The interplay between antimicrobial resistance, heavy metal pollution, and the role of microplastics Original paper

What was reviewed?

This paper reviewed how heavy metals and microplastics jointly intensify antimicrobial resistance (AMR) in environmental microbiomes by promoting co-selection, cross-resistance, and horizontal gene transfer. The authors framed heavy metals as long-standing evolutionary pressures that predate antibiotics and described microplastics as newer, widespread “substrates” that concentrate microbes into biofilms and accelerate gene exchange, especially in soil, rivers, drinking-water distribution biofilms, and landfill leachate reservoirs where resistance determinants can persist and spread.

Who was reviewed?

Rather than focusing on a single patient group, the review synthesized evidence across microbial communities and taxa that occupy contaminated water and soil interfaces, including biofilm-associated bacteria on microplastics (the “plastisphere”) and organisms in anthropogenically impacted systems such as wastewater-affected rivers and landfill leachates. It highlighted clinically relevant spillover risk by repeatedly tying environmental selection to opportunistic and foodborne pathogens that can colonize humans through water and food chains, including genera such as Escherichia, Klebsiella, Shigella, Salmonella, Vibrio, Campylobacter, Listeria, and Pseudomonas when they acquire or enrich resistance traits in these niches.

What were the most important findings?

The review’s core finding is that heavy metals (notably Pb, Hg, As, Cr, Cd, and Ni) and microplastics act as synergistic upstream drivers of AMR by selecting for resistance systems that also protect against antibiotics, then packaging these traits into mobile genetic elements that move across communities. It connected major microbial associations to resistance “signatures,” emphasizing that microplastics foster dense biofilms that function as genetic exchange hotspots, while metals increase selection pressure and can upregulate multidrug efflux and stress-response regulators that broaden resistance. It repeatedly pointed to coupled ARG–MRG patterns, including integron involvement (e.g., intI1) and co-occurrence between metal resistance determinants such as czcA/rcnA and antibiotic resistance classes such as β-lactamases and multidrug resistance, and it cited landfill leachate and river systems as reservoirs where genes like aadA, blaCTX-M/blaSHV, ermB, mefA, tetM/tetQ, and sul1/sul2 track with metal burdens. It also reinforced that community structure matters: the review described enrichment of potential pathogens in plastisphere communities and reported that taxa such as Pseudomonadota (Proteobacteria) frequently carry ARG–MRG combinations, consistent with a “hub” role for gene sharing under mixed-pollutant exposure.

What are the greatest implications of this review?

For clinicians, the main implication is that AMR risk does not originate only from antibiotic exposure; environmental co-exposures can amplify resistant pathogens and resistance genes before patients ever enter care. The review supports treating microplastics and heavy metals as actionable upstream levers in a One Health framework because reducing these exposures can plausibly reduce ARG abundance, slow resistance dissemination, and limit the environmental “seeding” of opportunistic pathogens that later cause hard-to-treat infections. Practically, it strengthens the rationale for integrating environmental surveillance (water systems, agricultural soils, landfill leachate, and food-production settings) into AMR prevention strategies, because these compartments can maintain and distribute clinically relevant resistance profiles through biofilms, mobile elements, and pollutant-driven selection even when antibiotic pressure appears low.