protecting raptors from rodenticides

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1 VOLUME XXVII, NUMBER 1-4, SPECIAL ISSUE 2011 (PUBLISHED JANUARY 2013) Protecting Raptors from Rodenticides

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Page 1: Protecting Raptors from Rodenticides

1

VOLUME XXVII, NUMBER 1-4, SPECIAL ISSUE 2011 (PUBLISHED JANUARY 2013)

Protecting Raptorsfrom Rodenticides

Page 2: Protecting Raptors from Rodenticides

2 Box 7414, Berkeley, CA 94707Common Sense Pest Control XXVII(1-4) Special Issue 2011

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© 2013 Bio-Integral Resource Center. All rights reserved. ISSN 8756-7881

Page 3: Protecting Raptors from Rodenticides

3Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

By William Quarles

Rats and mice have beenpests throughout recordedhistory. They eat and con-

taminate food, and help transmithuman diseases, including plague.Pest management as a professionstarted with rats and mice, andthey are common elements in litera-ture and in our cultural history.Who can forget The Plague by AlbertCamus, or the Pied Piper of Hamleinfolktale? (Corrigan 1997)The best way to control rodents is

by combining sanitation, exclusion,habitat management, and traps inan integrated control program. (Seethe second article in this issue.)This combination can work well forstructures, but urban conditionscan lead to rats breeding in sewers,vacant lots and other situations.Public health requires control, andoften, resources to provide urbancleanup and integrated manage-ment are not available (Olkowski etal. 1991). As a last resort, poisonbaits have been used to reduce ratpopulations. Poison has also beenused for voles, gophers, prairiedogs, ground squirrels and othersuch pests (Hygnstrom et al. 1994).

Primary and SecondaryPoisoning

Rodenticides should be used as alast resort because children, pets,and wildlife can be accidentallykilled or injured. Primary poisoningis a problem when a non-target ani-mal directly eats a rat bait, second-ary poisoning occurs when a preda-tor or scavenger eats a rodent thatis full of poison. The potential fornon-target poisoning can vary withthe active ingredient, with the for-mulation, and with the bait deploy-ment methods (see below) (see BoxA. Primary and SecondaryPoisoning). The purpose of this arti-cle is to identify the most problem-atic rodenticides and suggest lessharmful alternatives. Emphasis ison secondary poisoning of raptors.

Poisoning of People andPets

Each year about 13,000-20,000people in the U.S. are poisoned byrodenticides (See Table 1). Most ofthese are children under the age offive. About 78-83% of the exposuresand 76-82% of the hospitalizationsare due to second generation anti-coagulants, primarily brodifacoum(see Box A). Less than 6% of thehospitalizations are due to acutetoxicants such as bromethalin, vita-min D3, and zinc phosphide. Lessthan 2% are due to the first genera-tion anticoagulant, warfarin(Bronstein et al 2011; Watson et al.2005).About 95,000 pet poisonings due

to rodenticides were reported toAmerican Poison Control Centers in2010. About 75% of the animalspoisoned were dogs (Bronstein et al.2011). A study done by the HumaneSociety shows that 74% of their petpoisoning cases are due to secondgeneration anticoagulants, primarilybrodifacoum. Less than 14% aredue to acute toxicants such asbromethalin, vitamin D3, and zincphosphide. Only 2% are due to war-farin (Erickson and Urban 2004).Poisonings of children and dogs

have occurred probably because

consumers have been able to buyrodenticides formulated as treatedgrain or loose bait. This kind ofpackaging makes poisons easilyaccessible to children. To reduceexposures, the EPA in 2011required manufacturers to producebaits only in tamper resistant baitstations for the consumer market.Some companies have refused tocomply (EPA 2008; EPA 2011).

Poisoning of WildlifeAs well as people and pets, a wide

variety of wild bird and mammalspecies are being killed by rodenti-cides. Both primary and secondarypoisoning has occurred. Foxes, rac-coons, coyotes, opposums, squir-rels, bobcats, wild pigs, deer, evenmountain lions have been killed by

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Protecting Raptorsfrom Rodenticides

Barn owl, Tyto alba

Photocourtesy

MikeAtkinson

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4 Box 7414, Berkeley, CA 94707Common Sense Pest Control XXVII(1-4) Special Issue 2011

rodenticides (Stone et al. 1999;Hosea 2000; Eason et al. 2002).Raptors in the U.S., Canada,

France, Great Britain and elsewhereare dying from consuming rodentspoisoned with second generationanticoagulants such as brodifa-coum and bromadiolone. Owls,hawks, and eagles have been affect-ed (Albert et al. 2010; Stone et al.2003; Walker et al. 2008).

How do we Know Raptorsare Being Poisoned?

Direct information on the poison-ing problem has come from labora-tory experiments where birds arefed poisoned rodents, and from fieldstudies where birds are monitoredby radio tags after rodent baits aredeployed. Indirect evidence is com-ing from surveillance programswhere dead birds are found andturned in to a government agencyor a wildlife care clinic. Most of theproblems are due to the secondgeneration anticoagulant brodifa-coum (Erickson and Urban 2004).

Secondary Poisoning inthe Laboratory

The secondary poisoning threat ofbrodifacoum has been known sinceits registration. In one experiment,36 owls were fed rodents killed with6 different anticoagulants. Deadrats containing brodifacoum killed5 of 6 owls exposed (83%).Bromadiolone treated rats killedone of six owls (17%). Rats contain-ing other anticoagulants such asdiphacinone and chlorophacinone

caused bleeding, but not death(Mendenhall and Pank 1980). Inanother experiment, when six barnowls were fed brodifacoum mice,four of them died (66%). Just threemice were enough to cause death(Newton et al. 1990).An EPA review summarized labo-

ratory experiments with brodifa-coum in 2004. When 149 raptors orscavengers were fed brodifacoumpoisoned prey in the laboratory,42% of the birds died of secondarypoisoning (Erickson and Urban2004). So secondary poisoning ofpredatory birds and scavengerswith brodifacoum has been welldocumented by laboratory experi-ments.

Raptors Show IncreasedSensitivity

Part of the problem is that raptorsare relatively sensitive to anticoagu-lants. Rattner et al. (2011) studiedprimary poisoning of Americankestrels, Falco sparverius, withdiphacinone in the laboratory.Kestrels were 20-30 times moresensitive (LD50 = 96.8mg/kg) to thelethal effects of diphacinone thanthe Northern bobwhite, Colinus vir-ginianus; or mallards, Anasplatyrhynchos; bird species oftenused in EPA tests for toxic pesticideeffects.But diphacinone is much less of a

secondary poisoning problem thanbrodifacoum, and Rattner et al.(2011) calculated that secondarypoisoning “risk associated with asingle day exposure to diphacinonewould be low” for hawks and owls.The risk is low because diphacinone

is quickly eliminated, with a halflife of 22 hours. However, hawkscould show effects of sublethalexposure by as little as 3.5 g of liverfrom diphacinone poisoned rats(Rattner et al. 2011).

Field StudiesThere is also evidence of second-

ary poisoning of raptors from fieldstudies. In one experiment brodifa-coum scatter bait was used to con-trol voles, Microtus spp. in appleorchards. Radio transmitters wereattached to owls and hawks tomonitor their progress. Problems

occurred when raptors fed on volesin the treated orchards. If morethan 20% of the foraging range hadbeen treated with brodifacoum,minimum mortality of screech owls,Otus asio, was 58%. If less than10% of the foraging area had beentreated, mortality was 17%.Because of the severe impact, brod-ifacoum is not used for vole controlin the U.S. (Hegdal and Colvin1988).Secondary poisoning problems are

greatest when the target rodentspecies is a common food source forthe predator, and the poisoningoccurs inside the predator’s forag-ing range. In the experiment above,screech owls were affected, butbarred owls, Strix varia, foragedmostly in woodlands and avoidedthe treated orchards (Hegdal andColvin 1988).

