UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON D.C., 20460 

Statement of Reasons and Factual Basis for 

Notice Intent to Cancel Registrations of, and Notice of Denial of Applications for, 

Certain Rodenticide Bait Products

January 29, 2013 

This document provides the reasons and factual 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 registration applications of two rodenticide bait 

products, as required by 40 CFR §164.21(a). 

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

unreasonable adverse effects on the environment because 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 animals, 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.
   

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Further, EPA has determined that eight of the twelve registered rodenticide products also 

cause unreasonable adverse effects on the environment because they contain the active 

ingredients brodifacoum or difethialone and are sold for residential consumer use, as do the two 

products subject to denial. EPA bases this determination primarily on data and other information 

showing that these products cause unreasonable adverse 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 Notice of Denial pursuant to section 3(c)(6) of 

FIFRA. This document provides the reasons and 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 Cancellation 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 Resultant Health Effects ........................................ 31 

3. Comparison of SGAR and Bromethalin Poisonings .................................................. 34 

C. Characterization of Hazard to Domestic Animals ......................................................................... 40 

1. Sources of Domestic Animal 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 Assessment Approach .............................................................. 51 

3. Assessment Based on Calculated 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 risks ....................................................................... 87 

9. Incident Findings Related to Primary & Secondary Risk Analyses ........................... 89 

IV. Benefits ............................................................................................................................................... 100 

A. Methodology ................................................................................................................................ 102 

B. Target pests and use of rodent control measures ......................................................................... 103 

C. Usage Patterns .............................................................................................................................. 105 

D. Alternatives to Products Proposed 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 Rodenticide Products Meet the FIFRA Registration 

Criteria ................................................................................................................................................ 127 

A. Cancellation and Denial of Registrations of Rodenticides Containing Brodifacoum and 

Difethialone and Intended for Residential 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 Rodenticides Intended for Residential Consumer Use 

In Controlling Commensal Rodents In and Around Buildings In Forms That Do Not Adequately 

Protect Against Access By Children, Companion 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 requirements sufficient to allow it to determine whether 

new pesticides met the standard for registration. In 1972, Congress therefore directed EPA to 

assess all existing pesticides to determine whether 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 conducting a comprehensive review of all products 

registered before November 1, 1984 to determine whether these products had satisfied all 

applicable data requirements and the registration criteria of FIFRA section 3(c)(5). See FIFRA 

section 4(a), 7 U.S.C. § 136a-1(a). 

Shortly after passage of the 1988 amendments to FIFRA, EPA began the Section 4 

reregistration process for products registered for control of commensal rodents (i.e., house mice 

(Mus musculus), Norway rats (Rattus norvegicus), and roof rats (Rattus rattus)). These 

commensal rodents typically live in close association with humans, and are often found in and 

around homes as well as commercial establishments (Brooks, 1973; Timm 1994). The active 

ingredients in rodenticide products registered in the US to control 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 rodents that were tolerant of 

the previously developed FGARs (e.g., Hadler and Shadbolt, 1975; Dubock and Kaukeinen, 
   

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1978; Marsh, et al, 1980). FGARs currently registered 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 warfarin. 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 control in both agricultural and 

residential settings. 63 FR 48729, September 11, 1998. The “Rodenticide Cluster RED” 

contained eligibility decisions for the ingredients brodifacoum, bromadiolone, chlorophacinone, 

diphacinone, bromethalin, and pival (a FGAR for which all registrations now are canceled). The 

“Zinc Phosphide RED” addressed reregistration issues 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 reregistration unless their registrants adopted certain risk 

mitigation measures to reduce the risks they posed 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 eligible for reregistration, EPA 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 reducing exposures to children and pets” and to 

 

2

 The second generation anticoagulants, difethialone and difenacoum, and the acute toxin cholecalciferol, were first 

registered after November 1, 1984, and therefore were not subject to reregistration. 
   

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“develop workable mitigation measures to adequately protect children from accidental 

rodenticide exposures.” Id. at viii and 112. The group’s objectives included discussing long-term 

risk reduction measures and “decid[ing] on specific timing and other issues associated with bait 

dyes [and] bittering agents.” Reregistration Eligibility Decision for Zinc Phosphide (July 1998). 

In 1999, EPA formed the Rodenticide Stakeholders Workgroup (RSW) as a subcommittee of the 

federally-chartered advisory group, the Pesticide 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 Columbia 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 Association of Poison Control Centers, the National 

Pest Control Association, and several registrants of rodenticide products. 

The findings and recommendations of the RSW are contained in the November 15, 2000 

report, Recommendations for Managing Rodenticide Exposures to Children in the Home. EPA 

adopted those recommendations in a 2001 amendment 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 taste (via a bittering agent) and an indicator dye to rodenticide bait 

products registered for use in and around homes or at other sites where children might encounter 

them. An environmental group successfully challenged 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.
   

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EPA’s concerns regarding the effects of rodenticides on non-target wildlife also 

continued after issuing the 1998 REDs, leading the Agency to conclude that further evaluation of 

the ecological risks of rodenticides was necessary. As part of this work, the Agency developed a 

comparative ecological assessment for nine4

 rodenticide active ingredients. Between October 

1999 and December 2001, the comparative risk assessment 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 assessment, 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 associated with rodenticide products and EPA’s 

preliminary position on appropriate risk reduction 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 ecological 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).
   

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such bait products containing the SGAR active 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 Mitigation Decision at 4. Further, to decrease the 

possibility of children’s exposure to any rodenticide products used in homes, EPA proposed 

requiring that all commensal rodenticide bait products 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 mitigation measures for 120 days and received 

extensive comments from a wide range of stakeholders. During this comment period, the 

Rodenticide Registrant Task Force 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 difethialone. Brodifacoum also was implicated in a high percentage 

of reported non-target wildlife incidents. EPA concluded that if the lower toxicity and less 

persistent active ingredients replaced the higher toxicity and more persistent active ingredients 

for a portion of this market, there would be significant reduction in the adverse effects to nontarget wildlife. Based on the restrictions some municipalities place on restricted-use pesticides 

and concerns about imposing additional regulatory burdens on the poultry, livestock and pest 

control operator industries, and recognizing the importance of SGARs to these industries, EPA 

decided to employ sale and distribution limitations – rather than restricted-use classification – to 
   

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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 court’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 containing any of ten 

listed active ingredients. Among other things, EPA stated 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 come into contact with bait. RMD at 17-18. EPA also 

stated that rodenticides containing SGARs pose significant risks to wildlife and the environment, 

and that rodenticides containing those compounds 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 mitigation measures listed in the RMD, it “would 

present unreasonable risks inconsistent with FIFRA” and therefore should not remain registered. 

RMD at 15. 

The May 28, 2008, RMD announced EPA’s conclusions about rodenticide safety and 

signaled EPA’s intentions for the future completion of the reregistration process, but did not 

change the legal status of any rodenticide product. 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. 
   

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immediately remove from the market rodenticides that did not incorporate the specified 

mitigation measures. Instead, EPA asked registrants to adopt those mitigation measures 

voluntarily, on a schedule that would 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 rodenticide risks. Today, only twelve rodenticide products, all produced 

by Reckitt Benckiser, Inc., fail to meet the risk mitigation 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 these 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 rodenticide 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 February 4, 2011, EPA notified Reckitt Benckiser, Inc. 

(Reckitt Benckiser), of deficiencies in applications for two products (designated as 3282-RNL 

and 3282-RNU), and offered Reckitt 75 days to correct those deficiencies. Reckitt Benckiser’s 

April 19, 2011 response indicated that additional data to support their application would be 

submitted no later than May 20, 2011. Reckitt Benckiser’s May 20, 2011, letter offered several 

arguments supporting the applications, and provided revised draft labels that would prohibit 

outdoor use. Because these products do not meet the risk management goals of the RMD, EPA 
   

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is formally denying the applications for registration of those products. 

 Certain rodenticide registrants who have disagreed with the Agency’s positions regarding 

rodenticides have challenged aspects of the Agency’s actions in two court cases; however, 

neither case has addressed the merits of the scientific, economic, and 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 certain 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, generally 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 form7 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.
   

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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 mitigation measures that, if adopted, would 

make existing rodenticides eligible for reregistration. EPA is now proposing to cancel the 

rodenticide products identified above based on two of the most significant mitigation measures 

identified in the RMD: Removing SGARs from residential consumer products, and assuring that 

rodenticides available to residential consumers include bait stations designed to prevent children, 

domestic animals and non-target wildlife from being able to come into contact with the bait. 

Although the mitigation measures identified in the RMD are designed to act in concert, with each 

measure contributing towards safer outcomes, the bait station requirement is expected to protect 

children, domestic animals and non-target wildlife from exposures to commensal rodenticides 

generally, while the exclusion of SGARs from the homeowner market is expected to reduce 

environmental loading of SGARs and thereby reduce secondary poisonings among non-target 

wildlife. As currently labeled and sold, each of the rodenticide products identified above causes 

unreasonable risks to man or the environment owing to the lack of one or both of these 

mitigation measures. Individual products may also fail to meet the FIFRA registration criteria for 

other reasons. In order to focus a hearing on the most critical risk mitigation issues, the proposed 
   

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cancellations and the denials are based only on the presence of SGARs in products marketed for 

general consumer use in controlling commensal rodents in and around buildings, and/or on the 

rodenticide products being in forms that do not adequately protect against access by children, 

companion and domesticated animals, and non-target wildlife. 

EPA is proposing to cancel the registration of twelve rodenticide products sold in the 

general consumer market, and deny the applications for registration of two additional such 

products. The scope of this action is very narrow. Commercial, agricultural and professional 

users (including public health officials, pest control operators (PCOs), and other occupational 

applicators) are not affected because they are not significant users 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 cancel. Since its inception, EPA has 

been concerned that children, pets, and non-target wildlife are being unnecessarily exposed to 

rodenticides. This concern was expressed in Pesticide 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 Notice 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 animals, and/or non-target wildlife. Most of the 

children and pet incident concerns are occurring in and around homes, 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. These 

incidents can be significantly reduced if rodenticide products sold on the general consumer 
   

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market include bait stations designed to prevent 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 determined that it is appropriate to limit use of 

products containing the more toxic and persistent anticoagulants brodifacoum and difethialone. 

EPA has determined that the risks of use by residential consumers of rodenticides containing 

brodifacoum and difethialone outweigh the benefits of such use. There are over 30 alternative 

rodenticide products registered for sale in the general consumer market 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 addition, residential consumers also have access to 

mechanical control methods as well as the services of PCOs who will continue 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 commercial buildings, and in connection with 

agricultural and food processing establishments 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 professional, commercial or agricultural users. Products 

registered for the control of other types of rodents are also outside the scope of the NOIC. 

In making the determination that the products 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 stations designed to prevent 
   

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children, domestic animals and non-target wildlife from being able to come into contact with 

bait. For four of the products EPA proposes to cancel and the two applications EPA is denying, 

this determination additionally relies upon the substantial and well documented risks to nontarget wildlife from primary and secondary exposures to the active ingredients brodifacoum and 

difethialone. EPA also considered evidence and analyses relating to the benefits of continued use 

of the rodenticide products identified in the NOIC, and has determined that, based on the 

availability of adequate and affordable alternative rodenticide products and methods of 

commensal rodent control, the benefits linked specifically to the products identified in the NOIC 

are, at best, minimal. However, given the potential for exposure these products pose to children, 

coupled with risks to domestic animals and wildlife in the absence of further mitigation, EPA 

believes that this cancellation action would be warranted even if the anticipated costs of rodent 

control as a result of this action were somewhat greater than EPA has estimated. Accordingly, 

EPA is issuing a Notice of Intent to Cancel and a Notice of Denial of registrations of the 

consumer-use commensal rodenticide 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 Rodenticide 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 insecticides where adverse effects on mammals are 
   

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often different in nature than their effects on target pests. Rodenticides 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, diphacinone, diphacinone sodium salt, warfarin, and 

warfarin sodium salt, disrupt the production in the liver of vitamin K dependent bloodclotting factors II (prothrombin), VII, IX, and X, interfering with blood clotting and causing 

hemorrhages. Due to the long half-lives of the vitamin K-dependent clotting factors, the 

anticoagulant effect does not result in rodent mortality until after several days of ingestion. 

The onset of lengthened prothrombin time (PT) from 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 agents also increase permeability 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 rodents that consume the 

amount of bait equivalent to a single night’s feeding. 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 usually begin several days after ingestion, because 

of the long half-life of the 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 production of adenosine-5'-triphosphate (ATP) in the cells 

of the central nervous system by uncoupling oxidative phosphorylation in the 

mitochondria. Low levels of ATP reduce the efficiency of the enzyme Na/K ATPase, 

leading to increased intracellular sodium levels. 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 include headache, dizziness, nausea numbness, 

weakness, loss of coordination or balance, altered level of consciousness, respiratory 

depression, seizures, and death. 

• Cholecalciferol increases calcium absorption from food, and mobilizes calcium from bone 

which leads to hypercalcemia (increased calcium levels in blood). Hypercalcemia can 

cause formation of calcium crystals in internal 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 cholecalciferol poisoning may include fatigue, 

weakness, nausea, anorexia, headache and irregular heartbeats (Goldfrank et.al, 2010). 

Acute renal tubular injury due to hypercalcemia may cause excessive urination, increased 

water intake, protein in urine and increased 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 phosphine gas when it comes in contact with 

acids or water. Phosphine is thought to produce toxicity by blocking 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 jaundice 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 myocardial damage (Reigart J.R., 1999). 

