Recent advances in understanding the impact of microplastics on bacterial antibiotic resistance: mechanisms, evidence gaps, and One Health implications

Microplastic (MP) pollution and bacterial antimicrobial resistance are converging public health concerns. MPs provide persistent, mobile surfaces that can transport antibiotic-resistant bacteria and antibiotic resistance genes (ARGs). After aging and conditioning, MPs can develop biofilms in which resistance determinants accumulate, persist, and undergo horizontal transfer. This review conceptualizes MPs as mobile evolutionary interfaces and examines how particle properties and environmental conditions shape these processes. MP-associated biofilms increase cell density, retain extracellular DNA, and promote intercellular contact, facilitating plasmid conjugation and, in some experimental systems, transformation. Adsorbed antibiotics, metals, biocides, and plastic additives may exert selective or co-selective pressures, while oxidative stress, membrane perturbation, and SOS responses may alter gene-transfer potential. Studies of conventional and biodegradable MPs report enrichment of ARGs, MGEs, virulence-associated genes, and potential pathogens, however, neither enrichment nor biodegradability alone establishes health risk. Reports effects vary with polymer chemistry, particle size, concentration, aging, and microbial community composition. Evidence from wastewater, freshwater, estuarine, aquaculture, agricultural, landfill, food-processing, and tire-wear settings is organized within a six-level an evidence-to-risk framework, supplemented by comparisons of reported effect sizes. Field observations primarily demonstrate particle occurrence and ecological enrichment, whereas direct transfer is most convincingly shown in defined experimental systems; exposure-to-disease attribution remains unresolved. Future studies and One Health monitoring should prioritize realistic particle mixtures, standardized ARG quantification, linkage of resistance genes to viable bacterial hosts, and experimental confirmation of gene transfer under relevant conditions. Distinguishing molecular detection from functional spread is essential to avoid equating ARG presence with immediate clinical risk.