A new study reveals that microplastics accumulate in human bile, leading to cellular aging in the biliary system. Researchers found microplastics in bile samples from patients, with higher concentrations in those with gallstones. Exposure to microplastics in cell cultures led to cellular senescence and mitochondrial damage, findings that could lead to new understanding of the effects of microplastics on human health.
Plastic pollution is a significant environmental challenge, with microplastics now recognized as ubiquitous in our environment and increasingly found within the human body. These tiny particles, entering through food, drink, and air, have been detected in various organs and tissues, including the lungs, placenta, brain, semen, and feces.
This widespread presence raises concerns about the potential for long-term health effects, yet a crucial question remains largely unanswered: where do these particles ultimately go after entering the body, and how do they interact with the biological systems responsible for their processing and excretion? The enterohepatic circulation, involving bile, presents a particularly important avenue for investigation. Bile, a digestive fluid and key medium for substance excretion, is produced by the liver and stored in the gallbladder before being released into the small intestine. Disturbances in bile balance can contribute to gallstones and other disorders, making it a critical focus for studying microplastic accumulation and its associated toxicities within the body. In response to these challenges, researchers initiated an in-depth exploration of microplastic behavior within the biliary system. \Researchers from The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Sun Yat-sen University, Guilin Medical University, and collaborating institutions, conducted a study published in Environmental Science and Ecotechnology. The study, accepted on April 26, 2026, and pre-proofed in the journal, delves into the accumulation of microplastics in human bile and their impact on cholangiocytes, the cells lining the bile ducts. To investigate this, the research team collected bile samples from 14 patients undergoing surgery, including individuals with and without gallstones. Strict plastic-free protocols were implemented to minimize contamination and ensure the accuracy of the findings. Advanced analytical techniques were employed to characterize the microplastics present in the samples. Pyrolysis-gas chromatography-mass spectrometry (Py-GC/MS) was used to identify polymer types, laser direct infrared spectroscopy provided further insights, and scanning electron microscopy (SEM) was used to analyze particle size and morphology. The results revealed the presence of microplastics in all bile samples. Six different polymers were identified by Py-GC/MS, with PET (polyethylene terephthalate) accounting for the largest share at 68.05%, followed by PE (polyethylene) at 27.11%. Notably, patients with gallstones exhibited a significantly higher burden of microplastics, with a median bile concentration reaching 25.89 μg g−1, compared to 6.98 μg g−1 in the control group. The majority of the particles measured between 20 and 50 μm in size and displayed irregular, rod-like, and spherical shapes. \Further investigation involved modeling chronic exposure to microplastics in cultured human cholangiocytes using low-dose polystyrene nanoplastics. The researchers performed proteomic and cellular assays to examine the cellular impact. The results demonstrated an increase in senescence-related molecules, increased SA-β-gal activity, and G1 cell-cycle arrest, indicating cellular aging. Mechanistically, the exposure to microplastics was found to reduce ATP (adenosine triphosphate) levels, increase mitochondrial reactive oxygen species (ROS), promote Drp1-related mitochondrial fission, and lower mitochondrial membrane potential, all of which contribute to cellular damage and aging. Interestingly, the antioxidant melatonin was able to reverse much of the damage caused by microplastics, and it suppressed the release of inflammatory markers such as IL-6 and TNF-α. This finding is significant as it provides a potential avenue for intervention. An expert interpretation emphasizes that the study presents the biliary system as more than a passive transit site, suggesting bile may be a previously unrecognized reservoir and excretion route for microplastics. It also reveals that chronic exposure can cause aging in cholangiocytes due to mitochondrial injury. The study concludes that the biliary system may be a new target of microplastic-related health risks. The implications extend beyond gallstones, suggesting a new window into how plastic pollution may interact with digestive and liver-related health. The study also strengthens the case for better monitoring of microplastics, more realistic chronic-exposure models, and broader risk assessment for vulnerable populations. The authors also acknowledge the limitations of their study, including the small sample size and single-center origin of the samples. However, they emphasize the significance of their findings and the need for larger, multi-center studies to validate and expand upon these initial results. Overall, the work suggests that microplastics are present in the body and leave a measurable biological footprint in one of the most overlooked fluids
Microplastics Bile Cellular Aging Environmental Pollution Health Effects
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