or inflammatory pathways,⁹³ whereas some MPs show non-cytotoxic effects potentially because of pathogenic heterogeneity.⁹⁴ Furthermore, PS-NPs were reported to stimulate the pro-inflammatory phenotype of neutrophils with dysregulated recruitment in advanced three-dimensional human airway models.⁹⁵

Studies using A549 cells (alveolar epithelium mimics) exposed to PS-MPs demonstrate induction of oxidative stress, mitochondrial dysfunction, and activation of apoptotic pathways. Notably, PS-MPs trigger ferroptosis via the cGAS/STING signaling axis, substantially suppress proliferative capacity, and induce significant morphological alterations.⁹² While PS-NPs may not induce acute cytotoxicity, they disrupt critical cellular functions including surfactant production and cytokine secretion, indicating subtler pathophysiological perturbations.⁹⁶

Discussion

MPs appear to contribute to chronic respiratory diseases through an interconnected pathogenic network involving oxidative stress, inflammation, immune dysregulation, epithelial barrier dysfunction, ferroptosis, and abnormal tissue remodeling. Importantly, these mechanisms do not act independently but exhibit extensive crosstalk instead. For instance, MP-induced ROS production can simultaneously amplify inflammatory cytokine release, disrupt epithelial tight junctions, and induce ferroptosis, thereby generating a self-reinforcing cycle of injury, fibrosis, and impaired repair.^21,23,32,69 In asthma, Th2-dominant immune responses further interact with epithelial dysfunction and airway smooth muscle proliferation, suggesting that MPs may aggravate allergic sensitization and airway hyperresponsiveness.^22,26,27 In addition, MPs may alter the pulmonary microbiome, impair immune regulation and tissue repair, and serve as carriers for toxic chemicals, allergens, and pollutants, thereby amplifying respiratory toxicity and increasing susceptibility to infection and chronic inflammation.^31,97,98 Collectively, these findings suggest that MPs function not only as environmental irritants but also as multipliers of pre-existing pulmonary vulnerability.

Despite growing mechanistic evidence, the real-world respiratory health risks associated with chronic MP exposure remain incompletely understood. One key limitation is that most current experimental studies employ MP concentrations substantially exceeding environmentally relevant levels, thereby leading to an inadequate representation of clinical disease outcomes under chronic low‑dose conditions. This disparity is further evidenced by WHO technical reports⁵ and summarized in Table 3. Moreover, the lack of standardized sampling and analysis protocols restrains the consistency of environmental exposure levels and gaps the cross-study comparisons. In addition, existing analytical techniques are insufficient for accurately detecting respirable nano-sized MPs (<2.5 μm), which may represent the most biologically active fraction because of their deep alveolar penetration and high cellular uptake potential.^51,69 Given that particle size/type mainly influences lung concentration,¹⁹ missing evidence on the smallest MPs creates major uncertainty in exposure assessment. Future research should therefore prioritize standardized exposure assessment methods, environmentally relevant chronic exposure models, and longitudinal clinical studies integrating MP burden with respiratory outcomes. Sequential investigations should also clarify how MP characteristics, including size, shape, surface aging, polymer composition, and adsorbed pollutants, trigger pulmonary toxicity and immune responses.^35,93 Beyond single-agent toxicity, MPs may synergize with cigarette smoke, allergens, pathogens, or occupational pollutants, thereby amplifying airway inflammation, fibrosis, and immune dysregulation. Elucidating such combined exposures is essential for refining risk stratification, guiding evidence-based policy, and uncovering new therapeutic targets for chronic respiratory diseases.

Table 3.

Experimental versus environmental concentrations of microplastics.

