Late Lessons, Jensen Huang and AI
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LL2-12: Part B introduction (Emerging lessons from ecosystems) and Ch12 Booster biocide antifoulants: is history repeating itself?#

Late lessons from early warnings: science, precaution, innovation (EEA Report No 1/2013). Report pp. 261–278 (PDF pp. 263–280). The chapter itself runs pp. 265–278, with references on pp. 277–278.

Reading record: I read the full text extract (PDF 263 to 280, last marker “PDF PAGE 280 | REPORT PAGE 278”). I then checked the chapter summary box (p. 265), Table 12.1 and Box 12.1 (p. 268), Box 12.2 (p. 271), Tables 12.2 and 12.3 (p. 272), p. 273 and Table 12.4 (p. 276) against rendered PDF pages. Extraction problems I found:

For context and standpoint I also used a few other pages of the same PDF: the report introduction (p. 10), the author biographies in Annex 1 (pp. 696–697), and three later chapters that reuse this case (pp. 636, 644, 676). I checked later developments against primary sources where I could reach them: EUR-Lex, the IMO, and Europe PMC abstracts. These are marked [post-2013 / external] and kept separate from what the chapter says.

Authors and standpoint#

Authors. Andrew R. G. Price and James W. Readman (p. 265). The chapter page gives no affiliations. They come from the report’s Annex 1:

Insider account. Readman is a central actor in the story. He led the 1993 paper that first reported booster biocide contamination (Readman et al., 1993; pp. 267, 276). He sampled Bermuda in June 1995, and Box 12.2 names him in the third person: “In June 1995, Readman visited Bermuda…” (p. 271). He co-authored the phytoplankton toxicity work (Readman et al., 2004; Devilla et al., 2005), the UK post-ban evaluation (Cresswell et al., 2006), the Chagos baseline (Guitart et al., 2007, with Price) and the proposed EU monitoring approach (Price and Readman, 2006, a report to NERI Denmark and the EEA). By my count of the list on pp. 277–278, 13 of the chapter’s 41 references have Readman or Price as an author (count re-checked in this audit). Much of the key evidence therefore comes from the authors’ own research programme, although several pivotal studies are by others (Dahl and Blanck; Owen et al.; Jones; Voulvoulis et al.; Thomas et al., 2002; Thomas and Brooks). That is consistent with the EEA’s stated approach: authors “would not have been approached if they had not already extensively studied the case” (p. 10). The upside is expert, first-hand knowledge. The downside is little distance from the work being judged. For example, the success of the UK ban rests on a study Readman co-authored (Cresswell et al., 2006).

Stance. The chapter is written as marine-science synthesis, not as political or institutional history. Its tone is measured and technocratic. It names no companies, describes no lobbying, contested science or doubt-manufacturing, and spends almost no space on regulatory politics. That sets it apart from the Part A chapters, whose shared themes (per the report introduction, p. 10) include “slow and sometimes obstructive behaviour by businesses”. The chapter’s main commitments are:

  1. Both banned and permitted agents (the substitutes as well as what they replaced) should be monitored (p. 274).
  2. Monitoring should be tied to action thresholds.
  3. PBT (persistence, bioaccumulation, toxicity) criteria should guide targeted bans.
  4. Non-toxic alternatives should be developed.

“Precaution” appears only a few times and in a practical sense: monitoring “with an appropriate degree of precaution” (p. 274), further legislation “as an additional measure of precaution” (p. 274), and the UK having “taken precautionary action” (p. 275). The precautionary principle is not discussed as a doctrine.

Imported TBT lessons. The TBT background appears to draw on Santillo et al., the Volume 1 (2001) TBT chapter. The list of reasons TBT hazards were underestimated (p. 267) follows directly after the sentence citing Santillo et al. (2001) for “the complexities surrounding TBT, its ban and the delay in controls”, though the chapter does not explicitly attribute the list to them. The citation year is inconsistent: “2002” on p. 266 (“now infamous (Santillo et al., 2002)”) and in the reference list (p. 278), “2001” on pp. 266–267. From general knowledge, not from this chapter: Santillo and Johnston were at the Greenpeace Research Laboratories, and Langston at the Marine Biological Association. That background is relevant to standpoint, but the Volume 1 chapter was an EEA-commissioned, edited review, and the chapter’s own TBT facts are separately referenced (Alzieu, Vos, Labare, Evans, Smith).

Panels. Chapter 12 has no panels or commentaries. No industry or regulator response is included.

Part B “introduction”. Pages 261–264 hold no introductory prose. They contain:

The 16.1/16.2 exchange is the only explicit industry-versus-author panel pair in Part B.

The framing of Part B is in the report introduction instead (p. 10, outside this section’s page range). Part B “focuses on emerging lessons from the degradation of natural systems and their wider implications for society”. It covers “the issues of scientific evidence as the basis for action/inaction, the multiple, often complex factors and feedback loops in play”, and the interfaces between science, policy and society “in the context of heightened systemic risks and substantial unknowns” (p. 10).

Section-by-section notes#

Chapter summary box (p. 265)#

12.1 Introduction (pp. 266–267)#

12.1.1 The need for antifoulants (p. 266). - Hull coatings go back to Ancient Greece (Yebra et al., 2004). Early coatings were physical barriers against the gribble (Limnoria) and the Teredo worm, which could reduce hardwood planking “to pulp within a matter of months”. Fouling also slowed sailing ships and made it harder to sail to windward. For naval ships this “could mean losing sea battles” (p. 266). - The economic case, quantified: - “A layer of algal slime only 1 mm thick will increase hull friction by 80 % and cause a 15 % loss in ship speed”. - “a 5 % increase in fouling for a tanker weighing 250 000 deadweight tonnes will increase fuel usage by 17 %” (p. 266; MER, 1996; Evans et al., 2000). - Source note: MER (1996) is titled “Environmental benefits of TBT antifoulants” (Marine Engineering Review; p. 277). The fuel-penalty figures therefore come partly from a trade-journal source whose title indicates it made the case for TBT (they are also attributed to Evans et al., 2000). The chapter does not comment on this. - “Antifouling agents, applied as paint, are the most economically efficient solution found so far. Yet they come at an environmental cost, as graphically illustrated by… (TBT)” (p. 266).

12.1.2 The rise and fall of TBT (pp. 266–267). - TBT became common “Shortly after World War II”, especially in “‘self‑polishing’ formulations which, by design, release toxic persistent substances into the environment” (p. 266). Table 12.4 dates organotins to the late 1950s or early 1960s (p. 276), a small inconsistency. - TBT was valued because it allowed longer intervals between dry-dockings and did not cause galvanic corrosion on aluminium hulls. By the 1980s it was “recognised as a global pollutant” (p. 266). - Harms: - Oyster shell malformations. In Arcachon Bay, France, TBT caused an estimated loss of USD 147 million through reduced Crassostrea gigas production (Alzieu, 1991) (p. 266). - Imposex (female gastropods developing male sex organs), documented in about 150 species worldwide (Vos et al., 2000). It was “first discovered in the early 1970s”, but “Because of limited analytical capabilities… the physiological and ecological consequences were only attributed to TBT in the 1980s when many gastropod populations had declined” (p. 266). - Molluscs are affected at “less than 10 billionths of a gram per litre (10 ng/L)” (p. 266). - “By the late 1980s, the TBT problem was global.” Steps to ban it were taken “because of its unacceptable toxic effects on commercial shellfish (especially oysters) and other non‑target organisms” (p. 266). - Regulation: EC Directive 89/677/EEC (1989) banned TBT on boats under 25 m (mainly pleasure craft). For larger vessels, the IMO International Convention on the Control of Harmful Anti-fouling Systems (cited as IMO, 2008) (p. 266). - Why TBT hazards were initially underestimated, “for both technical and socioeconomic reasons” (p. 267): - “it was incorrectly assumed that an environmental quality target (EQT) of 20 ng/l would be sufficiently protective”; - persistence, accumulation and wider dissemination were underestimated; - organotin bioaccumulation was underestimated (Labare et al., 1997); - “the geographical scale of the problem was not fully appreciated (inadequate data collection)”; - “imposex observed in 1970 in predatory gastropods in Arcachon Bay was considered acceptable — it had no immediately obvious economic cost — whereas the failure of the oyster stocks soon after was not acceptable”; - the transboundary nature was not fully appreciated until continuing TBT problems in Japan, “despite a national ban in the late 1990s”. - The authors take from this “the value of recognising potential environmental hazards early, and introducing protocols for monitoring and appropriate regulatory measures” (p. 267).