B. Characterization of Hazard to Human Health 

The products subject to the NOIC each contain one of three rodenticide active 

ingredients: warfarin, brodifacoum, and difethialone. Warfarin 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 phosphorylation whose effects are manifested as 

cerebral edema. The symptoms of anticoagulant poisoning can be treated with vitamin K1, 

although the SGARs may require repeated administration 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 poisoning, however clinicians and veterinarians can 

treat the symptoms of bromethalin toxicity in the 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 block the production of active vitamin K which is essential 

for the synthesis of several clotting factors. The first sign of anticoagulant poisoning is an 

increase in the time it takes blood to clot (prothrombin time), although this would only be 

observed through tests in a medical facility. Because it takes time for the body’s ordinary 

metabolic processes to clear vitamin K-dependent 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 from almost any tissue 

such as gums, nose, urinary tract, gastrointestinal tract, etc. Patients 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. Symptoms resulting from FGAR exposure are likely to pass within 

24 hours with treatment; symptoms of SGAR exposure could persist for months, even with 

treatment. 

A fourth active ingredient, bromethalin, is also relevant to the Agency’s cancellation 

decision, inasmuch as that decision is based on the comparative risks of the products subject to 

the NOIC and the registered, available alternative rodenticide products. Bromethalin is not an 

anticoagulant and produces no unique or definitive symptoms, but instead produces the same 

constellation of potential symptoms as other uncouplers of oxidative phosphorylation. At low 

doses, a poisoned individual might exhibit fever, vomiting, dizziness, mental confusion or 

dullness. At higher doses, as cerebrospinal pressure increases, there may be indications of 

weakness in limb strength. Very high doses can cause general paralysis or convulsions, and 

ultimately death. These effects are likely to become 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 values and other relevant parameters reported in the studies. 

Warfarin. Warfarin is a FGAR. The acute oral LD50 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 LD50s for warfarin: “Reported oral LD50 values for warfarin in rats vary by a 

considerable magnitude. Values of 11 mg/kg body weight (Lund, 1982), 58 mg/kg body weight 

(Thomson, 1988) and 58 mg/kg (female) and 323 mg/kg (male) (Hagan & Radomski, 1953) have 

been reported.” (http://www.inchem.org/documents/ehc/ehc/ehc175.htm). Another study reports 

a large difference between the acute toxicity of warfarin to male and female rats with the LD50 

for males reported to be between 450 and 680 mg/kg and the LD50 for females reported as 

between 5 and 10 mg/kg (MRID 00143093). 

Brodifacoum. Brodifacoum is a SGAR. The oral (gavage) LD50 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 (MRID 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 revealed 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 the known anticoagulant activity of 

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

 

8 The LD50 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 and 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 half life of difethialone in rat liver from a single oral dose at 

0.5 mg/kg is 175 days for males and 98 days for females (MRID 42065010). In an acute lethality 

study, the oral (gavage) LD50 of difethialone in rats was 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 died at 0.8 mg/kg. The two acute studies are 

consistent with each other and support an LD50 value of 0.55 mg/kg for 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 LD50 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) (MRID 44775101). Another study (MRID 00241521) lists 

the LD50 for females as 9.1 mg/kg and the LD50 for males as 10.7 mg/kg. 

EPA routinely characterizes the risk to humans posed by pesticides with uses in or around 

the home. An important part of a residential assessment 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 residues (hand to mouth activity), or by mouthing an object with 

pesticide residue on it, or by picking up and eating solid particles 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 available toxicity data 

and other information such as physical and chemical properties of the pesticide, and activity 

patterns of potentially exposed persons, EPA estimates a level of exposure that would not cause 

harm (referred to in this analysis as the “exposure level of concern”), and compares that level to 

the amount of exposure people would get as a consequence 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 and Cosmetic Act (FFDCA), although in that 

context, the safety of the exposure is considered independently of any pesticidal benefits. 

EPA relies primarily on toxicity studies conducted 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 matches 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 available for the subject rodenticides are acute LD50 studies. 

Acute LD50 studies are not designed to identify sublethal toxic effects, 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 LD50. However, in the absence of a more appropriate toxicity 

data, the acute oral LD50 studies were used as the effect of concern for this assessment. 
   

~ 25 ~ 

 

To derive an exposure level of concern, EPA typically divides the point of departure (i.e., 

the exposure level that corresponds to the toxic effect of concern, here the acute oral LD50) by 

appropriate uncertainty factors. The uncertainty factors are intended to account for possible 

differences in sensitivity between humans and laboratory animals, for differences between 

humans, and in this case, to account for the likelihood of sublethal adverse effects. Using these 

uncertainty factors, EPA identifies a level of exposure that, with reasonable certainty, would not 

cause harm to humans because the difference between predicted exposures and the levels that 

cause adverse effects is large enough that no harm 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, the amount of the exposure and the 

sensitivity of the individual person. To address the possibility that the pesticide may generally be 

more toxic to humans than animals and the possibility that variations in human sensitivity may 

be greater than seen in the test animals, the Agency 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 additional uncertainty factors to account for the 

limitations of the toxicity database including the absence of a “no observed adverse effect level” 

(NOAEL). 

Owing to the paucity of data on sublethal effects 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 toxicity database with appropriate studies of 

sublethal effects with clearly established NOAELs, EPA would apply to that endpoint an 

uncertainty factor of at least 100 (i.e., a level of concern 100 times lower than the NOAEL) for 

each active ingredient to account for interspecies and intraspecies variability. If EPA had all the 
   

~ 26 ~ 

 

same studies, but the study showing the most sensitive 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 toxicity effect of concern (death) is severe and 

its relationship to sublethal acute adverse effects is unknown. In view of these uncertainties, EPA 

is unable to say with confidence that there is any finite level of exposure to the subject 

rodenticides that can be considered reasonably likely to cause no harm. Nevertheless, with the 

caveat that this undoubtedly understates the risks of sublethal adverse effects, Table 3 below 

shows the LD50 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 LD50s. 

Table 3. Surrogate Exposure Level of Concern 

Rodenticide LD50 

(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 their 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 bite (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 issue greatly exceeds possible safe 
   

~ 27 ~ 

 

levels, without even considering potential sublethal effects. Table 4 below shows how the 

estimated child exposure from taking one bite of rodenticide bait compares to the surrogate 

exposure levels of concern for each of the subject rodenticides. 

Table 4. Surrogate Exposure Level of Concern 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 toxicity data is consistent with information 

from reports of incidents of human poisonings. Children who have accidentally ingested 

quantities of the subject rodenticides have displayed symptoms that 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. Accidental ingestion of anticoagulants can lead to coagulopathy 

(impairment of the body's ability to stop bleeding) in a child; although the child is initially 

asymptomatic they have the potential to bleed excessively (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 their ability to stop bleeding is impaired. 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, unless use and exposure patterns are changed, 

children could easily ingest quantities of the subject rodenticides that would contain sufficient 

amounts of active ingredient to exceed levels that EPA would consider 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 risks of such use. Nevertheless, 

the FFDCA criteria for 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 pesticide use might be to agricultural producers – it is reasonable to infer that 

children should not suffer the same levels of exposures through other routes 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 been 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 frequent exposure of children to rodenticides, 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 toxicity 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 effects and exposure of registered pesticides may 

be collected and analyzed. In assessing the risks of products subject to the NOIC, EPA analyzed 

human observational data, or incidents, from the following sources: summary data from the 

American Association of Poison Control Centers (AAPCC), human incident (poisoning) data 

from such sources as OPP’s Incident Data System (IDS) database, National Institute for 

Occupational Safety and Health (NIOSH) Sentinel Event Notification System for Occupational 

Risks (SENSOR), the EPA-sponsored National Pesticide Information Center (NPIC), 

California’s Pesticide Incident Surveillance Program (PISP), and additional review of the open 

literature. 

Incident data can provide important information about actual real-world exposures and 

risks associated with pesticide products. Incident data are collected systematically, but 

differently, by a number of organizations. The databases used by the Agency differ with respect 

to such issues as coverage, certainty/confidence, fields/parameters reported, and usability. These 

five pesticide incident data sources in combination with additional data from the open literature 

provide useful content and historical 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 additional utility and were not relied upon for the development of 

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

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

~ 30 ~ 

 

In regard to children’s exposures to household products such as rodenticide baits, the 

AAPCC reports are the most applicable and complete, 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 discerning trends and patterns in incident poisonings 

associated with the following rodenticides used for commensal rodent control in bait form: 

brodifacoum, bromadiolone, bromethalin, chlorophacinone, cholecalciferol, difethialone, 

diphacinone, diphacinone sodium salt, warfarin, warfarin sodium salt, and zinc phosphide. 

Although these incident reporting databases can provide important information regarding the 

frequency, distribution and severity of adverse effects, they are far from comprehensive. EPA 

estimates that only one quarter of the total number of pesticide poisoning incidents are reported 

to the AAPCC or state counterparts. (Blondell and Spann, 06/03/1999, D256673). 

The AAPCCis a non-profit, national organization 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 control center are answered by a medical professional 

trained to answer questions about poisons. Additionally, AAPCC reports provide clearly 

summarized information on pesticide incidents within the context of other poisoning events. 

AAPCC produces an annual summary report giving statistics and information on all the 

poisonings reported to poison control centers in a calendar year. AAPCC ranks the severity of 

human exposure incidents as follows: 

• Death, 

• Major – symptoms are life-threatening or result in residual disability or disfigurement 

(coma, cardiovascular instability, repeated seizures), 
   

~ 31 ~ 

 

• Moderate – symptoms are more pronounced, prolonged, or more of a systemic nature 

than minor symptoms with no residual disability. Usually some form or treatment is 

indicated (high fever, disorientation), 

• Minor – symptoms are minimal with no residual 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 sources, as well as the open literature, 

rodenticides are found to be involved in numerous reported incidents, especially those involving 

children less than 6 years old. While all the sources (IDS, NPIC, PISP, NIOSH SENSOR) 

demonstrated that humans are being exposed to rodenticides, it is most evident 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 per year) of these 17,000 exposures occurred to 

children under 6 years old over the 11 year period analyzed (Table 5).10 Approximately 16% of 

all reported exposures to pesticides in the AAPCC data are related 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-related exposure incidents 

to children under 6 years old, for all pesticides, approximately 26% of the 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 products were the subject of 

the reported exposures, very few, if any, rodenticide products marketed to general consumers 

during this timeframe included bait stations intended to prevent children’s exposure. 

Table 5. AAPCC Reported Pesticide Exposure 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 available 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 children’s exposures to rodenticides, demonstrates 

that approximately 3,686 children less than 6 years old were treated at a health 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 years old from 1999 to 2005, approximately 39% of 

those seen in a health care facility are related to rodenticide exposure and 13% of hospitalization 

cases are related to rodenticide exposure. Fortunately, 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 result 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 rodenticides were applied. In other cases, it appears that the 

exposed children were visiting a different environment (such as grandparents, friends, or 

neighbors) and their parent or guardian was unaware that the baits were accessible. Most 

incidents involving rodenticide exposures among adults appear to be due to suicide or malicious 

intent. Accidental exposures, although rare, occasionally occur for adults. 

c. Resultant effects 

The majority of the rodenticide exposures reported to AAPCC did not result in significant 

symptoms based on those cases which received follow up to determine medical outcome. 

However, given the high number of children exposed to rodenticides, the small percentage 

experiencing significant symptoms is still a matter 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 while their ability to stop bleeding is impaired. 

Moreover, while exposures to rodenticides generally result in no detected clinical signs in 

children, the Agency believes that the number of non-symptomatic exposure incidents is 

unacceptably high because of the social and other costs (medical care, worry) 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 occur. The AAPCC data from 1999-2005 indicates 

that, compared to other pesticide exposures, rodenticide exposures are much more likely to 

receive medical treatment, accounting for 39% of all pesticide-related cases seen in a health care 

facility and 13% of all hospitalized cases involving children less than 6 years old. From 1999-

2005, 894 cases were reported having minor, moderate, 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 are likely the result of rodenticide exposure. 

* The categories are not mutually exclusive (i.e. a person could report 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 anticoagulant or a bromethalin rodenticide is of 

significantly less importance to human health than whether the exposure occurs in the first place. 

EPA is concerned about both SGAR and bromethalin poisonings and believes that packaging 

rodenticide bait products in tamper-resistant bait stations 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 toxic 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 containing 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 LD50 (mg/kg) 2.6 0.42 (male) 

MOE based on rat LD50 52 17 

Rat LD50 expressed as a human equivalent dose 

(mg/kg) 0.65 0.10 

MOE based on human equivalent LD50 13 4.2 

Ounces of bait containing the HED LD50 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 Association 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 total of 173,262 SGAR exposures, of which AAPCC 

classified 269 as moderate and 29 as major incidents. When evaluating differences in these 

incident counts during the period analyzed, it is important to recognize that many more units of 

SGAR baits were sold and used than were bromethalin baits. But assuming that users are equally 

likely to call a poison control center in the event of an exposure incident, regardless of what 

active ingredient the rodenticide contains, the rate of non-minor incidents 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 bromethalin, the rate of non-minor incidents was 26 

per 10,000 exposure calls, while for SGARs, the rate of non-minor incidents was 17 per 10,000 

exposure calls. Because the difference is not statistically 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 consistent with the results of animal studies that 

suggest that ingestion of 5 grams 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
   

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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 bruising and bleeding (including blood in urine, 

bleeding from the nose and gums, coughing blood and, depending on the amount consumed, 

bleeding into the joints and brain), but those symptoms do not appear until several days after 

ingestion. Thus, neither type of rodenticide (i.e., either 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 gastric decontamination could be an 

effective treatment. Sufficiently high exposures to both bromethalin and the anticoagulants 

(particularly the SGARs) have the potential to result in patients being admitted to intensive care 

units at considerable harm and expense to the patient. Because the persistent SGARs are 

metabolized more slowly by the body, compared to bromethalin, and due to the different mode 

of toxic action, SGARs result in longer-term medical effects and 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 anticoagulant rodenticide poisonings. Although emergency room physicians 

are more likely to have treated an anticoagulant 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 respiration 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 event, and in particular when the identity of the 

specific product or active ingredient is known. Initial emergency room treatment for known 

ingestion of a toxic dose of either 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 charcoal. However, the opportunity for decontamination is short (2 

hours or less), and after that, treatment methods diverge. In SGAR poisoning cases where 

bleeding is evident, the patient would be treated with repeated doses of vitamin K and, 

depending on the severity of the bleeding, fresh frozen plasma and clotting factor therapy such as 

recombinant activated factor VII therapy. In bromethalin cases, the 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 osmotic diuretics and steroids. In cases where 

exposure is unknown or uncertain, neither 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 gastric 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 prolonged 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 months 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 severe 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 incidents 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 concern, because any time a child can access 

rodenticide bait, there is the potential 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 would 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 any of the rodenticides 

subject to the NOIC is sufficient to cause adverse health effects. Symptomatic exposures – 

diagnosed or undiagnosed – are a matter 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 while their ability to stop bleeding is impaired. In addition to 

concerns about the actual health impacts of exposure 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.wikispaces.com/Anticoagulant+Rodenticides_Oral._logPs are 8.5 (brodifacoum, an SGAR) and 4.26 

(bromethalin) Rodenticide Cluster RED (1998).
   

