Are microplastics in food a risk factor for obesity: Current evidence, mechanistic pathways and emerging health risks associated with human exposure

Current evidence suggests that microplastics (MPs; ≤5 mm) and nanoplastics (NPs; <100 nm) are pervasive environmental contaminants to which humans are exposed predominantly through food, drinking water, and inhalation. MPs have been detected in multiple human tissues—including blood, urine, stool, placenta, breast milk, lungs, kidneys, liver, and semen—and can cross biological barriers. These particles may provoke inflammation, oxidative stress, immune dysregulation, endocrine disruption, and genotoxicity. MPs and their associated chemicals (phthalates, bisphenols, organotins) may contribute to metabolic dysfunction through hormonal signalling interference, adipogenesis, gut-microbiome disruption, and chronic inflammation. Although animal and in-vitro studies support a plausible link between MPs/NPs and adiposity, no longitudinal human epidemiological studies have demonstrated causality. Human evidence remains limited or “suspected”, with major methodological gaps noted in quantification, exposure assessment and harmonisation. MPs may also act as vectors for additional pollutants, potentially exacerbating metabolic effects. Emerging findings suggest maternal–foetal transfer and early developmental impact, although long-term effects remain unestablished. Stronger prospective human studies are needed to clarify whether MPs constitute a direct risk factor for obesity.