12.1.3 Effects of the TBT ban (p. 267; Table 12.1, p. 268). - “EU and national legislative prohibitions on using TBT for small craft reduced pollution substantially.” In Arcachon Bay, TBT fell from 900 ng/L in 1983 to below 10 ng/L in the late 1980s. The oyster beds recovered and commercial harvesting resumed (p. 267). [external, general knowledge] The Arcachon decline mostly predates the 1989 EC directive; France’s national ban on TBT paints for vessels under 25 m came in 1982. - “The (limited) controls imposed were hailed by some as a ‘solution’ to the TBT problem” (p. 267). UK dogwhelks recovered generally (Evans et al., 2000), “partially confirming this claim”. Elsewhere in Europe recovery was “mixed, or slower than expected” (p. 267). - The chapter introduces New Zealand as illustrating the “complex interactions between TBT inputs, concentrations, accumulation and biological effects and, most importantly, the beneficial effects of legislation” (p. 267). The table itself, though, lists mainly complications. Smith (1996) is titled “Selective decline in imposex levels… following a ban” (p. 278). - Table 12.1 (p. 268; source Smith, 1996; studies from 1988/1989 and 1994/1995) sets out New Zealand complexities: - How big the effect looks depends on the imposex metric (% imposex, or relative penis length). - Sediment re-release and TBT’s sediment half-life of 2.5–3 years “Can obscure actual TBT levels and the effectiveness of legislation”. - After the 1989 small-craft ban, imposex did not fall at Evans Bay marina (Wellington) because a commercial wharf nearby was still leaching TBT. - A 1993 law banned TBT for New Zealand vessels but not for foreign ships. - Sampling strategy matters. - The shared implications cell ends: “Continual monitoring needed to determine the effectiveness of legislation for larger ships” (p. 268). - “the ban on TBT does not seem to have been very effective everywhere. Levels are still going up in Asia, implying either that it is still being used or that there are issues surrounding persistence and transportation that are not yet fully understood” (p. 267).

12.2 Early warnings, actions and inactions (pp. 267–269)#

12.3 Early warnings: the science on antifouling agents (pp. 269–271)#

12.3.1 Persistence and toxicity (pp. 269–270). - Concern “arose because of the high concentrations reported at an increasing number of areas, coupled with findings regarding their toxicity to periphyton (at equivalent concentrations)” (p. 269). The warning combined exposure data with effect data. - Leaching from vessels keeps marina concentrations high, and there antifouling use “normally dominates the total input”. Removal routes are listed (biodegradation, photodegradation, hydrolysis, sedimentation, volatilisation, bioaccumulation) (p. 269). - The MAM-PEC model (van Hattum et al., 1999), developed separately and then validated against the ACE data, “can now be applied to predict future concentrations” (p. 269). Monitoring data therefore made a prospective assessment tool usable. - Half-lives (Thomas et al., 2002; Thomas and Brooks, 2010) (p. 269):

Substance Half-life
Irgarol 1051 100 days
dichlofluanid 18 hours
chlorothalonil 1.8 days
Sea-Nine 211 under 24 hours
zinc pyrithione under 24 hours
TCMTB 740 hours (Box 12.1 spells it “TCMBT”)
zineb 96 hours
diuron no degradation over 42 days when bound to paint particles; 14-day half-life otherwise

Diuron and Irgarol are singled out as “substantially resistant to degradation” (p. 269). - Toxicity (pp. 269–270): - Dahl and Blanck (1996): long-term periphyton effects at 0.25–1 nM (63–250 ng/L), “within the range of concentrations reported for coastal waters”. - Readman et al. (2004): 72-hour EC50 of 70 ng/L for natural phytoplankton (endpoint: selective reduction of the pigment 19’-hexanoyloxyfucoxanthin), “well within the range of concentrations reported in coastal waters” (p. 270). - Devilla et al. (2005): sensitivities differ by species (p. 270). Synechococcus was more tolerant than E. huxleyi of zinc pyrithione (NOEC 1,000 vs EC50 540 ng/L) and Sea-Nine 211 (NOEC 900 vs EC50 350 ng/L), but more sensitive to diuron (EC50 550 vs 2,260 ng/L). Irgarol hit both (EC50 160 and 250 ng/L). - Later studies are cited as confirming algal vulnerability: Okamura et al., 2003; Jacobson and Willingham, 2000; Fernandez-Alba et al., 2002 (p. 269). Source note [external]: Jacobson and Willingham (2000) were at Rohm and Haas, the maker of Sea-Nine. Their paper’s title calls Sea-Nine “an environmentally acceptable alternative to organotin antifoulants” (p. 277). Its abstract reports a microcosm half-life under 1 hour, no chronic or reproductive toxicity to marine species, and essentially no bioaccumulation (Europe PMC abstract; affiliation “Rohm and Haas Company” re-checked in this audit). The paper may well contain algal toxicity data that support the chapter’s use of it. But the chapter cites it as confirming vulnerability without noting its manufacturer source or its reassuring overall conclusion. - Endocrine disruption. Assessed within ACE: “None of the antifoulants evaluated (Irgarol 1051, Sea‑Nine, chlorothalonil, diuron, dichlofluanid, maneb and ziram) showed a strong estrogenic response” (p. 270). Thomas et al. (2001) identified persistence and toxicity as the critical risk features (p. 270). Analytical note: the reported result is for oestrogenic response only, and it says no strong response, which leaves weaker responses open. The chapter does not say whether ACE tested other endocrine endpoints. TBT’s signature harm, imposex, is masculinisation of females. An oestrogenicity screen would not by itself rule out TBT-like effects. Yet the summary turns this narrow result into the general statement that booster biocides “do not threaten to have endocrine disrupting properties similar to TBTs” (p. 265), and the conclusions say “Significant endocrine disruption… was not found” (p. 275). See the bias check below. - Residual uncertainty. Voulvoulis et al. (2002) judged that more data were still needed to evaluate Irgarol, diuron, Sea-Nine 211 and chlorothalonil. They “cautioned against the use of TCMS pyridine, TCMTB and dichlofluanid”, while “again identif[ying] a lack of appropriate data”. In their initial evaluation zinc pyrithione and zineb looked least hazardous, “However, analytical constraints for these latter booster biocide compounds render environmental assessment difficult” (p. 270).

12.3.2 Adverse ecological effects on corals (pp. 270–271). - Irgarol 1051 is herbicidal: it inhibits photosystem II. That raises concern for zooxanthellae, the symbiotic algae in warm-water corals (p. 270). - The context is the 1998 Indian Ocean bleaching, caused by the 1997–98 warming, with “mortality of over 90 % to considerable depths in the Maldives, Seychelles and Chagos” (Sheppard et al., 2002) (p. 270). - Irgarol inhibits photosynthesis of isolated zooxanthellae and of zooxanthellae inside coral tissue “at environmentally relevant concentrations (as low as 60 ng/L)” (Owen et al., 2002, 2003; Jones, 2005). Many harbours report Irgarol at or above this level (Konstantinou and Albanis, 2004). “This creates the possibility that antifouling agents will disperse to offshore sites, including coral reefs” (p. 270). The exposure link from harbour to reef is stated as a possibility, not shown. - Diuron and Irgarol “will also cause bleaching”, possibly through the same photosynthetic route as thermal bleaching (Jones, 2005). Crucially: “The notion that Irgarol and diuron contamination could exacerbate bleaching caused by elevated water temperatures has not yet been tested” (p. 270). - Jones (2005): at low levels and short exposures, herbicide bleaching can be reversible. Higher concentrations, exposure in light, or longer exposure bring “sustained long‑term reduction of the photochemical efficiency” (chronic photo-inhibition) (p. 270). - Jurisdiction. European corals lack symbiotic algae, so coral toxicity “is not directly relevant within the EU”. But European countries have dependent territories with significant reefs. For France, the Netherlands and some UK territories, local environmental law is closely tied to the home country’s. Chagos (British Indian Ocean Territory) is “more independent” (pp. 270–271). - Chagos as a clean reference. It was “virtually pristine and contaminant free” in studies more than 10 years earlier (Everaarts et al., 1999; Readman et al., 1999), despite the military base on Diego Garcia. It was sampled for booster biocides in early 2006 (Guitart et al., 2007) and offers a “useful international baseline or standard” (p. 271). The chapter adds that recent studies highlight Chagos as a “‘clean’ control site” (SOFI, 2009; Sheppard et al., 2009, the latter co-authored by Price), and that environmental monitoring is a requirement of agreements to which the British Indian Ocean Territory is party (p. 271). Source note: the Guitart et al. (2007) paper, co-authored by both chapter authors, is titled “Negligible risks to corals from antifouling booster biocides and triazine herbicides in coastal waters of the Chagos Archipelago” (p. 277).