Extended Exposures in theFood Chain

If baits are deployed for roof rats,predator species that do not eatroof rats should not be at risk.

4

Bald eagle,Haliaeetusleucocephalus

American kestrel,Falco sparverius

Photocourtesy

University

ofMinnesota

Eastern screech owl, Otus asio

Photocourtesy

BobJacksy

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5Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

Unfortunately, non-target rodentsoften consume rat baits. Forinstance, Brakes and Smith (2005)found that woodmice, field voles,and bank voles were being poisonedby rat bait boxes. Populations ofthese animals dropped, exposingtheir predators both to secondarypoisoning and a reduced food sup-ply.Insectivorous birds have died

after eating insects feeding on brod-ifacoum bait in bait stations (Hosea2000). Secondary poisoning canalso occur in humans when rodentsare a food source, though this isnot a problem in the U.S. (Fiedler1990). Secondary poisoning ofhumans is possible when deer, wildpigs, and other game animals havebeen poisoned with anticoagulants.The poison is not destroyed bycooking (Eason et al. 2002; Stone etal. 1999).

Sublethal EffectsRaptors are dying from lethal

exposures, but also sublethalamounts are making them moresusceptible to disease and acci-dents (Lemus et al. 2011; Stone etal. 2003). According to Stone et al.(2003), “Sublethal hemorrhage mayinterfere with locomotion, predis-posing animals to predation, acci-dental trauma, and reduced foodintake.” There is also the “possibili-ty of toxic injury to the liver.”Synergistic effects between anti-

coagulants and disease have alsobeen found in mammals. Forinstance, one study in SouthernCalifornia showed that 90% of bob-cats, Lynx rufus, in the area hadbeen poisoned with anticoagulants.Anticoagulants correlated with inci-dence of lethal mange, and 100% ofbobcats dead from mange had beenexposed. Two mountain lions in the

study area had also died from anti-coagulants (Riley et al. 2007).There can also be sublethal

effects on reproduction in raptors.Nestling barn owls, Tyto alba, intest areas baited with brodifacoumweighed 13% less than those inuntreated areas. Wingspans (15%)and tail lengths (18%) were alsoshorter. One nestling had mal-formed feathers, rendering it flight-less (Naim et al. 2010). It is wellknown that anticoagulants causebirth defects in humans, so repro-ductive effects of secondary poison-ing in raptors should be investigat-ed further (Stevenson et al. 1980).

Persistence a ProblemAlthough first generation antico-

agulants are eliminated fairly quick-ly, second generation productslinger in the bloodstream, and theliver acts like a sponge. Large

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There are two general kinds of ratpoisons—acute poisons and chronicpoisons (Meehan 1984). Until 1950,only acute poisons were available.With an acute poison, one encounterwith the bait is enough to kill a rat.Various compounds such as arsenic,strychnine, red squill powderobtained from the lily, Urginea mar-itima, sodium monofluoroacetate(Compound 1080), vitamin D3(cholecalciferol; Terad3®), zinc phos-phide (ZP Rodent Bait®; Ridall®),and bromethalin (Tom Cat®) have allbeen used (Meehan 1984; Ericksonand Urban 2004).There are three problems with

acute baits. One, Norway rats,Rattus norvegicus; and roof rats,Rattus rattus, tend to view with sus-picion any new item in their environ-ment (neophobia). Two, if they con-sume a sublethal amount of anacute bait, they will avoid eating anymore (bait shy). The other problemis that acute baits are extremelydangerous to pets and children, asone encounter can make them verysick or kill them (Meehan 1984).Non-target poisoning with acutebaits is called primary poisoning, asthe animal directly eats the bait(Erickson and Urban 2004).

AnticoagulantsThe need to provide added safety

for rat baits led to the invention ofthe anticoagulants. Early first gener-ation anticoagulants include war-farin, chlorophacinone, and diphaci-none. Most anticoagulants arechronic baits, and with many of theolder first generation compounds,daily doses over several days areneeded to kill a rat or a non-targetanimal. All the anticoagulants workin the same way; enzymatic synthe-sis of vitamin K is blocked. VitaminK is essential for proper clotting ofblood, and once vitamin K levelsdrop below a critical threshold,internal bleeding occurs and deathfollows.The first-generation anticoagulants

are much safer than acute poisonsbecause several encounters are gen-erally needed to produce a problemin a non-target species, and vitaminK is an antidote to anticoagulantpoisoning (Hadler and Buckle 1992).

Secondary PoisoningAlthough anticoagulants reduce

the risk of primary poisoning, therisk of secondary poisoning increas-es. Secondary poisoning resultswhen a predator or a scavenger eatsa poisoned rodent. Both mammals

and birds are affected by secondaryexposures in laboratory tests (Littrell1990; Mendenhall and Pank 1980).Effects of secondary poisoning fromfirst generation anticoagulants areminimized because the poison isquickly eliminated by the rodent,and amounts do not accumulate(Hadler and Buckle 1992).Secondary poisoning became a

real problem with the development ofsecond generation anticoagulantssuch as brodifacoum, bromadiolone,and others. These are more acutelytoxic and are extremely persistent.One feeding on a second generationbait provides a lethal dose. Butbecause a rat does not die rightaway, repeated feeding can occur,leading one rat to accumulate 20-40lethal doses (Erickson and Urban2004).Since predators prefer to eat live

rats, quick-acting acute poisons pro-duce very few secondary poisonings.Rats die slowly from anticoagulantbaiting, however, and the possibilityof secondary poisoning increaseswith time. Poisoned rats tend to diein the open, and may be movingslowly and erratically just beforedeath. Such rats make good targetsfor predators such as owls and foxes(Meehan 1984; Cox and Smith1992).

Box A. Primary and Secondary Poisoning

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6 Box 7414, Berkeley, CA 94707Common Sense Pest Control XXVII(1-4) Special Issue 2011

amounts accumulate in the liver ofrodents, and subsequently in thelivers of predators. Repeated feed-ings allow an accumulation of tox-ins to lethal levels over time(Erickson and Urban 2004).Second generation anticoagulants

are also extremely persistent. Forinstance, after field populations ofvoles in France were baited withbromadiolone, 50-80% of survivingvoles had detectable residues 135days later. About 59% of theresidue was concentrated in the liv-ers. Longterm persistence in thepest population can lead to cumula-tive risk for predators (Sage et al.2008). According to a review byEason et al. (2002), sublethalamounts of brodifacoum and bro-madiolone are likely to persist 6-12months.

Surveillance ProgramsAnother source of information

about secondary poisoning is gov-ernment surveillance programs.Dead birds found in the environ-ment are submitted to monitoringagencies. Birds are then analyzedfor poison. For instance, anticoagu-lant rodenticides were found in thelivers of 48% of 265 raptors collect-ed in New York. Of those exposed,anticoagulants were related to theirdeaths in about 22% of the cases(Stone et al. 2003).Also, 37% of 351 owls in Great

Britain and 72% of 164 owls inCanada had detectable concentra-tions of anticoagulant rodenticidesin their livers (Ratner et al. 2011).Concentrations in at least 21% ofthe Canadian owls were largeenough to be life threatening (Albertet al. 2010).Wildcare, an animal rehabilitation

center in Marin County, CA is see-ing poisoning in 58% of the birdand mammal patients. InMassachusetts, of 161 raptorsadmitted to a wildlife clinic, 86%had brodifacoum anticoagulantresidues in their livers (Murray2011).Cases from surveillance programs

are likely the tip of the iceberg, asmany bird poisonings go unnoticed,since the corpses decay quickly inout of the way locations. Toxic car-casses are also eaten by scavengersor predatory mammals, and these

animals are also poisoned (Eason etal. 2002).

