Microplastics and polycyclic aromatic hydrocarbons frequently co-occur in aquatic and terrestrial ecosystems, where their combined biological effects remain incompletely understood. Although both stressors exhibit well-documented individual toxicities, co-exposure studies report highly variable outcomes, ranging from enhanced or reduced toxicity to neutral responses. This review synthesizes findings from 45 peer-reviewed studies examining single and combined microplastic–PAH exposures across aquatic vertebrates, invertebrates, plants, microorganisms, and cell-based systems. Rather than introducing novel toxic mechanisms, microplastics primarily modulate the probability, magnitude, and timing of conserved biological response pathways. Across taxa, oxidative stress, metabolic disruption, immune modulation, developmental impairment, and behavioral alterations emerge as recurrent endpoints, with responses strongly shaped by context. Particle size, polymer type, exposure concentration and duration, and organismal traits consistently determine whether microplastics enhance PAH bioavailability, reduce effective exposure through sorption, or result in mixed or negligible effects. Overall, the evidence indicates that microplastics function as dynamic modifiers of chemical stress rather than universal toxicity amplifiers. These findings underscore the limitations of single-contaminant risk frameworks and highlight the need for biology-centered, mixture-based approaches that account for exposure pathways, life-history traits, and conserved stress-response systems in ecological risk assessment.
Arcadio et al. (Wed,) studied this question.