UNITED STATES ENVIRONMENTAL PROTECTION AGENCY WASHINGTON D.C., 20460

Statement of Reasons and Factual Basis for Notice Intent to Cancel Registrations of, a nd Notice of Denial of Applications for, Certain Rodenticide Bait Products

January 29, 2013

This document provides the reasons and f actual basis for the U.S. Environmental Protection Agency’s (EPA’s) Notice of Intent to Cancel the registrations of twelve rodenticide bait products and EPA’s Notice of Denial of regi stration applications of two rodenticide bait products, as required by 40 CFR §164.21(a).

EPA has determined that all of these r odenticide products cause, or would cause,

unreasonable adverse effects on the environment becau se they are sold for residential consumer use in controlling commensal rodents in and around buildings in forms and for means of placement that do not adequately protect against access by children, companion and domesticated animals, and non-target wildlife. EPA bases this determination on data and other information showing that these products cause, or would cause, unreasonable risks to children, companion and domesticated anim als, and non-target wildlife. 1

1 The risk assessments that form the basis for the denials of registration are essentially the same as those that form the basis for the cancellations. In order to make the remainder of this document somewhat easier to read, EPA will generally dispense with “or would cause” and similar phrases that specifically pertain to the products that have not been introduced into commerce. However, note that the discussion that follows concerning the risks and benefits of the 12 registered products also applies to the two products subject to the denials of registration.

### ~ 2 ~ Further, EPA has determined that eight of th e twelve registered rodenticide products also

cause unreasonable adverse effects on the e nvironment because they contain the active ingredients brodifacoum or difeth ialone and are sold for residen tial consumer use, as do the two products subject to denial. EPA bases this dete rmination primarily on data and other information showing that these products cause unreasonable a dverse effects to non-target wildlife. EPA is therefore issuing a Notice of Intent to Cancel pursuant to section 6( b) of the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA) and Noti ce of Denial pursuant to section 3(c)(6) of FIFRA. This document provides the reasons an d factual basis for the Agency’s actions. Although each of the products at issue differs in some respects from the others, the reasons and

factual basis for cancellation or denial articulated here apply to each of the products, except as expressly noted. Please see FRL-9377-7 for the Notice of Intent to Cancel Registrations of, and Notice of Denial of Applications for, Certain Rodenticide Bait Products (hereinafter “NOIC”). The NOIC and other documents supporting the NOIC, including this document, are available through www.regulations.gov in docket number EPA-HQ-OPP-2013-0049.

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Contents I. Regulatory History ......................................................................................................... ........................ 5 II. Scope of Intended Ca ncellation and Denials ................................................................................ ........ 12 III. Risks Associated with Exposure to Rodenticide Products Subject to the NOIC (Humans, Domestic Animals, and Non-target Wildlife) ............................................................................................. .......... 17 A. Effects on Mammals and Birds ............................................................................................... ....... 17 B. Characterization of Hazard to Human Health ................................................................................ 20 1. Sources of Human Incident Data ................................................................................ 29 2. Observed Human Exposures and R esultant Health Effects ........................................ 31 3. Comparison of SGAR and Bromethalin Poisonings .................................................. 34 C. Characterization of Hazard to Domestic Animals ......................................................................... 40 1. Sources of Domestic Anim al Incident Data ............................................................... 40 2. Observed Domestic Animal Exposure and Resultant Health Effects ......................... 42 D. Characterization of Hazard to Non-Target Wildlife ...................................................................... 45 1. Routes of exposure ..................................................................................................... 46 2. EPA’s Deterministic As sessment Approach .............................................................. 51 3. Assessment Based on Calcul ated Residues in Prey ................................................... 69 4. Whole Carcass Residue Analysis ............................................................................... 75 5. Secondary Feeding Studies ........................................................................................ 77 6. Estimation of number of prey animals equal to median lethal dose in secondary animals ....................................................................................................................... 80 7. Probabilistic Analysis ................................................................................................. 83 8. Summary of secondary exposure ri sks ....................................................................... 87 9. Incident Findings Related to Pr imary & Secondary Risk Analyses ........................... 89 IV. Benefits .................................................................................................................. ............................. 100 A. Methodology ................................................................................................................ ................ 102 B. Target pests and use of rodent control measures ......................................................................... 10 3 C. Usage Patterns ............................................................................................................. ................. 105 D. Alternatives to Products Pr oposed to be Cancelled ..................................................................... 108 1. House Mouse Control Products ................................................................................ 108 2. Rat Control Products ................................................................................................ 114 E. Impacts of Cancellation on Residential Consumers .................................................................... 119

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1. Incremental costs of house mouse control................................................................ 120 2. Incremental costs of commensal rat control ............................................................. 122 3. Socio-Economic Equity Assessment ........................................................................ 124 F. Potential for Resistance ................................................................................................... ............. 126 V. Conclusions Regarding Whether Subject Roden ticide Products Meet the FIFRA Registration Criteria ...................................................................................................................... .......................... 127 A. Cancellation and Denial of Registrations of Rodenticides Containing Brodifacoum and Difethialone and Intended for R esidential Consumer Use. ................................................................ 128 1. Effective alternatives to brodifacoum and difethialone are available. ..................... 128 2. Alternatives to brodifacoum and difethialone are affordable. .................................. 129 3. Residential consumer use of brodifacoum and difethialone causes adverse effects to non-target wildlife that could be avoided. ................................................................ 129 4. Conclusion. ............................................................................................................... 132 B. Cancellation and Denial of Registration of R odenticides Intended for Residential Consumer Use In Controlling Commensal Rodents In and Around Bu ildings In Forms That Do Not Adequately Protect Against Access By Children, Compani on And Domesticated Animals, And Non-Target Wildlife. ..................................................................................................................... ......................... 134 1. Rodenticides in bait stations that meet the standards of the RMD are effective alternatives to rodenticides without bait stations. ..................................................... 136 2. Rodenticides in bait stations that meet the standards of the RMD are affordable alternatives to rodenticides without bait stations. ..................................................... 137 3. Rodenticides without bait stations cause adverse effects to children, non-target wildlife and domesticated and companion animals that could be avoided. .............. 139 4. Conclusion. ............................................................................................................... 143 VI. Citations.................................................................................................................. ............................ 145

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I. Regulatory History Many pesticides were originally registered well before EPA came into existence or before EPA identified a complete set of data requirement s sufficient to allow it to determine whether new pesticides met the standard for registra tion. In 1972, Congress therefore directed EPA to assess all existing pesticides to determine whet her they would qualify for the new standard of registration adopted in the 1972 amendments to FIFRA. This process of assessing existing pesticides against current standards is known as “reregistration”. In1988, Congress established a formal five-phase process for EPA to use in co nducting a comprehensive review of all products registered before November 1, 1984 to determ ine whether these products had satisfied all applicable data requirements and the registration criteria of FI FRA section 3(c)(5). See FIFRA section 4(a), 7 U.S.C. § 136a-1(a).

Shortly after passage of the 1988 amendmen ts to FIFRA, EPA began the Section 4 reregistration process for products registered for control of co mmensal rodents (i.e., house mice ( Mus musculus ), Norway rats ( Rattus norvegicus ), and roof rats ( Rattus rattus )). These commensal rodents typically live in close associ ation with humans, and are often found in and

around homes as well as commercial establis hments (Brooks, 1973; Timm 1994). The active ingredients in rodenticide products registered in the US to cont rol commensal rodents include a variety of anticoagulants and three chemicals with other, more rapid modes of action (bromethalin, cholecalciferol, and zinc phosphide). The anticoagulants are commonly classed as first generation anticoagulant rodenticides (FGARs) or second generation anticoagulant rodenticides (SGARs). SGARs were developed, in part, to control r odents that were tolerant of the previously developed FGARs (e.g., Hadl er and Shadbolt, 1975; Dubock and Kaukeinen,

### ~ 6 ~ 1978; Marsh, et al, 1980). FGARs currently re gistered in the US include: chlorophacinone, diphacinone, and warfarin. SGARs registered in the US include brodifacoum, difenacoum, difethialone, and bromadiolone. 2

In 1991, EPA issued a Reregistration Eligibility Decision (RED) for rodenticide products containing the active ingredient warfari n. In July 1998, after making comprehensive reassessments of data relating to the use and effects of the remaining commensal rodenticide products subject to reregistration, EPA issued two REDs addressing seven different active ingredients that previously had been registered for rodent c ontrol in both agricultural and residential settings. 63 FR 48729, Septembe r 11, 1998. The “Rodenticide Cluster RED” contained eligibility decisions for the ingred ients brodifacoum, bromadiolone, chlorophacinone, diphacinone, bromethalin, and pival (a FGAR for which all registrations now are canceled). The “Zinc Phosphide RED” addressed reregistration issu es for the ingredient zinc phosphide. In these 1998 REDs, EPA issued FIFRA section 4(g)(2)(A) determinations that certain rodenticide products would not be eligible for reregistrati on unless their registrant s adopted certain risk mitigation measures to reduce the risks they pos ed to human health and the environment.

While the 1998 REDs identified certain measures intended to reduce children’s exposure as necessary in order for the rodenticides to be el igible for reregistration, EP A also stated at that time that “new, safer rodenticide use technology ” was needed to further reduce child and pet exposures. Rodenticide Cluster RED at viii. EPA announced that it would form a stakeholder group to “discuss means of significantly reducin g exposures to children and pets” and to

2 The second generation anticoagulants, difethialone and di fenacoum, and the acute toxin cholecalciferol, were first registered after November 1, 1984, and therefore were not subject to reregistration.

### ~ 7 ~ “develop workable mitigation measures to adequately protect children from accidental rodenticide exposures.” Id. at viii and 112. The gr oup’s objectives included discussing long-term risk reduction measures and “decid[ing] on specifi c timing and other issues associated with bait dyes [and] bittering agents.” Re registration Eligibility Decision for Zinc Phosphide (July 1998). In 1999, EPA formed the Rodenticide Stakeholde rs Workgroup (RSW) as a subcommittee of the federally-chartered advisory group, the Pestic ide Program Dialogue Committee (the “PPDC”). 3 The RSW included members from EPA, the US Consumer Product Safety Commission, the US Department of Agriculture, the District of Colu mbia Department of Health, Maryland Public Interest Research Group, the California Department of Food and Agriculture, the State of Maine, the Children’s National Medical Center, the Associ ation of Poison Control Centers, the National Pest Control Association, and several registrants of rodenticide products.

The findings and recommendations of the RS W are contained in the November 15, 2000 report, Recommendations for Managing Roden ticide Exposures to Children in the Home . EPA adopted those recommendations in a 2001 amen dment to the REDs. 66 Fed. Reg. 59,425. One of the recommendations adopted by EPA was to rescind the 1998 RED determination that registrants should add a bitter tast e (via a bittering agent) and an indicator dye to rodenticide bait products registered for use in a nd around homes or at other sites where children might encounter them. An environmental group successfully chal lenged EPA’s 2001 rescission of the bittering agent requirement, and a district court remanded it to EPA. West Harlem Env. Action v. EPA , 380 F. Supp. 2d 289, 294-295 (S.D.N.Y. 2005).

3 The PPDC is the principal stakeholder advisory body to EPA’s Office of Pesticide Programs and was established pursuant to the Federal Advisory Committee Act.

### ~ 8 ~ EPA’s concerns regarding the effects of rodenticides on non-target wildlife also continued after issuing the 1998 REDs , leading the Agency to concl ude that further evaluation of the ecological risks of rodenticides was necessary. As part of this work, the Agency developed a comparative ecological assessment for nine 4 rodenticide active ingred ients. Between October 1999 and December 2001, the comparative risk asse ssment was drafted by Agency scientists, received both internal and external peer review as well as review by the Rodenticide Registrant Task Force. Based on input from these reviews, the comparative risk assessment was revised. There were two public comment periods in 2003 and 2004 and the Agency reviewed and responded to the public comments and revised the risk assessment based upon those comments.

In September 2004, the Agency opened Phase 5 of the reregistration public participation process by publishing the revised comparative ecological risk a ssessment, which incorporated new ecological incident data and reflected revisions made in response to public comments on the preliminary version of the assessment. 5 Along with the revised ecological assessment, EPA also published a document discussing the benefits asso ciated with rodentic ide products and EPA’s preliminary position on appropriate risk re duction options. EPA accepted public comments on those documents through January 2005.

In January 2007, EPA issued a Proposed Risk Mitigation Decision for public comment.

Based on an evaluation of the eco logical risks associated with the use of rodenticide bait products containing these nine active ingredients, and consideration of the public health and other important benefits of the use of commensal rodenticide baits, EPA proposed to classify all

4 The active ingredient difenacoum was first registered in the U.S. in 2007 and therefore, was not included in the Comparative Analysis or the 2007 Proposed Risk Mitigation.

5 The public process for reregistration is described in 69 Fed.Reg. 26819 (May 14, 2004).

### ~ 9 ~ such bait products containing the SGAR activ e ingredients brodifacoum, bromadiolone, and

difethialone as restricted-use pesticides, which “would limit their use to certified applicators who have had sufficient training to know when to use the products and how to use them in order to limit risks [and] would result in marked overall reduction in exposure to and adverse effects from those compounds.” 2007 Proposed Risk Mitigati on Decision at 4. Further, to decrease the possibility of children’s exposure to any rode nticide products used in homes, EPA proposed requiring that all commensal rodenticide bait produc ts available for sale to consumers be sold only in tamper-resistant bait stations with solid bait blocks as the only permissible bait form.

EPA took comment on the proposed mitigati on measures for 120 days and received extensive comments from a wide range of st akeholders. During this comment period, the Rodenticide Registrant Task For ce surveyed their constituents. The survey indicated that in 2004, there were 105 million bait placements and in 2005, the number had increased to 115 million bait placements distributed on the consumer market. Based on anecdotal evidence from several sources, EPA believed that the majority of products sold on the consumer market

contained brodifacoum and difeth ialone. Brodifacoum also was im plicated in a high percentage of reported non-target wildlife incidents. EPA concluded that if the lower toxicity and less persistent active ingredients repl aced the higher toxicity and more persistent active ingredients for a portion of this market, there would be si gnificant reduction in th e adverse effects to nontarget wildlife. Based on the restrictions some municipalities place on restricted-use pesticides and concerns about imposing additional regulato ry burdens on the poultry, livestock and pest control operator industries, and recognizing the importance of SG ARs to these industries, EPA decided to employ sale and distri bution limitations – rather than re stricted-use classification – to

### ~ 10 ~ accomplish the same purpose of reducing the use of SGARs in settings where the risks outweigh the benefits (most residential consumer uses).

On May 28, 2008, in response to the district c ourt’s remand order, EPA issued the “Risk Mitigation Decision for Ten Rodenticides” (RMD). 6 The RMD explained EPA’s section 4(g)(2)(A) conclusions about the reregistration eligibility of rodenticides cont aining any of ten listed active ingredients. Among other things, EPA stat ed that rodenticide baits sold to residential consumers must be packaged in a bait station designed to prevent children, domestic animals and non-target wildlife from being able to co me into contact with bait. RMD at 17-18

. EPA also stated that rodenticides containing SGARs pose si gnificant risks to wildlife and the environment, and that rodenticides containing those compoun ds should only be sold to pest control professionals (i.e., governmental, commercial, and agricultural users)—not residential consumers—and then only with additional risk mitigation measures. Id. EPA stated that unless a rodenticide product incorporates the risk mitig ation measures listed in the RMD, it “would present unreasonable risks inconsistent with FIFR A” and therefore should not remain registered.

RMD at 15.

The May 28, 2008, RMD announced EPA’s conclu sions about rodenticide safety and signaled EPA’s intentions for the future comple tion of the reregistrati on process, but did not change the legal status of any rodenticide pr oduct. Recognizing that design and production of bait stations conforming to the RMD requirements would take some time, EPA did not attempt to

6 The RMD did not reinstate either the bittering agent or indicator dye requirement for a number of reasons. After review of all the available information, EPA concluded that, among other things, neither bittering agents nor indicator dyes would provide risk reduction comparable to a bait station requirement, because neither prevents exposure. At best, bittering agents might reduce consumption, and indicator dyes might provide a signal of an exposure event.

### ~ 11 ~ immediately remove from the market rodentic ides that did not incorporate the specified mitigation measures. Instead, EPA asked regist rants to adopt those mitigation measures voluntarily, on a schedule that w ould allow registrants until June 4, 2011 to convert their products. RMD at 26.

By June 4, 2011, most rodenticide registrants had voluntarily amended their registrations or replaced them with new registrations meeting the risk mitigation goals of the RMD, thereby significantly reducing rode nticide risks. Today, only twelve rodenticide products, all produced by Reckitt Benckiser, Inc., fail to meet the risk mitig ation goals of the RMD. As set forth in this document, EPA intends to achieve the necessary risk reduction identified in the RMD by cancelling and denying the registrations of thes e remaining Reckitt-Benckiser rodenticide products that do not include mitigation measures sufficient to prevent unreasonable risks to man

and the environment.

Since the issuance of the RMD, EPA has received a number of applications for registration of new commensal r odenticide products intended for the general consumer market. Most of these applications meet the risk management goals of the RMD and those products have been registered, but some have not. On Febr uary 4, 2011, EPA notified Reckitt Benckiser, Inc. (Reckitt Benckiser), of deficiencies in applic ations for two products (designated as 3282-RNL and 3282-RNU), and offered Reckitt 75 days to co rrect those deficiencies. Reckitt Benckiser’s April 19, 2011 response indicated th at additional data to suppor t their application would be submitted no later than May 20, 2011. Reckitt Benc kiser’s May 20, 2011, letter offered several arguments supporting the applicatio ns, and provided revised draf t labels that would prohibit outdoor use. Because these products do not meet the risk management goals of the RMD, EPA

### ~ 12 ~ is formally denying the applications for registration of those products.

Certain rodenticide registrant s who have disagreed with the Agency’s positions regarding rodenticides have challenged aspects of the Agency’s actions in tw o court cases; however,

neither case has addressed the mer its of the scientific, economic, a nd policy questions at issue in this cancellation proceeding. See generally, Reckitt Benckiser, Inc. v. Jackson , 762 F. Supp. 2d 34, 46 (D.D.C. 2011)(concerning the scope of EPA’s authority to pursue enforcement action in lieu of a cancellation proceeding), and Woodstream Corp. v. Jackson , 845 F.Supp.2d 174 (D.D.C 2012) (concerning EPA’s authority to place cert ain conditions on pesticide registrations).

II. Scope of Intended Cancellation and Denials

For the reasons set forth in Sections III and IV, below, EPA has determined that certain registered rodenticide bait products, when used in accordance with widespread and commonly recognized practice, genera lly cause unreasonable adverse effects on humans and the environment. Accordingly, EPA intends to cancel the registrations of the following pesticide products:

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Table 1. Pesticide Products Subject to the Notice of Intent to Cancel.

Product EPA Reg. No. Registrant Active Ingredient Deficiency D-Con Concentrate Kills Rats & Mice 3282-3 Reckitt Benckiser, Inc. Warfarin Consumer product in a powder form 7 and packaged without a protective bait station D-Con Ready Mixed Kills Rats & Mice 3282-4 Reckitt Benckiser, Inc. Warfarin Consumer product in a pelleted form and packaged without a protective bait station D-Con Mouse Prufe Kills Mice 3282-9 Reckitt Benckiser, Inc. Warfarin Consumer product in a pelleted form and packaged without a protective bait station D-Con Pellets Kills Rats & Mice 3282-15 Reckitt Benckiser, Inc. Warfarin Consumer product in a pelleted form and packaged without a protective bait station

D-Con Mouse Prufe II 3282-65 Reckitt Benckiser, Inc. Brodifacoum Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

D-Con Pellets Generation II 3282-66 Reckitt Benckiser, Inc. Brodifacoum Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

D-Con Bait Pellets II 3282-74 Reckitt Benckiser, Inc. Brodifacoum Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR D-Con Ready Mixed Generation II 3282-81 Reckitt Benckiser, Inc. Brodifacoum Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

D-Con Mouse-Prufe III 3282-85 Reckitt Benckiser, Inc. Difethialone Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

D-Con Bait Pellets III 3282-86 Reckitt Benckiser, Inc. Difethialone Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR D-Con II Ready Mix Baitbits III 3282-87 Reckitt Benckiser, Inc. Difethialone Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

D-Con Bait Packs III 3282-88 Reckitt Benckiser, Inc. Difethialone Consumer product: 1) in a pelleted form and packaged without a protective bait station, and 2) containing a SGAR

7 EPA Reg. No. 3282

‐ 3 is not itself a rodenticide bait, but rather, a general use rodenticide concentrate bearing label directions requiring that the user mix it with suitable bait materials before placement. Accordingly, this product shares the same risks as the other products, plus the additional risks associated with the characteristics and use of a pesticide concentrate.

### ~ 14 ~ For the same reasons, EPA intends to deny applications for registration of the following pesticide products:

Table 2. Pesticide Product Applications Subject to Denial.

Product EPA Application No. Registrant Active Ingredient Deficiency D-Con Bait Station XV Kills Mice 3282-RNU Reckitt Benckiser Inc. Brodifacoum Consumer product containing an SGAR D-Con Bait Station XVI Kills Mice 3282-RNL Reckitt Benckiser Inc. Brodifacoum Consumer product containing an SGAR

In the RMD, EPA identified a number of m itigation measures that, if adopted, would make existing rodenticides eligible for rere gistration. EPA is now pr oposing to cancel the rodenticide products identified above based on two of the most significant mitigation measures identified in the RMD: Removing SGARs from re sidential consumer produc ts, and assuring that

rodenticides available to resident ial consumers include bait stations designed to prevent children, domestic animals and non-target wildlife from bei ng able to come into contact with the bait. Although the mitigation measures identified in the RM D are designed to act in concert, with each measure contributing towards safer outcomes, the bait station require ment is expected to protect children, domestic animals and non- target wildlife from exposure s to commensal rodenticides generally, while the exclusion of SGARs from the homeowner market is expected to reduce environmental loading of SGARs and there by reduce secondary poisonings among non-target wildlife. As currently labeled a nd sold, each of the rodenticid e products identified above causes

unreasonable risks to man or the environment ow ing to the lack of one or both of these mitigation measures. Individual products may also fa il to meet the FIFRA registration criteria for other reasons. In order to focus a hearing on the most critical risk mitig ation issues, the proposed

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cancellations and the denials are based only on the presence of SG ARs in products marketed for general consumer use in cont rolling commensal rodents in an d around buildings, and/or on the rodenticide products being in forms that do no t adequately protect against access by children, companion and domesticated anim als, and non-target wildlife. EPA is proposing to cancel the registration of twelve rodenticide products sold in the general consumer market, and deny the applica tions for registration of two additional such products. The scope of this action is very na rrow. Commercial, agricu ltural and professional users (including public health o fficials, pest control operator s (PCOs), and other occupational applicators) are not affected b ecause they are not significant user s of the products identified in

the NOIC and will continue to have access to the same types of rodenticide products that they had prior to June 4, 2011. Residential consumers will see a different mix of rodenticide products that conform to the RMD on retail store shelves, but will continue to find effective rodenticide products at prices comparable to those that EPA proposes to can cel. Since its inception, EPA has been concerned that children, pets, and non-targ et wildlife are being unnecessarily exposed to rodenticides. This concern was expressed in Pe sticide Registration (PR) Notice 83-5, setting criteria for “tamper-proof” bait stations nearly 30 years ago. That notice was followed 11 years later by PR Notice 94-7, which updated PR Noti ce 83-5 with label text intended to increase compliance with requirements to use bait stations if bait placements were to be made in areas within the reach of children, pets, domestic animal s, and/or non-target wi ldlife. Most of the children and pet incident concerns are occurri ng in and around homes, despite mandatory label statements requiring use in tamper-resistant (o r tamper-proof) bait stations where placements otherwise would be accessible to children, domes tic animals, and/or non-target wildlife. These incidents can be significantly reduced if rodenticide products sold on the general consumer

### ~ 16 ~ market include bait stations designed to pr event children, domestic animals and non-target wildlife from being able to come into contact with bait, rather than relying on consumers to separately purchase and use such bait stations . Further, based on the reported incidents of wildlife exposures to rodenticides, EPA has determ ined that it is appropriate to limit use of products containing the more toxi c and persistent anticoagulants brodifacoum and difethialone. EPA has determined that the risks of use by re sidential consumers of rodenticides containing brodifacoum and difethialone outweigh the benef its of such use. There are over 30 alternative rodenticide products registered for sale in the general consumer ma rket that can provide effective rodent control, that fully conform to the RMD, and that meet the no unreasonable adverse effects

on the environment standard of FIFRA. In addi tion, residential consumers also have access to

mechanical control methods as well as the services of PCOs who will conti nue to have access to a broader range of products. The NOIC includes only rodenticides intended to control the commensal rodents: the Norway (brown or sewer) rat, the roof (black or ship) rat, and the house mouse. Control of these commensal rodents in sewers, in and around co mmercial buildings, and in connection with agricultural and food processing establishmen ts will not be affected by the proposed cancellations, because the products EPA proposes to cancel are marketed to general consumers in small sizes unlikely to be used by professiona l, commercial or agricultural users. Products registered for the control of other types of r odents are also outside the scope of the NOIC. In making the determination that the produc ts subject to the NOIC do not meet the FIFRA registration criteria, EPA has relied upon evidence and analyses demonstrating significant exposure to children, domestic animals, and non-target wildlife from the use of consumer use rodenticide products which are not protected in bait stati ons designed to prevent

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children, domestic animals and non-ta rget wildlife from being able to come into contact with bait. For four of the products EPA proposes to cancel and the two appl ications EPA is denying, this determination additionally relies upon th e substantial and well documented risks to nontarget wildlife from primary a nd secondary exposures to the ac tive ingredients brodifacoum and

difethialone. EPA also considered evidence and anal yses relating to the bene fits of continued use of the rodenticide products id entified in the NOIC, and has determined that, based on the availability of adequate and affordable al ternative rodent icide products and methods of commensal rodent control, the benefits linked sp ecifically to the products identified in the NOIC are, at best, minimal. However, given the poten tial for exposure these pr oducts pose to children, coupled with risks to domestic animals and wild life in the absence of further mitigation, EPA

believes that this cancellation action would be warra nted even if the antici pated costs of rodent

control as a result of this ac tion were somewhat greater than EPA has estimated. Accordingly, EPA is issuing a Notice of Intent to Cancel a nd a Notice of Denial of registrations of the

consumer-use commensal rodenticid e products listed in above. See FRL-9377-7 for the NOIC. The NOIC and other documents supporting the NOIC, including this document, are available through www.regulations.gov in docket number EPA-HQ-OPP-2013-0049.

III. Risks Associated with Exposure to Rode nticide Products Subject to the NOIC (Humans, Domestic Animals, and Non-target Wildlife)

A. Effects on Mammals and Birds Rodenticides are designed to kill mammals, and so their effects on humans, birds, and non-target mammals are qualitatively the same as their effects on target pests, unlike other pesticides such as herbicides and certain in secticides where adverse effects on mammals are

### ~ 18 ~

often different in nature than th eir effects on target pests. Roden ticides can be divided into three

broad classes in terms of their effects: FGARs, SGARs, and non-anticoagulants. The nonanticoagulant rodenticides work in different ways to cause death. Each of these is discussed

below:

• The FGARs, such as chlorophacinone, diphacino ne, diphacinone sodium salt, warfarin, and warfarin sodium salt, disrupt the production in the liver of vitamin K dependent bloodclotting factors II (proth rombin), VII, IX, and X, interfer ing with blood clotting and causing hemorrhages. Due to the long half-lives of the vitamin K-dependent clotting factors, the anticoagulant effect does not resu lt in rodent mortality until af ter several days of ingestion. The onset of lengthened prothrombin time (PT) fr om a toxic dose may occur within 24 hours,

and reach a maximum in 36-72 hours at a dose much lower than the dose that can cause hemorrhage (Reigart J.R. et.al, 1999). These ag ents also increase perm eability of capillaries throughout the body, leading to widespread internal hemorrhage.

• The SGARs such as brodifacoum, bromadiolone , difenacoum, and difethialone are more toxic than FGARs and are more likely to cause lethal effects to rode nts that consume the amount of bait equivalent to a single night’s fe eding. These chemicals block the formation of

the active form of vitamin K in the same manner as warfarin and warfarin sodium; however, SGARs have much longer half-lives in the body (Batten and Bratt, 1990 ). Similar to the FGARs, the toxic effects of these agents usua lly begin several days after ingestion, because of the long half-life of th e coagulation factors.

Three other active ingredients that are not anticoagulants are registered for use as rodenticides, although only one – bromethalin – is registered for use against the commensal

### ~ 19 ~

rodents that are at issue in this action. Each of the non-anticoagulants has a distinct mode of

action:

• Bromethalin causes decreased pr oduction of adenosine-5'-tri phosphate (ATP) in the cells of the central nervous system by unc oupling oxidative phosphorylation in the

mitochondria. Low levels of ATP reduce the efficiency of the enzyme Na/K ATPase, leading to increased intracellular sodium le vels. This in turn draws more water into neuronal cells (cerebral edema) and increases intracranial pressure which can be lethal. Symptoms and signs of cerebral edema in clude headache, dizziness, nausea numbness, weakness, loss of coordination or balance, altered level of consciousness, respiratory depression, seizures, and death.