Owls in CanadaWhen 164 owl carcasses in west-

ern Canada were analyzed for anti-coagulants, 72% had residues of atleast one anticoagulant in their liv-ers. Frequency varied with species:barn owls (62%), Tyto alba; greathorned owls (70%), Bubo virgini-anus; and barred owls (92%), Strixvaria. Barred owls encountered poi-soned rodents more often becausethey hunt mostly in urban and sub-urban sites (Albert et al. 2010).Brodifacoum and bromadiolone

were the most frequently detectedanticoagulants at liver concentra-tions up to about 1 mg/kg. Levels

of anticoagulants were high enoughto cause bleeding in 92% of thecases. Anticoagulants were directlythe cause of death in 3.6% of thecases, 6% had liver concentrations(>0.6 µg/g) known to correlate withdeath, and 15% had liver concen-trations (>0.2 µg/g) likely to corre-late with death (Newton et al.1999). About 32% of the owls hadliver concentrations (>0.1 µg/g) thatsome studies have associated withlethal risk in owls (Thomas et al.2011; Newton et al. 1998).From these data, if dead owl sam-

ples were representative of the gen-eral owl population, at least 11%and up to 23% of the owl popula-tion in western Canada from 1988

to 2003 was at risk of death fromanticoagulants especially brodifa-coum and bromadiolone (Albert etal. 2010).Another Canadian study used a

statistical method to estimate thatabout 11% of the great horned owlpopulation of Canada was at risk ofbeing killed by second generationanticoagulants (Thomas et al.2011).

Raptors in New YorkWhen 265 dead raptors from 12

species were collected and analyzedin New York (1998-2001), anticoag-ulant residues were found in 49%.Brodifacoum was detected in 84%of the positive cases, and was con-sidered the principal or probablecause of death in 27 of 28 deathsattributed to anticoagulants. Ofraptors exposed, brodifacoum mayhave killed 21% of them. If thesample was representative of theraptor population, then very rough-ly at least 10% of New York raptorsthat died during this sampling peri-od were likely killed by brodifa-coum. (There was no systematicmonitoring across the state. But theestimate is likely to be a lower limitbecause dead birds die in out of theway locations, and few are broughtin by the public for analysis.Scavengers also feed on thecorpses.)Some species are more at risk

due to food preferences and sensi-tivity to brodifacoum. Anticoag-ulants were found in 81% of greathorned owls, Bubo virginianus, and58% of red tailed hawks, Buteojamaicensis. Brodifacoum was theprincipal or probable cause of deathin about 21% of the great hornedowls and about 27% of the redtailed hawks exposed to anticoagu-lants (Stone et al. 2003).Bromadiolone was detected in

22% of the positive anticoagulantcases, but was likely involved inonly two deaths. Chlorophacinone,diphacinone, and warfarin weredetected in some cases, but led tono deaths (Stone et al. 2003).

Raptors in California andMassachusetts

California Department of Fish andGame collected 74 animals from

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Barred owl, Strix varia

Photocourtesy

JoeVincent

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7Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

1994-1999. Residues of anticoagu-lants were found in 74% of themammals and 68% of the birds col-lected. About 61% of the mammalsand 55% of the birds containedbrodifacoum. About 19% of thebirds were exposed to bromadi-olone, 10% contained diphacinone,and 10% chlorophacinone. Mostfrequently exposed were coyote,Canis latrans; bobcats, Lynx rufus;golden eagles, and barn owls. Aboutone-third of the birds exposed wereowls, about 55% other predatorybirds (Hosea 2000).Of 161 raptors collected in a

Massachusetts wildlife clinic from2006-2010, 85% tested positive forbrodifacoum. Species included red-tailed hawks, Buteo jamaicensis;barred owls, Strix varia, easternscreech owls, Megascops asio, andgreat horned owls, Bubovirginianus. At least 6% of the birdshad died from poisoning (Murray2011).

Raptors in Europe and theUK

In Demark, a total of 430 raptorsfrom 11 species were analyzed foranticoagulants. Frequency of anti-coagulant liver residues varied withspecies, but residues were found in84-100% of the bird species ana-lyzed. Amounts also varied byspecies, but about 13-37% ofresidues in the livers were largeenough to have caused poisoningsymptoms or death (Christensen etal. 2012).In Britain, 20% of the tawny owl,

Strix aluco, population had been

exposed to second generation anti-coagulants over a five year observa-tion period (Walker et al. 2008).Over a 15 year period, 28% of deadbarn owls, Tyto alba, containedresidues of these anticoagulants.About 48% of the owls had diedfrom auto accidents and 31% fromstarvation. The residues increasedover the years, and 40% of thebirds were positive for the anticoag-ulants at the end of the experimentin 1998 (Newton and Wylie 2002).When 401 wild or domestic ani-

mals were examined in Spain,about 39% had been exposed toanticoagulants, either through pri-mary or secondary poisoning. Ofthose exposed, 90% had died fromthe poison. About 62% of dead rap-tors and 38% of carnivorous mam-mals had died from the poison.Widespread exposure occurredthrough treated grain spread on thesoil surface (Sanchez-Barbudo et al.2012).

Raptors in New ZealandBrodifacoum and second genera-

tion anticoagulants are widely usedin New Zealand. Aerial applicationsare used to clear islands of rats.With island applications, 80-90% ofsome bird species were killed by acombination of primary and second-ary poisoning. On one island, about21% of the native owl morepork,Ninox sp., were presumably killedby secondary poisoning.

On the mainland in areas wherebrodifacoum is used, 63% of deadbirds have residues in their livers.Mammals are also at risk, as 60%of wild pigs, 33% of deer, 80% ofwildcats, and 85% of stoats sam-pled have residues in their livers.Deer poisoning is likely primarypoisoning from feeding directly onthe bait (Eason et al. 2002).

Where are RodenticidesUsed?

Rodenticides are used in urbansituations to reduce rat popula-tions. They are used in agriculturalsituations to remove gophers andvoles from crops, and in wildlife sit-uations to reduce populations ofprairie dogs, and ground squirrels.But second generation anticoagu-lants are registered only for struc-tural pest control in the U.S. Firstgeneration chlorophacinone anddiphacinone baits are used forvoles, gophers, and ground squir-rels (Erickson and Urban 2004;Hygnstrom et al. 1994).

Declining RaptorPopulations

Secondary poisoning effects onbird and mammal populations arelocalized to the treated area. Birdsor mammals must be feeding on thetreated rodents to get poisoned. Inthe case of brodifacoum, one ratcan contain 30-40 times a lethaldose (Erickson and Urban 2004).But if large areas are treated,

predator populations in large areas

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Great horned owl,Bubo virginianus

Photocourtesy

GeorgeJameson

Red tailed hawk,Buteo jamaicensis

Photocourtesy

Patricia

Velte

Tawny owl, Strix aluco

Photocourtesy

MarkPayne-Gill

Page 8: Protecting Raptors from Rodenticides

8 Box 7414, Berkeley, CA 94707Common Sense Pest Control XXVII(1-4) Special Issue 2011

can be affected. Owls in westernCanada are declining (Albert et al.2010). Kestrels and some owlspecies are declining in the U.S.(Smallwood et al. 2009).Various published studies cited

above have found these species areoften exposed to secondary rodenti-cide poisoning (Stone et al. 2003;Hosea 2000; Albert et al. 2010).Predatory birds such as kestrels aremore sensitive to anticoagulantsthan grain eaters such as bob-whites or mallards (Rattner et al.2011). Rodenticides are likely onefactor in areawide populationdecline.

Raptors are the SolutionRaptors should be encouraged as

part of an integrated rodent controlprogram. In Malaysia on 188 oilpalm plantations where barn owlboxes were built, there was adecline in rat numbers and damage(Basri et al. 1996). Barn owl boxeson a rice plantation reduced ratdamage from about 6.5% to 2.5%(Mohamad and Goh 1991). Anotherexperiment showed that barn owlboxes were most effective whenrodent numbers were low (Chia etal. 1995). Barn owl boxes and blue-prints for their construction areavailable on the Internet.

