### UNITEDSTATES ENVIRONMENTAL PROTECTION AGENCY WASHINGTON, D.C. 20460


### OFFICE OF PREVENTION, PESTICIDES AND TOXIC SUBSTANCES PC Code No.: 098801 DP Barcode: 323825 Date: June 30,2006 SUBJECT: Environmental fate and ecological risk assessment for re-registration of chlorflurenol methyl ester (ME), an herbicideiplant growth regulator for use on ornamentals, hedge and fence rows, turf, shade trees, woody shrubs and vines, and to produce planting material for pineapple production. 

### TO: Tawanda Spears, Chemical Review Manager Michael Goodis, Branch Chief SpecialReview and Re-registration Division (7508P) 

# I FROM: ERB V Team for Chlorflurenol ME: Jennifer Leyhe, M.S., Biologist, Ecological Effects Reviewe Larry Liu, Ph.D., Chemist, Environmental Fate Reviewer Environmental Fate and Effects Division (7507P) 

### THROUGH: Karen Whitby, Ph.D., Acting Branch Chief Environmental Risk Branch V Environmental Fate and Effects Division (7507P) The attached document contains the Environmental Fate and Effects Division's (EFED) screening-level environmental risk assessment for ChlorflurenolME. Therisk assessmenthas been conductedin accordance with the Agency guidance on ecological risk assessment and the OPP ecological risk assessment Overview document. Chlorflurenol ME is used as an herbicidelplant growth regulator on ornamentals, hedge and fence rows, turf, shadetrees, woody shrubs and vines, andto produceplantingmaterial forpineapple production. An evaluation of environmental risk to aquatic and terrestrial organismsasaresult oftheuseof chlorflurenol ME is summarized in the Executive Summary and the Risk Characterization sections of the attached document. This assessment was conducted with minimal data and therefore contains major uncertainties. outs tan din^ Data Reauirements and Data Gavs Environmental Fate: The environmental fate data gaps are listed in Table 1 (also Appendix 

### H, the attached environmental risk assessment document). In order to meet data requirements and reduceuncertainty, the registrant is requested to conduct: 1) 16 1 

### - 1 Hydrolysis 2) 161-2Aqueous photolysis 3) 16 1-3 Soil photolysis 4) 162-1 Aerobic soil metabolism5) 162-2 Anaerobic soil metabolism 6) 162-3 Anaerobic aquatic metabolism 7) 163-1 Adsorption/desorption 8) 164-1 Terrestrial field dissipation 9) 165-4Fish bioaccumulation 10) 20 1-1 Droplet Size Spectrum 11

) 202-1 Drift Field Evaluation Ecological Effects: The screening-level risk assessment for chlorflurenol 

### ME has been conducted, despite unfulfilled guideline requirements and existing data gaps. Table 2 (also Appendix 

### H,the attached environmental risk assessment document) lists the status of the ecological effects data requirements for chlorflurenol ME. In orderto reduce uncertainty in this risk assessment, we are requesting that the registrant submit the following: 1 ) Guideline 72-1: Acute freshwater fish. 2) Guideline 72-2: Acute freshwater invertebrate. 3) Guideline 72-3: Acute estuarineimarine fish and invertebrate. 4) Guideline 72-4: Chronic fish. 5) Guideline 7 1-4: Avian reproduction. 6) Guideline 123-1: Terrestrial plant seedling emergence and vegetative vigor. 7) Guideline 123-2 Aquatic plant growth 8) Guideline 141-1 : Honey bee acute contact toxicity. Uncertainties Environmental Fate: Theregistrant has submitted three studies to support the environmental fate data requirements; however, these studies were considered either supplemental or unacceptable (see reasons below). As a result, the uncertainty analysis could not be performed with confidence. Guideline 161 -1: The study was conducted at pHs 3, 6 and 

### 9 rather than pHs 5, 7 and 9 as required in Subdivision N Guidelines. This study was determined to be supplemental. Thehydrolysis data requirements have not been fulfilled. A new study including pH 7 is required. Guideline 162-1: The study was conducted outdoors in the summer where the environmental conditions, soil aerobicity, microbial viability, and soil moisture were neither controlled nor reported. Subdivision N Guidelines require that the study be conducted in the dark at 25 It 1"C. This study was determined to be unacceptable. The aerobic soil metabolism data requirements have not been fulfilled. A new study is required. Guideline 163-1: Only one test soil type was used in the adsorption study and it could not be determined if this German soil was comparable to soils found in typical use areas in the United States. Subdivision N guidelines specify that four different soil types should be used. This study was determined to be supplemental. The adsorptionldesorption data requirements have not been fulfilled. A new study including three soils is required. Ecological Effects:1) Acute oral and dietary toxicity studies in birds and acute oral toxicity studies in mammals failed to establish defmitive acute LD50/LCso values (i.e., the LCsO was expressed as "greater than" the highest dietary concentration tested); thus, significant uncertainty was introduced into the avian oral- and dietary-based and mammalian oral-based acute RQ calculations. 2) The study testing oral toxicity to birds did not state which components were included in the test material. EFED assumes the test material contained all three components which may underestimate risk to birds on an acute oral basis if in fact the test material only contained one ofthe three components. 3) The mammalian chronic RQs are based on a developmental study that shows evidence of delayed skull ossification and cleft palates in young rats. These endpoints are not adequate for determining risk to the survival and fecundity of a population. However, without other studiesEFED used these data. Therefore, the RQs may not accurately portray chronic risk to mammals. Risk may be under- or overestimated. 4) Application interval and number of applications per year are not indicated on the label. For multiple application scenarios, the 

### T-REX model requires both of these parameters in order to estimate exposure to terrestrial organisms. In the absence of these numbers an application interval of 28 days and 8 applications per year (as derived by HED, Appendix B, attached risk assessment document) were used. HED used information provided on the labels along with knowledge of the croplweed growth cycles, pest pressure timing, etc. to determine the application interval and yearly number of applications. Since these numbers are considered "likely" applications per year, risk to terrestrial organisms may be underestimated. EFED Label Recommendations The EFED recommends the following changes in hazard labeling: End Use Products This pesticide is toxic to birds and mammals. This pesticide is toxic to fish and aquatic invertebrates. Thisproduct ishighlytoxic to bees exposed to direct treatment on blooming crops or weeds. Do not apply this product or allow it to drift to blooming crops or weeds while bees are actively visiting the treatment area. Do not apply directly to water, or to areas where surface water ispresent or to intertidal areas below the mean high water mark. Do not contaminate water when disposing of equipment washwater or rinsate. Drift may be hazardous to aquatic organisms in water adjacent to treated areas. Manufacturing Use: Donot dischargeeffluent containing this product into lakes, streams, ponds, estuaries, oceans, or other waters unless in accordance with therequirements ofaNational Pollutant Discharge Elimination System (NPDES)permit and thepermitting authority has been notified in writing prior to discharge. Do not dischargeeffluent containing this productto sewer systems without previously notifying the local sewage treatment plant authority. For guidance contact your State Water Board or Regional Office of the EPA.Table 1. Environmental Fate Data Requirements. Date: Case No: n/a Chemical No: 09880 1 Data Requirelnents
Dewadation Studies -Lab:
TGAI or 161-1 Hydrolysis 161 -2 Photolysis in Water

Metabolism 

## I PAIRA 

## 1 3, 10, 11 

## 1 43595403 

## 1 was used) 

## I environment) 162-2 Anaerobic Soil 

## I TGAI or 

### ' 158.290 ENVIRONMENTAL FATE CHLORFLURENOL ME DATA REQUIREMENTS FOR THE ENVIRONMENTAL FATE AND EFFECTS DIVISION

161-3 Photolysis in Soil 

## I PAIRA ~om~osition'

Supplemental (pH 7 was not PAIRA TGAI or PAIRA TGAI or Yes (a study should be conducted at

10

Metabolism 162-3 Anaerobic Aquatic Metabolism Mobilitv Studies:
163-1Leaching and adsorptionJdesorption Dissi~ation Studies 

### - Field: 164-1 Terrestrial Field Dissipation 164-3 Forestry Use pattern'

3, 10, 11

3, 10 

## I Yes Metabolism Studies - Lab:



### ' 158.440 SPAY DRIFT 162- 1 Aerobic Soil

PAIRA TGAI or PAIRA
TGAI or PAIRA

TEP TEP

20 1-1 Droplet Size Spectrum 202-1 Drift Field Evaluation Bibliographic Citation

43496201

TGAI or

Yes Waived 3 10
3, 10, 11

3, 11

10 Accumulation Studies:

3, 11 3, 11 Study Classification

used)

165-4 Fish Bioaccumulation 165-5 Aquatic Non-Target Organisms

Yes yes Additional Data Required Under FIFRA?

pH 7) Yes

Unacceptable (an open study system

43496202 Yes (a study should be conducted under the controlled

Reserved TGAI or PAIRA TEP Ground Water Monitoring Studies: Supplemental (one German soil was used)

3, 10

10 166-1 Small Scale Prospective Groundwater Study Yes Yes Yes (three additional soils should be used)
Yes Waived

TEP 3, 11I. Composition: TGAl = Technical grade of the active ingredient; PA1 = Pure active ingredient; PAlRA = Pure active ingredient. radiolabeled; TEP = Typical end-use product. 2. Use Patterns: 1 = Tcrrestrial/Food; 2 = Terrestrial!Feed; 3 = Terrestrial Non-Food; 4 = Aquatic Food; 5 = Aquatic NonFood (Outdoor); 6 = Aquatic Non-Food (Industrial); 7 = Aquatic Non-Food (Residential); 8 = Greenhouse Food; 9 = Greenhouse Non-Food; 10 = Forestry; 1 1 = Residential Outdoor; 12 = Indoor Food; 13 = Indoor Non-Food; 14 = Indoor Medical; 15 = Indoor Residential.
Table 2. Ecological

Guideline#

71- 1

7 1-2

7 1-4

72- 1

72-2

72-3(a) Are additional data needed for ecological risk

assessment?
No

No

Yes

Yes

No

Yes

Yes Effects Data Requirements Data Requirement

Avian Oral LDco

Av~an Dietary LCSO

Avian Reproduct~on

Freshwater Fish LCio

Freshwater Invertebrate Acute LCFo
EstuarineIMarine F~sh LCi0 for Chlorflurenol ME. Test Substance

TGAI

TGAl MRlD # or Citation

43595401 43623601 43623602 Study Classification

Acceptable
Acceptable

No Data Submitted - Data Gap

TGA1

TEP

TGAl

No Data Submitted - Data Gap 120852100047 185 140979 45 137401 45242602 4524260 1 45 137402

90289 1 199251120889 120870 45 137403 45242603 Invalid

Invalid

InvalidTable 2. Ecological
Guideline #

72-3(b)

- 72-3(c)
72-4(a)
72-4(b) 72-4(c)

72-5 123-l(a)

123-1(b)

123-2

141- 1

141-2
81-1

83-I b 83-3a Effects Data Requirements for ChlorflurenolME. Data Requirement Test Substance Are additional data needed for ecological risk

assessment? MRID # or

Citation

Yes

Yes

Yes

Yes

Yes
Yes
Yes

Yes

Yes

Yes

No

Yes
Yes
Yes EstuarineIMar~ne

Mollusk ECjo EstuarinelMarine

Shr~mp ECjo Freshwater Fish Early Life-Stage Aquat~c Invertebrate L~fe-Cycle (freshwater) Aquatic Invertebrate L~fe-Cycle (marine) F~sh Full Life-Cycle Seedl~ng Emergence (T~er 11) Vegetat~ve Vigor (Twr 11) Aquatic Plant Growth (Tler 11) Honey Bee Acute

Contact LDjo Honey Bee Residue on Foliage Acute Oral Toxicity to Rat Dog Chronic Study Prenatal Developmental

Toxicity Study - Rat Study Classification

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap
No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap
Acceptable
Acceptable Acceptable TGAl

TGAI TGAI 43355402

00082863 45 190901UNI'I'EI) STti'IES ENVIRONMEN'I'AL, PRO'TECTIONAGENCY ,+TED ST47c0 \4'ASf IING'I'ON, D.C. 20460 OFFICE OF PREVENTION, PESrI'ICIUk:S, AN11 'I'OXIC SUBS'I'ANCES 

# Environmental Fate and Ecological Risk Assessment for ChlorflurenolMethyl Ester Reregistration

Prepared by: Jennifer Leyhe, M.S. Larry Liu, Ph.D. Reviewed by: Karen Whitby, Ph.D. United StatesEnvironmental Protection Agency Office of Pesticide Programs Environmental Fate and Effects Division Environmental Risk Branch V 1200Pennsylvania Ave. Mail Code 7507P Washington, D.C. 20460

## Table of Contents I

# . Executive Summary
.............................................................................................................................. 3 A

# . Nature of Chemical Stressor


### ........................................................................................................ 3 B

## . Potential Risks to Non-target Organisms


### ................................................................................... 4 C

# . Conclusions


### . Exposure Characterization


### .................................................................................. 5 D

# . Conclusions


### . Effects Characterization


### ....................................................................................... 5 E

# . Data Gaps and Uncertainties


### ....................................................................................................... 5

...................................................................................................................... 1



# . Environmental Fate 6



### .......................................................................................................................... 2

# . Ecological Effects 6 F

## . Summary of Endangered Species
................................................................................................7 I1

## . Problem Formulation


### ....................................................................................................................... 8 A

# . Stressor Source and Distribution


### ................................................................................................ 8 1

# . Source and Intensity
....................................................................................................................8 2

# . Physicochemical, Fate, and Transport Properties
................................................................. 8

............................................................................... 3

# . Pesticide Type, Class, and Mode of Action 10



### ...................................................................................................... 4

# . Overview of Pesticide Usage 10

..................................................................................................................................... B

# . Receptors 10

........................................................................................................................ 1



# . Ecological Effects 10

.................................................................................................................... a

# . Aquatic Effects 10



### ............................................................................................................... b

# . Terrestrial Effects 10

...................................................................................................................... 2

# . Ecosystems atRisk 10

................................................................................................................ C

## . Assessment Endpoints 11

....................................................................................................................... D

# . Conceptual Model 12



### .......................................................................................................................... 1



# . Risk Hypotheses 12 2

# . Diagram
....................................................................................................................................... 12

............................................................................................................................... E

## . Analysis Plan 13



### ...... 1

## . Methods for Conducting Ecological Risk Assessment and Identification of Data Gaps 13 2

# . Measures to Evaluate Risk Hypotheses and Conceptual Model


### ............................................. 15 a

# . Measures of Exposure


### ........................................................................................................ 15 b

## . Measures of Effect


### .............................................................................................................. 15 c

# . Measures of Ecosystem and Receptor Characteristics


### .................................................... 16 I11

# . Analysis


### ............................................................................................................................................ 16 A

# . Use Characterization


### .................................................................................................................. 16 B

# . Exposure Characterization


### ........................................................................................................ 17 1

# . Environmental Fate and Transport Characterization


### ............................................................ 17 2

## . Measures of Aquatic Exposure


### .................................................................................................. 17 a

# . Aquatic Exposure Modeling
............................................................................................... 18 b

# . Aquatic Exposure Monitoring (Field Data)


### ..................................................................... 18 3

## . Terrestrial Exposure Assessment


### .............................................................................................. 18 a

# . Terrestrial Animal Exposure Modeling


### ............................................................................ 18 b

# . Terrestrial Exposure Monitoring (Field Data)


### ................................................................. 20 4

## . Non-Target Plant Exposure Assessment
.................................................................................. 20 C

## . Ecological Effects Characterization


### .......................................................................................... 20 1

# . Aquatic Effects: Animals and Plants


### ......................................................................................... 20 2

# . Terrestrial Effects
....................................................................................................................... 20 a

## . Terrestrial Animals


### ............................................................................................................. 21 b

# . Terrestrial Plants
................................................................................................................22 IV

# . Risk Characterization


### .................................................................................................................... 22 A

# . Risk Estimation 

### - Integration of Exposure and Effects Data


### .................................................. 22 1

# . Non-target Aquatic Animals and Plants
................................................................................... 22 a

# . Acute and Chronic Risk to Animals


### ................................................................................. 22 b

# . Aquatic Plants


### ..................................................................................................................... 22 2

## . Non-target Terrestrial Animals


### ................................................................................................. 23.................................................................................... 

## . a Acute Risk to Birds and Mammals 23

................................................................................ b

# . Chronic Risk to Birds and Mammals 23



### ....................................................................................... c

# . Riskto Terrestrial Invertebrates 24 3

## . Non-target Terrestrial and Semi-Aquatic Plants


### ..................................................................... 24



### .................................................................. B

## . Risk Description 

### - Interpretation of Direct Effects 24



### ....................................................................................................... 1

## . Risks to Aquatic Organisms 24

.................................................................................................. 2

# . Risks to Terrestrial Organisms 25



### .................................................................................... a

# . Acute Risk to Birds and Mammals 25

................................................................................ b

# . Chronic Risk to Birds and Mammals 25

................................................................................ c

# . Non-target Terrestrial Invertebrates 26



### ................................................................................................................ d

## . Terrestrial Plants 26 3

# . Review of Incident Data


### ............................................................................................................. 26 4

# . Endocrine Effects


### ...................................................................................................................... 27



### ....................................................................... 5

# . Threatened and Endangered Species Concerns 27



### .......................................................................................................................... a

## . Action Area 27 b

# . Taxonomic Groups Potentially atRisk
............................................................................. 28 i

# . Discussion of Risk Quotients


### .............................................................................................. 28 ii

# . Probit Dose Response Relationship


### .............................................................................. 29 c

## . Indirect Effects Analysis


### .................................................................................................... 30 d

## . Critical Habitat
................................................................................................................... 31 e

# . Co-occurrence Analysis
...................................................................................................... 32 C

# . Description of Assumptions, Limitations, Uncertainties, Strengths and Data Gaps


### ............ 33 1

# . Assumptions, Limitations, Uncertainties, Strengths and Data GapsRelated toExposure For All Taxa


### ............................................................................................................................................... 33 2

# . Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Exposure For Aquatic Species


### ................................................................................................................................... 33 3

# . Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Exposure For Terrestrial Species
.............................................................................................................................. 34 a

# . Location of Wildlife Species
...............................................................................................34 b

# . Routes of Exposure
............................................................................................................. 34 c

# . Incidental Pesticide Releases Associated with Use
......................................................... 35 d

# . Residue Levels Selection
.....................................................................................................35 e

# . Dietary Intake

## - The Differences Between Laboratory and Field Conditions


### ............... 36 4

## . Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Effects Assessment


### ........................................................................................................................................... 36 a

# . Age Class and Sensitivity of Effects Thresholds
............................................................... 37 b

# . Lack of Effects Data for Amphibians and Reptiles


### .......................................................... 37 c

# . Use of the Most Sensitive Species Tested


### .......................................................................... 38 5

## . Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to the Acute and Chronic LOCs


### .............................................................................................................................. 38 V

## . Literature Cited
.............................................................................................................................. 39 

## I

# . Executive Summary A

# . Nature of Chemical Stressor Chlorflurenol methyl ester 

### (ME) is used as an herbicide and plant growth regulator to control perennial and annual weeds and grasses


### . It is applied to ornamentals. hedge and fence rows. turf. shade trees. woody shrubs. and vines. and also is used to produce plantingmaterial for pineapples


### . It is formulated as an emulsifiableconcentrate. which is applied as a spray; or as a granule. which is broadcast with a spreader


### . Chlorflurenol

### MEpenetrates into herbaceous plants (via foliage andlor roots) and moves freely inside the plant (acro and basipetal transport)


### . Growth and development of growing tips and buds of herbaceous plants are blocked or slowed down


### .Chlorflurenol ME consists ofthree components. The major component is methyl 2-chloro-9- 

### hydroxyfluorene-9-carboxylate(PC code 098801). The minor components are methyl 

### 2,7- dichloro-9-hydroxyfluorene-9-carboxylate (PC code 098803) and methyl 9-hydroxyfluorene-9- carboxylate (PC code 098802). The latter (PC code 098802) is used as the starting material for the production of the major component (PC code 098801) and the former (PC code 098803) is obtained as a byproduct during the manufacture of the latter compound (PC code 098802). Since the chemical structures for these two minor components are very similarto that of the major component, it is reasonable to believe that they all have herbicidal activity. According to the registrant, these three components are inseparable and are synthesizedin a relatively constant ratio. For example, the ratio amongPC code 098801, PC code 098802, and PC code 098803 on the label EPA Reg. No. 69361-1 are 5.6: 1.4:1 whereas the corresponding ratio on the label EPA Reg. No. 69361-6 are 5.5: 1.3:

### 1. As a result, althoughmany environmental fate and ecological studies stated that 

### methyl-2-chloro-9-hydroxyfluorene-9-carboxlate (the major component) was used as the test substance, EFED assumed that a mixture of all three components was used. Therefore, this ecological risk assessment is based on this assumption. The environmental persistence of chlorflurenol

### ME is difficult to determine with any certainty due to the limited number of studies available, and the deficiencies within these studies. Based onthese limited data, chlorflurenol ME appearstobehighly to very highly mobile in soil, and hydrolytically stable at pH 6. The study submittedby the registrant in order to fulfill the aerobic soil metabolism data requirements was determined to be unacceptable because the study was conducted outdoors. However, since this aerobic soil metabolism study could be considered supplemental as a small-scale quasi field dissipation study, its results could be interpreted qualitatively. Chlorflurenol 

### ME appears to degrade rapidly under field conditions. 

### B. Potential Risks to Non-target Organisms This is the Environmental Fate and Effects Division's (EFED) national screening-level ecological risk assessment for the proposed re-registration of chlorflurenol

### ME. 'I'able 1 summarizes the major conclusions and uncertainties ofthis assessment for aquatic and terrestrial receptors. The results suggest the potential for acute risk to listed terrestrial birds, reptiles, and mammals, and chronic risk to mammals. In addition, there is the potential for acute risk to non-listed terrestrial birds and reptiles from restricted use applications. Functionally, the estimated risks may translate to reduced survival and reproduction of impacted species with subsequent effects at higher levels ofbiological organization. 

