Microplastics that accumulate in the body may 'clog up' immune cells
Microplastics that break off polystyrene food containers might prevent immune cells from fighting infections and clearing away dead cells, as well as reducing sperm counts, a mouse study hints.
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Microplastics that accumulate in the body can disrupt the immune system by preventing immune cells from gobbling up microbes and clearing dead cells, a new study in mice and lab dishes shows. Although it's still unclear how this might play out in the human body, experts say the study has potential implications for human health.
Microplastics are tiny particles that break off of plastic products, like water bottles, food storage containers and freezer bags. Although these undigestible particles accumulate in the body, scientists remain unsure how they contribute to illness. The new study revealed that these tiny particles can clog up and disrupt the function of macrophages, cells that engulf and destroy potentially harmful viruses, bacteria or fungi, as well as dead cells.
Microplastics contaminate air, soil and water; are abundant in food and drinks; and have been detected in various human tissues and fluids, including blood, breast milk, the brain, the liver and reproductive organs. Eliseo Castillo, who researches how microplastics affect health at the University of Mexico but was not involved with the study, told Live Science in an email that "because plastic production continues to increase and these materials slowly fragment over time, microplastic pollution is expected to keep rising in the future."
Article continues belowThe buildup of microplastics in the body has been correlated with atherosclerosis, in which plaque builds up in the inner walls of arteries, causing them to become narrow and rigid; neurodegeneration; and cancer, said Justin Perry, an immunologist at Memorial Sloan Kettering Cancer Center and senior author of the study, which was published March 10 in the journal Immunity.
Nonetheless, researchers have not proved that microplastics directly cause disease. "I think that really set off myself and other colleagues in the field to try and understand this," Perry told Live Science. For the new study, he and his colleagues focused on polystyrene, a common plastic that is used in food containers and breaks down into microplastic particles that can be as small as a virus or as large as a grain of sand.
The team focused on macrophages, which engulf material, such as dead cells and infectious microbes, from their surroundings and break them down into sugars, amino acids and fats that the cells can recycle. Scientists have shown in mice and humans that macrophages actively take up microplastics but can't break them down.
"That's kind of scary, because that means that we really haven't evolved a response to them," Perry said, so it's possible that cells hoard increasing volumes of microplastics throughout a person's lifetime, he added.
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At this time, there is no clear public health evidence directly linking microplastic exposure to increased infections in humans.
Eliseo Castillo, microplastics researcher at the University of Mexico
Perry and his colleagues administered this nonbiodegradable plastic to human macrophages cultured in lab plates. They also inserted the microplastic particles into the airways of mice, euthanized them and extracted their lungs to image on a microscope.. Cells that took up the particles struggled to engulf and destroy dead cell matter or infectious microbes like bacteria or fungi, the team discovered.
To determine if microplastics could prevent macrophages from fighting infections, the team administered the fungus Aspergillus fumigatus, which causes respiratory infections in immunosuppressed people, to the mice's lungs. They found that the mice that were given microplastics struggled to clear the infection and experienced worse disease.
"Whether this leads to higher infection rates in people is still unknown," Castillo said. "At this time, there is no clear public health evidence directly linking microplastic exposure to increased infections in humans."
Microplastics also stopped macrophages from engulfing and destroying dead cell matter, potentially causing litter to build up in tissues. Perry said people lose 2% of their body mass per day due to cell death, and it's up to macrophages to clear away the dead litter. "It's about 3 million [dying] cells per second. If you really do the math, it's quite a large burden [for macrophages]," Perry added
A pileup of dead cell material like DNA can alarm the immune system because it signals that a threat such as an infection may be causing tissue damage. This could trigger inflammation, potentially precipitating autoimmune disorders, Castillo said.
Microplastics might also reduce fertility when taken up by macrophages in the testes. Perry and his colleagues exposed male mice to regular doses of microplastics and found that their sperm counts decreased over 18 weeks. He speculated that microplastics may partly account for the drop in sperm count seen globally in the human population. The study didn't explore the potential impact of these particles on female fertility.
Although the researchers demonstrated that human macrophages engulf microplastics when cultured in lab dishes, researchers still don't know how readily the cells would do so in the body.
Perry plans to study samples taken from humans — specifically, how microplastics might contribute to atherosclerotic plaques that clog up blood vessels. It's already known that macrophages loaded with undigested material accumulate in these blood-flow-stopping plaques, so he and his colleagues hypothesize that microplastics may exacerbate the problem, he said.
This article is for informational purposes only and is not meant to offer medical advice.
Codo, A. C., Romero-Pichardo, J. E., Wang, Z., Aufiero, M. A., Lazarov, T., Saitz Rojas, W., Walker, N. S., Nair, A., Cole, R. F., Adkins, S., Dong, E., Fadojutimi, K., Martínez de la Torre, C., David, Y., Hohl, T. M., Geissmann, F., Keshari, K. R., Lucas, C. D., & Perry, J. S. A. (2026). Polystyrene microplastic-induced pathophysiology is driven by disruption of efferocytosis. Immunity, 59(3). https://doi.org/10.1016/j.immuni.2026.01.009

Kamal Nahas is a freelance contributor based in Oxford, U.K. His work has appeared in New Scientist, Science and The Scientist, among other outlets, and he mainly covers research on evolution, health and technology. He holds a PhD in pathology from the University of Cambridge and a master's degree in immunology from the University of Oxford. He currently works as a microscopist at the Diamond Light Source, the U.K.'s synchrotron. When he's not writing, you can find him hunting for fossils on the Jurassic Coast.
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