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The Plasticene Paradigm: Microplastics, Gut Dysbiosis, and Food Allergy — A Critical Commentary

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This paper reviews existing research on whether microplastics in food might disrupt gut bacteria and contribute to food allergies. It notes that most evidence comes from animal studies using much higher plastic doses than people are estimated to encounter, limiting conclusions about human risk, and calls for more human-based research.

Body Systems
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Lindong Shi,1,* Peiqin Wang,2,* Bin Wu,2 Congfu Huang21Department of Pediatrics, Longgang District Central Hospital, Shenzhen, People’s Republic of China; 2Department of Pediatrics, Longgang District Maternity & Child Healthcare Hospital of Shenzhen City (Longgang Maternity and Child Institute of Shantou University Medical College), Shenzhen, People’s Republic of China*These authors contributed equally to this workCorrespondence: Congfu Huang, Email 78333755@qq.comBackground: The increasing prevalence of food allergy (FA) in industrialized regions cannot be fully explained by traditional hygiene and biodiversity frameworks, suggesting the involvement of new environmental triggers. Microplastics (MPs), which are dietary contaminants now consistently found in human biological samples, have been proposed as a potential threat to gut-immune balance. However, direct evidence for this link in humans is still lacking.Main Body: This commentary critically examines and advances the "Plasticene Paradigm”, which hypothesizes that dietary MP exposure disrupts the beneficial relationship between the host and its microbiota, thereby promoting the development of FA through microbiota-dependent mechanisms. The central mechanism proposed involves MP-induced dysbiosis, characterized by a reduction in short-chain fatty acid (SCFA) -producing bacteria. This reduction subsequently impairs the differentiation of regulatory T cells (Tregs), disrupts the balance between Th2 and Treg cells, and compromises the integrity of the intestinal barrier. While studies involving fecal microbiota transplantation in animal models offer causal evidence under experimental conditions, this evidence primarily comes from studies using supraphysiological doses of pristine polymers (mg/kg/day range). These doses exceed mass-based estimates of human daily intake (μg/kg/day range) by several orders of magnitude, although direct quantitative comparison is complicated by the use of heterogeneous exposure metrics (mass-based vs particle-count-based) across different estimation approaches. This significant difference in dosage fundamentally limits the applicability of these findings to human exposure levels found in the environment. We identify four obstacles to translating these findings: dose relevance, exposure complexity, challenges in model extrapolation, and analytical constraints. These barriers currently prevent drawing definitive conclusions about human risk.Conclusion: The current evidence, which is predominantly preclinical, is constrained by issues of dose relevance, exposure complexity, and gaps in model extrapolation, with human data largely showing only associations. We propose a three-pronged research agenda: (I) establishing prospective birth cohorts with specific biomonitoring for polymers; (II) conducting mechanistic studies using environmentally relevant MP mixtures in FA models; and (III) developing microbiome-targeted interventions as needed. This framework aims to transform the Plasticene Paradigm from a hypothesis-driven mechanistic narrative into one supported by a stronger evidence base. This evidence may ultimately inform public health policy, food safety regulations, and precise prevention strategies for FA in an era of widespread plastic contamination.Keywords: microplastics, food allergy, gut microbiota, short-chain fatty acids, intestinal barrier, translational research, exposome

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