Microplastics and nanoplastics (MPs/NPs), emerging as pervasive environmental contaminants, have raised growing concern due to their potential implications for human health. Among their diverse biological effects, recent evidence highlights their capacity to cross biological barriers, accumulate in tissues, and interact with cellular components in ways that may promote carcinogenesis. MPs/NPs can cause oxidative stress, inflammation, and epithelial barrier dysfunction, leading to cellular homeostasis disruption. Their interaction with endothelial cells and immune components further exacerbates pro-tumorigenic processes, including angiogenesis, immune evasion, and epithelial–mesenchymal transition (EMT), thereby potentially facilitating tumor initiation and progression. At the cellular level, these particles are internalized through various endocytic pathways, where they are associated with oxidative stress, inflammation, DNA damage, and barrier dysfunction—processes that have been linked to carcinogenesis. This review synthesizes current evidence on the cellular and molecular mechanisms through which MPs/NPs may contribute to cancer development, with particular emphasis on their interactions with endothelial cells and the tumor microenvironment. It highlights the need for further mechanistic and epidemiological studies to clarify the potential role of these particles in carcinogenesis. Given the increasing global production and environmental ubiquity of plastic particles, understanding their direct contribution to cancer development is critical for advancing both public health strategies and environmental regulations.

Resumen Carta al editor (sin resumen)

Microplastics and nanoplastics (MPs/NPs) are increasingly recognized as biologically active interfaces that may reshape host–microbe interactions in carcinogenesis. This review proposes a hypothesis-generating mechanistic framework in which MPs/NPs may influence cancer-related processes through the integration of environmental exposure, epithelial barrier disruption, immune dysregulation, and tumor microenvironment remodeling. Although applicable to multiple epithelial interfaces, the framework primarily focuses on the intestinal mucosa, where the most substantial evidence exists. Through plastisphere formation, MPs/NPs adsorb pollutants, virulence factors, and microbial communities, potentially facilitating pathogen persistence, horizontal gene transfer, and antibiotic resistance enrichment. Upon host exposure, MPs/NPs have been associated with compromised epithelial integrity, enhanced microbial translocation, and activation of inflammatory pathways involving pattern recognition receptors, NF-κB, and the NLRP3 inflammasome. At the microbiome level, MPs/NPs may promote dysbiosis, alter microbial metabolism, and favor pro-inflammatory and genotoxic metabolites that could reinforce oncogenic signaling. These processes may converge to sustain chronic inflammation, immune evasion, extracellular matrix remodeling, angiogenesis, and tumor-permissive niches. While experimental and biomarker-based evidence support this axis, direct human data remain limited. Collectively, this review provides a conceptual basis for understanding environmentally associated carcinogenesis through MPs/NPs as ecological mediators bridging the environmental exposures, microbiome, and cancer biology.