12.4 The lessons drawn (pp. 271–276)#

12.4.1 Permitted agents (pp. 271–272). - “Controls and legislation have been developed to address the accumulation of booster biocides in the marine environment and the marked toxicity of certain agents” (p. 271). - Tables 12.2 and 12.3 are described as the legislative position “as of 2002”. In fact Table 12.2 is ACE 2002 and Table 12.3 is an October 2008 update (p. 271–272). Details: - The UK now permits only three organic boosters and prohibits diuron and Irgarol. - Sweden is more restrictive. - The Netherlands, France, Greece and Spain permit more agents, and Dutch files were under review. - Denmark banned diuron and Irgarol on pleasure craft in 2000. - A Danish risk analysis found PEC/PNEC below 1 for Sea-Nine 211 and zinc pyrithione in most cases, “indicating an acceptable risk” (p. 271). Some substitutes were judged acceptable, a point the chapter does not dwell on. - Table 12.2 (p. 272; ACE 2002 via Readman 2006): booster biocides permitted on yachts under 25 m.

Country Number permitted Which
UK 3 zinc pyrithione, dichlofluanid, zineb
France 5 diuron, Irgarol, zinc pyrithione, dichlofluanid, chlorothalonil
Greece 7 as France, plus ziram and folpet
Spain 5 diuron, Irgarol, zinc pyrithione, dichlofluanid, Sea-Nine
Sweden 1 Irgarol 1051
Denmark 2 zinc pyrithione, Sea-Nine
Netherlands 5 diuron, Irgarol, dichlofluanid, ziram, zineb

The table also covers metallic antifoulants. Copper(I) oxide is permitted in all seven countries; copper thiocyanate in all but Greece and Spain; copper powder only in Sweden and Denmark; and chromium trioxide only in the Netherlands (p. 272). The chapter does not discuss the metallic rows.

Footnotes that matter: - France, Greece and Spain have “Very limited/no approval scheme (in principle, all can be used)”. Their “permitted” counts are therefore not real approvals. - Sweden regulates copper leach rates on the west coast and bans copper on the east coast. - Denmark approved Sea-Nine, but the product was “not used on pleasure craft”. - Denmark and the Netherlands: “Regulations currently under debate”.

Observation: in 2002 the single booster biocide Sweden allowed was Irgarol, which the UK and Denmark had banned. National regimes differed in which substances they judged worse, not just in how strict they were. The chapter reports the difference without comment. - Table 12.3 (p. 272; IYP, 2008; the abbreviation is not expanded): - EU-wide, all antifoulings must be notified or authorised. - Under the Biocidal Products Directive (BPD) 98/8/EC, the review of antifouling biocides was “well under way” and “Decisions on the acceptability of these biocides are expected shortly”. Products deemed unacceptable “will be removed from the EU market”. - TBT application is banned under 76/769/EEC. Under Regulation (EC) No 782/2003, EU-flagged ships may not use TBT, and ships with active TBT coatings may not enter EU ports. There are certification rules for ships over 400 GT and self-certification for ships over 24 m and under 400 GT. - Sweden: case-by-case risk assessment. - Denmark: copper release limits (200 μg Cu/cm² in the first 14 days, 350 μg/cm² in the first 30 days) for pleasure craft of 200 kg and above. Biocidal paint is banned for pleasure craft under 200 kg, with exemptions for wooden boats and some harbours. Irgarol and diuron are banned on pleasure craft. - UK: Irgarol and diuron banned. - Netherlands: diuron banned. - The BPD harmonises data requirements for existing and new biocides, with antifoulants as product type 21. Companies had to notify in 2002 with a base data set, but “Time scales for submitting additional necessary data have not been established” (p. 271). - Bermuda (Box 12.2, p. 271). - June 1995: Readman’s samples show high Irgarol in some harbours, raising “fears of damage to coral endosymbiotic algae” (Readman, 1996). Extended data followed (Connelly et al., 2001). - The Bermuda Government (Ministry of the Environment) funded toxicology at the Bermuda Biological Station for Research that “demonstrated the vulnerability of the corals” (Owen et al., 2002, 2003). - 1 July 2005: Irgarol- and diuron-based paints were banned by amending BR 20/1989. - In the main text: “Within a period of 10 years, harmful booster biocides were identified in some harbour areas and, because of their potential harm to corals, were banned in the entire territory” (p. 271). The ban rested on potential harm.

12.4.2 Effects of banning selected booster biocide agents (p. 273). This summarises Cresswell et al. (2006). - The section opens: “While the positive impact of banning TBT has been well demonstrated in European waters and elsewhere, the effectiveness of legislation outlawing specific booster biocides has been determined only recently” (p. 273). That is more confident about TBT than p. 267, where recovery outside the UK was “mixed, or slower than expected” and the ban “does not seem to have been very effective everywhere”. - In 2001 the UK limited small-vessel (under 25 m) antifouling paints to dichlofluanid, zinc pyrithione and zineb. This took diuron and Irgarol off the small-craft market. - Resampling sites with good pre-restriction data showed “a clear reduction in water concentrations of Irgarol 1051 (by 10–55 % of levels in pre‑restriction studies)” (p. 273). - Source check [external; re-verified in this audit via Europe PMC]: the Cresswell et al. (2006) abstract says “(between 10% and 55% of that found during pre-restriction studies)”. Residual concentrations were 10–55% of earlier levels, which is a 45–90% reduction. The chapter’s “by 10–55 % of levels” is ambiguous rather than plainly wrong: “of levels” points to the correct reading, but “by” invites the reading of a 10–55% reduction, a much smaller effect. - No comparable diuron data were reported. Chlorothalonil, dichlofluanid and Sea-Nine 211 were all below detection (under 1 ng/L) (p. 273). Zinc pyrithione and zineb, two of the three permitted substances, are not reported. Section 12.3.1 had already noted that they are analytically hard to measure (p. 270). - The remaining Irgarol might come from ongoing use, hulls painted before the ban, non-UK vessels, or persistence: “It is likely to be a combination of all these factors” (p. 273). - Retail compliance was imperfect. “small amounts of Irgarol 1051‑based paints were still being sold and… there was no routine monitoring of retailers”. Even so, by regulating production and distribution “at the manufacturer level”, the UK Health and Safety Executive brought concentrations “below the proposed Environmental Quality Standard, EQS, of 24 ng/L”. The survey supports “removing Irgarol 1051‑based paints from the market using simple regulations targeted at manufacturers” (p. 273).

12.4.3 History repeats itself? (pp. 273–274). - The authors set out a five-step cycle common to TBT, earlier antifoulants and booster biocides (p. 273): 1. “identification of new antifouling agents to replace older supposedly more toxic or less effective products (although the relative efficacy and toxicity of antifouling paints can only be determined by subsequent monitoring to establish whether initial suppositions/hypotheses were correct)”; 2. monitoring of distribution, accumulation and toxicity “to determine whether the initial supposition or hypotheses about the net benefits of new products were correct”; 3. concern, debate and review; 4. “banning of the most harmful agents”; 5. “search for less toxic solutions”. - “Detailed toxicity tests have not been undertaken for all booster biocides.” Diuron and Irgarol show exposure and potential vulnerability, since photosynthesis is affected “at extraordinarily low concentrations, i.e. in the ‘parts per trillion’ (ng/L) range” (p. 273). Short exposures may be reversible; longer or higher exposures reduce algal photochemical efficiency. In corals this can mean bleaching and “lengthy recovery times”. “Hence, booster biocides can impact the base of food chains, which are linked to seafood production and many other ecosystem services” (p. 273). - The mechanism. Diuron and Irgarol act “at the herbicide binding site (by definition) of PSII”, via the QB site on the D1 protein. D1 is “a remarkably conserved area”: 98% amino acid homology among higher plants and 85–90% across PSII-containing species (p. 273). “This conservation, and the fact that it is the base of the food chain, means that, like TBT, booster biocides can potentially have far‑reaching consequences” (p. 274). - “Whereas TBT acted quite specifically in causing imposex and shell abnormalities, through endocrine disruption, the booster biocides that replaced TBT have more broad‑spectrum impacts” (p. 274). - “The wider ecological impacts… remain poorly understood but of considerable potential concern. The message is clear: there is a need to develop and apply non‑toxic and less toxic solutions” (p. 274).