• Cholecalciferol increases calcium absorption fr om food, and mobilizes calcium from bone which leads to hypercalcemia (increased calci um levels in blood). Hypercalcemia can cause formation of calcium crystals in inte rnal organs such as blood vessels, kidneys, stomach wall and lungs (Chavhan S.G., et .al, 2011). Abnormal heart conduction and irregular heartbeats can also occur since the heart tissue is sensitive to changes in blood calcium levels. Symptoms and signs of c holecalciferol poisoning may include fatigue, weakness, nausea, anorexia, headache and ir regular heartbeats (G oldfrank et.al, 2010). Acute renal tubular injury due to hypercalcemia may cause excessive urination, increased water intake, protein in urine and increas ed blood urea levels. Prolonged hypercalcemia may eventually cause kidney failure due to formation of kidney stones and calcium deposition in kidney tissues.

### ~ 20 ~

• Zinc phosphide can quickly produce toxic phosph ine gas when it comes in contact with acids or water. Phosphine is thought to pr oduce toxicity by blocki ng cytochrome oxidase and, inhibiting oxidative phosphorylation which may lead to cell death (Perry H.E., 1998). Most of the tissue damage can occur in liver, kidneys and heart. Patients may present with symptoms such as, severe gastrointestinal irritation, nausea, vomiting (with fishy odor), chills, tightness of chest, difficulty in breathing and cough (from pulmonary edema). Development of liver failure can cause ja undice and excessive hemorrhage. Symptoms such as delirium, convulsions and coma from toxic encephalopathy were reported. Renal tubular damage and renal failure can occur. A common cause of death is from ventricular arrhythmias and shock due to myocar dial damage (Reigart J.R., 1999).

B. Characterization of Hazard to Human Health

The products subject to the NOIC each c ontain one of three rodenticide active ingredients: warfari n, brodifacoum, and difethialone. Warf arin is a FGAR; brodifacoum and difethialone are SGARs that are very similar in structure to each other. Bromethalin is not an anticoagulant but an uncoupler of oxidative phos phorylation whose effects are manifested as cerebral edema. The symptoms of anticoagula nt poisoning can be treated with vitamin K 1 , although the SGARs may require repeated administ ration over many days or weeks, transfusion with fresh frozen plasma, and clotting factor therapy (e.g., recombinant activated factor VII). There is no specific antidote for bromethalin pois oning, however clinicians and veterinarians can treat the symptoms of bromethalin toxicity in th e same manner as other toxins causing cerebral edema, such as aspirin and ibuprofen. Treatment , if needed, typically lasts for several hours, depending on the level of exposure.

### ~ 21 ~ Anticoagulant rodenticides bl ock the production of active vi tamin K which is essential for the synthesis of several clotting factors. The first sign of anticoa gulant poisoning is an increase in the time it takes blood to clot (p rothrombin time), alt hough this would only be observed through tests in a medi cal facility. Because it takes time for the body’s ordinary metabolic processes to clear vitamin K-depende nt clotting factors from the blood, changes in prothrombin time resulting from an anticoagulant ’s inhibition of the replenishment of those factors would not be apparent until 24 hours or more after exposure. Significant adverse effects begin 2-3 days after exposure, and include easy bruising and bleeding fr om almost any tissue such as gums, nose, urinary tract, gastrointestinal tract, etc. Patie nts may also have symptoms of anemia, including fatigue and dyspnea on exertion. In severe cases, there is massive loss of blood leading to shock and death. Symp toms resulting from FGAR exposur e are likely to pass within 24 hours with treatment; symptoms of SGAR expo sure could persist for months, even with

treatment. A fourth active ingredient, bromethalin, is al so relevant to the Agency’s cancellation decision, inasmuch as that decision is based on th e comparative risks of the products subject to the NOIC and the registered, available alternativ e rodenticide products. Bromethalin is not an anticoagulant and produces no unique or definiti ve symptoms, but instead produces the same constellation of potential sympto ms as other uncouplers of oxi dative phosphorylation. At low doses, a poisoned individual might exhibit feve r, vomiting, dizziness, mental confusion or dullness. At higher doses, as cerebrospinal pre ssure increases, there may be indications of weakness in limb strength. Very high doses can cause general paralysi s or convulsions, and ultimately death. These effects are likely to be come manifest within 2 to 8 hours, and the sublethal effects pass within 1 to 4 days.

### ~ 22 ~ The acute toxicity of each of the four rodenticides is discussed briefly below with the focus being on acute toxicity valu es and other relevant paramete rs reported in the studies.

Warfarin. Warfarin is a FGAR. The acute oral LD 50 for warfarin in rats is reported as 3 mg/kg (males only) (Gaines, T. B. 1969). 8 Another source indicates there is considerable variability in reported rat LD 50 s for warfarin: “Reported oral LD 50 values for warfarin in rats vary by a considerable magnitude. Valu es of 11 mg/kg body weight (L und, 1982), 58 mg/kg body weight (Thomson, 1988) and 58 mg/kg (fem ale) and 323 mg/kg (male) (H agan & Radomski, 1953) have been reported.” (http://www.inchem.org/docum ents/ehc/ehc/ehc175.htm). Another study reports a large difference between the acute toxicity of warfarin to male and female rats with the LD 50 for males reported to be betw een 450 and 680 mg/kg and the LD 50 for females reported as between 5 and 10 mg/kg (MRID 00143093).

Brodifacoum. Brodifacoum is a SGAR. The oral (gavage) LD 50 of brodifacoum in rats is 0.42 mg/kg in males and 0.56 mg/kg in females. There were no mortalities or signs of toxicity in male and female rats at a dose of 0.25 mg/kg (M RID 42687501). Signs of toxicity at 0.5 and 0.75 mg/kg included pallor, bleeding from the nose and/or rectum and/or other sites. Deaths occurred in the period from 3-8 days after dosing. Post mortem examination of those animals that died or

were sacrificed in extremis and/or showed signs of bleeding re vealed the presence of free or

clotted blood in the abdominal and/or thoracic cavity. Discoloration or pallor of a number of organs was also observed. These findings are consistent with th e known anticoagulant activity of

brodifacoum. The liver half-life for brodif acoum is long – up to 350 days (MRID 42007502).

8 The LD 50 is the median lethal dose, which is the quantity of a toxin that is estimated to kill half the members of an exposed population.

### ~ 23 ~

Difethialone. Difethialone is a SGAR. Difethialone a nd brodifacoum have similar structures, differing only in the hetero atom in the coumarin ring. Like brodifacoum, difethialone has a long half-life in the body. The estimated ha lf life of difethialone in rat liver from a single oral dose at 0.5 mg/kg is 175 days for males and 98 days fo r females (MRID 42065010). In an acute lethality study, the oral (gavage) LD 50 of difethialone in rats wa s 0.55 mg/kg (males) and 0.58 mg/kg ((females) (MRID 40268903). Animals died in 4- 8 days with symptoms of anticoagulant toxicity. There were no deaths for either males or females at 0.4 mg/kg, indicating a very steep dose response curve. There was a second acute lethality study in rats (MRID 40268903) in which 0/10 rats died at 0.4 mg/kg and 10/10 rats di ed at 0.8 mg/kg. The two acute studies are consistent with each other and support an LD 50 value of 0.55 mg/kg fo r acute lethality of

difethialone in rats.

Bromethalin. Bromethalin is not an anticoagulant but an uncoupler of oxidative phosporylation in which the the most apparent manifestation of toxicity involves the central nervous system. The

oral LD 50 in rats for bromethalin is reported as 3.2 mg/kg (males), 2.1 mg/kg (females) and 2.6 mg/kg (combined males and females) (M RID 44775101). Another study (MRID 00241521) lists

the LD 50 for females as 9.1 mg/kg and the LD 50 for males as 10.7 mg/kg. EPA routinely characterizes the risk to humans posed by pestic ides with uses in or around the home. An important part of a residential asse ssment is consideration of potential “incidental oral” exposure. The incidental oral assessment seeks to determine the exposure and risks to young children who may ingest pesticide by putting their hands in their mouths after touching objects bearing pesticide residue s (hand to mouth activity), or by mouthing an object with pesticide residue on it, or by pi cking up and eating solid particle s of pesticide applied in and

around the home.

### ~ 24 ~ EPA has developed a quantitative approach to evaluating whether a pesticide poses risks to those who might be exposed as a consequence of pesticide uses. Using av ailable toxicity data and other information such as physical and chemi cal properties of the pesticide, and activity patterns of potentially exposed persons, EPA esti mates a level of exposure that would not cause harm (referred to in this analysis as the “exposur e level of concern”), and compares that level to the amount of exposure people would get as a cons equence of pesticide use. If the estimated exposure exceeds the exposure level of concern, the use of the pesticide poses risks that may or may not be unreasonable, depending on the benefits of the use. EPA uses a similar logic in determining whether dietary risks are of concern when evaluating exposure to pesticides in food under section 408 of the Federal Food, Drug a nd Cosmetic Act (FFDCA), although in that context, the safety of the exposure is consider ed independently of any pesticidal benefits. EPA relies primarily on toxicity studies conduc ted with laboratory animals to derive exposure levels of concern for pesticide active ingredients. First, EPA examines all of the

available hazard studies and identifies the most sensitive toxic effect caused by a pesticide for the route and duration of exposure that ma tches the proposed exposure scenario. For rodenticides, EPA is primarily concerned about the hazards of a single instance of oral exposure. The only acute oral exposure studies availabl e for the subject rodenticides are acute LD 50 studies.

Acute LD 50 studies are not designed to identify sublethal toxic effect s, but instead, to determine the amount of exposure that will cause death to 50 % of the test animals after a single exposure.

Because most chemicals cause adverse effects at dose levels well below the median lethal dosage, EPA typically would base a human health risk assessment on toxicity effects that occur at dosages lower than the acute LD 50 . However, in the absence of a more appropriate toxicity data, the acute oral LD 50 studies were used as the effect of concern for this assessment.

### ~ 25 ~ To derive an exposure level of concern, EPA t ypically divides the point of departure (i.e., the exposure level that corresponds to the toxi c effect of concern, here the acute oral LD 50 ) by appropriate uncertainty factors. The uncertainty factors are intended to account for possible differences in sensitivity between humans a nd laboratory animals, for differences between humans, and in this case, to acc ount for the likelihood of sublethal adverse effects. Using these uncertainty factors, EPA identifies a level of e xposure that, with reason able certainty, would not

cause harm to humans because the difference be tween predicted exposures and the levels that cause adverse effects is large enough that no ha rm would reasonably be expected. It should be noted that an exposure at a level above the exposure level of concern may not elicit any discernible symptoms, depending on the nature of the effect, th e amount of the exposure and the sensitivity of the individual pers on. To address the possibility that the pesticide may generally be more toxic to humans than animals and the possib ility that variations in human sensitivity may be greater than seen in the test animals, the Agen cy usually applies uncertainty factors of at least 100, meaning that in order to be presumed safe , an exposure should be at least 100 times lower than the toxicity endpoint. Often, EPA applies ad ditional uncertainty fact ors to account for the limitations of the toxicity databa se including the absence of a “no observed adverse effect level” (NOAEL). Owing to the paucity of data on sublethal eff ects of the subject rodenticides, EPA cannot confidently establish exposure levels of concern for acute human exposure to the subject rodenticides. However, if EPA had a complete t oxicity database with appropriate studies of

sublethal effects with clearl y established NOAELs, EPA would apply to that endpoint an uncertainty factor of at least 100 (i.e., a leve l of concern 100 times lower than the NOAEL) for each active ingredient to account fo r interspecies and intraspecies variability. If EPA had all the

### ~ 26 ~ same studies, but the study showing the most se nsitive toxic effect failed to establish a NOAEL, EPA would, in all likelihood, use an uncertainty factor of 1000. In the present case, all of these uncertainties are present, and moreover, the acute t oxicity effect of concer n (death) is severe and its relationship to sublethal acute adverse effects is unknown. In view of these uncertainties, EPA is unable to say with confiden ce that there is any finite le vel of exposure to the subject rodenticides that can be considered reasonably likely to cause no harm. Nevertheless, with the caveat that this undoubtedly understa tes the risks of sublethal a dverse effects, Table 3 below

shows the LD 50 values for each of the rodenticides and what the exposure level of concern would be if EPA applied an uncertainty factor of 1000 to derive a level of concern based on rat LD 50 s.

Table 3. Surrogate Exposure Level of Concern

Rodenticide LD 50 (mg/kg) Provisional Uncertainty Factor Surrogate Exposure Level of Concern (mg/kg) Warfarin 3 mg/kg 1000 0.003 mg/kg Brodifacoum 0.42 mg/kg 1000 0.00042 mg/kg Difethialone 0.55 mg/kg 1000 0.00055 mg/kg Bromethalin 2.6 mg/kg 1000 0.0026 mg/kg

After deriving an exposure level of concern, EPA would estimate potential exposure of different population groups. As is evident from human poisoning and suspected poisoning events, and corroborated by studies of children’ s behavior, young children will pick up and put

small amounts of food-like material into thei r mouths. In the 1998 Rodenticide Cluster RED, EPA had cited a poison specialist’s estimate that a child weighing 10 kg would consume approximately 5 grams of rodenticide bait in one b ite (less than a quarter of an ounce). In the current analysis, EPA’s estimate of the potential exposure to children eating a single, 5-gram bite of rodenticide bait containing any of the active ingredients at issu e greatly exceeds possible safe

### ~ 27 ~ levels, without even considering potential subl ethal effects. Table 4 below shows how the estimated child exposure from taking one bite of rodenticide bait compar es to the surrogate exposure levels of concern for each of the subject rodenticides.

Table 4. Surrogate Exposure Level of Co ncern for 5 gm Rodenticide Bait.

Rodenticide % active ingredient in a bait product Rodenticide ingested in a 5 gm bite of bait by a 10 kg child Surrogate Exposure Level of Concern (UF = 1000) Warfarin 0.025% 9 0.13 mg/kg 0.003 mg/kg Brodifacoum 0.005% 0.025 mg/kg 0.00042 mg/kg Difethialone 0.0025% 0.0125 mg/kg 0.00055 mg/kg Bromethalin 0.01% 0.05 mg/kg 0.0026 mg/kg

This quantitative analysis based on animal toxi city data is consistent with information from reports of incidents of human poisoni ngs. Children who have accidentally ingested quantities of the subject rodentic ides have displayed symptoms th at are consistent with exposure to toxic levels of these compounds. Symptoms for the anticoagulants include hematological effects such as bruising, and bleeding from gums, nose and other tissues. Symptoms from bromethalin poisoning may include fever, dizziness, dullness, and tremors.

Anticoagulant poisonings present additional risks: Even initially asymptomatic children may experience a period of increased risk of excessive bleeding following exposure to anticoagulant rodenticides. Acci dental ingestion of anticoagula nts can lead to coagulopathy (impairment of the body's ability to stop bleedi ng) in a child; although the child is initially asymptomatic they have the potential to bleed ex cessively (internally or externally) if they

9 One warfarin product subject to cancellation (EPA Reg. No. 3282-9) contains 0.054% active ingredient.

### ~ 28 ~ experience bodily trauma while thei r ability to stop bleeding is im paired. This potential is not limited to easily recognized locations. Bleeding can take place within a less easily recognized location, such as the brain. In sum, EPA’s analysis shows that, unl ess use and exposure patterns are changed, children could easily ingest quantities of the subj ect rodenticides that would contain sufficient amounts of active ingredient to ex ceed levels that EPA would c onsider safe. Consequently, EPA could not conclude that exposure to the subject rodenticides was reasonably certain not to cause harm. EPA fully appreciates that rodenticides are governed by the FIFRA risk-benefit standard rather than the FFDCA reasonable certainty of no harm standard, and that any hearing on the

NOIC must consider the benefits of rodenticide use against the ri sks of such use. Nevertheless, the FFDCA criteria for unsafe exposures to pes ticides in food provide a meaningful benchmark: If Congress would not allow these levels of pesticide exposure in food – no matter how beneficial the pesticide use might be to agricult ural producers – it is reas onable to infer that

children should not suffer the same levels of e xposures through other ro utes absent important countervailing benefits.

The rodenticide active ingredients in products subject to the NOIC are man-made chemicals designed to kill rodents and are highly toxic to all mammals. Consequently, the nature

and extent of their effects in humans has not b een studied in detail. Much of the available information on their potential risk to humans and domestic animals comes from the numerous reported incidents detailing the fr equent exposure of children to r odenticides, and observations of the serious consequences to companion animals exposed to rodenticides . These incidents are

discussed in the next sections.

### ~ 29 ~

1. Sources of Human Incident Data EPA generally relies on toxici ty studies conducted on animals and exposure information based on the pesticide’s use pattern when registering a pesticide. After a pesticide is registered, however, human observational data about the effect s and exposure of registered pesticides may be collected and analyzed. In assessing the risk s of products subject to the NOIC, EPA analyzed human observational data, or in cidents, from the following s ources: summary data from the

American Association of Poison Control Center s (AAPCC), human incident (poisoning) data from such sources as OPP’s Incident Data Sy stem (IDS) database, Na tional Institute for Occupational Safety and Health (NIOSH) Sentinel Event Notifi cation System for Occupational Risks (SENSOR), the EPA-sponsored Nationa l Pesticide Information Center (NPIC), California’s Pesticide Incident Surveillance Prog ram (PISP), and additional review of the open

literature. Incident data can provide important informa tion about actual real -world exposures and risks associated with pesticide products. Inci dent data are collected systematically, but differently, by a number of organizations. The data bases used by the Agency differ with respect to such issues as coverage, certainty/confidence, fields/parameters report ed, and usability. These five pesticide incident data sources in combina tion with additional data from the open literature provide useful content and histor ical perspective. Various other comparable sources of data are available (e.g. the Bureau of Labor Statistics, emergency room outpatient surveillance, etc.) but

are believed to be of limited a dditional utility and were not relied upon for the development of

this document. Information from all 5 databa ses and open literature is provided in the

Rodenticides Tier II: Review of Human Incidents, November 1, 2011 Memorandum.

### ~ 30 ~ In regard to children’s expos ures to household products such as rodenticide baits, the AAPCC reports are the most applicable and co mplete, and are therefore the focus of this discussion. By looking across the data sources which were used, the Agency is confident that the data are adequate and appropriate for discerni ng trends and patterns in incident poisonings associated with the following rodenticides used for commensal rodent control in bait form: brodifacoum, bromadiolone, bromethalin, chlo rophacinone, cholecalciferol, difethialone, diphacinone, diphacinone sodium salt, warfarin, warfarin sodium salt, and zinc phosphide. Although these incident reporting databases can provide importan t information regarding the frequency, distribution and severity of adverse effects, they ar e far from comprehensive. EPA estimates that only one quarter of the total number of pesticide poi soning incidents are reported to the AAPCC or state counterparts. (Blondell and Spann, 06/03/1999, D256673). The AAPCCis a non-profit, national organiza tion founded in 1958 that represents the poison control centers of the United States and the interests of poison prevention and treatment of poisoning. All of the calls to a poison cont rol center are an swered by a medical professional trained to answer questions about poisons. Additionally, AAPCC reports provide clearly summarized information on pesticide incidents wi thin the context of other poisoning events. AAPCC produces an annual summary report gi ving statistics and information on all the poisonings reported to poison control centers in a calendar year. AAPCC ra nks the severity of human exposure incidents as follows:

• Death,

• Major – symptoms are life-threatening or resu lt in residual disabil ity or disfigurement (coma, cardiovascular instabil ity, repeated seizures),

### ~ 31 ~

• Moderate – symptoms are more pronounced, pr olonged, or more of a systemic nature than minor symptoms with no residual disabi lity. Usually some form or treatment is indicated (high fever, disorientation),

• Minor – symptoms are minimal with no residua l disability (skin irritation, drowsiness, mild gastrointestinal symptoms), or

• None – patient developed no symptoms as a result of exposure.

2. Observed Human Exposures and Resultant Health Effects

a. Prevalence When looking across human incident data s ources, as well as the open literature,

rodenticides are found to be involved in numerous reported incidents, es pecially those involving children less than 6 years old. While all th e sources (IDS, NPIC, PISP, NIOSH SENSOR) demonstrated that humans are being exposed to r odenticides, it is most ev ident in the Agency’s examination of the AAPCC rodenticide data from 1999 to 2009. The 1999-2009 AAPCC data showed that on average 17,000 human exposures to rodenticides were reported annually. Approximately 85% (i.e., approximately 15,000 pe r year) of these 17,000 e xposures occurred to children under 6 years old over the 11 year period analyzed (Table 5). 10 Approximately 16% of all reported exposures to pestic ides in the AAPCC data are re lated to rodenticide exposure. Approximately 26% of all reported pesticide exposures among children under 6 in the AAPCC data are related to rodenticide exposure. Out of all reported pesticide-re lated exposure incidents to children under 6 years old, for all pesticides , approximately 26% of th e exposures are due to

10 It should be noted that there has been a decrease over a number of years and the in 2010 there were 10,966 incidents reported to AAPCC occurring to children under 6 years old for all rodenticides (there were 406 bromethalin incidents, 8966 SGAR incidents, and 210 FGAR incidents).

### ~ 32 ~ rodenticides. Although incident data generally do not specify which product s were the subject of the reported exposures, very few, if any, rode nticide products marketed to general consumers during this timeframe included bait stations intended to prevent children’s exposure.

Table 5. AAPCC Reported Pesticide Expo sure Incidents Involving Children <6 years old by Pesticide Category from 1999-2009

Pesticide Category Total reported exposure incidents Number of reported incidents involving children <6 years old % Reported pesticide incidents that involved children Disinfectants 224,578 122,868 55% Fungicides 14,308 3,593 25% Herbicides 101,832 26,774 26% Insecticides 474,149 192,745 41% Organophosphates 84,931 24,877 29% Other pesticides 150,196 98,309 65% Rodenticides 195,263 166,250 85%

While certain AAPCC data are publicly ava ilable through 2010, EPA purchased access to the raw data and ancillary information for the years 1999 to 2005. More detailed analysis of AAPCC raw data from 1999 to 2005 of the childre n’s exposures to rodenticides, demonstrates that approximately 3,686 children less than 6 years ol d were treated at a h ealth care facility for the seven year period analyzed. The analysis also demonstrates that on average for this seven year period approximately 128 cases per year (or 1%) of the exposures to children result in a medical outcome classified by the AAPCC as minor , moderate or major. Also, of all pesticiderelated cases involving children less than 6 y ears old from 1999 to 2005, approximately 39% of

those seen in a health care faci lity are related to rodenticide exposure and 13% of hospitalization cases are related to rodenticide exposure. Fort unately, no deaths to children under 6 years old have been reported in these AAPCC data from 1999 to 2010.

### ~ 33 ~

b. Circumstances Incidents involving children appear to resu lt primarily from their picking up unprotected

baits in the home. These incidents may result from failure to follow label directions to keep bait away from children, though in some cases, baits might have been moved by rodents from appropriate placement locations. In some cases, it appears that parents underestimated children’s abilities to access places where r odenticides were applied. In othe r cases, it appears that the exposed children were visiting a different envi ronment (such as grandparents, friends, or neighbors) and their parent or guardian was una ware that the baits were accessible. Most incidents involving rodenticide expo sures among adults appear to be due to suicide or malicious intent. Accidental exposur es, although rare, occasionally occur for adults.

c. Resultant effects The majority of the rodenticide exposures re ported to AAPCC did not result in significant symptoms based on those cases which receiv ed follow up to determine medical outcome. However, given the high number of children e xposed to rodenticides, the small percentage experiencing significant symptoms is still a matt er of concern, both for the symptoms themselves and (in the case of anticoagulants) on account of the risk of excessive bleeding (internally or externally) in response to subsequent trauma wh ile their ability to stop bleeding is impaired. Moreover, while exposures to rodenticides gene rally result in no detect ed clinical signs in children, the Agency believes that the numb er of non-symptomatic exposure incidents is unacceptably high because of the social and other costs (medical care, wo rry) associated with evaluating and treating children who might have been exposed.

### ~ 34 ~ Although most symptomatic exposures do not result in lasting harm, severe outcomes from human exposures to rodenticides do o ccur. The AAPCC data from 1999-2005 indicates that, compared to other pesticide exposures, rodenticide exposures are much more likely to receive medical treatment, accounti ng for 39% of all pesticide-relate d cases seen in a health care facility and 13% of all hospitalized case s involving children less than 6 years old. From 1999- 2005, 894 cases were reported having minor, modera te, or major effects (Table 6). For cases reporting moderate or major effects, the most common effect reported was hematological, 37% and 55% respectively. These symptoms are likely a result from anticoagulant rodenticides’ abilities to interfere with blood clotting and ar e likely the result of rodenticide exposure.

* The categories are not mutually exclus ive (i.e. a person could re port both a neurological and renal symptom). No cardiovascular symptoms were reported.

3. Comparison of SGAR and Bromethalin Poisonings Whether a particular exposure is to an an ticoagulant or a bromethalin rodenticide is of significantly less importance to human health than whether the exposur e occurs in the first place.

EPA is concerned about both SGAR and bromet halin poisonings and believes that packaging rodenticide bait products in tamper-resistant bait st ations will result in dramatic reductions in Table 6. AAPCC Reported Exposure Symptoms for Symptomatic Children Less Than 6 Exposed to Rodenticide from 1999-2005 Level of Effect Total Expo sures Reported Exposure Symptoms*Neurological Ocular Renal Respiratory Misc. Dermal GI Hematological Minor effect 727 15 (2%) 17 (2%) 0 20 (3%) 180 (25%) 18 (2%) 277 (38%) 36(5%) Moder ate effect 147 7 (5%) 1 (1%) 4 (3%) 2 (1%) 22 (15%) 8 (5%) 34 (23%) 55 (37%) Major effect 20 1 (5%) 0 0 2 (10%) 5 (25%) 2 (10%) 4 (20%) 11 (55%)

### ~ 35 ~ exposures. In comparing bromethalin to the SGARs, animal acute toxicity data indicate that one

bite of bromethalin bait is one third as t oxic as one bite of brodifacoum bait (an SGAR), 11 and bromethalin clears from the body more quickly than the SGARs. Table 7 compares the toxicological properties of bromethalin and brodifacoum, one of the SGARs.

Table 7. Comparative properties of consumer products containi ng bromethalin and brodifacoum for rat and mouse control Property Bromethalin Brodifacoum Formulations - % active ingredient 0.010% 0.005% mg active ingredient consumed per 5 gm bite 0.5 0.25 dose to a 10 kg child (mg/kg/bite) 0.05 0.025 Acute lethality - Rat oral LD 50 (mg/kg) 2.6 0.42 (male) MOE based on rat LD 50 52 17 Rat LD 50 expressed as a human equivalent dose (mg/kg) 0.65 0.10 MOE based on human equivalent LD 50 13 4.2 Ounces of bait containing the HED LD 50 2.3 0.7 Estimated human acute lethality (mg/kg) 0.33 0.25 (est.) MOE based on case studies 6.6 10 Ounces of bait containing a lethal dose 1.2 1.8 Repeated dose toxicity - study 90 day subchronic developmental - species rat, dog rabbit - NOAEL mg/kg/day 0.025 0.002 - LOAEL mg/kg/day 0.125 0.005 MOE based on rept. dose NOAEL 0.5 0.08 Plasma half-life 5.6 days (rat) 16 -36 days (human) Range (time) of anticoagulant action N/A 51 days - 8 months Time to onset of clinical effects 6.5-8 hours 24-36 hours

11 This determination is based on the assumption that “one bite” is 5 grams of bait, which contains either 0.025 mg of brodifacoum or 0.05 mg bromethalin. The predicted dose of 0.05 mg bromethalin produces a margin of exposure (MOE) of 52, based on the acute oral LD50s in the rat (2.6 mg/kg). For brodifacoum, the MOE based on a rat LD50 is 17.

### ~ 36 ~

a. Incident Data Incident data presented in the American A ssociation of Poison Control Centers National Poison Data System (AAPCC-NPDS) for 1993 through 2005 show 4,271 total calls reporting exposure to bromethalin for children less than six years of age. Only eleven of the 4,271

incidents with bromethalin were classified as “moderate” and none were classified as “major.” Over the same time period, there were a to tal of 173,262 SGAR exposures, of which AAPCC classified 269 as moderate and 29 as major in cidents. When evaluating differences in these incident counts during the period analyzed, it is important to r ecognize that many more units of

SGAR baits were sold and used than were brom ethalin baits. But assuming that users are equally likely to call a poison control cen ter in the event of an exposur e incident, regardless of what active ingredient the rodenticide contains, the rate of non-minor in cidents involving a particular chemical per 10,000 calls relating to that chemical can provide a useful basis for comparison of

the likelihoods of non-minor incidents. For brom ethalin, the rate of non-minor incidents was 26 per 10,000 exposure calls, while for SGARs, th e rate of non-minor incidents was 17 per 10,000 exposure calls. Because the difference is not st atistically significant, these incident reports support a conclusion that bromethalin exposures are not significantly more likely to result in non-minor incidents than are SGAR exposures.

