Abstract
Plastic residues have become a persistent structural component of arable land, and the microbial films that develop on their surfaces have been proposed as concentrated sites for the accumulation and exchange of antibiotic resistance genes. This review critically examines the evidence that microplastics act as hotspots for antibiotic resistance gene dissemination in agricultural soils, the mechanisms invoked to explain that behaviour, and the environmental and agronomic conditions that modulate it. Literature was identified through structured searching of open bibliographic and scholarly indexes, supplemented by backward and forward citation tracking and by checks for corrections and retractions, with priority given to soil-based experimental and field studies, mechanistic work on gene transfer, and multi-site surveys. The evidence consistently shows that plastic surfaces recruited from soil support communities that differ compositionally from the surrounding matrix and that carry a higher relative abundance of resistance determinants and mobile genetic elements. Confidence in the stronger interpretation, that plastic itself selects for resistance, is weaker. Comparisons are most often drawn between a colonised surface and bulk soil rather than against inert or natural particulate controls, and the single study identified that included wood and glass comparators found that a natural substrate enriched resistant organisms to a similar degree as polystyrene. Mechanistic support is strongest for physical proximity within biofilms, for host community reassembly towards taxa that already carry multidrug determinants, and for stress-mediated stimulation of conjugative transfer through reactive oxygen species and altered membrane permeability. Biodegradable polymers, rather than conventional ones, produce the largest and most reproducible increases in soil resistance gene abundance, which complicates their promotion as a straightforward substitute. Manure and long-term organic fertilisation, metal and biocide co-contamination, particle size, ageing and soil reaction emerge as the principal modulators. Translation from gene abundance to demonstrated resistance transfer into pathogens under field conditions remains unresolved, and quantitative risk statements should be treated as provisional.