12.4.4 Why monitoring should continue (p. 274). - The reasons: “the legacy of TBT, our understanding now that booster biocides are far from ‘risk free’, and the recognition that developing non‑toxic alternatives may take years or decades” (p. 274). - Monitoring should cover at least selected constituents of the newer agents. It must be robust enough to detect spatial and temporal trends “with an appropriate degree of precaution… to ensure that any ‘clean bill of health’ given to existing and new booster biocides is environmentally warranted” (p. 274). Both banned and permitted agents should be monitored to decide whether further legislation is needed “as an additional measure of precaution” (p. 274). - Reference sites: the report’s Minamata chapter shows how hard it is to find pollution-free baselines. Chagos is proposed as a reference area (p. 274). - Proposed programme (Price and Readman, 2006): a scaled-down ACE. Sampling regions: Norway and the Faroes, the Baltic, the North Sea, the Mediterranean (north and south), the Black Sea, the Barents Sea, the English Channel, the Celtic region and Irish Sea, and the Iberian Peninsula (p. 274). - Start with Irgarol 1051 because of its “widespread use, marked toxicity” and because “it can be traced to antifouling paints since it is not used as a herbicide (unlike diuron)”. The ACE project’s 800 samples serve as baseline (p. 274). - Monitoring must be tied to action. “Any future monitoring programme should be firmly linked to an action plan and catalyse management activities if contaminant levels or other metrics of ecosystem health fall to some predetermined threshold level(s). Otherwise, monitoring can easily become an essentially scientific or academic pursuit” (p. 274). The analogy offered is oil-spill clean-up criteria for when to start and stop (p. 274). - The counterweight: “the detection of imposex at least partly resulted from initially academic work, rather than monitoring of toxic effects. Academic activities may thus play a role, not least in identifying possible emerging issues” (p. 274).

12.4.5 New-age antifouling: is there a non-toxic way? (pp. 274–275). - “Given the undeniable (and necessarily) toxic nature of biocidal antifouling agents, there is a case for further research and fast‑track development of more environmentally benign solutions” (p. 274). - Options considered: - Controlled slow release through polymer design: “only a ‘stop‑gap’”. It might be better to keep biocides “permanently in the paint, assuming they could still be sufficiently effective, to enable recovery and disposal on land” (p. 274). The authors flag the effectiveness assumption themselves. - Natural products or synthetic analogues (terpenoids, steroids, heterocyclics, alkaloids, polyphenolics), which interfere with foulers’ metabolism or adhesives. These have “not… been commercially exploited”. The chapter notes that natural products are not all hazard-free (strychnine, aflatoxins), but says their release “is not perceived to pose a serious environmental threat by the general public” (p. 275). This is an argument from public perception. - Non-stick (foul-release) coatings of fluoropolymers or silicones. They appeal environmentally but perform modestly, needing “relatively high speeds” to shed fouling. Some are on the market for some vessel classes, but cost, poor hull adhesion and damage susceptibility mean “widespread commercial application seems unlikely without further advances in technology” (p. 275). - Innovation dynamics. The BPD and other instruments consider substitutes. “However, it is normally existing manufacturers of antifouling products that seek to innovate in response to such instruments and they tend to devise solutions with which they are familiar — typically more biocide. The result is incremental change, such as the shift to booster biocides after TBT use was outlawed” (p. 275). Alternatives such as “non‑stick coatings and polishing robots” exist, “but the companies that could develop more innovative solutions are generally unaware of the emerging market” (p. 275). No evidence or citation is given for either claim.

12.4.6 Hindsight, foresight and conclusions (pp. 275–276). - “TBT, now in demise, has been a highly effective antifouling agent but is among the most toxic synthetic compounds ever produced.” Small-craft use was banned in Europe in the late 1980s and early 1990s, ships took longer, and “a total ban has come into force” through the international convention and linked EU law (p. 275). - TBT’s early warnings are “important reminders” for booster biocides: recognise hazards early, monitor, regulate appropriately. Analytical limits and poor baselines “do not constrain understanding of antifouling residues as they did twenty or more years ago” (p. 275). - “Recent research has demonstrated the significant toxicity of booster biocides at extremely low concentrations” (p. 275). The chapter recaps the ACE results, the data gaps, the Voulvoulis caveats and the finding that “Significant endocrine disruption, the major problem associated with TBT, was not found for booster biocides (ACE, 2002)”. Instead, booster biocides are “often photosystem II inhibitors” affecting “the base of food chains and their dependencies (e.g. symbiotic algae and host corals)” (p. 275). - Two small shifts in the recap. The data gap is now “negligible data are available for other biocides” (p. 275), where p. 269 said other regions. And the recap repeats that zinc pyrithione and zineb “appeared the least hazardous options” but drops the p. 270 caveat that analytical constraints make their assessment difficult. - “Like several other countries, the United Kingdom has taken precautionary action”, and Cresswell et al. (2006) indicates the legislation “appears to have been effective in reducing environmental concentrations” (p. 275). - “Even for prohibited (but still used) toxic substances, it is fair to assume that a release into the environment is often inevitable. The preference should always be for non‑toxic, competitively priced alternative approaches” (p. 276). - Booster biocides “must be monitored to gather more data on accumulation, toxicity and the impact of legislation”. There “appears to be a strong case and market demand for further research and fast‑track development of more environmentally benign solutions… such as natural products and non‑stick coatings” (p. 276). Note the hedge “appears to be”. This sits awkwardly with p. 275, where potential innovators are “unaware of the emerging market”. - Thomas and Brooks (2010) report that “even today DDT is used in China as an antifoulant”. The novel compounds phenylborane pyridine, Econea, capsaicin and medetomidine “are almost uninvestigated, with very little information available on them in the public domain” (p. 276). - Closing paragraphs (p. 276) repeat the summary box and add: “Policy has proven effective in, for example, Bermuda and the United Kingdom, where banning selected agents lowered concentrations and limited adverse ecological impacts”. The chapter gives concentration evidence only for the UK, and no ecological-outcome evidence for either jurisdiction. - Table 12.4, “Early warnings and actions” (p. 276). This is a long history: from Ancient Greek lead sheathing and copper nails through Arab lime-and-mutton-fat coatings (about 800 AD), Columbus’s pitch and tallow, Royal Navy tar and sulphur, copper sheathing (late 1700s), copper paints (mid 1800s), and “Copper, arsenic and mercury paints” (mid 1900s). Each is described as having “caused no environmental concern” or “no or limited environmental concern”. Then:

Date Event
Late 1950s/60s–1990s Organotins/TBT cause “increasing environmental warnings and actions”
1989 EC TBT small-boat ban, “triggering the development and use of booster biocides”
1993 First report of booster biocides in coastal waters
1996 First toxicity at environmental levels
1997 Expanded research
1999 ACE funded
2000 BPD review begins (in force 14 May 2000); UK HSE begins phasing out all boosters except dichlofluanid, zinc pyrithione and zineb
2002–2005 Coral zooxanthellae toxicity concern “leading to bans on specific agents in several countries”
“Today” Natural products and fluoropolymer/silicone non-stick coatings

Observations: - The mid-1900s entry, “Copper, arsenic and mercury paints caused no or limited environmental concern”, records the absence of concern, not the absence of harm. - The UK entry here is 2000, when the HSE “began phasing out” boosters; pp. 273 and 275 date the legislation to 2001. The two dates may refer to different steps, so this is not necessarily an inconsistency. - The table says the BPD “entered into force on 14 May 2000”. [external, general knowledge; not re-verified in this audit] Directive 98/8/EC was adopted on 16 February 1998 and, as I understand it, entered into force in May 1998; 14 May 2000 was the deadline for member states to transpose it. The table probably conflates the two dates.

Case timeline#

Dates are from the chapter unless marked [external]. Lag calculations are mine.

