Monitoring agricultural rodenticide use and secondary exposure of raptors in Scotland

Abstract

Despite the documented risk of secondary poisoning to non-target species by anticoagulant rodenticides there is no statutory post-approval monitoring of their use in the UK. This paper presents results from two Scottish monitoring schemes for the period 2000-2010; recording rodenticide use on arable farms and the presence of residues in raptor carcasses. More than three quarters of arable farms used anticoagulant rodenticides; predominately the second generation compounds difenacoum and bromadiolone. There was widespread exposure to anticoagulant rodenticides in liver tissues of the raptor species tested and the residues encountered generally reflected agricultural use patterns. As found in other studies, Red Kites (Milvus milvus) appeared to be particularly vulnerable to rodenticide exposure, 70 % of those sampled (n = 114) contained residues and 10 % died as a result of rodenticide ingestion. More unexpectedly, sparrowhawks (Accipiter nisus), which prey almost exclusively on birds, had similar exposure rates to species which prey on rodents. Although, with the exception of kites, confirmed mortality from rodenticides was low, the widespread exposure recorded is concerning. Particularly when coupled with a lack of data about the sub-lethal effects of these compounds. This raises questions regarding whether statutory monitoring of use is needed; both to address whether there are deficiencies in compliance with approval conditions or whether the recommended risk management procedures are themselves adequate to protect non-target wildlife.

Poisoning by Anticoagulant Rodenticides in Humans and Animals: Causes and Consequences

“…The delayed action of ARs, inherent to its mechanism, allows rodents to eat several times the LD50 dose between the irst bait intake and the death [1] and may as well increase the risk of secondary exposition. Pesticide usage has been correlated with non-target wildlife exposition [74,75], and the intensity of treatment was related to incidence on local fox populations in France [80]. Finally, the diet is certainly going to inluence secondary exposition and species like raptors, foxes and mustelids largely feeding on rodents when abundant are consequently the most at risk, as demonstrated for the red kite (Milvus milvus) [81].…”

“…Wildlife expositions or intoxications to ARs have been reported around the world for many mammals such as minks [70], bobcats [71], stoats and weasels [72], foxes [73,74] and boars [67] and as well for many birds [75][76][77]. Exposition of ish was reported near an island where an eradication of rodent with brodifacoum was performed and the risk for human through the consumption appeared very low [78].…”

Development of an Ecofriendly Anticoagulant Rodenticide Based on the Stereochemistry of Difenacoum

“…Because of this increased persistence in animal tissues, especially in liver (Langford et al, 2013), the use of SGARs is associated with an increased risk of secondary poisoning for predators and scavengers feeding on contaminated rodents. Evidence of secondary poisoning was confirmed in predatory bird species such as barn owl (Tyto alba), buzzard (B. buteo), kestrel (Falco tinnunculus), Red kyte (Milvus milvus), and tawny owl (Strix aluco) (Christensen et al, 2012 ;Hughes et al, 2013 ;Geduhn et al, 2015), in predatory mammals such as red foxes (Vulpes vulpes) (Sage et al, 2010), European mink (Mustela lutreola) (Fournier-Chambrillon et al, 2004), weasels (Mustela nivalis) (Elmeros et al, 2011). Therefore, ARs were identified by the European Union as candidates for future comparative risk assessment and substitution in view of their unacceptable risk of secondary poisoning for wildlife.…”

Adaptative evolution of theVkorc1gene inMus musculus domesticusis influenced by the selective pressure of anticoagulant rodenticides

“…The emergence of such resistance to anticoagulants belonging to the first generation (i.e., warfarin, diphacinone, coumatetralyl, chlorophacinone) led to the development of new AVK belonging to the second‐generation molecules (i.e., bromadiolone, difenacoum, flocoumafen, brodifacoum, and difethialone) in the 1970s and 1980s. Nevertheless, the use of such molecules, excessively persistent, exacerbated the risk of primary and secondary poisoning of nontarget species (Caloni, Cortinovis, Rivolta, & Davanzo, 2016; Hughes, Sharp, Taylor, Melton, & Hartley, 2013; Jacquot et al., 2013). Therefore, such molecules should be carefully used.…”