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.

Micro- and nanoplastics (MNPs) are gaining prominence as human-made pollutants that continuously enter the human body through ingestion, inhalation, and iatrogenic routes. Current analytical technologies utilizing vibrational chemical imaging and thermal degradation mass spectrometry have established that these materials enter blood circulation and accumulate in the human cardiovascular system (blood, arteries, plaques, thrombi, and myocardium). MNPs function as a unique combination of solid and chemical pollutants since the materials contain an insoluble polymer core, formulation-specific additives, such as phthalates and bisphenols that can leach into the surrounding milieu, and contaminants that adsorb to the surface. This phenomenon, called the “Trojan horse” effect, explains this property of MNPs. Experimental studies have demonstrated their ability to degrade the endothelial glycocalyx and uncouple endothelial nitric oxide synthase. MNPs also trigger mitochondrial stress, which activates the NLRP3 inflammasome pathway. These mechanisms can contribute to multiple cardiovascular diseases like atherosclerotic cardiovascular disease (ASCVD), acute coronary syndromes (ACS), heart failure, arrhythmia, and thromboembolism. The findings from human surgical cohorts show that there is a connection between polymer accumulation in plaques, the development of vascular inflammation, the structural vulnerability of plaques, and the incidence of major adverse cardiovascular events. However, it is important to understand that these results are not sufficient for establishing definitive clinical causality. Most human data come from cross-sectional studies that can suffer from reverse causation, such as when inflamed, hyperpermeable vascular walls allow the entrance of the pollutants without them being the direct cause of the disease. To reach a definite conclusion about the connection between MNPs and cardiovascular diseases, it is essential to conduct intervention studies and establish prospective longitudinal exposure cohorts.