~ 40 ~ 

 

is mindful of both the potential medical costs associated with children’s exposure to rodenticides 

in the home and the anxiety to parents (and perhaps children as well) caused by the exposure of 

children to poisons in the home. 

C. Characterization of Hazard to Domestic Animals 

Rodenticides are highly toxic to mammals and 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 species 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 effects and exposure of registered 

pesticides may be collected and analyzed. In assessing 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 System (IDS) database, 

• The EPA-sponsored National Pesticide 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 days a year resource for animal poison-related 

emergencies. Calls to the APCC are triaged by specially trained veterinary toxicologists. The 

Pet Poison Helpline, another poison reporting center which is available throughout the U.S., 

Canada and the Caribbean, is managed by veterinary specialists who also help triage animal 

poisoning events. The veterinary specialists include board-certified veterinary internal medicine 

emergency critical care specialists, and veterinary toxicologists. 

OPP Incident Data System (IDS) 

The OPP IDS database of pet exposure information includes reports of alleged incidents from 

various sources, including FIFRA Section 6(a)(2) reports from registrants and reports from other 

environmental agencies and individual consumers. The IDS exposure severity types for 

domestic animals, as defined by 40 CFR 159.184, are as follows:

• DA – Death – if the domestic animal 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 exhibited or was alleged to have exhibited 

symptoms which are more pronounced, more prolonged or of a more systemic nature than 

minor symptoms and included some treatment 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, science-based pesticide information and respond to 

inquiries from the public and to incidents. NPIC receives approximately 25,000 calls per year, 

with about 4000 of these being related to pesticide exposure incidents. NPIC collects the 

information about the incidents and records that information in a database. NPIC is a source of 

national incident information; but generally receives fewer reports than IDS. Regardless, NPIC 

can provide an additional source of incident information. Unlike IDS, incidents reported to 

NPIC are assigned a certainty classification, which helps ascertain whether the exposure and 

reported outcome are related. 

2. Observed Domestic Animal Exposure 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 toxicants 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 and insect bait stations) and the fourth most common class of 

toxicants involved in cat poisonings (after lilies, canine permethrin insecticides and household 

cleaners). 

Both the IDS and NPIC data indicate that the number of reported incidents of pet 

exposure to rodenticides is increasing over time. However, different rodenticides are associated 
   

~ 43 ~ 

 

with this increase in the different databases. 

IDS reports that the number of reported 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 trend may be a result of increased usage or increased reporting, 

rather than an increase in the likelihood that use of a product results 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 this 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 minimizes 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 gain access to baits placed in and around homes. 

EPA believes the main reason these incidents are occurring is because rodenticide baits are being 

placed in areas accessible to pets without use of pet-resistant bait stations required by the 

products’ labels.
   

~ 44 ~ 

 

c. Resultant effects 

The IDS data reflect that, although most rodenticide incidents appear to result in lower 

severity outcomes, there were a substantial number 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 incidents that actually occur because 

many incidents go unreported. 

The IDS data also allow rodenticide active ingredients to be ranked 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 ingredient. The rodenticide with the highest number of incidents 

ranked DA (death) and DB (major) over the period 1999-2010 was brodifacoum (710 incidents), 

followed by bromadiolone (355), bromethalin (292) and diphacinone and its sodium salt (262). 

Together, the SGARs brodifacoum and bromadiolone 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 cause 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 bromadiolone result in a death or 

major incident, indicating that brodifacoum exposures 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 analysis shows some differences in the likelihood of death or major 

outcomes for the different rodenticides, large percentages 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 for pet resistance would reduce the frequency of pet 

exposures to rodenticides. Although such products have been available in the commercial and 

agricultural pest-control markets for nearly 30 years, 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 application of additional effects and exposure data, 
   

~ 46 ~ 

 

use of additional exposure modeling, and quantitative risk assessment techniques for the four 

rodenticide active ingredients (brodifacoum, difethialone, warfarin and bromethalin) contained in 

products subject to the NOIC and for two rodenticides (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. Rodenticide exposures and mortalities have been 

documented for mammals and birds that are 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-target organism. Use of rodenticide baits around 

structures is likely to result in primary exposures among non-target wildlife. 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. Incident reports document rodenticide exposures 

among a number of species that are likely to be primary consumers of bait, including quail, 

turkeys, squirrels, opossums, raccoons, skunks, and deer. 

Secondary consumers were defined for purposes of the ecological risk assessment as 

those animals that prey upon or scavenge primary consumers of bait. Rodenticide baits pose 

potential secondary poisoning risks, because predators 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 secondary 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 consumers for this analysis. 

EPA is concerned with both the primary and 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 lines 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 animals through secondary exposure to rodenticides, 

including an evaluation using probabilistic risk assessment techniques; (3) an evaluation of 

available feeding studies as they relate to secondary exposure risks; and (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 conclusions 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 chemicals 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 high potential for adverse effects to birds, although 

the relatively short blood half-life and the tendency of animals 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, diphacinone, and bromethalin; however, the toxicity differences 

between chemicals are much more pronounced for birds. 

• For primary exposure to birds, all or a majority 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 directly consume bait. For both bait 

concentrations of warfarin (0.025 and 0.054%), the deterministic risk assessment indicates that 

some weight classes of birds are likely to be adversely affected if they directly consume bait; 

however, the additional lines of evidence indicate that the required feeding times and bait 

consumption quantities are greater than for brodifacoum, 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 LD50 (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 suggest that mammals are likely to be adversely affected if they directly 

consume bait. 

• 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 
   

~ 49 ~ 

 

chemicals. The most notable exception is bromethalin, as only a few incidents were reported; 

however, bromethalin is not often included 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 mice or rats in diet required to consume the 

equivalent of an LD50, results of a limited probabilistic analysis, and results of available 

secondary feeding studies) indicate that birds are likely to be adversely affected by brodifacoum 

if birds consume contaminated prey (incident data confirms that birds have been adversely 

affected by consuming contaminated prey). Similar conclusions can be made for difethialone: 

the predominance of the evidence is that difethialone adversely affects birds if they consume 

contaminated prey, but a few exposure scenarios (larger birds consuming prey with low 

contamination levels) are less likely to result in adverse effects than is the case for brodifacoum. 

Evidence that predators or scavenger may be adversely affected by secondary exposure to 

warfarin, chlorophacinone, diphacinone, and bromethalin is equivocal, suggesting 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 contaminated prey (incident data confirms that 

mammals have been adversely affected by consuming contaminated prey) for brodifacoum. Bait 

containing difethialone, bait containing 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 result 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 secondary 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 bromethalin, as no secondary exposure incidents were 

reported; however, bromethalin is not often included in tissue residue analyses. 

Table 9. Ecological risk conclusions 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 All 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 Equivocal 

Chlorophacinone 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 All 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 data No data All lines Equivocal 

Warfarin 

(0.054%) All lines Predominant All lines No data No data All lines Predominant 

Chlorophacinone 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 result in those adverse effects. 

“Equivocal” = Equivocal evidence that risk exceeds concern levels and effects are likely to occur 

“Little” = Little evidence that risk exceeds concern levels or that effects are likely to occur
   

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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 adversely affect non-target wildlife. These lines of 

evidence include the following: 

• Risk quotients (RQs), 

• Evaluation of primary and secondary exposure studies, 

• Measures to determine the feasibility 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 subsequent sections. The RQ is a unitless value that 

is the ratio of exposure to the toxicity endpoint. For example, in the context of acute avian risk 

estimates (e.g., mortality), an RQ of 1 would mean that 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 tests (specifically, the LD50 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 potential to cause risks of concern to non-target 

organisms. 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 risks to species listed as threatened or endangered 

(LOC = 0.1); however, for simplicity, this analysis 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 deterministic assessment is intended to serve as a screening tool for identifying 

a potential for adverse effects, it is somewhat limited and conservative by design. As a result, 

EPA does not believe that the RQs derived in this assessment can be used as a precise measure of 

the magnitude of effects that will occur, but rather serve as tools for addressing 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 evidence to characterize the 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 absorption, distribution and elimination in the body), 

concentration of active ingredient in the bait, and availability of bait for consumption. For each 

of the evaluated chemicals, risk was assessed in several ways. RQs were calculated assuming: 

• Single day dose-based exposure to bait, based on allometric equations that allow for 

differentiation among taxa and body size, is compared to acute oral LD50 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 LD50 toxicity values; and 
   

~ 53 ~ 

 

• Diet-based exposure, based on the concentration of rodenticide active ingredient in bait, 

is compared to acute dietary LC50 values. 

 Further lines of evidence were evaluated, including: 

• An analysis of the number of days of bait 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 method, exposure was calculated by dividing the 

dose (in milligrams of active ingredient) by the body weight (in kilograms) of the consuming 

individual for three standard weight classes of birds and mammals. Allometric equations that 

relate food consumption to body weight (Wildlife Exposures Handbook, USEPA 1993) were 

used to determine potential exposures for typical birds and mammals of varying sizes. 

Allometric equations were used for the generic bird and mammal. In addition, allometric 

equations for passeriform birds and rodent mammals were also used as these would best 

approximate those individuals with high potential for consuming bait and they would give 

conservative exposure estimates. Animal exposure 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 LD50 values for birds and mammals were used as the measure of toxicity 

to non-target species. The toxicity values selected for this assessment for birds were the most 
   

~ 54 ~ 

 

sensitive LD50 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 LD50 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 LD50 values for non-target animals. Although there 

are numerous studies addressing the toxicity of one or more rodenticides in a wide variety of 

non-target species, these standard test species are the only ones for which studies are available on 

all of the rodenticides of interest. Therefore, in order to provide a uniform basis of comparison 

between rodenticides, EPA’s analysis focused on these standard test species. However, this 

method may be less conservative if other non-target species are more sensitive to rodenticide 

exposure than are the standard test species. 

Scaling factors were used to modify the available avian and mammalian toxicity data to 

account for differences in sensitivity between animals of different body weights. For example, 

when using the default scaling factor, smaller birds are estimated to be more sensitive compared 

to larger birds. Scaling factors, 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 scaling factor was available for brodifacoum 

(0.76) from Mineau et al. (1996), and for all other chemicals where such a specific value is 

unavailable, the default scaling factor (1.15) was used to adjust the avian LD50s. 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 LD50 values were calculated using the “body weight 3⁄4” adjustment (USEPA 1995, 

2011). EPA’s assessment for primary exposure and risk 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 bird and mammal body weights used in by EPA for 

ecological risk assessments (T-REX 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 were calculated by estimating body burden based on 

the assumption that bait was consumed 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 LC50. The LC50 (mg a.i./kg-diet) is obtained from 5-day exposure 

dietary toxicity studies. RQs are calculated as a ratio of a.i. concentration and the LC50. Risk 

results that agree between this method and the multiple day accumulated dose method described 

above provide an enhanced degree of confidence in risk conclusions for a given chemical. 

As noted above, EPA also evaluated further lines 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 consume 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 LD50 through consuming 100% of its daily diet as bait. The second line of 

evidence involved calculating the amount of bait that would need to be consumed to be 

equivalent to the LD50. These additional lines of evidence represent useful tools for comparing 

risks among chemicals. The greatest concerns for non-target primary risk are with those 

pesticides for which little feeding 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 consumption are necessary over a protracted period of 

time to cause death. 

ii. Risk Characterization 

Variation in toxicity among the chemicals and sensitivity across taxonomic groups, 

species, and exposure methods are evident when examining the available toxicity endpoints 

(Figures 1-4). Generalized conclusions based on the available acute oral (LD50) 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, followed by bromethalin, followed by warfarin, 

chlorophacinone, and diphacinone; and (5) for mammals, an approximate toxicity ranking is 

brodifacoum and difethialone, followed by bromethalin, warfarin, chlorophacinone, and 

diphacinone. 

Although fewer toxicity endpoints are available for the acute dietary (LC50) studies, the 

general conclusions are similar: (1) mammals are more 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 among species and/or laboratories; (4) for birds, an approximate 

toxicity ranking is brodifacoum and difethialone, followed by bromethalin, warfarin, 

chlorophacinone, and diphacinone; and (5) for mammals, the central tendencies and ranges in 

toxicity appear very similar across all chemicals for which data are available. 
   

