Micro- and Nanoplastics and Liver Disease: Mechanistic Insights, Experimental Evidence, and Pathways to Hepatic Inflammation, Fibrosis, and Carcinogenesis

Micro–nanoplastics (MNPs) have emerged as a critical environmental pollutant with significant potential implications for the development of liver disease. These MNPs can accumulate in the liver, initiating a series of detrimental biological responses. One of the main mechanisms is the initiation of oxidative stress, which is marked by overproduction of reactive oxygen species harming cellular structures. This oxidative damage is closely linked to hepatic inflammation, where immune responses are triggered, exacerbating tissue injury and disrupting normal liver function. As a result, hepatic metabolism, detoxification, and immune regulation become compromised due to persistent MNPs exposure. Although in vitro and vivo models effectively show direct cellular toxicity, oxidative stress, and metabolic disruption, direct evidence from human studies is mostly confined to tissue detection and cross-sectional correlations. As a result, advanced pathological outcomes like the progression of hepatic fibrosis and the development of cancer are considered mechanistic hypotheses grounded in biological plausibility rather than confirmed human causation.