Microplastics Can Silence or Sharpen a Toxic Pollutant in Freshwater Algae

A new study has revealed a strikingly counterintuitive relationship between two of the world’s most ubiquitous aquatic pollutants: depending on how much plastic is in the water, microplastics can either amplify or neutralize the toxicity of benzo[a]pyrene, one of the most dangerous hydrocarbons contaminating freshwater ecosystems. The research, conducted by a Brazilian team of ecotoxicologists and published in the journal Ecotoxicology, focused on the green microalga Raphidocelis subcapitata, a cornerstone species at the base of aquatic food webs. The findings suggest that ecological risk assessments built on the assumption that contaminants act independently may substantially misjudge the real dangers facing freshwater environments.

Benzo[a]pyrene, often abbreviated BaP, belongs to the polycyclic aromatic hydrocarbons, a family of compounds assembled from fused aromatic rings and generated mainly by the combustion of fossil fuels, plant biomass, and petroleum derivatives. These molecules are persistent, highly lipophilic, and notorious for their affinity for particulate surfaces. In aquatic organisms they are associated with narcosis, cardiac dysfunction, mutagenicity, and carcinogenicity, and BaP in particular ranks among the most potent genotoxic and bioaccumulative agents known in aquatic toxicology. Microplastics, meanwhile, have become so widespread that measuring their effects in isolation increasingly misses the point. Contaminants in rivers and lakes rarely arrive alone, and microplastic particles, with their vast hydrophobic surface areas, are prime candidates to interact chemically with hydrocarbons dissolved in the water.

The research team, led by Yuuri Gabriel de Souza Santos of Universidade Santa Cecília together with colleagues from Universidade Santa Cecília and the Universidade Federal de São Paulo, designed a full-factorial exposure experiment to disentangle these interactions. Cultures of Raphidocelis subcapitata were exposed for 72 hours under tightly controlled conditions of temperature, light, and agitation to low-density polyethylene microplastics at three concentrations: 5, 50, and 500 milligrams per liter. The lowest of these reflects concentrations actually reported in freshwater environments, while the higher doses were intended to simulate more extreme pollution scenarios. Each microplastic treatment was tested alone and in combination with the median effective concentration of BaP, the dose that inhibits algal growth by fifty percent, which the team first determined experimentally for this species.

That determination produced a sobering baseline. The calculated EC50 for BaP in R. subcapitata was approximately 21 micrograms per liter, with a 95 percent confidence interval of 20 to 25 micrograms per liter. Even the lowest concentration tested, 3 micrograms per liter, caused statistically significant growth inhibition, marking it as the lowest observed effect concentration under the study’s conditions. At the highest dose of 39 micrograms per liter, growth inhibition approached 90 percent. The estimated EC50 falls squarely within the range of BaP concentrations documented in contaminated freshwater systems worldwide, where water column values typically span from less than a hundredth of a microgram to roughly 2.4 micrograms per liter, and sediments can hold far higher burdens. In other words, the toxicological benchmark established in the laboratory is uncomfortably close to what polluted rivers actually deliver.

The mechanism behind BaP’s damage to algae is thought to involve both photosynthetic disruption and direct membrane interactions. As a lipophilic compound, BaP binds readily to the lipid bilayers of algal cells, and polycyclic aromatic hydrocarbons can drive excessive production of reactive oxygen species through interference with cellular electron transport. Prior work has also shown that high hydrocarbon loads impair chlorophyll production, starving cells of photosynthetic capacity. Intriguingly, during routine microscopic examination the researchers occasionally observed clumps of lipids forming on the outer surfaces of BaP-exposed cells, a response consistent with previous reports that green algae increase membrane lipids as a defensive strategy against cytotoxic hydrocarbon damage.

When the microplastics were tested on their own, the results defied simple dose-response logic. At 5 and 50 milligrams per liter, the polyethylene particles significantly reduced algal density, an effect the authors attribute largely to chemical additives incorporated into the polymer, such as plasticizers, antioxidants, UV stabilizers, lubricants, and pigments. Because these additives are not covalently bound to the plastic matrix, they can leach into the surrounding water and exert their own toxicity; benzotriazole UV stabilizers, for example, have previously been shown to harm the freshwater alga Chlamydomonas reinhardtii. Yet at 500 milligrams per liter, toxicity vanished entirely and algal biomass actually exceeded the control by 3.7 percent, surpassing the lower-dose treatments by more than 40 percent. The most plausible explanation is that the enormous particle surface area at high concentrations provided an ideal substrate for biofilm formation, effectively turning the plastic into a growth platform for the microorganisms it would otherwise harm.