The small number of moderate incidents and the absence of major incidents for

bromethalin in the AAPCC-NPDS data are consiste nt with the results of animal studies that suggest that ingestion of 5 gram s of bromethalin bait is unlikely to cause adverse effects in a 10 kilogram (22 pound) child. 12

12 In two 90

‐ day sub

‐ chronic studies with bromethalin in the rat (MRID 43582102) and dog (MRID 43582101), there

### ~ 37 ~

b. Exposure and Treatment Neither bromethalin nor the anticoagulants produce symptoms that would serve to immediately alert a parent who is unaware that his or her child has ingested a rodenticide. If a toxic dose is ingested, bromethalin will, within hours of ingestion, cause non-specific symptoms including fever, dizziness, and, depending on the amount consumed, tremors. A toxic dose of an anticoagulant causes somewhat more distinctive br uising and bleeding (incl uding blood in urine, bleeding from the nose and gums, coughing bl ood and, depending on the amount consumed, bleeding into the joints and brain), but those sy mptoms do not appear until several days after ingestion. Thus, neither type of rodenticide (i.e., either antico agulant or bromethalin) is more likely than the other to produce symptoms that w ould alert parents or hea lth care workers of a rodenticide poisoning within the critical first hou rs when gastric decontamination could be an effective treatment. Sufficiently high exposur es to both bromethalin and the anticoagulants (particularly the SGARs) have the potential to re sult in patients being admitted to intensive care units at considerable harm and expense to th e patient. Because the persistent SGARs are metabolized more slowly by the body, compared to bromethalin, a nd due to the different mode of toxic action, SGARs result in longer-term medical effects a nd necessitate longer treatment regimes, at greater costs to the patient. Bromethalin poisonings are treatable, and do not present greater concerns or difficulties than treatment of anticoagulan t rodenticide poisoni ngs. Although emergency room physicians are more likely to have treated an anticoagulan t poisoning than a bromethalin poisoning in recent

were no effects in either the rat or dog after 90 days of continuous daily exposure to bromethalin at a dose of 0.025 mg/kg/day. For comparison, the No Observed Adverse Effects Level (NOAEL) for maternal effects in a rabbit developmental study with brodifacoum was 0.002 mg/kg/day (MRIDs 00052442 and 40307201).

### ~ 38 ~ years, specific experience with bromethalin is not important to successful treatment. Like aspirin, indomethacin and ibuprofen, bromethalin is an uncoupler of oxidative phosphorylation, and clinicians are experienced in the appropriate emergency care for exposure to other common chemical substances that act in the same way as bromethalin and require the same treatment. Uncoupling of electron transport is a reversible effect. Once the uncoupler is removed from the system, normal mitochondrial resp iration resumes. Transient effects associated with the uncoupling are not associated with long term neurological damage. Regardless of the rodenticide at issue, treatment outcomes are likely to be better when the symptoms are linked to a rodenticide exposure even t, and in particular when the identity of the specific product or active ingr edient is known. Initial emerge ncy room treatment for known ingestion of a toxic dose of e ither type of rodenticide would, however, be the same. In both cases, physicians would work to limit the quantity absorbed by gastric decontamination, and

administration of activated char coal. However, the opportunity for decontamination is short (2 hours or less), and after that, treatment met hods diverge. In SGAR poisoning cases where bleeding is evident, the patient would be trea ted with repeated doses of vitamin K and, depending on the severity of the bleeding, fresh fro zen plasma and clotting factor therapy such as

recombinant activated factor VII therapy. In bromethalin cases, th e patients would be treated for symptoms such as fever and dizziness and, in severe cases with cerebral edema and increased intracranial pressure, treatment would include os motic diuretics and steroids. In cases where exposure is unknown or uncertain, ne ither type of rodenticide (i.e ., anticoagulant or bromethalin) is more likely than the other to produce symptoms that would alert parents or health care workers of a rodenticide poisoning within the critical first hours when ga stric decontamination could be

an effective treatment.

### ~ 39 ~ Although Vitamin K treatment can compensate for reduced levels of active vitamin K resulting from anticoagulant poisoning, a prolonge d treatment regime may be necessary because of the long half-lives of the SGARs. 13 Coagulopathy, a reduction in the blood’s ability to clot when there is bleeding, can last for several mont hs while the anticoagulant is cleared from the body. Patients will often need repeated vitamin K treatments, based on prothrombin time and hemoglobin level determinations . Clinical effects from seve re bromethalin poisonings are typically present for a shorter period of time as compared with the SGARs. Data from AAPCCNPDS indicate that for the 9 bromethalin incident s mentioned previously, the duration of clinical effects was from 2 to 8 hours, and the incident reports do not indicate any lasting effects. Every child’s exposure event is of con cern, because any time a child can access rodenticide bait, there is the poten tial for the child to swallow some or all of it. A single 5 gram bite (less than a quarter of an ounce) of any rodenticide bait w ould result in a pesticide exposure that greatly exceeds levels considered safe as a dietary exposure for a child weighing 10 kg, and the quantity of active ingredient contained in a single placement of a ny of the rodenticides subject to the NOIC is sufficient to cause adve rse health effects. Symptomatic exposures – diagnosed or undiagnosed – are a matter of concern, both for the symptoms themselves and (in the case of anticoagulants) on accoun t of the risk of excessive bleed ing (internally or externally) in response to subsequent trauma while their abil ity to stop bleeding is impaired. In addition to concerns about the actual health impacts of expo sure of children to any rodenticide, the Agency

13 Bromethalin half-life is 5.6 days (MRID 000146583). SGAR half-lives range from 11-170 days: brodifacoum half-life is 16-36 days (Blood, Vol76. 1990: pp 2555-2559; bromadiolone half-life is 8-170 days (biphasic) http://www.inchem.org/documents/pds/pds/pest88_e. htm; difenacoum half-life is 11-42 days http://toxwiki.wikisp aces.com/Anticoagulant+Rodenticid es_Oral._logPs are 8.5 (brodifac oum, an SGAR) and 4.26 (bromethalin) Rodenticide Cluster RED (1998).

### ~ 40 ~ is mindful of both the potential medical costs asso ciated with children’s e xposure to rodenticides in the home and the anxiety to parents (and perh aps children as well) caused by the exposure of children to poisons in the home.

C. Characterization of Ha zard to Domestic Animals Rodenticides are highly toxic to mammals a nd birds, and have much the same effects on domestic animals as they do on humans and on target mammals, as discussed above. Species may differ somewhat in sensitivity to particular rodenticides; however, in the absence of reliable data on relative sensitivities, it is reasonable to presume that all vertebrate pet sp ecies are highly

vulnerable to all rodenticides.

1. Sources of Domestic Animal Incident Data EPA generally relies on toxicity studies conducted on laboratory animals and exposure information relevant to the pesticide’s use pattern when initially registering a pesticide. After a pesticide is registered; however, observational data about the eff ects and exposure of registered pesticides may be collected and analyzed. In as sessing the risks of products subject to the NOIC, pet observational data, or incidents, from the following sources were analyzed:

• Information from the National Animal Poison Control Center (APCC), the Pet Poison Helpline, and the open literature.

• OPP’s Incident Data Sy stem (IDS) database,

• The EPA-sponsored National Pesticid e Information Center (NPIC),

### ~ 41 ~ Animal Poison Control Center and Pet Poison Helpline The American Society for the Prevention of Cruelty to Animals (ASPCA) Animal Poison Control Center (APCC) is a 24 hours a day, 365 da ys a year resource for animal poison-related emergencies. Calls to the APCC are triaged by sp ecially trained veterinary toxicologists. The Pet Poison Helpline, another po ison reporting center which is available throughout the U.S., Canada and the Caribbean, is managed by veterina ry specialists who also help triage animal poisoning events. The veterinary specialists include board-certified veterina ry internal medicine emergency critical care specialists, and veterinary toxicologists. OPP Incident Data System (IDS) The OPP IDS database of pet exposure informati on includes reports of al leged incidents from various sources, including FIFRA Section 6(a)(2) re ports from registrants and reports from other environmental agencies and individual consum ers. The IDS exposure severity types for domestic animals, as define d by 40 CFR 159.184, are as follows:

• DA – Death – if the domestic anim al died or was euthanized;

• DB – Major – if the domestic animal exhibited or was alleged to have exhibited symptoms which may have been life-threatening or resulted in residual disability;

• DC – Moderate – if the domestic animal e xhibited or was alleged to have exhibited symptoms which are more pronounced, more prol onged or of a more systemic nature than minor symptoms and included some treatme nt and return to pre-exposure state;

• DD – Minor – if the domestic animal was alleged to have exhibited symptoms, but they were minimally bothersome and resolved rapidly;

• DE – Unknown – if symptoms are unknown or not specified. 14

14 Some exposures are classified as “D” in IDS, which is a classification used before 1998 (at which point reporting requirements were updated) or used to indicate the severity is undetermined; as the focus of this assessment is on incidents occurring in 1999 or later, we assume all “D” exposures are “DE” and have undetermined severity.

### ~ 42 ~ National Pesticide Information Center (NPIC) NPIC is a cooperative effort between Oregon State University and EPA which is funded by EPA to serve as a source of objective, scie nce-based pesticide info rmation and respond to inquiries from the public and to incidents. NP IC receives approximately 25,000 calls per year, with about 4000 of these being related to pest icide exposure incidents. NPIC collects the

information about the incidents a nd records that information in a database. NPIC is a source of national incident information; but generally recei ves fewer reports than IDS. Regardless, NPIC can provide an additional source of incident information. Unlik e IDS, incidents reported to NPIC are assigned a certainty classification, wh ich helps ascertain whether the exposure and reported outcome are related. 2. Observed Domestic Animal Expos ure and Resultant Health Effects

a. Prevalence The American Society for the Prevention of Cruelty to Animals (ASPCA) Animal Poison Control Center (APCC) website identifies the top ten pet toxi cants of 2010 based on the number of calls received. Out of the approximately 167,000 phone calls about pet exposures they received during 2010, rodenticides were listed as the third most frequent reason for calls to the APCC (after human medications and insecticides ). Another 24-hour hotline, the Pet Poison Helpline, in 2009 identified rodenticides as the third most common class of toxicants involved in dog poisonings (after chocolate a nd insect bait stations) and the fourth most common class of toxicants involved in cat poisoning s (after lilies, canine permethr in insecticides and household cleaners).

Both the IDS and NPIC data indicate that the number of repor ted incidents of pet exposure to rodenticides is incr easing over time. However, differe nt rodenticides are associated

### ~ 43 ~

with this increase in the different databases. IDS reports that the number of reporte d pet exposures involving FGARs and nonanticoagulant rodenticides was relatively stable from 1999 to 2009, whereas reported exposures involving SGARs (chiefly bromadiolone) increased over time, from approximately 200 per year to approximately 1400 per year, primarily in the moderate, minor and unknown outcome categories. The overall upward tr end may be a result of increased usage or increased reporting,

rather than an increase in the likelihood th at use of a product resu lts in an incident. By contrast, NPIC reports that the number of reported pet exposures involving FGARs and SGARs was relatively stable from 1999 to 2010, whereas reported exposures involving nonanticoagulants (chiefly zinc phosphide) increased over time, from approximately 5 per year to approximately 180 per year. To the extent that th is increase is associated with use of zinc phosphide, it is not relevant to the proposed cancellation because zinc phosphide is not registered

for commensal rodent control in and around homes. The only zinc phosphide products registered for general consumer use are for mole and pocket gopher control, and must be manually applied below ground to maximize exposure to target species, which mini mizes exposure to non-target

animals. b. Circumstances The narrative information available regarding these incidents and EPA’s review of the scientific literature indicate that many pets ga in access to baits placed in and around homes.

EPA believes the main reason these incidents are o ccurring is because roden ticide baits are being placed in areas accessible to pets without use of pet-resistant bait st ations required by the products’ labels.

### ~ 44 ~

c. Resultant effects The IDS data reflect that, although most roden ticide incidents appear to result in lower severity outcomes, there were a substantial numbe r of fatalities (1209) and major outcomes (565) from 1999 to 2009. These numbers indicate that rodenticides cause, on average, about 160 severe (death or major effect) domestic animal incidents every year. EPA believes that the IDS data are likely to significantly underestimate the number of incide nts that actually occur because many incidents go unreported.

The IDS data also allow rodenticide active ingredients to be ra nked according to the severity of domestic animal incidents reported. Although the data may be influenced by market share, focusing on those exposures resulting in severe outcomes provides an indication of the hazard of a particular active ingr edient. The rodenticid e with the highest number of incidents ranked DA (death) and DB (major) over the pe riod 1999-2010 was brodifacoum (710 incidents), followed by bromadiolone (355), bromethalin (292 ) and diphacinone and its sodium salt (262). Together, the SGARs brodifacoum and bromadiol one accounted for 60% of the major and fatal domestic animal incidents (DA+DB) attributed to rodenticides. Comparing the major and fatal incidents (DA+ DB) per active ingredient as a percentage

of total incidents for that same active ingredient provides a way to judge whether a particular active ingredient is more or less likely to cau se serious adverse effects (i.e., major or fatal incidents) than another. For example, 22% of reported exposures to brodifacoum result in a pet death or major incident, but only 8% of reported exposures to brom adiolone result in a death or major incident, indicating that brodifacoum e xposures are more likely to cause severe consequences than bromadiolone exposures.

### ~ 45 ~

Table 8: IDS - Rodenticides as a Percentage of Severe Outcomes, 1999-2009

Rodenticide Category Percentage of Death + Major Incidents out of Total Exposure Count Total Exposure Count Diphacinone and diphacinone, sodium salt First generation anticoagulant 22% 1,192 Warfarin and warfarin, sodium salt 22% 151 Chlorophacinone 21% 29 Brodifacoum Second generation anticoagulant 22% 3,229 Bromadiolone 8% 4,661 Difethialone 13% 144 Difenacoum 27% 11 Bromethalin Nonanticoagulant 12% 2,460 Zinc phosphide 18% 258 Cholecalciferol 23% 209

The incident data show that all rodenticides have caused death or major adverse health effects to pets. Although this an alysis shows some differences in the likelihood of death or major

outcomes for the different rodentic ides, large percentage s of pets exposed to a rodenticide are likely to experience severe outcomes, regardless of the category or identity of the rodenticide.

Use of bait stations that meet EPA’s criteria fo r pet resistance would reduce the frequency of pet exposures to rodenticides. Alt hough such products have been av ailable in the commercial and agricultural pest-control markets for nearly 30 year s, they were virtually absent from consumeroriented markets until the June 4, 2011, RMD compliance date.

D. Characterization of Hazard to Non-Target Wildlife This discussion summarizes the ecological risk concerns that form part of the basis of EPA’s decision to cancel and deny registrations for the commensal rodent control products identified above in the NOIC. EPA has updated its previous risk assessment findings conducted in support of the May 2008 RMD through the applic ation of additional effects and exposure data,

### ~ 46 ~ use of additional exposure modeling, and quantita tive risk assessment te chniques for the four rodenticide active ingredients (bro difacoum, difethialone, warfarin and bromethalin) contained in products subject to the NOIC and for two rodent icides (chlorophacinone and diphacinone) that are potential alternatives to brodifacoum and difethialone in the consumer rodenticide market. Rodenticide baits are intended to be lethal to rodents and a few other small mammals, but the active ingredients are not selective to target species. All mammals and birds are vulnerable to adverse effects, including mortality, from rodenticides, although different species and individuals may have differing sensitivities. R odenticide exposures and mortalities have been

documented for mammals and birds that ar e primary and secondary consumers.

1. Routes of exposure For the purpose of the ecological risk assessment, primary exposure was defined as consumption of rodenticide treated bait by non-tar get organism. Use of rodenticide baits around structures is likely to result in primary e xposures among non-target wi ldlife. Many factors influence which non-target animals might be exposed directly to baits. For instance, birds and mammals that are attracted to seeds and grains may consume grain-based rodenticide baits and baits in forms similar to seeds and grains. Some non-target animals will readily consume

rodenticide baits that have a block form. In cident reports document rodenticide exposures among a number of species that are likely to be primary cons umers of bait, including quail, turkeys, squirrels, opossums, raccoons, skunks, and deer. Secondary consumers were defined for purpos es of the ecological risk assessment as those animals that prey upon or scavenge prim ary consumers of bait. Rodenticide baits pose potential secondary poisoning risks, because predat ors and scavengers are likely to be attracted

### ~ 47 ~ to dead or dying rats, mice, and poisoned non- target animals. Incident reports document rodenticide exposures among a number of seco ndary consumer species including larger mammals such as bobcats and foxes, and numerous bird species such as hawks, eagles and owls. Omnivores were considered as both primary and secondary consumer s for this analysis. EPA is concerned with both the primary a nd secondary risks to birds and non-target mammals from exposure to the commensal rodent control products subject to the NOIC. This concern is based upon consideration of several li nes of evidence, including (1) an assessment of the risks to non-target animals associated with primary exposure to rodenticides; (2) an assessment of the risks of non-target animal s through secondary expos ure to rodenticides, including an evaluation using probabilistic risk assessment techniques; (3) an evaluation of available feeding studies as they relate to s econdary exposure risks; a nd (4) an evaluation of reported wildlife incidents as they relate to primary and secondary mortality events for nontarget species in a variety of land use settings , including urban, suburban, and rural settings. Table 9 provides a summary of EPA’s conc lusions on primary and secondary risks for each chemical based on an analysis of the above lines of evidence. Across all lines of evidence, the evaluated data suggest that all assessed chemi cals pose risk to wildlife that exceeds levels of concern. For birds, brodifacoum and difethialone stand out as posing the greatest potential for

adverse effects. Bromethalin also exhibits a hi gh potential for adverse effects to birds, although the relatively short blood half -life and the tendency of an imals to stop eating bait after consuming a toxic dose of bromethalin reduces the potential for secondary exposure. For mammals, the ranking of relative chemical risk is similar; however, there is much less differentiation in risk among the chemicals as might be expected given that rodenticides were

### ~ 48 ~ developed with the goal of mammal mortality. For the individual lines of evidence, EPA concludes the following: a. Primary Exposure Risk

• Brodifacoum and difethialone are more toxic to birds and mammals than are warfarin, chlorophacinone, dipha cinone, and bromethalin; howeve r, the toxicity differences between chemicals are much more pronounced for birds. • For primary exposure to birds, all or a majo rity of lines of evidence (i.e., results of the deterministic risk assessments, days required to consume the bait equivalent of an LD50, and quantity of bait required to consume an LD50) for brodifacoum, difethialone, and bromethalin indicate that birds are likely to be adversely affected if they dire ctly consume bait. For both bait concentrations of warfarin (0.025 and 0.054%), the deterministic risk asse ssment indicates that some weight classes of birds are likely to be adversely affected if they directly consume bait; however, the additional lines of evidence indi cate that the required feeding times and bait consumption quantities are greater than for br odifacoum, difethialone, and bromethalin. For chlorophacinone and diphacinone, the analysis suggests that birds do have the potential to be adversely affected following primary consumption of bait, but the estimated days of feeding on

bait to reach an LD 50 (ranging from 16 to >365 days) are much greater than for the other

evaluated rodenticides. • For primary exposure to mammals, all or a majority of lines of evidence for all

evaluated rodenticides s uggest that mammals are likely to be a dversely affected if they directly

consume bait. • Analysis of the available reported wildlif e incidents indicated that for both birds and mammals, consumption of bait does occur re sulting in mortality across a majority of the

### ~ 49 ~ chemicals. The most notable exception is bromet halin, as only a few inci dents were reported; however, bromethalin is not often in cluded in tissue residue analyses. b. Secondary Exposure Risk For secondary exposure to birds, all lines of evidence (i.e., results of the deterministic risk assessments, quantity of contaminated mi ce or rats in diet required to consume the equivalent of an LD50, results of a limited pr obabilistic analysis, and results of available secondary feeding studies) indicat e that birds are likely to be a dversely affected by brodifacoum if birds consume contaminated prey (incident da ta confirms that birds have been adversely affected by consuming contaminated prey). Sim ilar conclusions can be made for difethialone: the predominance of the evidence is that difethia lone adversely affects birds if they consume contaminated prey, but a few exposure scenar ios (larger birds cons uming prey with low contamination levels) are less likely to result in adve rse effects than is the case for brodifacoum. Evidence that predators or scavenger may be adversely affected by secondary exposure to warfarin, chlorophacinone, diphacinone, and bromet halin is equivocal, sugge sting that risks may be dependent on the sensitivity of individual species or a rodenticide’s potential for accumulation in prey animals. For secondary exposure to mammals, all lines of evidence indicate that mammals are likely to be adversely affected if exposed to co ntaminated prey (incident data confirms that mammals have been adversely affected by consum ing contaminated prey) for brodifacoum. Bait containing difethialone, bait cont aining the higher concentration of warfarin (0.054%), and bait containing bromethalin also may adversely affect mammals that consume contaminated prey; but a few exposure scenarios are less likely to resu lt in adverse effects than in the case of brodifacoum. Also, bromethalin appears to have lower potential to accumulate and be retained

### ~ 50 ~ in prey relative to the other assessed chemicals, which reduces the second ary exposure potential. Analysis of the available reported wildlife incidents indicated that for both birds and mammals, consumption of bait does occur resulting in mortality across a majority of the chemicals. The most notable exception is bromet halin, as no secondary exposure incidents were reported; however, bromethalin is not ofte n included in tissue residue analyses.

Table 9. Ecological risk conclusi ons from all lines of evidence

Chemical RQs and Opportunity for Exposure Incident Data Overall Conclusion Primary

Risk Secondary Risk Primary Secondary Urban/ Suburban Primary Secondary Birds Brodifacoum All lines All lines All lines All lines A ll lines All lines All lines Difethialone All lines Predominant No data All lines All lines All lines Predominant Warfarin (0.025%) Equivocal Equivocal All lines All lines All lines Equivocal Equivocal Warfarin (0.054%) Equivocal Equivocal All lines All lines All lines Equivocal EquivocalChlorophacinone Equivocal Little All lines All lines All lines Equivocal Equivocal Diphacinone Little Equivocal All lines All lines All lines Equivocal Equivocal Bromethalin Predominant Equivocal No data No data No data Predominant Equivocal Mammals Brodifacoum All lines All lines All lines All lines A ll lines All lines All lines Difethialone All lines Predominant All lines All lines All lines All lines Predominant Warfarin (0.025%) All lines Equivocal All lines No da ta No data All lines Equivocal Warfarin (0.054%) All lines Predominant All lines No da ta No data All lines PredominantChlorophacinone Predominant Equivocal All lines All lines All lines Predominant Equivocal Diphacinone All lines Equivocal All lines All lines All lines All lines Equivocal Bromethalin All lines Predominant All lines No data No data All lines Predominant “All Lines” = All lines of evidence suggest risk exceeds concern levels and effects are likely to occur “Predominant” = The predominance of the evidence is that the chemical causes adverse effects, but a few exposure scenarios are less likely to resu lt in those adverse effects. “Equivocal” = Equivocal evidence that risk exceeds concern levels and effects are likely to occur “Little” = Little evidence that risk exceeds conc ern levels or that effects are likely to occur

### ~ 51 ~ 2. EPA’s Deterministic Assessment Approach In conducting both the primary and secondary risk assessments, EPA utilized several independent lines of evidence to determine whether and to what extent the commensal rodenticides at issue in this proceeding advers ely affect non-target wild life. These lines of evidence include the following:

• Risk quotients (RQs),

• Evaluation of primary and s econdary exposure studies,

• Measures to determine the feasibi lity of an effect occurring, and

• Incident data. The RQ is briefly described in this section, and other lines of evidence evaluated in this assessment are described in greater detail in subse quent sections. The RQ is a unitless value that is the ratio of exposure to the to xicity endpoint. For example, in the context of acute avian risk estimates (e.g., mortality), an RQ of 1 would mean th at non-target birds may be exposed in the environment to an amount of the pesticide that would be expected to result in 50% mortality based upon laboratory test s (specifically, the LD 50 dose). EPA compares RQs to the Agency’s levels of concern (“LOC”) for non-target species. The LOC represents the exposure levels at which, in EPA’s judgment, a pesticide has the pote ntial to cause risks of concern to non-targetorganisms. Thus, when the RQ for a pesticide exceeds the LOC for a particular category of nontarget species, the Agency believes there is a risk of concern for species in that category. In this assessment, risk quotients were compared with the acute level of concern that EPA regularly uses in assessing risks to non-target wildlife generally (LOC = 0.5). Additional levels of concern may also be used to evaluate potential ri sks to species listed as threatened or endangered (LOC = 0.1); however, for simplicity, this analys is only used the LOC of 0.5. Therefore,

### ~ 52 ~ conclusions made with respect to the LOC of 0.5 may not apply to listed species.

Because this deterministi c assessment is intended to serve as a screening tool for identifying a potential for adverse effects, it is somewhat li mited and conservative by design. As a result, EPA does not believe that the RQs deri ved in this assessment can be used as a precise measure of the magnitude of effects that will occur, but rather se rve as tools for addre ssing whether or not a chemical poses a risk to assessed animals at a level of concern to the Agency. As a result, direct comparisons between chemicals on the basis of RQs can be misleading. Therefore, in this assessment, the Agency also uses other lines of ev idence to characterize th e relative risks of the rodenticides that are subject to the NOIC and the alternatives considered here, as described in succeeding sections.

a. Primary Exposure and Risk

i. Methodology For the purpose of this assessment, primary exposure is defined as non-target organism consumption of rodenticide treated bait. Primary exposure risk is influenced by factors including toxicity, toxicokinetics (chemical absorpti on, distribution and elimination in the body), concentration of active ingredient in the bait, an d availability of bait for consumption. For each of the evaluated chemicals, risk was assessed in several ways. RQs we re calculated assuming:

• Single day dose-based exposure to bait, base d on allometric equations that allow for differentiation among taxa and body size , is compared to acute oral LD 50 toxicity values;

• Six day dose-based exposure to bait, based on metabolism rate in the body and allometric equations that allow for differentiation among taxa and body size, is compared to acute

oral LD 50 toxicity values; and

### ~ 53 ~

• Diet-based exposure, based on the concentrati on of rodenticide active ingredient in bait, is compared to acute dietary LC 50 values.

Further lines of evidence were evaluated, including:

• An analysis of the number of days of ba it consumption required to reach the median lethal dose of rodenticide;

• The amount of bait individuals would need to consume in order to accumulate the median lethal dose; and

• Incident data.

