A team led by Sunday Amos Onikanni of the Federal University of Rio de Janeiro, publishing in Environmental Science and Pollution Research, argues that the entire risk-assessment playbook for this chemical is outdated. Their central claim is provocative: Irgarol’s toxicity cannot be predicted from its measured concentration alone. Instead, the authors propose an Exposure–Transformation–Response (ETR) framework that treats toxicity as a dynamic ecological process, shaped by how long the compound persists, how it chemically transforms, how it moves between sediments, water, particles, and organisms, and how each species uniquely responds. The framework reframes a familiar regulatory assumption, that degradation equals detoxification, as a dangerous oversimplification.

The evidence for that reframing begins with the compound’s stubborn persistence. Unlike biocides engineered for rapid breakdown, Irgarol lingers in marina waters, estuarine sediments, and paint particulates, remaining bioavailable for years. Paint flakes and polymeric residues shed from hulls act as secondary reservoirs, slowly releasing the biocide long after its initial application. Field studies have detected Irgarol in sediments, porewaters, and coastal waters worldwide, and residues have now been found in geographically isolated regions, including remote and polar environments, far from any local source. Hydrodynamic transport carries dissolved and particle-bound Irgarol toward the open sea, while storms and tides churn it between the water column and underlying sediment. The result is a chemical whose exposure history in a given ecosystem cannot be captured by a single water sample.

Perhaps the most unsettling finding concerns what happens when Irgarol degrades. Photochemical and microbial processes convert it into metabolites, most notably M1, or descyclopropyl-Irgarol, which frequently persists alongside the parent compound. In several coastal ecosystems, M1 has been measured at concentrations equal to or exceeding those of Irgarol itself. These transformation products are not inert leftovers. Their altered structure changes polarity, partitioning behavior, sorption characteristics, and how they interact with biological targets. The review frames this as a chemical lineage: a parent molecule giving rise to a second generation of biologically active descendants with distinct mobility and toxicity. Monitoring programs that track only the parent compound may therefore systematically underestimate the true toxicological burden in the water.

Bioavailability, the authors argue, is not a fixed property of a molecule but a moving target that transformation continuously reshapes. Two ecosystems carrying identical total Irgarol burdens could present radically different biological risks depending on the transformation status of the contaminant pool. This is where microplastics enter the story with particular force. Antifouling paint releases polymer fragments that adsorb Irgarol, and aging processes such as ultraviolet exposure and biofilm formation roughen plastic surfaces, increasing chemical uptake. These particle-bound reservoirs shield the biocide from photodegradation, extend its residence time, and follow transport pathways similar to microplastics, including surface drift, long-range suspension, and vertical settling. When organisms ingest contaminated particles, the acidic, surfactant-rich environment of the gut promotes desorption, delivering higher internal doses than dissolved exposure alone would predict. Experiments and field surveys confirm that animals feeding on pollutant-laden particles accumulate more contaminant in their tissues than animals exposed to the same dissolved concentration.

The biological consequences reach far beyond photosynthetic inhibition. While Irgarol remains best known as a photosystem II poison that suppresses algal growth, emerging studies implicate it in endocrine disruption. Research on larval and juvenile fish shows altered thyroxine levels and suppressed expression of genes in the thyroid signaling axis, impairing growth and development. Other work links exposure to disrupted insulin signaling and lipid balance, suggesting effects on hormone receptors in nonphotosynthetic species. Irgarol and its transformation products also induce hepatic stress: elevated reactive oxygen species, lipid peroxidation, dysregulation of cytochrome P450 detoxification enzymes, and shifts in triglyceride and lipid profiles in exposed fish and bivalves. The structural resemblance between Irgarol and chlorinated s-triazine herbicides such as atrazine, a well-documented endocrine disruptor, raises the possibility that the triazine scaffold itself carries mechanistic risks beyond photosynthesis, a question the authors say demands urgent investigation.

