Figure 1.

Representative schematic summarizing the intestinal and peripheral effects of oral microplastic exposure. (A) Pre-clinical evidence indicates that in the gut lumen, microplastics have been shown to have three major effects: (1) microbial dysbiosis, characterized by poorer diversity and compositional instability [41,42,43,44,45], and (2) increased gut permeability due to intestinal cell damage (namely enterocytes) [44,47,48,57,65]. These microplastic-induced disruptions to the microbiome and gut barrier contribute to gastrointestinal inflammation (3), leading to the translocation of pro-inflammatory cytokines, bacterial toxins (lipopolysaccharide, LPS), and mucosal immune cells from the gut into peripheral circulation microplastics [31,33,56,63]. After oral microplastic exposure, studies also report peripheral effects: microplastic circulation, microplastic deposition in peripheral organs, elevated serum LPS, and systemic inflammation [33,45]. (B) Notably, clinical evidence using human biopsy samples and post-mortem samples, microplastics have been isolated from the heart, saphenous vein, liver, spleen, kidney, gut, lower limb joints, and reproductive organs (represented by green zones) [8,10,53,83,84,85,86,87,88]. Figure created with Biorender.com.