For the single-day dose-based exposure met hod, exposure was calcul ated by dividing the dose (in milligrams of active i ngredient) by the body we ight (in kilograms) of the consuming

individual for three standard we ight classes of birds and mammals . Allometric equations that relate food consumption to body weight (W ildlife Exposures Handbook, USEPA 1993) were used to determine potential exposures for t ypical birds and mammals of varying sizes. Allometric equations were used for the gene ric bird and mammal. In addition, allometric equations for passeriform birds and rodent ma mmals were also used as these would best approximate those individuals with high poten tial for consuming bait and they would give conservative exposure estimates. Animal exposur e was determined based on daily food intake rates (dry weight), assuming 100% of their diet consisted of dry bait. It was assumed for this

assessment that the form of the bait would not influence rate of intake or total intake. Weight-adjusted LD 50 values for birds and mammals were used as the measure of toxicity to non-target species. The toxicity values sele cted for this assessment for birds were the most

### ~ 54 ~

sensitive LD 50 values available for Northern bobwhite quail ( Colinus virginianus ) or mallard

duck (Anas platyrhynchos ). The toxicity values selected for this assessment for mammals were

the most sensitive LD 50 values available for the Norway rat ( Rattus norvegicus ). For this assessment, EPA used standard bird (bobwhite quail and mallard duck) and mammal (Norway rat) test species to estimate weight-adjusted LD 50 values for non-target animals. Although there are numerous studies addressing the toxicity of one or more roden ticides in a wide variety of non-target species, these standard test species are the only ones fo r which studies are available on all of the rodenticides of interest. Therefore, in order to provide a uni form basis of comparison between rodenticides, EPA’s analysis focused on these standard test species. However, this method may be less conservative if other non-targ et species are more sensitive to rodenticide exposure than are the st andard test species. Scaling factors were used to modify the av ailable avian and mammalian toxicity data to account for differences in sensitivity between an imals of different body weights. For example, when using the default scaling factor, smaller bird s are estimated to be more sensitive compared to larger birds. Scaling f actors, derived from Mineau et al . (1996) for birds are used in this assessment, which is consistent with the Agency ’s terrestrial animal risk assessment model TREX v.1.4.1 (U.S. EPA 2008). A chemical-specific s caling factor was ava ilable for brodifacoum (0.76) from Mineau et al . (1996), and for all other chemical s where such a specific value is unavailable, the default scaling factor (1.15) was used to adjust the avian LD 50 s. Using additional data, Mineau et al . (2001) provided an alternative scaling factor for brodifacoum (0.88) and a chemical-specific scaling factor for chlorophacinone (-0.53). Mammalian weightadjusted LD 50 values were calculated using the “body weight 3⁄4 ” adjustment (USEPA 1995, 2011). EPA’s assessment for primary exposure and ri sk utilized default weight classes of birds

### ~ 55 ~ (small (20 g), medium (100 g), and large (1000 g)), and mammals (small (15 g), medium (35 g), and large (1000 g)). These are the standard bi rd and mammal body weights used in by EPA for ecological risk assessments (T-R EX version 1.4.1, U.S. EPA 2008). The six day dose-based exposure assessment utilized the same toxicity information discussed above, but in this assessment RQs we re calculated by estimating body burden based on the assumption that bait was cons umed exclusively for six days . Body burden concentrations (milligram active ingredient per kilogram body weight [mg a.i./kg-bwt]) were based on feeding

rates and elimination rates from liver half-life estimates. For the diet-based primary exposure assessment, EPA evaluated the concentration of a.i. in the bait and the dietary LC 50. The LC 50 (mg a.i./kg-diet) is obt ained from 5-day exposure dietary toxicity studies. RQs are calculated as a ratio of a.i. concentration and the LC 50 . Risk results that agree between this method and the multiple day accumulated dose method described above provide an enhanced degree of confiden ce in risk conclusions for a given chemical. As noted above, EPA also evaluated further li nes of evidence, including an analysis of the number of days of bait consumption required to reach the median lethal dose of rodenticide

and the mass of bait animals would need to consum e in order to reach the median lethal dose,

and incident data. The first line of evidence involved calculation of the number of days it would take an individual non-target bird or mammal (assuming the standard body weights described above) to reach the LD 50 through consuming 100% of its daily diet as bait. The second line of evidence involved calculating th e amount of bait that would n eed to be consumed to be equivalent to the LD 50. These additional lines of evidence re present useful tools for comparing risks among chemicals. The greatest concerns for non-target primary risk are with those pesticides for which little feedi ng time or only a small amount of treated material is necessary for

### ~ 56 ~ mortality to occur. Mortality to non-target primary consumers becomes less likely when consistent feeding or large amounts of consump tion are necessary over a protracted period of

time to cause death.

ii. Risk Characterization Variation in toxicity among the chemi cals and sensitivity across taxonomic groups, species, and exposure methods are evident when examining the availabl e toxicity endpoints (Figures 1-4). Generalized conclusions based on the available acute oral (LD 50 ) studies are: (1)

mammals are more sensitive to these rodenticides than are birds; (2) there is a larger variation in toxicity to rodenticides for birds than there is for mammals; (3) within a chemical, significant variation is present among species and/or laboratories; (4) for birds, an approximate toxicity ranking is brodifacoum and difethialone, fo llowed by bromethalin, followed by warfarin, chlorophacinone, and diphacinone; and (5) for mamma ls, an approximate toxicity ranking is brodifacoum and difethialone, followed by bromethalin, warfarin, chlorophacinone, and diphacinone.

Although fewer toxicity endpoints are av ailable for the acute dietary (LC 50 ) studies, the general conclusions are similar: (1) mammals are mo re sensitive than birds; (2) there is a larger variation in toxicity to rodenticides for birds than there is for mammals; (3) within a chemical, significant variation is present am ong species and/or laboratories; (4) for birds, an approximate toxicity ranking is brodifacoum and dife thialone, followed by bromethalin, warfarin, chlorophacinone, and diphacinone; and (5) for mamma ls, the central tendencies and ranges in toxicity appear very similar across all ch emicals for which data are available.

### ~ 57 ~

Figure 1. Avian acute oral LD 50 (mg a.i./kg-bwt) values for all evaluated chemicals. Only toxicity values obtained using the technical material were included. Circles represent the lowest toxicity value obtained from a standard test species (bobwhite quail or mallard duck); these values were used for RQ calculation. Triangles represent toxicity values obtained from non-standard test species or less sensitive standard test species.

Figure 2. Mammalian acute oral LD 50 (mg a.i./kg-bwt) values for all evaluated chemicals. Only toxicity values obtained using the technical material were included. Circle s represent the lowest toxicity value obtained from a standard test species (laboratory rat); these values were us ed for RQ calculation. Triangles represent toxicity values obtained from non-standard test species or less sensitive standard test species 0.1 1 10 100 1000 10000

0.1 1 10 100 1000 Brodifacoum

Difethialone

Chlorophacinone Diphacinone

Bromethalin Warfarin

LD 50 (m g a.i./k g -bwt)

LD 50 (m g a.i./k g -bwt) Di p hacinone

Bromethalin Chloro p hacinone Warfarin Difethialone Brodifacoum

### ~ 58 ~

Figure 3. Avian acute dietary LC 50 (mg a.i./kg-diet) values for all evaluated chemicals. Only toxicity values obtained using the technical material were included. Circ les represent the lowest toxicity value ob tained from a standard test species (bobwhi te quail or mallard duck); these values were us ed for RQ calculation. Triangles represen t toxicity values non-standard test specie s or less sensitive standard test species

Figure 4. Mammalian acute dietary LC 50 (mg a.i./kg-diet) values for all evaluated chemicals. Only toxicity values obtained using the technical material were included. Circles represent the lowest toxicity value obtained from a standard test species (laboratory rat); these values were used for RQ calculation. Tr iangles represent toxicity values non-standard test species or l ess sensitive standard test species. No data were available for di fethialone; data for bromethalin were not acceptable for RQ calculation. 0.1 1 10 100 1000 10000

0.1 1 10 100 1000 Warfarin

Chlorophacinone Brodifacoum

Difethialone

Di p hacinone

Bromethalin

LC 50 (m g a.i./k g -diet)

Brodifacoum

Difethialone

Warfarin

Chloro p hacinone Diphacinone

Bromethalin

LC 50 (m g a.i./k g -diet)

### ~ 59 ~ The risks identified by the determ inistic analyses and the other lines of evidence for each of

the rodenticides considered in the EPA assessm ent are characterized below. Tables 10 and 11 include the RQs for primary exposures of birds and mammals (respectively) to rodenticides.

These tables also include the estimated number of days required to reach the LD 50 through 100% consumption of bait and the mass of bait to be consumed for an individual to reach the LD 50 .~ 60 ~Table 10. Bird risk assessment: primaryexposure of passerine birds to bait.Bodyweights(g)Second GenerationAnticoagulantsFirst Generation AnticoagulantsNon-anti-coagulantBrodifacoumDifethialoneWarfarin(0.025%)Warfarin(0.054%)ChlorophacinoneDiphacinoneBromethalin

Risk QuotientsSingleday doseRQ20 20* 30*0.230.50*0.07 0.017.8*100 23* 18*0.14 0.31 0.04 0.014.8*1000 28* 9.2*0.07 0.16 0.02 <0.012.4*Six daydose RQ20 120* 170* 1.4* 2.9*0.40 0.05NA100 140* 100* 0.84* 1.8*0.25 0.03NA1000 170* 52*0.420.91*0.12 0.01NADietaryRQNA38* 45*0.400.86* 0.89*0.06 0.48

Additional lines of evidenceDays toconsumesufficientbait toreach theLD5020<1<14-5 1-216-17>365 <1100<1<17-8 3-430-31>365 <11000<1<114-15 6-7117-118>365 <1Gramsbaitconsumedto reachthe LD5020<1<125 1086>1800 <1100<11.1160 80620>7300 4.210005152100 99017000>52000 59NA = not applicable ND = no data* RQ exceeds acute risk LOC = 0.50~ 61 ~NA = not applicable ND = no data * RQ exceeds acute risk LOC = 0.50Table 11. Mammal risk assessment: primary exposure of rodents to bait.Bodyweights(g)Second GenerationAnticoagulantsFirst Generation AnticoagulantsNon-anti-coagulantBrodifacoumDifethialoneWarfarin(0.025%)Warfarin(0.054%)ChlorophacinoneDiphacinoneBromethalin

Risk QuotientsSingleday doseRQ15 9.9* 4.3* 8.4* 18* 0.82* 2.0* 5.1*35 8.5* 3.7* 7.1* 15* 0.70* 1.7* 4.4*1000 4.6* 2.0* 3.8* 8.3*0.380.90* 2.4*Six daydose RQ15 59* 24* 49* 110* 4.7* 12* NA35 51* 21* 42* 90* 4.0* 9.9* NA1000 27* 11* 22* 48* 2.1* 5.3* NADietaryRQNA94*ND57* 120* 44* 22* ND

Additional lines of evidenceDays toconsumesufficientbait toreach theLD5015<1 <1 <1 <1 1-2 <1 <135<1 <1 <1 <1 1-2 <1 <11000<1 <1 <1 <1 2-3 <1 <1Gramsbaitconsumedto reachthe LD5015<1 <1 <1 <1 6 1.1 <135<1 1.3 <1 <1 9 2.1 1.110006.7 16 8.0 3.7 61 25 13

### ~ 62 ~ RQs exceed the LOC for all mammals exposed to brodifacoum and difethialone. These pesticide active ingredients were developed to kill rode nts; they pose a lethal primary risk to non-target small mammals that eat bait containing either of thes e rodenticides. However, the quantitative assessment also demonstrates that ba it containing these two rodenticides constitutes a primary exposure risk concern for larger mammals as well as all avian size classes – that is, species that are plainly not the intended targets of these products. This conclusion is consistent across all primary exposure risk analyses performe d (single oral dose, six-day accumulated dose, dietary concentration and the feed ing period- lethality assessment ). EPA’s analysis indicates birds and mammals could attain a lethal dose (LD 50 ) of either brodifacoum or difethialone upon feeding for less than one day on treated bait. The brevity of feeding required to reach a potentially lethal exposure repres ents an increased opportunity (rela tive to all other rodenticides assessed) for non-target animals – especially bi rds -- to chance upon bait and consume a lethal

dose of either brodifacoum or difethialone. Warfarin, as expected for al l rodenticides, also demonstrates a primary exposure risk

concern to small mammals. The assessment of wa rfarin also indicates a risk to large mammals for all assessment methods employed as well. EP A’s analysis indicates th at feeding on treated bait for less than a day is sufficient to attain a lethal dose in all evaluated size classes of mammals, suggesting a similar opportunity, relati ve to brodifacoum and difethialone, for nontarget mammals to chance upon treated bait and consume a lethal dose. In contrast to brodifacoum and difethialone, warfarin’s primar y exposure risk for birds is limited to small passeriformes and other medium sized birds. While a single day dose risk assessment suggests only a risk to small passeriformes from the high est concentration formulation, accounting for the potential for multiple day accumulation on a dose basis expands the concerns to include

### ~ 63 ~ passeriformes and other small and medium sized bird s at all formulation concentrations assessed. The dietary assessment does not consider body weight as a determinant factor. However, this assessment method still predicts a risk concern at the highest formulation concentration. EPA

estimates that birds would attain a lethal warfarin dose after 1 to 7 days of feeding (0.054% warfarin bait) or after 4-15 days of feeding (0.02 5% warfarin bait). Th is finding suggests that, for birds there is less of an opportunity for cons uming a lethal dose of warfarin by chance when compared with brodifacoum and difethialone, since it would generally require multiple days of feeding on warfarin treated bait to reach a lethal dose in birds. For bromethalin, as can be expected for a relatively fast acting compound (target mortality occurs 1 to 7 days after initial exposure, Pitt et al . 2011, and registrant-submitted studies), acute risk concern levels are exceeded for all mammalian size classes feeding on treated bait regardless of the assessment method EPA em ployed. In addition, bromethalin exceeds risk

concern levels in a ll assessment methodologies with the exception of the dietary exposure methodology. EPA’s analysis indica tes that less than a single day’ s feeding on bromethalin bait

is sufficient to attain a lethal dose in birds and mammals, sugges ting (again like brodifacoum and difethialone) adverse effects to non-target wildlife are likely fro m primary exposure events with

treated bait. Two anticoagulant alternatives , chlorophacinone and diphacinone, also present primary exposure risk concerns for nearly all mamma l sizes assessed using all primary exposure assessment methods (however, large rodents, greater than 1000 g, consuming chlorophacinone bait for one day are not expected to experience risks of concern). EPA’s analysis indicates that <1 day (diphacinone) and <1 to 3 days (chlor ophacinone) of feeding on bait are sufficient to

attain the median lethal dose in mammals. Thes e periods are not materially different from the

### ~ 64 ~ other rodenticides with respect to the opport unity for non-target mammals to chance upon and ingest a lethal dose of treated ba it. In contrast to mammals, pr imary avian risk is below concern levels for these two compounds. This finding may be due to a limitation in the analysis of primary exposure models which had them termina ting at six days (i.e., longer exposure periods might provide sufficient exposure to bait for ad verse accumulation to occur). However, the analysis indicates that, unlike brodifacoum and di fethialone, a very cons istent and protracted feeding period for either diphacinone or chloroph acinone is required to at tain a lethal dose in birds (i.e., daily feedings over weeks to months).

b. Secondary Exposure and Risk The toxicity of each of the rode nticides and a variety of fact ors concerning their fate and effects in biological systems influence their poten tial for risk to secondary consumers, i.e., nontarget wildlife that may ingest living or dead an imals that have consumed rodenticide bait. These characteristics can be compared to predict the rodenticid es’ relative potential for such secondary risk. The elimination rate, potential to accu mulate within body tissues, time to death, and toxicity to both primary and secondary consumers influence exposure and risk. A compound that is rapidly me tabolized or excreted from a primary consumer likely results in a lesser secondary ri sk to non-target predators a nd scavengers than one that accumulates with repeated exposure, even if re peated exposure occurs weeks or months after initial exposure (Eason and Mu rphy 2000). Compounds that more rapidly clear from the body are less likely to pose secondary risk because the r odenticide is less able to accumulate to a level sufficient to affect a secondary consumer. Time to death also influences the potential for exposure, because compounds that kill rapidly would prevent the primary consumer from

### ~ 65 ~ continuing to eat bait, thereby consuming a dose th at would be toxic to a secondary consumer.

Rodenticides that are slower to cause death also prolong the period when contaminated (and potentially more vulnerable) prey are available to predators. The toxicity of the rodenticide to the secondary consumer would also affect the risk of adverse effects that would result from exposure. Based on these characteristics, rodentic ides that are eliminated more slowly and have greater potential to accumulate within body tissues, take longer to kill the primary consumer, and have greater toxicity to seconda ry consumers are expected to pr esent greater secondary exposure

risk. Below is an evaluation of the elimin ation and accumulation potential for each of the

assessed chemicals. i. Accumulation and Elimination

Information available from residue studies in primary consumers indicates that, of the anticoagulants, brodifacoum and difethialone accumula te in body tissues to a greater extent than warfarin, chlorophacinone, and diphacinone. Data fr om these types of studi es are not available for bromethalin, but the opportunity for primar y consumers to feed on bromethalin bait and

accumulate the rodenticide is limited due to th is chemical's rapid mode of action and the likelihood that target animals will stop feeding after a toxic dose is reached (Pitt et al. 2011). In addition, an available secondary feeding study shows that dogs consuming 600 g of bromethalincontaminated rat meat for 14 days did not show ove rt signs of bromethalin toxicity. While rats in this study were exposed to one half of the bromethalin found in currently registered bromethalin baits, these data suggest that bromet halin is not likely retained in body tissues in toxicologically significant amounts.

Available toxicokinetic data also indicate that , of the anticoagulants, brodifacoum is more persistent in animal tissue than all of the other ro denticides considered in this assessment. In one

### ~ 66 ~ study, brodifacoum was detected in rat livers up to 200 days post exposure to a single oral dose of 0.2 mg a.i./kg (Hawkins et al . 1991), and up to 11.7% was detected in livers of rats after 104 weeks following a single dose of 0.15 mg a.i./ kg (Batten and Bratt 1990 ). Other studies reviewed by the Agency provide further evidence of the long-term retention of brodifacoum in body tissues, and half-lives range up to 307.4 days in liver tissue and 91.7 days in plasma (Vandenbroucke et al. 2008). The study by Vandenbroucke et al. (2008) shows that difethialone may be much less persistent in the body than brodifacoum, with a liv er half-life of 28.5 days and a plasma half-life of 38.9 days. However, other studies submitted to EPA (Belleville 1986 and 1991, MRID#s 42065010 and 42065009 respectively) indi cate that the half-life of dife thialone may be several times greater than Vandenbroucke et al (2008). Belleville (1991) calculat ed a half-life for difethialone of 74 days in liver. Biological persistence data available for warfarin show variation among the species tested; however, most of the information on tissue retention indicates that it is generally less persistent in the body than brodifacoum and difeth ialone. A liver half-life of up to 66.8 days has

been calculated for warfarin in rats (Vandenbroucke et al. 20 08), and other estimates are less

than this value. Most data indicate that the plasma half-lives are less than 1 day (Pyrola 1968, Breckenridge et al. 1985, a nd Eason et al. 1999). Available data also show that chlorophacinone and diphacinone are mo re persistent than warfarin, but less persistent than brodifacoum and difethialone. Liver and plasma half-lives for chlorophacinone are 35.4 days and 11.7 days (Va ndenbroucke et al. 2008), respectively and a plasma half-life of 0.4 days has also been calculated (Belleville 1991). Half-lives for

### ~ 67 ~ diphacinone have been estimated to be shorter in some species (ranging from 3 – 5.43 days), but

liver retention times in cattle were determined to be >90 days (Fisher 2006, Fisher et al. 2003, Bullard et al. 1976).

Available data on the non-antico agulant rodenticide bromethalin suggest that it is rapidly eliminated by the body. While there are no data on the elimination half-l ife of bromethalin in liver, a metabolism study conducted in rats in dicated a plasma half-life of 5.6 days. Owing to the lack of available whole-body elim ination data for all assessed rodenticides,

liver half-lives were selected fr om the range of available data as a conservative representation of whole body elimination in animals consuming bait. If liver half-lives were not available, as in the case of bromethalin, the blood plasma half-life was used. In order to allow for comparisons of half-lives among chemicals, liver half-lives for brodifacoum , difethialone, warfarin, and chlorophacinone from the same study (by Vandenbr oucke et al. (2008)) were selected. Although this approach reduces variability due to differences attributed to laboratories, it is not necessarily the most conservative approach. For instance, th e liver half-life value for difethialone reported by Vandenbroucke (28 days) is lower than provided in other studies (74 days from Belleville, 1991). Though a liver half-life value is availabl e for diphacinone, it is based on a study on pigs,

rather than the rats used in the other studies. There is some indi cation from the available half-life studies that different sp ecies react differently to anticoagulant rodenticides. Therefore, the pig value may overestimate or underestimate the liv er half-life of rats for diphacinone. For bromethalin, there are no available data on the liv er half-life, so a blood plasma value was used instead. It is uncertain how a blood plasma half- life would differ from the liver half-life for this

chemical. The half-lives that were used to es timate doses of each rodenticide in non-target and target animals are provided in Table 12.

### ~ 68 ~

ii. Potential to Accumulate a Lethal Dose Many of the assessed rodentic ides typically cause mortality several days after exposure, which may allow target rodents to feed for se veral days upon rodenticide bait before dying. Such repeated feeding can lead to doses that far exceed the lethal dose. To compare the extent to which an accumulated dose may exceed the median lethal dose of target animals, EPA calculated estimated doses at the time of death assuming that target rodents continued to consume anticoagulant baits at the same rate until the da te when mortality was observed in acute oral toxicity studies. For rodents exposed to bait s containing 0.25% warfarin , doses were estimated to be 4 to 94 times the LD 50 at the time of death. For rode nts exposed to chlorophacinone and diphacinone, estimated doses at the time of death ranged from 3 to 13 times the LD 50 . In contrast, for rodents exposed to brodifacoum an d difethialone, estimated doses at the time of death ranged from 9 to 82 times the LD 50 . 15 This analysis indicates that target rodents that

15 For rodents exposed to bromethalin, similar calculations would predict estimated doses at the time of death ranging from 2 to 16 times the LD 50 . However, bromethalin is not expected to result in elevated levels in target rodents because one effect of bromethalin poisoning is that the animals stop feeding soon after attaining a lethal dose. Table 12. Elimination half-lives for certain rode nticides based on elimin ation rates from liver. Rodenticide Elimination half-life (days) References Brodifacoum 307.4 Vandenbroucke et al. 2008 Difethialone 28.5 Vandenbroucke et al. 2008 Warfarin 66.8 Vandenbroucke et al. 2008 Chlorophacinone 35.4 Vandenbroucke et al. 2008 Diphacinone 5.4 Fisher 2006 Bromethalin 5.6* MRID 0004724 *Value is based on elimination from blood plasma.

### ~ 69 ~ continue consuming anticoagulant rodenticide ba it after reaching a lethal dose may accumulate rodenticide doses that are many times the levels th at are sufficient to cause mortality. Elevated residues resulting from repeated consumption of bait poses in creased risk for secondary consumers that prey upon poisoned rodents becau se the secondary consumers receive high doses of rodenticides. Although all anticoagulants present risks that target rodents may bear

rodenticide concentrations in exces s of the lethal dose, this risk is clearly higher for the SGARs

difethialone and brodifacoum.

3. Assessment Based on Calcul ated Residues in Prey

a. Methodology Exposure for secondary consumers was estimated by calculating the amount of rodenticide in target rodents (i.e., house mouse an d Norway rat) that repr esent potential prey. As with the primary assessment, EPA’s secondary risk assessment estimated exposure using allometric equations of da ily food intake from the W ildlife Exposure Factors Handbook (EPA 1993). Rodenticide intake base d on consumption of bait by the primary consumers (prey) was calculated for the house mouse (23 g) and Norway rat (485 g). For this analysis, rodenticide accumulation in prey over three different time pe riods (1, 3 and 6 days) was calculated. These time periods were used as representative time pe riods that target rodents may survive after the initial daily dose of a pesticide (based on availabl e toxicity studies) and in order to bracket the available data from residue studies submitted to the Agency and reported in open literature. Accumulation was determined based on daily food intake rates for the prey, conservatively assuming 100% of their diet consis ted of dry bait. It was assumed that the form of the bait would not influence intake. Based on the assumed weight of the primary consumers, the percent active

### ~ 70 ~ ingredient in the bait, and daily food intake, the concentration with in the prey animal at the end of a day’s feeding was determined. Accumulati on of rodenticide within the prey animal over time was calculated using an elimination rate constant based on the liver half-lives for each chemical (described above). This analysis is expected to produce a c onservative estimate of

exposure. In addition to the estimates of rodenticide re sidues in target rodent s representing prey of secondary consumers, empirically measured rode nticide concentrations in carcasses of rodents were used to represent potential exposure va lues for secondary cons umers. Although this method of representing concentrations of rodentic ides in prey of secondary consumers would be expected to be less conservative than the estimates described in the previous paragraph, both analyses produced similar findings. Dose-based exposure to secondary consumer s was assessed for mammals weighing 50g, 1000g, or 3000g, and birds weighing 100g, 1000g, or 5000g. These weights were selected based on the range of secondary consumers identified in rodenticide incidents in the Environmental Incident Information System (EIIS) database. The generic bird and mammal equations for food intake (Wildlife Exposure Factors Handbook ) were used to calculate the daily rodenticide intake for predator/scavenger birds and mammals consuming house mice and Norway rats exposed to

rodenticide bait for three or si x days. Dose-based RQs were calculated by dividing the dosebased exposure values from the es timated dose by the adjusted LD 50 values. In addition, dietary-based RQ s were calculated for secondary consumers. This was accomplished by dividing the estimated concentrati ons of rodenticides in target rodents by the

LC 50 values for birds or mammals.

### ~ 71 ~

b. Risk Estimation Based on acute exposure of predator and scaven ger birds to rodenticides accumulated in prey organisms, RQs for brodi facoum and difethialone exce ed the Agency’s acute LOC regardless of assessed weight class, prey orga nism consumed, or accumulation scenario. RQs calculated for warfarin, diphacinone, and chlorophacinone do not exceed the acute LOCs for birds, except for small predator and scavenge r birds consuming prey exposed to the higher concentration of warfarin (0.054%) bait for six days . The results for bromethalin fall in between the two anticoagulant groups, as bromethalin RQs exceed the acute LOC for all predator and scavenger birds consuming small prey animals (i.e., house mice), but do not exceed the acute LOC for large predator and scavenger mammals consuming large prey animals (i.e., Norway rats). When considering dietary- based exposures of predator and scavenger birds to rodenticides, brodifacoum and difethialone RQs exceed the acute LOC, while warfarin, chlorophacinone, diphacinone, and bromethalin RQs do not exceed the acute LOC. Secondary bird RQs are provided in Table 13. Although warfarin, chlorophacinone, and di phacinone RQs for secondary birds do not exceed the acute LOC, there is uncerta inty associated with th ese values. Available data suggest that some predatory birds may be substantially more sensitive to diphacinone exposure compared to the bobwhite quail and mallard ducks that are the source of th e majority of the avian toxicity data. If bobwhite quail and mallard ducks are significantly less sensitive to anticoagulant rodenticides than pr edatory birds, then the secondar y bird RQs calculated for these chemicals may not be conservative. For predator and scavenger mammals exposed to rodenticides accumulated in prey, RQs

for all assessed chemicals exceed the acute LO C, except for predator and scavenger mammals exposed to a three day accumulation of chlo rophacinone in large prey animals and small

### ~ 72 ~ predators/scavengers exposed to a six day accu mulation of chlorophacinone in large prey animals. Dietary-based RQs exceed the acute LOC for all of the assessed rodenticides for which

relevant data were available. Dietary toxicity data in mammals are not available for difethialone

or bromethalin so these chemical s were not included in this an alysis. Secondary exposure RQs for birds are provided in Table 13; secondary exposure RQs for mammals are provided in Table

14.~ 73 ~Table 13. RQs from the bird risk assessment: secondary exposure of predator/scavenger birds to residues in consumedrodents.Bodyweights (g)Second GenerationAnticoagulantsFirst Generation AnticoagulantsNon-Anti-CoagulantBrodifacoumDifethialoneWarfarin(0.025%)Warfarin(0.054%)Chloropha-cinoneDipha-cinoneBromethalin

Secondary exposure to carnivores and scavengersHouse mouseconsumption:3 dayaccumulation inprey RQ100 20* 17*0.14 0.30 0.04 0.014.1*1000 15* 5.4*0.04 0.09 0.01 <0.011.3*5000 13* 2.4*0.02 0.04 0.01 <0.010.58*Norway ratconsumption:3 dayaccumulation inprey RQ100 5.3* 4.5*0.04 0.08 0.01 <0.011.1*10004.1*1.4*0.010.02<0.01<0.010.345000 3.4* 0.64*0.01 0.01 <0.01 <0.01 0.15House mouseconsumption:6 dayaccumulation inprey RQ100 39* 33*0.270.58*0.08 0.01NA1000 31* 10*0.09 0.19 0.02 <0.01NA5000 16* 4.7*0.04 0.08 0.01 <0.01NANorway ratconsumption:6 dayaccumulation inprey RQ100 10* 8.7*0.07 0.15 0.02 <0.01NA1000 8.1* 2.8*0.02 0.05 0.01 <0.01NA5000 6.8* 1.2*0.01 0.02 <0.01 <0.01NAHouse mouseconsumption:dietary RQNA18* 21*0.19 0.41 0.32 0.02 0.20Norway ratconsumption:dietary RQNA4.7* 5.5*0.05 0.11 0.09 <0.01 0.05NA = not applicable ND = no data* RQ exceeds acute risk LOC = 0.50~ 74 ~Table 14. RQs from the mammal risk assessment: secondary exposure of predator/scavengermammals to residues inconsumed rodents.Second GenerationAnticoagulantsFirst Generation AnticoagulantsNon-Anti-CoagulantBodyweights (g)BrodifacoumDifethialoneWarfarin(0.025%)Warfarin(0.054%)Chloro-phacinoneDipha-cinoneBromethalin

Secondary exposure to carnivores and scavengersHouse mouseconsumption:3 dayaccumulation inprey RQ50 11 * 4.7* 8.8* 19* 0.84* 2.5* 4.3*1000 14* 5.9* 11* 24* 1.0* 3.1* 3.5*3000 15* 6.4* 12* 26* 1.1* 3.4* 5.8*Norway ratconsumption:3 dayaccumulation inprey RQ50 2.9* 1.3* 2.3* 5.0*0.220.66* 1.1*1000 3.7* 1.6* 2.9* 6.3*0.270.82* 1.4*3000 4.0* 1.7* 3.1* 6.8*0.300.89* 1.5*House mouseconsumption:6 dayaccumulation inprey RQ50 22* 9.2* 17* 37* 1.6* 4.2* NA1000 27* 11* 22* 47* 2.0* 5.2* NA3000 30* 12* 23* 50* 2.2* 5.6* NANorway ratconsumption:6 dayaccumulation inprey RQ50 5.9* 2.4* 4.6* 9.9* 0.43 1.1* NA1000 7.3* 3.0* 5.7* 12* 0.53* 1.4* NA3000 7.9* 3.3* 6.2* 13* 0.58* 1.5* NAHouse mouseconsumption:dietary RQNA45*ND27* 58* 20* 10* NDNorway ratconsumption:dietary RQNA11*ND7.0* 15.23* 5.4* 2.7* NDNA = not applicable ND = no data * RQ exceeds acute risk LOC = 0.50

### ~ 75 ~

4. Whole Carcass Residue Analysis

a. Methodology As discussed above, EPA also assessed sec ondary risks by analyzi ng residues in test

animals that had consumed contaminated carca sses. This analysis differs from the carcass concentration-based risk assessment described pr eviously in that it makes use of measured residues in intoxicated target organisms as a basis for dietary exposur e in scavengers and predators. Using actual animal concentrations el iminates some uncertainty associated with bait feeding, absorption, and elimination rates used in the previous assessment. However, alone, this method is limited by the types and magnitude of r odenticide exposure in th e prey base (i.e., the animals intoxicated at the primary exposure leve l). A concordance of risk conclusions made using this method with conclusions based on the previous method allows for more confidence in the risk conclusions overall; howev er, if the empirically-based RQs calculated in this section do not exceed the LOC, risk cannot necessarily be pr ecluded, especially if th e previously estimated RQs do exceed the LOC. In field and laboratory studies, rodenticide whole-carcass residues were determined in mammals after exposure to bait. Data are avai lable for a variety of small and medium sized mammalian granivores and omnivores exposed to brodifacoum, difethialone, warfarin, chlorophacinone and diphacinone. No such residue data were identified for bromethalin. These

measured residue concentrations were also us ed as the exposure component of the RQ for predators and scavengers in the same manner as the calculated residue values previously

described.