New EPA RegulationsFrom the information above, it is

clear that second generation antico-agulants, and especially brodifa-

coum, are the major cause of acci-dental poisonings in humans andpets. They are also causing second-ary poisoning of wildlife and espe-cially raptors. The EPA reviewedproblems with rodenticides in 2008.As a result, second generation anti-coagulants were banned in the con-sumer market, and bait stationswere required for all rodenticidessold in this market. The rules wereimplemented in June 2011. Manycompanies have complied, but threecompanies are fighting the new reg-ulations (EPA 2008; EPA 2011).The new EPA regulations do not

affect the professional market andapplications on farms. Althoughsecond generation anticoagulantsare not registered for agriculturalpests such as gophers and voles,farmers are allowed to use them forrat and mouse control in andaround structures (EPA 2011).

Best Methods for RodentsThe best way to control rodents is

with an IPM program featuring sev-eral different methods. Habitatmanagement, sanitation, and exclu-sion can be combined with trap-ping. (see the next article)Rodenticides should be used as a

last resort because accidental poi-sonings can occur, and deadrodents can lead to odors in struc-tures and production of other pestssuch as flies (Olkowski et al. 1991).If a rodent bait is necessary, first

generation materials such as war-farin, diphacinone, or chlorophaci-none should be used. Whererodents are known to be resistantto warfarin, acute baits such asbromethalin or vitamin D3 may beneeded. All baits used by con-sumers should be contained withina tamper resistant bait station.

ConclusionThousands of children in the U.S.

are exposed to rodenticides eachyear. About 76% of the hospitaliza-tions are due to brodifacoum andsecond generation anticoagulants.About 74% of pet poisonings areprimarily due to brodifacoum. Inareas where brodifacoum is used,at least 11% of the raptors may beat lethal risk from secondary poi-soning. First generation anticoagu-lants such as warfarin, chloropha-cinone, and diphacinone are caus-ing sublethal effects, but are rarelydetermined to be a direct cause ofdeath in raptors, and cause only asmall percentage of human poison-ings. To reduce exposures, all man-ufacturers should follow EPA regu-lations that eliminate second gener-ation anticoagulants and mandatetamper resistant bait stations forthe consumer market.

ReferencesAlbert, C.A., L.K. Wilson, P. Minaeau, S. Trudeau

and J.E. Elliott. 2010. Anticoagulant roden-ticides in three owl species from westernCanada, 1988-2003. Arch. Environ. Contam.Toxicol. 58:451-459.

Basri, M.W., S. Ismail and N. Kamarudin. 1996.The extent of biological control of rats withbarn owls in Malaysian oil palm plantations.Planter 72(838):5-8. [CAB Abstracts]

Borrecco, J.E. and R.E. Marsh. 1992.Proceedings of the Fifteenth Vertebrate PestConference. University of California, Davis,California. 415 pp.

Brakes, C.R. and R.H. Smith. 2005. Exposure ofnon-target small mammals to rodenticides:shortterm effects, recovery and implicationsfor secondary poisoning. J. Appl. Ecol.42(1):118-128.

Bronstein, A.C., D.A. Spyker, L.R. Cantilena, J.L.Green, et al. 2011. 2010 Annual Report ofthe American Association of Poison ControlCenters’ National Poison Data System (NPDS):28th Annual Report. Clin. Toxicol. 49:910-941.

Chia, T.H., J.L. Lim and B. Buckle. 1995. Barnowls for rat control on oil palm plantations-

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Dimensions of a barn owl box

Courtesy

USDA

American Bird Conservancy, POBox 249, The Plains, VA20198; 202-234-7181,www.abcbirds.org

Golden Gate Audubon, 2530 SanPablo Ave, Ste G, Berkeley, CA94702; 510-843-9912, www-goldengateaudubon.org

Golden Gate Raptor Observatory,Bdlg 1064, Ft. Cronkhite,Sausalito, CA 94965; 415-331-0730, www.ggro.org

Hungry Owl Project, 179 TheAlameda, San Anselmo, CA94960; 415-454-4587,www.hungryowlproject.org

Raptors are the Solution,www.raptorsarethesolution.org

Rodenticide Free Project, PO Box892. Bolinas, CA 94924; 415-786-8467, www.rodenticide-freeproject.org

Wildcare, 76 Albert Park Lane,San Rafael, CA 94901; 415-456-7283, www.wildcareb-yarea.org

Resources

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9Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

do they work? Planter 71(828):109-117.[CAB Abstracts]

Christensen, T.K., P. Lassen and M. Elmeros.2012. High exposure rates of anticoagulantrodenticides in predatory bird species inintensively managed landscapes inDenmark. Arch. Environ. Contam. Toxicol.63:437-444.

Corrigan, R. 1997. Rats and mice. In: Mallis, A.1997. Handbook of Pest Control, 8th ed. S.A.Hedges, ed. Mallis Handbook and TechnicalTraining Company. pp. 11-105 of 1453 pp.

Cox, P. and R.H. Smith. 1992. Rodenticide eco-toxicology: pre-lethal effects of anticoagu-lants on rat behavior. In: Borrecco andMarsh, pp. 165-169.

Davis, L.R., R.E. Marsh and D.E. Beadle. 1990.Proceedings of the Fourteenth Vertebrate PestConference. University of California, Davis,California. 372 pp.

Eason, C.T., E.C. Murphy, G.R.G. Wright andE.B. Spurr. 2002. Assessment of risks ofbrodifacoum to non-target birds and mam-mals in New Zealand. Ecotoxicol. 11:35-48.

EPA (Environmental Protection Agency). 2008.Risk mitigation decision for ten rodenticides.60 pp. www.epa.gov/oppsrrd1/reregistra-tion/rodenticides/finalriskdecision.htm

EPA (Environmental Protection Agency). 2011.Cancellation process for certain rodenticides.3 pp. www.epa.gov/pesticides/mice-and-rats/rodent-bait-station.html

Erickson, W. and D. Urban. 2004. Potential risksof nine rodenticides to birds and non-targetmammals: a comparative approach. Office ofPrevention, Pesticides and Toxic Substances,EPA, Washington, DC. 230 pp. www.regula-tions.gov, docket no. EPA-HQ-OPP-2006-0955

Fiedler, L.A. 1990. Rodents as a food source. In:Davis et al., pp. 149-154.

Hadler, M.R. and A.P. Buckle. 1992. Forty fiveyears of anticoagulant rodenticides—past,present and future trends. In: Borrecco andMarsh, pp. 149-155.

Hegdal, P.L. and B.A. Colvin. 1988. Potentialhazard to eastern screech owls and otherraptors of brodifacoum bait used for volecontrol in orchards. Environ. Toxicol. Chem.7:245-260.

Hosea, R.C. 2000. Exposure of non-targetwildlife to anticoagulant rodenticides inCalifornia. In: T.P. Salmon and A.C. Crabb,eds. 19th Vertebrate Pest Conference. UCDavis, Davis, CA.

Hygnstrom, S.E., R.M. Timm and G.E. Larsen,eds. 1994. Prevention and Control of WildlifeDamage. University of Nebraska, Lincoln. 2vols.

Lemus, J.A., C. Bravo, M. Garcia-Montijano etal. 2011. Side effects of rodent control onnon-target species: rodenticides increaseparasite and pathogen burden in great bus-tards. Sci. Total Environ. 409:4729-4734.

Littrell, E.E. 1990. Effects of field vertebrate pestcontrol on nontarget wildlife. In: Davis et al.,pp. 59-61.

Meehan, A.P. 1984. Rats and Mice: Their Biologyand Control. Rentokil, East Grinstead, WestSussex, United Kingdom. 383 pp.