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Figure 1. Avian acute oral LD50 (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 LD50 (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 (laboratory rat); these values were used 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 

LD50 (mg a.i./kg-bwt)

LD50 (mg a.i./kg-bwt)

Diphacinone 

Bromethalin 

Chlorophacinone 

Warfarin 

Difethialone 

Brodifacoum 
   

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Figure 3. Avian acute dietary LC50 (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 (bobwhite 

quail or mallard duck); these values were used for RQ calculation. Triangles represent toxicity values non-standard test species or 

less sensitive standard test species 

Figure 4. Mammalian acute dietary LC50 (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. Triangles represent toxicity values non-standard test species or less 

sensitive standard test species. No data were available for difethialone; 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 

Diphacinone 

Bromethalin 

LC50 (mg a.i./kg-diet)

Brodifacoum 

Difethialone 

Warfarin 

Chlorophacinone 

Diphacinone 

Bromethalin 

LC50 (mg a.i./kg-diet)
   

~ 59 ~ 

 

The risks identified by the deterministic analyses and the other lines of evidence for each of 

the rodenticides considered in the EPA assessment 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 LD50 through 100% 

consumption of bait and the mass of bait to be consumed for an individual to reach the LD50. 

 
~ 60 ~ 

Table 10. Bird risk assessment: primary exposure of passerine birds to bait. 

Body weights (g) 

Second Generation 

Anticoagulants First Generation Anticoagulants 

Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chlorophacinone Diphacinone 

Risk Quotients 

Single day dose RQ 

20 20* 30* 0.23 0.50* 0.07 0.01 

100 23* 18* 0.14 0.31 0.04 0.01 1000 28* 9.2* 0.07 0.16 0.02 <0.01 

Six day dose RQ 

20 120* 170* 1.4* 2.9* 0.40 0.05 

100 140* 100* 0.84* 1.8* 0.25 0.03 1000 170* 52* 0.42 0.91* 0.12 0.01 

Dietary RQ NA 38* 45* 0.40 0.86* 0.89* 0.06 

Additional lines of 

evidence 

Days to consume sufficient bait to reach the LD50

20 <1 <1 4-5 1-2 16-17 >365 

100 <1 <1 7-8 3-4 30-31 >365 1000 <1 <1 14-15 6-7 117-118 >365 

Grams bait consumed to reach the LD50

20 <1 <1 25 10 86 >1800 

100 <1 1.1 160 80 620 >7300 1000 5 15 2100 990 17000 >52000 

NA = not applicable ND = no data * RQ exceeds acute risk LOC = 0.50 
~ 61 ~ 

NA = not applicable ND = no data * RQ exceeds acute risk LOC = 0.50 Table 11. Mammal risk assessment: primary exposure of rodents to bait. 

Body weights (g) 

Second Generation 

Anticoagulants First Generation Anticoagulants 

Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chlorophacinone Diphacinone 

Risk Quotients 

Single day dose RQ 

15 9.9* 4.3* 8.4* 18* 0.82* 2.0* 

35 8.5* 3.7* 7.1* 15* 0.70* 1.7* 1000 4.6* 2.0* 3.8* 8.3* 0.38 0.90* 

Six day dose RQ 

15 59* 24* 49* 110* 4.7* 12* 

35 51* 21* 42* 90* 4.0* 9.9* 1000 27* 11* 22* 48* 2.1* 5.3* 

Dietary RQ NA 94* ND 57* 120* 44* 22* 

Additional lines of 

evidence 

Days to consume sufficient bait to reach the LD50

15 <1 <1 <1 <1 1-2 <1 

35 <1 <1 <1 <1 1-2 <1 1000 <1 <1 <1 <1 2-3 <1 

Grams bait consumed to reach the LD50

15 <1 <1 <1 <1 6 1.1 

35 <1 1.3 <1 <1 9 2.1 1000 6.7 16 8.0 3.7 61 25 
   

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RQs exceed the LOC for all mammals exposed to brodifacoum and difethialone. These 

pesticide active ingredients were developed to kill rodents; they pose a lethal primary risk to 

non-target small mammals that eat bait containing either of these rodenticides. However, the 

quantitative assessment also demonstrates that bait 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 performed (single oral dose, six-day accumulated dose, 

dietary concentration and the feeding period- lethality assessment). EPA’s analysis indicates 

birds and mammals could attain a lethal dose (LD50) 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 represents an increased opportunity (relative to all other rodenticides 

assessed) for non-target animals – especially birds -- to chance upon bait and consume a lethal 

dose of either brodifacoum or difethialone. 

Warfarin, as expected for all rodenticides, also demonstrates a primary exposure risk 

concern to small mammals. The assessment of warfarin also indicates a risk to large mammals 

for all assessment methods employed as well. EPA’s analysis indicates that 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, relative 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 primary 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 highest concentration formulation, accounting for the 

potential for multiple day accumulation on a dose basis expands the concerns to include 
   

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passeriformes and other small and medium sized birds 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 (0.025% warfarin bait). This finding suggests that, 

for birds there is less of an opportunity for consuming 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 employed. In addition, bromethalin exceeds risk 

concern levels in all assessment methodologies with the exception of the dietary exposure 

methodology. EPA’s analysis indicates that less than a single day’s feeding on bromethalin bait 

is sufficient to attain a lethal dose in birds and mammals, suggesting (again like brodifacoum and 

difethialone) adverse effects to non-target wildlife are likely from primary exposure events with 

treated bait. 

Two anticoagulant alternatives, chlorophacinone and diphacinone, also present primary 

exposure risk concerns for nearly all mammal 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 (chlorophacinone) of feeding on bait are sufficient to 

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

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other rodenticides with respect to the opportunity for non-target mammals to chance upon and 

ingest a lethal dose of treated bait. In contrast to mammals, primary 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 terminating at six days (i.e., longer exposure periods 

might provide sufficient exposure to bait for adverse accumulation to occur). However, the 

analysis indicates that, unlike brodifacoum and difethialone, a very consistent and protracted 

feeding period for either diphacinone or chlorophacinone is required to attain a lethal dose in 

birds (i.e., daily feedings over weeks to months). 

b. Secondary Exposure and Risk 

The toxicity of each of the rodenticides and a variety of factors concerning their fate and 

effects in biological systems influence their potential for risk to secondary consumers, i.e., nontarget wildlife that may ingest living or dead animals that have consumed rodenticide bait. These 

characteristics can be compared to predict the rodenticides’ relative potential for such secondary 

risk. The elimination rate, potential to accumulate within body tissues, time to death, and 

toxicity to both primary and secondary consumers influence exposure and risk. 

A compound that is rapidly metabolized or excreted from a primary consumer likely 

results in a lesser secondary risk to non-target predators and scavengers than one that 

accumulates with repeated exposure, even if repeated exposure occurs weeks or months after 

initial exposure (Eason and Murphy 2000). Compounds that more rapidly clear from the body 

are less likely to pose secondary risk because the rodenticide 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 that 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, rodenticides 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 secondary consumers are expected to present greater secondary exposure 

risk. Below is an evaluation of the elimination 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 accumulate in body tissues to a greater extent than 

warfarin, chlorophacinone, and diphacinone. Data from these types of studies are not available 

for bromethalin, but the opportunity for primary consumers to feed on bromethalin bait and 

accumulate the rodenticide is limited due to this 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 overt 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 bromethalin 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 rodenticides 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 liver 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) indicate that the half-life of difethialone may be several times 

greater than Vandenbroucke et al (2008). Belleville (1991) calculated 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 difethialone. A liver half-life of up to 66.8 days has 

been calculated for warfarin in rats (Vandenbroucke et al. 2008), 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, and Eason et al. 1999). 

Available data also show that chlorophacinone and diphacinone are more 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 (Vandenbroucke 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-anticoagulant rodenticide bromethalin suggest that it is rapidly 

eliminated by the body. While there are no data on the elimination half-life of bromethalin in 

liver, a metabolism study conducted in rats indicated a plasma half-life of 5.6 days. 

Owing to the lack of available whole-body elimination data for all assessed rodenticides, 

liver half-lives were selected from 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 Vandenbroucke 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, the 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 available for diphacinone, it is based on a study on pigs, 

rather than the rats used in the other studies. There is some indication from the available half-life 

studies that different species react differently to anticoagulant rodenticides. Therefore, the pig 

value may overestimate or underestimate the liver half-life of rats for diphacinone. For 

bromethalin, there are no available data on the liver 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 estimate doses of each rodenticide in non-target and 

target animals are provided in Table 12. 
   

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ii. Potential to Accumulate a Lethal Dose 

 Many of the assessed rodenticides typically cause mortality several days after exposure, 

which may allow target rodents to feed for several 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 date when mortality was observed in acute oral 

toxicity studies. For rodents exposed to baits containing 0.25% warfarin, doses were estimated 

to be 4 to 94 times the LD50 at the time of death. For rodents exposed to chlorophacinone and 

diphacinone, estimated doses at the time of death ranged from 3 to 13 times the LD50. In 

contrast, for rodents exposed to brodifacoum and difethialone, estimated doses at the time of 

death ranged from 9 to 82 times the LD50.

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 LD50. 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 rodenticides based on elimination 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 bait after reaching a lethal dose may accumulate 

rodenticide doses that are many times the levels that are sufficient to cause mortality. Elevated 

residues resulting from repeated consumption of bait poses increased risk for secondary 

consumers that prey upon poisoned rodents because the secondary consumers receive high doses 

of rodenticides. Although all anticoagulants present risks that target rodents may bear 

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

difethialone and brodifacoum. 

3. Assessment Based on Calculated Residues in Prey 

a. Methodology 

Exposure for secondary consumers was estimated by calculating the amount of 

rodenticide in target rodents (i.e., house mouse and Norway rat) that represent potential prey. As 

with the primary assessment, EPA’s secondary risk assessment estimated exposure using 

allometric equations of daily food intake from the Wildlife Exposure Factors Handbook (EPA 

1993). Rodenticide intake based 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 periods (1, 3 and 6 days) was calculated. These 

time periods were used as representative time periods that target rodents may survive after the 

initial daily dose of a pesticide (based on available 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 consisted 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 within the prey animal at the end 

of a day’s feeding was determined. Accumulation 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 conservative estimate of 

exposure. 

In addition to the estimates of rodenticide residues in target rodents representing prey of 

secondary consumers, empirically measured rodenticide concentrations in carcasses of rodents 

were used to represent potential exposure values for secondary consumers. Although this 

method of representing concentrations of rodenticides 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 consumers 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 six days. Dose-based RQs were calculated by dividing the dosebased exposure values from the estimated dose by the adjusted LD50 values. 

In addition, dietary-based RQs were calculated for secondary consumers. This was 

accomplished by dividing the estimated concentrations of rodenticides in target rodents by the 

LC50 values for birds or mammals. 
   

~ 71 ~ 

 

b. Risk Estimation 

Based on acute exposure of predator and scavenger birds to rodenticides accumulated in 

prey organisms, RQs for brodifacoum and difethialone exceed the Agency’s acute LOC 

regardless of assessed weight class, prey organism consumed, or accumulation scenario. RQs 

calculated for warfarin, diphacinone, and chlorophacinone do not exceed the acute LOCs for 

birds, except for small predator and scavenger 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 diphacinone RQs for secondary 

birds do not exceed the acute LOC, there is uncertainty associated with these 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 the majority of 

the avian toxicity data. If bobwhite quail and mallard ducks are significantly less sensitive to 

anticoagulant rodenticides than predatory birds, then the secondary 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 LOC, except for predator and scavenger mammals 

exposed to a three day accumulation of chlorophacinone in large prey animals and small 
   

~ 72 ~ 

 

predators/scavengers exposed to a six day accumulation 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 chemicals were not included in this analysis. 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 rodents. 

Body weights (g) 

Second Generation 

Anticoagulants First Generation Anticoagulants 

Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chloropha- cinone Dipha- cinone 

Secondary exposure to carnivores and scavengers 

House mouse consumption: 3 day accumulation in prey RQ 

100 20* 17* 0.14 0.30 0.04 0.01 

1000 15* 5.4* 0.04 0.09 0.01 <0.01 5000 13* 2.4* 0.02 0.04 0.01 <0.01 

Norway rat consumption: 3 day accumulation in prey RQ 

100 5.3* 4.5* 0.04 0.08 0.01 <0.01 

1000 4.1* 1.4* 0.01 0.02 <0.01 <0.01 5000 3.4* 0.64* 0.01 0.01 <0.01 <0.01 

House mouse consumption: 6 day accumulation in prey RQ 

100 39* 33* 0.27 0.58* 0.08 0.01 

1000 31* 10* 0.09 0.19 0.02 <0.01 5000 16* 4.7* 0.04 0.08 0.01 <0.01 

Norway rat consumption: 6 day accumulation in prey RQ 

100 10* 8.7* 0.07 0.15 0.02 <0.01 

1000 8.1* 2.8* 0.02 0.05 0.01 <0.01 5000 6.8* 1.2* 0.01 0.02 <0.01 <0.01 

House mouse consumption: dietary RQ 

NA 18* 21* 0.19 0.41 0.32 0.02 

Norway rat consumption: dietary RQ 

NA 4.7* 5.5* 0.05 0.11 0.09 <0.01 

NA = 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/scavenger mammals to consumed rodents. 

