Emamectin benzoate belongs to the avermectin group and is administered to the fish through feed. This preparation is manufactured by Schering-Plough Animal Health and is marketed under the name Slice® vet. Unless another source is given, the information comes from McHenery (1999), a report prepared on behalf of Schering-Plough.
Avermectins bind with high affinity to glutamate-regulated ion channels in invertebrates. Avermectins cause increased diffusion of chlorides through the cell membranes in the salmon louse and nerve impulse disruptions. The result is that the parasite is paralysed and dies. Emamectin benzoate is effective against several stages of the salmon louse, the copepodite, chalimus, mobile pre-adult and adult stages. Due to the spread of infectious salmon anaemia (ISA), it is desirous for the treatment to kill the salmon louse at all stages of its life, since the salmon louse can function as a carrier of ISA (Nylund et al., 1994).
Effective treatment of salmon lice is achieved by administering 50 μg per kilogram fish, per day for seven days.
Biodegradation in the environment
When giving feed with emamectin added, a small amount will fall to the bottom as feed spills, while most of it is added to the environment through excrement and is thus incorporated into the sediments. Dispersion will depend on local current and depth conditions. Various models have helped researchers estimate that feed spills and excrement disperse over an area of between 10,000 and 20,000 sq. m after treating twelve 15×15 m cages.
Biodegradation in seawater
The half-life of emamectin in water was found to vary between 0.7 days during summer conditions to 35.4 days during winter conditions. The difference is due to light-sensitivity, not temperature.
Biodegradation in sediments
Laboratory tests in which medicated pellets containing emamectin were added to anaerobic marine sediment samples showed than 66-68% of the administered dose had not biodegraded after 100 days. On the basis of this datum, a half-life in these samples was estimated to be between 164 and 175 days.
Modelling indicates that the concentration of emamectin in sediments is at 76 μg/kg directly beneath fish farms that have been medicated, falling to 1.7 – 16.7 μg/kg 75 metres away along the tidal axis. 100 m downstream from the fish farm, the concentration drops to 0.2-1.7 μg/kg. Field tests have established emamectin residues in one of ten sediment samples. The positive sample was taken ten metres downstream from the fish farm. The other nine samples yielded no traces. The likely reason that the field tests showed less residue than the modelling results is that the substance was quickly diluted in large quantities of seawater.
The toxicity of avermectins in general and emamectin in particular has been tested for a large number of organisms. In the following we will review examples of various categories of organisms, but for a complete survey, we refer to McHenery (1999).
Microorganisms and plants
Avermectins have neither antibacterial nor fungicidal properties, and no effect on microbial fauna in the soil has been recorded at concentrations of 5 mg/kg. Nor have microalgae been found to be sensitive to avermectins, with tests on Selenastrum capricornutum over 5 days at concentrations of up to 3.9 μg/litre showing no effect. Gibbous duckweed (Lemna gibba) exposed to concentrations of up 94 μg/litre over 14 days was not affected either. However, toxic effects were found for tomato roots that were dipped in a solution with a concentration of 192 mg/litre (McHenery, 1999).
Since emamectin is meant to kill salmon lice, which is a crustacean (subphylum: Crustacea), it is not surprising that this substance is also toxic to other crustaceans. The most vulnerable is Mysidopsis bahia (mysid shrimp), which had a mortality of 50% (LC50) after 96 hours in water with a concentration of emamectin of as little as 0.04 μg/l. At the opposite end of the scale we find Crassostrea virginica (a species of oyster, not relevant in Norway), which had an estimated mortality of 50% at a concentration of 665 μg/l. Similar results have been found in a number of other molluscs. Field tests in which mussels were placed near fish farms during treatment with emamectin showed no signs of toxic effects up to 4 and 12 months after treatment.
For Crangon crangon (common shrimp, sand shrimp) and Nephrops norvegicus (Norway lobster, ocean crayfish) mortality of 50% was registered after 192 hours at concentrations in the water of 166 μg/l and 572 μg/l, respectively. Such high concentrations will not be found under realistic conditions. No significant effect or mortality was seen in the same species after they were fed fish food with concentrations of 69.3 and 68.2 mg/kg, respectively.
Salmon that have ingested doses of emamectin through medicated feed of 356 μg/kg fish/day over 7 days, showed no mortality, and the No Effect Limit (NOEL) was found to be 173 μg/kg fish/day.
Tests of toxic effects on mammals have been done with regard to human health (see below).
A score of toxicological studies have been done on mice, rats and beagles. Mortality of 50% (LD50) occurred at doses varying from 22 to 120 mg/kg. In the study yielding the lowest NOEL, an experiment based on neurotoxicity with daily doses over 15 days in mice, a NOEL of 100 μg/kg body weight was found.
Based on the NOEL and a safety factor of 100, the acceptable daily intake (ADI) has been set at 1 μg/kg body weight. Thus, a person weighing 60 kg has an ADI of 60 μg/kg body weight. On this basis, the MRL has been set at 100 ?g/kg fish (EMEA, 1999).
Based on residue concentration tests in salmon, researchers in many countries have found no need for any retention period. This applies to the EU and Chile, for example. Nevertheless, the United Kingdom and Chile have a rule that fish may not be treated more than once during the 60 days before slaughtering, which is not really relevant in any case. In Norway there was once a requirement of zero residue instead of an MRL, and therefore a retention period of 120 days. The Norwegian system with the zero threshold was justified on the basis of marketing considerations whereby Norwegian fish would be able to be marketed as "completely" pure. In practice this meant that the detection threshold of the testing method in question was the applicable threshold. This has now been abolished and replaced with an MRL.