Washington, D.C.—Microplastics are not just pollutants, but also highly complex materials that facilitate antimicrobial resistance, even without antibiotics, according to a new study. The findings were published in Applied and Environmental Microbiology, a journal of the American Society for Microbiology.
“Addressing plastic pollution isn’t just an environmental issue—it’s a critical public health priority in the fight against drug-resistant infections,” said lead study author Neila Gross, a Ph.D. candidate in the lab of Professor Muhammad Zaman at Boston University.
As global plastic use has surged, microplastic contamination has become widespread, with wastewater emerging as a major reservoir. At the same time, antimicrobial resistance (AMR) is rising globally, with environmental factors playing a key role. Microplastics are well known to harbor bacterial communities on their surfaces—the “plastisphere.”
In the new study, researchers sought to quantify AMR at clinically relevant levels and explore how microplastic characteristics influence AMR development. The researchers used different plastic types (polystyrene, such as the packing peanuts used for shipping; polyethylene, found in plastic zip-top bags; and polypropylene, which is found in crates, bottles and jars) and sizes (from half a millimeter to 10 micrometers—similar scale to a typical bacterium) and incubated them with Escherichia coli for 10 days. Every 2 days, the researchers checked the minimum inhibitory concentrations (MICs), or how much antibiotic is required to kill an infection, for 4 widely used antibiotics to determine if the bacteria were growing in resistance or not.
The researchers found that microplastics, regardless of the tested size and concentration, facilitated multidrug resistance in 4 tested antibiotics (ampicillin, ciprofloxacin, doxycycline and streptomycin) in E. coli within 5-10 days of exposure.
The researchers demonstrated that microplastics alone can facilitate increased AMR development. “This means that microplastics substantially increase the risk of antibiotics becoming ineffective for a variety of high impact infections,” Gross said. Prior research primarily focused on antibiotic-driven resistance, without considering the role of environmental pollutants like microplastics. Studies with microplastics looked mostly at resistance factors such as antibiotic-resistant genes (ARGs) and biofilms, not the rate or magnitude of AMR via their minimum inhibitory concentration to different antibiotics.
The researchers found that resistance induced by microplastics and antibiotics was often significant, measurable and stable, even after antibiotics and microplastics were removed from the bacteria. Ultimately, this means that microplastic exposure may select for genotypic or phenotypic traits that maintain antimicrobial resistance, independent of antibiotic pressure.
“Our findings reveal that microplastics actively drive antimicrobial resistance development in E. coli, even in the absence of antibiotics, with resistance persisting beyond antibiotic and microplastic exposure,” Gross said. “This challenges the notion that microplastics are merely passive carriers of resistant bacteria and highlights their role as active hotspots for antimicrobial resistance evolution.” Given that polystyrene microplastics facilitated the highest levels of resistance, and that biofilm formation—known to enhance bacterial survival and drug resistance—was a key mechanism, the results underscore the urgent need to address microplastics pollution in antimicrobial resistance mitigation efforts.
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Journal
Applied and Environmental Microbiology