The combined exposures produced the study’s most consequential findings. BaP alone at 21 micrograms per liter inhibited roughly 57.6 percent of algal growth. But when the same BaP concentration was paired with 50 or 500 milligrams per liter of microplastics, inhibition dropped sharply to about 34.9 and 22.8 percent respectively, both statistically distinct from BaP alone. The interpretation is that at these higher particle densities, the hydrophobic hydrocarbon preferentially sorbs onto plastic surfaces, sequestering it away from the water column and lowering its effective bioavailability to the algae. This protective sorption effect mirrors previous observations in gammarids, cladocerans, sea urchins, and mysids, and echoes a study of juvenile common gobies in which microplastics delayed pyrene-induced mortality from 48 to 60 hours. Plastic, in these scenarios, acts as a temporary chemical sponge.

At the environmentally relevant concentration, however, the picture reversed into genuine concern. When just 5 milligrams per liter of microplastics accompanied the BaP, inhibition remained essentially unchanged from BaP alone, at about 58.3 percent, and both treatments were significantly more toxic than controls. This dose of plastic was evidently too low to strip a meaningful fraction of BaP from solution, leaving the hydrocarbon free to attack cell membranes. Since 5 milligrams per liter reflects concentrations documented in real freshwater systems, the message for regulators is troubling: at realistic pollution levels, microplastics do nothing to buffer hydrocarbon toxicity, while the plastic itself independently inhibits growth at that same dose.

The authors emphasize that this is the first study to evaluate combined BaP and microplastic effects in Raphidocelis subcapitata, and that their generalized linear model analyses confirmed a statistically significant interaction between the two contaminants, meaning the impact of each depends on the level of the other. The relationship is explicitly nonlinear: microplastics can either enhance or mitigate BaP toxicity depending on their concentration, rendering simple additive assumptions obsolete. Fourier transform infrared spectroscopy confirmed the test particles were linear low-density polyethylene, the polymer characteristically identified by split methylene peaks and methyl-group bands in its spectrum, matching the manufacturer’s specification.

The ecological stakes extend well beyond a single algal species. As primary producers, freshwater microalgae drive oxygen production, nutrient cycling, and energy transfer through food webs, and both microplastics and hydrocarbons can bioaccumulate in algal cells before moving to higher trophic levels. Green algae such as R. subcapitata are also valued agents of PAH bioremediation, and the new results raise questions about whether plastic contamination could undermine that cleanup capacity by altering hydrocarbon bioavailability. The authors acknowledge limitations: BaP adsorption onto the particles was not directly quantified, and responses such as chlorophyll content, oxidative stress, and gene expression were not measured. Notably, prior work on marine invertebrates found that even when survival appeared unaffected by combined exposures, surviving organisms carried DNA damage and elevated lipid peroxidation, hinting that growth-based endpoints may understate harm. The team calls for future research on chronic effects, trophic transfer, and additional freshwater species under environmentally realistic conditions, and concludes that microplastics cannot be treated as inert particles in aquatic systems. Their concentration, not merely their presence, may determine whether they worsen or mask the toxicity of the organic pollutants they travel with.

Subject of Research: Interactive toxicity of low-density polyethylene microplastics and benzo[a]pyrene in the freshwater microalga Raphidocelis subcapitata

Article Title: Interactive effects of low-density polyethylene microplastics and benzo[a]pyrene on the growth of the freshwater microalgae Raphidocelis subcapitata

Article References: de Souza Santos, Y. G., Choueri, R. B., Nobre, C. R., Simões, F. R., & Gusso-Choueri, P. K. (2026). Interactive effects of low-density polyethylene microplastics and benzo[a]pyrene on the growth of the freshwater microalgae Raphidocelis subcapitata. Ecotoxicology, 35(7), Article 161. https://doi.org/10.1007/s10646-026-03143-3

Image Credits: AI Generated

DOI: 10.1007/s10646-026-03143-3

Keywords: microplastics, benzo[a]pyrene, Raphidocelis subcapitata, freshwater ecotoxicology, polycyclic aromatic hydrocarbons, low-density polyethylene, algal growth inhibition, bioavailability, sorption, additive leaching, biofilm formation, ecological risk assessment