Mendenhall, V.M. and L.F. Pank. 1980.Secondary poisoning of owls by anticoagu-lant rodenticides. Wildl. Soc. Bull. 8(4):311-315.

Mohamad, C. and N.S. Goh. 1991. The use ofbarn owl (Tyto alba) to control ricefield rats-an experience in Seberang Perak. MAPPSNewsletter 15(2):20. [CAB Abstracts]

Murray, M. 2011. Anticoagulant rodenticideexposure and toxicosis in four species ofbirds of prey presented to a wildlife clinic in

Massachusetts, 2006-2010. J. Zoo Wildl.Med. 42(1):88-97.

Naim, M. H.M. Noor and A. Kasim et al. 2010.Growth performance of nestling owls in ratbaiting area in Malaysia. J. Agric. Biol. Sci.5(6):1-13. [CAB Abstracts]

Newton, I., I. Wyllie and P. Freestone. 1990.Rodenticides in British barn owls. Environ.Pollution 68:101-117.

Newton, I., L. Dale, J.K. Finney et al. 1998.Wildlife and Pollution: 1997/1998 AnnualReport, JNCC Rpt. No. 285. [cited in Albertet al. 2010]

Newton, I., R.F. Shore, I. Wiley et al. 1999.Empirical evidence of side effects of rodenti-cides on some predatory birds and mam-mals. In: D.P. Cowan and C.J. Feare, eds.Advances in Vertebrate Pest Management.Filander Verlag, Furth, pp. 347-367.

Newton, I. and I. Wyllie. 2002. Rodenticides inBritish barn owls. In: I. Newton, R.Kavanagh, J. Olsen et al. eds. Ecology andConservation of Owls, pp. 286-295.

Olkowski, W., S. Daar and H. Olkowski. 1991.Common Sense Pest Control. Taunton Press,Newtown, CT. 715 pp.

Rattner, B.A., K.E. Horak, S.E. Warner et al.2011. Acute toxicity, histopathology, andcoagulopathy in American kestrels (Falcosparverius) following administration of therodenticide diphacinone. Environ. Toxicol.Chem. 30(5):1213-1222.

Riley, S.P.D., C. Bromley and R.H. Poppenga etal. 2007. Anticoagulant exposure andnotoedric mange in bobcats and mountainlions in urban southern California. J. Wildl.Manag. 71(6):1874-1884.

Sage, M., M. Coeurdassier, R. Defaut et al. 2008.Kinetics of bromadiolone in rodent popula-tions and implications for predators afterfield control of the water vole, Arvicola ter-restris. Sci. Total Environ. 407:211-222.

Sanchez-Barbudo, I.S., P.R. Camarero and R.Mateo. 2012. Primary and secondary poison-ing by anticoagulant rodenticides of non-tar-get animals in Spain. Sci. Total Environ.420:280-288.

Smallwood, J.A., M.F. Causey, DH. Mossop et al.2009. Why are American kestrel (Falcosparverius) populations declining in NorthAmerica? Evidence from nest-box programs.J. Raptor Res. 43(4):274-282.

Stevenson, R.E., M. Burton, G.J. Ferlauto andH.A. Taylor. 1980. Hazards of oral anticoag-ulants during pregnancy. JAMA 243:1549-1551.

Stone, W.B., J.C. Okoniewski and J.R. Stedelin.1999. Poisoning of wildlife with anticoagu-lant rodenticides in New York. J. Wildl. Dis.35(2):187-193.

Stone, W.B., J.C. Okoniewski and J.R. Stedelin.2003. Anticoagulant rodenticides and rap-tors: recent findings from New York, 1998-2001. Bull. Environ. Contam. Toxicol. 70:34-40.

Thomas, P.J., P. Mineau, R.F. Shore et al. 2011.Second generation anticoagulant rodenti-cides in predatory birds: probabilistic char-acterization of toxic liver concentrations andimplications for predatory bird populationsin Canada. Environ. Int. 37:914-20.

Walker, L.A., A. Turk, S.M. Long et al. 2008.Second generation anticoagulant rodenti-cides in tawny owls from Great Britain. Sci.Total Environ. 392(1):93-98.

Watson, W.A., T.L. Litovitz, G.C. Rodgers, Jr. etal. 2005. 2004 Annual Report of theAmerican Association of Poison ControlCenters Toxic Exposure Surveillance System.Am. J. Emerg. Med. 23(5):589-666.

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length, the roof rat’s tail is longer than the head andbody. Including the tail in the measurement, both ratsgrow to an overall length of about 16 inches (40 cm) atadulthood. The Norway rat is a larger, heavier rat, buthas smaller eyes and a blunter snout than the roof rat(Ingles 1965; Meehan 1984). House mice are muchsmaller than rats. Their bodies and tails are each about3.5 inches (9 cm) long, and they can gain entrancethrough holes as small as a dime. Mice can be distin-guished from immature rats by their large ears, andtheir heads and feet are smaller relative to their bodysize (Olkowski et al. 1991).If rats are not seen, the species involved can be

deduced from their excrement. Norway rat droppingsare larger and more ovoid than roof rat droppings,which tend to be longer and more cylindrical (Weber1982). Each pest has a different biology and manage-ment methods must take this into account. Due tospace limitations, rodent biology will not be coveredhere. The reader is referred to other sources (Olkowskiet al. 1991; Corrigan 1997; Simon and Quarles 2004).Presented here is an IPM blueprint that can lead toeffective rat management and reduction of rodenticides.

An IPM ApproachThe best approach to rat management is a combina-

tion of monitoring, exclusion, habitat management andsanitation to prevent infestations. Once an infestationoccurs, exclusion efforts should be intensified, and res-ident rats should be removed by traps. In some cases,a rodenticide may be necessary (Frantz and Davis1991).Until rat problems are under control, any attractive

food, even closed packages of crackers or candy, can betemporarily stored in the refrigerator. Since hungry ratswill eat nearly anything, even bars of soap may have tobe refrigerated.Large bags of flour, grain, dry pet or livestock food

that are stored in basements or sheds should be placedon open-wire metal shelving that offers little rat harbor-age and is elevated at least 18 inches (45.7 cm) fromthe floor (Olkowski et al. 1991; Timm 1994).

Outdoor Garbage ManagementProper disposal of organic garbage is essential to

keep rats at bay. Organic wastes should be separated

By William Quarles

Rodents most often encountered as structuralpests include the Norway rat, Rattus norvegicus;the roof rat, Rattus rattus; and the house mouse,

Mus musculus. The Norway rat, considered the mostimportant pest rat in the U.S., is also known as thebrown, wharf, house, grey, or sewer rat. (Albino formsof the Norway rat are used for scientific research.) Itoccurs in every state and is widely distributed aroundthe world. The roof rat, also known as the ship or blackrat, occurs mainly in the coastal U.S., including thePacific Coast states, the Gulf states, and the Southeastand some Middle Atlantic states. The house mouse isfound throughout the U.S. (Marsh 1994; Corrigan1997).Both Norway rats and roof rats are omnivores, and

will feed on almost anything. Unlike mice, rats requirewater daily, and prefer to nest where water is available.In general, Norway rats build their nests in under-ground burrows or in ground level areas in buildings.Roof rats prefer living in elevated areas and build nestsin trees, vine-covered fences, and roofs, attics, andwalls, although they will nest at ground level if arborealhabitat is limited. Roof rats often enter buildings fromthe roof or via overhead utility lines, which they use totravel from area to area. They are often found living onthe second floor of buildings, whereas Norway rats aremore likely to occupy the first or basement floor(Meehan 1984). Mice prefer to nest inside dwellings—wall voids, cabinets, furniture, and appliances arefavorite targets (Olkowski et al. 1991).

How to Identify a RatThe Norway rat and the roof rat differ from other rats

and mice in that their tails are noticeably scaly. TheNorway rat’s tail is shorter than its head and body

Roof rats, Rattus rattus, have longtails and slender bodies.

