The scale of the problem begins with plastic production itself. Since the mid-twentieth century, synthetic polymers such as polyethylene, polypropylene, polystyrene, polyvinyl chloride, and polyethylene terephthalate have been manufactured in enormous quantities, and a substantial fraction has escaped into the environment. Through ultraviolet radiation, mechanical abrasion, and thermal stress, larger plastic items fragment into microplastics, particles generally defined as smaller than five millimeters. Weathering does not merely shrink these materials; it fundamentally alters their surface chemistry. Oxidation introduces oxygen-containing functional groups onto polymer surfaces, increases surface area through cracking, and changes surface charge, all of which influence how strongly other molecules adhere to the plastic. The review emphasizes that aged, weathered microplastics often behave very differently from pristine laboratory particles, generally adsorbing contaminants more readily because of their roughened, chemically activated surfaces.

The chemistry of contaminant adsorption onto microplastics is governed by several interacting mechanisms. Hydrophobic organic contaminants, including polycyclic aromatic hydrocarbons, polychlorinated biphenyls, organochlorine pesticides such as DDT, and polybrominated diphenyl ethers, tend to partition onto the hydrophobic surfaces of polyethylene and polypropylene in much the same way they bind to soil organic matter. Heavy metals such as lead and cadmium interact through electrostatic attraction, surface complexation with oxidized functional groups, and, in some cases, bridging via biofilm exudates. Pharmaceuticals and antibiotics display variable behavior depending on water chemistry, pH, and ionic strength. Per- and polyfluoroalkyl substances, the so-called forever chemicals prized for their water and grease resistance, present a particular paradox: although their fluorinated tails repel both water and oil, certain PFAS compounds nonetheless adsorb appreciably to microplastic surfaces, particularly where biofilms have colonized the plastic and extracellular polymeric substances provide additional binding sites.

That last point highlights one of the most dynamic aspects of microplastic contamination: the plastisphere. When microplastics enter aquatic or terrestrial environments, they rapidly acquire microbial biofilms, creating a distinct ecological niche on an artificial substrate. These biofilms change the game in multiple ways. They add sticky extracellular polymeric substances that enhance the capture of both organic chemicals and metals, they can alter local pH and redox conditions at the plastic surface, and they facilitate horizontal gene transfer, raising concerns that microplastics act as vectors for antibiotic resistance genes. Recent in situ studies cited in the review show that biofilm development on microplastics measurably increases PFAS adsorption in aquatic environments, meaning that a plastic particle drifting through a river is not a chemically inert object but an evolving platform whose cargo changes over time.

Once contaminant-laden microplastics form, they become mobile. Ocean currents, riverine flow, atmospheric transport, and even agricultural practices such as the application of sewage sludge and plastic mulch films distribute these particles across the planet, including to remote regions such as Antarctica and the deep ocean. Atmospheric modeling has suggested that airborne transport is a major pathway delivering microplastics to distant ecosystems, and indoor air itself carries a significant load of textile-derived synthetic fibers. Along this journey, microplastics transfer their chemical cargo through food webs. Plankton ingest particles, small predators eat contaminated plankton, and trophic transfer compounds exposure at higher levels, a phenomenon documented in littoral predators and in commercially harvested seafood such as mussels and fish. Because many of the adsorbed pollutants are persistent, bioaccumulative, and toxic, the review notes that plastic-mediated transport can move chemicals to locations and organisms that would otherwise experience far lower exposures.

Human exposure occurs through three principal routes: ingestion, inhalation, and dermal contact. Microplastics have been detected in table salt, bottled water, beer, honey, and seafood, and food packaging is a recognized source of contamination. Indoor environments, where synthetic textiles shed fibers continuously, contribute substantially to inhalation exposure; breathing simulation studies using thermal manikins have quantified the inhalation of airborne microplastic fibers in realistic indoor settings. Perhaps more striking is the accumulating evidence that these particles penetrate deep into the human body. Researchers have identified microplastics in human blood, lung tissue obtained during bronchoscopy, cirrhotic liver tissue, human stool, breast milk, placenta, and even the oral cavity. Particle size is a critical determinant of fate: larger fragments are likely to pass through the gut, while micrometer-scale and nanoplastic particles can be internalized by intestinal M cells, cross epithelial barriers, be taken up by macrophages, and distribute to distant organs. In the respiratory tract, modeled deposition patterns suggest that inhaled particles settle in different airway regions depending on size and shape, with the smallest particles reaching the alveolar region.

The toxicological question that the review frames most carefully is whether microplastics serve as meaningful vectors for chemical exposure, or whether the chemicals they carry would enter the body anyway through water and food. Earlier critical work, notably a model-supported reinterpretation of empirical studies, argued that for many hydrophobic organic contaminants, transfer from ingested plastic is minor compared with other dietary routes. The new review does not dismiss that caution, but it highlights scenarios in which the carrier role could matter substantially. Laboratory studies simulating human digestion have shown that PAHs adsorbed on microplastics can desorb in the gastrointestinal tract, and heavy metals bound to plastics can similarly be released under the acidic, enzyme-rich conditions of the gut. Weathered particles with high contaminant loads, or particles that concentrate chemicals locally at epithelial surfaces, may deliver boluses of toxicants that chronic low-level background exposure does not. Combined particle-chemical exposure has been associated in cell and animal studies with oxidative stress, generation of reactive oxygen species, inflammatory signaling, intestinal barrier damage, and apoptosis, effects that may exceed the sum of exposures to particles and chemicals separately.

A distinctive contribution of the review is its argument for bringing physiologically based pharmacokinetic modeling, or PBPK, into microplastic risk assessment. PBPK models divide the body into tissue compartments and use physiological parameters, blood flows, and tissue partitioning to simulate how a chemical is absorbed, distributed, metabolized, and excreted. The approach is well established in pharmaceutical development and has been applied by the same research group to compounds such as diethyl phthalate, nonylphenol, and isothiazolinone preservatives. Applied to microplastics, such models could predict internal doses of both the particles themselves and the chemicals desorbing from them, bridging the gap between environmental concentrations measured in water, food, and air and the concentrations that actually reach target tissues. The authors argue that this modeling framework, combined with better data on desorption behavior under digestive and pulmonary conditions, is essential for moving the field from hazard identification toward quantitative human health risk assessment.

The implications extend beyond human toxicology to ecosystem management and policy. Microplastics in soil plastispheres have been identified as hotspots of antibiotic resistance genes, linking plastic pollution to one of the most pressing public health threats of the century. Tire wear particles, an often-overlooked category of microplastic pollution, add another contaminant stream to marine and freshwater systems. Because adsorption depends on polymer type, degree of weathering, and environmental chemistry, the review suggests that risk assessments relying on pristine, spherical, laboratory-grade particles may systematically misrepresent real-world exposures. Water treatment plants remove some microplastics, but the smallest fractions largely pass through conventional systems, and no current technology eliminates the chemical cargoes that particles carry once dispersed.

The authors conclude that microplastic-mediated contaminant exposure has become an emerging concern in environmental health sciences that demands integrated research approaches. Understanding the full risk requires connecting environmental chemistry, microbial ecology, toxicology, and human pharmacokinetics in a single analytical framework. As evidence of microplastics in human tissues continues to mount, the question is no longer whether people are exposed to these particles and their chemical hitchhikers, but how much of that combined exposure translates into internal dose and, ultimately, disease. The review makes clear that answering that question will require the kind of quantitative, mechanistic, cross-disciplinary effort that has transformed risk assessment in pharmaceutical science, now applied to one of the most diffuse pollution problems of the modern age.