The Toxic Afterlife of a Boat Paint Biocide Is Rewriting Risk Assessment

Irgarol 1051 was designed to solve a narrow engineering problem: keep algae, barnacles, and slime off ship hulls so vessels glide through water with less drag and burn less fuel. When tributyltin, the notorious organotin antifoulant, was banned worldwide for its catastrophic effects on marine mollusks, Irgarol stepped in as a supposedly safer booster biocide. It worked by selectively inhibiting photosystem II, the molecular engine of photosynthesis, in the algae that colonize hulls, marina pilings, and aquaculture nets. For years, that selectivity was treated as a guarantee of safety. But two decades of environmental monitoring have told a different story. Irgarol did not vanish once it leached off a hull. Instead, it entered a long ecological afterlife of persistence, transformation, redistribution, and biological interaction that now extends from harbor sediments to polar snow, and, according to a sweeping new review, potentially to human exposure through the seafood on our plates.

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in Environmental Science and Pollution Research, argues that the entire risk-assessment playbook for this chemical is outdated.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