Abstract The pervasive contamination of microplastics (MPs) and nanoplastics (NPs) in the environment has emerged as a critical public health concern, with the gastrointestinal (GI) tract being the primary route of human exposure. This comprehensive review synthesizes current knowledge on the metabolic risks and toxicological mechanisms of microplastic-induced GI system damage, drawing from recent studies conducted across Spain, Germany, China, Japan, and the United States. Microplastics have been detected in 94-98% of human fecal samples and accumulate at higher concentrations in colorectal cancer (CRC) tissues compared to adjacent normal tissues. The review elucidates multiple molecular mechanisms underlying GI toxicity, including oxidative stress, inflammatory responses, intestinal barrier disruption, gut microbiota dysbiosis, and metabolic dysfunction. Size-dependent toxicity analysis reveals that smaller particles (20-100 nm) exhibit significantly higher intestinal toxicity compared to larger counterparts. Furthermore, the disruption of tight junction proteins and activation of the NF-kappaB/NLRP3 signaling pathway have been identified as critical mechanisms mediating microplastic-induced intestinal barrier dysfunction. This review highlights significant research gaps, including the need for standardized detection methods, long-term exposure studies at environmentally relevant concentrations, and therapeutic interventions. The findings underscore the urgent need for policy development and regulatory frameworks to address microplastic contamination and protect public health.
Zhang et al. (Mon,) studied this question.