Norway rats, Rattus norvegicus, have short tailsand stout bodies.

Managing Ratsand MinimizingRodenticides

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11from metal, glass and plastic. In some locations, greenrecycling cans are provided for organic waste. Checkevery evening to make sure there is no garbage lying onthe ground around the cans, and lids are securely inplace. Outdoor cans with holes or lids that do not fittightly should be replaced or repaired. Where rat prob-lems are compounded by raccoons or dogs tipping overgarbage cans, spring-type or stretchy fasteners can beused to keep lids tightly closed (Olkowski et al. 1991;Timm 1994).

Reducing Landscape HabitatBoth Norway and roof rats can harbor in dense vege-

tation, which provides them both habitat and food.Keep woody shrubs and ground covers adjacent tobuildings pruned to expose the lower 18 inches (45.7cm) of trunk. This facilitates inspection for burrows

and discouragesrat harborage byexposing the areato light (Frantz1988). Large leafAlgerian ivy,Hedera canarien-sis, is a favoritehiding place forrats, particularlywhen grown indense monocul-tures and allowedto cover fencesand trees. Roofrats also feed onthe ivy berries. Ifyou have this

plant in your landscape, it should be trimmed to aheight of at least 30 cm (11.8 in), or replaced withEnglish ivy, Hedera helix (Frantz and Davis 1991).Avoid planting large areas of uniform ground cover

that allows rats to run for long distances unseen.Break up existing dense plantings with exposed path-ways, stretches of lawn or very low ground cover. Ratsdo not like to move across areas where they can beeasily seen.Fallen fruit, nuts and similar foods may be feeding

rats around buildings. They should be shoveled, rakedor swept up and put into rat-proof garbage containersor green recycling cans. Trees such as date palms offerboth food and harborage for roof rats. These treesshould be thinned, the low-hanging branches prunedoff, and a rat guard attached around each trunk. Ratguards on trees should be checked annually andreleased as necessary to prevent girdling (Frantz andDavis 1991; Olkowski et al. 1991). Rats will also feedon cat, dog, and horse feces, so these must be pickedup daily around infested areas.A gap of at least one meter (3 ft) should be main-

tained between buildings and adjacent trees andshrubs so that branches do not enable rats to jump toand from roofs or ledges (Frantz and Davis 1991).Debris heaps, woodpiles or construction debris nearbuildings should also be removed. Power lines running

into the upper portions of buildings and trees that arebrushing up against the structure give rodents accessto the roof (Marsh 1994).

Rat-Proofing BuildingsExclusion of rodents by rat-proofing a building is very

important. Entry points into buildings should be thor-oughly rat-proofed by plugging holes larger than 1/2inch (1.3 cm) in diameter, installing guards to preventrats from moving along pipes and wires, screeningdrains in basement and shower room floors, and plac-ing barriers between and within walls to prevent rodenttravel. Wooden doors should have metal kickplates atthe bottom to discourage rodents from gnawing theirway inside along the bottom corners of the door (Scott1991; Timm 1994). Rodent-proofing against roof ratsusually requires more time to find entry points than forNorway rats because of their greater climbing ability(Marsh 1994).Storage rooms should be reorganized to eliminate as

much clutter as possible to facilitate inspection andreduce rat harborage. Broken sewer pipes should berepaired as rats can dig into them and swim up thetrap in a toilet to enter a building. Toilet bowl drainscan be rat-proofed by feeding the pipe from the toiletbowl into a pipe section of larger diameter (Frantz andDavis 1991).

The Better Rat TrapWhen rats are present inside the house, trapping

should be the primary approach used in an IPM pro-gram (Hedges 1995). There are a number of advantagesto traps compared to poisons. Traps provide physicalevidence of capture, and there is less risk to non-targetorganisms. They are also usually quicker in riddingyour house of rats. When poison is used, there is thepossibility that rats may die in wall voids and sub-floors, where it is difficult to find and remove them.These carcasses cause unpleasant odors and attractflies, carpet beetles, and other pests.

Traps should be placed in attics, basements, orlocked storage rooms where children and pets or othernon-target animals will not have access to them. If thisis impossible, traps can be placed in tamper resistantbait stations.

Garbage cans should betightly closed.

Roof vents shouldbe screened.

Entry points around plumb-ing should be secured.

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Traps should be set along walls or other runwaysleading to the holes. Other good trap locations include:near droppings, gnaw marks or other signs of rat dam-age; under and behind objects likely to harbor rats; indark corners; along rafters or other protected areaswhere rats are likely to travel. Note that traps or baitsplaced on the ground or floor may catch very few roofrats unless they are positioned at the very points thatrats traverse from above down to a food source (Marsh1994).A sufficient number of traps must be used in order to

be effective. Depending on the size of the infestation, ahouse may require a dozen traps. In an active corner ofa room, 5 to 10 traps should be set. Three traps set ina row ensures that a rat trying to jump over the trapswill be caught. If rat activity in an area is unknown,traps should be set 10 to 20 feet apart (3.0 to 6.0 m)along possible runways (Timm 1994).Traps must be checked daily and fresh bait added as

needed. Moving traps after three or four days is advisedif there is no sign of activity.If there are many rats in the house and most of the

rats have been trapped, it can be hard to catch the lastfew because they may be trap-shy. In such cases, thetraps can be removed for a week, then set in new loca-tions using the pre-baiting method described below.Insecticides should not be sprayed on the traps and

they should not be stored with insecticides, rodenti-cides or application equipment. These smells canmake the rats avoid the traps when they are next used(Corrigan 1997; Olkowski et al. 1991).

Food BaitsTraps should be baited if food for rats is limited. If

there is plenty of food around, the traps will be moreeffective without bait. Alternatively, an extremelyattractive food bait can be used. Baits can be tied tothe trigger using string or dental floss to ensure thatthe rat will spring the trap when investigating the bait.Suggested baits for Norway rats are pieces of hot dog,bacon, liver, peanut butter or nut meats. Suggestedbaits for roof rats are nuts, dried fruits, or fresh fruitssuch as bananas or apples. Other baits include fruit,marshmallows, raisins, or peanut butter mixed withrolled oats. If rats are feeding on other foodstuffs pres-ent, these items can be tried as baits. Cereal (like oat-meal) can be sprinkled around the traps to make themmore attractive (Timm 1994; Marsh 1994).

Pre-baiting TrapsIf baited traps are initially unsuccessful, place baited

but unset traps out for one to three days so ratsbecome accustomed to them. Traps should be checkedto see if the bait is being eaten—if not, another bait

Rats are extremely wary of new objects in their envi-ronment. Traps, baits and bait stations may be avoid-ed for several days after initial placement. Even afterthis period, rats will be very cautious in approachingthem. If a rat nibbles on a bit of poison bait that latermakes it sick without killing it, the rat will avoid simi-lar baits or bait stations in the future, and, if it is afemale, will teach its young to do the same. Thus, it isdifficult to make a substantial long-term reduction in arat population through trapping and baiting alone(Olkowski et al. 1991; Timm 1994).

