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Molecular mechanisms and tissue targets of brominated flame retardants, BDE-47 and TBBPA, in embryo-larval life stages of zebrafish (Danio rerio).

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In this chapter we discuss the current understanding on chemical exposures and effects in wildlife for phthalates, the most widely used plasticisers, and two other major components of plastics, bisphenol A (BPA) – a plastic monomer and polybrominated diphenyl ethers (PBDEs) – incorporated as flame retardants. Ecotoxicity studies have shown that phthalates (and BPA) are generally not acutely toxic to wildlife at environmentally relevant exposures (in the low µg l−1 range), but chronic effects, including disruption of hormone systems and reproduction, have been reported in almost all animal groups studied. Although phthalates (and BPA) do not readily bioaccumulate and undergo rapid biodegradation, their continual release into the environment makes them pseudo-persistent. In contrast with phthalates and BPA, PBDEs are highly bioaccummulative, and developmental exposures to some PBDEs cause liver and kidney toxicity, immunotoxicity, neurotoxicity and endocrine disruption for environmentally relevant exposures in various wildlife phyla. Many of the effects of PBDEs in vertebrates occur due to disruptions to the thyroid hormone system. Concern relating to both human and wildlife exposure and (eco)toxicological effects has recently led to various regulations restricting the use of certain phthalates, bisphenols and PBDEs in plastics.

Anti-parasitic drugs used to control sea lice infestations in the salmonid aquaculture industry are a growing environmental concern due to their potential impacts on non-target crustacean species. This study examined the lethal effects of teflubenzuron, a common in-feed pharmaceutical drug used on Norwegian salmon farms, on a non-target species, rockpool shrimp Palaemon elegans, following an extended exposure period. The standard daily dose for treating salmon is 10 µg teflubenzuron g −1 fish. Adult shrimp were fed 1 of 6 low doses of teflubenzuron (0, 0.0025, 0.005, 0.05, 0.094, 0.188 and 1.88 µg g −1) twice a week for a period of 66 d. Cumulative mortality reached 15, 27, 82 and 100% amongst shrimp exposed to the highest treatment groups (0.05, 0.094, 0.188 and 1.88 µg g −1 , respectively). Cumulative mortality amongst shrimp exposed to the 2 lowest teflubenzuron doses and control feed was low (5%). Dose response curves based on measured concentrations within the shrimp were used to calculate a series of lethal threshold concentrations (LC x). The LC 5 , LC 50 and LC 90 concentrations of teflubenzuron causing low, median and high levels of mortality in rockpool shrimp were estimated to be 1.2, 18.4 and 150.6 ng g −1 , respectively. These concentrations are similar to those reported in wild crustacean species, including shrimp species in the vicinity of Norwegian fish farms, both during and after teflubenzuron medication, suggesting that exposure to low doses of this compound can pose a significant risk to wild shrimp populations.