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Dietary Components as Promising Candidates for Mitigating Micro- and Nanoplastic-Associated Metabolic Dysfunctions.

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This review summarizes existing research on micro- and nanoplastics found in human tissues and their links to effects seen in cell and animal studies, including insulin resistance, liver changes, and cardiovascular injury. It also discusses dietary strategies that might counteract these effects, noting such approaches remain hypothetical with limited clinical evidence.

Global plastic production has potentially led to pervasive micro- and nanoplastic (MNP) exposure across environmental, agricultural, and biological systems, now detected in every human tissue examined, from blood and placenta to brain and cardiovascular plaque, raising potential public health concerns. Given their small size and physicochemical properties, MNPs can infiltrate soil and water, enter plants and animals, and transfer along food and water systems, potentially reaching human tissues. In preclinical models, ingested MNPs appear to persist in the gastrointestinal tract and alter microbiota homeostasis and epithelial barrier integrity. Upon entering circulation, MNPs appear to acquire protein coronas, which may impact how they are distributed in organs and potentially impact cellular function. In cell culture and in animal studies, MNPs have been associated with insulin resistance, hepatic steatosis, cardiovascular injury, reproductive dysfunction, and neurological damage. In human studies, MNPs detected in carotid plaque have been associated with a higher risk of cardiovascular events, although direct causal data are absent, and associative data are limited by differences in detection approaches, size limits, reporting units, and other analytic factors. This review summarizes current evidence on the health effects of MNP exposure and identifies key gaps in the literature. Because MNPs move continuously across environmental, agricultural, and human systems, these gaps are best addressed through a One Health framework that integrates evidence from cell, animal, and human studies along this shared exposure pathway. Within this framework, we evaluate dietary and nutritional strategies that may counteract MNP-associated injury by strengthening gut barrier integrity, restoring redox balance, modulating inflammatory signaling, and promoting MNP excretion. Although dietary strategies remain hypothetical and clinical evidence is limited, we propose that such strategies are promising and worth pursuing in future translational and clinical investigations to determine their potential use as complementary approaches alongside efforts to mitigate MNP exposure.

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