### ~ 76 ~

b. Risk Estimation The acute LOC was exceeded for secondary exposure risk to birds for brodifacoum and difethialone; however, RQs for secondary exposure risk to birds exposed to warfarin did not exceed the acute LOC. RQs for secondary exposure risk to birds exposed to chlorophacinone or diphacinone on an acute basis did not exceeded the acute LOC. Carnivore/scavenger mammalian RQs for brodifacoum and difethialone exceeded the acute LOC. For warfarin, chlorophacinone, and diphacinone, RQs did not exceed the acute LOC, as shown in Table 15.

Table 15. Secondary Acute RQs based on a Single-dose of Rodenticide through Consumption of Contaminated Carcasses Predator Birds Mammals Predator Weight Class 100 g 1000 g 5000 g 50 g 1000 g 3000 g

Brodifacoum 6.4* 5.0* 4.2* 3.6* 4.5* 4.8* Difethialone 4.6* 1.5* 0.66* 1.4* 1.8* 1.9* Warfarin < 0.01 < 0.01 < 0.01 0.26 0.32 0.34 Chlorophacinone < 0.01 < 0.01 < 0.01 0.07 0.08 0.08 Diphacinone < 0.01 < 0.01 < 0.01 0.19 0.23 0.25 Bolded (*) RQs exceed acute risk LOC (0.5).

Avian and mammalian RQs based on five-day di etary studies are provided in Table 16. Carnivore and scavenger bird RQ s for brodifacoum and difethial one exceeded acute risk LOCs. Warfarin RQs for carnivore and scavenger bird s did not exceed any LOCs. RQs for birds exposed to chlorophacinone and diphacinone in th eir diet do not exceed acute risk LOCs. For carnivore and scavenger mammals , RQs for brodifacoum, warfarin and chlorophacinone exceed

the acute risk LOC. There are no availabl e mammalian dietary data for difethialone, bromethalin, or diphacinone.

### ~ 77 ~

Table 16. Secondary Dietary RQs based on a 5-day Exposure of Rodenticide through Consumption of Contaminated Carcasses Birds Mammals Brodifacoum 5.3* 13* Difethialone 5.5* ND Warfarin < 0.01 0.67* Chlorophacinone 0.02 1.4* Diphacinone < 0.01 ND ND = no data Bolded (*) RQs exceed ac ute risk LOC (0.5).

5. Secondary Feeding Studies Secondary feeding studies address a number of uncertainties associated with the quantitative dose-based risk estimation methods us ing estimated or empirically based prey-base

concentrations estimates of rodenticide. Th e feeding studies empirically account for primary organism feeding, absorption and elimination un certainties surrounding the estimated dose-based assessment. They also account for uncertainties associated with biol ogical availability of rodenticide from consumed prey and assumpti ons of predator/scavenger sensitivity to the rodenticide which are present in both of the dos e-based risk estimation methods. Concordance

between risk conclusions between all three methods constitutes enhanced confidence in the

overall risk conclusions made for predators and scavenging wildlife. Concerns for secondary risks with brodif acoum are supported by available data from secondary toxicity studies show ing mortality in 63% of predat or/scavenger birds and 42% of predator/scavenger mammals fed brodifacoum cont aminated target organisms. No secondary feeding data are available for difethialone. In the case of warfarin, mammalian sec ondary feeding studies involving mammal predators/scavengers show mixed results and fo r some species the differences extended to a

### ~ 78 ~ dose-dependent response. No mo rtalities were observed in ra ccoons and European ferrets (no dose dependency and bait concentrations equal to or higher than levels found in US registered products). Other studies showed mortalities in mink, least weas els and dogs, although the results often involved few test organisms. Avian second ary feeding studies of wa rfarin involved testing of four species. In three of the four species tested ther e was no observed mortality. Interestingly, the results from feeding tests do not completely parallel the results of the quantitative secondary risk assessment where risks were expected for small birds exposed to prey contaminated with higher concentrations of warfarin bait. For example no mortality was observed in the feeding studies with black-b illed magpies (~170 g bodyweight) while the risk assessment suggests a concern for a 100 gram bir d. Conversely, mortality results were mixed in larger birds of similar weights (death in barn owls but not in tawny owls both ~400-500 g body weight). These discrepancies s uggest that allometric relations hips for predicting effects of warfarin toxicity may incompletely explain th e factors contributing to species sensitivity variability. Bromethalin secondary feeding studies are limited to a single cas e. In that study involving domestic dogs fed intoxi cated rats there were no morta lities (n=4). The number of species tested is limited; therefore, there is in sufficient evidence from these data alone to make definitive conclusions regarding the accuracy of the secondary quantitative risk assessment

results. While these data are not sufficient to make definitive conclusi ons, they do indicate that bromethalin may not be retained in body tissu es in toxicologically significant amounts as discussed previously. No bird feeding studies were available for bromethalin. Chlorophacinone secondary toxicity results in clude studies with five mammal species. Mortality responses were variable and ranged fr om approximately 50 percent to 100 percent of

### ~ 79 ~ individuals tested. In one singl e species, European ferret, di fferent studies yielded highly variable results, ranging from zero to 100 percent mortality. It should be noted again that all

these studies involve a low number of test individuals and differences in perceived sensitivity may be as much a product of low number of i ndividuals as from real differences in toxic response across species. Avian feeding studies with chlorophacinone span 10 species with a wide range of bodyweights (170 to 4400 g). In no cases were mortalities observed. This finding is consistent with the secondary risk assessment. Diphacinone secondary feeding data span studies from seven mammal species. The effects range from 0 to 100 percen t mortality. Of particular not e is the study i nvolving actual secondary feeding with rats. This study is of note because (1) the secondary exposure risk assessment used a rat acute toxicity endpoint as a surrogate for predators and scavengers and (2) the assumed prey item concentrations in the ri sk assessment were 10 to 20 times higher than tested in the feeding study. The feeding study wi th rats yielded a 50 percent mortality response under conditions of similar toxicity and lower ex posure than modeled conditions showing risk. Looking back on the quantitative risk results, substituting the modeled diphacinone dietary

concentrations with the actual concentrations used in the feeding study would still trigger secondary acute risk concerns. These results are considered supportive of the secondary risk assessment with mammals. Avian feeding studies with diphacinone span five species of varying bodyweights. In three species th ere were no mortalities, consiste nt with the secondary risk assessment results. In the case of two owl species, mortalities were observed contrary to what the risk assessment results suggested. As discus sed earlier, the toxicity endpoint relied upon in the risk assessment may underestimate the sensitiv ity of raptoral species to this chemical.

### ~ 80 ~ 6. Estimation of number of prey animals equal to median lethal dose in secondary animals As evaluated in the secondary exposure ri sk assessment, residues were estimated and observed to reach levels in target organisms th at, when consumed by predators and scavengers

can result in death. When consid ering those risks among the assesse d rodenticides it is important to consider the likelihood of predators and s cavengers encountering e nough intoxicated target prey to reach potential lethal doses. Furthering the evalua tion of secondary exposure of

rodenticides are the resu lts of analyses of the number of i ndividual target organisms necessary for dietary consumption to achieve a lethal dos e in predators and scavengers. The fewer the number of intoxicated target organisms necessary to reach a lethal dose, the less efficiently and intently a predator or scavenger must locate and consume these organisms to reach lethal body burdens. The analysis considered different bodyweights of predator/scavengers consuming either rats or mice which have ingested ba it for a single day or up to six days. Again, compounds that can present a lethal dose to predat ors and scavengers after consumption of target organisms with only a single day of exposure ar e likely to represent greater opportunities for lethal secondary exposure events than those which require multiple days of target organism

exposure. Analyses were conducted to determine the number of rodenticide-intoxicated target organism a predator/scavenger mammal would n eed to consume in order to trigger lethal incidents (Table 17). Based on these analyses , every size predator/scavenger mammal exposed to brodifacoum through consumption of rats woul d only need to consume a fraction of a single target organism to reach lethal endpoint exposur es, even if the rat fed on brodifacoum bait for just one day. Comparing brodifacoum results for predator/scavenger mammals to other assessed

### ~ 81 ~

rodenticides does not reveal a marked differen ce among the chemicals. Owing to their smaller size, consumption of brodifacoum intoxicated mi ce must be slightly more intensive for the predator/scavengers to r each lethal endpoint exposure (<1 to 5 organisms) as compared to rats. These results are not atypical of the results fo r difethialone, warfarin and bromethalin assessed rodenticides. However, the amount of brodifaco um that must be consumed to reach lethal exposure is substantially lower than diphacinone and chlorophacinone.

Table 17. Secondary Exposure to Predator and Scavenger Mammals: Number of animals consumed to reach the LD 50 Body Weights (g) Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chlorophacinone Diphacinone Brometh -alin 1-Day Accumulation in Prey

House Mice 100 <1 <1 <1 <1 3 <1 <1 1000 2 5 3 1 27 8 5 5000 5 11 6 3 60 18 11

Norway

Rats 100 <1 <1 <1 <1 <1 <1 <1 1000 <1 <1 <1 <1 5 1 <1 5000 <1 2 1 <1 11 3 2 6-Day Accumulation in Prey*

House Mice 50 <1 <1 <1 <1 <1 <1 <1 1000 <1 <1 <1 <1 5 2 2 3000 <1 2 <1 <1 11 4 4

Norway

Rats 50 <1 <1 <1 <1 <1 <1 <1 1000 <1 <1 <1 <1 <1 <1 <1 3000 <1 <1 <1 <1 2 <1 <1 * For bromethalin, numbe rs are based on 3-day accumulation in prey

Similar analyses were conducted to determine the target organism numbers necessary to trigger lethal incidents in scav enger/predator birds (Table 18 ). Brodifacoum results show consumption of only a fraction of an intoxicated rat, regardless of rat exposure duration, is needed to reach lethal endpoint exposures in all bird sizes modeled. These results with

brodifacoum are similar to results with difeth ialone, but are greater for the other assessed

### ~ 82 ~ rodenticides, particularly for warfarin. Because house mice are much smaller than Norway rats, avian predators or scavengers ge nerally must ingest more house mice than Norway rats in order

to attain a lethal dos e, but ingestion of only <1 to 5 house mice intoxicated by brodifacoum would be sufficient to cause lethal secondary poi soning. With difethialone, consuming less than one intoxicated house mouse would be expected to kill a 100-g avian predat or or scavenger, but

the numbers of mice needed to kill birds at th e 1000-g and 5000-g sizes are somewhat greater with difethialone than brodifacoum. Depending on the size of the predator or scavenger bird, slightly to many times more br omethalin-intoxicated mice would be needed to cause lethal secondary poisoning than would be the case with either of the SGARs brodifacoum or difethialone. However, similar analyses conducted with warfarin, chlorophacinone, and diphacinone reveal that avian predators and s cavengers must consume many more intoxicated mice to reach lethal exposure endpoints than is the case with brodifacoum or difethialone. When taken together, these analyses suggests that brod ifacoum has a substantia lly greater opportunity than these other active ingredients to result in lethal incidents following exposure of a predator/scavenger bird to int oxicated target organisms.

### ~ 83 ~

Table 18. Secondary Exposure to Predator and Scavenger Birds: Number of animals consumed to reach the LD 50 Body weights (g) Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chlorophacinone Diphacinone Brometh -alin 1-Day Accumulation in Prey

House Mice 100 <1 <1 38 18 130 821 1 1000 2 4 539 249 1836 11602 16 5000 5 27 3429 1587 11690 73852 104

Norway

Rats 100 <1 <1 7 3 23 147 <1 1000 <1 <1 97 45 329 2079 3 5000 <1 5 614 284 2094 13232 17 6-Day Accumulation in Prey*

House Mice 50 <1 <1 7 3 23 183 <1 1000 <1 <1 92 43 321 2590 6 3000 <1 5 586 271 2045 16483 39

Norway

Rats 50 <1 <1 1 <1 4 33 <1 1000 <1 <1 17 8 58 464 1 3000 <1 <1 105 49 366 2953 7 * For bromethalin, numbe rs are based on 3-day accumulation in prey

7. Probabilistic Analysis EPA conducted a probabilistic analysis that a ddressed the two comparative variables of whole body half life and toxicity to inform the level of confidence and explore uncertainty in the likelihood that a randomly selected predator or sc avenger birds may achieve a lethal rodenticide dose. This was accomplished using a Monte Carl o simulation with a distribution of possible outcomes that were analyzed to allow for more thorough unders tanding of the uncertainties

associated with the available data. The modeli ng exercise was performed by varying selected parameters for liver or blood-plasma half-life and the LD50 or LC50. The metric for comparing chemicals was based on probability density functions for percentage of species with RQs above the acute LOC value of 0.5. This represents the likelihood that a bird feeding on prey containing

rodenticide could receive a dose of that roden ticide that may pose a risk to the secondary

### ~ 84 ~ consumer. Although the results presented below focus on bird s at risk through secondary exposure, an equivalent analysis was c onducted for predator/scavenger mammals. The probabilistic assessment for mammals at risk through secondary exposur e sheds no new light on the issues in the proposed cancella tions, as it simply confirms, as did the Agency’s deterministic assessment, that rodenticides designed to target mammalian speci es will be toxic to mammals regardless of whether they are primary or second ary consumers. However, the enhanced toxicity and extended residence time in non-target anim als suggests that bioaccumulation potential and resulting secondary poisoning potential of brodif acoum and difethialone are greater relative to the other assessed rodenticides. The probabilistic analysis conducted by EPA is described in more detail in “Probabilistic Analysis A ssociated with Avian Risks from Exposure to Brodifacoum, Difethialone, Chlorophacinone, Di phacinone, Warfarin, or Bromethalin” (Riley 2013). Ten thousand RQs were calculated for 100- g, 1000-g, and 5000-g birds consuming mice or rats that are primary consumers of rode nticides based on 10,000 randomly sampled LD50 and

half-life values. For each rodenticid e, the values in Table 19 provide the percentage of calculated RQs that were above the LOC for birds when t oxicity and exposure parameters were randomly sampled. These percentages allow for the comp arison of risks among chemicals where larger percentage values suggest a highe r likelihood that a randomly select ed bird may achieve a lethal dose under the assumptions of this analysis. Base d on this analysis, birds have a high likelihood of receiving a dose sufficient to pose a risk of mortality when consuming prey species

intoxicated with brodifacoum or difethialone, even after 1 da y of accumulation in the prey. However, the likelihood of risk from exposure to di fethialone is less than the likelihood of risk from exposure to brodifacoum, especially for larg e birds consuming intoxicated prey animals.

### ~ 85 ~

Relative to the risks of brodifacoum and dife thialone, there is a lower likelihood for birds consuming prey contaminated with warfarin to receive a dose sufficient to pose a risk of mortality. Chlorophacinone and diphacinone have a low likelihood of posing a risk of mortality,

relative to the other assessed rode nticides. However, it should be noted that sensitive 100-g birds (e.g., American kestrels) feeding on small mammal s exposed to diphacinone bait for an extended period of time may be at risk. For bromethalin, there is a high likelihood of risk exceeding concern levels for small birds consuming small mammals exposed to bromethalin bait for 1 day. However, small birds consuming large prey organisms and larger bird s consuming either small or large prey items have a low likelihood of risk exceeding concer n levels from exposure to bromethalin. In addition, it is important to note that several factor s suggest that bromethali n poses a lower risk to birds from secondary exposure, relative to brodi facoum and difethialone. These factors include: 1) target animals tend to stop feed ing after consumption of toxic dos es of bromethalin; therefore, they are less likely to carry residue levels in exces s of toxic doses; and 2) available data suggests that bromethalin is eliminated quickly from ta rget and non-target animal s relative to the other chemicals; therefore, brometha lin levels are not likely to increase after long-term low-dose exposure, like chemicals with longer half-lives.

### ~ 86 ~

Table 19. Percentage of Secondary Avian Acute Do se-Based RQs that are G reater than the LOC (0.5)

Prey Prey Exposure Type Brodifacoum Difethialone Warfarin (0.025%) Chlorophacinone Diphacinone Bromethalin 100-g Birds

house mice 1 day 99% 60% 5% ~0% ~0% 95% 6 days 100% 80% 50% ~0% ~0% NA 14 days 100% 85% 75% ~0% 1% NA

Norway

rats 1 day 70% 40% ~0% ~0% ~0% 10% 6 days 100% 65% 10% ~0% ~0% NA 14 days 100% 75% 30% ~0% ~0% NA 1000-g Birds

house mice 1 day 95% 40% ~0% ~0% ~0% 10% 6 days 100% 65% 15% ~0% ~0% NA 14 days 100% 75% 40% ~0% ~0% NA

Norway

rats 1 day 60% 25% ~0% ~0% ~0% ~0% 6 days 100% 50% ~0% ~0% ~0% NA 14 days 100% 60% 40% ~0% ~0% NA 5000-g Birds

house mice 1 day 95% 30% ~0% ~0% ~0% ~0% 6 days 100% 55% 5% ~0% ~0% NA 14 days 100% 65% 15% ~0% ~0% NA

Norway

rats 1 day 50% 15% ~0% ~0% ~0% ~0% 6 days 99% 35% ~0% ~0% ~0% NA 14 days 100% 50% ~0% ~0% ~0% NA NA- not applicable. Animals consuming bromethalin are not ex pected to continue feeding on bromethalin bait for six or fourteen days, therefore these numbers were not calculated.

For each rodenticide, the values in Table 20 provide the percentage of calculated dietarybased RQs that exceeded the LOC for birds wh en toxicity and exposure parameters were randomly sampled. Based on this analysis, bird s have a high likelihood of receiving a dose sufficient to pose a risk of mortality when cons uming prey species intoxicated with brodifacoum

### ~ 87 ~ and difethialone on a dietary basis. For warfar in and chlorophacinone th ere is little chance of predator/scavenger birds receiving a dose that may pose a risk of mortality, except under high accumulation scenarios. Again, birds feeding on diphacinone and bromethalin contaminated animals have a lower likelihood of exceeding concer n levels relative to th e other rodenticides

evaluated.

Table 20. Percentage of Acute Dietary-Based RQ s for Birds that are G reater than the LOC.

Prey Exposure Type Brodifacoum Difethialone Warfarin Chlorophacinone Diphacinone Bromethalin

House Mouse as prey 1 day 100% 100% ~0% ~0% ~0% ~0% 6 days 100% 100% 1% 15% ~0% NA 14 days 100% 100% 15% 60% ~0% NA Norway Rat as prey 1 day 95% 50% ~0% 0% ~0% ~0% 6 days 100% 100% ~0% 0% ~0% NA 14 days 100% 100% ~0% 5% ~0% NA NA- not applicable. Animals cons uming bromethalin are not expected to continue feeding on bromet halin bait for six or fourteen days.

8. Summary of secondary exposure risks The assessment of secondary exposure risks fo r wildlife involved a series of assessment methodologies that encompassed both estimated accumu lation of rodenticides in a prey base as well as empirical measurements of rodenticide re sidues in prey. This assessment concluded that all of the assessed rodenticides pose a risk of mortality to predator and scavenger mammals via secondary exposure. In addition, so me of the rodenticides pose a risk of mortality to predator and scavenger birds via secondary exposure. Based on the analysis of the number of prey

### ~ 88 ~ organisms that would have to be consumed in or der for predators and scav engers to receive an

LD 50 dose and the probabilistic analysis, the following conclusions can be made for risk to birds:

• Brodifacoum and difethialone po se greater secondary exposure risk to birds relative to the other chemicals assessed rega rdless of exposure scenario.

• Bromethalin may pose secondary exposure risk to certain sensitive species ( i.e., small birds consuming small prey animals); however, potential for secondary risk is somewhat

limited due to the lower likelihood of continuous feeding of prey af ter reaching a lethal threshold and rapid mortality observed in primary feeding studies with bromethalin. Risks to small birds consuming large prey an imals and risks to medium and large birds consuming small or large prey animals are s ubstantially lower than for brodifacoum and

difethialone.

• Warfarin may pose risk to certain sensitiv e species, especially under high accumulation scenarios; however, the likelihood of seconda ry exposure to exceed the LOC for warfarin is substantially lower than for brodifacoum and difethialone.

• Diphacinone does not have a high likelihood of triggering secondary risk concerns regardless of accumulation scenario assessed. However, results of the probabilistic analysis indicate that there is a possibility that the most sensitive smaller secondary avian consumers modeled may be at risk fr om diphacinone poisoning under the highest accumulation scenario. Secondary exposure risk s for diphacinone are substantially lower

than for brodifacoum and difethialone.

• For chlorophacinone, results for the acute dos e-based exposure scenarios demonstrate a low likelihood of secondary exposure concer ns. However, results of the probabilistic assessment conducted for dietary-based exposur e indicate that chlorophacinone may have

### ~ 89 ~ a greater likelihood of posi ng risk to predator/scave nger birds under the higher accumulation scenarios than the one-day accu mulation scenario. While these results represent a departure from the other analys es, the likelihood of s econdary exposure risk for chlorophacinone is still subs tantially lower than for brodifacoum and difethialone.

9. Incident Findings Related to Pr imary & Secondary Risk Analyses The quantitative risk assessment does not eval uate the actual potential for wildlife to come into contact with treated bait; it simply evaluates the consequences of exposure. To determine if any documented adverse effects have been reported, indicating complete exposure pathways, EPA looks to available incident and exposure information from a variety of sources, including state and local governme nts and pesticide registrants. The majority of available reported incidents for the rodenticides assessed are included in EPA’s Environmental Incident Information System (Version 2.1) EIIS. EPA believes these data offer strong support for the

conclusion that residential use of rodenticides in urban/suburban a nd rural areas provide complete exposure pathways for a variety of wildlife, and that both primary and secondary exposures can cause mortality in non-target w ildlife. Table 21 presents the total number of reported incidents associated with each of the rodenticides co nsidered in EPA’s assessment. Where possible, EPA distinguished between inci dents resulting from primary and secondary exposures. Additional details on these incidents are tabulated in Compilation of Rodenticide Wildlife Mortality Incidents Re ported Between 1971-2012 (EPA 2013).

### ~ 90 ~

Table 21. Total Number of Wildlife Incide nts by Rodenticide Ac tive Ingredient and Exposure Type, Occurring between 1971 and 2012. Rodenticide Active Ingredient Exposure Type Total Primary Secondary Unknown

Brodifacoum 72 202 39 313 Birds

4 Mammals 68 Birds 176 Mammals 26 Birds 21 Mammals 18 Birds 201 Mammals 112

Difethialone 1 5 0 7 Birds

0 Mammals 1 Birds 5 Mammals 1 Birds 0 Mammals 0 Birds 5 Mammals 2Chlorophacinone 6 5 3 14 Birds

3 Mammals 3 Birds 3 Mammals 2 Birds 1 Mammals 2 Birds 7 Mammals 7 Diphacinone 11 9 1 21 Birds

1 Mammals 10 Birds 5 Mammals 4 Birds 0 Mammals 1 Birds 6 Mammals 15

Warfarin 6 5 0 11 Birds

1 Mammals 5 Birds 5 Mammals 0 Birds 0 Mammals 0 Birds 6 Mammals 5

Bromethalin 2 0 0 2 Birds

0 Mammals 2 Birds 0 Mammals 0 Birds 0 Mammals 0 Birds 0 Mammals 2

Totals 98 227 43 368 Birds

9 Mammals 89 Birds 194 Mammals 33 Birds 22 Mammals 21 Birds 225 Mammals 143 * Incident counts exclude incidents with certainty levels of “unrelated” and “unlikely,” incidents known to be associated with intentional misuse, and incide nts associated with other active ingredients.

In evaluating EPA’s incident database fo r rodenticides, it is important to understand that reported incidents likely re present only a fraction of the incidents that have occurred. Because of the delay between consumption of a lethal dose and death associated with the anticoagulant rodenticides considered in this analysis (all assessed rodenticides except bromethalin), the deaths of anim als killed by these rodenticides typically occur at a distance, both spatially and temporally, from the site wh ere the rodenticide was used. As a result, the cause of death generally is not obvious to persons finding animals killed by these rodenticides. Only when the mortality is reported to an author ity, typically a state fish and wildlife office, and that agency conducts an investigat ion into the cause of death is an incident likely to be linked to

### ~ 91 ~ rodenticide exposure. The investigating state ag ency may then take tissue samples from the animal, normally from the liver, and have labora tory analyses performed to screen for the presence of various rodenticides, as well as va rious other pesticides. Only when the residue analysis finds one or more rodent icides in the tissue of the dead animal does the incident become diagnosed as a suspected or confirmed rodent icide incident. Because the linkage between wildlife mortalities and exposur e to the rodenticides subject to the NOIC depends on thorough investigations, includ ing residue analysis of ti ssue samples, incident re porting rates vary greatly from state to state and likely depend largely on whether the state has the personnel and resources to conduct and report inve stigations. Only two states, New York and California, have had programs that have systematically analyzed and reported wildlife mortality incidents, and thus are responsible for the majority of known rodentic ide incidents. Many states have never reported any wildlife mortality incidents related to rodenticides. Given th ese considerations, and the fact that most dead or dying animals are never seen by humans, EPA believes the vast majority of wildlife incidents from exposure to rodenticides go unreported. The general character of the reported incidents for each chemical are briefly discussed below. Notwithstanding the likely extent of underreporting of wildlif e incidents, the available data support the quantitative risk assessment’s conclusion that both pr imary and secondary exposure to brodifacoum poses leth al risk to a variety of sizes of mammals and birds. Mortality incidents likely to have resulted from prim ary exposure to brodifacoum include non-target mammalian wildlife ranging in size from chipmunks to white-tailed deer. This range is consistent with the size classes pred icted to be at risk from brodifacoum in EPA’s analysis above. For birds, mortality incidents likely to have resulted fr om primary exposure to brodifacoum involved species ranging in size from robins to geese, ag ain consistent with the risk model predictions.

### ~ 92 ~ Incidents representing likely secondary exposure of mammals to brodifacoum range from kit foxes to mountain lions, consistent with the mode led size classes predicted to be at risk from brodifacoum in EPA’s analysis above. Between 1971 and 2012, there were 176 total incidents of bird mortality attributed to s econdary exposure to brodifacoum. For birds, incidents likely to have resulted from secondary exposur e involve a variety of raptors, again consistent with the risk model predictions for larger birds. These incidents occurred in urban/suburb an and rural habitats. In summary, incident data indi cate that both primary and seco ndary exposures to brodifacoum are likely to cause mortaliti es among non-target wildlife in rural, suburban, and urban

environments.

The incident data set for difethialone is much more limited than that for brodifacoum. Analysis of the toxicity and re tention time of difethialone indi cates that it is toxicologically similar to brodifacoum, suggesting that the small nu mber of reported incident s for this ingredient could be due to the relatively low use of difethial one or to other factors not related to the intrinsic risk of the chemical. Nevertheless, one lethal in cident apparently resulting from direct exposure

to difethialone treated bait has been reported, involving Key deer in a suburban environment. Lethal exposures such as this incident are c onsistent with the conclusions of the mammalian primary exposure risk assessment. Although th ere are no reported incidents involving bird species and primary exposure to difethialone, th e absence of reported incidents neither supports nor refutes the findings of the av ian primary exposure risk assessmen t. Lethal incidents involving predatory birds and mammals and difethialone have been reported, consistent with the

conclusions of the mammalian and avian secondar y exposure risk assessments. All the reported

difethialone incidents are associ ated with urban/suburban areas.

