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Further Studies in Translatable Model Systems are Needed to Predict the Impacts of Human Microplastic Exposure
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This review highlights that humans are inevitably exposed to microplastics through food, drink, and air, but most toxicity studies have been done in aquatic species at unrealistically high doses. The authors call for better experimental models that reflect realistic human exposure before health risks can be fully assessed.
Microplastics are a pervasive environmental contaminant that have been found in many media including water sources, soils, and foodstuff. Due to the worldwide presence and persistence of microplastic debris, human exposure is inevitable. Human exposure occurs predominantly through ingestion, although dermal and inhalation exposures are probable. Microplastic single exposure studies in aquatic species and fish have shown various toxic effects including those on reproduction and survival. In addition to potential intrinsic toxicity, microplastics often have chemicals adsorbed to their surfaces. Studies report that these chemicals can have innate toxicity that is modulated by the composition of microplastics. Both the impacts of microplastics alone and co-exposures with adsorbed chemicals exhibit size dependent effects. Analysis of the current literature has revealed published studies predominantly investigate the toxicity of microplastic exposure in fish and other aquatic species, with limited knowledge about the effects in mammals and cell lines. Toxicity has been shown to vary widely between taxonomic groups, suggesting inferring human health relevance will require model systems where human routes of exposure can be mimicked. Although it may be difficult to extrapolate the results from aquatic model systems to relevant human health impacts, they may suggest effects to investigate. In order to best estimate the short- and long-term impacts of human microplastic exposure, it is imperative that studies in model systems with increased similarity to human anatomy and cellular processes be done.
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This review argues that better animal models are needed to accurately predict the health impacts of microplastic exposure on humans, noting that current studies using aquatic organisms and fish may not translate well to human biology. The authors call for more research using mammalian models and for studies that test environmentally realistic exposure conditions including the chemical cocktails associated with plastic particles.
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This comprehensive review examines microplastic exposure pathways in humans, methods of detection, and the potential toxic effects on various biological systems. The study highlights growing evidence that microplastics can enter the body through ingestion, inhalation, and dermal contact, and may affect multiple organ systems, though significant uncertainties remain about long-term health outcomes.
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This review synthesizes evidence on how microplastics are distributed throughout the environment, the routes by which people are exposed (food, water, and air), and the health effects documented in experimental studies. The authors find significant links between microplastic exposure and adverse health outcomes and call for urgent regulatory action and more research into long-term human health risks.
Microplastic Exposure and Human Health: Advancing Risk Assessment and Future Research Directions
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This review synthesizes recent evidence that microplastics are present in human blood, respiratory tissue, placenta, and gut, examines proposed toxicological mechanisms, and identifies priorities for improving risk assessment frameworks and exposure measurement methods.
Microplastics and human health: a narrative review of current evidence, knowledge gaps, and future research directions
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Researchers synthesized a decade of evidence on human microplastic exposure and found that ingestion and inhalation are the primary routes, with experimental data pointing to oxidative stress, inflammation, and potential gastrointestinal and reproductive effects — while calling out inconsistent detection methods and the absence of long-term epidemiological data as critical gaps.
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