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

## TL;DR

This review explores how microplastics may contribute to metabolic syndrome and colorectal cancer through various biological mechanisms.

## Contribution

The study provides a systematic synthesis of mechanistic, epidemiological, and experimental evidence linking microplastics to metabolic and colorectal cancer pathways.

## Key findings

- MP exposure is linked to insulin resistance, obesity, and dyslipidemia.
- Chronic MP exposure increases colonic inflammation and tumorigenic markers like β-catenin and COX-2.
- Altered gut microbiota and epithelial barrier dysfunction are observed with MP exposure.

## Abstract

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.

This systematic review aims to evaluate current human, animal, and in vitro evidence on the dual impact of MP exposure on metabolic dysregulation and pathways involved in colorectal carcinogenesis.

A systematic search was performed across PubMed, Scopus, Web of Science, and EMBASE in accordance with PRISMA 2020 guidelines. The review incorporated 45 studies: 18 observational studies involving humans, 17 animal studies, and 10 in vitro investigations. The outcomes analyzed included components of MetS, precursors to colonic neoplasia, and relevant biological mechanisms.

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).

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.