Microplastics and nanoplastics in inflammatory bowel disease: Mechanistic plausibility, human evidence and future research priorities

Abstract

Microplastics and nanoplastics (MNPs) are increasingly recognized as ubiquitous environmental contaminants with unavoidable human exposure through ingestion and inhalation. The gastrointestinal tract is an important interface between MNPs and the intestinal microbiota, epithelium and immune system. Interest in the effects of MNPs on human health has been increasing particularly in inflammatory bowel disease (IBD), a chronic immune-mediated disease in which environmental factors are thought to contribute to disease pathogenesis. Experimental studies have suggested that intestinal MNP exposure may promote several pathways relevant in IBD including dysbiosis, mucus disruption, impaired epithelial integrity, intestinal permeability and activation of immune pathways. Current evidence is largely translational and is dominated by experimental models that do not reflect real world human exposures. Human studies in IBD are currently limited to a small number of observational studies with data vulnerable to confounding and reverse causation. Despite increasing mechanistic plausibility, there is still no direct evidence that MNPs cause IBD or alter the disease course. In this narrative review we summaries the current knowledge on human MNPs exposures, we examine experimental evidence for biologically plausible pathways through which MNPs may influence intestinal inflammation and the emerging human evidence in IBD. We also explore the major analytical and methodological limitations in the field.

Keywords: Inflammatory bowel disease; Ulcerative colitis; Crohn’s disease; Microplastics; Nanoplastics

Core Tip: Microplastics and nanoplastics are emerging as ubiquitous environmental contaminants of potential relevance in inflammatory bowel disease (IBD). Experimental evidence suggests that intestinal exposure may promote dysbiosis, mucus barrier disruption, epithelial permeability and immune activation, all pathways implicated in IBD pathogenesis. Current evidence supports biological plausibility but is limited to simplified preclinical models and small observational human studies. Prospective human studies are needed to investigate whether micro- and nanoplastics may contribute to IBD onset, activity or progression.