### ~ 93 ~ Warfarin incidents involving non-target wildlif e generally parallel the findings of the quantitative risk assessment for primary exposure to this chemical in that primary exposure incidents have been reported, confirming that e xposure pathways are complete. No incidents of secondary poisonings to non-target mammals have been reported for warfarin; however, reported incidents of birds exposed to warfarin include a variety of raptoral sp ecies presumed to be secondary consumers. These secondary exposure in cidents are consistent with the quantitative secondary risk assessment and ar e in partial agreemen t with the available secondary feeding toxicity studies (warfarin seconda ry feeding studies showed mixed results as described in the Risk Estimation Section). Incident data indicate that secondary exposure to warfarin can cause mortalities among non-target wildlife in ru ral, suburban and urban environments. The incident data set for primary exposure of animals to bromethalin is limited to two reported mortality incidents of small mammals. This limited information is consistent with a quantitative risk assessment that indicates a risk to small mammals exposed to treated bait, yet provides little support for the risk assessment predictions for larger mammals. There are no reported incidents involving bird species that appear to have re sulted from primary exposure to bromethalin-treated bait, and no incidents involving either mamma ls or bird species that appear to have resulted from secondary exposure. In cidents involving this chemical may be under reported because, as discussed in the incident section of the ecological risk assessment, bromethalin is not commonly assayed for in inves tigations of wildlife mortality incidents. Thus, the lack of reported secondary exposure incidents involving brom ethalin can neither support nor

refute conclusions of the mammalian a nd avian secondary risk assessments. There are few reported incidents where there is high certainty that mammal mortalities resulted from primary exposure to chlorophacin one bait. Reports of mo rtalities in squirrels

### ~ 94 ~ (Central Park, New York) are in agreement with the primary exposure risk assessment predictions for small mammals. No larger mammal incidents attributable to primary exposure to this chemical have been reported. An incident report where a bird (California quail in an orchard) is likely to have received a lethal dose of chlorophacinone th rough primary exposure suggests the possibility that chlorophacinone pr esents greater primary exposure ri sk to birds than indicated in the primary exposure risk assessment. Chloropha cinone incidents of hi gh certainty involving likely secondary exposures of mammals and bird s are also scarce, but include reports of mortalities in wild felids (bobcats) and raptor s (red-tailed hawk). The mammal incidents are consistent with the secondary exposure risk asse ssment findings. The bird incident, however, is inconsistent with the secondary exposure risk assessment, which did not predict secondary exposure risk to birds. It is possible that raptors may be more sensitive to both chlorophacinone and diphacinone than the test species employed in the risk assessment. If the chlorophacinone secondary exposure risk assessment were adjusted for this possible incr eased sensitivity in raptors by assuming a 20-fold in crease in sensitivity, as has been observed for diphacinone (Rattner et al. , 2011), then the conclusions of the dietary subacute portions of the secondary exposure risk assessment would then be consiste nt with reported incidents. However, the incident report would still be in consistent with the single oral dos e risk assessment. On balance, incidents indicate that chlorophacinone may cause secondary lethalities to birds, but because of

attendant uncertainties inherent in incident data interpretation, th ey do not necessarily refute the conclusion of the risk assessments that chloropha cinone presents negligible risk to birds, and they are consistent with the conclusion th at the secondary risks of chlorophacinone are considerably less than those of brodifacoum and difethialone.

### ~ 95 ~ The diphacinone incident data set for mammals with primary exposure is similar to that for chlorophacinone in that four incidents invo lved poisoning of squirrels in urban/suburban settings, but is different in th at incidents have also been re ported of large mammals being poisoned (two incidents of mortality of white-tailed deer in New York). The reported incidents are consistent with the prediction of the risk a ssessment of risk to small mammals from primary exposure. Diphacinone incidents of high certa inty involving mammals and birds of likely secondary exposure are limited but include reports of mortalities in wild canids, mustilids and felids (fox, coyote, raccoon, and mo untain lion) and raptors (snow y and barred owls, red-tailed hawk). The mammal incidents are consistent with the secondary e xposure risk assessment findings. The bird incidents are inconsistent with the modeling portions of secondary exposure risk assessment, which did not pred ict significant secondary risk to birds, but are consistent with available feeding studies, especially for owls. If the diphacinone secondary exposure risk assessment were adjusted for the possible increased sensitivity in raptor s, the secondary risk conclusions would still yield risk quotients below concern levels. On balance, incidents indicate that diphacinone may cause secondary lethalities to birds, but becau se of attendant uncertainties inherent in incident data interp retation, those incidents do not nece ssarily refute th e conclusion of the risk assessments that diphacinone presents neg ligible risk to birds, and they are consistent

with the conclusion that the sec ondary risks of diphacinone are c onsiderably less than those of

brodifacoum and difethialone.

a. Implications for Risk Mitigation The proposed cancellations would limit the avai lability of brodifacoum and difethialone in ways expected to limit their use in urban and suburban areas to commercial and professional users. This change in the availability and us e of brodifacoum and difethialone will reduce the

### ~ 96 ~ potential for wildlife to encounter these rodentic ides, because residential consumers have been responsible for a large proportion of the use of these chemicals. As the quantitative risk assessment concludes, these two rodenticides present greater risk to non-target species – particularly to birds – than ot her rodenticides registered fo r general consumer use against commensal rodents. The incident reports support the quantitative risk assessment finding that bromethalin, chlorophacinone, diphacinone and warf arin present considerably less risk of primary and secondary poisoning than brodifacoum and difethialone. While the use of tamper resistant bait stations could effectively mitigat e primary exposure to birds and larger mammals for all rodenticides, secondary poisoning would remain a concern for wildlife that consumes commensal mice and rats or other primary consum ers that enter and consume bait from stations

sized to accommodate commensal rats and/or house mice. In this regard, brodifacoum and difethialone present a greater risk of secondary poisoning when compared to other commensal rodenticides. Limiting sales of brodifacoum and dife thialone in the consumer market is expected

to cause most consumers to turn to one of the ot her available rodenticides or to use alternative mechanical controls, thereby reducing overall us e of -- and wildlife exposure to -- brodifacoum and difethialone. While the replacement compounds may still present some risk of secondary poisoning, EPA believes that this change will grea tly reduce the risk of adverse effects to nontarget wildlife. The NOIC also proposes the cancellation of cer tain consumer commensal rodent control products because they are not sold in or with ba it stations reasonably anti cipated not to release rodenticide bait. Although labels of these produ cts currently require c onsumers to use tamper resistant bait stations if bait is placed wher e it would otherwise be accessible to non-target wildlife, it is readily apparent that such label requirements have been unsuccessful in preventing

### ~ 97 ~ harmful exposures to non-target animals. EP A expects that eliminating from the general consumer market all commensal rodenticides except for those sold in or with bait stations will reduce rodenticide exposures among birds and am ong non-target mammals larger than target

rodents. As bait stations ar e optimized for the body sizes of either house mice or Norway and roof rats, larger mammals are physically limited by the station portal size preventing them from reaching the bait within, and most birds will not en ter a small, confined space. Bait stations also reduce rodenticide risks to predat ors: Reducing the number and types of prey species likely to be

contaminated with rodenticides should reduce the proportion of rode nticide-contaminated prey in a predator’s diet and reduce th e total quantity of a rodenticid e available to the predator. Moreover, limiting the availability of bait form s such as pellets, granules, grain and meal is likely to reduce the spatial extent of bait disp ersal across the landscape. Bait in forms such as pellets, granules, grain and meal is easily scattered, offering non-target wildlife increased opportunities for rodenticide exposure when compar ed with a more focally placed bait station. Limiting access to rodenticide baits in the form of pellets, granules, grain and meal is likely to reduce bait scattering, resulting in a reduction of encounters of wild life directly with rodenticides. This may be especi ally significant for chemicals such as brodifacoum, difethialone,

bromethalin and warfarin where only a few feeding episodes are su fficient to cause mortality.

Measures that make rodenticid e baits less available to non-target wildlife that are primary consumers are also likely to re sult in a reducti on of predatory and scav enger wildlife encounters with intoxicated prey species, because the number and range of affected prey species should be

reduced if less scattered bait is available. Although the proposed cancellations will not lim it use of bait forms such as pellets, granules, grain and meal by professional, commerc ial and agricultural users, it is EPA’s belief

### ~ 98 ~ that such users (including persons who routinely apply pesticides as a minor part of their job, as well as full-time pesticide applicators) are more likely to choose a method of pest control appropriate for the specific circumstances, more likely to have reusable tamper-resistant bait stations, more likely to appreciate the consequences and liability of pesticide misuse, and in most cases acutely sensitive to the economic conse quences of overuse. Fo r these reasons, EPA believes that pesticides generally pose less risk when applied by profe ssional, commercial and agricultural users than wh en applied by the general public. In the case of rodenticides containing brodifacoum and difethialone (ac tive ingredients that ar e not registered for field uses, except for certain restricted use products registered to USDA/APHIS for very li mited island conservation uses by or under the supervision of agencies of the U.S. government), EPA believes that this difference is significant enough to warrant taking steps to lim it access to these products to professional, commercial a nd agricultural users.

b. Endangered Species Considerations for Rodenticide Active Ingredients The Agency has concluded that the roden ticides subject to the NOIC pose risks of concern to non-target wi ldlife. By extension, these chemicals would also pose risks of direct effects to federally listed threatened and enda ngered species and designa ted critical habitat. Further, potential indirect effect s to any species dependent upon a species that experiences effects

from use of rodenticide activ e ingredients cannot be preclu ded based on the deterministic ecological risk assessment. These findings are based solely on EPA’s deterministic assessment and, because they do not take into account such f actors as whether the species would be expected to be exposed to rodenticide active ingredients, do not in themselves constitute “may affect” findings under the Endangered Species Act. EPA pr eviously consulted with the Fish and Wildlife

### ~ 99 ~ Service (the Service) under the Endangered Spec ies Act on certain uses of rodenticides, and in 1993, as part of that consultation, the Service issued a biological opinion finding that a number of rodenticides, including several addressed and analyzed in this action, will likely jeopardize a number of animal species. (A more recent biol ogical opinion and consultations regarding the prairie dog bait products Rozol and Kaput-D are not applicable here, as those products are not registered for use against commensal rodents.) EPA has not in large measure implemented recommended measures provided in that 1993 op inion, but in March 2005, initiated informal consultation. That informal consultation for produc ts containing one of the nine rodenticide active ingredients registered for comme nsal rodents at that time wa s for the purpose of obtaining technical assistance in identifying the full suite of listed species that may be affected by the full range of uses of these products, to determine whether further, formal consultation would be necessary and if so, to explore possible mitigation relative to specific species that may be affected. Several reported incide nts have involved Federally list ed threatened and endangered species, for example the San Joaquin kit fox and northern spotted owl. In addition, reported incidents include the bald eagle, which is pr otected under the Bald and Golden Eagle Act. Although the action EPA is taking in the NOIC will likely reduce risks to a number of protected species, this action is not intended to resolve th e need for mitigation to address federally listed and other protected species. If EPA determines, as a result of its own further assessment, or through consultation with the Service, that additi onal restrictions on use are necessary to address adverse impacts to listed and ot her protected species or designat ed critical habitat, EPA may initiate other appropriate ac tion to address such impacts.

### ~ 100 ~

IV. Benefits FIFRA requires that, when determining wh ether a non-dietary pesticide use causes unreasonable adverse effects, EPA must ta ke into account the economic, social and environmental costs and benefits of the pesticid e use. This sense of the term “benefit” is

therefore different from its use in a benefit – cost analysis. In the FIFRA c ontext, the benefits of the rodenticide products that EPA proposes to cancel are equivalent to the impacts of

cancellation on their users. The im pacts of cancelling certain products are also representative of the foregone benefits of denying registration to products of si milar nature. EPA examined several potential impacts of the proposed cancellation of the r odenticide products identified in the NOIC, including:

• Whether residential consumers can achieve similar levels of control over rodent

infestations.

• Whether it may take longer for residential cons umers to achieve cont rol of their rodent problems.

• Whether the cost of rodent control, in cluding non-monetary costs, may increase.

• Whether the proposed cancellations will increase resistance to anticoagulant rodenticides.

Overall, EPA concludes that cancellation of products subject to this NOIC will not result in the loss of a residential consumer’s ability to control commensal rodents nor increase the time required to control commensal rodents. Residen tial consumers will still have a wide variety of options for rodent control, including several non-ch emical options as well as multiple rodenticide active ingredients. The performa nce of all commensal rodent control measures can vary widely according to external environmental conditions, st ate of the residence, and the behavior of individual rodents, but there is no evidence that SGARs consisten tly out-perform all other active

### ~ 101 ~ ingredients, or that unprotected ba it consistently out-performs bait in bait stations, regardless of

circumstances. Residential consumers who w ould otherwise use a product subject to the NOIC may experience a slight increase in the cost of house mouse control, of about $0.25 per placement or in the range of $1.50 to $3.00 per infe station. Cost increases such as these are unlikely to induce consumers who would use roden ticides to switch to non-chemical measures. Currently, rat control products that conform to the RMD and are available on the market are $7.00 to $8.00 more expensive per placement ($42 to $48 for a minor infestation) than the products proposed to be cancelled. However, si nce the issuance of the RMD, registrants have been able to develop technologies for pr oducing RMD-conforming house mouse products at substantially lower cost than was seen in 2008. T hus, it is possible that pr ices for conforming rat products will similarly decline. At the moment, the increase in cost may induce some residential consumers to use lower-cost, mechanical control options, but these measures would entail some additional non-monetary costs, su ch as disposing of dead rats (although the labels of the products subject to cancellation also requi re the disposal of dead rodent s if found). These cost impacts arise because of the requirement that bait be contained in bait stati ons; the choice of active ingredient does not affect the per-unit cost or the cost of control. The a dditional cost is generally less than two percent of the monthly non-housing in come for a family of three at the poverty line, and a considerably smalle r proportion for the majority of residential consumers. When comparing these costs against the expe cted risk reduction, EPA regards these cost increases as only affecting thos e residential consumers who do not use rodenticides where children, pets or non-target wildlif e might gain access. For other residential consumers, products with included, RMD-conforming bait stations are likely to provide a cost savings relative to the costs of obtaining products subject to the NOIC plus the tamper-resistant bait stations (which are

### ~ 102 ~ unlikely to be available at the same retail establ ishment) necessary for use consistent with those products’ existing labels. The following sections provide an overview of the methodology used in EPA’s impact assessment, target pests, the use and advantag es of the rodenticide products EPA intends to cancel and their alternatives, a nd expected impacts on households that would be affected by the proposed cancellation.

A. Methodology EPA’s impact analysis (Cook and Hill, 2011) explored the potential impacts incurred by households currently using products EPA proposes to cancel; specifically, rodenticides marketed

to residential consumers containi ng SGARs and/or unprotected bait, i.e. , not confined to a bait station reasonably anticipated not to release rodenticide bait. Th e analysis distinguishes between impacts on consumers treating for mice and for ra ts and also on consumers facing a single or sporadic infestation and those f acing chronic or repeated infesta tions. Chronic infestations may occur in situations where rodent populations ar e particularly high due to favorable external environmental conditions such as readily availa ble food and shelter. Examples include urban environments where food refuse (e.g., restaurant and residential waste) collects and rural areas where there may be readily available food (e.g., fiel ds or livestock feed) and harborage (barns or natural sites). In these situations, sanitation a nd exclusion are difficult and infestations can be prolonged and recurring. To assess the impacts of the proposed cancellati ons, EPA identified the target rodents and how the products are used. The Agency then identified available alternatives and compared their performance in terms of ability and time needed to achieve co ntrol of an infestation. EPA also compared other factors that may be considered advantageous or disadvantageous, such ease of

### ~ 103 ~ use and disposition of carcasses, and compared control costs. Fi nally, these factors formed the

basis for EPA’s conclusions about the most likel y alternatives to the products proposed for cancellation and the impacts of cancellation.

B. Target pests and use of rodent control measures The products subject to the NOIC bear label cl aims for control of one or more of three commensal rodents: the house mouse, Norway rat, and roof rat. The house mouse is by far the most common of these rodent pests. Of househol ds reporting seeing signs of rodents, 86 percent reported signs of mice, nine per cent reported signs of rats, and another five percent could not identify the rodent (Census Bur eau, 2011). Most rat problems in th e United States are likely to be Norway rats, as the roof ra t appears limited to Hawaii and relatively warm and coastal areas in the contiguous 48 states (Mar sh, 1994). Options to control these pests include various rodenticides, non-chemical methods such as snap traps and glue boards, and professional pest control operators (PCOs). According to the American Housing Survey (Census Bureau, 2011), slightly more than six percent of U.S. households reported having seen signs of a rodent in the three months that preceded the survey. Extrapolating over the whole year suggests that as much as 25 percent of U.S. households could see rodent signs. This is likely an overestimate of affected households since, as noted above, some households face chroni c or recurring problems. Market survey data (IRI, 2012b) indicate that rodenticides account for approximately 30 percent of sales, by unit, of rodent control products, with m echanical traps accounting for al most 40 percent of the market and glue boards for the remaining 30 percent. If 25 percent of households treat for rodents each year and 30 percent of those households choose rodenticides, then about 7.5 percent of all households would use rodenticides each year.

### ~ 104 ~ Residential consumers with commensal rat pr oblems may, in general, choose different control options than those with house mouse pr oblems. It seems likely, for example, that someone with a commensal rat problem would be mo re likely to call a professional pest control service than someone with a house mouse probl em, but specific data are not available. Rodenticides can, in general, be used to target either mice or rats alt hough bait stations for mice would typically be too small for rats to enter. Re sults of a market survey indicate that nearly 90 percent of rodenticide sales in the residential consumer market were for the elimination of house mice (Kline & Company, 2006). EPA’s review of annual production data for 2007 and 2008 supports this figure: EPA estimates that over 95 pe rcent of commensal roden ticide bait sold is in products intended for use against house mice. Glue boards come in differe nt sizes; market data from 2010 (IRI, 2010) indicate that mouse-sized glue boards account for almost 88 percent of sales. However, as the larger, rat-sized board s are also capable of entrapping house mice, it is possible that some users of large-size glue board are actually targeting mice. Snap traps are sized specifically to catch either mice or rats, an d sales data indicate only two percent of the sales for these products are for rat-sized units (IRI, 201 0). Together these data indicate that 90 percent or more of rodent control problems involve house mi ce. Given that only 7 percent of residences have rodent problems, these data imply that less than one percent of US residents face problems

with commensal rats. A summary of market survey data for the ye ar ending in July, 2012, indicate that SGAR pellets are the dominant form of mouse baits w ith just over 65 percent of the market (IRI, 2012a). Single-use, disposable bait stations, wh ich primarily contain br omethalin, account for about 12 percent of the market, while refillable bait stations, also mostly with bromethalin, account for 15 percent. The remaining portion of the market comprises various other forms

### ~ 105 ~ including baits of vari ous active ingredients and forms (e.g., blocks) not in stations and a few bait stations containing SGARs such as bromadio lone. EPA has recently conducted an informal check of available products whic h suggest that products targeti ng rats are more likely to be SGARs in block form than in pellet form. Some blocks contain bromethalin or an FGAR such as diphacinone. A disposable bait station containi ng bromethalin was recently registered for rat control. However, data on sales or use of recen tly registered products ar e not yet available.

C. Usage Patterns Rodenticides are formulated in baits designed to be sufficiently appe aling to rodents that even marginal feeders will return and eat enough to reach a lethal dose. Regardless of form (e.g., block or pellet, unprotected or in stations), the locations and amounts of bait placements will essentially be the same. Labels for commen sal rodenticides, includ ing those proposed for cancellation, direct users to place bait in the ar eas where the rodents ar e active, typically along walls or other likely routes of travel. When used to control h ouse mice, these labels typically direct that bait placements be made at intervals of 8 to 12 feet. When used to control commensal rats, these labels typically direct that bait placements are to be spaced 15 to 30 feet apart. All products subject to the NOIC bear labels that requ ire that placements that would be accessible to children, pets, domestic animals and/or non-target wildlife must be in tamper-resistant bait stations. With one exception, all pr oducts subject to the NOIC bear la bels that require the user to

check the condition of the bait af ter placement, replenish consumed bait, and collect and dispose

of unused bait and dead rodents. 16 Directions for use for non-chemical methods like snap traps

16 EPA Reg. No. 3282

‐ 3 does not require collection and disposal of unused baits, although it does require that users check perishable baits daily, and replace contaminated or spoiled bait immediately. The requirement to treat for rats for at least 10 days, and to treat for mice for at least 15 days, is effectively a replenishment requirement.

### ~ 106 ~ and glue boards also call for placem ents in similar locations. Not all target rodents will be gin to feed on bait immediately. Two or more weeks may be required to kill all rodents in an infestation, rega rdless of the active ingred ient in the rodenticide used. The longer treatment times are more lik ely where food items other than the bait are available to the rodents. From the time targ et rodents begin feeding on them, anticoagulant

rodenticides take at least three to five days to kill their first vi ctims, and two or more weeks to kill all of the rodents that will ultimately be ta ken. The acute rodenticide bromethalin typically causes death within two days from the onset of feeding, although it may take a few more days for some lethally exposed individuals to die. Thus, under good conditions (especially lack of alternate food sources), a successful rodenticide baiting program w ill typically last from one to

several weeks. Because it is difficult to determ ine how many rodents are present in a residential infestation, it is prudent for users to continua lly monitor for fresh signs of rodents during the course of control operations – regardless of th e method of control – and continue baiting until

new evidence of rodent activ ity is no longer detected. Effective use of rodenticides depends on a number of factors in cluding the size and complexity of the infested area and the size of the infestation. Use of multiple bait placements

will increase the likelihood that rodents will find th em and consume a lethal dose of rodenticide. To characterize the likely range of use, EP A evaluated scenarios for minor and major infestations, reflecting smaller and larger numbers of rodents and areas to be treated. By minor infestation, EPA means several individual rodents, which is the most common scenario. Rodents will typically take up residence near a supply of food (e.g., kitchen cupboards or pantry) where, despite their nocturnal habits, they will be notic ed either by their movement, by the consumption of food, or by their droppings. A major infestat ion might occur if rodent s find a food source that

### ~ 107 ~ is rarely disturbed, such as a large supply of pet food in a base ment, and can establish a sizable population (e.g., a half dozen or more individuals with active breeding) before being observed. Such an infestation would be relatively uncommo n, especially with rats. EPA also evaluated one-time infestation and repeated in festations in each of these scen arios. Repeated infestations may occur because environmental conditions in areas adjacent to the residential unit support large rodent populations. Examples of such areas are urban alleys with trash receptacles filled with food waste from nearby restaurants and ru ral settings where livestock feed provides an abundant food supply for rodents. EPA has no data on the frequency of recurring infestations, but it is likely to vary widely. Many househol ds may observe a seasonal pattern where rodents

seek shelter in late fall and winter . Major infestations in occupied residences are likely to be rare because most residents will observe signs and take action before a sizable population is

established. For purposes of comparison, EPA assumed that a user would make six bait placements (e.g., a block, packet, or baited st ation) in the case of a minor infestation of rodents, and 12 placements for a major infestation of rodents. These assumptions are based on university agricultural extension agencies and government recommendations for homeowners to control rodents (CDC 2010; Pierce 1993; Koehler and Kern, 2008; Hovanic et al., 2010; Illinois Department of Public Health undated), which EPA is confident will not underestimate use. The number of placements encompasses a variety of s ituations where bait pla cements are used both spatially and sequentially. For example, si x placements could represent a case where the user sets three placements around the kitchen ar ea and replaces each one time as the bait is

consumed.

### ~ 108 ~

D. Alternatives to Products Proposed to be Cancelled The anticipated effects of the cancellations proposed in the NOIC are the removal from the general consumer market, and from residential consumer use, of rodenticide bait products where the bait is not protected in a bait station meeting the crit eria announced in the RMD, and rodenticide bait products containing SGARs. EP A concludes that the proposed cancellations will not impair the ability of residential consum ers to control commensal rodents, because the

alternative control methods discus sed below remain available.

1. House Mouse Control Products

a. Rodenticides There are currently more than 30 rodentic ide products that conform to the RMD registered for general consumer use against co mmensal rodents. A regularly updated list of RMD-conforming consumer use products appears at http://www.epa.gov/pesticides/mice-andrats/rodent-bait-station.html . All are registered for use agains t house mice, despite the fact that the names of several products only mention rats . These currently registered, RMD-conforming products each use one of three different active ingredients (bromethalin, chlorophacinone, and diphacinone). At least four of these products contain refillable bait stations with replacement bait blocks, and the rest consist of bait in single-use, disposable bait stations. The bait components of these products meet th e efficacy testing requirements that EPA has established for registration of commensal rodenticide baits under FIFRA. In order to

demonstrate the effectiveness of a rodenticide active ingredient, EPA requires (1) acute oral toxicity testing with wild-type ro dents of the targeted species; (2 ) laboratory efficacy screening of one or more bait formulations with wild-typ e rodents of the targeted species; (3) indoor and outdoor field efficacy trials involving the targeted species in actual use situations in different

### ~ 109 ~ regions of the U.S. 17 In addition to these requirements fo r registering an new active ingredient for controlling commensal rodents, each new bait formulation must be screened for effectiveness in laboratory efficacy tests. These tests are not designed to rank the efficacy of the various rodenticide products, but instead to establish whether each produc t meets the efficacy threshold that EPA considers necessary to support registration. According to market research (IRI, 2012a), RMD-conformi ng products currently make up about 27 percent of the market for mouse rode nticides. EPA’s informal check of products and prices, conducted in the fall of 2011, suggests that most of the available RMD-conforming products contain the active ingred ient bromethalin, which is not an anticoagulant. Like most SGARs, bromethalin products are formulated such that a mouse could consume a lethal dose in a single feeding. A mouse consuming bromethalin will typically die in two to three days (Corrigan, 1997), a period that is somewhat shorter than the three to five days typical of SGARs. The major difference in performance is that a mouse will stop feeding once it consumes a lethal dose of bromethalin; in that respect, less bromethalin bait is needed to cont rol an infestation than anticoagulant bait because each individual mouse consumes less bromethalin bait before it dies. The rest of the RMD-conforming products curr ently available contain chlorophacinone or diphacinone, which are FGARs. They are less acutely toxic th an SGARs and often require a mouse to feed multiple times over several nights be fore it will obtain a lethal dose. In studies, however, the time to death is approximately th e same for FGARs as for SGARs (Dubock and Kaukeinen, 1978; Kaukeinen and Rampaud, 1986; Pitt, et al. , 2011; Witmer, 2007a,b). The need for multiple feedings may suggest that the user w ould have to make greater effort to maintain

fresh bait and reduce the availa bility of other food options in comparison to SGARs or

17 General guidance for the design of such studies appears on pages 307-310 of Subdivision G of EPA’s Pesticide Assessment Guidelines, Office of Pesticides and Toxic Substances, Washington, DC, 1982.

### ~ 110 ~ bromethalin. In practice, however, the differen ce is likely minimal, because the amount of bait applied (assuming use in accordance with label di rections) is more than the amount likely to be consumed in one night by the number of house mi ce in typical infestations. Infestations are likely to consist of more than one house mouse, and users cannot be sure that all individuals will take bait on the first night regardless of what rodentic ide product is used. As a result, most labels for all types of commensal rodenticides direct users to continue to provide fresh bait and sanitation for ten days or more. In a review of the literature, Clapperton ( 2006) found several studies demonstrating that block baits were preferred and se veral others showing that pelle ts or meals were preferred. Prescott (2011) reported that bait-block form ulations from many countries tended not to be accepted as well as pelleted baits when tested un der similar conditions. However, these reports do not address whether the products subject to the NOIC perform better than the registered, RMD-conforming alternatives. Kaukeinin and Marsh (2009) report that improved manufacturing processes and EPA’s bait-specifi c efficacy data requirements have led to the production in the U.S. of bait blocks that are high ly palatable to commensa l rats and mice. EPA requires that all commensal rodenticide bait form s (e.g., pellets, meals, pastes, powders, block baits) meet the same efficacy criteria for regist ration for use in and around residences (Jacobs, 2011). There is no basis for presuming that certai n bait forms offer faster control or a higher degree of control. Protective bait stations do not appear to affect the acceptance of bait by mice (e.g., Kaukeinin and Marsh, 2009). In fact, protective bait stations may provide several advantages over the use of uncontained bait. They may protec t bait from dust and moisture, thereby keeping the bait palatable longer. They provide mice w ith a protected place to feed leading to greater

### ~ 111 ~ consumption and a higher likelihood of obtaining a lethal dose (Vantassel et al. , 2006; Corrigan, 1997). Blocks anchored in bait stations will not be moved and cached by individual mice, and thus are more likely to remain available for consumption by the whole mouse population. Although bait station size may prevent placement in some locations, many recently registered bait station products are approximately the same size as the cardboard box in which one of the best-selling commensal rodenticides is appl ied, D-Con Mouse Proof II, EPA Reg. No. 3282-65. Although some may argue for the desi rability of being able to toss a packet of pellets or loose

blocks in wall crevices or attic spaces, such placement would not increase the level or speed of control of house mice because they forage for huma n and pet food where it is stored or spilled. Such places are typically in living areas, which consequently, are the most appropriate locations for placing any rodenticide (or a ny trap) intended to control a hous e mouse infestation. House mice tend to move through living spaces along walls and behind appliances, places where bait stations can easily be placed. Moreover, placemen t in wall voids or other places from which bait

cannot be checked or retrieved is not allowed under the use directi ons on the labels of any of the products subject to the NOIC. Tossing baits wh ere they cannot be monitored or retrieved precludes compliance with label directions to monitor bait co nsumption and to collect and dispose of uneaten bait. Inability to do so can result in inefficient rodent control and insect

infestations. On the basis of these considerations, EPA concludes that residential consumers will be able to achieve essentially th e same level of control of house mouse infestations, within essentially the same time frame, and with esse ntially the same level of effort, using other currently registered rodenticide products that conform to the RM D as they would with products subject to this NOIC.