The global monitoring record illustrates why a single regulatory threshold cannot capture this complexity. Surface waters in Southeast Florida have shown Irgarol concentrations up to 241 nanograms per liter, with submerged aquatic vegetation bioaccumulating both the parent compound and M1. In São Marcos Bay, Brazil, water concentrations ranged from below 0.8 to 89.4 nanograms per liter, yet researchers still classified the ecological risk as high because chronic exposure and sensitive primary producers amplify harm at low levels. By contrast, the Golden Horn Estuary in Turkey recorded 7.62 micrograms per liter, roughly thirty-two times the Florida maximum, and a 2026 assessment of Brazilian ports at São Luís, Santos, and São Vicente found surface water concentrations between 1.98 and 5.70 micrograms per liter, with species-sensitivity-distribution analysis flagging potential risks to primary producers. Environmentally relevant concentrations of 1 to 1000 nanograms per liter frequently exceed chronic effect thresholds for sensitive algae, whose no-observed-effect concentrations sit between 5 and 20 nanograms per liter, producing risk quotients above 1 in many maritime settings.

A regulatory paradox emerges from the Danish data. A survey of thirteen Danish marinas found Irgarol in every sediment sample but only half of the water samples, with concentrations lower than historical records, a decline attributed to the Danish and European Union bans in place since 2016. Yet sediment continues to act as a legacy reservoir, sustaining exposure through resuspension, diffusion, and benthic contact. The International Maritime Organization’s 2023 controls under the Anti-Fouling Systems Convention, which mandate removal or sealing of cybutryne-containing coatings, are expected to gradually reduce new inputs, but legacy coatings, shipyard residues, and environmental stability mean contamination will persist. Reduced usage, in other words, does not translate into a disappearing environmental burden. Meanwhile, a 2026 zebrafish study found that at environmentally relevant concentrations, Irgarol left survival, hatching, and morphology intact but measurably altered heart rate and swimming behavior, with larvae flipping from hyperactivity to hypoactivity after a recovery period, a reminder that sublethal endpoints often reveal harm before mortality does.

The ETR framework translates these findings into a concrete regulatory program. The authors propose complementing conventional metrics like predicted environmental concentrations and risk quotients with new indicators: a Transformation Burden Index combining parent compound and relevant metabolites, a Transformation Persistence Index, a Bioavailable Exposure Index, a Transformation Toxicity Ratio, and a Biological Response Index integrating molecular, organismal, and ecological data. A tiered monitoring scheme would start with routine parent-compound quantification, add targeted metabolite analysis, deploy suspect and non-target high-resolution mass spectrometry to catch emerging degradation products, and finish with effect-based assays testing whether transformation actually reduces biological activity. The framework extends naturally to replacement biocides such as diuron, DCOIT, chlorothalonil, dichlofluanid, and pyrithiones, whose transformation pathways deserve prospective evaluation before substitution is assumed to be safe. The deeper lesson reaches beyond one chemical: environmental contaminants are not static entities whose risks are fixed at release. They evolve, and twenty-first-century stewardship, the authors conclude, must shift from controlling chemical residues to managing chemical development, treating risk as a trajectory rather than a threshold, and grounding the next generation of antifouling design in transformation-safe, systems-level toxicology.

Subject of Research: Environmental persistence, transformation products, and human exposure risks of the antifouling biocide Irgarol

Article Title: Rethinking Irgarol toxicity: a unified framework linking environmental fate, bioactivity, and human exposure

Article References: Onikanni, S. A., Ropke, R., Olayinka, O. S., Murucci, M. D., Aribigbola, T., Fortunato, R. S., Dao, T. N. P., de Carvalho, D. P., Amos, O. E., Openiyi, E. O., Soares, P., & Miranda-Alves, L. (2026). Rethinking Irgarol toxicity: a unified framework linking environmental fate, bioactivity, and human exposure. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38294-7