Date Event Page
~1945–1960s TBT enters antifouling paints; self-polishing formulations release it by design pp. 266, 276
1970 Imposex seen in predatory gastropods in Arcachon Bay; “considered acceptable” because it had no obvious economic cost p. 267
Early 1970s Imposex “first discovered” p. 266
Soon after 1970 Arcachon oyster stocks fail; judged “not acceptable” p. 267
1982 [external, general knowledge] France bans TBT paints on vessels under 25 m (first national ban) —
1983 Arcachon TBT at 900 ng/L; falls below 10 ng/L by the late 1980s after “EU and national legislative prohibitions”; oysters recover p. 267
1980s Imposex attributed to TBT, after many gastropod populations had declined (delay blamed on analytical limits) p. 266
1989 EC Directive 89/677/EEC bans TBT on vessels under 25 m. This creates the market for booster biocides pp. 266, 267, 276
1989, 1993 New Zealand bans TBT on small craft (1989), then on NZ vessels but not foreign ships (1993) p. 268
1993 First warning (exposure): Irgarol at up to 1,700 ng/L on the Côte d’Azur, found by chance in a survey of agricultural triazines (Readman et al.) pp. 267, 276
June 1995 Readman samples Bermuda; high Irgarol in harbours p. 271
1996 Second warning (effects): Dahl and Blanck show periphyton effects at environmental Irgarol levels; Readman (1996) asks “Antifouling herbicides — a threat to the marine environment?” pp. 267–269, 276, 278
1997 Expanded research p. 276
1998 BPD 98/8/EC adopted; Indian Ocean mass bleaching (context) pp. 270–271
1999 MAM-PEC exposure model p. 269
1999–2002 EC-funded ACE project, 800 samples; Europe-wide picture; no strong oestrogenic response pp. 268–270, 274, 276
14 May 2000 BPD “entered into force” per Table 12.4; EU review of all biocides begins. [external: probably the transposition deadline, with entry into force in 1998; see Table 12.4 observations] p. 276
2000 Denmark bans diuron and Irgarol on pleasure craft; UK HSE begins phase-out pp. 271, 276
2001 UK legislation limits small-craft boosters to dichlofluanid, zinc pyrithione and zineb pp. 273, 275
2001 [external] IMO AFS Convention adopted, 5 October 2001 IMO
2002 BPD notification deadline for antifouling actives; Voulvoulis et al. risk evaluation calls for more data pp. 270–271
2002–2005 Coral zooxanthellae toxicity at about 60 ng/L (Owen et al.; Jones) leads to bans on specific agents in several countries pp. 270, 276
2003 Regulation (EC) 782/2003: TBT banned on EU-flagged ships; TBT-coated ships barred from EU ports p. 272
1 July 2005 Bermuda bans Irgarol- and diuron-based paints (government-funded local toxicology) p. 271
2006 Cresswell et al. find UK Irgarol at 10–55% of pre-restriction levels (reading confirmed from the Cresswell abstract; the chapter’s wording is ambiguous); Chagos baseline sampled; Price and Readman propose an EU monitoring indicator pp. 271, 273, 274
2008 IMO convention cited; [external] entered into force 17 September 2008. EU BPD decisions “expected shortly” (Oct 2008) pp. 266, 272
2010 Thomas and Brooks: novel boosters almost uninvestigated; DDT still used as an antifoulant in China p. 276
[external] 2013 Directive 2013/39/EU adds cybutryne (Irgarol 1051) as a Water Framework Directive priority substance. AA-EQS 0.0025 µg/L (2.5 ng/L), MAC-EQS 0.016 µg/L; good status required by 22 Dec 2027. Diuron remains a priority substance (AA-EQS 0.2 µg/L, MAC 1.8 µg/L) EUR-Lex
[external] 2015–2016 EU Biocidal Products Regulation approvals for product-type 21: tralopyril (Econea) from 1 Apr 2015 (Reg. 1091/2014); DCOIT (Sea-Nine 211) from 1 Jan 2016 (Reg. 437/2014); medetomidine from 1 Jan 2016 as a “candidate for substitution” (Reg. 2015/1731); copper pyrithione from 1 Oct 2016 (Reg. 2015/984). All carry containment conditions for application EUR-Lex
[external] 27 Jan 2016 Commission Implementing Decision (EU) 2016/107: cybutryne not approved for product-type 21. The environmental risk assessment “identified unacceptable risks” EUR-Lex
[external] 2021 → 1 Jan 2023 IMO MEPC amendment adds cybutryne to the AFS Convention; application banned from 1 Jan 2023; existing coatings removed or sealed within 60 months IMO

Lags (my calculations):

What was known when. - By 1996 the chapter’s account had both exposure (1993) and effect at environmental levels (1996). By 2002 the European exposure picture (ACE) was comprehensive. - The harmful mode of action was knowable in advance. Diuron is an agricultural herbicide and Irgarol a triazine. Both act “at the herbicide binding site (by definition) of PSII” (p. 273). - The chapter says almost nothing about pre-market assessment of the substitutes before or around 1989. It implies none that settled the question: relative toxicity “can only be determined by subsequent monitoring” (p. 273). The only data requirements it describes came later, under the BPD (notification and a base data set in 2002, p. 271). It also calls for future biocidal products to be “better appraised” (p. 265). - Field-level ecological damage, as distinct from lab, microcosm and in-symbio effects plus harbour concentrations above effect levels, is not documented in the chapter. The case for action rested on hazard plus exposure at effect-relevant levels.

Harms and costs. TBT: USD 147 million oyster loss in Arcachon (p. 266), and imposex in about 150 species with population declines (pp. 266, 267). Booster biocides: no quantified harm or cost. Harms are framed as risks to primary producers, corals and food-web bases (pp. 265, 273–274, 276). The cost of the controls (fuel, performance, industry costs) is not discussed.

The authors’ own lessons and conclusions#

A. Lessons the authors draw from their evidence.

  1. TBT hazards were underestimated for technical and socioeconomic reasons: a wrong protective threshold, underestimated persistence and bioaccumulation, missed geographic scale, harm tolerated until it had an economic cost, and missed transboundary spread (p. 267). These are “useful reminders” for booster biocides (pp. 267, 275).
  2. History is repeating in pattern (p. 273). The cycle is: new replacement assumed better; post-deployment monitoring; concern; bans of the worst agents; a new search for alternatives.
  3. Booster biocides relocate rather than remove harm (my phrasing; the chapter says they have “more broad‑spectrum impacts” and “like TBT… can potentially have far‑reaching consequences”, p. 274). They swap a specific endocrine disruptor for broad-spectrum PSII inhibitors that hit the base of food chains, given the conserved D1 target (pp. 273–274). Ecological consequences “remain poorly understood” (pp. 265, 274, 276).
  4. Targeted national bans work to reduce concentrations. UK Irgarol fell after the 2001 restriction (Cresswell et al., 2006), and regulating manufacturers worked despite weak retail enforcement (p. 273). Bermuda acted within 10 years of detection (p. 271).
  5. Analytical capacity is no longer the binding constraint it was for TBT (p. 275).
  6. Warnings can come from untargeted work. Irgarol was found during an agricultural herbicide survey (p. 267). Imposex was detected through “initially academic work” (p. 274).
  7. Mobile sources and national differences undermine bans. Examples: Irgarol in Australia (p. 267), residual UK Irgarol possibly from non-UK vessels (p. 273), TBT in Japan and rising in Asia (p. 267), and varying national rigour (p. 265; Tables 12.2 and 12.3).

B. Recommendations and advocacy.

  1. Keep monitoring both banned and permitted antifoulants, with robust trend-detection designs, reference sites (Chagos) and a scaled-down ACE programme across named European regions, starting with Irgarol (p. 274).
  2. Link monitoring to an action plan with predetermined thresholds that trigger management (p. 274).
  3. Use PBT criteria to rank biocides and target legislation (pp. 265, 276).
  4. Address geographic disparities in regulation, and appraise future biocidal products and novel approaches better (p. 265).
  5. Fast-track research into, and development of, non-toxic or less toxic solutions: natural products, non-stick coatings, perhaps biocide retention in paint for disposal on land. Treat controlled release as a stop-gap (pp. 274–276).
  6. Prefer “non‑toxic, competitively priced alternative approaches” (p. 276), and use “lateral thinking” (pp. 265, 276).
  7. Innovation policy should reach beyond incumbent manufacturers, who default to “more biocide” (p. 275). This is implied rather than framed as a formal recommendation.

The chapter does not recommend a general ban on biocidal antifouling, shifting the burden of proof, liability, or specific institutional reforms, beyond monitoring plus targeted bans plus research. On pre-market testing it goes only as far as saying future products “should be better appraised” (p. 265) and that PBT criteria can rank biocides; it sets out no specific testing requirements. By contrast, the report’s closing chapter, drawing on this case among others, calls for “hazard screening of alternatives” (p. 676, outside this section).

Mechanisms and dynamics#

1. Regulation-induced substitution and “regrettable substitution”. The 1989 TBT ban “trigger[ed] the development and use of booster biocides” (p. 276). Substitutes were chosen from chemistry already registered elsewhere: agrochemical herbicides, existing biocides, and a shampoo antifungal (p. 267). They were “believed to be less damaging” (p. 265), and that belief was tested only after release (p. 273). The substitution moved the harm from molluscs, through endocrine disruption, to primary producers, through photosynthesis inhibition (pp. 265, 274). The report’s closing chapter uses this case in exactly this way: “Research, precaution, and exposure control also need to be applied to the substitutes or alternatives to hazardous agents”, citing Ch12 among others, and suggests avoiding persistence, bioaccumulation and large spatial range, plus “hazard screening of alternatives” (p. 676; quote verified in this audit).

