Microplastic Exposure and Its Dual Impact on Metabolic Syndrome and Pathways of Colorectal Carcinogenesis: A Systematic Review of Epidemiological, Experimental, and Mechanistic Evidence

Background: Microplastics (MPs) and the endocrine-disrupting chemicals associated with them, including bisphenol A (BPA) and phthalates, have been identified as potential factors contributing to the increasing rates of metabolic syndrome (MetS) and colorectal carcinogenesis. Despite rising concerns in this area, a thorough synthesis of the mechanistic and epidemiological data connecting MPs to these health issues is currently absent. For consistency in this review, early-onset colorectal cancer is defined as colorectal cancer diagnosed before the age of 50 years, in line with recent epidemiological studies. Chronic exposure to MPs is defined as sustained exposure lasting at least 8 weeks in animal models or multiple years in human observational studies. These standardized definitions ensure clarity when comparing outcomes across diverse study designs. Objective: evidence on the dual impact of MP exposure on metabolic dysregulation and pathways involved in colorectal carcinogenesis. Methods: investigations. The outcomes analyzed included components of MetS, precursors to colonic neoplasia, and relevant biological mechanisms. Results: Exposure to MPs correlated with an increased risk of insulin resistance, obesity, and dyslipidemia. It also contributed to heightened inflammatory responses, alterations in gut microbiota composition, and dysfunction of the epithelial barrier. Furthermore, chronic exposure led to colonic inflammation and an elevation in tumorigenic markers, such as β-catenin (a key oncogenic protein in the Wnt signaling pathway) and COX-2 (an inflammatory enzyme implicated in tumor progression). Conclusion: The results indicate a biologically plausible connection between MP exposure and the development of both MetS and colorectal carcinogenesis pathways, rather than a direct clinical association with early-onset colorectal cancer.