Kinds of TrapsThere are three types of traps—snap traps, live traps

and glue boards. Live traps are not generally recom-mended for rat removal. Sometimes, pest control pro-fessionals use them so that the rat can be checked forectoparasites or disease. Glue boards may not be effec-tive for rats, and when used for mice can produceinhumane results. Snap traps are probably the best touse in a rat infestation, although they may requiresome care, time, and persistence (Hedges 1995;Corrigan 1997). These traps capture and instantly killsingle rats, and can be placed on floors for Norway ratsor nailed to beams for roof rats. When handling traps,gloves should always be worn for protection from dis-eases. Care should be taken because snap traps havevery strong springs, and accidental release may dam-age an exposed hand or foot. Always keep them out ofthe reach of children and pets (Olkowski et al. 1991).A rat trap called the Rat Zapper® provides an alter-

native to a snap trap as long as infestations are limited.The trap uses 4 AA batteries to power an electric shockunit. It is a covered trap and can be used outside aswell as inside. A bit of dry pet food is used to lure arodent inside the trap. The shape of the rodent triggersa lethal electroshock. A red light goes on that signalsthe trap is in use. The rodent slides easily out of thetrap into a plastic sack or a garbage can. According tocompany literature, it is safe for children and non-tar-get organisms. It is difficult for children or pets to trig-ger it; the electroshock causes a reflex withdrawal of ahand or a paw, and current transfer is limited becauseit is battery operated (AgriZap 2012). Woodstream alsosells an electric trap for mice (see Resources).

Setting and Placing Traps

Set traps with triggers toward the wall or set twotraps in parallel with triggers in opposite directions.

A baited snap trap

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13Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

should be tried. Once bait is being eaten, the trapsshould be rebaited and this time set (Timm 1994).

Biological ControlPredators and diseases can produce substantial

reductions in rat populations, but the effect is usuallytemporary (Frantz and Davis 1991). Snakes, owls andother birds of prey, coyotes, dogs and cats are naturalenemies of rats. It should be noted that beneficial pred-ators can be killed by consuming poisoned rats. Inaddition, rats may cache (hide) food that may or maynot be eaten, taking the poison bait to a place whereother animals can find it, or to other locations the labeldoes not allow. Thus, trapping is preferred over baitingfor rat suppression activities (Hedges 1995).

When to BaitPesticides must be used properly in accordance with

their label directions. Protective gear should always beworn during pesticide applications. Outdoors, poisonbaits should be used only when trapping is not effec-tive; in emergency situations where there are very highnumbers of rats; and to prevent rats from migrating toneighboring areas when a building is being rat-proofedor demolished. Poisons are also justified where rat pop-ulations are carrying plague (Zinsser 1935; McNeill1976; Weber 1982; Craven et al. 1993).

Use Bait StationsWhen used, poison baits must be placed in high pro-

file, tamper-resistant bait stations that lock (seeResources). Bait stations are useful because they pro-tect the bait from moisture and dust; provide a protect-ed place for rats to feed, making them feel more secure;keep other animals and children away from the poison;allow placement of bait in locations where it would oth-erwise be difficult; help prevent accidental spilling ofbait; and allow easy inspection of bait to see if rodentsare feeding on it. Waxy bait blocks that can beanchored to the bait station are the best formulation(Timm 1994; Corrigan 1997).

Which Rat Baits?When possible, warfarin (Kaput®), chlorophacinone

(Rozol®)or other first-generation anticoagulants are pre-ferred. They present less hazard to humans and petsthan second-generation anticoagulants (Frantz 2004).First generation anticoagulants also present fewerproblems for wildlife, including raptors, as secondarypoisoning problems are minimized (Erickson and Urban2004).Where rodent resistance to warfarin seems sure, an

acute bait such as bromethalin (Tom Cat®) or vitaminD3 (Terad3®) may be necessary. Research results up tonow show that secondary poisoning of raptors, pets,

13

The first step in a rat management program is findingareas of infestation. Try to identify as many of the areasas possible that provide rodents harborage, food, waterand access to the building. Check doorways for gaps orholes and note windows without screens or glass. Lookfor other openings in the house such as holes, ventswithout screens, holes around pipe and electrical wireentry points. Entry points can be openings as small as1/2 inch (1.2 cm) in diameter in walls, around pipeentries, sewer outlets, and under doors. Unscreenedsewer outlets and even toilets can give rats access tobuildings. Inspect all planters, woodpiles, vegetation.Look for water leaks and rooms where water condens-

es on the walls. Rodents like to follow edges; inspectthese areas for feces, rub marks, urine or other indica-tions of activity. [Note: Rub marks are grease spotsresulting from repeated contact of a rat with a surface.]After checking the main floor of the house, particularlythe kitchen, continue into the basement and attic tolook for holes, nests, feces, and rub marks. As notedearlier, Norway rats tend to seek harborage on lower lev-els and roof rats on higher levels of a building.Always be on the lookout for piles of trash, clutter, or

other debris. Nests are often composed of things likeshredded paper, pieces of plastic, and bits of fabric gath-ered together into a 5 inch (12.7 cm) diameter mass formice and 8 to 12 inch (20.3 to 30.5 cm) diameter forrats. If you find clothing or paper that looks torn orshredded but doesn’t look like a nest, you will most like-ly find the nest nearby.

Check for leaks and any standing water such as irriga-tion or drainage ditches, stagnant pools, ornamentalponds, and fountains. On the roof, check air condition-ing units that might provide water and harborage forrats (Corrigan 1997; Olkowski et al. 1991; Timm 1994).

Monitoring Tools and TechniquesAll potential rat habitats and areas of activity such as

attics, basements, garbage cans, and stored materialsshould be thoroughly inspected. It may be useful to dothis at night, when the rats are most active. For night-time inspections, use a powerful flashlight with a red fil-ter, which is less likely to scare rats away from view.If holes are found, they should be temporarily closed

with soil, aluminum foil, sawdust or crumpled paper,and inspected 24 hours later to see whether they havebeen reopened or if the paper has been moved orchewed. If so, it can be assumed that the hole is activelybeing used by one or more rats.If necessary, talcum powder can be sprinkled near

suspected harborage or entry points to gain furtherinformation. Rat footprints and rattail drag lines acrossthe powder confirm an infestation. A piece of whitepaper or cardboard can be temporarily placed in dark orhard-to-reach areas, and inspected for fecal pellets orother signs of rat activity. Rat signs, including drop-pings and sawdust from gnawed wood should be sweptup. If new droppings or other clues are found a couple ofdays later, an active infestation is confirmed (Olkowskiet al. 1991; Timm 1994).

Box A. Monitoring and Locating Rats

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14BIRC (Bio-Integral Resource Center). 2012. The

2012 Directory of Least-Toxic Pest ControlProducts. IPM Practitioner 25(11/12): 1-52.

Corrigan, R.M. 1997. Rats and mice. In: Mallis,pp. 11-105.

Craven, R.B., G.O. Maupin, M.L. Beard, T.J.Quan and A.M. Barnes. 1993. Reportedcases of human plague infections in theUnited States, 1970-1991. J. Med. Entomol.30(4):758-761.

EPA (Environmental Protection Agency). 2008.Risk mitigation decision for ten rodenticides.60 pp. www.epa.gov/oppsrrd1/reregistra-tion/rodenticides/finalriskdecision.htm

EPA (Environmental Protection Agency). 2011.Cancellation process for certain rodenticides.3 pp. www.epa.gov/pesticides/mice-and-rats/rodent-bait-station.html

Erickson, W. and D. Urban. 2004. Potential risksof nine rodenticides to birds and non-targetmammals: a comparative approach. Office ofPrevention, Pesticides and Toxic Substances,EPA, Washington, DC. 230 pp. www.regula-tions.gov, docket no. EPA-HQ-OPP-2006-0955

Frantz, S.C. 1988. Architecture and commensalvertebrate pest management. In: Kundsin,pp. 228-295.

Frantz, S.C. and D. Davis. 1991. Bionomics andintegrated pest management of commensalrodents. In: Gorham, pp. 243-313.

Frantz, S.C. 2004. Personal communication. NewYork State Department of Health, WadsworthCenter, Division of Infectious Disease,Empire State Plaza, PO Box 509, Albany, NY12201.

Gorham, J.R. 1991. Ecology and Management ofFood-industry Pests. FDA Technical Bull. 4.Association of Official Analytical Chemists.Arlington, VA.

Hedges, S. 1995. What’s for supper? Pest ControlTechnology 23(8):30, 31,35, 36, 86, 98.