2. The useful function is the hazard. Antifouling works by killing or deterring organisms. The chapter says so directly: “undeniable (and necessarily) toxic nature” (pp. 274, 276). TBT’s self-polishing paints release toxicant “by design” (p. 266). Substituting within the same functional principle, a biocide that leaches, tends to move harm around rather than end it. The authors see real improvement as needing a different principle: non-stick surfaces, mechanical polishing robots, or keeping the biocide in the coating (pp. 274–275).

3. Incumbent innovation and lock-in. Existing manufacturers “tend to devise solutions with which they are familiar — typically more biocide”, giving “incremental change”. Potential outside innovators “are generally unaware of the emerging market” (p. 275). Performance, cost and adhesion lock in toxic coatings: non-stick coatings need high speeds, are expensive and damage easily (p. 275). The economics are strong. The fuel and speed penalties of fouling (p. 266) make antifouling “essential for the shipping industry” (p. 266), and non-toxic alternatives “may take years or decades” (p. 274). The incumbent-innovation claim is asserted without citation.

4. How warnings arose. - By chance, from nearby work: Irgarol turned up in a herbicide survey because the analytical protocol was shared (p. 267). - From academic curiosity rather than monitoring: imposex (p. 274). - From combining exposure and effect data: concentrations at more and more sites, “coupled with findings regarding their toxicity to periphyton (at equivalent concentrations)” (p. 269). - From analytical capacity: TBT attribution was delayed by “limited analytical capabilities” (p. 266). Booster biocides were detectable in the ng/L range from the start, and conversely some substances (zinc pyrithione, zineb) remain hard to measure (p. 270).

5. Detectability shapes risk ranking. Voulvoulis et al. (2002) rated zinc pyrithione and zineb least hazardous but noted that analytical constraints make their environmental assessment difficult (p. 270). Two of the three substances the UK permitted from 2001 (p. 273) are those hard-to-measure compounds. The UK decision predates the Voulvoulis paper, so it was not based on it. Cresswell et al. reported no data on them (p. 273). The chapter does not draw the inference, but its facts are consistent with it: substances that are hard to measure can look better simply because less is known about them. In fairness, the short half-lives reported for zinc pyrithione, zineb and dichlofluanid (p. 269) give an independent reason to prefer them.

6. Economic salience decides what counts as harm. TBT imposex in 1970 “was considered acceptable — it had no immediately obvious economic cost — whereas the failure of the oyster stocks soon after was not acceptable” (p. 267). TBT was banned “because of its unacceptable toxic effects on commercial shellfish (especially oysters) and other non‑target organisms” (p. 266). Harm to species without market value did not trigger action; harm to a fishery did. (The p. 266 sentence does also name “other non‑target organisms” as a reason for the bans, so the chapter does not present the economic trigger as the only one.) For booster biocides, the most-cited endpoint (corals, pp. 270–271) sits mostly outside EU waters, “not directly relevant within the EU” (pp. 270–271). The chapter does not examine what drove Bermuda’s action (for example, reef-dependent economies).

7. Protective thresholds set too high. The TBT EQT of 20 ng/L “was incorrectly assumed” protective when molluscs are affected below 10 ng/L (pp. 266–267). For Irgarol, the chapter reports success in getting UK concentrations “below the proposed… EQS, of 24 ng/L” (p. 273). Its own figures, though, put long-term periphyton effects from 63 ng/L (p. 269), coral photosynthesis effects “as low as 60 ng/L” (p. 270) and a phytoplankton EC50 (a half-maximal effect, not a no-effect level) at 70 ng/L (p. 270). That is a margin below three-fold, which the chapter does not discuss. [external] In 2013 the EU set the cybutryne AA-EQS at 2.5 ng/L, about ten times lower than the UK figure the chapter uses as its benchmark. The chapter reports 24 ng/L only as a “proposed” standard and does not explicitly call it protective. Even so, the TBT pattern (a threshold later judged too lenient) is at least partly echoed in its treatment of the substitute. This is my inference.

8. Partial and national controls, mobile sources and legacy stocks. - The small-craft-only TBT ban was confounded by nearby commercial shipping and by re-release from sediments (half-life 2.5–3 years), which “Can obscure actual TBT levels and the effectiveness of legislation” (Table 12.1, p. 268). - Early partial success was “hailed by some as a ‘solution’” (p. 267). - Ships move pollutants and regulatory differences across borders (pp. 267, 273). - National regimes varied from strict approval (UK, Sweden, Denmark) to “Very limited/no approval scheme (in principle, all can be used)” (France, Greece, Spain; p. 272). National authorities also disagreed about which substances were worse (Sweden’s sole permitted booster was the one the UK banned; p. 272). - Overseas territories with coral reefs, where the most sensitive endpoint lies, may sit under separate environmental law (pp. 270–271).

9. Institutional pace. The BPD harmonised data requirements, but “Time scales for submitting additional necessary data have not been established” (p. 271). In 2008 decisions were still “expected shortly” (p. 272). Products stayed on the market meanwhile. [external] The cybutryne non-approval came in January 2016 and the IMO ban took effect in 2023. Faster action came from small or single jurisdictions (Denmark, the UK, Bermuda) using simple instruments.

10. Effective levers. - Regulating at the choke point. Rules on production and distribution at manufacturer level worked even without retail monitoring (p. 273). - A small jurisdiction funding its own science. The Bermuda Government funded local coral toxicology, then banned the substances (p. 271). - EU-funded monitoring (ACE). It produced a baseline and validated a predictive model (MAM-PEC) that allows prospective exposure assessment (p. 269).

11. Uncertainty and ignorance framing. The chapter’s language is cautious and graded: “potentially”, “possibility”, “poorly understood but of considerable concern”, “not yet tested” (pp. 265, 270, 273–274). It openly lists data gaps: no toxicity tests for all boosters, negligible data outside Europe, North America and Japan, novel compounds “almost uninvestigated” (pp. 269, 273, 276). It is not framed as a case of suppressed knowledge. It is a case of knowledge produced after deployment, with regulators acting on hazard plus exposure before field damage was shown. The burden-of-proof question is implicit. Substitutes entered the market on a presumption of relative safety, and the proof of harm fell to public-sector and academic science (ACE, PML, Bermuda’s government-funded studies). The report’s Chapter 26 on science for precautionary decision-making (p. 636, outside this section) notes that diuron and dichlofluanid “received only a little attention in independent research” (389 and 39 SciFinder links for 2000–2009). It calls “the paucity of complementary academic research publications” on compounds with “clear commercial interests” “unfortunate, although perhaps not surprising” (quotes verified in this audit).

12. How proponents and regulators thought (as far as the chapter shows). - Substitutes were assumed better because they were not TBT: “believed to be less damaging” (p. 265), “supposedly more toxic” old products (p. 273). - Partial controls were declared a “solution” (p. 267). - Some harm was judged “acceptable” if it lacked economic cost (p. 267). - A reassuring threshold was assumed protective (p. 267). - The chapter’s own sources suggest the manufacturer framing of one substitute (Sea-Nine: “an environmentally acceptable alternative”, p. 277). - The chapter gives no direct evidence about industry decision-making. Mental models are inferred from outcomes and from the titles of cited sources.

13. Distribution of costs and benefits. Shipping and boat owners gain fuel savings, speed and longer repaint intervals (p. 266). The costs fall on shellfisheries (Arcachon), non-target molluscs, primary producers, and possibly reefs far from the source, including in places where the chemical is not used (Irgarol in Australia, p. 267). The benefits of antifouling are quantified. The ecological costs of booster biocides are not.

14. Complexity and systems. The effects compound through food webs because the D1 target is conserved (pp. 273–274). There may be interactions with thermal stress (untested, p. 270). The same chemical comes from several sources, which blurs attribution (p. 268). There are degradation products (p. 269), sediment reservoirs (p. 268) and particle-bound persistence (diuron, p. 269).

Transferable insights (technology-neutral)#

  1. Banning a hazard creates a market for its substitutes, and those substitutes can inherit a presumption of relative safety that has not been tested in real-world use. When a harmful option is restricted, replacements come in quickly, often drawn from what is already available and familiar, and are assumed better because they are not the banned thing. Evidence: pp. 265 (“believed to be less damaging”), 267 (substitutes drawn from existing agrochemicals, biocides and personal-care products), 273 (“initial suppositions/hypotheses”), 275 (incumbents devise “more biocide”), 276 (Table 12.4, “triggering the development and use of booster biocides”); report synthesis p. 676. Strength: strong for the substitution sequence, which is documented, dated, uncontested in the chapter and matches other cases in the report. Moderate for the “untested presumption” part. The chapter never says who held the belief in relative safety or what pre-market data existed.