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38294-7

Keywords: Irgarol 1051, antifouling biocides, transformation products, endocrine disruption, microplastics, environmental persistence, ecotoxicology, photosystem II inhibition, sediment contamination, risk assessment, maritime pollution, systems toxicology

The story begins with biofouling, the relentless settlement of organisms on any submerged surface. On commercial vessels, fouling can increase fuel consumption by up to 40 percent, accelerate hull corrosion, and hitchhike invasive species across the globe along shipping routes. To fight it, the shipping industry turned to antifouling paints, first based on copper and zinc oxides, then on organotin compounds such as tributyltin. TBT was devastatingly effective but also devastatingly toxic, inducing imposex in gastropods and wreaking hormonal havoc in ship traffic zones, which led the International Maritime Organization to ban it. The replacements, a new generation of so-called booster biocides including Irgarol, Diuron, DCOIT, chlorothalonil, and dichlofluanid, were assumed to be safer. Whether that assumption holds for tropical ecosystems has remained largely untested.

Dichlofluanid, formally N-dichlorofluoromethythio-N′,N′-dimethyl-N-phenylsulfamide, is a non-metallic organochlorine compound with low water solubility and a strong tendency to associate with particles, reflected in its octanol-water partition coefficient of 3.7. It is also used as a fungicide and has previously been linked to mutagenic and carcinogenic effects in non-target marine invertebrates. Because it degrades rapidly in water, with a half-life of just a few hours and by-products including DMSA and dichloromethane aniline, organisms in ports and marinas are exposed to a shifting cocktail of the parent compound and its transformation products. Yet toxicity data for tropical species, which may be more sensitive to contaminants than their temperate counterparts, have been scarce.

To fill that gap, a team led by Ana Carolina Feitosa Cruz of São Paulo State University designed a two-pronged experiment. In the water-based arm, brown mussels Perna perna, a classic sentinel species sourced from an aquaculture farm at Cocanha Beach, were exposed for 96 hours to five nominal dichlofluanid concentrations ranging from 0.01 to 100 micrograms per liter, a span that brackets measured environmental levels of up to 3.37 micrograms per liter in seawater. Solutions were renewed every 24 hours to mimic the dynamic exposure that rapid degradation creates in nature. In the sediment arm, clams Anomalocardia flexuosa, collected from the Cananéia region, spent 21 days in sediments spiked with 1 to 10,000 nanograms per gram of the biocide. Crucially, the researchers used two sediment types from the protected Cananéia-Iguape Peruíbe Estuarine Complex: one with roughly 4 percent organic matter and another with about 10 percent, to test whether organic carbon changes the story.

The team then read the animals’ biochemical diaries through a battery of biomarkers. In mussels, the neutral red retention time assay revealed that hemocyte lysosomes, the cellular recycling centers whose membrane stability is a frontline indicator of chemical stress, lost integrity at 10 and 100 micrograms per liter after 96 hours. Retention times fell from 97.5 minutes in the acetone control to 33 and 15 minutes respectively, a dose-dependent collapse of lysosomal stability. Notably, the authors point out that TBT produced cytotoxicity in the mussel Mytilus edulis at concentrations above 0.5 micrograms per liter, suggesting dichlofluanid is less acutely cytotoxic than its banned predecessor, though still far from benign.

The biochemical picture in mussels was one of a defense system working overtime. Glutathione S-transferase activity rose in the digestive glands at the highest concentrations, while gills responded with elevated glutathione levels and glutathione peroxidase activity. This makes mechanistic sense: dichlofluanid’s primary mode of action involves reactions with cellular thiols, and glutathione is precisely the sulfhydryl-containing molecule the compound attacks. The pro-oxidant properties of the biocide and its metabolite DMSA can imbalance the glutathione pool and generate reactive oxygen species, which enzymes like GPx then scramble to neutralize. Lipid peroxidation in digestive glands actually dropped below control levels, and no DNA damage or neurotoxicity appeared, suggesting the antioxidant machinery largely kept oxidative damage in check. Principal component analysis, which explained nearly 65 percent of the variance, cleanly separated animals exposed above 0.1 micrograms per liter from controls, indicating a metabolic shift beginning at concentrations well within the environmental range.