### ~ 112 ~

b. Non-chemical Methods

The most common forms of non-chemical c ontrol methods are snap traps and glue

boards. Other non-chemical cont rol methods (e.g., live traps, devi ces that electrocute mice) are also marketed, however, EPA’s alternatives anal ysis focused on the more commonly used lethal measures: snap traps and glue traps. Snap traps have a long history of use, are an effective way to control mice and have a number of advantages over rodenticides. Snap traps are relatively inex pensive and they may be reused. In most cases, death is essentially instantaneous. Some disadvantages include the time and effort of baiting and setti ng the traps and, once sprung, a trap will not work until reset. The user must dispose of the dead mouse, whic h may be an unpleasant task (although users of rodenticides are also required to dispose of dead rode nts if they find them). On the other hand, the presence of the dead mouse offers a concre te measure of success, and enables the user to dispose of the carcass immediately, thus avoiding odor from decomposing mice, which can be a non-monetary cost associated with the use of r odenticides. Because snap traps can be deployed with different food items or other attractive objects , they may be more effective than rodenticide

baits in situations where other available food sources cannot be eliminated. Glue boards have a sticky substance to cat ch and hold rodents that run across them. Some consumers may like the ease of glue boards, as there are no triggers or baits to set, and as trapped rodents can be disposed along with the used trap. Glue traps may be useful to kill snap trap-wary mice and are sometimes used in conjunc tion with snap traps (Illinois Department of Public Health, undated). However, dampness, dust, and even temperature extremes will diminish the efficacy of the glue boards (Illinois Department of Public Health, undated). Since rodents trapped on glue boards do not die quickly, they can use their urine, feces, and fur to

### ~ 113 ~ escape (Corrigan 1997). Rodents have been observed to use paper, dirt, or leaves to essentially create bridges over the sticky su rfaces (Corrigan 1997). The Cent ers for Disease Control does not recommend glue boards because often the tra pped rodents are not dead when users collect the used glue boards, thereby increasing the pote ntial for disease transmission or rodent bites (CDC 2010). Despite these apparent drawbacks, glue boards account for about 30 percent of the rodent control market (IRI, 2012b.) In summary, snap traps and glue boards are commonly used and both provide similar

levels of control as rodenticid es within a similar time frame. In comparison to rodenticides, there may be some non-monetary co sts associated with their use, e.g. , the effort to bait snap traps and monitoring of and disposal of dead or dyi ng rodents from snap tr aps or glue boards. Considering the Centers for Disease Controls’ co ncerns about glue boards, EPA concludes that snap traps are the most appropriate alternative to rodenticides.

c. Professional Pest Control Operators Many residential consumers routinely rely on professional pest control operators (PCOs)

to treat their homes for rodent s and other pests, even though PCO services are more expensive than do-it-yourself pest control. Products rou tinely used by PCOs are not subject to the NOIC, therefore consumers currently using PCO servic es will not be impacted by this action. According to a market survey, 56 percent of PCOs use rodenticides as their primary method of

control for their residential acc ounts, 24 percent use mechanical traps, and 16 percent use glue boards (Curl, 2012). 18 There is a similar distributi on across commercial accounts, which

18 A recent survey indicates that 100 percent of PCOs use tamper proof bait stations for exterior rodenticide applications (the survey did not ask about indoor applications), so it is clear that PCOs have access to, and regularly use, tamper proof bait stations. This same survey also indicates that 79 percent of PCOs use rodenticides in bait

### ~ 114 ~ includes apartment buildings and condominiums. The SGAR bromadiolone is the rodenticide most commonly used by PCOs, accounting for about 45 percent of PCO rodenticide use (measured by expenditures), and difethialone acc ounted for about 20 percent of PCO rodenticide use, with all other rodenticides combining to account for the remaining 35 percent (Curl, 2012).

The source of these market data did not di stinguish between mous e and rat control.

2. Rat Control Products

a. Rodenticides Currently, there are only three rodenticide pr oducts that conform to the RMD registered for general consumer use against commensal rats. Two of these products ar e baits in single-use, disposable bait stations and one consists of a refillable bait station and multiple bait block refills. The RMD-conforming consumer use products are listed at http://www.epa.gov/pesticides/miceand-rats/rodent- bait-station.html . All of these products contai n bromethalin, which, as discussed above, is an acute rodenticide. Each product is formulated so that a rat may consume a lethal dose in a single night’s feeding. The rat will gene rally cease feeding at th at time and die in two to three days. Thus, the typical time to death is shorter than those t ypical of anticoagulants. There are currently no RMD-compliant F GAR products currently registered for residential consumer use in controlling commensal rats, but there are no a pparent impediments to the adaptation of currently registered bait bloc k formulations containi ng FGARs for use in bait

stations that conform to the RMD and are sized appropriately for baiti ng commensal rats. As noted in the discussion of mouse control produc ts, feeding on FGARs over several nights might

stations for residential rodent control sometimes, often, or all the time, and 13 percent use loose baits for residential rodent control sometimes, often, or all the time. The survey clearly supports an inference that use of bait stations is widespread among PCOs. ASPCRO/NPMA, Rodenticide Use Survey of Pest Management Professionals, 2013.

### ~ 115 ~ be necessary for a rat to obtain a lethal dose. Ti me to death with FGARs, however, is similar to

that of SGARs.

Blocks are an effective bait form for rat cont rol, as evidenced by their widespread use by PCOs and public health programs. Bait blocks are not novel pest management tools and they are the preferred bait form of professional applicators in residen tial settings (Lublinkhof 2011). Bait

blocks have been on the residential consumer markets as far back as the late 1980s. EPA’s informal check of products and prices also f ound more examples of bl ock baits than pelleted baits among products marketed to general consum ers for commensal rat control. Of course, many pellet forms are likely marketed for both rat and mouse control. As discussed above, EPA requires both block and pelleted co mmensal rodent baits to meet the same criteria in efficacy screening tests (except for bait blocks limited by labeling to use exclus ively in wet or damp areas), so there is no basis for presuming that pe lleted or meal baits offer faster control or a higher degree of control. Unlike house mice, which tend to explore new items, commensal rats tend to avoid new objects (Timm, 1994; Corrigan, 2001). Such “n eophobia”, defined as “new object reaction ...consists of avoiding an unfamiliar object in familiar surroundings." (Barnett, 1958) includes a reluctance to enter a station to consume bait, a nd is affected by a broad array of factors. Although neophobia can delay an indi vidual rat’s entry into a bait station and consumption of bait, it is unlikely that it will noticeably affect either the ability or time to control a rat

infestation. Bait-stations have been employed in effectiv e urban rat control projects for many years,

and have also been used in successful eradica tions of commensal rats from offshore islands, indicating that satisfactor y levels of control can be achieved using bait stations. For several

### ~ 116 ~ decades, pesticides registered for use to contro l commensal rodents have had label statements requiring use in tamper-resistant (or tamper-pro of) bait stations where placements otherwise would be accessible to children, pets, domestic animals, and/or non-target wildlife, and commercial and professional users generally achieve effective rodent control while complying with this requirement. There are several reasons suppor ting EPA’s conclusion that the bait station requirement will not noticeably increase the time required for control of a residential rat problem. First, rats’ tendency to avoid new objects is not confined to bait stations. The introduction of a new bait block or packet of pellets into the rats’ envir onment is also likely to induce some neophobia. Second, most rats will explore a new bait stat ion after a few days (Corrigan, 2001). This potential delay is small relative to the variation in time to mortality of an individual rat and the

variation in the time to control an infestation. Th ird, entering a container of some sort would not

be a new behavior for rats that are accust omed to entering boxes and cans containing food

leftovers or buckets and bins of animal feed. Moreover, each rat that enters and leaves a bait station safely leaves behind scent clues that dimi nish neophobia of other ra ts. Fourth, rats will not likely be fully accustomed to a human-occupied residence before the resident notices their presence and takes action. In such circumstance s, rats may not perceive a bait station as new

relative to other features of their environment. Achieving control of an infest ation using rodenticide baits wi thout bait stations (such as the products proposed to be cancelled) will generally take ten days to two weeks, and in some cases considerably longer. It can take severa l days for all of the rodents to find the bait placements; it can take multiple days for a rat to consume a lethal dose (even of those baits formulated to deliver a lethal dose in a single night’s feeding), and there can be differences of

### ~ 117 ~ several days in the lengt h of time between consumption of a lethal dose and death. The potential

variation in these factors for an individual rat is far greater than the potential variation in time between acceptance of bait in a bait station and acceptance of unprot ected bait, and this difference is even more pronounced for a group of several rats considered collectively. Given the long and highly variable treatment period needed to achieve control of an infestation even without bait stations, neophobia asso ciated with use of a bait station is unli kely to lead to a noticeable extension of the treatment period. Note , too, that many of the a lternative rodenticides currently registered all contain bromethalin, which typically kills one to three days faster than anticoagulants. Finally, for bait placements in areas accessible to children, pets, domestic animals and/or nontarget wildlife, use of RMD-conforming bait stations is not likely to lead to an increase in treatment duration in comparison with use of the tamper-resistant bait stations already required by the labels of the products subject to th e NOIC. In conclusion, available rodenticides with RMD-conforming bait stations for rats will perform similarly to the products subject to the NOIC in terms of level of control, the time to achie ve control, and the effort required of the user.

b. Non-chemical Methods As with house mice, non-chemical control met hods include snap traps and glue boards as

well as other devices. Data are not available to discern the relative mark et shares of various methods in the control of rats, which is a re latively small proportion of the rodent problems among residential consumers. Snap traps for rats are distinctly larger than snap traps for mice, and owing to their size, they are unlikely to kill mice. Only about two pe rcent of all snap traps sold are rat-sized (IRI, 2010, via Bell Labs). Since about ten percent of households re porting identifiable signs of rodents report rats, it ap pears that consumers with rat problems are either more likely to hire

### ~ 118 ~ PCOs or less likely to use snap traps than are t hose with mouse problems. It is reasonable to think that the perceived disadvantag es of snap traps, including th e effort of baiting and disposing of dead rats, are relatively larger than for rats than for mice. One advantage of traps – the likelihood of locating and disposing of the carcass – is also relative ly larger for rats, as the odors of decomposing rats are more pow erful and longer-lasting than t hose of mice. Regardless of the relative weights attached to thes e advantages and disadvantages, traps are an effective means of

control and could address a reside ntial infestation in a similar time frame as would rodenticides. Glue boards, like snap traps, are sold in sizes appropriate for catching commensal rats. According to market research, approximately 13 percent of glue board sales are of rat-sized products. Unlike snap traps, however, the larger rat-sized glue boards also could be used to catch mice. As with snap traps, it is reasonable to think that the advantages and disadvantages of glue boards, especially disposing of a trapped – but not necessarily dead – rat, are relatively higher for rats than for mice. In terms of perf ormance, however, extensive use of glue boards by PCOs suggests that glue boards are an effective form of control. As with any rodenticides, the performance of non-chemical methods for rat control will be subject to the wariness that characterizes the behavior of individual ra ts. Thus, the level of

control and the time to achieve control with non-chem ical methods will likely be similar to that

obtained with rodenticides. As with mouse c ontrol, non-chemical methods may require more effort on the part of the user to ba it snap traps and to dispose of rats.

c. Professional Pest Control Operators

The market data available to EPA concer ning PCO rodent control activities do not distinguish between treatments for rats versus mi ce. Treatments for commercial accounts, which include apartment buildings or condominiums, are for control of both rodents, along with other

### ~ 119 ~ pests (Curl, 2012). Treatments for residential accounts are typically for mice (Curl, 2012), but this may simply reflect the fact that about 90 percent of rodent problems involve mice (Census Bureau, 2011). It is reasonable to think th at reliance on PCOs is relatively higher among households with rat problems than with mice. Products typically used by PCOs are not subject to the NOIC, so PCOs and consumers currently us ing such services will not be affected by the proposed cancellations. It is also worth noting that most PCOs repor t that they routinely use bait stations when using rodenticides in residences (A SPCRO/NPMA 2013).

E. Impacts of Cancellation on Residential Consumers Based on the information present in IV.4., EP A concludes that the cancellation of the products identified in the NOIC will not significantly impact either the level of rodent control that residential consumers will obtain or the length of time it takes to achieve control. Since this action does not affect products typically used by professional users (e.g., PCOs, commercial and agricultural users, government agencies), there w ill be no impact on such users, or on others who rely on their services. The impact on consumers w ill likely be limited to any change in the cost

of control due to differences in the cost of compliant products relative to non-compliant products. Impacts will include any incremental ch ange in monetary expenditures as well as any non-monetary costs such as an increase in the effo rt needed to use an al ternative method or to dispose of carcasses. This section summarizes EPA’s analysis comp aring control costs of rodenticides that would be cancelled to the control costs using av ailable alternatives (Cook and Hill, 2011). This analysis addresses commensal mouse and rat contro l across a range of situ ations differing in the size of the infestation (minor or major) and the frequency of infest ation (one-time or repeated) as

described in IV.3.

### ~ 120 ~

1. Incremental costs of house mouse control Overall, EPA expects that incremental co sts of using RMD-conforming rodenticide products for mouse control in lieu of products proposed to be cancelled will be small. The rodenticide active ingredient used does not appear to significan tly affect the price of rodenticide products, so the incremental cost of the propos ed cancellations will be driven by the RMD bait station criteria. EPA obtained summary data from a national market survey covering the 52 weeks ending July 8, 2012 (IRI, 2012a), showing average prices weighted by quantity sold. The cost per placement for rodentic ide products that include disposable bait stations for mice was $1.63 while the cost per placement for SGAR pellet products (the product type that accounts for a majority of sales of mouse control products ) was $1.66, suggesting that consumers would face

no incremental costs associated with the cancell ation of the registrati ons of pelleted products. In a 2011 analysis of both mouse and rat pr oducts then on the market, EPA identified differences in the average price of RMD-conf orming and non-conforming products that would

indicate a cost increase for a one-time in festation ranging from around $2.00 for a minor infestation to as much as $12.00 for a major infestation (Cook and Hill, 2011). Using pellet products of the type that accounted for a majori ty of sales of mouse control products as the baseline, EPA’s 2011 analysis indicated that most residential consumers would be expected to see an average increase in cost of $1.50 in a minor infestation and $3.00 in a major infestation, or $0.25 per placement with the use of rodenticide pr oducts that include disposable or single use bait stations. These price data were based on a check of local s ources and national chains with internet pricing and represent simple averages of prices. In situations where infestations are expected to recur, residential consumers may find it less expensive to buy rodenticides in larger qua ntities of 16 to 28 placements per package.

### ~ 121 ~ EPA’s check of stores found a per placement price of about $0.75. Th e average cost of rodenticide products that include reusable bait stations, which pr ovide a bait station and six to eight blocks, implies a per-placement cost of le ss than $1.00. More recent information from the market survey indicates a cost per placement for products that include reusable bait stations of about $0.90 (IRI, 2012a), but did not provide a price for bait blocks that might be purchased in quantities of 16 to 28 placements per package. Using these figures, the incremental cost

associated with reusable bait st ations is about $0.15 to $0.25 per placement, similar to the onetime infestation scenario. In conclusion, market survey data suggest that for house mouse control there is no difference between the cost of products proposed to be cancelled and register ed rodenticides that conform to the RMD. Data generated by EPA su ggest that consumers may face a cost increase of about $0.25 per placement or an additional cost of $1.50 for a minor infestation to about $3.00 more to control a major infestation. Costs per infestation would be similar regardless of the frequency at which the infestation occurs. This ve ry modest increase in price is not likely to induce any changes in consumer behavior. If a consumer would typically use one of the products proposed to be cancelled, such as a SGAR in pellet form, the incremental cost of using

an alternative rodenticide in a bait station would not likely in duce him or her to purchase a nonchemical method instead. Thus, EPA does not antici pate an increase in the use of snap traps or glue boards by consumers treating for house mice. Again, mice account for approximately 90 percent of commensal rodent pr oblems in U.S. households. It is worth noting that the house mouse c ontrol market has undergone considerable changes in recent years. When the RMD wa s announced in 2008, few rodenticides were available in ready-to-use bait st ations, despite a long-standing requi rement on labels that tamper

### ~ 122 ~

resistant bait stations be used where children, pets or non-target wildlife could otherwise have access to the bait. Stand-alone, reusable, tamper-r esistant bait stations were very expensive and available mainly through vendor s catering to professional user s. Since the RMD, however, several manufacturers have developed rodentic ide products with single- use and reusable bait

stations that are similar in price to unprotected baits.

2. Incremental costs of commensal rat control As with mouse control products , the choice of active ingredie nt used does not appear to significantly affect the price. For residential consumers treating for commensal rat infestations, EPA’s 2011 analysis indicated that incremental costs of using a lternative rodenticide products with single-use bait stations for rats instead of products proposed to be cancelled would be about $8.00 per placement. For a one-time problem, this implies a cost increase ranging from $46 in a minor infestation to $92 in a major infestation. Note that rat problems are relatively rare, comprising about ten percent of rodent problems annually, and that major infestations would be exceedingly rare because the infestation would have to go untreated for some time in order for a population to become established. See the discus sion in IV.3. EPA does not have market data for rodenticide products intended to control rats as it do es for rodenticides intended to control

house mice. The incremental cost per treatment is similar for situations regarding repeated infestations. Stand-alone, reusable, tamper-resi stant bait stations are very expensive and available mainly through vendor s catering to professional user s. A new rodenticide product containing a rat-sized, reusable bait station wa s registered in October 2012 and may soon be

available in retail ou tlets, but the price of the prod uct is presently unknown. Improving technology rapidly has led to decreas es in the price of mouse-sized bait stations and the same

### ~ 123 ~ could happen for rat control products. Compared to the purchase of small quantities of rat bait blocks, EPA’s informal check of prices (Cook and Hill, 2011) indicates that purchases of rat bait blocks in large quantities do not substantially lower the per-placement cost, and hence produce little change in the cost of treatment or the in cremental cost of using disposable stations for repeated infestations.

The estimated increase in the cost of commens al rat control products as a result of the proposed cancellations could induce consumers to seek other rat control options. Snap traps, according to EPA’s informal check of prices , average $2.00 to $2.25 more per placement than the products proposed to be canceled (Cook a nd Hill, 2011). Glue boards average about $1.00 more per placement than the products proposed to be canceled. Thus, control of a minor rat

infestation is estimated to increase in co st by about $6.00 more with glue boards and $12.00 more with snap traps. Snap traps are recomm ended by the CDC, but glue boards are not. There are non-monetary costs associated with the use of both types of traps (i.e., regular monitoring and resetting, disposal of dead rodents, possibly th e dispatching of rats trapped but not killed). The disposal of dead rats, however, may be le ss of a disadvantage than with mice because the decomposing bodies of poisoned rats are likely to give off strong and unpleasant odors for a prolonged time, and poisoned rodents may be difficult to loca te and recover. For repeated infestations, snap traps are re usable, suggesting an ove rall per-infestation

cost similar to or lower than the roden ticide products proposed to be cancelled. In conclusion, the limited number and hi gher cost of RMD-conforming rat control products will result in incrementa l costs of addressing a rat infe station ranging from $46 in a minor infestation to $92 in a major infestation, or $8 per placement. Only a small proportion of residential consumers are expected to incur th ese costs, however, as commensal rats make up

### ~ 124 ~ about ten percent of residentia l rodent problems and only a po rtion of those problems would typically be addressed with rode nticide products proposed to be can celled. Use of snap traps or glue boards, rather than RMD-co mpliant rodenticides, would result in a lower incremental cost of rat control, but may entail additional non-monetary costs.

3. Socio-Economic Equity Assessment Changes in the per-unit cost of rodent contro l do not completely describe the impacts that may arise from the proposed cancellations. To place the estimated incremental cost in context, EPA has considered how the proposed cancellations would affect households that are at the poverty threshold. This concern is not only that these households have less income with which to purchase rodent control produc ts, but also that, as according to the U.S. Census Bureau’s American Housing Survey (Census Bureau, 2011) , households below the poverty-threshold have a greater likelihood of r odent problems. The AHS reports that about 14 percent of U.S. households are below the poverty line, but they account for a lmost 20 percent of households observing signs of rodents. To assess the per household impacts of can cellation, EPA compared the incremental costs, as presented in the previous section, lik ely to result from the pr oposed cancellations to household disposable income (i.e., excluding hous ing costs) at the poverty threshold. The poverty-threshold income varies depending on hous ehold size; this analysis used the income threshold for a three-person household as a refe rence, which is considered the average size household in the United States (C ensus Bureau, 2012). The poverty th reshold is higher for larger household, thus the analysis is al so representative of larger household at the poverty line. Monthly income rather than a nnual income was considered for two reasons. First, many low income households may lack savings or other met hods for spreading the cost of rodent control

### ~ 125 ~ across time and will have to pay for it from i mmediate cash resources. Second, some households will face recurring rodent control co sts rather than one-time or annua l costs. The Census Bureau (2012) reports that households at or below th e poverty line spend 42 percent of income on housing. Thus, for this analysis, EPA calcu lates monthly disposab le income at $900.For house mouse control, the average incremental costs for consumers using RMDconforming rodenticide products instead of prod ucts proposed to be cancelled ranges from zero to two percent of monthly non-housing income at the poverty threshold. For commensal rat control, incremental costs for consumers at th e poverty threshold range from five percent of monthly non-housing income in a minor infestation to 11 percent in a majo r infestation if they use the RMD-conforming rodenticides that are curre ntly available. Use of glue boards or snap traps would result in incremen tal costs of one percent or ov er three percent of monthly nonhousing income, respectively, plus non-monetary co sts associated with th e effort to set and monitor traps and dispose of d ead or trapped rats. Again, because those low income househol ds facing rodent problems overwhelmingly have mouse problems (88% of rodent infesta tions are mice, per Census Bureau, 2011), it is expected that impacts on most low-income residential consumers will be equivalent to zero to two percent of monthly non-housing income. More over, because less than ten percent of low income households report having seen signs of rodents within the pre ceding three month period, it is a small proportion of low income househol ds that would be subject to this burden. It is also worth repeating here that if these households have, or are visited by, young children (or pets), they already s hould be using bait station products and the potential cost of the

cancellation action on these users sh ould not be relevant to the ca ncellation decision. In fact, by making bait stations more easily available (and possi bly cheaper as they become more available),

### ~ 126 ~ the cancellation action may actually economically benefit lower income households with young

children.

F. Potential for Resistance

EPA considered the risks of increased resist ance to anticoagulant rodenticide products due to the proposed cancellation of certain c onsumer-oriented products containing SGARs and

concluded that the risks are mini mal. Resistance refers to gene tic changes in a rodent population

as a result of tolerant indivi duals being more likely to repr oduce and pass that trait on to subsequent generations, as a result of rodent icides removing large portions of susceptible individuals. EPA recognizes that there is the potential for rodents to develop resistance to anticoagulants, as there is with most pest-pes ticide combinations. However, residential consumer use of the conforming anticoagulant rode nticides will not be so widespread, frequent, and repetitive that enough anticoagulant tolerant individuals will be sele cted to result in a resistant population. First, relatively few residential consumer s face rodent problems. Current housing statistics show that only six percent of U.S. households report seei ng rodent signs in the preceding 3 months (Census Bureau, 2011). W ith such a low percentage of households observing rodent signs nationwide at any one time, and given the widespread distribution of rodents, few sites are subject to widespread, frequent, and repeti tive use of rodent control in general. Second, rodenticides as a whole make up a relatively small proportion of residential control products. Market data i ndicate that traps account for about 70% of retail sales of rodent control products, with rodenticides account fo r the remaining 30% of sales (IRI, 2012b). And

after SGARs are removed from the residentia l consumer market, the 30% of residential

### ~ 127 ~

consumer rodent control that relies upon rodenticides appear s likely to be divided between rodenticides containing active i ngredients with two very different modes of action: FGARs and

bromethalin. Finally, residential consumers are not the only persons controlling rodents. Some households will hire professional applicators who can utilize additional products, including

SGARs. The external rodent populations from which residentia l infestations arise are also subject to control by commercial applicators and public health officials using SGARs. These personnel, along with natural pr edators, will exert their own selection pressures on rodent populations, further diminishing the likelihood of an anticoagulant tolerant individual surviving treatment by a residential consumer altering the genetic makeup of the rodent population. Considering the lack of selection pressure resulting from the activities of residential

consumers treating their own premises, EPA concl udes that cancellation of the products identified in the NOIC presents, at most, a minimal risk of increasing the frequency of resistance-conferring alleles within U.S. populations of commensal rodents, even in areas with chronic rodent problems.

V. Conclusions Regarding Whether Subject Rodenticide Products Meet the FIFRA Registration Criteria Despite mandatory label statements requiring use in tamper-resistant (or tamper-proof) bait stations where placements otherwise would be accessible to children, domestic animals, and/or non-target wildlife, each of these groups experience significant rodenticide exposures that

cause risks of adverse effects. The rodenticide produc ts identified in the NOIC (and listed in Tables 1 and 2 of this document) present signif icantly greater risks to domestic animals and nontarget wildlife than other rodenticide products registered for the same uses, owing to various

### ~ 128 ~ factors. Chief among these factors are the pres ence of the active ingredients brodifacoum and

difethialone and/or the absen ce of a bait station conforming to the criteria of the RMD in products registered for general consumer use in the control of commensal rodents. The exposures to children and risks to the environment caused by the rodenticide products identified in this document are unreasonable because they are avoidable through th e use of alternative products that are eff ective and affordable.

A. Cancellation and Denial of Registra tions of Rodenticides Containing Brodifacoum and Difethialone and Intended for Residential Consumer Use.

1. Effective alternatives to brodifacoum and difethialone are available. All active ingredients and all or nearly a ll bait formulations containing them that are registered for use to control commensal rodents ha ve met the applicable criteria for registration that EPA has established under FIFRA, including data requirements addressing the effectiveness of the products against wild-type rodents of the target species. Products containing bromethalin and FGARs rodenticides have been register ed based on reliable studies demonstrating satisfactory effectiveness against target rodents. EPA conclude s that cancellation of products subject to the NOIC will not cause residential cons umers to lose the ability to control commensal rodents and will not increase the time required to control commensal rodents. Currently registered rodenticide products th at contain bromethalin or FGAR s, when used in combination with prudent sanitation and excl usion measures, are effective for general consumer use for the

control of commensal rodent s in and around buildings.

### ~ 129 ~ 2. Alternatives to brodifacoum an d difethialone are affordable. The rodenticide active ingredient used does not appear to significantly affect the price of rodenticide products, so the replacement of products containing the active ingredients brodifacoum and difethialone with products contai ning other active ingredie nts will not increase the price of rodenticides. Inasmuch as residential consumers will be able to achieve essentially the same level of control of rodent infestations, within essentially the sa me time frame, and with essentially the same level of effort, using othe r currently registered rodenticide products, the cancellation of products containing the active ingr edients brodifacoum and difethialone will not measurably increase the co st of rodent control.

3. Residential consumer use of brodifaco um and difethialone causes adverse effects to non-target wildlife that could be avoided.

Rodenticides that accumulate in rodents in quantities greatly exceeding the dose needed to kill the target pest, or that accumulate in predators and scavenge rs that consume target rodents, pose greater risks to non-target wild life than rodenticides that do so to a lesser degree. Available

toxicokinetic data indicate th at the SGARs brodifacoum and difethialone are much more persistent in animal tissue than the FGARs chlorophacinone, diphacinone and warfarin. The available information on bromethalin supports a conc lusion that it is rapidl y eliminated from the body. These findings concur with the results of wildlife monitoring studies (analysis of animals

that died from causes unknown or unrelated to rodenticide poisoning) , which show that accumulation of brodifacoum residues is prevalent in many species of avian and mammalian predators and scavengers. Accumulation of difethia lone also appears to be fairly prevalent in some areas, especially when considering the rela tively low usage of this rodenticide in the United States. Species in which widespread accum ulation of anticoagulant rodenticides in liver

### ~ 130 ~

tissue has been observed include owls, hawks, vul tures, mustelids, bobcats, and mountain lions. Notably, rodenticides were detected in 100% of the great horned owls tested in one study in central Massachusetts and 100% of mountain lions tested in a st udy in southern California. Inasmuch as products containing brodifacoum and di fethialone are only regi stered for use against

commensal rodents in and around bu ildings and are not registered for field uses or use against other rodent species, all non-targ et wildlife exposures to brodi facoum and difethialone are believed to result from commensal rodent produ cts registered for use in and around buildings. 19 Cancellation of brodifacoum and difethialone produc ts sold to residential consumers is expected to reduce environmental loading of these highly toxic and persis tent chemicals and to thereby reduce secondary poisonings amon g non-target wildlife. Inform ation from several lines of evidence (i.e., predictions from toxicity and me tabolism studies, whole ca rcass residue studies, secondary feeding studies, wildlif e incident reports) indicate that brodifacoum and difethialone accumulate in body tissues to a greater extent, an d persist for a longer time, than do warfarin, chlorophacinone, diphacinone, and bromethalin. The high retention of brodifacoum and difethialone in the tissue of prey animals, comb ined with the high toxicity of these chemicals, presents significant risks of secondary expos ure to non-target predators and scavengers. Moreover, the potential for target rodents to consume a lethal dose of brodifacoum or difethialone in one night’s feeding, and then to continue to consume additional bait for 3 or more additional days, can result in rodents with brodi facoum and difethialone body burdens well in

excess of the dose lethal to the target pest, and in many cases in excess of the lethal dose for nontarget predators and scavengers.

