Microplastics (MPs), environmental pollutants resulting from the degradation of plastic products and industrial processes, have become ubiquitous in global ecosystems. MPs can enter the human body through ingestion, inhalation, and dermal contact subsequently accumulating in vital tissues such as the liver, lungs, blood, and placenta. This review systematically evaluates the metabolic fate of MPs in humans, emphasizing their translocation across biological barriers and organ-specific deposition. We elaborated on the direct damage of MPs on the intestinal mucosal barrier and while simultaneously remodelling the gut microbiota, and focuses on the regulatory role of gut microbiota in the process of MPs-induced human health damage. Ingestion of MPs induces mechanical damage to the intestinal mucosa, epithelial cell apoptosis, and inflammation. It also alters gut microbial composition, that most notably increasing Firmicutes while decreasing Bacteroidetes and Actinobacteria , as well as disrupts metabolite production, including short-chain fatty acids and bile acids. These microbiota-mediated changes propagate via the gut-liver or gut-brain axis, contributing to obesity, cardiovascular diseases, neurological disorders, and reproductive impairments. This review clarifies the potential mechanism of MPs affecting human health through gut microbiota, and clearly identifies gut microbiota regulation as a potential therapeutic strategy to mitigate MP-induced diseases, and provides practical guidance for reducing MP-related health risks. This study systematically elaborates the pathways of human exposure to microplastics (MPs) via oral ingestion, inhalation, and dermal contact, as well as how microparticles cross biological barriers to enter the circulatory system and extensively accumulate in the intestine, lung, heart, liver, and brain. Meanwhile, it summarizes that MPs regulate the gut-liver/brain axis by reshaping the gut microbiota (e.g., the abundance of Firmicutes/Bacteroidetes) and interfering with microbial metabolites (short-chain fatty acids, bile acids, and amino acids), thereby participating in the occurrence and development of various diseases, including inflammatory bowel disease (IBD), obesity, cardiovascular diseases, neurodegenerative diseases, and reproductive impairment. • MPs invade the human body and bioaccumulate in tissues and cross multiple biological barriers. • MPs damage the intestinal mucosal barrier, trigger chronic low-grade inflammation and induce gut microbial dysbiosis. • MPs mediate the occurrence of human diseases by reshaping the gut microbiota and regulating related metabolites.
Chen et al. (Fri,) studied this question.