Second Generation 

Anticoagulants First Generation Anticoagulants 

Body weights (g) Brodifacoum Difethialone Warfarin (0.025%) Warfarin (0.054%) Chloro- phacinone Dipha- cinone 

Secondary exposure to carnivores and scavengers 

House mouse consumption: 3 day accumulation in prey RQ 

50 11 * 4.7* 8.8* 19* 0.84* 2.5* 

1000 14* 5.9* 11* 24* 1.0* 3.1* 3000 15* 6.4* 12* 26* 1.1* 3.4* 

Norway rat consumption: 3 day accumulation in prey RQ 

50 2.9* 1.3* 2.3* 5.0* 0.22 0.66* 

1000 3.7* 1.6* 2.9* 6.3* 0.27 0.82* 3000 4.0* 1.7* 3.1* 6.8* 0.30 0.89* 

House mouse consumption: 6 day accumulation in prey RQ 

50 22* 9.2* 17* 37* 1.6* 4.2* 

1000 27* 11* 22* 47* 2.0* 5.2* 3000 30* 12* 23* 50* 2.2* 5.6* 

Norway rat consumption: 6 day accumulation in prey RQ 

50 5.9* 2.4* 4.6* 9.9* 0.43 1.1* 

1000 7.3* 3.0* 5.7* 12* 0.53* 1.4* 3000 7.9* 3.3* 6.2* 13* 0.58* 1.5* 

House mouse consumption: dietary RQ 

NA 45* ND 27* 58* 20* 10* 

Norway rat consumption: dietary RQ 

NA 11* ND 7.0* 15.23* 5.4* 2.7* 

NA = 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 secondary risks by analyzing residues in test 

animals that had consumed contaminated carcasses. This analysis differs from the carcass 

concentration-based risk assessment described previously in that it makes use of measured 

residues in intoxicated target organisms as a basis for dietary exposure in scavengers and 

predators. Using actual animal concentrations eliminates 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 rodenticide exposure in the prey base (i.e., the 

animals intoxicated at the primary exposure level). 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; however, if the empirically-based RQs calculated in this section do 

not exceed the LOC, risk cannot necessarily be precluded, especially if the 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 available 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 used 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 dietary studies are provided in Table 16. 

Carnivore and scavenger bird RQs for brodifacoum and difethialone exceeded acute risk LOCs. 

Warfarin RQs for carnivore and scavenger birds did not exceed any LOCs. RQs for birds 

exposed to chlorophacinone and diphacinone in their 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 available 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 acute 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 using estimated or empirically based prey-base 

concentrations estimates of rodenticide. The feeding studies empirically account for primary 

organism feeding, absorption and elimination uncertainties surrounding the estimated dose-based 

assessment. They also account for uncertainties associated with biological availability of 

rodenticide from consumed prey and assumptions of predator/scavenger sensitivity to the 

rodenticide which are present in both of the dose-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 brodifacoum are supported by available data from 

secondary toxicity studies showing mortality in 63% of predator/scavenger birds and 42% of 

predator/scavenger mammals fed brodifacoum contaminated target organisms. No secondary 

feeding data are available for difethialone. 

In the case of warfarin, mammalian secondary feeding studies involving mammal 

predators/scavengers show mixed results and for some species the differences extended to a 
~ 78 ~ 

 

dose-dependent response. No mortalities were observed in raccoons 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 weasels and dogs, although the results 

often involved few test organisms. Avian secondary feeding studies of warfarin involved testing 

of four species. In three of the four species tested there 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-billed magpies (~170 g bodyweight) while the risk 

assessment suggests a concern for a 100 gram bird. 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 suggest that allometric relationships for predicting effects of 

warfarin toxicity may incompletely explain the factors contributing to species sensitivity 

variability. 

Bromethalin secondary feeding studies are limited to a single case. In that study 

involving domestic dogs fed intoxicated rats there were no mortalities (n=4). The number of 

species tested is limited; therefore, there is insufficient 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 conclusions, they do indicate that 

bromethalin may not be retained in body tissues in toxicologically significant amounts as 

discussed previously. No bird feeding studies were available for bromethalin. 

Chlorophacinone secondary toxicity results include studies with five mammal species. 

Mortality responses were variable and ranged from approximately 50 percent to 100 percent of 
~ 79 ~ 

 

individuals tested. In one single species, European ferret, different 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 individuals 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 percent mortality. Of particular note is the study involving 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 risk assessment were 10 to 20 times higher than 

tested in the feeding study. The feeding study with rats yielded a 50 percent mortality response 

under conditions of similar toxicity and lower exposure 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 there were no mortalities, consistent 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 discussed earlier, the toxicity endpoint relied upon in 

the risk assessment may underestimate the sensitivity 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 risk assessment, residues were estimated and 

observed to reach levels in target organisms that, when consumed by predators and scavengers 

can result in death. When considering those risks among the assessed rodenticides it is important 

to consider the likelihood of predators and scavengers encountering enough intoxicated target 

prey to reach potential lethal doses. Furthering the evaluation of secondary exposure of 

rodenticides are the results of analyses of the number of individual target organisms necessary 

for dietary consumption to achieve a lethal dose 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 bait for a single day or up to six days. Again, 

compounds that can present a lethal dose to predators and scavengers after consumption of target 

organisms with only a single day of exposure are 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 need 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 would only need to consume a fraction of a single 

target organism to reach lethal endpoint exposures, 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 difference among the chemicals. Owing to their smaller 

size, consumption of brodifacoum intoxicated mice must be slightly more intensive for the 

predator/scavengers to reach lethal endpoint exposure (<1 to 5 organisms) as compared to rats. 

These results are not atypical of the results for difethialone, warfarin and bromethalin assessed 

rodenticides. However, the amount of brodifacoum 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 LD50 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, numbers are based on 3-day accumulation in prey 

Similar analyses were conducted to determine the target organism numbers necessary to 

trigger lethal incidents in scavenger/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 difethialone, 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 generally must ingest more house mice than Norway rats in order 

to attain a lethal dose, but ingestion of only <1 to 5 house mice intoxicated by brodifacoum 

would be sufficient to cause lethal secondary poisoning. With difethialone, consuming less than 

one intoxicated house mouse would be expected to kill a 100-g avian predator or scavenger, but 

the numbers of mice needed to kill birds at the 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 bromethalin-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 scavengers 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 brodifacoum has a substantially greater opportunity 

than these other active ingredients to result in lethal incidents following exposure of a 

predator/scavenger bird to intoxicated target organisms. 

 
~ 83 ~ 

 

Table 18. Secondary Exposure to Predator and Scavenger Birds: Number of 

animals consumed to reach the LD50 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, numbers are based on 3-day accumulation in prey 

7. Probabilistic Analysis 

EPA conducted a probabilistic analysis that addressed 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 scavenger birds may achieve a lethal rodenticide 

dose. This was accomplished using a Monte Carlo simulation with a distribution of possible 

outcomes that were analyzed to allow for more thorough understanding of the uncertainties 

associated with the available data. The modeling 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 rodenticide that may pose a risk to the secondary 
~ 84 ~ 

 

consumer. Although the results presented below focus on birds at risk through secondary 

exposure, an equivalent analysis was conducted for predator/scavenger mammals. The 

probabilistic assessment for mammals at risk through secondary exposure sheds no new light on 

the issues in the proposed cancellations, as it simply confirms, as did the Agency’s deterministic 

assessment, that rodenticides designed to target mammalian species will be toxic to mammals 

regardless of whether they are primary or secondary consumers. However, the enhanced toxicity 

and extended residence time in non-target animals suggests that bioaccumulation potential and 

resulting secondary poisoning potential of brodifacoum and difethialone are greater relative to 

the other assessed rodenticides. The probabilistic analysis conducted by EPA is described in 

more detail in “Probabilistic Analysis Associated with Avian Risks from Exposure to 

Brodifacoum, Difethialone, Chlorophacinone, Diphacinone, 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 rodenticides based on 10,000 randomly sampled LD50 and 

half-life values. For each rodenticide, the values in Table 19 provide the percentage of calculated 

RQs that were above the LOC for birds when toxicity and exposure parameters were randomly 

sampled. These percentages allow for the comparison of risks among chemicals where larger 

percentage values suggest a higher likelihood that a randomly selected bird may achieve a lethal 

dose under the assumptions of this analysis. Based 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 day of accumulation in the prey. 

However, the likelihood of risk from exposure to difethialone is less than the likelihood of risk 

from exposure to brodifacoum, especially for large birds consuming intoxicated prey animals. 
~ 85 ~ 

 

Relative to the risks of brodifacoum and difethialone, 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 rodenticides. However, it should be noted that sensitive 100-g birds 

(e.g., American kestrels) feeding on small mammals 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 birds consuming either small or large prey items 

have a low likelihood of risk exceeding concern levels from exposure to bromethalin. In 

addition, it is important to note that several factors suggest that bromethalin poses a lower risk to 

birds from secondary exposure, relative to brodifacoum and difethialone. These factors include: 

1) target animals tend to stop feeding after consumption of toxic doses of bromethalin; therefore, 

they are less likely to carry residue levels in excess of toxic doses; and 2) available data suggests 

that bromethalin is eliminated quickly from target and non-target animals relative to the other 

chemicals; therefore, bromethalin 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 Dose-Based RQs that are Greater 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 expected 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 when toxicity and exposure parameters were 

randomly sampled. Based 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 
~ 87 ~ 

 

and difethialone on a dietary basis. For warfarin and chlorophacinone there 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 concern levels relative to the other rodenticides 

evaluated. 

Table 20. Percentage of Acute Dietary-Based RQs for Birds that are Greater 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 consuming bromethalin are not expected to continue feeding on bromethalin bait for six or fourteen

days. 

8. Summary of secondary exposure risks 

The assessment of secondary exposure risks for wildlife involved a series of assessment 

methodologies that encompassed both estimated accumulation of rodenticides in a prey base as 

well as empirical measurements of rodenticide residues 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, some 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 order for predators and scavengers to receive an 

LD50 dose and the probabilistic analysis, the following conclusions can be made for risk to birds: 

• Brodifacoum and difethialone pose greater secondary exposure risk to birds relative to 

the other chemicals assessed regardless 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 after reaching a lethal 

threshold and rapid mortality observed in primary feeding studies with bromethalin. 

Risks to small birds consuming large prey animals and risks to medium and large birds 

consuming small or large prey animals are substantially lower than for brodifacoum and 

difethialone. 

• Warfarin may pose risk to certain sensitive species, especially under high accumulation 

scenarios; however, the likelihood of secondary 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 from diphacinone poisoning under the highest 

accumulation scenario. Secondary exposure risks for diphacinone are substantially lower 

than for brodifacoum and difethialone. 

• For chlorophacinone, results for the acute dose-based exposure scenarios demonstrate a 

low likelihood of secondary exposure concerns. However, results of the probabilistic 

assessment conducted for dietary-based exposure indicate that chlorophacinone may have 
~ 89 ~ 

 

a greater likelihood of posing risk to predator/scavenger birds under the higher 

accumulation scenarios than the one-day accumulation scenario. While these results 

represent a departure from the other analyses, the likelihood of secondary exposure risk 

for chlorophacinone is still substantially lower than for brodifacoum and difethialone. 

9. Incident Findings Related to Primary & Secondary Risk Analyses 

 The quantitative risk assessment does not evaluate 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 governments 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 and rural areas provide 

complete exposure pathways for a variety of wildlife, and that both primary and secondary 

exposures can cause mortality in non-target wildlife. Table 21 presents the total number of 

reported incidents associated with each of the rodenticides considered in EPA’s assessment. 

Where possible, EPA distinguished between incidents resulting from primary and secondary 

exposures. Additional details on these incidents are tabulated in Compilation of Rodenticide 

Wildlife Mortality Incidents Reported Between 1971-2012 (EPA 2013). 

 
~ 90 ~ 

 

Table 21. Total Number of Wildlife Incidents by Rodenticide Active 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 

2 

Chlorophacinone 

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 incidents associated with other active ingredients.

 In evaluating EPA’s incident database for rodenticides, it is important to understand 

that reported incidents likely represent 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 animals killed by these rodenticides typically occur at a distance, 

both spatially and temporally, from the site where 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 authority, typically a state fish and wildlife office, and 

that agency conducts an investigation into the cause of death is an incident likely to be linked to 
~ 91 ~ 

 

rodenticide exposure. The investigating state agency may then take tissue samples from the 

animal, normally from the liver, and have laboratory analyses performed to screen for the 

presence of various rodenticides, as well as various other pesticides. Only when the residue 

analysis finds one or more rodenticides in the tissue of the dead animal does the incident become 

diagnosed as a suspected or confirmed rodenticide incident. Because the linkage between 

wildlife mortalities and exposure to the rodenticides subject to the NOIC depends on thorough 

investigations, including residue analysis of tissue samples, incident reporting rates vary greatly 

from state to state and likely depend largely on whether the state has the personnel and resources 

to conduct and report investigations. 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 rodenticide incidents. Many states have never reported 

any wildlife mortality incidents related to rodenticides. Given these 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 wildlife incidents, the available 

data support the quantitative risk assessment’s conclusion that both primary and secondary 

exposure to brodifacoum poses lethal risk to a variety of sizes of mammals and birds. Mortality 

incidents likely to have resulted from primary 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 predicted to be at risk from brodifacoum in EPA’s analysis above. For birds, 

mortality incidents likely to have resulted from primary exposure to brodifacoum involved 

species ranging in size from robins to geese, again 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 modeled 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 secondary exposure to brodifacoum. For birds, incidents likely to 

have resulted from secondary exposure involve a variety of raptors, again consistent with the risk 

model predictions for larger birds. These incidents occurred in urban/suburban and rural habitats. 

