Micro- and nanoplastics in gastric cancer: A narrative review

Micro- and nanoplastics (MNPs), defined as plastic particles smaller than 5 mm and 1 μm, respectively, are ubiquitous environmental contaminants detected in human tissues and typically ingested through food and drinking water. No threshold for adverse health effects has been established. This narrative review synthesizes current evidence on the molecular mechanisms, interactions with Helicobacter pylori, and experimental findings from 2D and 3D gastric cancer models relevant to MNP-induced gastric carcinogenesis. Particle size, shape, polymer type, surface charge, and weathering status influence toxicity. Proposed mechanisms include oxidative stress, mitochondrial dysfunction, chronic inflammation, genotoxicity, gastric dysbiosis, and ferroptosis, mediated by dysregulation of NF-κB, Wnt/β-catenin, MAPK, PI3K/Akt/mTOR, and cGAS-STING signaling. Nanoplastics (~100 nm) may induce ferroptosis via Fosl1 and p53, whereas larger microplastic fragments may activate YAP signaling and promote proliferation. MNPs may also carry persistent organic pollutants and toxic metals and may act synergistically with H. pylori to potentiate mucosal damage. In conclusion, MNPs can plausibly promote gastric carcinogenesis through mechanisms demonstrated in experimental systems, but a causal role in human gastric cancer has not been established. Standardized analytical methods, environmentally realistic exposure models, and large-scale epidemiological studies are needed.