The clam results were more alarming, and they overturned the researchers’ initial hypothesis. The team had expected organic matter to bind dichlofluanid and reduce its bioavailability, softening the blow to burrowing bivalves. Instead, clams in the organically richer Ariri sediment fared distinctly worse. In their gills, high-organic sediment triggered increased GST and EROD activities at the top concentration, depleted GSH, and elevated GPx and acetylcholinesterase activities at 100, 1,000, and 10,000 nanograms per gram, alongside lipid peroxidation at concentrations as low as 1 and 10 nanograms per gram. Digestive glands showed enhanced GST at intermediate concentrations, increased EROD and lipid peroxidation at 10,000 nanograms per gram, and DNA damage at just 10 nanograms per gram. In low-organic sediment, most biomarkers barely moved. The pattern suggests that dichlofluanid adsorbed onto organic particles is effectively delivered to filter- and deposit-feeding clams through ingestion, turning the sediment itself into a contamination route.

The integrated biomarker sequence in clams tells a coherent toxicological story: phase I biotransformation via EROD, conjugation via GST, consumption of glutathione, and then, when the antioxidant system proves insufficient, lipid peroxidation and DNA damage. Signs of neurotoxicity also emerged, with altered acetylcholinesterase activity in both tissues, an enzyme whose induction has been linked to cellular apoptosis. These findings echo earlier work in rat hepatocytes, where dichlofluanid induced lipid peroxidation and cytotoxicity above 25 micromolar, and in ascidians, where hemocytes showed apoptosis, shrinkage, and reduced phagocytic activity at 3.33 to 33.3 micrograms per liter. The authors caution that dichlofluanid’s rapid degradation, quantified at 87 percent within six hours at the 1,000 nanograms per gram level, complicates dose-response interpretation, since animals may have experienced transient exposure to the parent compound alongside potentially toxic transformation products.

The bottom line is a regulatory headache. Effects in mussels appeared from 0.1 micrograms per liter in water, comfortably below the maximum measured environmental concentration of 3.37 micrograms per liter, while clam effects began at 1 nanogram per gram in sediment, near the reported environmental maximum of 0.8 micrograms per gram. In scenarios of localized contamination near ports, marinas, and shipyards, ecological risk appears likely, and the authors argue that regulatory action is needed. More broadly, the study demonstrates that the organic content of sediments, a factor often overlooked in toxicity assessments, can amplify exposure to hydrophobic antifouling biocides, just as it does for diuron and TBT. As the shipping industry continues to rely on booster biocides to keep hulls clean, this research delivers a clear early warning: the chemicals replacing TBT are not harmless, and the tropical benthic ecosystems they drift into are paying attention.

Subject of Research: Ecotoxicological effects of the antifouling biocide dichlofluanid on tropical marine bivalves

Article Title: Effects of dichlofluanid in tropical marine bivalves exposed to water and spiked sediments: an assessment of biomarker responses

Article References: Cruz, A. C. F., Gusso-Choueri, P. K., Pauly, G. D. F. E., de Campos, B. G., Perina, F. C., de Castro, Í. B., & de Souza Abessa, D. M. (2026). Effects of dichlofluanid in tropical marine bivalves exposed to water and spiked sediments: an assessment of biomarker responses. Ecotoxicology, 35(8), Article 180. https://doi.org/10.1007/s10646-026-03164-y

Image Credits: AI Generated

DOI: 10.1007/s10646-026-03164-y

Keywords: dichlofluanid, antifouling biocides, marine bivalves, biomarkers, ecotoxicology, Perna perna, Anomalocardia flexuosa, sediment contamination, organic matter, oxidative stress, tropical marine ecosystems, lysosomal stability