# Microplastics as a Modifier of Polycyclic Aromatic Hydrocarbon (PAH) Toxicity: A Review on Context-Dependent Effects Across Organisms

**Authors:** Cris Gel Loui A. Arcadio, Jay Rumen U. Maglupay, Andros M. Po, Jhosin Jaik B. Pardillo, Hernando P. Bacosa

PMC · DOI: 10.3390/biology15060455 · Biology · 2026-03-11

## TL;DR

Microplastics can change how harmful certain chemicals are to organisms, depending on factors like plastic type and exposure conditions.

## Contribution

The study reveals that microplastics act as dynamic modifiers of chemical toxicity rather than universal amplifiers.

## Key findings

- Microplastics modulate biological responses by altering chemical exposure rather than introducing new toxic mechanisms.
- Outcomes depend on plastic size, polymer type, exposure conditions, and organism traits.
- Findings suggest a need for biology-centered approaches in assessing environmental risks.

## Abstract

Microplastics and toxic chemicals called polycyclic aromatic hydrocarbons are now found together in water, soil, and living organisms. Scientists are concerned because plastics can carry these chemicals and may change how harmful they are to plants and animals. However, past studies have reported different results, making it unclear whether plastics always make chemical pollution more dangerous. This review aimed to understand why these differences occur by examining how living organisms respond when exposed to plastics and these chemicals at the same time. By comparing studies across fish, plants, and microorganisms, we found that plastics do not create new types of harm but instead change how often and how strongly normal stress responses in living organisms are triggered. Sometimes plastics increase harm by helping chemicals enter the body, while in other cases they reduce harm by trapping chemicals and limiting exposure. The outcome depends on the size and type of plastic, how exposure occurs, and the traits of the organism. These findings help explain conflicting results in earlier studies and support more realistic approaches to studying pollution. This knowledge is valuable to society because it improves how environmental risks are assessed and supports better decisions to protect ecosystems and human health.

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.

## Full-text entities

- **Genes:** cyp1a (cytochrome P450, family 1, subfamily A) [NCBI Gene 140634] {aka cyp1a1, wu:fb63b04, zfCYP1A, zgc:109747}
- **Diseases:** immune impairment (MESH:D020274), alterations (MESH:D004408), injury to (MESH:D014947), developmental abnormalities (MESH:D006130), inflammation (MESH:D007249), developmental defects (MESH:D000094602), developmental impairment (MESH:D007805), carcinogenic (MESH:D011230), developmental and physiological impairments (MESH:D012735), neurotoxicity (MESH:D020258), Toxic (MESH:D064420), immunological impairment (MESH:D007154), cardiotoxicity (MESH:D066126)
- **Chemicals:** benzo[a]pyrene (MESH:D001564), PVC (MESH:D011143), PE (MESH:D020959), oxygen (MESH:D010100), PS (MESH:D011137), Polymer (MESH:D011108), plastics (MESH:D010969), fluoranthene (MESH:C007738), reactive oxygen species (MESH:D017382), MP-PAH (-), phenanthrene (MESH:C031181), benz[a]anthracene (MESH:C030935), chrysene (MESH:C031180), lipid (MESH:D008055), water (MESH:D014867), PAH (MESH:D011084), MP (MESH:D000080545), PP (MESH:D011126), pyrene (MESH:C030984)
- **Species:** Glycine max (soybean, species) [taxon 3847], Triticum aestivum (bread wheat, species) [taxon 4565], Oryzias melastigma (Indian medaka, species) [taxon 30732], Danio rerio (leopard danio, species) [taxon 7955], Ipomoea aquatica (Chinese water-spinach, species) [taxon 89636], Zea mays (maize, species) [taxon 4577], Lolium perenne (perennial ryegrass, species) [taxon 4522], Skeletonema costatum (species) [taxon 2843], Carassius auratus (goldfish, species) [taxon 7957], Daphnia magna (species) [taxon 35525], Spinacia oleracea (spinach, species) [taxon 3562], Pinna nobilis (species) [taxon 111169], Tegillarca granosa (species) [taxon 220873], Lates calcarifer (Asian seabass, species) [taxon 8187], Ruditapes philippinarum (Japanese littleneck, species) [taxon 129788], Phaeodactylum tricornutum (species) [taxon 2850], Oryzias latipes (Japanese medaka, species) [taxon 8090], Hediste diversicolor (species) [taxon 126592], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13023439/full.md

## References

129 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023439/full.md

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Source: https://tomesphere.com/paper/PMC13023439