URBANA, Ill. (U.S.A.) -- Nanoplastics are everywhere. These fragments are so tiny they can accumulate on bacteria and be taken up by plant roots; they’re in our food, our water, and our bodies. Scientists don’t know the full extent of their impacts on our health, but new research from University of Illinois Urbana-Champaign food scientists suggests certain nanoplastics may make foodborne pathogens more virulent.
“Other studies have evaluated the interaction of nanoplastics and bacteria, but so far, ours is the first to look at the impacts of microplastics and nanoplastics on human pathogenic bacteria. We focused on one of the key pathogens implicated in outbreaks of foodborne illness — E. coli O157:H7,” said senior study author Pratik Banerjee, associate professor in the Department of Food Science and Human Nutrition and an Illinois Extension Specialist; both units are part of the College of Agricultural, Consumer and Environmental Sciences at Illinois.
Banerjee’s team found that nanoplastics with positively charged surfaces were more likely to cause physiological stress in E. coli O157:H7. Just as a stressed dog is more likely to bite, the stressed bacteria became more virulent, pumping out more Shiga-like toxin, the chemical that causes illness in humans.
The researchers expected positively charged nanoplastics to impact E. coli because the bacteria’s surface carries a negative charge. To test their opposites-attract hypothesis, they created nanoplastics from polystyrene — the material in those ubiquitous white clamshell-style takeout boxes — and applied positive, neutral, or negative charges before introducing the particles to E. coli either free-floating in solution or in biofilms.
“We started with the surface charge. Plastics have an enormous ability to adsorb chemicals. Each chemical has a different effect on surface charge, based on how much chemical is adsorbed and on what kind of plastic,” Banerjee said. “We didn’t look at the effects of the chemicals themselves in this paper — that’s our next study — but this is the first step in understanding how the surface charge of plastics impacts pathogenic E. coli response.”
The bacteria exposed to positively charged nanoplastics showed stress in multiple ways, not just by producing more Shiga-like toxin. They also took longer to multiply when free-floating and congregated into biofilms more slowly. However, growth eventually rebounded.
Biofilms give bacterial cells a measure of protection thanks to an extracellular coating they develop. To test whether this coating protected against nanoplastic-induced stress, the team dunked comparatively large microplastic particles into the bacterial soup and gave E. coli a week or two to colonize. Then, they introduced the same charged nanoplastics.
The positively charged particles still caused stress — and enhanced Shiga-like toxin production — in biofilm-bound E. coli.
“Biofilms are a very robust bacterial structure and are hard to eradicate. They’re a big problem in the medical industry, forming on inserts like catheters or implants, and in the food industry,” Banerjee said. “One of our goals was to see what happens when this human pathogen, which is commonly transmitted via food, encounters these nanoplastics from the vantage point of a biofilm.”
Interactions with plastic particles may be doing more than increasing E. coli’s toxicity; other studies have shown biofilms on microplastics may serve as hotspots for the transfer of antibiotic resistance genes, making the bacteria harder to manage. Banerjee’s group has studies underway to look at resistance gene transfer and changes in virulence and transmission patterns of major foodborne pathogens in food products and other environments such as soil.
The study, “Nanoplastics-mediated physiologic and genomic responses in pathogenic Escherichia coli O157:H7,” is published in the Journal of Nanobiotechnology [DOI: 10.1186/s12951-025-03369-z]. The research was supported in part by a USDA National Institute of Food and Agriculture grant [# ILLU-698-981].
Banerjee is also affiliated with the Carl R. Woese Institute for Genomic Biology and the Center for South Asian and Middle Eastern Studies at U. of I.