  2. If the useful function is the hazard, swapping to another agent that works the same way tends to move harm to other targets rather than remove it. Real improvement usually needs a change of operating principle. Evidence: pp. 266 (“by design”), 273–274 (broad-spectrum PSII mechanism, conserved target), 274–276 (“necessarily toxic”; non-stick, robots, retention). Strength: moderate. Strong for the shift from TBT to boosters. The claim that other principles are viable is thinly evidenced (modest performance, no commercial uptake of natural products).

  3. The hazard profile of a substitute is often foreseeable from its known mode of action, even if nobody asks before deployment. Herbicides used as antifoulants predictably threaten primary producers. Evidence: pp. 267 (agrochemical origins), 269, 273 (“by definition” herbicidal binding site). Strength: moderate. This is my inference from the chapter’s facts. The chapter itself stresses that comparative risk is only settled by monitoring after deployment (p. 273).

  4. Pre-deployment judgements of comparative risk are hypotheses, and only post-deployment monitoring tests them. Monitoring therefore needs to be designed in from the start and cover both what is permitted and what is banned. Evidence: pp. 273 (“initial suppositions/hypotheses”), 274 (“clean bill of health”). Strength: moderate. Well illustrated here. As a general claim it is argued, and it may understate what earlier testing could show.

  5. Early warnings often come from untargeted or adjacent work, such as shared analytical methods or curiosity-driven research, not from designed surveillance. Keeping broad scientific capacity pays off. Evidence: pp. 267 (Irgarol found in a herbicide survey), 274 (imposex from academic work). Strength: moderate. Two concrete, well-sourced instances, but a small sample.

  6. Monitoring changes outcomes only when tied to predetermined action thresholds. Without that link it drifts into academic exercise. A counterpoint: open-ended research is also where new problems are first spotted. Evidence: p. 274. Strength: asserted. A reasoned recommendation, backed by an analogy (oil-spill criteria) rather than evidence from this case. The chapter itself supplies the counterpoint.

  7. What gets counted as harm depends on economic visibility. Damage to things without market value is tolerated until something with market value is hit. Evidence: pp. 266–267 (imposex “acceptable”, oyster failure not; bans driven by effects on “commercial shellfish (especially oysters) and other non‑target organisms”). Strength: moderate. Explicit in the chapter for one case (TBT at Arcachon), but it is a single, uncited judgement, apparently inherited from Volume 1. The chapter does not test it for booster biocides.

  8. Early protective thresholds, set on limited data, have tended to be too lenient and later revised down. Benchmarks that declare success can outlast the evidence. Evidence: pp. 266–267 (TBT EQT 20 ng/L versus effects below 10 ng/L); p. 273 (Irgarol “proposed EQS” 24 ng/L) against p. 270 (effects at 60–70 ng/L). [external] EU AA-EQS 2.5 ng/L (2013). Strength: moderate. Two instances, one relying on post-2013 evidence.

  9. Things that are hard to measure can look safer because they are under-observed. Choices made under data asymmetry can favour the least visible options. Evidence: p. 270 (zinc pyrithione and zineb “least hazardous” but analytically hard); p. 273 (UK permitted list; no post-ban data on them). Strength: suggestive. My inference. The chapter supplies the facts but not the argument, and short half-lives give an independent reason for the choice.

  10. Partial, national or segment-limited controls leak when the source is mobile and legacy stocks persist. Effects of intervention can be masked, and early partial success invites premature claims of a “solution”. Evidence: pp. 267 (“hailed by some as a ‘solution’”; Japan; Asia; Australia), 268 (Table 12.1), 273 (residual UK Irgarol), 265 and 272 (national disparities). Strength: moderate. Several independent observations. Mostly descriptive, without quantified leakage.

  11. Simple rules at a supply choke point can work where downstream enforcement is weak. Evidence: p. 273 (manufacturer-level regulation cut Irgarol despite some retail sales and no retailer monitoring). Strength: moderate. One study, co-authored by a chapter author. A consistent concentration decline, but it is a before–after comparison with no control sites reported, and it has no ecological endpoint.

  12. Small or single jurisdictions that pay for their own evidence can act much faster than harmonised regimes, which may take decades. Evidence: pp. 271 (Bermuda: sampling 1995, government-funded toxicology, ban 2005), 271 and 272 (BPD timescales “not established”, decisions “expected shortly”), 276 (UK and Denmark 2000–2001). [external] EU 2016, IMO 2023. Strength: moderate. The dates are clear. Effectiveness in Bermuda is asserted, not shown.

  13. Incumbents answering a restriction usually innovate incrementally within their existing competence. More radical alternatives come from actors who may not see the opportunity, so the direction of innovation, not just its pace, needs attention. Evidence: p. 275. Strength: asserted. Plausible and consistent with the substitution history, but no citation or data. It sits awkwardly with the claim of “market demand” on p. 276.

  14. Where the most sensitive receptors lie outside the regulating jurisdiction, risk assessment and law can miss the worst harm. Evidence: pp. 270–271 (corals are “not directly relevant within the EU”; dependent territories with more independent law); p. 267 (contamination where the chemical is not used). Strength: suggestive. Identified by the authors but not developed.

  15. Once a harmful thing is in circulation, prohibition reduces but rarely ends release. Planning should assume some continued release. Evidence: p. 276 (“fair to assume… release… is often inevitable”); p. 273 (continued retail sales); p. 267 (TBT rising in Asia); p. 276 (DDT still used as an antifoulant in China). Strength: suggestive. Several anecdotes; framed by the authors as an assumption.

Limitations, contestation and bias check#

Advocacy versus analysis. The chapter is mostly descriptive science synthesis. It reads less as advocacy than many chapters in the report, and it does not accuse industry. Its recommendations (monitoring, PBT criteria, research into alternatives) are moderate. The advocacy is in the framing:

Harm is largely potential. The evidence of harm is laboratory, microcosm and in-symbio photosynthesis inhibition, plus harbour concentrations at or above effect levels. The exposure link from harbour to reef is a “possibility” (p. 270). At the one remote reef system the authors sampled, the co-authored paper concludes “Negligible risks to corals” (p. 277; pp. 269, 271). Yet the summary says boosters “threaten a variety of habitats — from coral reefs…” (pp. 265, 276). In fairness, Chagos was chosen because it is remote and pristine, as a clean reference site. A negligible-risk finding there says little about reefs near harbours and moorings, such as Bermuda, where Irgarol was high in some harbour areas (p. 271). Still, the chapter presents no measurements of booster biocides on reefs near boating areas, so the strong “threaten” framing runs ahead of the demonstrated field exposure at reefs.

Unsupported effectiveness claim. “Policy has proven effective in… Bermuda and the United Kingdom, where banning selected agents lowered concentrations and limited adverse ecological impacts” (p. 276). The chapter gives no post-ban data for Bermuda and no ecological-outcome data for either place. The UK evidence covers Irgarol concentrations only, from one study co-authored by Readman.

Ambiguous figure. “by 10–55 % of levels in pre‑restriction studies” (p. 273) versus the source’s “between 10% and 55% of that found during pre-restriction studies”. The chapter’s wording is ambiguous and easily misread as a 10–55% reduction, which would understate the UK reduction (really 45–90%). Any misreading runs against the authors’ own argument, which suggests loose drafting rather than slant.

Endocrine claim wider than the evidence. “do not threaten to have endocrine disrupting properties similar to TBTs” (p. 265) rests on an oestrogenicity screen of seven compounds (p. 270). TBT’s harm (imposex) is masculinising, so that screen does not directly address TBT-like effects. [external] Later work reported endocrine effects of DCOIT (Sea-Nine 211) in marine medaka: raised oestradiol and lowered testosterone in males, called “a potent endocrine disruptive chemical” (Chen et al., 2014, Aquatic Toxicology). Caveats: those authors were comparing DCOIT with butenolide, a candidate antifoulant from their own research group. The 2014 abstract does not state exposure concentrations, but a companion study by the same group (Chen et al., 2015, Environmental Science & Technology) used 2.55 µg/L (about 2,550 ng/L) for 28 days. That is far above the sporadic Sea-Nine concentrations the chapter reports, so environmental relevance is doubtful. The 2015 study found vitellogenin induction in males, an oestrogenic effect, so the effect reported in fish is feminising rather than TBT-like masculinisation. (Abstracts re-checked via Europe PMC in this audit.) This later evidence qualifies, but does not overturn, the chapter’s reassurance.

