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Can Micro- and Nanoplastics Modify Food-Allergy-Relevant Pathways?—A Comprehensive Narrative Review

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This review pulls together existing lab and animal research suggesting that tiny plastic particles from our food, water, and packaging could interfere with digestion, gut health, and immune signals in ways that might make food allergies worse, especially in babies, whose guts are still developing and who often use plastic bottles and feeding gear. However, this is based on test-tube and animal studies only; no research has yet confirmed whether microplastics actually increase allergy rates or severity in real people, so more human studies are needed before drawing firm conclusions.

Study Type In vitro

Micro- and nanoplastics (MNPs) are widely detected in food, drinking water, food-contact materials, and human biological samples. This narrative review evaluates whether experimental evidence supports a role for MNPs as modifiers of food-allergen digestion, intestinal-barrier function, microbiota composition, and immune tolerance. In vitro studies indicate that protein-corona formation can alter allergen conformation, epitope accessibility, and proteolysis, although effects vary by polymer, particle size, dose, and digestive model. Rodent studies provide evidence that MNP exposure can disrupt epithelial integrity, induce oxidative and inflammatory signaling, and modify microbiota-dependent immune regulation. More direct food-allergy models have reported exacerbation of ovalbumin- and cow’s-milk-allergic responses, including Th2 polarization and changes in dendritic cell and regulatory T-cell compartments. Infants may represent a susceptible and highly exposed population because of immature digestive and barrier function and the use of plastic feeding equipment; however, the available pediatric evidence is limited to exposure studies and simulated digestion. The effect of MNP exposure on the incidence of food allergies, reaction thresholds, or clinical severity in humans has not yet been studied. Accordingly, current findings support biological plausibility and identify research priorities, but they do not establish causality in humans.

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