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The contaminant levels in Norwegian farmed salmon have generally decreased between 1999 and 2011. Excluding other dietary sources, the levels of dioxins and dioxin-like PCBs in 2011 allowed consumption of up to 1.3kg salmon per week to reach the tolerable weekly intake. The group of contaminants which was the limiting factor for safe consumption of Norwegian farmed salmon, based on currently established TWI values, is the sum of dioxins and dioxin-like PCBs.

Brominated flame-retardants (BFRs) such as polybrominated diphenyl ethers (PBDE) and hexabromocyclododecane (HBCD) are considered hazardous to human health. Due to their persistence, they are still present in the environment and in biota and seafood is major contributor of BFRs to human exposure. Here, we used data from >9700 samples of wild and farmed fish, fish feed and fish feed ingredients collected from the North Atlantic between 2006 and 2016 aiming to investigate factors influencing the risk assessments of BFRs. Due to most representative number of analyses, PBDEs were the main focus of investigation. Mean ∑PBDE in fillet samples ranged from below quantification in Atlantic cod fillet to 2.0 μg kg in Atlantic halibut. The main congener contributing to the ∑PBDE in all species was BDE 47. Factors affecting the level of BFR in seafood were multifaceted, and the levels were within species mainly determined by fish age, geographical origin and time of sampling. BDE 47, 99, 153 and HBCD were selected for margin of exposure (MOE) evaluation. When other sources of BFR than seafood were excluded, our risk assessment showed low risk at the current dietary intake of seafood. However, the dietary intake of BDE 99 may be of concern for toddlers when all sources are considered. The choice of fish species, dietary studies, choice of statistics, as well as exposure from other sources than seafood, were all factors that influenced the final MOE of BFRs. We propose the use of regression on order statistics as a tool for risk assessment, to illustrate means and spreads in large surveillance datasets to avoid the issue of measurements below the limit of quantification. A harmonized, updated evaluation of the risk associated with exposure to BFRs from diet, air and dust is warranted, where the fish species most commonly consumed also is taken into consideration.

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Methylmercury (MeHg) is a ubiquitous environmental contaminant which bioaccumulates in marine biota. Fish constitute an important part of a balanced human diet contributing with health beneficial nutrients but may also contain contaminants such as MeHg. Interactions between the marine n-3 fatty acids eicosapentaenoic acid (20:5n-3, EPA) and docosahexaenoic acid (22:6n-3, DHA) with MeHg-induced toxicity were investigated. Different toxic and metabolic responses were studied in Atlantic salmon kidney (ASK) cell line and the mammalian kidney-derived HEK293 cell line. Both cell lines were preincubated with DHA or EPA prior to MeHg-exposure, and cell toxicity was assessed differently in the cell lines by MeHg-uptake in cells (ASK and HEK293), proliferation (HEK293 and ASK), apoptosis (ASK), oxidation of the red-ox probe roGFP (HEK293), and regulation of selected toxicological and metabolic transcriptional markers (ASK). DHA was observed to decrease the uptake of MeHg in HEK293, but not in ASK cells. DHA also increased, while EPA decreased, MeHg-induced apoptosis in ASK. MeHg exposure induced changes in selected metabolic and known MeHg biomarkers in ASK cells. Both DHA and MeHg, but not EPA, oxidized roGFP in HEK293 cells. In conclusion, marine n-3 fatty acids may ameliorate MeHg toxicity, either by decreasing apoptosis (EPA) or by reducing MeHg uptake (DHA). However, DHA can also augment MeHg toxicity by increasing oxidative stress and apoptosis when combined with MeHg.

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