Omissions and underweighted counter-arguments. - Copper is the dominant antifoulant (p. 267) and the base that “boosters” are added to. It is treated as background (“no or limited environmental concern”, Table 12.4). Yet Table 12.2 and 12.3 footnotes show Sweden and Denmark regulating copper leach rates (p. 272). Copper’s environmental role is not discussed. - Risk–risk trade-offs are absent. Less effective antifouling means more fuel use and emissions (the chapter’s own fuel figures, p. 266) and, from general knowledge, more transfer of invasive species on hulls. Neither the chapter’s recommendations nor its preference for “non-toxic” options weigh these. - No cost analysis of harms or controls. - Industry perspective is absent. There is no panel and no manufacturer or regulator response. A manufacturer paper is cited only as evidence of vulnerability, without its source or reassuring conclusion (Jacobson and Willingham, 2000; p. 269). - The fuel figures come from a pro-TBT trade article (MER, 1996) without comment (p. 266). - The claim about innovation dynamics (p. 275) is uncited. - Natural products are promoted partly on public perception that they are benign (p. 275), which does not fit the report’s general emphasis on evidence.

Insider standpoint. Much of the evidence comes from the authors’ own work (13 of 41 references). They are well placed to know the case. But the chapter is effectively the principal investigators assessing their own research programme, and some judgements (the UK ban’s success, Chagos as benchmark, the proposed monitoring programme under Price and Readman, 2006) promote that programme. There is no counter-voice.

Staleness in a 2013 report. - The legislative tables date from 2002 and 2008 (p. 272). - The most recent effectiveness study is 2006. The most recent literature cited is 2010. - The chapter does not mention the Biocidal Products Regulation (EU) 528/2012 that replaced the BPD, adopted in May 2012, a year before the report’s May 2013 publication. [external] Nor does it mention the proposed Water Framework Directive priority listing of cybutryne. That listing was in train (Commission proposal 2012) but was only adopted as Directive 2013/39/EU in August 2013, after publication, so its absence is understandable. - It says the IMO convention was cited as 2008 and that a “total ban has come into force” (p. 275). That is broadly right for TBT.

Hindsight. The list of TBT underestimations (p. 267) is written with hindsight and inherited from Volume 1 (Santillo et al.). The chapter does not ask whether the 20 ng/L threshold was reasonable given what was known at the time.

Internal inconsistencies (minor). - UK action dated 2000 (Table 12.4, HSE “began phasing out”) and 2001 (legislation, pp. 273, 275). These may be different steps rather than a true inconsistency. - TBT uptake “Shortly after World War II” (p. 266) versus the late 1950s/60s (Table 12.4). - Santillo cited as both 2001 and 2002 in the text (p. 266 has both), and as 2002 in the references. - The data-gap sentence says “other regions” on p. 269 but “other biocides” on p. 275. - The ecological concern is “considerable potential concern” on p. 274 but “considerable concern” in the summary and conclusion (pp. 265, 276). - The TBT ban’s positive impact is “well demonstrated” (p. 273) versus recovery “mixed, or slower than expected” and a ban “not… very effective everywhere” (p. 267). - Table 12.4’s BPD date (“entered into force on 14 May 2000”) probably conflates entry into force with the transposition deadline (see Table 12.4 observations; external, not re-verified). - “TCMBT” versus “TCMTB”. - The legislative position is said to be “as of 2002”, but Table 12.3 is 2008. - “Burnham Warf” (Table 12.1). - Japan’s national TBT ban is dated to “the late 1990s” (p. 267). I have not verified this against sources, and it may be imprecise.

Case selection. This is a well-documented, fairly fast-moving case in which regulators acted within about 7–10 years nationally. It is a reasonable illustration of regrettable substitution and of monitoring-led correction. It is weak evidence for the report’s broader themes of industry obstruction or suppressed warnings, and the chapter does not claim otherwise.

Fair in the other direction. The chapter is candid about uncertainty. It reports reassuring findings (no oestrogenicity, acceptable Danish PEC/PNEC for two substitutes, negligible Chagos concentrations, short half-lives for several agents). It recognises the economic necessity of antifouling (p. 266) and the limits of current alternatives (p. 275). Its recommendations are modest and practical.

Notable quotes#

  1. “They were believed to be less damaging to aquatic life than TBT. Subsequently, however, it has been established that booster biocides can also create significant environmental risks.” (p. 265)
  2. “imposex observed in 1970 in predatory gastropods in Arcachon Bay was considered acceptable — it had no immediately obvious economic cost — whereas the failure of the oyster stocks soon after was not acceptable” (p. 267)
  3. “The (limited) controls imposed were hailed by some as a ‘solution’ to the TBT problem.” (p. 267)
  4. “These high levels were actually discovered during a survey of agricultural triazine herbicides, which are measured using the same analytical protocol.” (p. 267)
  5. “the relative efficacy and toxicity of antifouling paints can only be determined by subsequent monitoring to establish whether initial suppositions/hypotheses were correct” (p. 273)
  6. “Whereas TBT acted quite specifically in causing imposex and shell abnormalities, through endocrine disruption, the booster biocides that replaced TBT have more broad‑spectrum impacts.” (p. 274)
  7. “Any future monitoring programme should be firmly linked to an action plan… Otherwise, monitoring can easily become an essentially scientific or academic pursuit.” (p. 274)
  8. “they tend to devise solutions with which they are familiar — typically more biocide. The result is incremental change” (p. 275)
  9. “Even for prohibited (but still used) toxic substances, it is fair to assume that a release into the environment is often inevitable.” (p. 276)
  10. “novel compounds, such as phenylborane pyridine, Econea, capsaicin and medetomidine, are almost uninvestigated, with very little information available on them in the public domain.” (p. 276)

Open questions#

  1. Did the substitutes get any pre-market assessment? What testing, if any, did booster biocides undergo before or after 1989, and who held the data? The chapter is silent. Linked question: were some boosters (such as Irgarol) already on the market before 1989? The chapter says Irgarol was “previously registered” (p. 267).
  2. Who are the actors? Who manufactured the main boosters, and how did they engage with the national bans and the BPD review? The chapter names no companies. Were there disputes over the UK and Danish bans? Primary sources would be UK HSE and Danish EPA decision documents.
  3. What happened in Bermuda after the ban? Did concentrations fall? Did coral indicators change? The claim that ecological impacts were limited (p. 276) needs evidence.
  4. What have long-term European monitoring trends shown for Irgarol and diuron after the UK, Danish, EU (2016) and IMO (2023) measures, especially against the 2.5 ng/L AA-EQS? Was the proposed Europe-wide indicator (Price and Readman, 2006) ever adopted?
  5. Was the untested temperature–herbicide interaction (p. 270) confirmed? [external] Later work treats thermal stress and PSII herbicides as combined stressors in setting guideline values (Negri et al., 2020, Environmental Science & Technology, on diuron and copper). The specific findings need checking.
  6. How did the novel substitutes fare? Econea (tralopyril), medetomidine and DCOIT were approved under the BPR in 2015–2016, medetomidine as a candidate for substitution. What post-approval monitoring or evidence of harm exists? Is the cycle the chapter describes repeating a third time?
  7. Did non-stick and foul-release coatings, hull-cleaning robots and similar alternatives spread after 2013, against the chapter’s prediction that widespread use “seems unlikely without further advances in technology” (p. 275)? Did the innovators come from outside the incumbent manufacturers (p. 275)?
  8. How should the risk–risk trade-offs be weighed: fuel and emissions, and invasive species on hulls, against toxic coatings? What do post-2013 assessments conclude?
  9. What is diuron’s status for product-type 21 in the EU? I could not verify it in this session.
  10. What is “IYP (2008)”? It is the source of Table 12.3, cited as “‘Antifoulings — the legislative position by country’” (p. 277), and is not expanded. It may be a yacht-paint manufacturer’s publication (unverified). If it is, the regulatory summary has an industry source.
  11. Did TBT levels in Asia stop rising (p. 267) after the AFS Convention came into force in 2008? Did DDT use as an antifoulant in China (p. 276) end, for example under Stockholm Convention exemptions?
  12. Is the Japan “late 1990s” TBT ban date accurate (p. 267)?
  13. What was Readman’s role in the ACE project (1999–2002), which supplies the chapter’s European baseline? The chapter cites ACE (2002) as a corporate author and does not say who led it. If a chapter author coordinated ACE, the insider share of the evidence base is larger than the 13-of-41 reference count suggests.
  14. When exactly did the BPD enter into force? Table 12.4 says 14 May 2000; check this against the Official Journal text of Directive 98/8/EC.

External sources consulted (post-2013 checks)#

Audit log#

Independent fact-check against the text extract (PDF 263–280, all pages read) and rendered PDF pages 263, 270, 274 and 278.