In summary, incident data indicate that both primary and secondary exposures to brodifacoum 

are likely to cause mortalities 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 retention time of difethialone indicates that it is toxicologically 

similar to brodifacoum, suggesting that the small number of reported incidents for this ingredient 

could be due to the relatively low use of difethialone or to other factors not related to the intrinsic 

risk of the chemical. Nevertheless, one lethal incident 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 consistent with the conclusions of the mammalian 

primary exposure risk assessment. Although there are no reported incidents involving bird 

species and primary exposure to difethialone, the absence of reported incidents neither supports 

nor refutes the findings of the avian primary exposure risk assessment. Lethal incidents involving 

predatory birds and mammals and difethialone have been reported, consistent with the 

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

difethialone incidents are associated with urban/suburban areas. 
~ 93 ~ 

 

Warfarin incidents involving non-target wildlife 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 exposure 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 species presumed to be 

secondary consumers. These secondary exposure incidents are consistent with the quantitative 

secondary risk assessment and are in partial agreement with the available secondary feeding 

toxicity studies (warfarin secondary 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 rural, 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 resulted from primary exposure to 

bromethalin-treated bait, and no incidents involving either mammals or bird species that appear 

to have resulted from secondary exposure. Incidents 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 investigations of wildlife mortality incidents. Thus, 

the lack of reported secondary exposure incidents involving bromethalin can neither support nor 

refute conclusions of the mammalian and avian secondary risk assessments. 

There are few reported incidents where there is high certainty that mammal mortalities 

resulted from primary exposure to chlorophacinone bait. Reports of mortalities 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 through primary exposure suggests the 

possibility that chlorophacinone presents greater primary exposure risk to birds than indicated in 

the primary exposure risk assessment. Chlorophacinone incidents of high certainty involving 

likely secondary exposures of mammals and birds are also scarce, but include reports of 

mortalities in wild felids (bobcats) and raptors (red-tailed hawk). The mammal incidents are 

consistent with the secondary exposure risk assessment 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 increased sensitivity in 

raptors by assuming a 20-fold increase 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 consistent with reported incidents. However, the 

incident report would still be inconsistent with the single oral dose risk assessment. On balance, 

incidents indicate that chlorophacinone may cause secondary lethalities to birds, but because of 

attendant uncertainties inherent in incident data interpretation, they do not necessarily refute the 

conclusion of the risk assessments that chlorophacinone presents negligible risk to birds, and 

they are consistent with the conclusion that 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 involved poisoning of squirrels in urban/suburban 

settings, but is different in that incidents have also been reported 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 assessment of risk to small mammals from primary 

exposure. Diphacinone incidents of high certainty 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 mountain lion) and raptors (snowy and barred owls, red-tailed 

hawk). The mammal incidents are consistent with the secondary exposure risk assessment 

findings. The bird incidents are inconsistent with the modeling portions of secondary exposure 

risk assessment, which did not predict 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 raptors, 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 because of attendant uncertainties 

inherent in incident data interpretation, those incidents do not necessarily refute the conclusion of 

the risk assessments that diphacinone presents negligible risk to birds, and they are consistent 

with the conclusion that the secondary risks of diphacinone are considerably less than those of 

brodifacoum and difethialone. 

a. Implications for Risk Mitigation 

The proposed cancellations would limit the availability 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 use of brodifacoum and difethialone will reduce the 
~ 96 ~ 

 

potential for wildlife to encounter these rodenticides, 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 other rodenticides registered for general consumer use against 

commensal rodents. The incident reports support the quantitative risk assessment finding that 

bromethalin, chlorophacinone, diphacinone and warfarin present considerably less risk of 

primary and secondary poisoning than brodifacoum and difethialone. While the use of tamper 

resistant bait stations could effectively mitigate 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 consumers 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 difethialone in the consumer market is expected 

to cause most consumers to turn to one of the other available rodenticides or to use alternative 

mechanical controls, thereby reducing overall use 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 greatly reduce the risk of adverse effects to nontarget wildlife. 

The NOIC also proposes the cancellation of certain consumer commensal rodent control 

products because they are not sold in or with bait stations reasonably anticipated not to release 

rodenticide bait. Although labels of these products currently require consumers to use tamper 

resistant bait stations if bait is placed where 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. EPA 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 among non-target mammals larger than target 

rodents. As bait stations are 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 enter a small, confined space. Bait stations also 

reduce rodenticide risks to predators: Reducing the number and types of prey species likely to be 

contaminated with rodenticides should reduce the proportion of rodenticide-contaminated prey in 

a predator’s diet and reduce the total quantity of a rodenticide available to the predator. 

Moreover, limiting the availability of bait forms such as pellets, granules, grain and meal 

is likely to reduce the spatial extent of bait dispersal 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 compared 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 wildlife directly with 

rodenticides. This may be especially significant for chemicals such as brodifacoum, difethialone, 

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

Measures that make rodenticide baits less available to non-target wildlife that are primary 

consumers are also likely to result in a reduction of predatory and scavenger 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 limit use of bait forms such as pellets, 

granules, grain and meal by professional, commercial and agricultural users, it is EPA’s belief 
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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 consequences of overuse. For these reasons, EPA 

believes that pesticides generally pose less risk when applied by professional, commercial and 

agricultural users than when applied by the general public. In the case of rodenticides containing 

brodifacoum and difethialone (active ingredients that are not registered for field uses, except for 

certain restricted use products registered to USDA/APHIS for very limited 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 limit access to these products to 

professional, commercial and agricultural users. 

b. Endangered Species Considerations for Rodenticide Active 

Ingredients 

 The Agency has concluded that the rodenticides subject to the NOIC pose risks of 

concern to non-target wildlife. By extension, these chemicals would also pose risks of direct 

effects to federally listed threatened and endangered species and designated critical habitat. 

Further, potential indirect effects to any species dependent upon a species that experiences effects 

from use of rodenticide active ingredients cannot be precluded 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 factors 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 previously consulted with the Fish and Wildlife 
~ 99 ~ 

 

Service (the Service) under the Endangered Species 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 biological 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 opinion, but in March 2005, initiated informal 

consultation. That informal consultation for products containing one of the nine rodenticide active 

ingredients registered for commensal rodents at that time was 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 incidents have involved Federally listed 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 protected 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 the 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 additional restrictions on use are necessary to address 

adverse impacts to listed and other protected species or designated critical habitat, EPA may 

initiate other appropriate action to address such impacts. 
~ 100 ~ 

 

IV. Benefits 

FIFRA requires that, when determining whether a non-dietary pesticide use causes 

unreasonable adverse effects, EPA must take into account the economic, social and 

environmental costs and benefits of the pesticide use. This sense of the term “benefit” is 

therefore different from its use in a benefit – cost analysis. In the FIFRA context, the benefits of 

the rodenticide products that EPA proposes to cancel are equivalent to the impacts of 

cancellation on their users. The impacts of cancelling certain products are also representative of 

the foregone benefits of denying registration to products of similar nature. EPA examined 

several potential impacts of the proposed cancellation of the rodenticide 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 consumers to achieve control of their rodent 

problems. 

• Whether the cost of rodent control, including 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. Residential consumers will still have a wide variety of 

options for rodent control, including several non-chemical options as well as multiple rodenticide 

active ingredients. The performance of all commensal rodent control measures can vary widely 

according to external environmental conditions, state of the residence, and the behavior of 

individual rodents, but there is no evidence that SGARs consistently out-perform all other active 
~ 101 ~ 

 

ingredients, or that unprotected bait consistently out-performs bait in bait stations, regardless of 

circumstances. Residential consumers who would 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 infestation. Cost increases such as these are 

unlikely to induce consumers who would use rodenticides 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, since the issuance of the RMD, registrants have 

been able to develop technologies for producing RMD-conforming house mouse products at 

substantially lower cost than was seen in 2008. Thus, it is possible that prices 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, such as disposing of dead rats (although the labels of the products 

subject to cancellation also require the disposal of dead rodents if found). These cost impacts 

arise because of the requirement that bait be contained in bait stations; the choice of active 

ingredient does not affect the per-unit cost or the cost of control. The additional cost is generally 

less than two percent of the monthly non-housing income for a family of three at the poverty 

line, and a considerably smaller proportion for the majority of residential consumers. 

When comparing these costs against the expected risk reduction, EPA regards these cost 

increases as only affecting those residential consumers who do not use rodenticides where 

children, pets or non-target wildlife 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 establishment) 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 advantages of the rodenticide products EPA intends to 

cancel and their alternatives, and 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 containing SGARs and/or unprotected bait, i.e., not confined to a bait 

station reasonably anticipated not to release rodenticide bait. The analysis distinguishes between 

impacts on consumers treating for mice and for rats and also on consumers facing a single or 

sporadic infestation and those facing chronic or repeated infestations. Chronic infestations may 

occur in situations where rodent populations are particularly high due to favorable external 

environmental conditions such as readily available 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., fields or livestock feed) and harborage (barns or 

natural sites). In these situations, sanitation and exclusion are difficult and infestations can be 

prolonged and recurring. 

To assess the impacts of the proposed cancellations, 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 control of an infestation. EPA also 

compared other factors that may be considered advantageous or disadvantageous, such ease of 
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use and disposition of carcasses, and compared control costs. Finally, these factors formed the 

basis for EPA’s conclusions about the most likely 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 claims 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 households reporting seeing signs of rodents, 86 percent 

reported signs of mice, nine percent reported signs of rats, and another five percent could not 

identify the rodent (Census Bureau, 2011). Most rat problems in the United States are likely to 

be Norway rats, as the roof rat appears limited to Hawaii and relatively warm and coastal areas in 

the contiguous 48 states (Marsh, 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 chronic 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 mechanical traps accounting for almost 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 problems may, in general, choose different 

control options than those with house mouse problems. It seems likely, for example, that 

someone with a commensal rat problem would be more likely to call a professional pest control 

service than someone with a house mouse problem, but specific data are not available. 

Rodenticides can, in general, be used to target either mice or rats although bait stations for mice 

would typically be too small for rats to enter. Results 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 percent of commensal rodenticide bait sold is in 

products intended for use against house mice. Glue boards come in different 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 boards 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, and sales data indicate only two percent of the sales 

for these products are for rat-sized units (IRI, 2010). Together these data indicate that 90 percent 

or more of rodent control problems involve house mice. 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 year ending in July, 2012, indicate that SGAR 

pellets are the dominant form of mouse baits with just over 65 percent of the market (IRI, 

2012a). Single-use, disposable bait stations, which primarily contain bromethalin, 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 various active ingredients and forms (e.g., blocks) not in stations and a few 

bait stations containing SGARs such as bromadiolone. EPA has recently conducted an informal 

check of available products which suggest that products targeting 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 containing bromethalin was recently registered for rat 

control. However, data on sales or use of recently registered products are not yet available. 

C. Usage Patterns 

Rodenticides are formulated in baits designed to be sufficiently appealing 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 commensal rodenticides, including those proposed for 

cancellation, direct users to place bait in the areas where the rodents are active, typically along 

walls or other likely routes of travel. When used to control house 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 require 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 products subject to the NOIC bear labels that require the user to 

check the condition of the bait after 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 placements in similar locations. 

Not all target rodents will begin to feed on bait immediately. Two or more weeks may be 

required to kill all rodents in an infestation, regardless of the active ingredient in the rodenticide 

used. The longer treatment times are more likely where food items other than the bait are 

available to the rodents. From the time target rodents begin feeding on them, anticoagulant 

rodenticides take at least three to five days to kill their first victims, and two or more weeks to 

kill all of the rodents that will ultimately be taken. 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 will typically last from one to 

several weeks. Because it is difficult to determine how many rodents are present in a residential 

infestation, it is prudent for users to continually monitor for fresh signs of rodents during the 

course of control operations – regardless of the method of control – and continue baiting until 

new evidence of rodent activity is no longer detected. 

Effective use of rodenticides depends on a number of factors including 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 them and consume a lethal dose of rodenticide. 

To characterize the likely range of use, EPA 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 noticed either by their movement, by the consumption 

of food, or by their droppings. A major infestation might occur if rodents find a food source that 
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is rarely disturbed, such as a large supply of pet food in a basement, 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 uncommon, especially with rats. EPA also evaluated 

one-time infestation and repeated infestations in each of these scenarios. 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 rural 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 households 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 station) 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 situations where bait placements are used both 

spatially and sequentially. For example, six placements could represent a case where the 

user sets three placements around the kitchen area 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 criteria announced in the RMD, and 

rodenticide bait products containing SGARs. EPA concludes that the proposed cancellations 

will not impair the ability of residential consumers to control commensal rodents, because the 

alternative control methods discussed below remain available. 

1. House Mouse Control Products 

a. Rodenticides 

There are currently more than 30 rodenticide products that conform to the RMD 

registered for general consumer use against commensal 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 against 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 the 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 rodents of the targeted species; (2) laboratory efficacy screening 

of one or more bait formulations with wild-type 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 for 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 product meets the efficacy threshold 

that EPA considers necessary to support registration. 

According to market research (IRI, 2012a), RMD-conforming products currently make 

up about 27 percent of the market for mouse rodenticides. 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 ingredient 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 control an infestation than 

anticoagulant bait because each individual mouse consumes less bromethalin bait before it dies. 

The rest of the RMD-conforming products currently available contain chlorophacinone or 

diphacinone, which are FGARs. They are less acutely toxic than SGARs and often require a 

mouse to feed multiple times over several nights before it will obtain a lethal dose. In studies, 

however, the time to death is approximately the 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 would have to make greater effort to maintain 

fresh bait and reduce the availability 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. 
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bromethalin. In practice, however, the difference is likely minimal, because the amount of bait 

applied (assuming use in accordance with label directions) is more than the amount likely to be 

consumed in one night by the number of house mice 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 rodenticide 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 several others showing that pellets or meals were preferred. 

Prescott (2011) reported that bait-block formulations from many countries tended not to be 

accepted as well as pelleted baits when tested under 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-specific efficacy data requirements have led to the 

production in the U.S. of bait blocks that are highly palatable to commensal rats and mice. EPA 

requires that all commensal rodenticide bait forms (e.g., pellets, meals, pastes, powders, block 

baits) meet the same efficacy criteria for registration for use in and around residences (Jacobs, 

2011). There is no basis for presuming that certain 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 protect bait from dust and moisture, thereby keeping 

the bait palatable longer. They provide mice with a protected place to feed leading to greater 
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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 applied, D-Con Mouse Proof II, EPA Reg. No. 3282-65. 

