Micro- and nanoplastics (MNPs) are emerging environmental immunotoxins with widespread human exposure through ingestion, inhalation, and dermal contact. Detected in the placenta, lungs, blood, bone marrow, and brain, MNPs accumulate in immune organs where they disrupt innate and adaptive cell functions. Experimental evidence shows that MNPs impair macrophage phagocytosis, skew dendritic cell maturation, trigger neutrophil extracellular traps, and alter T and B cell responses. Mechanistically, these effects are driven by oxidative stress, mitochondrial dysfunction, and activation of NF-κB, MAPK, and NLRP3 inflammasome pathways, leading to apoptosis, pyroptosis, and chronic low-grade inflammation. Barrier disruption and microbiome dysbiosis further compromise immune tolerance, linking MNPs exposure to autoimmune risk. Preclinical models demonstrate exacerbation of systemic lupus erythematosus, inflammatory bowel disease, and rheumatoid arthritis, though human causal data remain limited. Standardized protocols, advanced imaging and omics, and longitudinal cohorts are urgently needed to establish causal links and inform public health strategies.
Fan et al. (Fri,) studied this question.