### Acute and chronic riskto all aquatic invertebrates, fish, and terrestrial invertebrates, and chronic risk to birds cannot be precluded because data are not available. In addition, data are unavailablefor aquatic and terrestrial plants; however, since chlorflurenol 

### ME is used as an herbicidelplantgrowth regulator,risk to aquatic vascular and non-vascular plants and non-target terrestrial and semi-aquaticplants is expected.

nd Estuarinelmarine Fish andC. 

### Conclusions

# - Exposure Characterization Chronic Risk to Birds Acute Risk to Mammals Chronic Risk to Mammals
Terrestrial Plants Non-target Invertebrates

The registrant has submitted three studies to hlfill the environmental fate data requirements; however, these studies were considered to be either supplementalor unacceptable. As a result, the analysis could not be performed with confidence. No aquatic modelling was conducted due to lack of fate and toxicity data. derived because there are no definitive LD,,, values. Risk could not be precluded dueto lack of data. Definitive acute dose-based RQ values for mammalian receptors could not be derived because there are no definitive LD,, values. The reported RQ values are above the chronic LOC (1.O) for speciesthat feed on short grass, tall grass, and broadleaf plants/small insects (RQ range = 0.02 to 2.90). Risk could not be precluded due to lack of data. Risk could not be precluded due to lack of data.

To estimate exposure of terrestrial animals, terrestrial EECs were generated using the Tier 1 model T-REX for chlorflurenol ME spray use based on maximum application rates and use patterns. Granular application was not assessed. For foliar spray applications, EECs and acute and chronic RQs were estimated for residues on various forage categories (short grass, tall grass, broadleaf plantslsmall insects, fruitslpodsllargeinsects, and seeds). ChlorflurenolME concentrations were highest on the surfaces of short grass and lowest on the surfaces of fruits, pods, and large insects. 

### D. Conclusions

## - Effects Characterization Results of acute toxicity studies on birds suggestthat chlorflurenol

### ME is practically nontoxic on an acute oral basis (LDS0 >10,000 mg a.i./kg body weight) and practically nontoxic on an acute dietary basis (LCSo >5,000 mg a.i./kg diet). Mammalian data suggest that chlorflurenol ME is practically nontoxic (LDSo >5,000 mg a.i./kg body weight) on an acute oral basis. A chronic toxicity study with rats showed that the maternalNOAEL was 250 mg/kg bwlday. The maternal LOAEL is 750 mglkg bwlday based on body weight gain decrement and nominally decreased food efficiency. The developmentalNOAEL is 250 mglkgbwlday. The developmental LOAEL is 750 mglkg bwlday, based on treatment-related delayed ossification in skull bones (nasal and frontal) in fetuses and litters. No quantitative data are available to characterizerisks from exposure of chlorflurenol ME to freshwater and estuarinelmarine fish and invertebrates (acute and chronic risk), birds (chronic risk), and aquatic and terrestrial plants. EFED cannot preclude risk to these taxa. In addition, since chlorflurenol ME is used as an herbicide or a plant growth regulator, risk to non-target plants is expected. 

### E. Data Gaps and Uncertainties The screening-level assessment for chlorflurenolME has been conducted despite unfulfilled guideline requirements and existing environmental fate and ecological data gaps 

### (Tables 

### H1 and 

### H2, Appendix H). The following is a brief synopsisof the major environmental fate and ecological effects data gaps and uncertainties. Additional detail can be found in Section IV C, Description of Assumptions, Limitations, Uncertainties, Strengths and Data Gaps.

### 1. Environmental Fate Guideline 161-1 Hydrolysis (the submitted study (MRID 43496201) was determined to be supplemental and the hydrolysis data requirements have not been fulfilled. A new study includingpH 7 is required) Guideline 161-2 Aqueous photolysis Guideline 161-3 Soilphotolysis Guideline 162-1 Aerobic soil metabolism (the submitted study 

### (MRID 43595403) was determined to be unacceptable. A new study using four soils is required) Guideline 162-2 Anaerobic soil metabolism Guideline 162-3 Anaerobic aquaticmetabolism Guideline 163-1 Adsorptioddesorption (the submitted study (MRID43496202) was determined to be supplemental and the adsorptioddesorption data requirements have not been fulfilled. 

### A new study including three soils is required) Guideline 164- 1 Terrestrial field dissipation Guideline 165-4Fish bioaccumulation Guideline 20 1-1 Droplet Size Spectrum (a waiver request was denied by EPA on 3/2/05) Guideline 202-1 Drift Field Evaluation (a waiver request was deniedby EPA on 3/2/05) 2. 

### Ecological Effects Guidelines 72-1, 72-2, 72-3, 72-4: Acute and chronic data for freshwater and estuarinelmarinefish and invertebrates are not available; thereforerisk could not be assessed. Guideline 71-4: There are no avian reproduction studies available; therefore risk could not be assessed. Guideline 123-1, 123-2: TerrestrialPlant Seedling Emergence and Vegetative Vigor studies are not available. In addition, aquaticplant growth studies are not available; therefore risk could not be assessed. Since chlorflurenol ME is used as an herbicide and growth regulator, toxicity data on non-target plants are necessary to estimaterisk. Available literature suggeststhat chlorflurenol causesreproductive effects in terrestrial plants. Guideline 141-1: Honey Bee Acute Contact Toxicity;no data are available; therefore risk could not be assessed. Acute oral and dietary toxicity studiesin birds and acute oral toxicity to mammals failed to establish definitive acute LDSO/LC50 values (i.e., the LCso was expressed as "greater than" the highest dietary concentrationtested); thus, acute RQ could not be calculated. The study testing oral toxicity to birds did not statewhich components were included in the test material. EFED assumes the test material contained all three components which may underestimate risk to birds on an acute oral basis if in fact the test material only contained one of the three components. The mammalian chronicRQs arebased on a developmental studythat shows evidence of delayed skull ossification and cleft palates in young rats. These endpointsare not adequate for determiningrisk to the survival and fecundity of a population. However, without other studiesEFED used these data. Therefore, the RQs may not accurately portray chronicrisk to mammals. Risk may be under- or over-estimated. Application interval and number of applicationsper year are not indicated on the label. For multiple application scenarios, the T-Rex model requires both of these parameters in 6 

### -

### order to estimate exposureto terrestrial organisms. In the absence of these numbers an application interval of 

### 28 days and 

### 8 applications per year (as derivedby HED, Appendix 

### B) were used. HED used information provided on the labels along with their best professional judgment of the croplweed growth cycles,pest pressure timing, etc. to determine the application interval and yearly number of applications. EFED used the HED data to maintain consistency between EFED and HED. Since these numbers are considered "likely" applications per year, risk to terrestrial organisms may be underestimated. 

### F. Summary 

### ofEndangered Species 

### 'I'able 

### 2 summarizes the potential risk to listed species associated with the application of chlorflurenol. For all taxa except acute risk to birds and mammals and chronic risk to mammals, risk is presumed to occur due to lack of data.

Acute - Yes '; Chronic - Yes

### 11. 

## Problem Formulation Marinelestuarine crustaceans

A. 

### Stressor Source and Distribution 1. 

### Source and Intensity a We cannot preclude risk due to lack of data.

The reported RQ values are above the chronic LOC (1.O) for species that feed on short grass, tall grass, and broadleaf plantslsmall insects (RQ range = 0.02 to 2.90). 

### ' RQs could potentially exceed acute listed species LOCs unless the actual LDsovalues are established in laboratory studies to be greater than -16,715 mg a.i.1kg body weight or if the amount available in the environment was lowered below 500 ppm Yes

Chlorflurenol

### ME formulations are currentlyregistered for use on turf, fencerows, hedgerows, rights-of-ways, forests, industrial areas,recreational areas, and pineapples as ground or aerial sprays. The rates of applicationrange from 0.25 to 3.0 lb a.i./acrewith no maximum number of applications/season and no set intervalbetween applications specifiedonthe label. Yes

2. 

### Physicochemical, Fate, and Transport Properties Chlorflurenol

### ME is used as an herbicide and plant growth regulator. It consists of three components (see table below). The major component is methyl 

### 2-chloro-9-hydroxyfluorene-9- carboxylate (PC code 098801). The minor components are methyl 2,7-dichloro-9- 

### hydroxyfluorene-9-carboxylate(PC code 098803) and methyl 

### 9-hydroxyfluorene-9-carboxylate (PC code 098802). The latter (PC code 098802) is used as the startingmaterial for the production of the major component (PC code 098801) and the former (PC code 098803) is obtained as a byproduct during the manufacture of the latter compound (PC code 098802). Since the chemical structures for these two minor components are very similarto that ofthe major component,it is reasonable to believe that they all have herbicidal activity. According to the registrant, these three components are inseparableand are synthesized in a relatively constantratio. For examples, the ratio among PC code 098801,PC code 098802,and PC code 098803 on the label 

### EPA Reg. No. 69361-1 are 5.6:1.4:1 whereas the corresponding ratio on the label EPA Reg. No. 69361-6 are 5.5:1.3:1. As a result, althoughmany environmental fate and ecological studies stated that 

### methyl-2-chloro-9-hydroxyfluorene-9-carboxlate (the major component) was used as the test substance, 

### EFED assumedthat a mixture of all three components was used. Therefore, this ecological risk assessment is based on this assumption. 

### Chlorflurenol 

### ME A mixture of 65-70%

### methyl-2-chloro-9-hydroxyfluorene-9-carboxylate, 10-1 5%

### methyl-2,7-dichloro-9-hydroxyfluorene-9-carboxylate and 15-20% 

### methyl-9-hydroxyfluorene-9-carboxylate.

R2

# Qp,

HO O'R3 R1 0No information on the physical and chemical properties could be found for those two minor components (PC codes 098802 and 098803). Limited information was found for the major component (PC code 098801), which has very low water solubility and is moderately volatile: Common Name: ChlorflurenolME Chemical Name (IUPAC): 

### (RS)-2-Chloro-9-hydroxyfluorene-9-carboxylic acid methyl ester Chemical Name (CAS): 

### 2-Chloro-9-hydroxy-9H-fluorene-9-carboxylic acid methyl ester CAS NO.: 2536-3 1-4 PC Code: 098801 Molecular Formula: C15Hl lC103 Molecular Weight: 274.7 glmol Vapor Pressure (temperatureunknown): 2.5 x 10-5torr Water Solubility (temperature andpH unknown): 21.8 ppm The environmental persistence of chlorflurenol ME is difficultto determinewith any certainty due to the limited number of studies available, and the deficiencieswithin these studies. Based on these limited data, chlorflurenolME appears to be highly to very highly mobile in soil, and hydrolytically stable at pH 6. The study submitted by the registrant in order to fulfill the aerobic soil metabolism data requirementswas determined to be unacceptable because the study was conducted outdoors. However, since this aerobic soil metabolism study could be considered supplemental as a small-scale quasi field dissipation study, its results could be interpreted qualitatively. Chlorflurenol ME appears to degrade rapidlyunder field conditions. Efforts were made; however, no chemicalswhich have similarchemical structuresas chlorflurenol ME were found. Chlorflurenol ME degraded by hydrolysiswith 

### a half-life of 161.2 days and 0.2 days at pHs 6 and 9, respectively. The most environmentallyrelevant 

### pH of 7 for aquatic systemswas not tested. At study termination, 77.8% (50 days,pH 6), 55.6% (0.19 days, pH 9) and 41.7% (0.29 days, pH 9) of the applied chlorflurenol ME was undegraded. The major transformationproduct was 2- chloro-9-hydroxyfluorene-9-carboxylic acid; however, quantitative data and further details were not reported. Chlorflurenol ME degraded in sandy loam soil (pH 6.0) in outdoor plots with a half-life of 1.3 days. Chlorflurenol ME was completelydegraded by 26 days (studytermination). One major degradation product was detected, 2-chloro-9-fluorenone at 

### a maximum of 14.3%of the applied at 5- 12 days and was not detected at 26 days. 

### Ln laboratory mobility studies, chlorflurenolME was highly to very highly mobile in a sandy loam soil from Germany.

### 3. Pesticide Type, Class, and Mode of Action Chloflurenol ME is used as an herbicide and plant growth regulator. It consistsof three components. The major component is methyl 

### 2-chloro-9-hydroxyfluorene-9-carboxylate(11). The minor components are methyl 

### 2,7-dichloro-9-hydroxyfluorene-9-carboxylate (111) and methyl 

### 9-hydroxyfluorene-9-carboxylate(I). The latter (I) is used as the starting material for the production ofthe major component (11) and the former (111) is obtained as a byproduct during the manufactureofthe latter compound (I). This chemical readily penetrates into herbaceous plants (via foliage andlorroots). It moves freelyinside the plant (acro and basipetal transport). Growth and development of growing tips and buds of herbaceous plants are blocked or slowed down as a result of chlorflurenolME usage. 

### EFED could not find information on the mode of action for this chemical.
4. 

### Overview of PesticideUsage There are no data on the actual usage of chlorflurenolME. 

### B. 

### Receptors 1. Ecological Effects Each assessment endpoint requires one or more measures of ecological effect, which are defined as changes in the attributesof an assessment endpoint itself or changes in a surrogate entity or attribute in response to exposure to a pesticide. Ecological measures of effect forthis screeninglevel risk assessment are based on a suite ofregistrant-submitted toxicity studies performed on a limited number of organisms in broad groupings. 

### A complete discussion of all toxicity data available for this risk assessment and the resulting measures of effect selected for each taxonomic group are included in 

### Appendix D. 

### a. Aquatic Effects Toxicity data sufficient for use in a risk assessment for chlorflurenol

### ME are 

### not availablefor freshwaterfish and invertebrates, estuarinelmarine fish and invertebrates, algae, and vascular plants. No studies on chlorflurenol ME are available for acute or chronic exposurefor any of these taxa. In addition, since there are very limited fate data, no aquatic exposure models were run. Therefore,risk cannot be precluded. b. 

### Terrestrial Effects Registrant-submittedlaboratory studies on chlorflurenol ME formulations are availablefor acute exposure of birds and mammals. In addition chronic studies have been submitted for mammals but not for birds. 

### No toxicity studieson the effects of chlorflurenol ME on terrestrial plants or honeybees were submitted. Details of all registrant and open literature studies areprovided in 

### Appendix 

### D. Where data are lacking, risk could not be precluded. 2. 

### Ecosystems at Risk Ecosystems potentiallyat risk are expressed in terms ofthe selected assessment measures of effect. The typical assessment measures of effect for screening-level pesticide ecological riskassessments are reduced survival and reproductive and growth impairment for both aquatic and terrestrial animal species. Aquatic animal species ofpotential concern include freshwater fish and invertebrates,estuarine/marine fish and invertebrates, and amphibians. Terrestrial animal species of potential concern include birds, mammals, reptiles, and beneficial insects. For both aquatic and terrestrial animal species, acute and chronic exposures are considered. C. Assessment Endpoints This risk assessment considers the maximum application rate of chlorflurenol

### ME spray (granular was not assessed) on vulnerable soils as reported on the label, the likely number of applications as derived by 

### HED (Appendix 

### B), and the likely application intervals asreported by 

### HED (Appendix 

### B) to estimateexposure concentrations as a result ofthe use of chlorflurenol 

### ME. This assessment is not intended to represent a site or time-specific analysis. Likewise, the most sensitive toxicity endpointsareused from surrogate test speciesto estimate treatment-related direct effects on acute mortality and chronic reproductive, growth and survival assessment endpoints. Surrogateaquatic organisms include freshwater and saltwater fish and invertebrates. 

### In the absence oftoxicity data on amphibians, it is assumed that aquatic-phase amphibians are approximately as sensitive as fish to potential effects of a pesticide. Surrogateterrestrial animal species includebirds and mammals. Therisk assessment also assumes that reptiles and terrestrial-phaseamphibians are approximately as sensitiveto pesticide-induced effects as birds. These tests include short-term acute, subacute,and reproduction studies and are typically arranged in a hierarchical or tiered system that progresses frombasic laboratory tests to applied field studies. For plants in terrestrial and semi-aquatic environments,the screening assessment endpoint is the perpetuationofpopulationsof non-target species (crops and non-crop plant species). Endpoints assessed includeemergence of seedlings and vegetative vigor. Although it is recognized that the endpoints of seedling emergenceand vegetative vigor may not address all plant life cycle components,it is assumed that impacts at emergence and in active growth have the potential to impact individual competitive ability and reproductive success. For aquatic plants, the assessment endpoint is the maintenance and growth of standing crop or biomass. In order to protect federally endangered and threatened (listed) species, all assessment endpoints are measured at the individual level. They also provide insight about risks at higher levels of biological organization(e.g. populations and communities). For example, pesticide effects on individual survivorshiphave important implications for both population rates of increase and habitat carryingcapacity. The ecologicalrelevance of selecting the above-mentioned assessment endpoints is as follows: 

### 1) complete exposurepathways exist for these receptors; 

### 2) the receptors may be potentially sensitive to pesticides in affected media and in residues on plants, seeds, and insects; and 

### 3) the receptors could potentiallyinhabit areaswhere pesticides are applied, or areas where runoff andlor spray drift may impact the sites because suitablehabitat is available. Thetoxicity studies areused to evaluate the potential of chlorflurenol

### ME to cause adverse effects, to determinewhether further testing is required, and to determine the need for precautionarylabel statementsto minimize the potential adverse effects to non-target animals and plants (40 CFR $158.202,2002). A summary ofthe assessment endpoints and measures of effect selected to characterizepotential ecological risks associated with exposure to chlorflurenol 

### ME is provided in Table 

### 3.D. 

### Conceptual Model Table

### 3. 

### Summaryof

### AssessmentEndpoints

### andMeasurnof

### Effect

### for Chlorflurenol

### ME. 1

1. 

### Risk Hypotheses Assessmeat Endpoint 1. Abundance (i.e., survival, reproduction, and growth) of individuals and populations of birds.

2. Abundance (i.e., survival, reproduction, and growth) of individuals and populations of mammals. 3. Survival and reproduction of individuals and conlmunities of freshwater fish and invertebrates.

4. Survival and reproduction of individuals and communities of estuarinelmarine fish and invertebrates. 5. Survival of terrestrial invertebrate populations (beneficial insects and earthworms).