19 Minor exceptions are restricted use products registered to the U.S.D.A. Animal and Plant Health Inspection Service for its use in eliminating non-native rodents from islands where they are disrupting the ecosystem. “Field uses” refers to uses in crop land, non-crop areas, ditch ba nks, river banks, gullies, irrigation ditches, railroad tracks, fence lines, buffer strips, garbage dum ps, landfills, orchards, and rangelands.

### ~ 131 ~ Wildlife incident data suppor t the quantitative risk assessment’s conclusion that secondary exposure to brodifacoum poses lethal risk to predator and scavenger mammals and

birds. The incident data set fo r difethialone is much more lim ited than that for brodifacoum, which is not surprising given dife thialone’s lower extent of use in the United States. However, analysis of the toxicity and rete ntion time of difethialone indicates that its risks to predators and scavengers are more similar to those posed by brodifacoum than by warfarin, chlorophacinone, diphacinone, and bromethalin. Therefore, the l ack of reported incidents involving difethialone may well be due to the low use of difethialone or to other factors not related to risk. All the rodenticides subject to the NOIC present primar y poisoning risks to non-target vertebrates. Primary poisoning risk for large non-target mammals and for birds can effectively be eliminated through the use of tamper resistan t bait stations. However, the secondary exposure risk to predators and scavengers cannot be ad equately addressed through use of bait stations alone. Risks of secondary poisoning are greater for products containing the SGARs brodifacoum or difethialone than for those containing warf arin, chlorophacinone, diphacinone, or bromethalin. Brodifacoum and (to a lesser extent) difethial one have been widely used by residential consumers, and residential consumer use may contribute significantl y to brodifacoum and difethialone poisonings in non-target wildlife. Limiting availability of these chemicals in the consumer market will likely cause consumer s who would otherwise buy brodifacoum and difethialone products to buy other rodenticides, thereby reducing use and environmental loading of brodifacoum and difethialone – and hence, se condary exposure risks to non-target wildlife. While switching to alternative r odenticides will not completely eliminate secondary exposure risks, EPA believes that these risks to wildlife wi ll be significantly reduced if brodifacoum and

### ~ 132 ~

difethialone are not available to residential consumers but are limited to the professional, commercial and agricultural (structural only) markets.

4. Conclusion. Non-target wildlife exposed to rodenticid es containing brodifacoum or difethialone experience significant adverse effects. These ad verse effects occur despite label statements requiring use in tamper-resistant bait stations wh ere placements otherwise would be accessible to non-target wildlife. Brodifacoum and difethialone present greate r risks to non-target wildlife

than other rodenticides because they persist longer in the bodies of predators and scavengers, who may attain a lethal dose by consuming rodent s that individually contain less than the dose

that would be lethal to the s econdary consumer. Brodifacoum and difethialone also present greater risks to non-target wildlife than other rodenticides because target rodents can continue to consume bait for several days afte r attaining a lethal dose, increasing their toxicity to predators and scavengers. Products contai ning brodifacoum and difethialone are only registered for use against commensal rodents in and around buildin gs. Significant numbers of incidents of secondary rodenticide poisonings of non-target w ildlife involving brodifacoum and difethialone occur in urban and suburban areas, suggesting th at use of products containing brodifacoum and difethialone in these areas pose sign ificant risk to non-target wildlife. These adverse effects could be substantially reduced if the quantity of brodifacoum and

difethialone introduced in to the environment were reduced. Registered rodenticide products containing other active ingredients can provide essentially the same level of control of rodent infestations, within essentially the same time fram e, and with essentially the same level of effort, at essentially the same cost, and without the higher risks associated with brodifacoum and

difethialone.

### ~ 133 ~ Inasmuch as rodenticides containing the ac tive ingredients bromethalin, chlorophacinone, diphacinone, and warfarin are effective, afford able, and cause significantly less risk to the environment, EPA concludes that the risks caus ed by residential consumer use of rodenticide products containing brodifacoum or difethial one active ingredients cause risks that are unreasonable. Accordingly, the fo llowing rodenticide products regi stered for general consumer

use for the control of commensal rodents in and around buildings s hould be cancelled:

D- MOUSE PRUFE II, EPA Re g. No. 3282-65 (brodifacoum) D- PELLETS GENERATION II, EP A Reg. No. 3282-66 (brodifacoum) D- BAIT PELLETS II, EPA Reg. No. 3282-74 (brodifacoum) D- READY MIXED GENERATION II, EP A Reg. No. 3282-81 (brodifacoum) D- MOUSE-PRUFE III, EPA Re g. No. 3282-85 (difethialone) D- BAIT PELLETS III, EPA Re g. No. 3282-86 (difethialone) D- II READY MIX BAITBITS III, EP A Reg. No. 3282-87 (difethialone) D- BAIT PACKS III, EPA Re g. No. 3282-88 (difethialone) In addition, EPA denies applications fo r registration of the following products: D-CON BAIT STATION XV KILLS MI CE, EPA Application No. 3282-RNU (brodifacoum) D-CON BAIT STATION XV KILLS MI CE, EPA Application No. 3282-RNL (brodifacoum) EPA denies these applications on account of the same risk c oncerns that are the basis for the cancellation of the products de scribed above, and in addition, not es that because no one is currently relying on these unregiste red products for rodent control, denial of these registrations does not cause any impacts to consumers. Nor does denial result in any loss of future benefits that are not available through ot her registered products that do not cause unreasonable adverse

effects.

### ~ 134 ~ B. Cancellation and Denial of Regist ration of Rodenticides Intended for Residential Consumer Use In Contro lling Commensal Rodents In and Around Buildings In Forms That Do No t Adequately Protect Against Access By Children, Companion And Domesticated Animals, And Non-Target Wildlife.

Rodenticide baits are dir ectly accessible to children, domestic animals and non-target wildlife, unless the bait s are placed where children, domestic animals and non-target wildlife

cannot reach them or unless the baits are enclosed in bait stations that effectively prevent access by organisms larger than the target pests. In prac tice, it is difficult to pl ace rodenticides in or around residential structures in places where ch ildren, domestic animals and non-target wildlife

cannot reach them. Even if rodenticides are in itially well placed, rode nts often move unsecured, small-particle baits (e.g., pellets, granules, grain, meal) to other locations, which may be readily accessible to children, domestic animals and non-target wildlife. The labels of each of the rodenticide produc ts subject to the NOIC prohibit placement where children, domestic animals and non-target wildlife can reach them, unless they are enclosed in bait stations that qua lify as tamper resistan t. Although such bait stations exist, they are marketed primarily to commercial users, and they are seldom, if ever, available for purchase in retail stores where residential consumers typi cally purchase rodenticid es. Consequentially, the widespread and commonly recogn ized practice of residential consumers has been to apply rodenticides without tamper resist ant bait stations, in locations th at in many instances fall short of label requirements prohibiting placement where children, domestic animals and non-target

wildlife can reach them. That practice is becoming less common as registrants introduce new RMD-conforming products, but it likely continue s unabated among purchasers of the products

### ~ 135 ~ subject to the NOIC. Although some residential consumers might purchase tamper resistant bait stations from the companies that supply them to commercial users, EPA believes that the number who do so is negligible in comparison to the num ber who do not. Moreover, the products subject to the NOIC are not designed or expected to fit securely in such thir d-party bait stations. The primary exposures of children, domes tic animals, and non-target wildlife to rodenticides, and the resultant risks, can be substa ntially reduced if the bait is contained in a bait

station that meets the standards of the RMD. The RMD describes four types of bait stations varying in terms of resistance to children, dogs, and weather:

• Tier 1 - Tamper-Resistant and W eather-Resistant: These bait stations are resistant to weather and to tampering by children and dogs . Tier I bait stations meet the tamper resistance and weather resistance standards se t forth in Pesticide Registration Notice 94- 7, and have also satisfactorily demonstrated the ability to isolate bait from children and dogs in laboratory testing c onforming to EPA protocols.

• Tier 2 - Tamper-Resistant (but not weather resistant): Tier 2 bait stations have satisfactorily demonstrated the ability to isol ate bait from children and dogs in laboratory testing conforming to EPA protocols. Tier 2 ba it stations have not met weather resistance standards; therefore, ro denticide bait products that include Tier 2 bait stations must be labeled for indoor use only.

• Tier 3 – Tamper-Resistant for Children Only: Tier 3 bait stations have satisfactorily demonstrated the ability to isolate bait from children in laboratory testing conforming to EPA protocols. Tier 3 bait stat ions have not demonstrated the ability to isolate bait from dogs and have not met weather resistance standa rds; therefore, rode nticide bait products that include Tier 3 bait sta tions must be labeled for indoor use only and to prohibit placement where the product is accessible to dom estic animals and/or non-target wildlife.

• Tier 4 - Tamper-Resistance Unknown: Tier 4 ba it stations have not been demonstrated to meet the testing standards required of the hi gher tiers, but must be made of a material of sufficient rigidity such that the station is not easily crushed or opened by a child less

### ~ 136 ~ than 6 years of age, not easily chewed by targ et rodents, and not reas onably anticipated to release rodenticide bait except for bait remove d by target rodents and minor quantities of crumbs created by target rodents. Roden ticide bait products that include Tier 4 bait stations must be labeled for indoor use onl y and to prohibit placement where the product is accessible to children, domestic animals and/or non-target wildlife.

1. Rodenticides in bait stations that meet the standards of the RMD are effective alternatives to rode nticides without bait stations. In order to be registered in the U.S. for use in and around residen ces and other buildings, rodenticide baits – whether formulated as blocks, pellets, meal, etc. – must meet the same criteria in laboratory efficacy trials. Rodenticide products purchased by professional applicators (including public health offici als, pest control operators (PCOs), and other occupational applicators) are overwhelmingly in block fo rm (Lublinkhof 2012). There is no basis for presuming that pelleted or meal baits offer fa ster control or a highe r degree of control. Bait-stations are widely used by professional applicators and effective rodent control has been achieved using bait stati ons in a wide variety of circ umstances (Kaukeinen and Marsh 2009). For several decades, pesticides registered for use to control commensal rodents have had label statements requiring use in tamper-resistant (or tamper-proof) bait stations where placements otherwise would be accessible to childr en, pets, domestic animals, and/or non-target wildlife, and commercial and professional users ge nerally achieve effective rodent control while complying with this requirement. Some rodents (particularly Norway rats) are wary of any new objects in their environments, and may avoid a newl y introduced bait station for a period of time, however, the delay in initial entry is small comp ared to the variability in the other factors affecting the length of the treatm ent period needed to achieve cont rol of an infestation even

### ~ 137 ~ without bait stations. Conseque ntly, any delay in entry is un likely to cause an measureable increase in the time required to control a rat infestation.

2. Rodenticides in bait stations that meet the standards of the RMD are affordable alternatives to rode nticides without bait stations. Most residential consumers will not be affected by the proposed removal of rodenticides

without bait stations from the re sidential consumer market, because most residential consumers use mechanical methods of control, which will no t be affected by the proposed cancellations. Likewise, residential consumer s who prefer to use rodent control services provided by professional and commercial appl icators will not be affected by the proposed cancellations. Professional users (e.g., PC Os, commercial users, property ma nagers, public health officials) generally have access to tamper-resistant bait stati ons (required by existing rodenticide labels for use outdoors and where placements otherwise would be accessible to children, domestic animals, and/or non-target wildlife) and will continue to have access to many registered rodenticides intended for use in those bait stations, and in addition, will continue to have access to rodenticides formulated as pell ets, granules, grains, and meal if special circumstances might warrant their use. Inasmuch as these professiona l users will not be affected by the cancellations,

neither will residential consumer s who rely on thei r services. The only users likely to be affected by th e proposed cancellations are those residential consumers who purchase and use rodenticides fo r control of commensal rodents in and around buildings, and who prefer one or more of the products subject to the NOIC. Most such residential consumers are likely to experience only modest cost increases as a consequence of the proposed cancellation of rodenticid e products registered for the c ontrol of commensal rodents in and around buildings products with out bait stations conforming to the RMD criteria, because

### ~ 138 ~ there are multiple altern ative rodenticide produc ts conforming to the RMD and marketed at prices comparable to those of the products EPA pr oposes to cancel. And to the extent that these households have, or are visited by, young children and/or pets, they are already required to be using products in bait stations and the potential cost impact of the cancellation action on these

users should not be relevant to the cancellation decision. Mo reover, by making bait stations more easily available (and possibly cheaper as they become more available), the cancellation action may actually economically benefit lo wer income households with young children. For residential consumers currently using rode nticide products that do not conform to the RMD to control mice, data from a recent nationa l market survey shows the cost per placement for rodenticide products that in clude disposable bait stations for mice was $1.63 while the cost per placement for pellet products was $1.66, suggesting that consumers would face no

incremental costs associated with the cancellation of the registrati ons of pelleted products (IRI, 2012a). For the much smaller number of reside ntial consumers attemp ting to control rats (approximately10% of the consumer rodenticide market), the data suggest that some cost increases are likely. EPA estimates that the change in costs resulting from the proposed cancellations will range from $46 in a minor infestat ion to up to $92 in a major infestation. EPA has compared these changes in costs against monthly non-housing income for a family at the poverty threshold. For mouse control, incremental costs for control of a minor infestation would range from zero to two percent of monthly non-h ousing income at the povert y threshold. For rat control, incremental costs for consumers at th e poverty threshold range from five percent of monthly non-housing income in a minor infestation to 11 percent in a major infestation. Because those low income households facing rodent problems overwhelmingly have mouse problems (88% of rodent infestations are mice, per Ce nsus Bureau, 2011), it is expected that impacts on

### ~ 139 ~

most low-income residential consumers will be equivalent to zero to two percent of monthly non-housing income. Moreover, because less than ten percent of low income households report having seen signs of rodents within the precedin g three month period, it is a small proportion of

low income households that woul d be subject to this burden. Finally, in considering whet her the risks posed by these rodenticide products are unreasonable, EPA does not believe it appropriate to attribute any significance to potential cost increases for consumers who are currently using th e products subject to th e NOIC in violation of their label requirements, i.e., in circumstances where children, domestic animals, or non-target wildlife can get access to the product. Such uses pres ent unreasonable risks and cannot reasonably be viewed as benefits to society that would be lost as a result of the cancellations.

3. Rodenticides without bait stations ca use adverse effects to children, nontarget wildlife and domesticated and companion animals that could be avoided.

Bait stations that conform to the standards of the RMD are designed to prevent children, domestic animals and non-target wildlife from being able to come into contact with rodenticides. The rodenticide products proposed for cancellation lack significant engineering controls against contact by children, domestic animals and non-target wildlife, and therefore rely on users to only place the rodenticides where they would not be accessible to children, domestic animals, and/or non-target wildlife in order to prevent exposure and ingestion of roden ticides. Use of a bait station that substantially reduces exposure to the bait plainly poses less risk to children, domestic animals and non-target wildlife risk than presenta tions that allow direct contact with the bait. Many thousands of incidents of children being exposed to rodenticides have been reported. Although most exposures generally result in no clinical harm, these events are not risk-

### ~ 140 ~ free and should not be taken ligh tly. The high numbers of reports of exposed children are of concern because every exposure event presents th e possibility of significant adverse health effects. Approximately 85% of the rodenticide exposures repo rted to AAPCC involved children under 6 years old (i.e., approximately 15,000 per year during the period1999-2009; approximately 11,000 in 2010). These incidents may have resulted from failure to follow label directions to keep bait away from children, t hough in some cases, baits might have been moved by rodents from appropriate placement locations. In some cases, it appears that parents underestimated children’s abilities to access place s where rodenticides were applied. In other cases, it appears that the exposed children we re visiting a different environment (such as grandparents, friends, or neighbors) and their parent or guardian wa s unaware that the baits were accessible. Every child’s exposure event is of concern, because any time a child can access rodenticide bait, there is the potential for the child to swallow an amount sufficient to cause

adverse effects. Of the rodenticide incidents to reported to AAPCC from 1999 to 2005, approximately one percent of exposed children (an average of 128 cases per year) experienced a medical outcome classified by AAPCC as minor, moderate or major. Such symptomatic exposures – diagnosed or undiagnosed – are a matter of concern, both for the symptoms themselves and (in the case of anticoagulants) on accoun t of the risk of excessive bleed ing (internally or externally) in response to subsequent trauma. The advers e health consequences of these symptomatic exposures could be prevented throug h the use of tamper resistant bait stations, as could the social

and economic costs that arise from addre ssing children’s asymptomatic exposures to rodenticides, including economic costs to health care facilities and poi son control hotlines, and

social and economic costs to the fam ilies whose childre n are exposed.

### ~ 141 ~ EPA’s analysis shows that, unless use and e xposure patterns are ch anged, children could easily ingest quantities of the subject rodenticides that would contain suff icient amounts of active ingredient to exceed levels that EPA would cons ider safe. A single 5 gram bite (less than a quarter of an ounce) of any of the rodenticid e baits subject to the NOIC would result in a pesticide exposure that greatly ex ceeds levels considered safe as a dietary exposure for a child weighing 10 kg, and the quantity of active ingredient containe d in a single placement of rodenticide baits subject to the NOIC is sufficient to cause adverse health effects. Consequently, EPA could not conclude that expo sure to the subject rodenticides was reasonably certain not to cause harm. EPA fully appreciat es that the rodenticide products at issue are governed by the

FIFRA risk-benefit standard rather than the FFD CA reasonable certainty of no harm standard, and that any hearing on th e NOIC must consider the benefits of rodenticide use against the risks of such use. Nevertheless, the FFDCA criteria fo r unsafe exposures to pesticides in food provide a meaningful benchmark: If Congress would not allow these levels of pesticide exposure in food – no matter how beneficial the pes ticide use might be to agricultura l producers – it is reasonable

to infer that children should not suffer the same levels of exposures through other routes absent important countervailing benefits. Rodenticides are implicated in numerous reported accidental poisonings of domestic animals, which have the potential to result in de ath and other severe outcomes that have required veterinary care. In 2010, APCC identified rodentic ides as the third most likely cause of pet poisonings and the Pet Poison Helpline identified rodenticides as the third most common toxin involved in dog poisonings and the fourth most common toxin involved in cat poisonings. OPP’s IDS identifies two rodenticides (brodifaco um and bromadiolone) in the top 20 pesticides most likely associated with a domestic animal fata lity. OPP’s IDS indicates that in recent years

### ~ 142 ~ there are about 2000 reported incide nts per year of domestic anim als exposed to rodenticides. Many of these exposures result in severe outco mes -- on average 14% result in death or a major outcome -- which may necessitate veterinary care. The IDS data indicate that about 160 severe (death or major effect) domestic animal incidents attributable to rodenticides are reported every year, which EPA believes significantly underest imates the actual number of incidents. The various lines of evidence evaluated by EP A have led the Agency to conclude that risks to non-target wildlife from all the rodenticides addressed in the NOIC are significant. There is little question that non-target wildlife are being exposed to r odenticide bait products. Incident reports and exposure studies make clear that a wide range of mammalian and avian wildlife can

come into contact with the rodenticides from primary exposure, and these primary consumers can put predator and scavenger species at risk of secondary exposure. EPA’s quantitative assessment and the incident data provide eviden ce that rodenticide exposure causes non-target wildlife deaths. Although many non-target wildlife species av oid areas of human habitation, significant numbers of incidents of both primar y and secondary rodenticide poisonings of nontarget wildlife occur in urban and suburban areas. These data suggest that residential and

commercial uses of rodenticides for commensal r odent control pose significant risk to non-target

wildlife. Moreover, regardless of collection location, autopsies and biopsies of predatory and scavenging wildlife routinely show accumulation of rodenticide residues in liver tissue of numerous predatory and scavenging wildlife specie s, including owls, eagle s, hawks, vultures, mustelids, bobcats, and mountain lions. Nume rous monitoring studies conducted throughout the United States have found SGARs present in over 85% of individuals of one or more species studied. The prevalence of SGAR s in wildlife regardless of location of collection indicates that

### ~ 143 ~

rodenticides used in and around bui ldings for control of commensal rodents (the only lawful uses of SGARs) affect predatory and scavenging wildlife everywhere. Bait stations conforming to the RMD can prevent primary exposures to birds and to mammals larger than mice and rats by preventing th em from direct access to the bait. While bait stations cannot prevent secondary exposures to intoxicated prey, ba it stations can ensure that fewer intoxicated birds and mammals are available as prey.

4. Conclusion. The rodenticides subject to the NOIC are poi sonous to all mammals and birds. Exposure to these rodenticides is widespread among childre n, domestic animals, and non-target wildlife. If

rodenticides continue to be av ailable in the residential consum er market without bait stations, these exposures are likely to continue. Bait stations conforming to the RMD crit eria can significantly reduce rodenticide exposures among children, domestic animals, and non-target wildlife, co mpared to products without bait stations conforming to the RMD crite ria. EPA has determined that control of commensal rodents in and around buildings by residential consumers can be satisfactorily accomplished with rodenticides protected by bait st ations. For many years, labels for commensal rodenticides have required th at baits used where children, do mestic animals, and non-target wildlife might be exposed must be placed in tamper-resistant bait stations. Registered rodenticide products that include bait stations that meet the RMD criteria are now available on the market at costs comparable to the rodentic ide products subject to the NOIC, and, when used in combination with prudent san itation and exclusion measures, are effective for the control of commensal rodents in and around buildings.

### ~ 144 ~

Inasmuch as rodenticides in bait stations that meet the standards of the RMD are available, effective, affordable, and cause sign ificantly less risk to ma n or the environment, rodenticide products intended to control comm ensal rodents in and around structures and marketed for general consumer use cause unreasona ble risks unless they in clude a bait station

that meets the standards of the RMD. Accordingly, EPA proposes to cancel the following rodenticide products registered for the control of commensal rodents in and around buildings products without bait stations c onforming to the RMD criteria:

D-CON CONCENTRATE KILLS RATS & MICE , EPA Reg. No. 3282-3 (warfarin) D- READY MIXED KILLS RATS & MI CE, EPA Reg. No. 3282-4 (warfarin) D- MOUSE PRUFE KILLS MICE, EPA Reg. No. 3282-9 (warfarin) D- PELLETS KILLS RATS & MICE, EPA Reg. No. 3282-15 (warfarin) D- MOUSE PRUFE II, EPA Re g. No. 3282-65 (brodifacoum) D- PELLETS GENERATION II, EP A Reg. No. 3282-66 (brodifacoum) D- BAIT PELLETS II, EPA Reg. No. 3282-74 (brodifacoum) D- READY MIXED GENERATION II, EP A Reg. No. 3282-81 (brodifacoum) D- MOUSE-PRUFE III, EPA Re g. No. 3282-85 (difethialone) D- BAIT PELLETS III, EPA Re g. No. 3282-86 (difethialone) D- II READY MIX BAITBITS III, EP A Reg. No. 3282-87 (difethialone) D- BAIT PACKS III, EPA Re g. No. 3282-88 (difethialone)

Dated: January 29, 2013

Steven P. Bradbury, Ph.D. Director, Office of Pesticide Programs

### ~ 145 ~

VI. Citations ASPCRO/NPMA, 2013. Association of Structural Pest Control Regul atory Officials and National Pest Management Association, 2013, Rodenticide Use Survey of Pest Management Professionals, 2. http://library.constantcontact .com/download/get/file/1102861932245- 477/ASPCRO+PMP+Rodenticide+ Survey+Report+1-9-13.pdf Barnett, S.A. 1958. Experiments on ‘neophobia’ oin wild and laboratory rats . British Journal of Psychology, 49, 195-201. Batten, P. and H. Bratt. 1990. Brodifacoum: elim ination from the tissues of rats following administration of single oral doses. Unpubl. report submitted to EPA by ICI Americas, Inc., Wilmington, DE. 65 pp. Belleville, M. 1986. Toxi-kinetics and metabolism: 1. study performed with the molecule marked 14C; 2. study performed with the cold mo lecule. Unpubl. report submitted to EPA by LiphaTech, Inc., Milwaukee, WI. 133 pp. MRID# 42065010 Belleville, M. 1991. Compared hepatic kinetics of brodifacoum and di fethialone in the rat, after oral administration of 0.06 mg/kg once weekly for 4 consecutive weeks. Unpubl. Report submitted to EPA by LiphaTech, Inc., Milwaukee, WI. 39 pp. MRID# 42065009 Blondell, J. and Spann M.F. 1999. Review of Rodenticide Incident Reports Primarily Concerning Children DP Barc ode D256673, Chemical #112701, 112001, 067707, 067701, 086002, 088601. U.S. Environmental Protection Agency. Breckenridge, A.M., S. Cholerton, J.A.D. Hart, B.K. Park, and A.K. Scott. 1985. A study of the relationship between the pharmacokine tics and pharmacodynamics of 4- hydroxycoumarin anticoagulants, warfarin, dife nacoum, and brodifacoum in the rabbit. British J. Pharmacol. 84: 81.91. Brooks, J.E. (1973) A review of commensal rode nts and their control. Critical Reviews in Environmental Control , 3:4, 405-453. Buckle, A. and Prescott, C. 2012. The current status of anticoagulant resistance in rats and mice in the UK. Report from the Rodenticide Re sistance Action Group of the United Kingdom to the Health and Safety Executive , May 17, Rodenticide Resistance Action Group, 35. Bullard, R.W., R.D. Thompson, G. Holguin. 1976. Di phenadione residues in tissues of cattle. Journal of Agricultural and Food Chemistry. 24:261-263. Census Bureau (2012). Households and Fam ilies: 2010, 2010 Census Briefs. Available at: http://www.census.gov/prod/cen2010/briefs/c2010br-14.pdf Census Bureau (2011). Current Housing Reports, Series H150/09, American Housing Survey for the United States: 2009. U.S. Government Printing Office, Washington, D.C., 20401. Printed in 2011.

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CDC. 2010. Centers for Disease Control and Prevention. Rodents. Located at http://www.cdc.gov/rodents/ Accessed June 21, 2011. Clapperton, B.K. 2006. A review of current knowledge of rodent be haviour in relation to control devices. Science for Conservation 263, Scien ce & Technical Publishing, Department of Conservation, Wellington, NZ, 55 pp. Cook, C. and Hill, E. 2011. Impact assessment of th e draft notice of intent to cancel selected residential consumer rodenticide products to control commensal r odents. Biological and Economic Analysis Division, Office of Pestic ide Programs, Office of Chemical Safety and Pollution Prevention, U.S. Environmental Protection Agency, Washington, DC, 50 pp. plus appendices. Corrigan, R. M. 1997. Rats and mice. In: Handbook of Pest Control- Mallis, 8th ed. Mallis Handbook and Technical Training Company. Pp. 11-105. Corrigan, R. M. 2001. Rodent Control: A Practical Guide for Pest Management Professionals. GIE Media, Cleveland. 351 pp. Dubock, A.C. and Kaukeinen, D.E. 1978. Brodifac oum (TalonTM Rodenticide): a novel concept. Proc. 8th Vertebrate Pest Conf. (W.E. Howard and R.E. Marsh, eds.), University of California, Davis, CA, 8,127-137. Eason, C.T., M. Wickstrom, P. Turck, and G. R.G Wright. 1999. A review of recent regulatory and environmental toxicology studies on 1080: results and implications. New Zealand J. Ecol. 23:129.137. Eason, C.T. and E. Murphy. 2000. Recognising an d reducing secondary and tertiary risks associated with brodifacoum. Pages 157-163 in J. J. Johnston (ed.), Pesticides and Wildlife. American Chemical Society Symposium Series 771. Fisher, P., C. O’Connor, G. Wright, and C.T. Eason. 2003. Persistence of four anticoagulant rodenticides in the liver of laboratory rats. Doc Scien ce Internal Series 139. New Zealand Department of Conservati on, Wellington, NZ. 19 pp. MRID# 48190801 Fisher, P. 2006. Persistence of residual diphacinone concentrations in pig tissues following sublethal exposure. DOC Research & De velopment Series 249. Department of Conservation, Wellington. 19p. Gaines, T. B. 1969. Acute toxicity of pestic ides. Toxicol. Appl. Pharmacol. 14, 515-534 Hadler, M.R. and Shadbolt, R.S. 1975. Novel 4- hydroxycoumarin anticoagul ants active against resistant rats. Nature 253, 275-277. Hagan, E. C., and Radmoski. 1953. The toxici ty of 3-(acetonylbe nzyl)-4-hydroxycoumarin (warfarin) to laboratory animals. Journal of the American Pharmaceutical Association 42: 379– 382.

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