REDUCING RODENTICIDE HAZARDS TO HUMANS AND WILDLIFE: THE NEED FOR USE REGULATIONS MICHAEL FRY, Pesticides and Birds Program . American Bird Conservancy, Washington DC, USA Abstract: Rodenticide use poses significant exposure risks for children and poisoning risks for native wild birds and mammals in the United States. Poison Contro l Center reports document 15,000 calls annually identifying household rat poison ingestion , with 88% of cases for children under age six. Wildlife poisonings from ingestion of baits or treated grain may occur whenever birds or mammals have access to the products. This is especially true for broadcast baits and treated grain used above ground in agricultural settings, or when baits are distributed around structures or outside waste containers. Secondary poisoning of predators and scavengers occurs when target rodents are moribund or die above ground in locations accessible to predatory birds or mammals . Secondary poisoning risks appear to be highest for the "seco nd generation" anticoagulant rodenticides , becaus e rodents consume them in super-lethal doses in multiple feedings during the 4-6 days required for these poisons to kill the target rodents. These anticoagulants persist for long periods in tissues of scavengers and predators , increasing the risk of adverse effects from subsequent feedings on poisoned rodents. The risk of both human and wildlife poisonings can be greatly reduced by packaging rodenticides in bait stations and restricting the use of second generation product s to licensed pest control operators. Key words: anticoagulant rodenticides, brodifacoum , bromadiolone , chlorophacinone, diphacinone , rodent, seco ndary toxicity , strychnine, warfarin, zinc phosphide Proceeding s of the 12th Wildlife Dama ge Management Conference (D.L. Nolte, W.M. Arjo, D.H . Stalman, Eds). 2007 INTRODUCTION rodenticide products to children has resulted Commensal rodents pre sent public in many reported incident s to poison control hea lth and disea se risks to human cen ters, and the high toxicity to other population s, living in almost every urban vertebrates has resulted in both primary and rural region. Rodent s also damage poisoning of non-target mammals and birds stored crops and structures resulting in ingesting baits or treated grain, as well as economic loss and contamination of stored seco ndary poisonin g of carnivorous grains. Co ntrol of these populations is scave nging mammals and birds . neces sary, and effective rodenticide baits The poisoning of non-target animals and treated gra ins have been developed with and humans has been a major concern of the a variety of different mechanisms of action. US Env ironm ental Protection Agency Because these toxicants are designed (EPA) , which initiated regulatory review of for mammalian rodents , rather than insects nine rodenticides in 1998, resulting in a or plant pests, the chemicals are also toxic to comprehens ive risk assessme nt and human s, other mammals , and birds . The mitigation plan by the EPA in 2007 in an high availability of over-the-counter ll9 effort to mm1m1ze the exposure to non­ (FGAR) registered in the US include targets , including children. warfarin, and the indanedione derivative s chlorophacinone and diphacinone. These RODENTICIDES CURRENTLY ON have been marketed for the past 50 years. THE CONSUMER MARKET Rodent resistance to warfarin occurred in The EPA currently has ten many areas in the 1960s and a group of rodenticide active ingredients registered for highly toxic derivatives were developed as use in the US. The products available are alternatives for the first generation three "first generation" anticoagulants anticoagulants. Brodifacoum was described (warfarin, chlorophacinone, and by Hadler and Shadbolt (1975) and termed a diphacinone ), three "seco nd-generation" "superwarfarin" or "seco nd generation" anticoagulants (brodifacoum, difethialone , anticoagulant rodenticide (SGAR). Other bromadiolone ), and four non-anticoagulant SGARs registered in the US include compounds (zinc phosphide , bromethalin, difenacoum , difethialone and bromodialone. strychnine and cholecalciferol) . The They all are derivatives of coumarin, and act rodenticides are predominantly used to by the same mode of action as FGARs. The control commensal rats and mice in and SGARs are more toxic, and formulated in around buildings and other urban areas. Al! bait blocks at concentrations of 0.025 to are available as consumer products "ove r­ 0.005% active ingredient , and are generally the-counter", sold without restnct1ons, lethal to rodents after a single feeding. although the more concentrated formulations Since the mechanism of action is similar for of several are "restricted use " and available both first and second generation