Risk hypotheses are specific assumptions about potential adverse effects (i.e., changes in assessment endpoints) and may be based on theory and logic, empirical data, mathematical models, or probability models 

### (US EPA 2004). For this assessment, the risk is stressor-initiated, where the stressor 

### is the release of chlorflurenolME spray to the environment. The following risk hypothesis is presumed for this screening-levelassessment: 

### Me~ure ofEEect

, ,,, la. Bobwhite quail acute oral LDSO(guidelinerecommended species). lb. Bobwhite quail subacute dietary LCso (guideline-recommended species). 1 c. Avian chroniclreproduction:data gap 2a. Laboratoryrat acute oral LDSo. 2b. Rat developmental NOAEL 3a. Rainbowtrout and bluegill sunfish acute LC50 : data gap 3b. Water flea acute LCso:data gap 3c. Freshwater fish chronic: data gap 3d. Freshwater invertebrate chronic: data gap 4a. Estuarineimarinefish acute: data gap 4b. Estuarinelmarineinvertebrate acute: data gap 4c. Estuarine/marinefish chronic: data gap 4d. Estuarinelmarineinvertebrate chronic: data gap 5a. Honeybee acute contact LDSo: data gap



### Non-target aquatic and terrestrial plants and animalsmay be exposed to chlorflurenol 

### ME when it is applied in agricultural and/or non-agricultural settings to control unwantedplants. Based on available information regarding the persistence, mode of action, direct and indirect toxicity, chlo~urenol 

### ME may have the potential to compromise growth, reproduction, and/or survival ofnon-target terrestrial and aquatic animals andplants. LD50= Lethal dose to 50% of the test population. LCso(ECSo) = Lethal (effective) concentration to 50% of the test population.

Ecological receptors that may potentially be exposed to chlorflurenolME and its transformation products include terrestrial and semi-aquatic wildlife (i.e., mammals, birds, amphibians, and reptiles), terrestrial and semi-aquatic plants, and soil invertebrates. In addition, aquatic receptors (e.g., freshwater and estuarine/marine fish and invertebrates,and amphibians) may also be exposed as a result of potential migration of chlorflurenolME via spray drift and/or runofflerosion from the site of application to various watersheds and other aquatic environments. These data formed the basis for identifying potential endpoints, stressors, and ecological effects associated with uses of chlorflurenol ME. 

### 2. DiagramBased onthe preliminary iterative process of examining fate and effects data, the conceptual model or the risk hypothesis model for spray applicationto non-agricultural crops and pineapples has been established, refined and included in 

### Firrure 1. Granular application was not assessed. In establishing the diagram for the conceptual model it was necessary to go through an iterative process to identify: 

### (1) likely stressors/exposurepathways and 

### (2) organisms that are most relevant and applicable to this assessment.

.................................. ........................... .............................. .................................. 

### .. ._..... .. ._. . . . . . . . . . .

.Volatilization, Direct j

. j

. Spray f 

### ; Runoff1

. . 

### Transport 

### i /wind ) Deposition ] 

## i Drift j f Erosion

. . 

### Pathways Suspension ..- ] (Parent) -., . 

### i 

### i

. (Parent) ] ] (Parent 

## + Deg) 

### f

........ ....................... ""..

. . ................................. ,.. ......

" ............................ 

### ,. ................. 

### Stressor

Source1 Exposure Media Chlorflurenol applied as groundlaerialspray to turf, forests, recreational areas, industrial areas, right-of-ways,pineapples



### Exposure Point I 

# + t 1 

## * 4



### Receptors Leaching Infiltration/Percolation (Parent 

### + Deg)

.:
. . 

### i 

### I Riparian] 

## I

. 

## i

. Water Column, 

# 9 Groundwater. : : .................... ._..............., oil 

### j 

## 1 Wetland f i Sediment i

. . ........... .................................. ............. """ :

.......................................................
................................................................. Food Web j



# ................................... ...................... ..................... 

# ] E~OSUE .;



### ... Ingestion& Dermal 

### / j Direct contact and robt uptakeK 

## 1.

. . ... ...

....... ............................. Uptake ; ..................................... 

## t.

...................... i Birds, Mammals, Reptiles, Terrestrial i IIIVeILt

....................................................................... 

## / 

# I i Amnh .......... .......... ..... 

### / Wetland/ 

### / Aquatic j /

. . ] Riparian 

## . 

# I I Plants 

### i ] Aquatic 

### /

.......................... ,, ; 2: I...,-A., .brates tebrates j

. / 

### .....,.. ibians 'i ...............l.. .. .. ... . .... j Piscivorous ] 

## i Vertebrates 

## i 1 (Birds and j 

### f mammals) j

.............. ........................... i.. .: .: 

## I 

# I

...............................................

............................................................................ 

### i Plant population j 

# 1 

# 1: j Reduced j j IndividualAnimals j 

## 1 population 

### ; Reduced survival ] Reduced growth j growth 

### I

.............................................. % 2 Reduced reproduction :...................... :

.................. Dotted lines represent no data available Figure 1. Ecological conceptual exposure model for chlorflurenol.


### E. Analysis Plan 1. 

### Methods for Conducting Ecological Risk Assessment and Identification ofData Gaps The primary method used to assess risk in this screening-level assessment is the risk quotient (RQ) and follows closely methods outlined in the EPA Overview Document 

### (US 

### EPA, 2004). The RQ is the primary risk value for the screening-level assessment and is the result of comparingmeasures of exposureto measures of effect. A commonlyused measure of exposure is the estimated exposureconcentration (EEC) and commonly used measures of effect include toxicity values such as the LDSo or NOAEC. Assessment endpoints and their respective measures of effect are listed in 

### 'I'able3. Theresulting RQ is then compared to a specified level of concern (LOC), which represents a point of departure for concern; ifthe RQ exceeds the LOC, then risks are triggered. Although not necessarily a true estimate of risk since there is no estimated probability of effect, in general, the higher the RQ, the more certain the potential risks. Risk presumptions, along with the corresponding RQs, equations, and LOCs are summarized in 

### Appendix E. Levels of concern (LOC) are thepolicy tool for interpreting risks from direct pesticide effects and have a magnitude, duration,frequency, and spatial extent. The magnitude is set by the risk presumption for each endpoint.The frequency of potential risk is once every ten years for aquatic endpoints and reasonableupper bound for terrestrial risk. The spatial extent is defined by the use area, and the areas downstream and areaspotentially affected by spray drift. Generation of robust RQs is dependent on the quality of data from both fate and toxicological studies. The adequacyof the submitted data was evaluated relative to Agency guidelines. The followingidentified data gaps for ecological fate and toxicity endpoints result in a degree of uncertainty in evaluating the ecological risk of chlorflurenol ME. For fate and transport, 

### Table 

### H1 (Appendix H) lists the status ofthe fate and transport data requirements for chlorflurenol 

### ME. The adequacy ofthe submitted data was evaluated relativeto Agency guidelines. Data gaps identified for fate and transport include Guideline 

### 161 

## -1Hydrolysis Guideline 16

### 1-2 Aqueous photolysis Guideline 16 1-3 Soilphotolysis Guideline 162-1 Aerobic soil metabolism Guideline 162-2 Anaerobic soil metabolism Guideline 162-3Anaerobic aquatic metabolism Guideline 163-1Adsorptioddesorption Guideline 164-1Terrestrialfield dissipation Guideline 165-4Fishbioaccumulation Guideline201-1 Droplet Size Spectrum Guideline202-1 Drift Field Evaluation For the ecological assessment,

### Table 

### H2 (Appendix H) lists the status of ecological data requirements for chlorflurenol ME. Hereunder is a summary of identified data gaps and associateduncertainties: Guidelines72-1, 72-2, 72-3, 72-4: Acute and chronicdata for freshwater and estuarinelmarinefish and invertebrates are not available; therefore risk could not be assessed. Guideline 71-4: Avian reproduction studies are not available; thereforerisk could not be assessed. Guideline 123-1 (a, b), 123-2: Terrestrial plant seedling emergence and vegetativevigor studies are not available. In addition, aquatic plant growth studies are not available;thereforerisk could not be assessed. Since chlorflurenolME is used as an herbicide and growth regulator, toxicity data on non-target plants are necessary to estimaterisk. Guideline 

### 141-1:Data for honey bee acute contact toxicity are not available; therefore risk could not be assessed. Acute oral and dietary toxicity studies in birds and acuteoral toxicity studies in mammals failed to establish definitive acuteLDSo/LC50 values (i.e.,the LDSO/LC50 were expressed as "greater than" the highest concentration tested); thus, acute RQ could not be calculated. The mammalian chronic RQs arebased on a developmental study that shows evidenceof delayed skull ossification and cleft palates in young rats. These endpoints are not adequate for determining risk to the survival and fecundity of a population. However, without other studiesEFED used these data. Therefore, the RQs may not accurately portray chronicrisk to mammals. Risk may be under- or over-estimated. 2. 

### Measures 

### to EvaluateRisk Hypotheses and Conceptual Model a. Measures of Exposure Due to the absence of fate data and aquatic toxicity data, no aquatic exposure modeling was conducted for this assessment. 

### Exposure was assumed to occur. Measures of exposure for terrestrial mammals, birds, reptiles and amphibians incorporate maximumproposed use rates but rely less on fate properties. Terrestrial exposures were estimated using a number of methods. Acute and chronic terrestrial exposure estimates are derived directly from empiricallydetermined observations ofpesticide residues on various terrestrialfood items. The Kenaga nomogram, as modified by Fletcher et al., (Hoerger and Kenaga, 1972;Fletcher et al., 1994)is used to relatepesticide application rates to residues on terrestrial food items. The surface residue concentration(ppm) is estimatedby multiplying the applicationrate (pounds active ingredient (a.i.) per acre)by a value specificto each food item. For multiple applicationsof a given use, the exposuremodel incorporates a first-order decay rate dependent on the foliar dissipation half-lifeofthe chemical. 

### In the absence of data, a default foliar dissipation half-lifeof 35 days is used. The T-REX model was run for chlodurenol ME turf use with the maximum proposed application rate (3.0 Ib a.i./A; as stated on the label), a maximum of 

### 8 applications (HED derived with best professional judgment, see

### Appendix B), and a 28-day application interval (HED derived with best professional judgment, see 

### Appendix B) to assessrisk to terrestrial organisms. EFED used the HED data to maintain consistency between EFED and HED. The conceptualapproach taken to estimate residues (upper-bound and mean) on potential dietary sources for mammals and birds is presented in the model T-REX Version 1.2.3 (T-REX, 2005)(Formore details see 

### Appendix C and the Exposure Characterization section of this document). 

### b. Measures of Effect Measures of ecological effects are obtained from a suite of registrant-submitted guideline studies conducted with a limited number of surrogate species. The test species are not intended to be representativeof the most sensitivespecies but rather were selected based on their abilityto thveunder laboratory conditions. Measures of effect are based on deleterious changes in a receptor as a result of chemical exposure. Functionally, measures of effect typicallyused in risk assessments include changes in survival,reproduction, or growth as determined from standard laboratory toxicity tests. The focus on these effects for quantitative risk assessmentsis due to 15 

## -their clear relationshipto higher-order ecological systems such as populations, communities,and ecosystems. Monitoring data may also be used to provide supporting lines of evidence for the risk characterization. In addition,although effects other than survival, reproduction, and growth may be considered,rarely are they used quantitatively to estimate risks since, in many cases, the relationshipbetween these effects and higher-order processes is tenuous at best. Commonly used laboratory-derivedtoxicity values include estimates of acute mortality 

### (e.g.,LD50, LC50,or EC50) and estimatesof effects due to longer term, chronic exposures (e.g.,NOAEC, NOAEL). The latter can reflect changes seen in mortality, reproduction, or growth. In general, for a given assessment endpoint the lowest relevant measure of effect is used when calculating the RQ. Sincepreliminary review of the available ecological effects data suggests that chlorflurenol 

### ME is practicallynontoxic to birds and mammals on an acute exposure basis, acute effectsto non-listed birds and mammals are not expected. Chronic exposure studies indicate that mammals may be at chronic risk; no chronic avian toxicity data are available. No guideline data are availablefor aquatic species,terrestrial plants, and insects. However,there are literaturestudies that show reproductiveeffects on terrestrial plants. 

### A search of the open literatureusing EPA's Ecotoxicology database, ECOTOX, was conducted to identify studiesto fill the data gap for acute and chronic exposureof chlorflurenol ME to aquatic fish and invertebrates,terrestrial invertebrates; search ofthe ECOTOX database did not identify studiesto fill these data gaps. The ECOTOX search did identify additional chronic toxicity studies on the following: terrestrial plants (See section IV.B.2.d). 

### c. Measures of Ecosystem and Receptor Characteristics The ecosystems selected for modeling, using T-REX for the Tier 1terrestrial animal assessment, are intendedto be generally representative of any aquatic or terrestrial ecosystem associated with areas where chlorflurenol ME is used. Thereceptors addressedby the aquatic and terrestrialrisk assessments are summarized in 

### 'l'able3. For aquatic assessments, generally fish and aquatic invertebratesin both freshwater and estuarinelmarine environments are represented, when available. For terrestrial assessments, mammals are representedby three different size classes and fivepotential foraging categories(short grass, tall grass, broadleaf plantslsmall insects, fruitslpods/seeds/largeinsects, and seeds). For the three different size classes of small birds, four potential foraging categories are considered (short grass, tall grass, broadleaf plantslsmall insects, and fruitslpods/seeds/largeinsects). For terrestrial plants, generally both dicots and monocots are represented. Detailed information regardingthe data available for these various classes of aquatic and terrestrialreceptors is provided in 

### Appendix D. 

### 111. 

## Analysis A. 

### Use Characterization ChlorflurenolME 

### [(RS)-2-chloro-9-hydroxyfluorene-9-carboxylic acid methyl ester; CF 125, 12.5%a.i.1 is an herbicidelplant growth regulator 

### (PGR)used to control weeds and grasses for ornamentals,hedge and fence rows, turf, shadetrees, woody shrubs and vines, and is specifically used to produce planting material for pineapple production. The maximum application rate is 

### 3 lb a.i.1A for ornamental lawns, turf, and non-agricultural right-of-ways, fencerows, and hedgerows; 1 lb a.i./100 gal for shadetrees (dueto lack of information, EFED is unable to convert it to lb ai/A), woody shrubs and vines, forest conifers andjunipers, recreational areas and industrial areas(outdoors); and 

### 1.0875 lb a.i./A for pineapples. The labels indicatethat for optimum results, chlorflurenol ME can be used in conjunctionwith othertraditional herbicides. 

### B. Exposure Characterization 1. 

### Environmental Fate and Transport Characterization Environmental Persistence The environmental persistence of chlorflurenolME is difficult to determine with any certainty due to the limited number of studies available, and the deficiencieswithin these studies. However, based on these limited data, chlorflurenolME appears to be highly to very highly mobile in soil, and hydrolytically stable at pH 6. The study submitted by the registrant in order to fulfill the aerobic soil metabolism data requirementswas determined to be unacceptable because the study was conducted outdoor. However, sincethis aerobic soil metabolism study could be considered supplemental as a small-scale quasi field dissipation study, its results could be interpreted qualitatively. Chlorflurenol ME appearsto degraderapidly under field conditions. Theprimary route of dissipation could not be determined. Photodegradationmay also occur; however, no studies were submitted, so this degradation route could not be confirmed. 

### In buffered aqueous solutions, the half-life of chlorflurenol ME at pH 6 and pH 9 was 161.2 and 

### 0.20 days, respectively. The phototransformation of chlorflurenol ME could not be evaluated because no studies were submitted. In the registrant-claimed aerobic soil metabolism study (which was consideredby EFED as a small-scale quasi field dissipation study), chlorflurenol

### ME degraded with a half-life of 

### 1.3days in a sandy loam soil from Germany. However, these experimental plots were outdoorsunder uncontrolled environmental conditions,and without a phototransformation study to reference,it is uncertain to what extent degradation occurred due to microbial metabolism, and/or photodegradation. The metabolism of chlorflurenol ME under aerobic aquatic, anaerobic soil, and anaerobic aquatic conditions,and the potential for bioaccumulation could not be evaluated becauseno studieswere submitted in these areas. 

### Expected Mobility Chlorflurenol ME is highly to very highly mobile in sandy loam soil from Germany, with a 

### KFoc of 109. The field dissipation of chlorflurenolME could not be evaluated because no studies were submitted. 

### Environmental Metabolites Themajor transformationproduct of chlodurenol ME that was quantifiedwas 2-chloro-9- fluorenone (Compound

### IV; fluorenone). 

### 2-Chloro-9-hydroxyfluorene-9-carboxylicacid (Compound 11) was also identified as a major transformationproduct of hydrolysis,but was not quantified. Thetransformationpathway of chlorflurenol ME in the environment is difficult to determine with any certainty due to the limited number of studies available,and the deficiencies within these studies.

### 2. Measures of Aquatic Exposure

### a. Aquatic Exposure Modeling Since there are limited fate data for chlorflurenol 

### ME no aquatic modeling was conducted. 

### b. Aquatic Exposure Monitoring (Field Data) There are no aquatic exposuremonitoring data. 

### 3. TerrestrialExposure Assessment Terrestrial wildlife exposureestimates are typically calculated for birds and mammals, emphasizing a dietary exposure route for uptake ofpesticide active ingredients. These exposures are considered as surrogates for terrestrial-phase amphibians aswell as reptiles. For exposure to terrestrial organisms, such as birds and small mammals, pesticide residues on food items are estimated,based on the assumption that organisms are exposed to a singlepesticide residue in a given exposure scenario.


### a. Terrestrial Animal Exposure Modeling A primary concern with chlorflurenol ME is that birds and mammals may be exposed shortly after applicationthrough oral or dietary exposureto vegetativeplant material or insects when foragingin the treated fields for nesting material or food. Therefore estimation ofpesticide concentrationsin wildlifefood items focuses on quantifying possible dietary ingestionofresidues on vegetative matter and insects. The EFED terrestrial exposure model T-REX (T-REX, Version 1.2.3, dated August 8,2005) is used to estimate exposures and risks to avian and mammalian species. Input values for avian and mammalian toxicity as well as chemical applicationand foliar dissipation half-life data are required to run the model. The model provides estimatesof exposure concentrationsand risk quotients (RQs). Specifically,the model provides estimates of concentrations (upper-bound and mean) of chemical residues on the surface of different types of foliage and insects that may be dietary sourcesof exposure to avian,mammalian, reptilian, or terrestrial-phase amphibianreceptors. The surface residue concentration (ppm) is estimated by multiplying the application rate (pounds active ingredient per acre) by a value specific to each food item. These values (termed the Hoerger-Kenaga estimates) along with a more detailed discussion ofthe methodology implementedby T-REX, arepresented in 

### Appendix C (T-REX Model). For multiple applications, the EEC is determined by addingthe mass on the surfaceimmediately following the applicationto the mass of the chemical still present on the surfaces on the day of application (determined based on first order kinetics using the foliar dissipation half-life as the rate constant). Input valuesused for estimating avian and mammalian exposure risks to chlorflurenolME are summarized in 'Table 4.

Table4. Input parameters used in 

### T-REX v1.2.3 to determineterrestrial EECsfor the maximum ehlorflurenol

### ME spray applicationscenario. Input Variable Parameter Value Source Maximum application rate Likely # of applications per year Likely application interval 3.0 Ib a.i./A 8 28 days I X 

### - Product Label HED HED aTable 4. Input parameters used in T-REX v1.2.3 to determine terrestrial EECs for the maximum chlorflurenol

### ME spray applicationscenario. InputVariable Parameter Value Source Foliar dissipation half-life 35 days T-REX Default Value

a HED used information provided on the labels along with their best professional judgment of the croplweed growth cycles, pest pressure timing, etc. to determine the application interval and yearly number of applications. EFED used the HED data to maintain consistency between EFED and HED. Uncertainties in the terrestrial EECs are associated with a lack of data on dissipation from foliar surfaces. When data are absent, as in this case, EFED assumes a 35-day foliar dissipation halflife, based onthe work of Willis and McDowell(1987). In this respect, the EECs for chlorflurenol ME may be an overestimation of actual concentrationsifthe half-life under field conditions is lower than the default value. Because foliar dissipation data are not available, the extent to which EECs may be overestimatedor underestimated is uncertain. In addition, EFED used a "likely" applicationinterval and yearly application rate, since no information was provided on the label. Risks could be underestimated ifthe actual application rate, frequency of application,andlor number of applicationsarehigher than the input parameters used for the exposure scenariothat was modeled. For this risk assessment, the T-REX model was run for turf use with the maximum proposed application rate (3.0 lb a.i./A), 8 applications/year (derived by HED, see Appendix B), and a 28-day application interval (derivedby HED, see Appendix B), to assessrisk to terrestrial organisms. HED used informationprovided on the labels along with their best professional judgment of the croplweed growth cycles,pest pressure timing, etc. to determine the applicationinterval and yearly number of applications. EFED used the HED data to maintain consistencybetween EFED and HED. By comparing estimated exposure concentrations to acute and chronic toxicity reference values, RQs are calculated.TheEECs on food items may be compared directly with dietary toxicity data or converted to an oral dose, as is done for smallmammals. For mammals, the residue concentration is converted to daily oral dose based on the fraction ofbody weight consumed daily as estimated through mammalian allometric relationships. The screening-level risk assessment for chlorflurenol ME uses upper-bound predicted residues as the measure of exposure. Summaries ofthe predicted upper-bound and mean residues of chlorflurenol ME that may be expected to occur on selected avian or mammalian food items immediately following application for the maximum use scenario arepresented in Table 5. For the maximum chlorflurenolME application scenario, acute concentrations for different forage types ranged from 104.22to 1671.50

### ppm for upper-bound residues and 48.75 to 591.99 ppm for mean residues. Chlorflurenol ME concentrationswere highest on the surfacesof short grass and lowest on the surfaces of fruits, pods, and large insects.

