Microplastics, Nanoplastics, and Cancer: A Narrative Review

Microplastics and nanoplastics (MNPs) have become a cancer-relevant biomedical question because exposure is repeated, dietary and inhalational routes are difficult to avoid, and particles have been reported in multiple human fluids, tissues, and clinical settings. Cancer is a difficult endpoint in this field because latency is long, exposure mixtures are heterogeneous, and analytical methods differ across studies. This narrative review synthesizes evidence on the scope of the MNP problem, including human tissue distribution, mechanistic pathways linking particles and plastic-associated mixtures to carcinogenesis, and site-specific preclinical and clinical evidence in oncology. The strongest evidence supports exposure and biological plausibility. MNPs can interact with epithelial barriers, mitochondria, immune cells, microbial communities, endocrine pathways, and chemical co-contaminants. Preclinical studies report oxidative stress, inflammatory signaling, genotoxic and epigenetic stress, barrier injury, microbiome dysbiosis, altered metabolism, tumor promotion in colorectal and other models, and possible modulation of treatment response. Human evidence remains preliminary as MNP particles have been detected in stool, blood, urine, placenta, breast milk, lung, liver, colon, carotid plaque, reproductive tissues, and several tumor types, but detection does not establish causality. The most direct cancer epidemiology consists of early colorectal case-control and tumor-biomonitoring studies, which suggest that MNPs are plausible modifiers of cancer initiation, promotion, progression, and treatment response. However, additional research is needed to definitively establish them as human carcinogens, with priority given to standardized biomonitoring, internal-dose metrics, environmentally realistic mixtures, long-term cancer models, prospective cancer cohorts, and intervention studies that connect source reduction to validated changes in human MNP burden.