only to licensed pest control operators. anticoagulants, the time to death for Some products (zinc phosphide , strychnine , intoxicated target animals is very similar (5- chlorophacinone and diphacinone) also have 7 day s), even though only a single feedin g is regi strations for outdoor and agricultural required for the SGARs to be lethal. uses against rodent and small mammalian pests. Additionally , brodifacoum and Non-anticoagulant Rodenticides diphacinone hav e important island The four non-anticoagulant conservation uses on lands mana ged by the rodenticides currently registered in the US US Fish and Wildlife Service, US National include a variety of chemicals with diverse Park Service , and other agencies . modes of action. Two are neurotoxin s: strychnine and bromethelin . Strychnine Anticoagulant Rodenticides causes exc itation of all parts of the nervous Warfarin was patented by the system by blocking inhibitory neurons Wisconsin Alumni Research Foundation in resulting in convulsions. Bromethalin is a 1945 after a series of coumarin compounds disruptor of energy metabolism with central were isolated and synthesized by university nervous system effects that also causes researchers (Stahmann et al. 1941 ). convulsions and paralysis. Zinc phosphide Warfarin and other anticoagulants act by has been registered as a rodenticide since the disrupting blood clotting through inhibition 1940s, and liberates highly toxic phosphine of vitamin K synthesis. The inhibition and gas in the gut of exposed animals which depletion of clotting factors takes several adversely and rapidly affects major organ days , and intoxicated animals usually die 4- systems. Vitamin D 3, cholecalciferol, is 8 days after ingestion of baits . The "first registered as a rodenticide, and when fed in generation" anticoagulant rodenticides large amounts , disrupts nom1al calcium 120 metabolism, resulting in calcium compared to SGARs. A review of l 7 mobilization and deposition in many tissues studies , including all three first generation and, ultimately , kidney failure. anticoagulants (warfarin , diphacinone and chlorophacinone) , showed little mortality RISK OF FIRST AND SECOND from secondary exposure to many species of GENERATION ANTCCOAGULANT predatory birds. Mortality ranged from 0 to RODENTCCIDES TO NON-TARGET 9%. In eight chlorophacinone studies with 9 ANIMALS species of raptors , there was no · mortality Laboratory studies conducted EPA from consuming laboratory poisoned protocols for anticoagulants with first rodents. There was a 9% mortality in three generation ( chlorophacinone , diphacinone, diphacinone studies with five different warfarin) and second generation species of birds , and in four warfarin (bromodialone, brodifacourn, and studies, there was also a 9% mortality. For difethialone) ingredients have shown that all most studies , adverse effects such as compounds are greater than 90% effective, prolonged clotting time were observed in and time to death was very similar for all some surviving individuals. There were no compounds tested, with median times to observed sublethal effects in surviving birds death of 4.5-6 days (Erickson and Urban , exposed to warfarin. 2004). ln contrast to the relatively low Because time to death is similar , the mortality with first generation more acutely toxic second generation anticoagulants , EPA review of SGAR compounds have a greater potential to studie s demonstrated high mortality for overload target animals during successive predatory birds and mammals fed carcasses feedings , and they pose a significantly of brodifacoum-poisoned rodents . In eleven greater secondary toxicity hazard to raptors studies , an average of 63% of exposed and mammalian scavengers. predatory or scavenging birds died The potential for target rodents following ingestion of poisoned prey. accumulating super-lethal levels of SGARs About 33% of survivors showed signs of was report ed to EPA by the produc er (!Cl tox1c1ty. In five studie s with bromadiolone , Americas , Inc ., Gold sboro , NC) and however , mortality occurred in 8% of birds reported in Erickson and Urban (2004). exposed to poisoned prey . Brodifacoum (Talon™ , 50ppm) was fed to The se reviews indicate that SGARs , captive Norway rats (Rattu s nor vegicus) and especially brodifacoum , pose significant monitored for consumption . Rats were secondary risks to wild birds and mammals given bait alone or as a choice with when ever target rodent s are accessible untreated food , and fed until death, which outdoors . averaged 6.5 days. Rats fed only bait as food consumed an average of 80 lethal doses EXPOSURES TO CHILDREN AND before death , and rats given the choice of NON-TARGET ANIMALS baits and untreated food ingested an average of 40 lethal doses before