Table5. Upper-bound and mean terrestrial EECs estimatedfor the chlorflurenolME spray application scenario using Kenaga vahes. Forage Type Upper-bound Residues Mean Residues (PPW 

### @P@ short grass 1671.SO 591.99tall grass broadleaf plants and small insects fruitsipodsilargeinsects 104.22 48.75


### b. TerrestrialExposure Monitoring (Field Data) No data were identified to provide information on terrestrial monitoring. 4. 

### Non-Target Plant Exposure Assessment No toxicity data were identified to provide informationon terrestrial plants. 

### C. Ecological Effects Characterization In screening-levelecological risk assessments, effects characterization describes the types of effects a pesticide can produce in an aquatic orterrestrial organism. This characterization is based onregistrant-submitted studies that describe acute and chronic effects toxicity information for various aquatic and terrestrial animals and plants. 

### AppendixD summarizesthe results ofthe registrant-submittedtoxicity studies used to characterize effects for this risk assessment. Toxicity testing reported in this section does not represent all species ofbirds, mammals, or aquatic organisms. Only a few surrogate speciesfor both freshwater fish and birds areused to represent all freshwaterfish (2000+)and bird (680+) species in the United States. For mammals, acute studies are usually limited to Norway rat or the house mouse. Estuarinelmarine testing is usually limited to a crustacean, a mollusc, and a fish. Also, neither reptiles nor amphibians are tested. The risk assessmentassumes that avian and reptilian toxicities are similar. The same assumption is used for fish and aquatic amphibians. In general, categoriesof acutetoxicity ranging from "practically nontoxic" to "very highly toxic" have been establishedfor aquatic organisms (based on LC50and ECso values or limit of solubility),mammals (based on LD50values), avian species (based on LDsoand LCSO values), and non-target insects (based on LDSO values for honey bees) 

### (U.S. EPA 2001). These categories are presented in 

### Appendix 

### D. 1. 

### Aquatic Effects: Animals and Plants No aquatic animal or plant toxicity studies are available for chlorflurenol

### ME. There were several fish and aquatic invertebrate studies submitted; however they were considered unacceptable due to major deviations from guidelines. Therefore, effects cannot be determined. 

### 2. TerrestrialEffects The toxicity endpointsused to characterize risks of chlorflurenol

### ME exposure to birds and mammals are summarized in 

### Table 6. Results of all studies in terrestrial organisms are summarizedin 

### Appendix D, Tables Dl to 

### D3.

,

### Table 6. 

### GhloPaurenol

### ME Todcity

### ReferenceValues

### for Terr~eat Organisms. Speege SeSelIentifIc ToxteIty Effeets Refemnet! Name Rdemnce [Clmsifledltion)

### a. TerrestrialAnimals 

## I I 1 

## 1 V&U@ 

### 1 

## I

Mammalian Species Mammals Acute
Chronic

Birds Acute (D~~~- based) Acute(Dietarybased)

Chronic Plants

Results of an acute oral exposure study in laboratoryrats (MRID 43355402; Acceptable) show that the LD50 for chlorflurenol

### ME is >5,000 mg a.i./kg body weight; therefore, chlorflurenolME is categorized as practically nontoxic to mammalian species on an acute oral basis. EFED will use the acute oral LD50of >5,000 mg a.i.1kgbody weight to evaluate acute dose-based risk to mammalian species. In a developmental toxicity study 

### (MRID 45 190901),chlorfurenol-methyl ester was administered to pregnant SpragueDawley rats by gavage. The maternal NOAEL was 250 mg/kg bwlday. The maternal LOAEL is 750 mg/kg bwlday based on body weight gain decrement and nominally decreased food efficiency. The developmental

### NOAEL is 250 mg/kg bwlday. The developmental LOAEL is 750 mg/kg bwlday,based on treatment-related delayed ossification in skull bones [nasal and frontal] in fetuses and litters. 

### In addition a cleft palate was seen in each of two litters and one diaphragmatic hernia at 1000mglkg bwlday and one cleft palate at 750 mglkg bwlday (cleft palate is rare in rats). Acute 

### I Data gap Chronic 

### I Data gap Rat

Rat

Bobwhite Quail Bobwhite Quail
Mallard Duck Data gap



### Avian S~ecies Results of an acute oral exposure study in bobwhite quail (MRID 43595401;Acceptable) indicate that the LD50 for chlorflurenol

### ME is >10,000 mg a.i.1kgbody weight; therefore, chlorflurenol 

### ME is categorized as practicallynontoxic to avian species on an acute oral basis. EFED will use Rattus norveglcus

Raftus norvegfcw

Colfnus virgintanus Colfntrs v~rgnianus Anas Platyrhync hos 43355402 (Acceptable)

45 190901 (Acceptable)

4359540 1 (Acceptable) 43623601 (Acceptable) 43623602 (Acceptable) Acute Oral

Days 6-15 of gestation LDSo > 5000 mglkg body weight Maternal NOAEL = 250 mg/kg/day

- -

Developmental NOAEL = 250 mgkglday Mortality body weight gain decrement and nominally decreased food efficiency

- - - delayed ossification in skull bones
Mortality

Mortality Single Oral Dose

8 days LDS0 >10,000 mg a.i'kg weight

LC~o > 5,0°0 mg a.i./kg dietthe acute oral LDS0 of >10,000 mg a.i./kg body weight to evaluate acute dose-based risk to avian species. Results of subacute dietary studies in mallard ducks (MRID 43623602; Acceptable) and bobwhite quail (MRID 43623601; Acceptable), show that the acute dietary LCs0 value is ~5,000 mg a.i./kg diet, indicating that chlorflurenol ME is practically nontoxic on an acute dietary basis. EFED will use the LCso value of >5,000 mg a.i./kg diet to assess the risk of acute dietary exposure of birds to chlorflurenol ME. 

### Non-target Insects No data are available for non-target insects. b. 

### Terrestrial Plants No data are available for terrestrial plants. 

## IV. Risk Characterization Risk characterization is the integration of exposure and effects characterization to determine the ecological risk from the use of chlorflurenolME and the likelihood of effects on aquatic life, wildlife, and plants based on varying pesticide-use scenarios. Therisk characterization provides an estimation and a description of the risk; articulates risk assessment assumptions, limitations, and uncertainties; synthesizes an overall conclusion; and provides the risk managers with information to make regulatory decisions. 

### A. Risk Estimation

# - Integrationof Exposure and EffectsData Results of the exposure modeling and toxicity effects data are used to evaluate the likelihood of adverse ecological effects on non-target species. For the assessment of chlorflurenolME risks, the risk quotient (RQ) method is used to compare exposure and measured toxicity values (refer to 

### Appendix E). Estimated environmental concentrations (EECs) are divided by the most sensitive acute and chronic toxicity values. The RQs are then compared to the Agency's levels of concern (LOCs). These LOCs, summarized in 

### Appendix E, are the Agency's interpretive policy and are used to analyze potential risk to non-target organisms and the need to consider regulatory action. These criteria are used to indicate when a pesticide's use as directed on the label has the potential to cause adverse effects on non-target organisms. Details of all RQs are provided in 

### Appendix F. 

### 1. Non-targetAquatic Animals and Plants a. Acute and ChronicRisk to Animals 

### Acute and chronic risk to fish and invertebrates cannot be evaluated at this time because no toxicity data are available. Risk cannot be precluded. 

### b. Aquatic Plants 

### Risk to aquatic plants cannot be evaluated at this time because no toxicity data are available. Risk cannot be precluded.

### 2. Non-target TerrestrialAnimals a. Acute Risk to Birds and Mammals Mammalian S~ecies Definitive acute dose-basedRQ values for mammalian receptors could not be derived because all treated animals survived and gained weight in the submitted acute oral toxicity study on mammals (the oral LDso was >5000 mg a.i.1kg body weight). Based on these results, chlorflurenol ME TGAI is categorizedas practically non-toxic to mammals on an acute oral basis. 

### Avian S~ecies Definitive acute dose- and dietary-basedRQ values for avian receptors could not be derived because the acute effects data show that chlorflurenol ME is practically non-toxic to birds (LDSo >10,000 mg a.i./kgbodyweight and LCSo > 5,000 mg a.i./kg diet). b. 

### Chronic Risk to Birds and Mammals Mammalian S~ecies T-REX was used to calculate chronicRQs for mammals using the chronic toxicity value for the rat (MRID 45 190901). Dose- and dietary-based chronicRQs for mammals are summarizedin 

### 'Table 7 (also in Table F-4 of Appendix 

### F). Dose-based RQs exceed the chronic risk level (LOC 1)to mammalian species for 15-gand 35-g mammals that forage on short grass, tall grass, and broadleafplantslsmall insects (RQrange = 1.14to 2.90) and for 1000-g mammals that forage on short grass (RQ = 1.33). Dietary-basedRQs do not exceed chronicrisk (LOC 1)to mammalian species (RQ range =0.02 to 0.33). These RQs were calculated using upper-bound residues.



### Table 

### 7. Dose- andDietary-based ChronicRQs for Mammals Exposedto Chlorflurenol

### ME Based on UmerBound Residues as Calculated by T-REX CropUse (Application Rate) Body Weight (g)
Dose-based Chronic Mammalian RQs a 

### MammalianRisk 

### Quotients

Turf (3.0 lb a.i./A) 

### Short Grass

15 35 1,000 

### Tall Grass

Dietarv-based Chronic Mammalian RQs b 2.90 2.48 1.33

Turf (3.0 lb a.i.iA) 

### Broadleaf PlantsISmall Insects

1.33 1.14 0.61

0.33 

### FruitslPoddLarge Insects Seeds

1.63 1.39 0.75

0.15 0.18 0.15 0.08

0.19 0.04 0.03 0.02

0.02 NA

### Avian Suecies Table 

### 7. 

### Dose- andDietary-based ChronicRQs for Mammals Exposedto ChlorflurenolME Based onUauer Bound Residues as Calculated 

### by 

### T-REX.

No toxicity data are available to quantitatively assess chronic risk of chlorflurenolME exposure to birds. Risk cannot be precluded. 

### Crop Use (Application Rate)

c. Risk to TerrestrialInvertebrates No toxicity data are available to quantitatively assess risk of chlorflurenolME exposure to terrestrial invertebrates. Risk cannot be precluded.

a Chronic dose-based RQ = EECDIOAEL, where EEC values are upper bound residues expressed as equivalent dose (mg a.i./kg body weight) generated from T-REX and the toxicity value is the chronic dose-based NOAEL = 250 mg a.i./kg/day in the rat.

Chronic dietary-based RQ = EECMOAEC, where EEC values are upper bound residues expressed as dietary concentrations (mg a.i./kg diet) generated from T-REX and the toxicity value is the chronic dietary-based NOAEC = 5000 mg a.i./kg diet in rats (converted from the rat oral dose study).

RQs are above the LOC for chronic risk (LOC 1). 

### Body Weight (g)



### 3. Non-target Terrestrialand Semi-Aquatic Plants No toxicity data are available to quantitatively assess risk of chlorflurenolME exposure to terrestrial However, since chlorflurenolME is used as an herbicide and as a growth regulator, risk to non-target plants may occur. 

### MammalianRisk Quotients



### B. Risk Description

## - Interpretation ofDirect Effects There are no data on the usage of chlorflurenol

### ME; however, the registrant suggests it is used in low volumes. Therefore, even though RQs may indicate risk, exposure may be overestimated due to the low volume applied yearly across the contiguousUnited States. RQs, and therefore risk, may also be under- or over-estimated due to major uncertainties and gaps in the fate and toxicity data (see section 1V.C). In most instances RQs could not be calculated due to data gaps. 

### Seeds

1. 

### Risks to Aquatic Organisms FruitsflPodsLarge Insects Short Grass

There are no acceptable toxicity studies and little environmental fate data to evaluate potential exposure; therefore, EFED is unable to preclude risk to aquatic animals and plants. Since chlorflurenol ME is applied as a spray to non-food crops that are ubiquitous (i.e. turf, rights of ways, fence rows), a wide variety of non-target aquatic organisms may come into contact with chlorflurenol ME and its degradates in runoff or spray drift. Based on limited fate data, chlorflurenol ME may leach through the ground quickly decreasing the amount of chlorflurenol ME available for runoff to surface water. However, this study was conducted on sandy loam soils 

### Tall Grass Broadleaf PlantsiSmall Insectswhich do not occur throughout the 

### U.S. In addition, this does not account for chlorflurenol ME moving to aquatic systemsvia spray drift. This study was classified as supplemental due to guideline deviations which increases the amount of uncertainty. Once in the water, the fate cannot be determined. Therefore, if chlorflurenolME enters water systems,non-target aquatic organisms may be at risk. 2. 

### Risks to Terrestrial Organisms a. Acute Risk to Birds and Mammals Based onthe submitted acute oral toxicity studies on birds and mammals, chlorflurenol ME is categorized aspractically non-toxic to birds and mammals on an acute oral and/or dietary (birds only) basis (LDSo > 10000mg a.i./kg body weight for birds; LCso> 5000 mg a.i./kg diet for birds; LDSo > 5000 mg a.i./kg body weight for mammals). No effects were seen in the acute avian studies; however, the mammal study showed rats with hunched posture, lethargy and diarrhea. RQs could potentially exceed acute listed species LOCs unless the actual LDso values are established in laboratory studies to be greater than -1 6,715 mg a.i./kg body weight or if the amount available in the environment was loweredbelow 500 ppm (see 

### Appendix 

### C on how to calculate adjusted LDso values, dose-based EECs, and acute dose-based RQs). Therefore, some uncertainty concerning acute oral risk to birds and mammals as a result of exposure to chlorflurenol ME does exist. In addition,the studytesting oral toxicity to birds did not state which components were included in the test material. EFED assumes the test material contained all three components which may underestimaterisk to birds on an acute oral basis. b. 

### Chronic Risk to Birds and Mammals Relative to the use patterns identified in this assessment, exposure of chlorflurenol ME spray application is expected to result in chronicrisk to listed and non-listed mammals. As shown in 

### Table 7, some dose-basedRQs for chronicrisk to mammalian species are above the chronic risk LOC (1) for the maximum spray application scenarioconsidered in this risk assessment (RQ range =0.02 to 2.90). Specifically, chronic dose-based RQs exceed the LOC for mammals feeding on short grass (RQ range = 1.33to 2.90),tall grass (RQrange = 0.61 to 1.33),and broadleaf plants/small insects (RQrange = 0.75 to 1.63).The chronic LOC is not exceeded for mammals of any size feeding on fruits/pods/largeinsects (RQ range =0.08 to 0.18) or seeds (RQ range = 0.02 to 0.04). Chronic dietary-basedRQs do not exceed the chronicLOC for mammals (RQ range =0.02 to 0.33). To bound the estimates of risk to mammals resulting from chronic exposure to chlorflurenol ME, RQs using mean Kenaga residue values in additionto upper-bound values were calculated (See Table 

### F-5;Appendix F). Using the non-conservativemean residuevalues, implyingthat higher predicted residue values are expected half the time, only the RQ for 15gmammals that feed on short grass (RQ = 1.02) exceeds the chronic LOC. These RQs arebased on a developmental study that shows evidence of delayed skull ossification and cleft palates in young rats. These endpoints are not adequate for determiningrisk to the survival and fecundity of a population. However, without other studiesEFED used these data. Therefore, the RQs may not accuratelyportray chronic risk to mammals. Risk may be under- or over-estimated.There are uncertainties associated with the RQ values derived with T-REX, In the absence of foliar dissipation half-life data, application interval, and number of yearly applications, the default half-life and "likely" interval and yearly applications were used, which may have overestimated or underestimated the risk to terrestrial species. The dose-based approach considers the uptake and absorption kinetics of a gavage toxicity study to approximate exposure associated with uptake from a dietary matrix. Toxic response is a function of duration and intensity of exposure. For many compounds a gavage dose represents a very short-term high intensity exposure. Although the dose-based estimates may not reflect reality in that animals do not receive a gavage while feeding, it is possible that a short-duration, high-intensity exposure could occur associated with feeding on an agricultural field since many birds may gorge themselves when food items are available. mle the dietary-based estimates may suggest greater "realism," they too suffer from some uncertainties. Primarily, the dietarybased approach assumes that animals in the field are consuming food at a rate similar to that of confined laboratory animals despite the fact that energy content in food items differs between the field and the laboratory as does the energy requirements of wild and captive animals. No quantitative data are available to characterize chronic risks from application of chlorflurenol ME to birds; therefore, EFED cannot preclude chronic risk to birds. 

### c. Non-target Terrestrial Invertebrates No quantitative data are available to characterize risks from application of chlorflurenolME to terrestrial invertebrates. Since chlorflurenolME is applied in areas where there may be pollinators and other invertebrates,EFED cannot preclude risk to terrestrial invertebrates. d. 

### Terrestrial Plants No quantitative data from guideline studies are availableto characterize risks from application of chlorflurenol ME to terrestrial plants. However, since chlorflurenol

### ME is used as anherbicide and growth regulator, risk to terrestrial plants is assumed. Chlorflurenol ME has been shown to induce parthenocarpyin cucumbers (Robinson et al. 1971) and interrupt ovule development in muskmelons (Snyder et al. 1983). Robinson et al. (1971) stated that at lower concentrations (10 -20 ppm), parthenocarpy was induced when cucumber plants were treated in the flowering stage; however, at a higher concentration (40 ppm) parthenocarpy was induced two week prior to the flowering stage. In muskmelons, ovule development was halted when chlorflurenol was applied 10 - 12 days before anthesis (Snyder et al. 1983). Since parthenocarpic plants produce fruits with no seeds, sexual reproduction cannot occur. Nontarget plants that come in contact with chlorflurenolME may also suffer from increased parthenocarpy, severely limiting their ability to reproduce. 

### 3. Review of Incident Data Incident reports submitted to EPA since approximately 1994have been tracked by assignment of "incident numbers" in an Incident Data System (IDS), microfiched, and then entered into a second database, the Ecological Incident Information System (EIIS). An effort has also been made to enter information to EIIS on incident reports received prior to establishment of current databases. Incident reports are not received in a consistent format (e.g., states and various labs usually have their own formats), may involve multiple incidents involving multiple chemicals in 26 

### -one report, and may report only part of a given incident investigation (e.g., residues). While some progress has been made in recent years in getting incident reports submitted and entered, there has never been the level of resources assigned to incidents that therehas been assigned to the tracking and review of laboratory toxicity studies,for example. No incident reports involving aquatic or terrestrial exposure to chlorflurenol ME have been reported. 4. 

### Endocrine Effects Under the Federal Food, Drug and Cosmetic Act (FFDCA), as amendedby the Food Quality Protection Act (FQPA), EPA is required to develop a screening program to determine whether certain substances(including all pesticide active and other ingredients) "may have an effect in humans that is similarto an effect produced by a naturally-occurring estrogen, or other such endocrine effects as the Administrator may designate." Followingthe recommendations of its Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC),EPA determined that there was scientificbasis for including, as part ofthe program, the androgen- and thyroid hormone systems, in addition to the estrogen hormone system. EPA also adopted EDSTAC's recommendationthat the Program include evaluations ofpotential effects in wildlife. For pesticide chemicals,EPA will use FIFRA, to the extent that effects in wildlife may help determinewhether a substance may have an effect in humans, and the FFDCA authority to require the wildlife evaluations. As the science develops and the resources allow, screeningof additionalhormone systems may be added to the Endocrine Disruptor Screening Program (EDSP). When the appropriatescreening and or testing protocols being considered under the Agency's EndocrineDisruptor Screening Program have been developed, chlorflurenol ME may be subjectedto additional screeningand or testing to better characterize effects related to endocrine disruption. Results of the submitted developmental study in mammals show exposureto chlorflurenol ME produces adverse effects on reproductive parameters. Observed effects in the submitted mammalian study includematernal body weight gain decrement and nominally decreased food efficiency,as well as treatment related delayed ossification in skull bones (nasal and frontal) in fetuses and litters. Results of this developmental study suggest that chlorflurenol ME could be a candidate for additional screening and/ortesting to better characterize effects related to endocrine disruption. Chronic exposure studies on the effectsof chlorflurenol have not been conducted in aquatic organismsorbirds. Therefore,EFED must considerthe possibility that chlodlurenol ME may have detrimental effects on the endocrine system in these taxa. 5. 

