Publish date: January 7, 2009

Teflubenzuron is a salmon delousing agent that is added to medicated pellets at a concentration of 2g/kg of feed. The dosage is 10 mg/kg body weight each day over seven days. Teflubenzuron is marketed in Norway by Skretting under the name Ektobann. Teflubenzuron is for the moment not being used in Norway, which partly is due to the negative focus in 1998 on possible environmental effects and partly doe to the introduction of the product Slice, with emamectin as the active ingredient. Unlike teflubenzuron, Emamectin is effective against all stages of salmon lice. Owing to fears of the development of resistance in salmon lice against emamectin in particular, Skretting sees a certain possibility for a resumption in the use of teflubenzuron, even though the manufacturer does not currently have a commercial interest in this. This substance is approved for use in Norway, the United Kingdom, Ireland, Canada and Chile (Richie, 2002).



Teflubenzuron is a chitin synthesis inhibitor, that is, it disrupts chitin synthesis in shellfish and kills the louse by preventing moulting. The substance is effective on moulting on the larval stage and pre-adult lice, but has no effect on adult lice.


Fate in the environment

Teflubenzuron enters the environment chiefly via excrement and, to a certain extent, feed spills. The substance binds to particles and has low water-solubility. This leads to low concentrations in the water and there is no effect on aquatic organisms. Sedimentation of the particles is relatively rapid below and around the fish farm, with the result that high concentrations can be recovered only in a limited area.


Biodegradability in the sediment

Teflubenzuron biodegrades relatively slowly, and according to laboratory tests, has a half-life in sediment varying from 35 to 100 days. However, a field study that took place over a year in a location in Scotland showed a half-life of six months. The discrepancy with regard to the expected degradation time is attributed to the fact that the test location was a "worst-case" location in respect of water exchange and being burdened by organic material (SEPA, 1999).



Since teflubenzuron works on crustaceans by preventing moulting, the deleterious effects on crustaceans around the fish farm will be greatest if a lot of animals are moulting during and in the period following treatment.


Several field studies have been done to assess the effect that teflubenzuron use has on crustaceans such as crab and lobster. In an experiment conducted in Norway, three groups of crabs (Cancer pagarus) were set out. One was placed next to the fish farm, one 70 metres away and one was a control group. Mortality was 17.1 per cent next to the fish farm, 14.5 per cent 70 metres away and 17.5 per cent in the control group. Thus, mortality in crabs exposed to teflubenzuron does not deviate significantly from the control group. Nor were any significant differences found in the percentage of individuals that moulted successfully during the experiment.


In a similar Canadian experiment on lobster (Homarus americanus), mortality of 10% was found in lobster located under the fish farm and 13% in the group located 50 metres away. A group located 100 metres away had zero mortality, as did the control group. Here the difference in mortality is significant.


A Scottish study of lobster (H. gammarus) yielded significant differences in mortality between the control groups and the groups of lobster placed under the fish farm and 25 metres away from it. In this study there was also high mortality in the control group, which is attributed to high levels of organic material in the sediment.


Human health

A number of studies of toxic properties have been done to uncover possible risks to human health. The studies were reviewed by EMEA (1999b). No NOEL has been set, because the lowest dose studied, 487.3 mg/kg body weight/day, yielded effects in the form of increased liver size in mice and rats, for instance.


The carcinogenicity tests cited conclude that there is no significant difference in tumour development between treated rodents and the control group, and negative results of mutagenicity studies were cited.


Owing to a lack of knowledge of the NOEL a safety factor of 200 was used to set the ADI, which on the basis of dose-related effects in tissue from the carcinogenicity studies has been set at 0.01 mg/kg body weight. On the basis of residue concentration studies, the MRL has been set at 500 μg/kg fish.