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mary cummins, animal advocates, anticoagulant bait, rat poison, poison, anticoagulant, los angeles, california, wildlife, death, brodifacoum, fish, water, lake, ocean, sea |
A new study came out showing anticoagulant poison in trout, Brodifacoum causes coagulopathy, hemorrhages, and mortality in rainbow trout (Oncorhynchus mykiss) at environmentally relevant hepatic residue concentrations.
When I was accidentally poisoned by anticoagulant bait along San Buenvaventura beach in 2003 it also went into the water. The pest control operator admitted to free scattering the poison in the tidal areas in the rocks to kill ground squirrels. Within a week I found dead fish and a dead pelican on the beach. I sent the pelican to the lab. It had evidence of internal bleeding. I also found many, many dead birds on the beach and beach parking lot besides a dead cat. Sent the birds to the lab. They had four different types of anticoagulant bait in them. The ecoli level was so high in the water right there that they closed the beach for two weeks. Poison gets into the water directly and indirectly.
Study Highlights
•Brodifacoum doses ≥ 75 µg/kg bw disrupt blood coagulation of rainbow trout.
•Brodifacoum doses between 100 and 200 µg/kg bw cause mortality in rainbow trout.
•Test duration is a key factor assessing the effects of brodifacoum on fish.
•Brodifacoum doses ≥ 75 µg/kg bw disrupt blood coagulation of rainbow trout.
•Brodifacoum doses between 100 and 200 µg/kg bw cause mortality in rainbow trout.
•Test duration is a key factor assessing the effects of brodifacoum on fish.
•The lowest mean hepatic residue associated with effects in trout is 122.6 ng/g.
•Brodifacoum causes effects at environmentally relevant hepatic concentrations.
Abstract
•Brodifacoum causes effects at environmentally relevant hepatic concentrations.
Abstract
Widely used second-generation anticoagulant rodenticides like brodifacoum are classified as persistent, bioaccumulative, and toxic. Widespread exposure of terrestrial and avian non-target species is well-known and recently hepatic anticoagulant rodenticide residues have been detected in wild fish. However, no sufficient data exist to interpret the effects of these findings on fish health. In order to assess the potential impact of rodenticide residues on fish, we exposed rainbow trout (Oncorhynchus mykiss) to brodifacoum-spiked feed. In a first experiment, individually kept trout (body weight ca. 200 g) were exposed to a single dose of brodifacoum and observed for 15 days. In a second experiment, fish (body weight ca. 330 g) were kept in groups and fed every 7 or 8 days with brodifacoum-spiked feed for up to 60 days. Sampling of trout every 15 days over the 60 days period allowed monitoring of brodifacoum concentrations in serum, liver, and muscle tissue, as well as occurring effects over the course of the experiment. In both experiments, brodifacoum doses of ≥ 75 µg/kg body weight caused prolonged or non-measurable blood coagulation times. Disturbed hemostasis led to hemorrhages and anemia with significantly decreased albumin levels. In the 60 days-experiment, brodifacoum doses ≥ 100 µg/kg body weight caused additionally discoloration, apathy, and anorexia, resulting in reduced weight gain, and ultimately mortality. The delay until the onset of overt symptoms (14–17 days) highlights the importance of test duration while investigating effects of anticoagulant rodenticides in fish. The lowest hepatic brodifacoum concentration associated with effects in trout was on average 122.6 ng/g liver wet weight, which is in the range of previously reported brodifacoum residues in wild fish. These findings illustrate the risks associated with the use of anticoagulant rodenticides for freshwater fish and reinforce the need to stipulate all available and appropriate risk mitigation measures to prevent emissions at source.
Link to paper
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