Inhaled Micro- and Nanoplastics as Environmental Modifiers of Lung Carcinogenesis: Mechanistic Insights and Evidence Synthesis

The exponential rise in global plastic production has resulted in the widespread environmental dissemination of micro- and nanoplastics (MNPs) across air, water, and biological systems. Inhalation of airborne MNPs represents a biologically plausible pathway of pulmonary exposure, particularly within indoor and occupational environments. Experimental evidence indicates that inhaled MNPs deposit within distal lung compartments, where their small aerodynamic diameter and surface reactivity may favor cellular uptake, oxidative stress induction, inflammatory activation, and prolonged biopersistence. Experimental studies further indicate that MNP exposure may induce DNA damage, chromosomal instability, and the dysregulation of signaling pathways involved in genomic integrity, thereby providing additional mechanistic support for their potential role in carcinogenesis. Chronic redox imbalance, macrophage dysfunction, inflammasome activation, epithelial–mesenchymal transition, and dysregulated cell adhesion collectively resemble mechanisms implicated in inflammation-associated carcinogenesis. Emerging in vitro and in vivo data further suggest that nanoplastics may function as tumor promoters or co-carcinogenic modifiers, particularly under chronic low-dose exposure or in combination with other airborne toxicants. However, human epidemiological evidence remains limited, and causality has not been established. This review synthesizes current mechanistic evidence regarding inhaled MNPs as potential modifiers of lung carcinogenesis, compares them with established inhaled carcinogens, and outlines critical research priorities necessary to clarify exposure–response relationships and clinical relevance. Current evidence supports biological plausibility rather than confirmed carcinogenic classification.