Poisoning of Wildlife With Anticoagulant Rodenticides in New York

Abstract

From 1971 through 1997, we documented 51 cases (55 individual animals) of poisoning of non-target wildlife in New York (plus two cases in adjoining states) (USA) with anticoagulant rodenticides--all but two of these cases occurred in the last 8 yrs. Brodifacoum was implicated in 80% of the incidents. Diphacinone was identified in four cases, bromadiolone in three cases (once in combination with brodifacoum), and chlorophacinone and coumatetralyl were detected once each in the company of brodifacoum. Warfarin accounted for the three cases documented prior to 1989, and one case involving a bald eagle (Haliaeetus leucocephalus) in 1995. Secondary intoxication of raptors, principally great horned owls (Bubo virginianus) and red-tailed hawks (Buteo jamaicensis), comprised one-half of the cases. Gray squirrels (Sciurus carolinensis), raccoons (Procyon lotor) and white-tailed deer (Odocoileus virginianus) were the most frequently poisoned mammals. All of the deer originated from a rather unique situation on a barrier island off southern Long Island (New York). Restrictions on the use of brodifacoum appear warranted.

Second generation anticoagulant rodenticides in predatory birds: Probabilistic characterisation of toxic liver concentrations and implications for predatory bird populations in Canada

“…Diamond in the center of the box represents average, line is the median, box is the upper and lower quartiles and the whiskers are the standard deviation. Sources of the data are: Newton et al 1990Newton et al , 1998Newton et al , 2000Stone et al 1999Stone et al , 2003Albert et al 2010; EIIS 2010 download.…”

“…frequently than red-tailed hawks (Stone et al 1999(Stone et al , 2003. Additional studies and 368 monitoring of red-tailed hawk SGAR residues would strengthen our ability to estimate 369 the risk of toxicosis following exposure to SGARs.…”

“…These newer anticoagulant poisons differ from their 5 first-generation counterparts in that they are more acutely toxic at lower doses (often 6 allowing a lethal dose to be obtained in a single feeding), and are more persistent in 7 vertebrate livers (Parmar et al 1987, Stone et al 1999, Erickson and 8 Urban 2004. Greater acute toxicity increases the potential for primary poisoning 9 amongst non-target species while the longer tissue half-lives of SGARs enhance the 10 potential for bioaccumulation in non-target predators in particular, and so may increase 11 the risk of secondary poisoning.…”

“…SGARs bind and inhibit vitamin K epoxide reductase and persist for at least six 20 months in organs and tissues containing this enzyme such as the liver (Stone et al 1999, 21 Eason et al 2002. In an attempt to monitor exposure in non-target wildlife, the presence 22 of detectable SGAR residues as well as the magnitude of concentrations has been 23 measured in the livers of some Canadian, American and European predatory birds and 3 24 scavengers (Albert et al 2010, Newton et al 1990.…”

“…However, it is uncertain 41 whether these barn owl criteria would apply to other species. Liver residues associated 42 with SGAR poisonings in various species typically range over two orders of magnitude 43 and were reported to be as low as 0.01 mg/kg wet wt in one great horned owl that was 44 examined (Stone et al 1999 …”