Hygnstrom, S.E., R.M. Timm and G.E. Larson.1994. Prevention and Control of WildlifeDamage. USDA/APHIS, University ofNebraska Cooperative Extension, Lincoln,Nebraska.

Ingles, L.G. 1965. Mammals of the Pacific States.Stanford University Press, Stanford,California. 506 pp.

Kundsin, R.B., ed. 1988. Architectural Designand Indoor Microbial Pollution. Oxford Univ.Press, New York.

McNeill, W.H. 1976. Plagues and People.Anchor/Doubleday, Garden City, New York.340 pp.

Mallis, A. 1997. Handbook of Pest Control, 8thed. S. Hedges and D. Moreland, eds. MallisHandbook and Technical Training Company.Cleveland, OH. 1453 pp.

Marsh, R.E. 1994. Roof rats. In: Hygnstrom etal., pp. B-125 to B-132.

Meehan, A.P. 1984. Rats and Mice: Their Biologyand Control. Rentokil, East Grinstead, WestSussex, United Kingdom. 383 pp.

Olkowski, W., S. Daar and H. Olkowski. 1991.Common Sense Pest Control. Taunton Press,Newtown, Connecticut. 715 pp.

Scott, H.G. 1991. Design and construction:building out pests. In: Gorham, pp. 331-343.

Simon, L. and W. Quarles. 2004. Integrated ratmanagement. Common Sense Pest ControlQuarterly 20(1):5-16.

Timm, R.M. 1994. Norway rats. In: Hygnstrom etal., pp. B-105 to B-120.

Weber, W.J. 1982. Diseases Transmitted by Ratsand Mice. Thomson Publications, Fresno,California. 182 pp.

Zinsser, H. 1935. Rats, Lice and History. Little,Brown, and Company. 301 pp.

avoid the bait or cache it. When thebaiting program is over, all bait sta-tions should be collected and stored(Timm 1994).

ConclusionsWhen rat infestations are discov-

ered, there are five steps in an IPMprogram for controlling them: 1)improve sanitation and garbagemanagement practices; 2) ratproofbuildings and alter landscape plant-ings and other features that providerat access and harborage; 3) usetraps to reduce the existing rat pop-ulation; 4) if trapping is not effec-tive, supplement with poison baitsplaced in tamper-proof bait stationsand checked frequently; 5) continuemonitoring periodically to ensurethat rats are not recolonizing.

ReferencesAgriZap. 2012. The Rat Zapper.

www.agrizap.com

and wildlife is less of a problemwith these materials. Because thereare no convenient antidotes toacute baits such as these, theyshould always be used in tamperresistant bait stations, or in areaswhere children and pets will notencounter them (Erickson andUrban 2004; EPA 2008; EPA 2011;Meehan 1984).

Baiting ProceduresWhen baiting, leave a prominent

warning label on the bait stationbox, and posted in the immediatearea of baiting. Place bait stationswhere rats have been found to bemost active. In the case of roof rats,secure bait stations above theground in areas such as attics,roofs or trees, or at the base oftrees or other heavily vegetatedstructures such as fences over-grown with ivy. Space bait stations15 to 50 feet apart (4.6 to 15.2 m),and leave them in place for a fewdays to determine if the bait isbeing taken. Rats may take a weekto begin consuming the bait. If aftera week none of the bait has beenconsumed, move the station to anew location.Once it is observed that the bait

is being taken, the stations shouldbe left in place for a week or moresince the rats are now accustomedto them. Bait stations should bechecked and rebaited regularly—rats seldom feed on bait that isspoiled. The correct amount of baitshould be used—too little can makethe rats bait-shy or be ineffective;however too much will cause rats to

Bait Stations— Bell Laboratories Inc.,3699 Kinsman Blvd., Madison, WI53704; 608/241-0202, Fax608/241-9631; www.belllabs.com.JT Eaton & Company, Inc., 1393 E.Highland Rd., Twinsburg, OH44087; 800/321-3421, 330/425-7801, Fax 330/425-8353;www.jteaton.com. Lipha Tech, 3600W. Elm St. , Milwaukee, WI 53209;888/331-7900, 414/351-1476, Fax414/247-8166; www.liphatech.com

Bromethalin (0.01%) (Tom Cat®)— BellLabs, see above

Chlorophacinone (0.005%)(Rozol®)—Liphatech, see above

Diphacinone (0.005%)(Ditrac®)— BellLabs, see above

Rat and Mouse Traps (Victor®)—Woodstream Corp., 69 N. LocustSt., Lititz, PA 17543-0327;800/800-1819, 717/626-2125, Fax717/626-1912; www.woodstream-pro.com

Rat Zapper, Agrizap, www.agrizap.comVitamin D3 (Terad3®)—Bell Labs, see

aboveWarfarin (0.025%)(Kaput® Blocks)—

Scimetrics, PO Box 1045,Wellington, CO 80549; 866/442-3467, 970/482-1330, www.kaput-products.com

*A more complete list of products canbe found in the IPM Practitioner’s2012 Directory of Least-Toxic PestControl Products, BIRC, PO Box7414, Berkeley, CA 94707;www.birc.org

Resources

Rat baits should besecured in bait stations.

Photocourtesy

BellLabs

Page 15: Protecting Raptors from Rodenticides

15Common Sense Pest Control XXVII(1-4) Special Issue 2011 Box 7414, Berkeley, CA 94707

Bio-Integral Resource Center(BIRC) is now on Facebook and

TwitterFor BIRC members and others who

favor social media, BIRC is now onFacebook and Twitter. A convenientway to find us is to go to the BIRCwebsite, www.birc.org. There arelinks there to Facebook and Twittersocial media pages. We also estab-lished a crowdfunding appeal onCauseVox to help raise money forthis issue of the Quarterly. BIRCthanks Maggie Ruffo of the HungryOwl Project and Jennifer Bates ofBIRC for donations toward produc-tion of this Quarterly. We also thankBIRC members who responded toour annual appeal. Our publicationsare dependent on donations andmember support.

Six Million Voters in CaliforniaWant Genetically Engineered

Food LabeledCalifornia voters in November had

a chance to mandate labeling ofgenetically engineered food. A yesvote on Proposition 37 meant label-ing would be required. An early votecount on November 9 showed themeasure was defeated 4,326,770(47%) yes and 4,884,961 (53%) no.A final tally on the CaliforniaSecretary of State Website inJanuary 2013 that included absen-tee and provisional ballots showed6,088,714 (48.6%) yes and6,442,371 (51.4%) no.The election was swayed by nega-

tive advertising funded by food andchemical corporations. Early pollshad Proposition 37 winning beforethe advertising barrage started.Despite $46 million in negativeadvertising, the measure lost by only353,657 votes. The $46 million inadvertising represents almost $7 forevery no vote, and about $131 foreach deciding vote.The labeling measure generally

won in most of the urban Californiacounties, such as those in the SanFrancisco Bay Area and Los Angeles,and it generally lost in rural andagricultural counties.The fight for Genetically Modified

Organism (GMO) labels is not over.The vote in California is a preview ofa national effort. With nearly half ofvoters politically committed to GMOlabels, it is just a matter of timeuntil GMO labels are a reality.

15

Dear BIRC MembersDecreased income due to therecession has forced us to delaypublication dates, and to reducethe number of issues of theQuarterly that we produce eachyear. This Special Issue ofCommon Sense Pest ControlQuarterly will be the onlyQuarterly produced for 2011.

For the calendar year 2011,Quarterly Members have alsoreceived three Special Issues ofthe IPM Practitioner—the ProductsDirectory, Genetically EngineeredCrops, and Honey Bee Death andDecline.

We are slowly recovering from theeconomic downturn. We appreci-ate your support, and hope youwill continue as BIRC members.

Thank you,William Quarles, Ph.D.BIRC Executive Director

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