### Threatened and Endangered Species Concerns a. Action Area For listed species assessment purposes, the action area is considered to be the area affected directly or indirectlyby the Federal action and not merely the immediate area involved in the action. At the initial screening-level, the risk assessment considers broadly described taxonomic groups and so conservatively assumes that listed species within those broad groups are collocated with the pesticidetreatment area. This means that terrestrial plants and wildlife are assumed to be located on or adjacent to the treated site and aquatic organisms are assumed to be located in a 27 

### -surface water body adjacent to the treated site. The assessment also assumesthat the listed species are located within an assumed area which has the relatively highest potential exposure to the pesticide, and that exposures are likely to decrease with distancefrom the treatment area. Section III(A) of this risk assessment presents the pesticide use sitesthat are used to establish initial collocation of species with treatment areas. If the assumptions associated with the screening-level action area result in RQs that arebelow the listed species LOCs, a "no effect" conclusionis made with respect to listed species in that taxa, and no further refinement of the action area is necessary. Furthermore,RQs below the listed species LOCs for a given taxonomic group indicateno concern for indirect effects upon listed species that depend upon the taxonomic group covered by the RQ as a resource. However, in situations where the screening assumptionslead to RQs in excess ofthe listed speciesLOCs for a given taxonomic group, a potential for a "may affect" conclusion exists and may be associated with direct effects on listed speciesbelonging to that taxonomic group or may extend to indirect effects upon listed speciesthat depend upon that taxonomic group as a resource. In such cases, additional information onthe biology of listed species, the locations of these species, and the locations of use sites could be considered to determine the extent to which screening assumptions regarding an action area apply to a particular listed organism. These suhequent refinement steps could consider how this information would impact the action area for a particular listed organism and may potentially include areas of exposure that are downwind and downstream of the pesticide use site. b. 

### Taxonomic Groups Potentially at Risk The Level I screening assessment process for listed speciesuses the generic taxonomic groupbased process to make inferences on direct effect concerns for listed species. The first iteration of reporting the results of the Level I screeningis a listing of pesticide use sites and taxonomic groups for which RQ calculationsreveal values that meet or exceed the listed species LOCs. 

### In the majority of cases, the screening-level risk assessment process reports RQ calculations for the following broad taxonomic groupings: Birds (also used as surrogate for terrestrial-phase amphibians and reptiles) Mammals Freshwater fish (alsoused as a surrogatefor aquatic phase amphibians) Freshwater invertebrates Estuarinelmarine fish Estuarinelmarine invertebrates 

### Terrestrial plants Algae and aquatic plants i. Discussion of Risk Quotients Should estimated exposure levels occur in proximity to listed resources, the available screeninglevel information suggests a potential concern for direct effects to listed fish (freshwater and estuarinelmarine), aquatic invertebrate (freshwaterand estuarinelmarine), beneficial insect, avian, reptile, amphibian, and mammalian species associated with areas where chlorflurenol

### ME is used. More specifically, the available screening-level information indicates the following: Fish and Aquatic InvertebratesRisk quotients for acute and chronic effects to freshwater and estuarinelmarinefish and invertebrates could not be calculated because there are no acceptable toxicity studies. Aquatic Plants andAlgae Risk quotients for aquatic plants and algae could not be calculated because there are no acceptable toxicity studies. Birds Definitive acute dose- or dietary-based RQ values for avian receptors could not be derived because there are no definitive LDso or LCs0values. Risk quotients for chronic effects to birds could not be calculated because there are no acceptable toxicity studies. Mammals Definitive acute dose- or dietary-based RQ values for mammalian receptors could not be derived because there are no definitive LD50or LCsO values. 

### The use of chlorflurenol ME under the maximum application rate scenarios results in dose-based RQs for mammals exceeding the chronic risk LOC (1) for exposurevia short grass, tall grass, and broadleaf plantslsmall insects. Terrestrial Plants Risk quotients for terrestrial plants could not be calculated because there are no acceptable toxicity studies. ii. Probit Dose Response Relationship The probit slope response relationship is evaluated to calculate the chance of an individual event corresponding to the listed species acute LOCs.The analysis uses the EFED spreadsheet IECvl .l.xls, developed by Ed Odenkirchen (6122104). It is important to note that the IEC model output can go as low as 

### 1 x in estimating the event probability. This cut-off is a limit in the Excel spreadsheet environment and is not to be interpreted as an agreed upon lower bound threshold for concern for individual effects in any given listed species. If an LDSo or LCsO has been established for a particular taxonomic group,but information is unavailable to estimate a slope from a study, a default slope assumption of

### 4.5 is used as per original Agency assumptions of typical slope cited in Urban and Cook (1986). 

### Ln instances where an LCsoor LDSo has not been established for a particular taxonomic group, an individual effects probability is not estimated. Freshwater and EstuarineIMarineFish and Invertebrates No toxicity data are available to quantitatively assess individual risk of chlorflurenol ME exposureto aquatic organisms.

### Mammals and Birds Definitive LCSo/LDSos are not available to quantitatively assess individual risk of chlorflurenol ME exposure to terrestrial organisms. 

### c. Indirect Effects Analysis The Agency acknowledgesthat pesticideshave the potential to exert indirect effects upon the listed organismsby, for example, perturbing forageor prey availability, altering the extent of nesting habitat, and creating gaps in the food chain. In conducting a screen for indirect effects, direct effect LOCs for each taxonomicgroup areused to make inferences concerning the potential for indirect effects upon listed speciesthat rely upon non-listed organisms in these taxonomic groups as resources criticalto their life cycle. Species-specific concerns for chlorflurenol ME indirect effects to listed organisms will require a determinationof the coincidence of chlorflurenol ME use with locations of listed species and the biologically based resources upon which they depend. TheAgency uses the dose response relationshipfrom the toxicity study used for calculating the RQ to estimate the probability of acute effects associated with an exposure equivalent to the EEC (see Probit Dose response Relationship above). In instances where informationon the dose response is available, it serves as a guide to establish the need for and extent of additional analysis that may be performed using Services-provided "species profiles" as well as evaluations of the geographical and temporal nature of the exposure to ascertainif a "not likely to adversely affect" determination can be made. The degree to whlch additional analysesareperformed is commensurate with the predicted probability of adverse effects from the comparison of the dose response information with the EECs. The greater the probability that exposures will produce effects on a taxa, the greater the concern forpotential indirect effects for listed species dependant upon that taxa, and therefore, the more intensivethe analysis on the potential listed species of concern, their locations relative to the use site, and information regarding the use scenario (e.g., timing, frequency, and geographical extent of pesticide application). Relative to chlorflurenolME proposed usage, EFED's screeninglevel analysis showsthat there is a concern for indirect effects to listed speciesthat may depend upon other taxonomic group for their survival (e.g., invertebratesas a food source for listed fish, etc.). Screening-levelRQs for avian species potentially exceed the acute risk LOC and RQs for mammalian species exceed the acute and chronic risk LOC. Therefore, the nature of the toxicological endpoint, Servicesprovided "species profiles," and krther evaluation of the geographical and temporal nature of the exposure will need to be considered to determineif a rationale for a "not likely to adversely affect" determinationis possible. Using ourbest professional judgment, 

### EFED concludesthat due to the lack of toxicity data for fish, aquatic invertebrates, aquaticplants, birds (chronic), and terrestrial plants, risk cannot be precluded and there may be a potential concern for indirect effects to the following groups of organismsin the action area: Terrestrial plants Aquatic plants Birds Mammals Reptiles Aquatic Invertebrates FishAmphibians Terrestrial Insects For listed species that may potentially be indirectly affectedby the Federal action, see 

### Appendix G (Locates run). 

### d. Critical Habitat In the evaluation of pesticide effects on designated critical habitat, consideration is given to the physical and biological features (constituent elements) of a criticalhabitat identified by the U.S. Fish and Wildlife and National Marine Fisheries Services as essential to the conservation of a listed species and which may require special management considerationsor protection. The evaluation of impacts for a screening-level pesticide risk assessment focuses on the biological features that are constituent elements and is accomplished using the screening-level taxonomic analysis (risk quotients, RQs) and listed species levels of concern (LOCs) that areused to evaluate direct and indirect effects to listed organisms. The screening-level risk assessment has identified potential concerns for indirect effects on listed species for those organisms dependent upon aquatic fish and invertebrates (including benthic animals), birds, reptiles, and mammals. 

### In light of the potential for indirect effects, the next step for EPA and the Service(s) is to identify which listed species and critical habitat are potentially implicated. Analytically, the identification of such species and critical habitat can occur in either of two ways. First, the agencies could determine whether the action area overlaps critical habitat or the occupied range of any listed species. If so, EPA would examine whether the pesticide's potential impacts on non-listed species would affect the listed species indirectly, or directly affect a constituent element ofthe critical habitat. Alternatively, the agencies could determine which listed species depend on biological resources, or have constituent elements that fall into the taxa that may be directly or indirectly impacted by the pesticide. Then EPA would determine whether use of the pesticide overlaps the critical habitat or the occupied range of those listed species. At present, the information reviewed by EPA does not permit use of either analytical approach to make a definitive identification of species that arepotentially impacted indirectly or critical habitats that ispotentially impacted directlyby the use of the pesticide. EPA and the Service(s) are working together to conduct the necessary analysis. This screening-level risk assessment for critical habitat provides a listing of potential biological features that, ifthey are constituent elements of one or more critical habitats, would be of potential concern. These correspond to the taxa identified above as being of potential concern for indirect effects and include the following: terrestrial plants, aquatic plants, reptiles, birds, mammals, fish and aquatic invertebrates, terrestrial insects, and amphibians. This list should serve as an initial step in problem formulation for further assessment of critical habitat impacts outlined above, should additional work be necessary. -1'able 

### 8 provides a list of the taxa that may be directly or indirectly affected.

monocotse. Co-occurrenceAnalysis The goal ofthe analysis for co-locationis to determinewhether sites of pesticide use are geographically associated with known locations of listed species. At the screening level, this analysis is accomplishedusing the LOCATES database. The databaseuses location information for listed species at the county level and comparesit to agricultural census data for crop production at the same county level ofresolution. The product is a listing of federally listed species that are located within countiesknown to produce the crop upon which the pesticide will be used. Because the Level 

### I screeningassessment considers both direct and indirect effects across generic taxonomic groupings,it is not possible to exclude any taxonomic group from a LOCATES database run for a screeningrisk assessment. Given the extent of potential chlorflurenol ME usage across the U.S. and the expected large number of listed species that are likely to occur in counties where chlorflurenol 

### ME is used, a list of endangeredlthreatenedspecies Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes Terrestrial and semi-aquatic plants - dicots Insects
Birds
Terrestrial phase amphibians Reptiles
Mammals Aquatic vascular plants
Freshwater fish Aquatic phase amphibians
Freshwater crustaceans
Mollusks
Marineiestuarine fish
Marinelestuarine crustaceans

a We cannot preclude risk due to lack of

The reported RQ values are above the chronic LOC (I .0)for species that feed on short grass, tall grass, and broadleaf plantslsmall insects (RQ range = 0.02 to 2.90). 

### 'RQs could potentially exceed acute listed species LOCs unless the actual LDSo values are established in laboratory studies to be greater than -1 6,7 15mg a.i.1kg body weight or if the amount available in the environment was lowered below 500 ppm Yes a Yes a Acute - Yes '; Chronic - Yes a Yes a Acute -Yes '; Chronic - Yes a Acute - Yes '; Chronic - Yes
Yes a Yes a Yes a Yes a Yes a Yes a Yes a data.and crop acreage at the county level for the taxonomic groups and crops of concern is not included in this phase of the risk assessment process. Given that the potential extent of chlorflurenol ME usage includes every state, and that all taxonomic groups are included in the initial LOCATESrun for a screening-level risk assessment, 

### Appendix G provides the entire list of endangeredlthreatened species at the state level. The registrant must provide information on the proximity of federallylisted birds, fish, mammals, amphibians, crustaceans, reptiles, arachnids, insects,plants, snails, and clamsto the chlorflurenol ME use sites. This requirement may be satisfiedin one of three ways: 1)having membership in the FIFRA Endangered SpeciesTask Force (Pesticide Registration [PR]Notice 2000-2); 2) citing FIFRA Endangered Species Task Force data; or 3) independently producing these data, provided the information is of sufficient quality to meet FIFRA requirements. The informationwill be used by the OPP Endangered Species ProtectionProgram to develop recommendations to avoid adverse effects to listed species. C. 

### Description ofAssumptions, Limitations,Uncertainties, Strengthsand Data Gaps This risk assessment relies on best available estimates of environmental fate and physicochernical properties, maximum application rate of chlorflurenol ME, maximum number of applications,and the shortest interval between applications. However, several uncertainties and model limitations are noted and should be consideredin interpreting the results of this risk assessment. 1. 

### Assumptions, Limitations, Uncertainties,Strengths and Data Gaps Related to Exposure For All Taxa There are a number of areas of uncertaintyin the aquatic and terrestrialrisk assessments. There are no valid toxicity data for any aquatic species,birds (chronic only), terrestrial invertebrates, and plants. Thetoxicity assessment for terrestrial animals is limited by the number of species tested in the available toxicity studies. Use oftoxicity data on representative species does not provide information on the potential variability in susceptibility to acute and chronic exposures. 

### 2. Assumptions, Limitations,Uncertainties, Strengths and ~ata Gaps Related to Exposure For Aquatic Species Theregistrant has submitted three studies to support the environmental fate data requirements; however, these studies were considered either supplemental or unacceptable (see reasons below). As a result, the uncertainty analysis could not be performed with confidence. Guideline 161-1: The study was conducted at pHs 3,6and 

### 9 rather than pHs 

### 5,7and 

### 9 as required in SubdivisionN Guidelines. This studywas determined to be supplemental. The hydrolysis data requirementshave not been fulfilled. A new study including pH 

### 7 is required. Guideline 162-1:The study was conducted outdoorsin the summerwhere the environmental conditions, soil aerobicity, microbial viability, and soil moisture were neither controllednor reported. SubdivisionN Guidelines requirethat the study be conductedin the dark at 25

# * 1 OC. This study was determined to be unacceptable. The aerobic soil metabolism data requirements have not been fulfilled. A new studyusing four soils is required. Guideline 163-1: Only one test soil type was used in the adsorption study and it could not be determined if this German soil was comparable to soils found in typical use areas in the United States. Subdivision N guidelines specifythat four different soil types should be used. This studywas determined to be supplemental. The adsorption/desorption data requirements have not been fulfilled. A new study including three soils is required. 

### 3. Assumptions, Limitations, Uncertainties,Strengths and Data Gaps Related to Exposure For Terrestrial Species The dataset availableto support the terrestrial exposureassessment for chlorflurenol ME is substantially incomplete. Application interval,number of applicationsper year, and a foliar dissipation study, which are input variables for modeling of risks to birds and mammals (i.e., TREX), are lacking. The terrestrialmodeling for chlorflurenol ME was conducted using "likely" application intervals and yearly applications, as derived by HED. Also a default foliar dissipation half-life value of 35 days, based on the work ofWillis and McDowell(1987), was used. Therefore, if these values are lower or higher terrestrialEECs may be overestimated or underestimated. 

### a. Location ofWildlife Species For screening terrestrialrisk assessments, a generic bird or mammal is assumedto occupy either the treated field or adjacent areas receiving the pesticide at a rate commensurate with the treatment rate on the target field. This assumptionmay lead to an overestimationof exposureto species that do not occupy the treated field. The actual habitat requirements of any particular terrestrial species are not considered, and it is assumed that species occupy, exclusively and permanently, the treated area being modeled. This assumption leads to a maximum level of exposure in the risk assessment. 

### b. Routes of Exposure Screening-level risk assessments for spray applications ofpesticides consider dietary exposure alone, and assume that 100%ofthe diet is relegated to single food types foraged only from treated fields. These assumptions are likely to be conservative for many species and will tend to overestimate potential risks. The assumptionof 100% diet from a treated area may be realistic for acute exposures,but long-term exposuresmodeled as single food types composed entirely of material from a treated field is uncertain. Other routes of exposure, not considered in this assessment, are discussedbelow. 

### Incidental Soil InvestionEx~osure This risk assessment does not consider incidental soil ingestion. Available data suggest that up to 15%of the diet can consist of incidentallyingested soil depending on the species and feeding strategy (Beyer et al. 1994). A simple first approximation of soil concentration of pesticide from spray application showsthat ingestionof soil at an incidental rate ofup to 15% of the diet would not increase dietary exposure. 

### Inhalation Ex~osure The screening risk assessment does not consider inhalationexposure. Such exposuremay occur through three potential sources: 

### (1) spray material in droplet form at the time of application 

### (2) vapor phase pesticide volatilizingfrom treated surfaces, and 

### (3) airborne particulate (soil, vegetative material, and pesticide dusts).Available data suggest that inhalation exposureat the time of application is not an appreciable route of exposure for birds. According to research on mallards and bobwhite quail, respirable particle size in birds (particlesreaching the lung) is limited to a maximum diameter of 2 to 5 microns. Theoretically, inhalationof pesticide active ingredient in the vapor phase may be another source of exposure for somepesticidesunder some exposure situations. The impact from exposure to dusts contaminated with the pesticidecannot be assessed generically as partitioning issues related to application site soils and chemical properties render the exposure potential from this route highly situation-specific. 

### Dermal Ex~osure The screening assessment does not considerdermal exposure, except as it is indirectly included in calculations of RQs based on lethal dosesper unit of pesticide treated area. Dermal exposure may occur through three potential sources: (1) direct applicationof spray to terrestrial wildlife in the treated area or within the drift footprint, 

### (2) incidental contact with contaminated vegetation, or 

### (3) contact with contaminated water or soil. The available measured data related to wildlife dermal contact with pesticides are extremely limited. The Agency is actively pursuingmodeling techniquesto account for dermal exposure via direct application of spray and by incidental contact with vegetation. 

### drink in^Water Ex~osure Drinking water exposureto a pesticide active ingredient may be the result of consumption of surface water or consumption of the pesticide in dew or otherwater on the surfaces of treated vegetation. For pesticide active ingredientswith a potential to dissolvein runoff, puddles on the treated field may contain the chemical. 

### c. Incidental Pesticide ReleasesAssociated with Use This risk assessment is based on the assumptionthat the entiretreatment area is subject to chlorflurenol

### ME applicationat the rates specifiedon the label. In reality, there is the potential for uneven application of chlorflurenol

### ME through suchplausible incidents as changes in calibration of application equipment, spillage,and localized releases at specific areas of the treated field that are associated with specifics of the type of applicationequipment used (e.g., increased application at turnaboutswhen using older ground application equipment). 

### d. Residue Levels Selection As discussed earlier in the exposure sectionof this document, the Agency relies on the work of Hoerger and Kenaga 

### (1972) and Fletcher et al. 

### (1994) for setting the assumed pesticide residues in wildlife dietary items. The Agency believesthat these residue assumptionsreflect a realistic upper-bound residue estimate, although the degree to which this assumption reflects a specific percentile estimate is difficult to quantify. It is important to note that the field measurement efforts used to develop the Fletcher estimatesof exposure involvehighly varied sampling techniques. It is entirely possible that much of these data reflect residues averaged over entire above ground plants in the case of grass and forage sampling. Dependingupon a specific wildlife species' foraging habits, whole aboveground plant samples may either underestimate or overestimate actual exposure.