Experimental concentrations of microplastics
Study type		MP type	MP size	MP concentration		Reference
In vitro (Primary human alveolar macrophages, AT2 and TT1 cells)		PS-NPs	50 nm and 100 nm in diameter	1–100 μg/mL (exposure for 4 and 24 h)		[69]
In vitro (BEAS-2B cells)		PS-MPs	~1.72 μm (avg.), hydrodynamic diameter ~4.06 μm	1–1000 μg/cm² (test range) key tested doses: 10 μg/cm² (low) and 1000 μg/cm² (high)		[23]
In vivo (C57BL/6 male mice)		PS-NPs	40 nm	16, 40, and 100 μg/day via inhalation		[24]
In vitro (BEAS-2B cells; C57BL/6 male mice, asthma model)		PS-MNPs	Microparticles (~2.6 μm) and Nanoparticles (~213 nm)	BEAS-2B cells: 1–1000 μg/mL (test range); 30 and 300 μg/mL used for key mechanistic assays C57BL/6 male mice: 300 μg/mL administered intranasally		[26]
In vivo (C57BL/6 female mice, asthma model)		PE-MPs	1–5 µm	300 µg per dose, intranasally administered daily for 29 days		[27]
In vivo (Mouse, OVA-induced asthma model)		PS-MPs	0.2–0.5 μm	5 mg/kg bw/day (for 28 days)		[75]
In vitro (Human primary nasal epithelial cells, with/without macrophage co-culture)		PA-MPs	Length: 1–2 mm (cut fibers) Diameter: 0.08– 0.16 µm	Exposure dose: 200 µg/cm² (apical, 48h) Tested range: 0, 10, 100, 1000 µg/cm²		[22]
In vivo (rat, 28-day subacute inhalation)		PS-MPs	~0.1 μm (mean diameter)	Low: 0.75 × 10⁵ particle/cm³ Middle: 1.50 × 10⁵ particle/cm³ High: 3.00 × 10⁵ particle/cm³		[77]
In vivo (mouse, C57BL/6 male)		PS-MPs	5 µm	Main study: 1.25 and 6.25 mg/kg, intratracheal, 3×/week for 3 weeks Translocation study: 12 mg/kg (intratracheal) and 100 mg/kg (oral), daily for 7 days		[11]
In vivo and vitro (mouse, C57BL/6 female; A549 cells)		PS-MPs	1–5 μm; 10–20 μm	40 mg/kg/day (mice); 0–500 μg/mL (cells)		[31]
In vitro (MLE12 mouse alveolar epithelial cells)		PS-MPs	100 nm	0, 100, 200, 400 μg/mL for 48h		[78]
In vivo and vitro (mouse, C57BL/6 female; A549 cells)		PS-MPs	5 μm	0.5, 1, 2 mg/kg (mice); 0–200 μg/mL (cells)		[32]
In vitro (human bronchial epithelial BEAS-2B cells)		PET-MPs	Not mentioned	Long-term exposure: 50 μg/mL for 30 weeks Cytotoxicity test range: 25, 50, 100, 150, 200 μg/mL (24 h)		[34]
In vitro (A549, NCI-H1650 lung cancer cells; RAW 264.7, BMDC, P14 CD8+ T immune cells)		PP-MPs	<20 µm	In vitro cell exposure: 0.1, 0.5, 1, 10, 100 µg/mL Key dose for mechanistic studies: 100 µg/mL		[35]
In vivo (rat, Wistar)		PS-MPs	0.5 μm	0, 0.5, 5, 50 mg/kg/day, intragastric administration for 90 days		[86]
Environmental concentrations of Microplastics
Sample type	Predominant MP type	MP size	Particle concentration (average)	Number of particles in blanks (average)	Quality Score	Reference
Air (indoor and outdoor)	Indoor: PET, PA, PP Outdoor: PE, PS, PET	> 90% < 100 μm, the 5–30 μm fraction representing 54.1–65.2% of total	1583 ± 1181 MP/m³ (indoor); 189 ± 85 MP/m³	3.3 ± 1.8 MP/filter	¹⁸	[99]
Air (outdoor)	PE, PET, PS	73.5–96.6% represented by 5–30-μm fraction	282 ± 127 MP/m³ (range, 104–650)	3.9 ± 2.2 MP/filter	¹⁸	[100]
Air (indoor)	81% PET, 6% PE, 5% PA, 2% PP and 6% other polymers; non-synthetic, 95% protein, 5% cellulose; MP > 4% total particles	36 and 21 for the major and minor dimensions	9.3 ± 5.8 particles/m³	7.7 ± 3.8 MP/blank, data not corrected	¹⁵	[101]
Air (indoor and outdoor)	PS, PET, PE	Fiber lengths: indoors 641 μm; outdoor 616 μm; approx. 30% of fibers 100–300 μm Fragments: outdoors 104 μm; indoors 58.6 μm	Fiber lengths: indoors 641 μm; outdoors 616 μm; approx. 30% of fibers 100–300 μm Fragments: outdoors 104 μm; indoors 58.6 μm	2.4 fibers and 12.2 fragments per filter indoors; 0.4 fibers and 6.3 fragments per filter outdoors	¹⁵	[102]
Air (outdoor)	PET (51%), epoxy resin (19%), PE (12%), alkyd resin (8%); fibrous PET (87%)	246.52 μm (12.35–2191.32 μm)	0.41 MP/m³(0–2 MP/m³)	No MP in one blank collected	¹³	[103]
Deposition	PS (as fragments) followed by PE	Most MP < 50 µm, fiber lengths predominantly 100–200 μm and 200–300 μm (max, 3000 µm); films, 50–200 μm	365 ± 69 particles/m² per day (range, 29–462)	3 ± 1 fibers, 1 ± 1 film and 8 ± 1 fragments per filter	¹²	[104]

