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Abstract:Microplastics (MPs; <5 mm) and nanoplastics (NPs; <1000 nm) are pervasive environmental contaminants increasingly detected in food, water, and human biological samples. The gastrointestinal (GI) tract represents a primary site of exposure, yet the full scope of their impact on human health remains incompletely understood. This review synthesizes current evidence on the role of MPs and NPs in gastrointestinal disease, extending beyond microbiome disruption to include epithelial barrier dysfunction, immune activation, oxidative stress, and systemic effects. Experimental and emerging clinical data suggest that MPs compromise intestinal integrity by disrupting tight junction proteins and inducing reactive oxygen species, leading to increased permeability and chronic inflammation. These mechanisms are implicated in the pathogenesis of inflammatory bowel disease (IBD), colorectal cancer (CRC), irritable bowel syndrome (IBS), and other GI disorders. MPs also alter gut microbiota composition, promote dysbiosis, and interact with immune cells to drive pro-inflammatory signaling. Beyond the GI tract, MPs may contribute to systemic effects through the gut–brain axis and endocrine disruption. In addition to mechanistic insights, this review highlights emerging strategies for mitigation and intervention, including probiotic-based approaches, enzyme-mediated degradation of plastics, targeted delivery systems such as lipid nanoparticles, and polysaccharide-based binding agents. Advances in detection technologies for environmental and biological samples are also discussed as critical tools for exposure assessment and risk stratification. Together, these findings underscore the need for integrated approaches combining detection, prevention, and therapeutic intervention to address the growing burden of microplastic exposure and its implications for gastrointestinal and systemic health. Keywords: Microplastics (MPs), Gastrointestinal (GI) diseases, Intestinal barrier dysfunction, Gut microbiome, Inflammatory bowel disease (IBD), Oxidative stress Contact: Brian Devorkin, bxd290@case.edu