### e. Dietary Intake

# - The Differences Between Laboratory and Field Conditions The acute and chronic characterization of risk rely on comparisons of wildlife dietary residues with LCs0or NOAEC values expressed in concentrations of pesticides in laboratory feed. These comparisons assume that ingestion of food items in the field occurs at rates commensurate with those in the laboratory. Although the screening assessment process adjusts dry-weight estimates of food intake to reflect the increased mass in fresh-weight wildlife food intake estimates, it does not allow for gross energy and assimilative efficiency differences between wildlife food items and laboratory feed. On gross energy content alone, direct comparison of a laboratory dietary concentration- based effects threshold to a fresh-weight pesticide residue estimatewould result in anunderestimation of field exposure by food consumptionby a factor of 1.25

### - 2.5 for most food items. Only for seeds would the direct comparison of dietary threshold to residue estimate lead to an overestimate of exposure. Differences in assimilative efficiency between laboratory and wild diets suggest that current screening assessment methods do not account for a potentially important aspect of food requirements. Depending upon species and dietary matrix,bird assimilation of wild diet energy ranges from 23 

## - 80%, and mammal's assimilationranges from41 

### - 85% 

### (US.Environmental Protection Agency, 1993). If it is assumed that laboratorychow is formulated to maximize assimilative efficiency (e.g., a value of 85%), a potential for underestimation of exposure may exist by assuming that consumption of food in the wild is comparable with consumption during laboratory testing. In the screening process, exposuremay be underestimated because metabolic rates are not related to food consumption. Finally, the screening procedure does not account for situations where the feeding rate may be above orbelow requirements to meet free living metabolic requirements. Gorging behavior is a possibility under some specific wildlife scenarios (e.g.,bird migration) where the food intake rate may be greatly increased. Kirkwood (1983) has suggestedthat an upper-bound limit to this behavior might be the typical intake rate multipliedby a factor of 5. In contrast, there is the potential for avoidance, operationally defined as animals responding to the presence of noxious chemicals in their food by reducing consumption of treated dietary elements. This response is seen in nature where herbivores avoidplant secondary compounds. However, reduced food intake, particularly over an extended period, could result in reduced survival or reproductive output. 4. 

### Assumptions, Limitations, Uncertainties,Strengths and Data Gaps Related to Effects Assessment The dataset available to support the terrestrial and aquatic effects assessment for chlorflurenol ME is incomplete. Data gaps, uncertainties, and limitations are summarized as follows: Guidelines 72-1, 72-2, 72-3, 72-4: Acute and chronic data for freshwater and estuarinelmarine fish and invertebrates are not available; therefore, risk could not be assessed. Guideline 71-4: Avian reproduction studies are not available; therefore, risk could not be assessed. Guideline 123-1, 123-2: Terrestrialplant seedling emergence and vegetative vigor studies are not available. In addition, aquatic plant growth studies are not available;therefore risk could not be assessed. Since chlorflurenolME is used as an herbicide and growth regulator, toxicity data on non-target plants are necessaryto estimate risk. Guideline 141 -1 :Data for honey bee acute contact toxicity are not available; therefore, risk could not be assessed. Acute oral and dietary toxicity studies inbirds and acute oral toxicity studies in mammals failed to establish definitive acute LD50/LCs0 values (i.e., the LCs0was expressed as "greater than" the highest dietary concentration tested); thus, acute RQ could not be calculated. The study testing oral toxicity to birds did not state which components were included in the test material. EFED assumesthe test material contained all three components which may underestimate risk to birds on an acute oral basis if in fact the test material only contained one ofthe three components. The mammalian chronic RQs are based on a developmental study that shows evidence of delayed skull ossification and cleR palates in young rats. These endpoints are not adequate for determining risk to the survival and fecundity of a population. However, without other studies EFED used these data. Therefore, the RQs may not accurately portray chronic risk to mammals. Risk may be under- or over-estimated. Application interval and number of applications per year are not indicated on the label. For multiple application scenarios the T-REX model requires both of these parameters in order to estimate exposure to terrestrial organisms. In the absence of these numbers an application interval of 

### 28 days and 

### 8 applicationsper year were used as derived by HED 

### (Appendix

### B). HED used informationprovided on the labels along with best professional judgment of the croptweed growth cycles,pest pressure timing, etc. to determine the application interval and yearly number of applications. EFED used the HED data to maintain consistency between EFED and HED. Since these numbers are considered "likely" applications per year, risk to terrestrial organisms may be underestimated.


### a. Age Class and Sensitivityof Effects Thresholds It is generally recognized that test organism age may have a significantimpact on the observed sensitivity to a toxicant. The screening risk assessment acute toxicity data for fish are collected onjuvenile fish between 0.1 and 5 grams. Aquatic invertebrate acute testing is performed on recommended immature age classes 

### (e.g., first instar for daphnids, second instar for amphipods, stoneflies and mayflies, and third instar for midges). Similarly, acute dietary testing with birds is alsoperformed onjuveniles, with mallard being 5-10 days old and quail at 10-14days of age. Testing of juveniles may overestimate the toxicity of direct acting pesticides in adults. As juvenile organisms do not have fully developed metabolic systems, they may not possess the ability to transform and detoxify xenobiotics equivalent to the oldertadult organism.The screening risk assessment has no current provisions for a generally applied method that accounts for this uncertainty. 

### In so far as the available toxicity data may provide ranges of sensitivity information with respect to age class, the risk assessment uses the most sensitive life-stage information as the conservative screening endpoint. 

### b. Lack of EffectsData for Amphibians and Reptiles Currently, toxicity studies on amphibians and reptiles are not required for pesticide registration. Since these data are lacking, the Agency uses fish as surrogates for aquatic phase amphibians and birds as surrogates for terrestrial phase amphibians and reptiles. These surrogates are thought tobe reflective of or protective (more sensitive)ofherpetofauna. Amphibians are characterizedby a permeable skin. The most important route of exposure for aquatic amphibianswould likely be the dermal route. Using freshwaterfish may be suitable surrogates since exposure would likely be surface area dependent and the gill surface of many fish is a fairly large surface area. Also, both fish and amphibians are ectothermic so metabolic rates and demandswould likely be similar. For terrestrial species, however, the differencebetween amphibiansand birds and reptiles and birds is quite large. Terrestrial amphibiansand reptiles areboth ectothermic while birds are endothermic; birds have a higherbasal metabolic rate required to maintain constant body temperature. The higher metabolic demandsofbirds may be predispose birds to higher relative exposures. However, this does not address any potential differencesin toxicity. To date, there are few controlled studies on reptile speciesthat couldbe used to compare to similar studies on birds. A priori, there is no strong reason to think that one taxon is more or less sensitive than another. Therefore, it was assumedthat the use of surrogate effectsdata is sufficiently conservative to apply the broad of specieswithin taxonomic groups.If other speciesare more or less sensitive to chlorflurenolME than the surrogates,risks may be under- or overestimated, respectively. The Agency is not limited to a base set of surrogate toxicity informationin establishing risk assessment conclusions.The Agency also considers toxicity data on nonstandard test species when available.Further research is required to determinewhether, in general, reptiles and terrestrial-phase amphibians are suitablyrepresented by bird species in assessing risks for chlorflurenolME. 

### c. Use ofthe Most Sensitive SpeciesTested Although the screeningrisk assessment relies on a selectedtoxicity endpoint from the most sensitive species tested, it does not necessarily mean that the selected toxicity endpointsreflect sensitivity ofthe most sensitive species existing in a given environment. The relative position of the most sensitive species tested in the distribution of all possible species is a function of the overall variability among species to a particular chemical. The relationshipbetween the sensitivity of the most sensitivetested speciesversus wild species (including listed species) is unknown and a source of significantuncertainty. 

### In addition,in the case of listed species, there is uncertainty regarding the relationship of the listed species' sensitivity and the most sensitive species tested. The use of laboratory specieshas historicallybeen driven by availability and ease of maintenance. A widespread comparison of speciesis lacking, however, even variation within a species can be quite high. For example,in this assessment, acute studies on honey bees yielded different values. 5. 

### Assumptions,Limitations, Uncertainties,Strengths and Data Gaps Related to the Acute and ChronicLOCs The risk characterization section of the assessment document includes an evaluation of the potential for individual effects to listed species at an exposure level equivalent to the LOC. This evaluation is based on the median lethal dose estimate and doselresponserelationship established for the effects study corresponding to each taxonomic group for which the LOCs are exceeded. The slope of the probit-dose response is used to generate a probability of individual effects near the low end tail of the curve. Predictionsbased on low probability events areby nature highly uncertain. Moreover, for this assessment the dose-response curve representing a given taxon is generated from one study using one species. It is likely that the resulting dose-response relationship does not represent the response of all specieswithin a taxon. Calculating the probability of individual effects at the lower and upper bounds of the slope is designed to address

### this source of uncertaintybut the extent to which this captures the variability within a taxon is unknown. In some cases, a probit dose-responserelationship cannot be calculated.

### In these instances, event probabilities are calculatedbased on a default slope assumptionof 4.5 with upper and lower confidence intervals of 2 and 9 (Urban and Cook, 1986). 

### V. Literature Cited 

### Environmental Fate MRID Studies Submitted to EPA MRID 43496201 Darskus,R. 1977. Hydrolysis of chlorflurenol ME-methyl. Unpublished studyperformed by CELAMERCK. Gmbh & 

### Co. KG, Rhein, Germany, compiled and submitted by SRS International Corporation, Washington, DC, an agent for Nita Industries, Inc. StudyNo. CFM-NITA-1611. MRID 43496202b Doebbler, G.F. 198 1. Soil adsorption/desorptionofchlorflurenolMEmethyl ester. Unpublished studyperformed by Union Carbide Corporation Environmental Services, Tarrytown,NY; sponsored by 

### EM Industries, Inc., Elrnsford, NY; and submittedby Nita Industries,Inc., (location not reported). StudyNumber CFM-NITA-1631. UCCES ProjectNo. 11507- 86. EPA CaseNumber 2095. Active Ingredient Number 98801. MRID 43496202a Schliiter, H. 1981. Leaching of '4~-chlorflurenol ME-methyl. Unpublished study performed by CelamerckGmbH & 

### Co. KG, IngelheirnMein, Germany and submitted by Nita Industries,Inc., (locationnot reported). StudyNumber CFM-NITA-1631. CM Document No. 109AA-922-003. EPA CaseNumber 2095. Active Ingredient Number 98801. 

### MRID 43595403 Sieper, H. 1969. Aerobic soil metabolism study. Unpublished study performedby E. MERCK AG, Darmstadt,Germany, compiled and submittedby SRS International Corporation, Washington,DC, an agent for Nita Industries,Inc. Study No. CFM-NITA-1621. 

### Ecological Effects MRID Studies Submitted to EPA MRID 00082863 Frohberg, H., A. Metallinos, H. Pies, et al. 1975. Chronic Toxicity Test with IT 3456 in Beagle Dogs: Administration with the Food over a Period of Two Years. (Translation;unpublished studyreceived Apr 25, 1978 under 21 137-EX-3; prepared by E. Merck, West Germany, submittedby EM Laboratories,Inc., Elms- ford,N.Y.; CDL:097056-A) MRID 43355402 Wnorowski, G. 1994. Acute Oral ToxicityLimit Test: (ChlorflurenolME Methyl): Lab Project Number: 31 70. Unpublished study prepared by Product SafetyLabs. 16p. MRID 43595401 Estop, C. and R. Teske. 1969. Acute Oral Toxicity of ChlorflurenolME Methyl Ester in Bobwhite Quail: Lab Project Number: CFM-NITA-711A: S-404.Unpublished study prepared by Hill Top Research,Inc. 29 p.

### MRID 43623601 Pedersen, C. and A. Solatycki. 1995. 8-Day Acute Dietary LC50 Study with ChlorflurenolME Methyl in Bobwhite Quail: Lab Project Number: 152-001 -01. Unpublished study prepared by Bio-Life Associates, Inc. 48 p. MRID 43623602 Pedersen, C. and A. Solatycki. 1995. 8-Day Acute Dietary LC50 Study with ChlorflurenolME Methyl in Mallard Ducklings: Lab Project Number: 152-002-02. Unpublished studyprepared by Bio-Life Associates,Inc. 46 p. MRID 45190901 Muller, W. 2000. Chlorflurenol ME-Methyl, Technical Oral (Gavage) Teratogenicity Studyin the Rat: Lab Project Number: 926-460-028:460- 028. Unpublished studyprepared by Hazleton Laboratories Deutschland GmbH. 222 p. 

### Open Literature and Government Reports Beyer, W. N.; Connor, E; Gerould, S. 1994. Survey of soil ingestionby wildlife. Journal of Wildlife Management 58:375-382. Fletcher, J.S., J.E. Nellesson and T. G. Pfleeger. 1994. Literaturereview and evaluation of the EPA food-chain (Kenaga)nomogram, an instrument for estimating pesticide residues on plants. Environ. Tox. And Chem. 13(9):1383-1391. Hoerger, F. and 

### E.E. Kenaga. 1972. Pesticideresidues on plants: correlationof representative data as a basis for estimation of their magnitudein the environment. IN: 

### F. Coulston and F. Corte, eds., Environmental Quality and Safety: Chemistry, Toxicology and Technology. Vol 

### 1. George Theime Publishers, Stuttgart,Germany. pp. 9-28. Kirkwood, RC. 1983. Therelationship of metabolism studies to the modes of action of herbicides. Pestic. Sci. 14: 453-460. Robinson, R. W., D. J. 

### Cantliffe, and S. Shannon. 1971. Morphactin-induced parthenocarpyin the cucumber. Science 171: 

### 125 1-1252. Snyder, J. 

### C., C. Carter, and D. E. Knavel. 1983. ChlorflurenolME interruptsovule development of muskmelon. HortScience 18:345-347. T-REX. 2005. Terrestrial Residue ExposureModel (T-REX), Version 1.2.3. August 8,2005. Environmental Fate and Effects Division, Office of PesticidePrograms, U.S. Environmental Protection Agency, Washington, D.C. U.S. EPA. 1993. U. S. 

### Environmental ProtectionAgency. Wildlife Exposure Factors Handbook. Volume I of 11. EPA1600R-931187a.Office of Research and Development, Washington, D. C. 20460. U.S. EPA. 2001. U.S. Environmental Protection Agency. Ecological Risk Assessor Orientation Package. U.S. Environmental ProtectionAgency, Ecological Fate and Effects Division. Draft Version, August 2001. U.S. EPA. 2004. U.S. Environmental ProtectionAgency. Overview of the Ecological Risk Assessment Process in the Office of PesticidePrograms, U.S. Environmental ProtectionAgency:

### Endangered and Threatened SpeciesEffects Determinations. Office of Prevention, Pesticide, and Toxic Substances. January 23. Urban, D.J. and N.J. Cook. 1986.Hazard Evaluation Division Standard Evaluation Procedure Ecological Risk Assessment. EPA 54019-85-001.U.S. Environmental Protection Agency, Office of Pesticide Programs, Washington,DC. Willis and McDowell. 1987. Pesticide persistence on foliage. Environ. Contam. Toxicol. 100:23- 73.

### APPENDIX A. Environmental Fate and Transport Data

a.Degradation Hydrolysis (161-1): Thehydrolysis of non-radiolabeled chlorflurenol 

### ME applied at a rate of 1.8 or 18mg a.i./L (ppm) was studied in the dark at 25OC in sterilepH 3, pH 6 and pH 9 aqueous buffer solutions for up to 50 days 

### (MRID 43496201). Quantitative data for pH 3 buffer solution was not provided; however an extrapolated (not defined) half-life of 336 days was reported by the study author. In the pH 6 buffer, chlorflurenol ME applied at 18 ppm decreased only slightly from CLI. 94.4% of the applied at time 0 and 10 days, to 

### ca. 77.8% at 50 days posttreatment. In pH 9 buffer, chlorflurenol 

### ME applied at a rate of 18 ppm, decreased from 

### ca. 111.1 % of the applied at time 0, to 

### ca. 55.6% at 4.5 hours (0.19 days; study termination); applied at a rate of 1.8ppm, chlorflurenol ME decreased from 

### ca. 116.7% of the applied at time 0, to 

### ca. 41.7% at 7 hours (0.29 days; study termination). The only major transformation product reported was 2-chloro-9- hydroxyfluorene-9-carboxylic acid (Compound 11), however, quantitative data and further details were not reported. 

### MRID 43496201 was classified as supplemental because the material balance was incomplete, the analytical methods were inadequate, and tabular data for chlorflurenol ME and quantitative data for its transformation products were not reported.

Photodegradation in water (161-2): No photodegradation in water studies were submitted. Summary of Hydrolysis of Chlorflurenol 

### ME 

### (MRID 43496201)

Photodegradation in soil (161-3): No photodegradation in soil studies were submitted. At 25OC PH 6 PH 9

b. Metabolism Aerobic soil metabolism (162-1):Unlabeled chlorflurenol 

### ME (formulation CF125, 12.5% a.i.) applied at a rate of 8.75 kg a.i./ha to outdoor field plots degraded in sandy loatn soil from Germany (pH 6.0, organic matter 3.5%; soil moisture content not provided) with a linear and nonlinear half-life of 1.3 days, and an observed half-life of <5 days (MRID 43595403). Chlorflurenol ME decreased from 

### ca. 66.3% of the applied at time 0, to 

### ca. 4.5% at 5-12 days, and was not detected at 26 days (study termination). One major degradation product was confirmed by a colormetric method. 2-Chloro-9-fluorenone (Compound IV; fluorenone) increased to a maximum of 

### ca. 14.3%of the applied at 5-12 days and was not detected at 26 days. Linear Half-life (days) 161.2 0.19-0.20

MRID 43595403 was classified as unacceptable because the study was conducted outside where the environmental conditions were neither controlled nor reported, the material balance was incomplete, volatiles were not collected, the sampling intervals were inadequate to accurately establish a half-life, and the analytical method was inadequate at identifying all potential transformation products. Major Transformation Products 2-Chloro-9-hydroxyfluorene-9-carboxylicacid (Compound 11)Also it could not be determined if the German soil used was comparable to soils found in a typical chlorflurenol 

### ME use area in the 

### US. An aerobic soil metabolism study using 4 soils may be required.

Anaerobic soil metabolism (162-2): No anaerobic soil metabolism studies were submitted. Anaerobic aquatic soil metabolism (162-3): No anaerobic aquatic soil metabolism studies were submitted. Aerobic aquatic soil metabolism (162-4): No aerobic aquatic soil metabolism studies were submitted.

c. Mobility Mobility/Adsorption/Desorption (163-1): The column leaching of [phenyl-~-'4~]-labeled chlorflurenol ME was studied in unaged sand (A), sandy loam (B), and two loam (C and D) German soils and one aged sandy loam (B) German soil (MRID 43496202a). For the unaged soil columns, the application rate of the test substance to each soil column ranged from 50.26 pg to 53.70pg (not further specified); the test substance was applied to the aged soil at a rate of 1 pg/~nL. The unaged soil columns were leached under saturated conditions with 437 

### rnL of distilled water (equivalent to 20.6 hdcm rain) for up to 24 hours; the aged soil column was leached daily with 1I I~L distilled water (equivalent to 0.52 hdcmrain) for 45 days. In the treated soil layer of the unaged soil columns, chlorflurenol 

### ME comprised 1.5%of the applied radioactivity in the sand soil, 2.6% in the sandy loam soil, 1.3%in the loam soil (C), and 6.0% in the loam soil (D). In the soil segments of the unaged soil columns, chlorflurenol ME comprised 1.3% ofthe applied (0-20 cm) in the sand soil, 3.4% (0-10 cm) in the sandy loam soil, 29.3% (0-20 cm) in the loam soil (C), and <35.7% (0-15 cm) in the loam soil (D). The transformation product 2-chloro-9-hydroxyfluorene-9-carboxylic acid totaled 1.2%, 1.9%,0.2%, and 1.2%) of the applied in the treated sand, sandy loam, loam (C) and loam (D) soils, respectively; and 32.3% (0-30 cm), 27.2% (0-20 cm), 39.5% (0-30 cm), and 21.9% (0-30 cm), respectively in the soil columns. 2-Chloro-9-fluorene totaled 0.3%, 1.0%,0.4%, and 0.7% of the applied in the treated soils, respectively; and <0.8% (0-30 cm), 2.7% (0-10 cm), 4.1% (0-30 cm), and 4.2% (0-25 cm), respectively in the soil columns. In the leachate, 24.3% ofthe applied radioactivity was detected in the sand soil, and the transformation product 2-chloro-9- hydroxyfluorene-9-carboxylic acid was identified but not quantified in the leachate; 10.7%ofthe applied radioactivity was detected in the leachate in the other three soils. In the aged column leaching portion ofthe study, following the 30-day aging period under aerobic conditions, [14c]residues were 38.1% of the applied radioactivity, of which chlorflurenol ME cotnprised 0.6% of the applied. The transformation products 2-chloro-9-hydroxyfluorene-9- carboxylic acid and 2-chloro-9-fluorene were 11.5%and 1.8%of the applied, respectively. Following 45 days of leaching, an average of 18.0% ofthe applied radioactivity was recovered in the aged soil. Chlorflurenol 