Although some may argue for the desirability 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 human 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 any trap) intended to control a house mouse infestation. House 

mice tend to move through living spaces along walls and behind appliances, places where bait 

stations can easily be placed. Moreover, placement in wall voids or other places from which bait 

cannot be checked or retrieved is not allowed under the use directions on the labels of any of the 

products subject to the NOIC. Tossing baits where they cannot be monitored or retrieved 

precludes compliance with label directions to monitor bait consumption 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 the same level of control of house mouse infestations, within 

essentially the same time frame, and with essentially the same level of effort, using other 

currently registered rodenticide products that conform to the RMD as they would with products 

subject to this NOIC. 
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b. Non-chemical Methods 

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

boards. Other non-chemical control methods (e.g., live traps, devices that electrocute mice) are 

also marketed, however, EPA’s alternatives analysis 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 inexpensive and they may be 

reused. In most cases, death is essentially instantaneous. Some disadvantages include the time 

and effort of baiting and setting the traps and, once sprung, a trap will not work until reset. The 

user must dispose of the dead mouse, which may be an unpleasant task (although users of 

rodenticides are also required to dispose of dead rodents if they find them). On the other hand, 

the presence of the dead mouse offers a concrete 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 rodenticides. 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 catch 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 conjunction 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 
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escape (Corrigan 1997). Rodents have been observed to use paper, dirt, or leaves to essentially 

create bridges over the sticky surfaces (Corrigan 1997). The Centers for Disease Control does 

not recommend glue boards because often the trapped rodents are not dead when users collect 

the used glue boards, thereby increasing the potential 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 rodenticides within a similar time frame. In comparison to rodenticides, 

there may be some non-monetary costs associated with their use, e.g., the effort to bait snap traps 

and monitoring of and disposal of dead or dying rodents from snap traps or glue boards. 

Considering the Centers for Disease Controls’ concerns 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 rodents and other pests, even though PCO services are more expensive 

than do-it-yourself pest control. Products routinely used by PCOs are not subject to the NOIC, 

therefore consumers currently using PCO services 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 accounts, 24 percent use mechanical traps, and 16 percent use glue 

boards (Curl, 2012).18 There is a similar distribution 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
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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 accounted 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 distinguish between mouse and rat control. 

2. Rat Control Products 

a. Rodenticides 

Currently, there are only three rodenticide products that conform to the RMD registered 

for general consumer use against commensal rats. Two of these products are 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 contain 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 generally cease feeding at that time and die in two 

to three days. Thus, the typical time to death is shorter than those typical of anticoagulants. 

There are currently no RMD-compliant FGAR products currently registered for 

residential consumer use in controlling commensal rats, but there are no apparent impediments to 

the adaptation of currently registered bait block formulations containing FGARs for use in bait 

stations that conform to the RMD and are sized appropriately for baiting commensal rats. As 

noted in the discussion of mouse control products, 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.
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be necessary for a rat to obtain a lethal dose. Time to death with FGARs, however, is similar to 

that of SGARs. 

Blocks are an effective bait form for rat control, 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 residential 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 found more examples of block baits than pelleted 

baits among products marketed to general consumers 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 commensal rodent baits to meet the same criteria in efficacy 

screening tests (except for bait blocks limited by labeling to use exclusively in wet or damp 

areas), so there is no basis for presuming that pelleted 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 “neophobia”, 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, and is affected by a broad array of factors. 

Although neophobia can delay an individual 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 effective urban rat control projects for many years, 

and have also been used in successful eradications of commensal rats from offshore islands, 

indicating that satisfactory levels of control can be achieved using bait stations. For several 
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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 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 supporting 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’ environment is also likely to induce some neophobia. 

Second, most rats will explore a new bait station 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. Third, entering a container of some sort would not 

be a new behavior for rats that are accustomed 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 diminish neophobia of other rats. Fourth, rats will 

not likely be fully accustomed to a human-occupied residence before the resident notices their 

presence and takes action. In such circumstances, rats may not perceive a bait station as new 

relative to other features of their environment. 

Achieving control of an infestation using rodenticide baits without 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 several 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 
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several days in the length 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 unprotected 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 associated with use of a bait station is unlikely to lead to a 

noticeable extension of the treatment period. Note, too, that many of the alternative 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 the 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 achieve control, and the effort required of the user. 

b. Non-chemical Methods 

As with house mice, non-chemical control methods include snap traps and glue boards as 

well as other devices. Data are not available to discern the relative market shares of various 

methods in the control of rats, which is a relatively 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 percent of all snap traps sold are rat-sized (IRI, 

2010, via Bell Labs). Since about ten percent of households reporting identifiable signs of 

rodents report rats, it appears that consumers with rat problems are either more likely to hire 
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PCOs or less likely to use snap traps than are those with mouse problems. It is reasonable to 

think that the perceived disadvantages of snap traps, including the 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 relatively larger for rats, as the odors 

of decomposing rats are more powerful and longer-lasting than those of mice. Regardless of the 

relative weights attached to these advantages and disadvantages, traps are an effective means of 

control and could address a residential 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 performance, 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 rats. Thus, the level of 

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

obtained with rodenticides. As with mouse control, non-chemical methods may require more 

effort on the part of the user to bait snap traps and to dispose of rats. 

c. Professional Pest Control Operators 

The market data available to EPA concerning PCO rodent control activities do not 

distinguish between treatments for rats versus mice. Treatments for commercial accounts, which 

include apartment buildings or condominiums, are for control of both rodents, along with other 
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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 that 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 using such services will not be affected by the 

proposed cancellations. It is also worth noting that most PCOs report that they routinely use bait 

stations when using rodenticides in residences (ASPCRO/NPMA 2013). 

E. Impacts of Cancellation on Residential Consumers 

Based on the information present in IV.4., EPA 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 will be no impact on such users, or on others who 

rely on their services. The impact on consumers will 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 change in monetary expenditures as well as any 

non-monetary costs such as an increase in the effort needed to use an alternative method or to 

dispose of carcasses. 

This section summarizes EPA’s analysis comparing control costs of rodenticides that 

would be cancelled to the control costs using available alternatives (Cook and Hill, 2011). This 

analysis addresses commensal mouse and rat control across a range of situations differing in the 

size of the infestation (minor or major) and the frequency of infestation (one-time or repeated) as 

described in IV.3. 
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1. Incremental costs of house mouse control 

Overall, EPA expects that incremental costs 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 significantly affect the price of rodenticide 

products, so the incremental cost of the proposed 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 rodenticide 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 cancellation of the registrations of pelleted products. 

In a 2011 analysis of both mouse and rat products then on the market, EPA identified 

differences in the average price of RMD-conforming and non-conforming products that would 

indicate a cost increase for a one-time infestation 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 majority 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 products that include disposable or single use 

bait stations. These price data were based on a check of local sources 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 quantities of 16 to 28 placements per package. 
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EPA’s check of stores found a per placement price of about $0.75. The average cost of 

rodenticide products that include reusable bait stations, which provide a bait station and six to 

eight blocks, implies a per-placement cost of less 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 stations 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 registered rodenticides that 

conform to the RMD. Data generated by EPA suggest 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 very 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 induce him or her to purchase a nonchemical method instead. Thus, EPA does not anticipate 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 problems in U.S. households. 

It is worth noting that the house mouse control market has undergone considerable 

changes in recent years. When the RMD was announced in 2008, few rodenticides were 

available in ready-to-use bait stations, despite a long-standing requirement on labels that tamper 
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resistant bait stations be used where children, pets or non-target wildlife could otherwise have 

access to the bait. Stand-alone, reusable, tamper-resistant bait stations were very expensive and 

available mainly through vendors catering to professional users. Since the RMD, however, 

several manufacturers have developed rodenticide 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 ingredient 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 alternative 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 discussion in IV.3. EPA does not have market data 

for rodenticide products intended to control rats as it does for rodenticides intended to control 

house mice. 

The incremental cost per treatment is similar for situations regarding repeated 

infestations. Stand-alone, reusable, tamper-resistant bait stations are very expensive and 

available mainly through vendors catering to professional users. A new rodenticide product 

containing a rat-sized, reusable bait station was registered in October 2012 and may soon be 

available in retail outlets, but the price of the product is presently unknown. Improving 

technology rapidly has led to decreases in the price of mouse-sized bait stations and the same 
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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 incremental cost of using disposable stations for 

repeated infestations. 

The estimated increase in the cost of commensal 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 and 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 cost by about $6.00 more with glue boards and $12.00 

more with snap traps. Snap traps are recommended 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 the dispatching of rats trapped but not killed). 

The disposal of dead rats, however, may be less 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 locate and recover. 

For repeated infestations, snap traps are reusable, suggesting an overall per-infestation 

cost similar to or lower than the rodenticide products proposed to be cancelled. 

In conclusion, the limited number and higher cost of RMD-conforming rat control 

products will result in incremental costs of addressing a rat infestation 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 these costs, however, as commensal rats make up 
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about ten percent of residential rodent problems and only a portion of those problems would 

typically be addressed with rodenticide products proposed to be cancelled. Use of snap traps or 

glue boards, rather than RMD-compliant 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 control 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 products, 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 rodent problems. The AHS reports that about 14 percent of U.S. 

households are below the poverty line, but they account for almost 20 percent of households 

observing signs of rodents. 

To assess the per household impacts of cancellation, EPA compared the incremental 

costs, as presented in the previous section, likely to result from the proposed cancellations to 

household disposable income (i.e., excluding housing costs) at the poverty threshold. The 

poverty-threshold income varies depending on household size; this analysis used the income 

threshold for a three-person household as a reference, which is considered the average size 

household in the United States (Census Bureau, 2012). The poverty threshold is higher for larger 

household, thus the analysis is also representative of larger household at the poverty line. 

Monthly income rather than annual income was considered for two reasons. First, many low 

income households may lack savings or other methods for spreading the cost of rodent control 
~ 125 ~ 

 

across time and will have to pay for it from immediate cash resources. Second, some households 

will face recurring rodent control costs rather than one-time or annual costs. The Census Bureau 

(2012) reports that households at or below the poverty line spend 42 percent of income on 

housing. Thus, for this analysis, EPA calculates monthly disposable income at $900. 

For house mouse control, the average incremental costs for consumers using RMDconforming rodenticide products instead of products 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 the poverty threshold range from five percent of 

monthly non-housing income in a minor infestation to 11 percent in a major infestation if they 

use the RMD-conforming rodenticides that are currently available. Use of glue boards or snap 

traps would result in incremental costs of one percent or over three percent of monthly nonhousing income, respectively, plus non-monetary costs associated with the effort to set and 

monitor traps and dispose of dead or trapped rats. 

Again, because those low income households facing rodent problems overwhelmingly 

have mouse problems (88% of rodent infestations 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. Moreover, because less than ten percent of low 

income households report having seen signs of rodents within the preceding three month period, 

it is a small proportion of low income households 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 should be using bait station products and the potential cost of the 

cancellation action on these users should not be relevant to the cancellation decision. In fact, by 

making bait stations more easily available (and possibly cheaper as they become more available), 
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the cancellation action may actually economically benefit lower income households with young 

children. 

F. Potential for Resistance 

EPA considered the risks of increased resistance to anticoagulant rodenticide products 

due to the proposed cancellation of certain consumer-oriented products containing SGARs and 

concluded that the risks are minimal. Resistance refers to genetic changes in a rodent population 

as a result of tolerant individuals being more likely to reproduce and pass that trait on to 

subsequent generations, as a result of rodenticides 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-pesticide combinations. However, residential 

consumer use of the conforming anticoagulant rodenticides will not be so widespread, frequent, 

and repetitive that enough anticoagulant tolerant individuals will be selected to result in a 

resistant population. 

First, relatively few residential consumers face rodent problems. Current housing 

statistics show that only six percent of U.S. households report seeing rodent signs in the 

preceding 3 months (Census Bureau, 2011). With 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 repetitive use of rodent control in 

general. 

Second, rodenticides as a whole make up a relatively small proportion of residential 

control products. Market data indicate that traps account for about 70% of retail sales of rodent 

control products, with rodenticides account for the remaining 30% of sales (IRI, 2012b). And 

after SGARs are removed from the residential consumer market, the 30% of residential 
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consumer rodent control that relies upon rodenticides appears likely to be divided between 

rodenticides containing active ingredients 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 residential infestations arise are also 

subject to control by commercial applicators and public health officials using SGARs. These 

personnel, along with natural predators, 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 concludes 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 products identified in the NOIC (and listed in 

Tables 1 and 2 of this document) present significantly 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 presence of the active ingredients brodifacoum and 

difethialone and/or the absence 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 the use of alternative 

products that are effective and affordable. 

A. Cancellation and Denial of Registrations 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 all bait formulations containing them that are 

registered for use to control commensal rodents have 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 registered based on reliable studies demonstrating 

satisfactory effectiveness against target rodents. EPA concludes that cancellation of products 

subject to the NOIC will not cause residential consumers to lose the ability to control commensal 

rodents and will not increase the time required to control commensal rodents. Currently 

registered rodenticide products that contain bromethalin or FGARs, when used in combination 

with prudent sanitation and exclusion measures, are effective for general consumer use for the 

control of commensal rodents in and around buildings. 
~ 129 ~ 

 

2. Alternatives to brodifacoum and 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 containing other active ingredients 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 same time frame, and with 

essentially the same level of effort, using other currently registered rodenticide products, the 

cancellation of products containing the active ingredients brodifacoum and difethialone will not 

measurably increase the cost of rodent control. 

