Polytetrafluoroethylene (PTFE, Teflon) microplastics and nanoplastics induce oxidative stress, mitochondrial damage, and genotoxicity in human intestinal cells

Polytetrafluoroethylene (PTFE, Teflon™), widely used in non-stick cookware, can degrade into micro- and nanoplastics (MNPLs). This raises concerns about human exposure, which remain largely unexplored. In the present study, we used physiologically relevant in vitro intestinal monoculture and co-culture models (Caco-2/HT29-MTX) to systematically assess the effects of PTFE-MNPLs (∼250 nm and ∼2 µm) at concentrations of 50-200 µg/mL over 24-48 h. PTFE-MNPLs, particularly nanosized particles, readily entered both differentiated and undifferentiated cells. They interacted with nuclear membranes and mitochondria, inducing structural and physiological disturbances without significantly affecting cell viability. These interactions led to mitochondrial damage and triggered inflammation, oxidative stress, and DNA damage. The severity of these effects increased with particle size, dose, and exposure duration. These findings challenge the assumption that PTFE particles are biologically inert, highlighting hazards arising from their physical interactions, especially at the nanoscale. Given the relevance of the co-culture in vitro model of intestinal barrier to human intestinal physiology, the results underscore potential intestinal health risks from PTFE-MNPL exposure. Future studies should focus on chronic, low-dose exposures to elucidate the specific cellular pathways activated by PTFE-MNPL exposure.