### ME was not detected in the soil segments. 2-Chloro-9-fluorene-9- carboxylic acid totaled 1.O% ofthe applied in the aged soil and 1.9%in the soil segments (0-20cm); 2-chloro-9-fluorenetotaled 2.6% in the aged soil and 4.1% in the soil segments (0-20 cm). Unextractable residues totaled 27.9% of the applied. The leachate contained an average of 0.7% of the applied radioactivity, first detected at 22 days, and containing a maximum of 5.0 ng equivalents of ['4~]chlorflurenol ME/mL effluent at 44 days. MRID 43496202a was classified as supplemental because for both unaged and aged soil column leaching studies, it could not be determined ifthe German soil used was comparable to soils found in a typical chlorflurenolME use area in the US. In addition, for the aged soil column leaching study, the test substance was aged for longer than one half-life prior to use in the leaching portion of the study, and the material balances were incomplete (<90% of the applied). The adsorption of [I4C]chlorflurenol 

### ME was studied in sandy loam soil (pH 7.3; organic carbon 1.1%) from Germany in a batch equilibrium experiment (MRID 43496202b). Based on the McCall Classification System, chlorflurenol ME was high to very highly mobile. This study was classified as supplemental because it could not be determined if the German soil used was comparable to soils found in a typical chlorflurenol 

### ME use area in the 

### US and the material balances were not determined.

Laboratory volatility (163-2): No laboratory volatility studies were submitted. Field volatility (163-3): No field volatility studies were submitted.
d.Dissipation Terrestrial Field Dissipation (164-1): No terrestrial field dissipation studies were submitted.
e. Accumulation Fish bioaccumulation (165-4): No fish bioaccumulation studies were submitted.
J Special Field Studies Small-scale prospective groundwater study 

### (166-1): No small-scale prospective groundwater studies were submitted. g. degradates The table below summarized the degradates which were detected in the fate studies: Chlorflurenol ME and its transformation products.Transformation Product Name and Structure

pH 9, applied at 1.8

Table A-2. Chlorilurenol 

### ME: Parnet and Suspected transformation Productsin Laboratorv and Field Studies

Code Name Chemical Name Chlorflurenol ME 

### (RS)-2-Chloro-9-hydroxyfluorene-9-carboxylic (Chlorflurenol-methyl; Chlorflurenol-methyl acid methyl ester ester; Chlorflurecol-methyl; Clorflurecolmethyl ester; Compound I) Transformation Product 1 (Fluorenone; Compound IV) Transformation Product 2 (Chlorflurenol; Compound 11) 2-Chloro-9-hydroxyfluorene-9-carboxylic acid

### Confirmed Transformation Product Lab Results Max %AR' (Study) Chemical Structure Fluorenone

Chlorflurenol

%AR = % of applied radioactivity. 14(aerobic soil)

Not quantified. CI 0

CI

# a HO COOH /

### APPENDIX 

### B.

Occupational Uses

Turf: ornamental and lawns

Turf golf courses Weed Turf growing in culverts, ROW, median strips, ditches, under security fences Weed Hardwoods: growing under utility

lines, as screens or ground cover, adjacent to highways Weed Hedges: growing under utility lines, as screen

Weed Vines growing under utility

lines, as screens or ground cover, ROW, hedgerows Weed Gymnospernls
Trees: bark banding to inhibit growth 69361-1 water dispersible solution

69361-6 liquid 69361-1 water dispersible solution 69361-6 liquid

69361-6 liquid

69361-6 liquid

69361-6 liquid
69361-6 liquid 69361-6 liquid I I I 

### I Wait at least 4 weeks before 

### I 0.26 Ib ailacre 2"dapplication Apply anytime weeds actively
3.0 lb ailacre

1.0lb ailacre growing and temp is >60°F Apply when grass just beginning to green up. Apply throughout growing season.



# '"lb aillOO gallons Apply when weeds are actively growing

Retards growth up to 1 year

'O lb aiiloo gallons

depends on diameter & 8(FL)

Retards growth up to 2 months

# l61 60

0.25 lb ad100 gallons

tree type 40 (FL)

8 (FL) 40 (FL)

Must be treated before buds expand 1 10

# I Agricultural Uses 

# I
Turf: sod farms
Pineapple plants: forplant material production (non food use) 

## I planting material harvest. Residential Uses 69361-6 liquid

6936 1-6 (SLN) liquid

Turf: lawns 3.0 lb ailacre

1.0 lb ailacre

growing and temp is >60°F 69361-3 dry Apply throughout growing season beginning when turf is just beginning to green up. (RE148 hours) A 2"dapplication may be made after an interval of 10- 12 days. Apply to mature pineapple plants at time of forcing, and 6 months prior to desired

0.26 1b ailacre 6

2

Wait at least 4 weeks before 2"dapplication Apply anytime weeds actively 30

10

6 6

### APPENDIX 

### C. T-REX 

### Model (Version 

### 1.2.3, August, 

### 2005) I. Introduction This spreadsheet-based model calculates the residues on avian and mammalian food items along with the dissipation rate of 

### a chemical applied to foliar surfaces (for single or multiple applications) in order to estimate acute and reproductive risk quotients. LDso ft-2 values are calculated for both broadcast and banded (granular and liquid) applications using an adjusted LD50 method. Theresults are presented by weight class for various sized birds and mammals for each type of application. Avian and mammalian risk quotients are also calculated for seed treatment applications to various crop seeds. T-REX uses the same principle asthe batch code models FATE and TERREEC that calculate terrestrial exposure concentration estimates on plant surfaces following pesticide application. However, T-REXperforms a number of calculations that neither FATE nor TERREEC perform. For example, T-REX adjusts acute and chronic toxicity values based on the relative body weight of the animal being assessed compared with the animal used in the toxicity studies. T-REX also calculates risk quotients for granular applications and seed treatments. 11. Inputs Inputs needed to run T-REX include the following (inputs denoted with an 

## * are required; inputs denoted with a *C are required when multiple applications are being modeled: A. Pesticide Application Data Chemical name: Either the chemical or common name used in the assessment. Use: Thetype of use (e.g., turf, residential, crop, foliar, right-of-way, etc.) applicable, also provide crop name. Product name and 

### form: Thename ofthe formulated product as it appears on the subject label, including any indication of the form of the product (e.g. log - 10% granular, wp 

### - wettable powder, etc.) The %A.I. for the formulation (from the label). 

### If an application rate for a formulated product is used, use the % A.I. for the formulation. However, ifthe application rate to be entered has already been adjusted for % A.I., use 100 % in this cell. Application Rate*: The maximum label application rate (pounds ailacre). If your application rate has already been adjusted for active ingredient, make sure you have entered 100in the % A.I. cell above; otherwise, enter your application rate in lbs formulatiodAhere and then the %A.I. in the product in the above cell. Foliar Dissipation Half-life*: The foliar dissipation half-life in days. 

### EFED policy requires the risk assessor to consult availablemagnitude of residue (1 71-4), the reduction ofresidue (171-5) and the foliar dissipation (132-1) studies submitted by the registrant to 

### HED for determiningpesticide residue half-life for wildlife food items used for terrestrial wildlife exposure modeling. Another source for dissipation data for wildlife exposure modeling purposes is Willis and McDowell(1987; available at 

### F:\USER\SHARE\Models\Terrestrial Exposure\TREX). In the event that the above data sources do not provide a suitable halflife estimate, the EFED default value is 35 days. When using the defaults, the risk assessor is urged to evaluatethe effect of alternative assumptions of residue half life assumption on the outcome ofthe terrestrial wildlife risk assessment and include this evaluationin the discussion ofrisk assessment uncertainties. Application interval*^: The minimutn interval (days) between multiple applications (if any). Note: This version ofthe model can only accommodate uniform application intervals; subsequent models may incorporate a provision of intervals of varying length. The risk assessor may evaluate the effect of using application intervals other than the minimum interval on the label to explorepossible mitigation effort effects onrisk outcomes. Number of Applications*~: The number of applications. EFED policy states that screening risk assessments should consider the maximum number of applications specified on the product label. However, the risk assessor may elect other numbers of applications to explore possible mitigation effort effects on risk outcomes. B. Avian and Mammalian Endpoints To calculate risk quotients,user-supplied avian and mammalian toxicity endpoints need to be entered into the 'Endpoints' section of the Inputs worksheet. These endpoints can be found in avian acute oral LDjo,avian acute dietary LC50, avian reproduction NOAECIL, acute mammalian LD.50 or LC50, and mammalian reproduction NOAECIL toxicity studies. T-REX requires that both the chosen endpoint (entered in the blue cell) and the test speciesbe included (chosen from the drop-down menu options). For example, one would enter an avian LDSo of 500 mg/kg-bw and that this endpoint was based on a Bobwhite quail study (i.e., chosen from the drop-down menu immediately to the right ofthe LDSo input cell). Typically, endpoint data for bobwhite quail, mallard duck, and laboratory rats from submitted studies or open literature will be used. In the case where data on bird species other than bobwhite quail or mallard duck are assessed (e.g. Japanese quail), choose "other" from the species drop down menu and enter the body weight of the species. A similar option for mammals is not currently available in this version of T-REX. Calculations for animals other than rats need to be done by hand using equations included in this user's guide until the release of the next version of T-REX. Seethe progratn author for assistance if needed. 1. Avian Endpoints The following avian toxicity endpoints may be entered into T-REX : LDSU LDsofor dose-based acute effects endpoint (mglkg-bw).Lcso LCSo for dietary-based acute effects endpoint (mglkg-diet). Reported Chronic Endpoint NOAEL if reported in mglkg-bw or NOAEC if reported in mgikg-diet. Mineau Scaling Factor If chemical-specific data are available the user can specify the avian scaling factor (see Mineau, et a1.,1996) Otherwise, use the EFED default value of (1.15). T-REX will not run unless a Mineau scaling factor is entered. However, zero can be entered if the assessor believes that body weight does not influence toxicity of the chemical being assessed. EFED policy states that for screening risk assessments, the lowest LDjo,LC50, NOAEC andlor NOAEL from acceptable or supplemental studies be used. For non-screening risk assessments, the risk assessor may elect other values as necessary, but must document in the risk assessment why the lowest tested endpoint was not used. However, the assessor should determine that the lowest toxicity value from a laboratory study results in the lowest adjusted toxicity values for the various weight classes being assessed. This is important when the toxicity values from different species are similar to each other because T-REX adjusts the toxicity values based on body weight and food intake of the tested organism compared with the assessed organism. Therefore, when data are available from multiple species, adjusted LDSOs hould be calculated for all species and the lowest value should be used. The risk assessor should note that this version ofthe model assumes a set body weight for tested bobwhite quail (178 g) and mallard duck (1580 g) unless another body weight is entered to the right of this cell or "other" is selected for a test species. Use of "other" species or studies involving subject animals markedly different from the assumed body weights requires the risk assessor to provide the alternatebody weight and the species name. These data should be obtained from the study report if possible (time weighted average). Alternatively, reference body weight values may be obtained from a variety of sources including U.S. EPA (1993) and the testing laboratory.
2. Mammalian Endpoints The following mammalian endpoints may be entered into T-REX: LDso LD50(mg/kg-bw) for dose-based acute effects endpoint. Lcso LCso(mg/kg-diet) for dietary-based acute effects endpoint. Reported Chronic Endpoint NOAEL if reported in mglkg-bw or NOAEC if reported in mglkg-diet. 

### EITHER the NOAEL or the NOAEC. To the right ofthe cell is a drop down menu for the units in which the endpoint is expressed. The model will automatically make default adjustments for units to expressthe endpoint BOTH asNOAEC and NOAEL by assuming that a laboratory rat consumes 

### 5% of its body weight daily (i.e.,divide the concentration in food (ppm) by 20 to calculate the dose in mg/kg-bw). However,if a reproduction study reports toxicity values in units of dose (mglkg-bw) and dietary concentration (mglkg-diet), then both ofthese values should be used over the estimated values calculatedby T-REX. Because the current version of T-REX only allows for input of either a dose or dietary concentration (not both), T-REX needs to be run twice when a study reports toxicity values in terms of concentration (mglkgdiet) and dose (mglkg-bw). If a rat reproduction study is unavailable, the risk assessor may use the rat teratogenicity study NOAEL or NOAEC, but must identify this alternative endpoint use and must discuss in the risk description the limitations. Studies other than reproduction or developmental toxicity studies are not currently used by EFED to calculate risk quotients. The lowest LDSo, LCSn, NOAEC andlor NOAEL from acceptable or supplemental studies are used in screening-level risk assessment of mammals. For non-screening level assessments, the risk assessor may select other values as necessary, but must document in the risk assessment why the lowest tested endpoint was not used. Therisk assessor should note that this version of the model assumes a set body weight of 350 g for the tested organism, assuming they are laboratory rats. Use of other species, or studies involving subject animals markedly different from the assumed body weight of 350 g will result in inaccuracies when extrapolatingtest endpoints to modeled animals. Therefore, if a mammalian species other than rats is used (e.g. dog, rabbit, 

### mink), use the time-weighted average body weight of the animals that were tested in the experiment (from the DER or the original study report). Alternatively, reference body weight values may be obtained from a variety of sources including U.S. EPA (1993) and the testing laboratory. However, T-REX does not currently allow the use to enter body weights of mammals that differ from the 350-gram laboratory rat. Therefore, adjusted toxicity values would need to be performed by hand. C. Additional Inputs for LDS0 ft-2 analysis Chlorflurenol ME is not intended for use as a seed treatment. 

### D. Additional Inputs for Seed Treatment Analysis Chlorflurenol ME is not intended for use as a seed treatment. 111. Risk Estimation Based on Dietary Residue Concentrations (Foliar Spray) The methods used by T-REX to estimate risk from consumption of selected contaminated food items is described below. For this analysis, T-REX calculates EECs and risk quotients based on both the upper bound and mean residue concentrations aspresented by Hoerger and Kenaga (1972) and modified by Fletcher et al. (1994). These concentrations are determined using nomograms that relate application rate of a pesticide to residues remaining on dietary items of terrestrial organisms. The results ofthe upper bound and mean residue levels are presented in separate tabs ("upper bound Kenaga" and "mean Kenaga"); however, the methods used to calculate EECs and risk quotients are equivalent. Only RQs from the upper bound Kenaga worksheet are to be used for comparison to levels of concern in the assessment. The mean residues, and the RQs generated from them, presented in the mean Kenaga worksheet aretobe used only for risk description. Replacing the upper bound residues with the mean residues is not a valid mitigation approach when upper bound residues result in LOC exceedances. Based on theestimated dietary residue concentrations from the upper bound and mean Kenaga values, T-REX calculates the associated doses for various size classes of birds and mammals. Both the dietary concentration (mglkg-dietary item) and the resulting estimated doses (mglkg-bw) may be used for risk estimation. The resulting dietary based and concentration based risk quotients are discussed below. This section describes how T-REX estimates the following: (1) residue concentrations on selected food items (mglkg-dietary item); 

### (2) dose-based EECs (mglkg-bw) from dietary concentrations on selected food items; (3) adjusted toxicity values; and (4) risk quotients. A. Calculation ofDietary Concentrations on SelectedFood Items The spreadsheet calculates the pesticide residue concentrations on each selected food item on a daily interval for one year. When tnultiple applications are modeled, residue concentrations resulting from the final application and remaining residue from previous applications are summed. The maximum concentration calculated out ofthe 365 days is returned as the EEC used to estimate potential risk to birds and mammals asdescribed below. Dissipation of a chemical applied to foliar surfaces for single or multiple applications is calculated assuming a first order decay rate from the following first order rate equation:

or in log form:

Where CT = concentration at time T = day zero. C,= concentration, in parts per million (PPM), present initially (on day zero) on the surfaces. C,is calculated by multiplying the application rate, in pounds active ingredient per acre, by 240 for short grass, 110for tall grass, and 135 for broadleafed plants/small insects and 15 for fruits/pods/large insects based on the Kenaga nomogram (Hoerger and Kenaga, 1972) as modified by Fletcher (1994). For maximum concentrations, additional applications are converted from pounds active ingredient per acre to PPM on the plant surface and the additional mass added to the mass ofthe chemical still present onthe surfaces onthe day of application. 

### k = If the foliar dissipation data submitted to EFED are found scientifically valid and statistically robust for a specific pesticide, the 90% upper confidence limit of the mean half-lives should be used. When scientifically valid, statistically robust data are not available, EFED recommends using a default half-life value of 35 days. Theuse of the 35-day half-life is based onthe highest reported value (36.9 days), asreported by Willis and McDowell (Pesticide persistence on foliage, Environ. Contam. Toxicol, 100:23-73, 1987). T = time, in days, since the start of the simulation. The initial application is on day 0. The

simulation is designed to run for 365 days. The dietary concentrations estimated using the above methodology may be used directly to calculate risk quotients, but may also be used to calculate dose-based EECs (mglkg-bw) for various size classes of mammals and birds as below.

### B. Calculating EEC Equivalent Doses based on Estimated Dietary Concentrations on Selected Bird and Mammal Food Items EECs (mglkg-bw) for various size classes of mammals and birds may be calculated based on the dietary residue concentrations derived using the equations presented above. To allow for this type of analysis, the EECs and toxicity values are adjusted based on food intake and body weight differences sothat they are comparable for a given weight class of animal. The size classes assessed are small (20-gram), medium (100-gram), and large (1000-gram) birds, and small (15- gram), medium (35-gram), and large (1 000-gram) mammals. Equations used to calculate food intake (gramslday) and to adjust toxicity values for dose-based risk quotients are presented below. 

### Calculating Food Intake for Different Size Classes of Birds and Mammals: Daily food intake (glday) is assumed to correlate with body weight using the following empirically derived equation (U.S. EPA, 1993):

Avian consumption
where: 

### F = food intake in grams of fresh weight per day (giday) BW =body mass of animal (g) W = mass fraction of water in the food (EFED value = 0.8 for birds and herbivorous mammals, 0.1 for granivorous mammals)
Based on this equation, a 20-gram bird would consume 22.8 grams of food daily (114%of its body weight), a 100-grambird would consume 65 grams of food daily (65% of its body weight daily), and 1000-grambird would consume 290 grams of food daily (29% of its body weight). These data, together with the residue concentrations (mglkg-food item) on selected food items calculated from the Kenaga nomogram, are used to estimate the dose (mg/kg-bw) of residue consumed by the three size classes of birds as discussed below. Using a small (20-gram) bird as an example, a dietary concentration of 100mgtkg-diet (ppm) x 1.14kg dietlkgbw (1 14%)would result in an equivalent dose-based EEC of 114 mglkg-bw. T-REX calculates food intake based on dry weight and wet weight of food items. The dose-based assessment uses the wet weight food consumption values by assuming that dietary items are 80% water by weight. However, if dietary items of a species being assessed are known, then a refined dose-based EEC can be calculated using appropriate water fractions of the food items. A similar relationship between body weight and food intake has been derived for mammals (US. EPA 1993):

### 0.648

## * BW O 651 

### F = 

### (1-W) Mammalian food consumption (glday) where: 

### F = food intake in grams of fresh weight per day (glday) BW =body mass of animal (g) W = mass fraction of water in the food (EFED value =0.8 for birds and herbivorous mammals, 0.1 for granivorous mammals)
The scaling factors result in a percent body weight consumed presented in the following table for each weight class of mammal. These values are used in the same manner described for birds to calculate dose-based EECs (mglkg-bw). Note the difference in food intake of grainivores compared with herbivores and insectivores. This is caused by the difference in the assumed mass fraction of water in their diets.

" The first number in this colu~nn is specific to herbivores/insectivores.The second number is for granivores. These groups have markedly different consumption requirements. 

### Table C1. 

### Scaling factors and percent body weight consumedfor 3 weight classesofmammals.

T-REX calculates food intakebased on dry weight and wet weight of food items (wet weight is used for RQ calculations). The dose-based assessment uses the wet weight food consumption values by assuming that dietary items are 80% water by weight (10% for granivores). However, if dietary items of a species being assessed are known, then a refined dose-based EEC can be calculated using appropriate water fractions of the food items.

Organism and Body Weight
15 g 35 g I000 g

C. 

