The literature on plastics in human tissues is growing rapidly, and many reports suggest widespread occurrence.1,2 However, translating these findings into statements on systemic exposure still requires standardized analysis,3,4 and global assessments need harmonized protocols before drawing conclusions about risk.
Mass spectrometry methods are useful for providing mass quantification of polymers, yet they inherently lose information on particles (e.g., size, shape, color) and are difficult to implement due to significant matrix-dependent interferences. Human samples are challenging matrices. In blood, realistic detection limits for polymers can be up to 20 times higher than limits calculated in Milli-Q water once matrix suppression and recovery are considered. This is equally applicable to polyethylene and polyvinyl chloride. In particular, nonspecific products and matrix interferences hinder identification and quantification.5 Claims of plastics in human brain tissue also continue to be the subject of methodological debate and demand contamination-controlled procedures with rigorous QA/QC (quality assurance/quality control), validated digestion and recovery using well-characterized reference materials, confirmation by additional analytical approaches, and size and shape characterization.4 Consequently, the presence of plastics within the human body has prompted widespread discussion.3–5 In this context, current evidence points to the expected routes of entry, and the respiratory6 and gastrointestinal tracts7 are biologically plausible pathways.
The airway as the logical starting point: microplastics in the respiratory systemAerodynamic diameters govern deposition patterns across the respiratory tract. Particles with a mass median aerodynamic diameter >6μm deposit preferentially in the oropharynx.8 Particles 2–6μm deposit in the central airways and those <2μm can reach the peripheral small airways and alveoli.8 Thin fibers can also act as smaller particles from an aerodynamic perspective and can reach distal airways even when their geometric length is considerable. The well-established health risk of other types of particles (i.e., PM10, PM2.5 and asbestos) supports monitoring and risk assessment of plastics including fibers in the respiratory systems.
Microplastics (MPs; small plastic pieces less than 5mm long) have been detected throughout the respiratory tract from bronchoalveolar lavage fluid (BALF), sputum, pleural fluid, and lung tissue obtained at autopsies samples.6,9 Most studies use spectroscopic methods (LDIR, μFTIR, or μRaman) to identify polymers, characterize particle (size, shape, and color), and report quantitative burdens.10 Advancing the field requires harmonized and validated protocols with unified quality assurance/quality control (QA/QC), matrix-matched limit of detection/limit of quantification (LOD/LOQ), and consistent reporting units (e.g., per gram of tissue or per milliliter of BALF). Dual reporting (particle counts and polymer-specific mass) should be standard to support dose–response analysis and to align in vivo and in vitro assays with human exposure. Furthermore, a non-invasive upper-airway sampling strategy would enable routine population monitoring.
Respiratory health and plastic exposure: signal, not verdict (yet)Airborne MPs are practically ubiquitous in urban areas and inhalation exposure is continuous among the general population.11 Daily breathing therefore constitutes a constant route of contact, and this exposure could increase in occupational settings. Epidemiological evidence of respiratory effects has been reported since the late 20th century, but evidence remains very limited and associative.12,13 In polyvinyl chloride (PVC) manufacturing, exposure to PVC dust has been associated with a modest deterioration of lung function, mild chest-radiograph changes, and exertional dyspnea, but causality has not been established.12 Reports of MPs in human lungs alongside findings such as ground-glass nodules or suggestions of links to lung cancer risk should be considered preliminary, as most mechanistic insights still come from experimental models rather than population studies.10,13
Experimental evidence supports these signals. In vivo mammalian studies indicate that chronic MP exposure can impair pulmonary macrophage functions and promote persistent inflammation, which may be linked to fibrotic lesions.14 Future studies should evaluate long-term effects on lung function associated with realistic urban and indoor exposures (polymer type, size, shape, concentration). In parallel, in vitro assays can serve as a first screening step to prioritize the most harmful scenarios before advancing to in vivo assays.
What do we know and what do we still need to know?The presence of MPs within the human respiratory system is documented. However, prevalence in the general population remains unclear. Clinical sampling is sometimes invasive and methods are heterogeneous. These factors limit comparability across studies.
Further study calls for non-invasive upper-airway sampling with standardized protocols, strict contamination control, unified QA/QC, matrix-matched LOD/LOQ, consistent units, and dual reporting of counts and mass with size and shape characterization. These practices provide information (i.e., concentration, size and shape) to carry out assays in vivo and in vitro models with realistic exposure scenarios and computational modeling of deposition and dose.15 Furthermore, studies should also measure atmospheric suspended MPs in places where participants spend most of their time, with an emphasis on indoor environments. This paired design enables evaluation of the relationship between airborne MPs and the presence of MPs in respiratory systems. Evangelou et al.16 reported that previous global estimates of atmospheric MPs were greatly overstated, often by several orders of magnitude, and show that land-based sources dominate emissions, while oceanic contributions are much smaller than previously assumed. Taken together, these recommendations facilitate larger cohorts and improve comparability, helping identify the factors that drive MP presence and determine whether these materials pose health risks.
Beyond the polymers themselves, additional risks require assessment: for example, MPs can host microorganisms on their surfaces. Studies should test whether MPs act as vectors for viable and pathogenic taxa to the respiratory tract. MPs can also contain additives or sorbed chemicals. Researchers should quantify these chemicals, evaluate their release under airway-relevant conditions, and assess their effects on respiratory tissues.
In conclusion, standardized and streamlined measurement turns a signal into evidence. Such a framework supports risk assessment by identifying the specific MPs that drive hazards. This enables targeted mitigation, prioritizing the sources and physicochemical attributes with the highest impact. Ultimately, measurement is the shortest route from uncertainty to prevention.
Declaration on generative AI and AI-assisted technologies in the writing processDuring the preparation of this manuscript, the authors used Microsoft Copilot to enhance the language and improve the readability of the text. After using this tool, the authors thoroughly reviewed and manually edited the content as needed. The authors take full responsibility for the accuracy and integrity of the final version of the manuscript.
FundingThe authors acknowledge the financial support provided by the Spanish Government through Ministry of Science grants PID2024-155145OB-C21, PID2024-155145OA-C22, and RyC2021-034953-I, funded by the European Union “NextGenerationEU”/PRTR. Additional support was received from Seneca Foundation – Science and Technology Agency of the Region of Murcia (grant 21874/PI/22).
Authors’ contributionsConceptualization: Miguel González-Pleiter; Roberto Rosal; Carlos Baeza-Martínez; Gerardo Pulido-Reyes; Francisca Fernández-Piñas; Javier Bayo.
Methodology: Javier Bayo (detection and analytical methods); Roberto Rosal (chemical framing); Carlos Baeza-Martínez (clinical/medical framing); Gerardo Pulido-Reyes and Francisca Fernández-Piñas (biological framing).
Investigation (literature synthesis and checking): all authors.
Writing – original draft: Miguel González-Pleiter.
Writing – review & editing: all authors (all authors critically reviewed the manuscript and approved the final version).
Conflicts of interestThe authors declare that they have no known competing financial interests or personal relationships that may have influenced the work reported in this paper.
