When Sunlight Makes Plastic More Toxic: A Mussel Study

Plastic in the ocean does not stay the same plastic. Sunlight, waves, salt, and microbes slowly break it down — and a 2025 study suggests that this weathering does not just make plastic smaller. It can make it more toxic.

Researchers exposed the Pacific mussel Mytilus trossulus to microparticles of polymethylmethacrylate (PMMA), a common acrylic plastic, in both fresh form and after 120 hours of UV irradiation. The aged particles caused more DNA damage and more cellular stress than the fresh ones. [Toxics, 2025]

That distinction matters. Most microplastic toxicity research uses pristine, factory-fresh particles — but the plastic actually floating in the sea has been weathering for months or years. This study is a direct look at what that aging does.

Why acrylic plastic deserves attention

PMMA sits alongside polystyrene, polyethylene, and polypropylene as one of the plastics widely present in the environment. It shows up in marine debris because of how heavily it is used: optical lenses, touch screens, appliances, paint resins, abrasives, cosmetics, and prosthetic materials. [Toxics, 2025]

Yet it is less studied than those other polymers. That gap matters because PMMA is not chemically neutral. It is a product of the polymerization of acrylic acid derivatives, which are toxic, and PMMA itself is classified under current schemes as a potentially hazardous polymer. [Toxics, 2025]

Filter-feeding mussels are a logical test organism. By pushing large volumes of seawater through their gills, they concentrate micro- and nanoplastics, which can pass into the circulating hemolymph and accumulate in the digestive system. [Toxics, 2025]

What UV light did to the plastic

Before testing toxicity, the researchers characterized how the plastic itself changed. They irradiated PMMA granules for 120 hours under a UV lamp, then analyzed the particles with Fourier transform infrared spectroscopy (FTIR) and a laser diffraction particle analyzer.

The chemical signature shifted. The oxidation index — a measure of oxygen-containing groups in the polymer — rose from 5.15 ± 0.54 in fresh PMMA to 6.83 ± 0.46 after irradiation, an increase of almost 25%. That reflects oxidative degradation of the polymer chains. [Toxics, 2025]

~25%

The size distribution changed too. After irradiation, the proportion of large particles (500–1000 µm) fell, while the number of the smallest particles (50–125 µm) increased significantly — roughly twofold. [Toxics, 2025] Smaller particles are more bioavailable, meaning more of the aged plastic falls into the size range a mussel can actually take up.

Cell viability: lysosomes under strain

The team measured cell health using the neutral red retention assay, which tracks how well living cells hold dye inside their lysosomes. Damaged cells leak; dead cells don’t retain dye at all.

Both fresh and aged PMMA reduced dye retention in hemocytes — the mussel’s immune cells — to similar levels (55.2 ± 3.24% and 61.1 ± 1.99% of control, respectively). [Toxics, 2025] Hemocytes react instantly to foreign material, so a strong response there is expected.

The revealing difference appeared in gill and digestive gland cells. There, aged PMMA-UV reduced lysosomal membrane stability significantly more than fresh PMMA did. [Toxics, 2025] Because lysosomal membranes are highly sensitive to oxidative stress, and their destabilization can raise the risk to cell survival and even trigger apoptosis, this is a meaningful signal that the weathered particles are more damaging at the cellular level. [Toxics, 2025]

The DNA damage signal

The clearest evidence of increased toxicity came from the comet assay, which measures nuclear DNA fragmentation.

Fresh PMMA already raised DNA damage well above control levels across all three tissues: 19.0 ± 1.3% in the digestive gland, 10.1 ± 1.4% in hemocytes, and 7.8 ± 1.1% in gills, versus control values of 5.1%, 3.6%, and 4.6% respectively. [Toxics, 2025]

Aged PMMA-UV pushed those numbers higher. The effect was most pronounced in gill cells, where DNA damage reached 14.4 ± 2.9% — nearly double the damage from fresh particles. [Toxics, 2025]

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The distribution of damage tells the story more starkly than the averages. In mussels exposed to fresh PMMA, gill cells with more than 20% DNA damage made up no more than 5–6% of the population. After exposure to aged PMMA-UV, that fraction rose to 27%. And a population of severely damaged cells (>30% DNA in the comet tail) appeared only after aged-particle exposure — such cells were absent in mussels exposed to fresh PMMA. [Toxics, 2025]

A more complicated picture: the oxidative stress markers

Here is where the study earns credibility by not overselling itself. The biochemical stress markers did not line up cleanly, and the authors say so.

The response was tissue-specific. Integral antiradical activity — the cells’ capacity to neutralize peroxyl radicals — rose sharply in the digestive gland (by roughly 2× with fresh PMMA and 1.3× with aged PMMA versus control) but only slightly, and not significantly, in gill cells. [Toxics, 2025] Malondialdehyde, a marker of lipid peroxidation, rose in the gills after both exposures, but in the digestive gland it increased only after fresh PMMA. [Toxics, 2025]

This is worth sitting with. The headline — UV makes PMMA more toxic — holds for cell viability and DNA damage. But it is not a uniform effect across every biological measure, and the tissue-by-tissue variation suggests the mechanisms are still being worked out.

What this study does and doesn’t show

This is, by the authors’ account, the first study to demonstrate that UV exposure increases PMMA toxicity to M. trossulus, and it points to physicochemical changes in the plastic — oxidation and fragmentation — as the likely driver. [Toxics, 2025]

But the limits are real. The exposure concentration was 20 mg/L, which the authors themselves describe as an elevated level rather than a measured environmental one. They note that the genome’s vulnerability may persist at concentrations closer to ecologically relevant ones, citing a meta-analysis of microplastic genotoxicity, but that is an inference, not a direct measurement in this experiment. [Toxics, 2025] The study ran for 72 hours on a single mussel species in the lab. It is a mechanistic finding about how weathered plastic behaves in shellfish cells — not a measurement of ocean-scale risk, and not a human health study.

The practical takeaway

The useful idea to carry away is conceptual, not a shopping instruction. When we picture microplastic pollution, it is tempting to imagine inert fragments simply getting smaller. This study suggests weathering does two things at once: it multiplies the number of bioavailable particles and it chemically alters them in ways that raise their biological activity. [Toxics, 2025]

For anyone weighing the long-term footprint of plastic in the environment, that reframes the problem. The plastic already in the ocean is not static. Sunlight is not just breaking it down — under the conditions tested here, it is making acrylic microparticles both more abundant at bioavailable sizes and more genotoxic to the shellfish that filter our coastal waters. Understanding future risk, the authors argue, means studying not just how much plastic is out there, but how far it has weathered. [Toxics, 2025]