AT2, human alveolar type 2 epithelial cells; BEAS-2B, human bronchial epithelial cell line; MNP, micro/nanoplastic; MP, microplastic; NP, nanoplastic; OVA, ovalbumin; PA, polyamide; PE, polyethylene; PET, polyethylene terephthalate; PP, polypropylene; PS, polystyrene; TT1, human alveolar epithelial type I-like cell.

Conclusion

This review confirms that airborne MPs are detectable in human respiratory tissues and are associated with COPD, asthma, and pulmonary fibrosis via oxidative stress, inflammation, barrier disruption, and ferroptosis. However, the evidence is constrained by two major limitations: most experimental studies use MP concentrations far exceeding environmental levels, and research is disproportionately focused on PS, limiting generalizability to other high-risk polymers. Furthermore, conventional cytotoxicity assays have inherent limitations for complex particle risk assessment. Consequently, while MPs exhibit clear toxic potential in controlled settings, their definitive causal role in real-world respiratory disease remains to be established.

Perspectives

To bridge mechanistic evidence and real-world risk assessment, future research should prioritize three interconnected directions. Environmentally chronic exposure models using low-dose, long-term protocols and aged MPs are urgently needed. In addition, the development of standardized analytical methods is required to accurately detect respirable nano‑sized MPs (<2.5 μm) in human biospecimens, especially polymers beyond PS. Finally, exposomic approaches integrating coexisting pollutants are essential to elucidate synergistic effects. Addressing these priorities will refine risk stratification, inform regulatory policies, and support targeted interventions for MP-associated respiratory diseases.

Supplemental Material

sj-docx-1-tar-10.1177_17534666261465486 – Supplemental material for Evidence on microplastic exposure and respiratory health outcomes: a systematic review

Supplemental material, sj-docx-1-tar-10.1177_17534666261465486 for Evidence on microplastic exposure and respiratory health outcomes: a systematic review by Chen Chen, Ling Luo, Yanghong Zheng, Linxin Ran, Zhaoqi Li, Zhongliang Guo, Qiang Li, Yingqun Ji, Jing Hua and Na Wang in Therapeutic Advances in Respiratory Disease

Supplemental Material

sj-docx-2-tar-10.1177_17534666261465486 – Supplemental material for Evidence on microplastic exposure and respiratory health outcomes: a systematic review

Supplemental material, sj-docx-2-tar-10.1177_17534666261465486 for Evidence on microplastic exposure and respiratory health outcomes: a systematic review by Chen Chen, Ling Luo, Yanghong Zheng, Linxin Ran, Zhaoqi Li, Zhongliang Guo, Qiang Li, Yingqun Ji, Jing Hua and Na Wang in Therapeutic Advances in Respiratory Disease

Footnotes

Appendix

Acknowledgements

None.

Author note

Figures 2 and 3 were created by the authors. Figure 2 was prepared using Microsoft PowerPoint, and was created with BioRender.com.

Declarations

ORCID iDs

Chen Chen

Zhaoqi Li

Na Wang

Supplemental material

Supplemental material for this article is available online.

Artificial intelligence policy

We have not used AI or LLM tools for phrasing or editing the manuscript.

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