Nanoplastics (NPs) are increasingly recognized as persistent intracellular cargoes whose long-term effects may depend not only on chemical reactivity, oxidative stress, and inflammation, but also on how particle-containing vesicles are transported, positioned, and cleared. Because the positioning and movement of endosomes, lysosomes, autophagosomes, mitochondria, and NP-containing vesicles are extensively regulated by microtubule-based transport, prolonged NP retention has the potential to disrupt intracellular trafficking and organelle homeostasis. Here, we examine how NPs may influence microtubule dynamics, tubulin post-translational modifications, motor-dependent trafficking, and organelle positioning, with particular emphasis on their relationships to cellular senescence and ageing. We first summarize evidence that senescence and ageing are associated with alterations in microtubule organization, stability, acetylation, intracellular transport capacity, cytoplasmic physical properties, and neuronal microtubule integrity. We then evaluate emerging evidence linking NP exposure to altered microtubule states and trafficking-related dysfunction, while considering particle size, shape, surface chemistry, aggregation, exposure duration, and intracellular burden as important determinants of particle fate and cellular response. We propose microtubule-dependent trafficking congestion as a testable framework in which persistent NP-containing cargo progressively reduces intracellular transport efficiency, while distinguishing this state from simple particle retention or generalized organelle dysfunction. Potential mechanisms include increased cargo loading, altered kinesin-dynein balance, perinuclear lysosomal retention, changes in cytoplasmic crowding or viscosity, and dysregulation of tubulin-modifying enzymes. Direct evidence for NP-induced trafficking congestion remains limited, highlighting the need for quantitative live-cell measurements of vesicle mobility, velocity, run length, pausing, directionality, and recovery after exposure withdrawal. Finally, we discuss human biomonitoring and tissue-distribution evidence and emphasize the distinction between detection of plastic particles in human tissues and demonstration of pathological causality.