3. Residential consumer use of brodifacoum 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 scavengers that consume target rodents, 

pose greater risks to non-target wildlife than rodenticides that do so to a lesser degree. Available 

toxicokinetic data indicate that 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 conclusion that it is rapidly 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 difethialone also appears to be fairly prevalent in 

some areas, especially when considering the relatively low usage of this rodenticide in the 

United States. Species in which widespread accumulation of anticoagulant rodenticides in liver 
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tissue has been observed include owls, hawks, vultures, 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 study in southern California. 

Inasmuch as products containing brodifacoum and difethialone are only registered for use against 

commensal rodents in and around buildings and are not registered for field uses or use against 

other rodent species, all non-target wildlife exposures to brodifacoum and difethialone are 

believed to result from commensal rodent products registered for use in and around buildings.19 

Cancellation of brodifacoum and difethialone products sold to residential consumers is expected 

to reduce environmental loading of these highly toxic and persistent chemicals and to thereby 

reduce secondary poisonings among non-target wildlife. Information from several lines of 

evidence (i.e., predictions from toxicity and metabolism studies, whole carcass residue studies, 

secondary feeding studies, wildlife incident reports) indicate that brodifacoum and difethialone 

accumulate in body tissues to a greater extent, and 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, combined with the high toxicity of these chemicals, 

presents significant risks of secondary exposure 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 brodifacoum 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 banks, river banks, gullies, irrigation ditches, railroad tracks, 

fence lines, buffer strips, garbage dumps, landfills, orchards, and rangelands.
~ 131 ~ 

 

Wildlife incident data support 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 for difethialone is much more limited than that for brodifacoum, 

which is not surprising given difethialone’s lower extent of use in the United States. However, 

analysis of the toxicity and retention 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 lack 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 primary 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 resistant bait stations. However, the secondary exposure 

risk to predators and scavengers cannot be adequately 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 warfarin, chlorophacinone, diphacinone, or bromethalin. 

Brodifacoum and (to a lesser extent) difethialone have been widely used by residential 

consumers, and residential consumer use may contribute significantly to brodifacoum and 

difethialone poisonings in non-target wildlife. Limiting availability of these chemicals in the 

consumer market will likely cause consumers who would otherwise buy brodifacoum and 

difethialone products to buy other rodenticides, thereby reducing use and environmental loading 

of brodifacoum and difethialone – and hence, secondary exposure risks to non-target wildlife. 

While switching to alternative rodenticides will not completely eliminate secondary exposure 

risks, EPA believes that these risks to wildlife will be significantly reduced if brodifacoum and 
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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 rodenticides containing brodifacoum or difethialone 

experience significant adverse effects. These adverse effects occur despite label statements 

requiring use in tamper-resistant bait stations where placements otherwise would be accessible to 

non-target wildlife. Brodifacoum and difethialone present greater 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 rodents that individually contain less than the dose 

that would be lethal to the secondary 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 after attaining a lethal dose, increasing their toxicity to predators 

and scavengers. Products containing brodifacoum and difethialone are only registered for use 

against commensal rodents in and around buildings. Significant numbers of incidents of 

secondary rodenticide poisonings of non-target wildlife involving brodifacoum and difethialone 

occur in urban and suburban areas, suggesting that use of products containing brodifacoum and 

difethialone in these areas pose significant 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 frame, 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 active ingredients bromethalin, chlorophacinone, 

diphacinone, and warfarin are effective, affordable, and cause significantly less risk to the 

environment, EPA concludes that the risks caused by residential consumer use of rodenticide 

products containing brodifacoum or difethialone active ingredients cause risks that are 

unreasonable. Accordingly, the following rodenticide products registered for general consumer 

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

D- MOUSE PRUFE II, EPA Reg. No. 3282-65 (brodifacoum) 

D- PELLETS GENERATION II, EPA Reg. No. 3282-66 (brodifacoum) 

D- BAIT PELLETS II, EPA Reg. No. 3282-74 (brodifacoum) 

D- READY MIXED GENERATION II, EPA Reg. No. 3282-81 (brodifacoum) 

D- MOUSE-PRUFE III, EPA Reg. No. 3282-85 (difethialone) 

D- BAIT PELLETS III, EPA Reg. No. 3282-86 (difethialone) 

D- II READY MIX BAITBITS III, EPA Reg. No. 3282-87 (difethialone) 

D- BAIT PACKS III, EPA Reg. No. 3282-88 (difethialone) 

In addition, EPA denies applications for registration of the following products: 

D-CON BAIT STATION XV KILLS MICE, EPA Application No. 3282-RNU 

(brodifacoum) 

D-CON BAIT STATION XV KILLS MICE, EPA Application No. 3282-RNL 

(brodifacoum) 

EPA denies these applications on account of the same risk concerns that are the basis for 

the cancellation of the products described above, and in addition, notes that because no one is 

currently relying on these unregistered 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 other registered products that do not cause unreasonable adverse 

effects. 
~ 134 ~ 

 

B. Cancellation and Denial of Registration of Rodenticides Intended for 

Residential Consumer Use In Controlling Commensal Rodents In and 

Around Buildings In Forms That Do Not Adequately Protect Against Access 

By Children, Companion And Domesticated Animals, And Non-Target 

Wildlife. 

 Rodenticide baits are directly accessible to children, domestic animals and non-target 

wildlife, unless the baits 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 practice, it is difficult to place rodenticides in or 

around residential structures in places where children, domestic animals and non-target wildlife 

cannot reach them. Even if rodenticides are initially well placed, rodents 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 products 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 qualify as tamper resistant. 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 typically purchase rodenticides. Consequentially, the 

widespread and commonly recognized practice of residential consumers has been to apply 

rodenticides without tamper resistant bait stations, in locations that 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 continues 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 number who do not. Moreover, the products subject 

to the NOIC are not designed or expected to fit securely in such third-party bait stations. 

 The primary exposures of children, domestic animals, and non-target wildlife to 

rodenticides, and the resultant risks, can be substantially 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 Weather-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 set forth in Pesticide Registration Notice 94-

7, and have also satisfactorily demonstrated the ability to isolate bait from children and 

dogs in laboratory testing conforming to EPA protocols. 

• Tier 2 - Tamper-Resistant (but not weather resistant): Tier 2 bait stations have 

satisfactorily demonstrated the ability to isolate bait from children and dogs in laboratory 

testing conforming to EPA protocols. Tier 2 bait stations have not met weather resistance 

standards; therefore, rodenticide 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 stations have not demonstrated the ability to isolate bait from 

dogs and have not met weather resistance standards; therefore, rodenticide bait products 

that include Tier 3 bait stations must be labeled for indoor use only and to prohibit 

placement where the product is accessible to domestic animals and/or non-target wildlife. 

• Tier 4 - Tamper-Resistance Unknown: Tier 4 bait stations have not been demonstrated 

to meet the testing standards required of the higher 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 target rodents, and not reasonably anticipated to 

release rodenticide bait except for bait removed by target rodents and minor quantities of 

crumbs created by target rodents. Rodenticide bait products that include Tier 4 bait 

stations must be labeled for indoor use only 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 rodenticides without bait stations. 

In order to be registered in the U.S. for use in and around residences 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 officials, pest control operators (PCOs), and other occupational 

applicators) are overwhelmingly in block form (Lublinkhof 2012). There is no basis for 

presuming that pelleted or meal baits offer faster control or a higher degree of control. 

Bait-stations are widely used by professional applicators and effective rodent control has 

been achieved using bait stations in a wide variety of circumstances (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 children, pets, domestic animals, and/or non-target 

wildlife, and commercial and professional users generally 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 newly introduced bait station for a period of time, 

however, the delay in initial entry is small compared to the variability in the other factors 

affecting the length of the treatment period needed to achieve control of an infestation even 

 
~ 137 ~ 

 

without bait stations. Consequently, any delay in entry is unlikely 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 rodenticides without bait stations. 

Most residential consumers will not be affected by the proposed removal of rodenticides 

without bait stations from the residential consumer market, because most residential consumers 

use mechanical methods of control, which will not be affected by the proposed cancellations. 

Likewise, residential consumers who prefer to use rodent control services provided by 

professional and commercial applicators will not be affected by the proposed cancellations. 

Professional users (e.g., PCOs, commercial users, property managers, public health officials) 

generally have access to tamper-resistant bait stations (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 pellets, granules, grains, and meal if special circumstances might 

warrant their use. Inasmuch as these professional users will not be affected by the cancellations, 

neither will residential consumers who rely on their services. 

The only users likely to be affected by the proposed cancellations are those residential 

consumers who purchase and use rodenticides for 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 rodenticide products registered for the control of commensal rodents in 

and around buildings products without bait stations conforming to the RMD criteria, because 
~ 138 ~ 

 

there are multiple alternative rodenticide products conforming to the RMD and marketed at 

prices comparable to those of the products EPA proposes 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. Moreover, by making bait stations 

more easily available (and possibly cheaper as they become more available), the cancellation 

action may actually economically benefit lower income households with young children. 

For residential consumers currently using rodenticide products that do not conform to the 

RMD to control mice, data from a recent national market survey shows the cost per placement 

for rodenticide products that include 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 registrations of pelleted products (IRI, 

2012a). For the much smaller number of residential consumers attempting 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 infestation 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-housing income at the poverty threshold. For rat 

control, incremental costs for consumers at the 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 Census 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 preceding three month period, it is a small proportion of 

low income households that would be subject to this burden. 

Finally, in considering whether 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 the products subject to the 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 present 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 cause 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 rodenticides. 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 presentations 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 lightly. The high numbers of reports of exposed children are of 

concern because every exposure event presents the possibility of significant adverse health 

effects. Approximately 85% of the rodenticide exposures reported 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, 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 rodenticides were applied. In other 

cases, it appears that the exposed children were visiting a different environment (such as 

grandparents, friends, or neighbors) and their parent or guardian was 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 account of the risk of excessive bleeding (internally or externally) 

in response to subsequent trauma. The adverse health consequences of these symptomatic 

exposures could be prevented through the use of tamper resistant bait stations, as could the social 

and economic costs that arise from addressing children’s asymptomatic exposures to 

rodenticides, including economic costs to health care facilities and poison control hotlines, and 

social and economic costs to the families whose children are exposed. 
~ 141 ~ 

 

EPA’s analysis shows that, unless use and exposure patterns are changed, children could 

easily ingest quantities of the subject rodenticides that would contain sufficient amounts of active 

ingredient to exceed levels that EPA would consider safe. A single 5 gram bite (less than a 

quarter of an ounce) of any of the rodenticide baits subject to the NOIC would 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 

rodenticide baits subject to the NOIC is sufficient to cause adverse health effects. Consequently, 

EPA could not conclude that exposure to the subject rodenticides was reasonably certain not to 

cause harm. EPA fully appreciates that the rodenticide products at issue 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 risks 

of such use. Nevertheless, the FFDCA criteria for 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 pesticide use might be to agricultural 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 death and other severe outcomes that have required 

veterinary care. In 2010, APCC identified rodenticides 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 (brodifacoum and bromadiolone) in the top 20 pesticides 

most likely associated with a domestic animal fatality. OPP’s IDS indicates that in recent years 
~ 142 ~ 

 

there are about 2000 reported incidents per year of domestic animals exposed to rodenticides. 

Many of these exposures result in severe outcomes -- 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 underestimates the actual number of incidents. 

 The various lines of evidence evaluated by EPA 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 rodenticide 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 evidence that rodenticide exposure causes non-target 

wildlife deaths. Although many non-target wildlife species avoid areas of human habitation, 

significant numbers of incidents of both primary 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 rodent 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 species, including owls, eagles, hawks, vultures, 

mustelids, bobcats, and mountain lions. Numerous 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 SGARs in wildlife regardless of location of collection indicates that 
~ 143 ~ 

 

rodenticides used in and around buildings 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 them from direct access to the bait. While bait 

stations cannot prevent secondary exposures to intoxicated prey, bait stations can ensure that 

fewer intoxicated birds and mammals are available as prey. 

4. Conclusion. 

The rodenticides subject to the NOIC are poisonous to all mammals and birds. Exposure 

to these rodenticides is widespread among children, domestic animals, and non-target wildlife. If 

rodenticides continue to be available in the residential consumer market without bait stations, 

these exposures are likely to continue. 

 Bait stations conforming to the RMD criteria can significantly reduce rodenticide 

exposures among children, domestic animals, and non-target wildlife, compared to products 

without bait stations conforming to the RMD criteria. EPA has determined that control of 

commensal rodents in and around buildings by residential consumers can be satisfactorily 

accomplished with rodenticides protected by bait stations. For many years, labels for commensal 

rodenticides have required that baits used where children, domestic 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 rodenticide products subject to the NOIC, and, when used 

in combination with prudent sanitation 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 significantly less risk to man or the environment, 

rodenticide products intended to control commensal rodents in and around structures and 

marketed for general consumer use cause unreasonable risks unless they include 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 conforming to the RMD criteria: 

D-CON CONCENTRATE KILLS RATS & MICE, EPA Reg. No. 3282-3 (warfarin) 

D- READY MIXED KILLS RATS & MICE, 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 Reg. No. 3282-65 (brodifacoum) 

D- PELLETS GENERATION II, EPA Reg. No. 3282-66 (brodifacoum) 

D- BAIT PELLETS II, EPA Reg. No. 3282-74 (brodifacoum) 

D- READY MIXED GENERATION II, EPA Reg. No. 3282-81 (brodifacoum) 

D- MOUSE-PRUFE III, EPA Reg. No. 3282-85 (difethialone) 

D- BAIT PELLETS III, EPA Reg. No. 3282-86 (difethialone) 

D- II READY MIX BAITBITS III, EPA Reg. No. 3282-87 (difethialone) 

D- BAIT PACKS III, EPA Reg. 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 Regulatory Officials and 

National Pest Management Association, 2013, Rodenticide Use Survey of Pest 

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