Study reveals bile as reservoir for microplastics in humans

Plastic pollution has become one of the defining environmental issues of modern life, and microplastics are now known to enter the body through food, drink, and air. Previous studies have detected them in organs and tissues including the lungs, placenta, brain, semen, and feces, raising concern about long-term health effects. Yet one crucial question has remained largely unexplored: where do these particles go after entering the body, and how might they affect the systems that process and excrete them? Because bile is both a digestive fluid and a key medium for substance excretion in enterohepatic circulation, and because disturbances in bile balance can contribute to gallstones and other disorders, based on these challenges, in-depth research into microplastic accumulation and toxicity in the biliary system is needed.

Researchers from The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Sun Yat-sen University, Guilin Medical University, and collaborating institutions reported (DOI: 10.1016/j.ese.2026.100686) this study in Environmental Science and Ecotechnology as a 2026 journal pre-proof accepted on April 26, 2026, describing how microplastics accumulate in human bile and drive cholangiocyte senescence.

To answer that question, the team collected bile from 14 patients undergoing surgery, including five without gallstones and nine with gallstones, while using strict plastic-free protocols to avoid contamination. They combined pyrolysis-gas chromatography-mass spectrometry, laser direct infrared spectroscopy, and scanning electron microscopy to identify polymer types, estimate concentrations, and characterize particle size and morphology. Microplastics were found in all samples. Six polymers were identified by Py-GC/MS, with PET accounting for 68.05% and PE for 27.11%. Patients with gallstones carried far heavier burdens: median bile concentrations reached 25.89 μg g−1, compared with 6.98 μg g−1 in controls. Most particles measured 20-50 μm, and microscopy revealed irregular, rod-like, and spherical shapes. The researchers then modeled chronic exposure in cultured human cholangiocytes using low-dose polystyrene nanoplastics. Proteomic and cellular assays showed increased expression of senescence-related molecules, greater SA-β-gal activity, and G1 cell-cycle arrest. Mechanistically, the particles reduced ATP, increased mitochondrial reactive oxygen species, promoted Drp1-related mitochondrial fission, and lowered mitochondrial membrane potential. Melatonin reversed much of this damage and suppressed inflammatory markers including IL-6 and TNF-α.

"This study reframes the biliary system as more than a passive transit site," an expert might say. "It suggests that bile may act as a previously underrecognized reservoir and excretion route for microplastics, while also revealing that chronic exposure can age cholangiocytes through mitochondrial injury. Just as importantly, the finding that melatonin blunted these effects offers a biologically plausible starting point for protective intervention, even though larger human studies are still needed." This interpretation is consistent with the authors' conclusion that the biliary system may be a new target of microplastic-related health risk.

The implications extend beyond gallstones. By identifying bile as a potential accumulation and excretion hub, the study opens a new window into how plastic pollution may interact with digestive and liver-related health. It also strengthens the case for better monitoring of microplastics in drinking water and food systems, more realistic chronic-exposure models, and broader risk assessment for vulnerable populations. At the same time, the authors caution that their sample size was small and drawn from a single center, so the findings should be expanded in larger, multicenter studies. Even so, the work offers a compelling narrative: tiny plastic particles may be leaving a measurable biological footprint in one of the body's most overlooked fluids.