### CalculatingAdjusted Toxicity Values The dose-based EECs (mglkg-bw) derived above are compared with LDSO or NOAEL (mglkgbw) values from acceptable or supplemental toxicity studies that are adjusted for the size of the animal tested compared with the size of the animal being assessed (e.g., 20-gram bird). These exposure values are presented as mass of pesticide consumed per kg body weight of the animal being assessed (mglkg-bw). EECs and toxicity values are relative to the animal's body weight (mg residuelkg bw) because consumption ofthe same mass of pesticide residue results in a hlgher body burden in smaller animals compared with larger animals. For birds, only acute values (LDSos) are adjusted because dose-based risk quotients are not calculated for the chronic risk Food Intake (g day -') a 14.3 13.2 2315 1 150 134 PercentBody Weight Consumed (day -1) a 95 121 66 / 15 1513estimation. Adjusted mammalian LDSOs and reproduction NOAELs (mgikg-bw) are used to calculate dose-based acute and chronic risk quotients for 15-, 35-, and 1000-gram mammals. The following equations are used for the adjustment (U.S. EPA 1993): Adjusted avian LDS0: 

### AdjNOAEL or

### LD

# ,, = 

### NOAEL ov 

### LD 

# ,, - '25) where: Adj. LDso= adjusted LD5, (mgikg-bw) calculated by the equation LDSo = endpoint reported from bird study (mg/kg-bw) TW =body weight of tested animal (1 78g bobwhite; 1580gmallard; 350g rat) AW =body weight of assessed animal (avian: 20g, 100g,and 1000g) 

### x = Mineau scaling factor for birds; 

### EFED default 1.15 Adjusted mammalian NOAELs and LDSos (note that the same equation is used to adjust the NOAEL):

where: Adj. NOAEL or LDS0 = adjusted NOAEL or LDS0 (nlgikg-bw) NOAEL or LD5o= endpoint reported from bird study (mg/kg-bw) TW =body weight of tested animal (350g rat) AW =body weight of assessed animal (15g, 35g, 1000g) D. Calculating Risk Quotients Two types ofrisk quotients are calculated by 

### T-REX based onthe estimated dietary residue concentrations determined from the Kenaga nomogram: 

### (I) dietary based RQs; and (2) dose based RQs. These RQs are not equivalent. Dietary risk quotients are calculated by directly comparing the concentration of a pesticide administered (or estimated to be administered)to experimental animals in the diet in a toxicity study to the concentration estimatedto be on selected food items. Theserisk quotients do not account for the fact that smaller-sized animals need to consume more food relative to their body weight than larger animals or that differential amounts of food are consumed depending on the water content and nutritive value of the food. The dose-based risk quotients do account for these factors. The dose-based RQs incorporatethe ingestion rate-adjusted exposure from the various food items to the different weight classes of birds and the weight class-scaled toxicity endpoints. Formulas presented in Table C2 are used to calculate dose-based and dietary based risk quotients:These risk quotients are compared to the Agency's LOCs to determine if risk is greater than EFED's concern level.



### Table C2. 

### Formulas used to calculate dose- and dietary-based 

### risk quotients.

IV. 

### Actual Input Parameters

Duration
Acutc

Chron~c

A. 

### PesticideApplication Data The actual input parameters used to determine terrestrial EECs on food items for chlorflurenol ME are listed below in Table C4. Only one scenario was modeled using 

### T-REX; a foliar spray application for turf use. The label indicates that chlorflurenol ME can be applied at a maximum application rate of 3.0 lb a.i./A for turf use. Chlorflurenol ME is likely applied via foliar spray application 8 times per year and at a 28-day interval (as derived by HED). Dose orDietary RQ Dose-based Dietary-based Dietary-based Dose-based

Uncertainties in the terrestrial EECs are associated with a lack of data on dissipation from foliar surfaces. When data are absent, as in this case, EFED assumes a 35-day foliar dissipation halflife, based on the work of Willis and McDowell (1987). In this respect, the EECs for chlorflurenol ME may be an overestimation of actual concentrations if the half-life under field conditions is lower than the default value. Because foliar dissipation data are not available, the extent to which EECs may be overestimated or underestimated is uncertain. On the other hand, terrestrial EECs could be an underestimation of actual exposure concentrations in the environment. EFED used a "likely" application interval and yearly application rate, since no information was provided on the label. Risks could be underestimated if the actual application rates, frequency of application, or number of applications are higher than the input parameters used for the exposure scenariothat was modeled. Surrogate Organism
Birds and matnmals
Birds Birds and mammals Mammals



### Table C4. Input parameters used in 

## T-REX v1.2.3 

### to determine terrestrial.EECs for the maximum chlorflurenol

### ME spray application scenario. a Input Variable Parameter Value Source Equation Acute Daily Exposure (mgkg-bw) 1adjusted LD,, (mgikg-bw) Kenaga EEC (mgkg-food item) 1 LC5, (mglkg-diet) EEC (mglkg-food item) 1NOAEC (mgkg-diet) EEC (mgikg-bw) l Adjusted NOAEL (tnglkg-bw)

Maxi~nutn application rate 3.0 Ib a.i./A Product Label Maxitnu~n # of applicationsper year 8 HED Minimutn Application Interval 28 days HED Foliar hali-life 35 days T-REX Default Value
" Representative exposure scenariofor turf use.

### B. Avian and Mammalian Endpoints Discussion of the available endpoints and those used for determination ofrisk quotients for chlorflurenol ME are discussed extensively in Appendix D. V. Actual Terrestrial Estimated Environmental Concentrations (EECs) A summary of the predicted residues of chlorflurenol ME that may be expected to occur on selected avian or mammalian food items immediately following application for the maximum foliar spray application scenario are presented in Table C5.



### Table C5. 

### Upper-bound and mean terrestrialEECs estimated

### forthe maximum chlorflurenol

### ME spray application scenario using Kenagavalues. a Forage Type Upper-bound Residues Mean Residues (PP~) (PP~) short grass 1671.50 591.99 tall grass 766.10 250.72 broadleaf plants and small insects 940.22 313.41 fruitsipodsllargeinsects 104.22 48.75 '' EEC equivalent dose = Upper-bound Kenaga value * (%BW consu1nd100).%BW consumed = 114%. 65%, and 29% for small, medium. and large birds, respectively. V1. References Dunning, J.B. 1984. Body weights of 686 species ofNorth American birds. Western Bird Banding Assoc. Monograph No. 1. Fletcher, J.S., J.E.Nellesson and T. G.Pfleeger. 1994. Literature review and evaluation of the EPA food-chain (Kenaga) nomogram, an instrument for estimating pesticide residues onplants. Environ. Tox. And Chem. 13(9):1383-1391. Hoerger, 

### F. and E.E. Kenaga. 1972. Pesticide residues onplants: correlation of representative data as a basis for estimation oftheir magnitude in the environment. IN: 

### F. Coulston and 

### F. Corte, eds., Environmental Quality and Safety: Chemistry, Toxicology and Technology. Vol 1. George Theiine Publishers, Stuttgart, Germany. pp. 9-28. Mineau, P., B.T. Collins, A. Baril. 1996. On the use of scaling factors to improve interspecies extrapolation to acute toxicity in birds. Reg. Toxicol. Pharmacol. 24:24-29. Urban, D. J. 2000. Guidance for Conducting Screening Level Avian Risk Assessments for Spray Applications of Pesticides. OPPIEFED, USEPA. July 7, 2000. U.S. EPA. 1992. Comparative analysis of acute avian risk from granular pesticides. Office of Pesticide Programs. U.S. EPA. March 1992. USEPA. 1993. Wildlife Exposure Factors Handbook. Volume 

### I of 11. EPA/600/R-931187a. Office of Research and Development, Washngton, D. C. 20460.

### USEPA. 1995.Great Lakes Water Quality Technical Support Document for Wildlife Criteria. Office of Water, Washington D.C. Document Number EPA-820-B095-009. Willis and McDowell. 1987.Pesticide persistence on foliage. Environ. Contam. Toxicol. 100:23- 73.

### APPENDIX D. Ecological Effects Data I. Overview Thetoxicity testing required does not test all species of birds, fish, mammals, invertebrates, and plants. Typically, only two surrogate species for birds (bobwhite quail (Colinus virginianus) and mallard ducks (Anusplafyrhynclzos)) are used to represent all bird species (over 900 inthe U.S.), three species of freshwater fish (rainbow trout (Salrno gairdnevi), bluegill sunfish (Lepomis muci.oc/tii-us),and fathead minnow (Pimephalespromelas)) are used to represent all freshwater fish species (over 900 in the U.S.), and one estuarinelmarine fish species (sheepshead minnow (Cypi-inodonvariegutus)) is used to represent all estuarinelmarine fish (over 300 in the U.S.). The surrogate species for terrestrial invertebrates is the honey bee (Apis mellifera), for freshwater invertebrates the surrogate species isusually the waterflea (Daphnia magna), and for estuarinelmarine invertebrates the surrogate species are mysid shnmp (Mysidopsis bahia) and eastern oyster (Crassostt-eavirginica). These four species are used to represent all invertebrate species (over 10,000 in the U.S.). For plants, there are typically ten surrogate species used for all terrestrial plants and five surrogate species used for all aquaticplants. There are over 20,000 plant species in the U.S. which includes flowering plants, conifers, ferns, mosses, liverworts, hornworts and lichens with over 27,000 species of algae worldwide. The surrogate species testing scheme used in this assessment assumes that a chemicals mechanism of action and toxicity found for avian species is similar to that in all reptiles (over 300 species in the U.S.). The same assumption applies to amphibians (over 200 species in the U.S.) and fish; the tadpole stage of amphibians is assumed to have the same sensitivity as a fish. Therefore, the results from toxicity tests on surrogate species are considered applicable to other member species within their class and are extrapolated to reptiles and amphibians. The U.S. species numbers noted in this section were taken from: http://www.natureserve.orglsummary (Natureserve: An online encyclopedia of life [web application] 2000) and the worldwide species number fro111Ecological Planning and Toxicology, Inc. 1996. 11. Toxicity to Terrestrial Animals 

### In general, categories of acute toxicity for avian species canbe classified according to the toxicity reference value (LCSo) given by a study (EPA, 2001):

Similarly, categories of acute toxicity for avian and mammalian species can be classified according to the toxicity reference value (LD50) given by a study (EPA, 2001): 

# - LC50 (PP~)

<50 50-500 501--1000 1001-5000 >5000 

# I LD, (mg a.i./kg) 

# I Toxicity Category 

# I Toxicity Category Very highly toxic Highly toxic Moderately toxic Slightly toxic Practically nontoxica. Birds, Acute and Subacute <I0 10-50 5 1-500 50 1-2000 >2000

An acute oral toxicity study using the technical grade of the active ingredient (TGAI) is required to establish the toxicity of chlorflurenol ME to birds. The preferred test species is either mallard duck (Anasplutyrl~.ynchos; a waterfowl) or bobwhite quail (Colinus virginiunus; an upland gamebird). Results of an acute oral exposure study in bobwhite quail (MRID 43595401; Acceptable) are detailed below in Table D-1. Birds were dosed with 10,000mg a.i./kg bodyweight by oral gavage in corn oil. Onebird died and upon necropsy revealed the presence of a yellow creamy substance resembling the sample in the crop. Other necropsy results are listed in the table below. Results show that the LDsofor chlorflurenol ME is >10,000 nlg a.i./kg body weight; therefore, chlorflurenol 

### ME is categorized as practically nontoxic to avian species on an acute oral basis. EFED will use the acute oral LDso of >10,000 mg a.i./kgbody weight to evaluate acute dose-based risk to avian species. The guideline requirement [$71-11is fulfilled. 1 Very highly toxic Highly toxic Moderately toxic Slightly toxic Practically nontoxic

Two subacute dietary studies using the TGAI are required to establish the toxicity of chlorflurenol 

### ME to birds. Thepreferred test species are mallard duck (Anusplatyrhynchos) (Guideline $71-2(b), Acute Avian Diet, Duck) and northern bobwhite quail (Colinus virginiunus) (Guideline $71-2(a), Acute Avian Diet, Quail). Results of subacute dietary studies are tabulated below in Table D-2. 

### In both studies (mallard ducks MRID 43623602; Acceptable and bobwhite quail MRID 43623601; Acceptable) chlorflurenol ME was administered in the diet in at concentrations of 3 12, 625, 1250,2500, and 5000 ppm a.i. In both species, the acute dietary value was >5,000 mg a.i./kg diet, indicating that chlorflurenol 

### ME is practically nontoxic on an acute dietary basis. In both studies, no mortality was observed in any ofthe test groups and no clinical signs of toxicity were noted. Also, no gross pathology was noted in any of the birds that were subjected to gross pathological exam. EFED will use the LCso value of >5,000 mg a.i./kg diet to assess the risk of acute dietary exposure of birds to chlorflurenol ME. The guideline [$72- 11 is fulfilled. 

### Table Dl. 

### Acute oral toxicity ofchlorflurenol

### ME to birds. Species

Bobwhite Quail (Collntr~ l'~t~lt11flt11c~) Test Substance

(purity) TGAl (96% a.i ) Toxicity Category Practically ~~~~~~i~ Effects LDjo>I0,000 mg a.i /kg body weight 1 mortality Necropsies revealed pale livers, enlarged spleen, part~al loss of plumage, dry scaly skin texture Identification Number (Author, Year) 43595401 (Estop and Teske 1969) Study Classification Acceptableb. Birds, Chronic 

### Table D2. Acute dietary toxicity ofchlorflurenol 

### ME to birds.

Avian reproduction studies using the TGAI are required for chlorflurenol 

### ME because birds may be subject to continuous exposure to the pesticide, especially preceding or during the breeding season. The preferred test species are bobwhite quail (Colinus virginianus; an upland gamebird) and ~nallard duck (Anasplatyrhynchos; a waterfowl). No studies were submittedto the 

### USEPA; therefore this guideline requirement has not been filled. Species

Mallard Duck 04rius plirtyrl~yticho r)

Bobwhite Quall (Colrnrlc i.~rgltiiori~~c)



### c. Mammals, Acute and Chronic Wild mammal testing is required on a case-by-case basis, depending on the results of lower tier laboratory mammalian studies, intended use pattern and pertinent environmental fate characteristics. In most cases, rat or mouse toxicity values obtained from the Agency's Health Effects Division (HED) substitute for wild mammal testing. These toxicity values are reported below in Table D3. Test Substance

(purity) TGAl (98.77% a.i.)

TGAI (98 77% a I.)

In an acute study (MRID 43355402) chlorflurenol ME was adninistered in corn oil to laboratory rats by gavage at a dose of 5,000 mglkg of bodyweight. All the rats survived and gained weight. Eight of the ten rats exhibited hunched posture, lethargy, piloerection, soft feces, diarrhea, andlor ano-genital staining. Gross necropsy findings at terminal sacrifice were generally unremarkable. The LDjofor chlorflurenol ME is >5,000 mg a.i./kgbody weight; therefore, chlorflurenol 

### ME is categorized aspractically nontoxic to mammalian species on an acute oral basis. EFED will use the acute oral LDjoof >5,000 mg a.i.1kgbody weight to evaluate acute dose-based risk to mammalian species. In a chronic toxicity study (MRID 00082863) chlorflurenol 

### ME technical was administered to 4 Beagle dogs/sex/group in the diet at dose levels of 0, 300, 1000 or 3000 ppm ( for malelfemale, equivalent to 010, 8.7/8.8,30.6129.9 or 94.0194.4 mglkg bwlday, calculated from test material consumption) for 104weeks. Body weight appeared to be slightly reduced by month 13 at the highest dose tested [HDT]. Dogs showed this body weight decrement at month 13 when compared with initial body weights for males [the HDT gained 0% vs. 22.3% for control weight] and for females [the HDT gained 6.6% Effects LCso 5,000 mg a.i./kg diet No lnortality was observed. No gross pathology was noted in any b~rds LCso> 5,000 mg a.i.ikg diet No mortality was observed. No gross pathology was noted in any b~rds. Identification Number (Author, Year) 43623602 (Pedersen and Solatycki 1995)

43623601 (Pedersen and Solatycki 1995) Toxicity Category Practically Nontoxic

Practically Nontoxic Study Classification Acceptable

Acceptablevs. 20.3% for control body weight]. Male body weight gain appeared to be reduced for the remainder of the study. Male body weight gain was decreased at 104 weeks [body weight gain was 0.8 kg at the HDT and 2.5 kg for controls]. At the end ofthe study female body weight gain was the same as control weight gain. Food consumption was unaffected in both sexes. Erythrocytes [ERY],hemoglobin concentration [Hb] and hematocrit [Ht] values appeared to be slightly decreased at the HDT in males and females starting at week 4 [the first time period evaluated] and male dogs maintained a decreasethrough out the study. The ERY, Hb and

Ht values [difference between measured values and week -2 values] appeared to decrease in males and fernales at the HDT starting at week 4 and male dogs maintained the decrease through out the study. This decrease is consistent with the slightly higher incidence andlor severity of siderous in the spleen, liver and Kupffer cells at the HDT. Hemosiderin in the 1000ppm group was not considered sufficiently consistent to show that the mid dose group was affected. In addition the values for ERY, Hb and Ht from the 1000ppm group of animals did not show consistent effects. From week 26-52 to termination, the values for ERY, Hb and Ht for treated female dogs did not appear to differ from control. The NOAEL was 30.6129.9mglkglday for maleslfemales. The LOAEL was 94.0194.4 mglkglday for malelfemales based on decreased erythrocytes, hemoglobin and hematocrit by week 4 in males and females, supported by hemosiderin deposits in liver and increased incidence of gastritis and possible decreased body weight in males and females by month 13of the study, but not in females by study termination at 24 months. In a developmental toxicity study (MRID 45 190901)with chlorfurenol-methyl ester was administered to 31pregnant female, Crl:CD(SD):BR strain of SpragueDawley ratslgroup by gavage at dose levels of 0,250,750 or 1000mg a.i./kgbwlday from days 6 through 15 of gestation. Doses were administered in 1%carboxymethyl cellulose/water in a volume of 5 mLlkgIday. Maternal toxicity was evaluated and fetal evaluations were conducted on one-half of the fetuses viscerally or skeletally. Maternal toxicity was seen as a statistically significant decrement in body weight gain during gestational days 6 to 16at 750 and 1000mglkgtday, and at 1000mglkgiday during gestational days 6-9. Supporting this body weight decrement was nominally decreased food efficiency at 750 and 1000 mglkg bwlday. The maternal NOAEL was 250 mglkg bwlday. Thematernal LOAEL is 750 mgikg bw/day based on body weight gain decrement and nominally decreased food efficiency. Delayed ossification was seen in skull bones of fetuses. The incidence of incompletely ossified nasal bones and frontal bone was increased at 750 and 1000 mglkg bwlday (60.9-63.0% vs. 28.6% in control and 55.6%-60.9% vs. 33.3% in control, respectively). Intrauterine death was borderline statistically significant [p = 0.05291at 1000mglkg bw/day [1.7 vs. 0.3 in control]. The post-implantation loss and early resorptions, which were nominally increased at 1000 mglkglday, supported the intrauterine death at 1000 mglkg bw/day. The developmental NOAEL is 250 tnglkg bwlday. The developmental LOAEL is 750 mglkg bwlday, based on treatmentrelated delayed ossification in skull bones [nasal and frontal] in fetuses and litters.



### Table D3. 

### Toxicity of chlorflurenol

### ME to mammals. SpeciesITest Type Test Substance (purity) Toxicity Value and Affected Endpoints Identification Number (Author,Year) Study Classificationd. Terrestrial Insects and Mites: Acute Contact and Foliar Residue Studies 

### Table D3. SpecieslTest Type Laboratory Rat Acute

Dolnestlc Dog Chron~c

7Laboratory Rat

Develop~nental

A honey bee acute contact study using the TGAI is required for chlorflurenol ME because its outdoor treatment use may result in honey bee exposure. The acute contact 

### LD50, using thehoney bee,Apis mellifei-a,is an acute contact, single-dose laboratory study designed to estimate the quantity oftoxicant required to cause 

### 50% mortality in a test population of bees. The 

### TGAI is administered by one of two methods: whole body exposure to technical pesticide in a nontoxic dust diluent or topical exposure to technical pesticide via micro-applicator. The median lethal dose 

### (LDSo) is expressed in micrograms of active ingredient per bee (pg a.i./bee). The following toxicity category descriptions were developed by Atkins (1981)and have been used by EFED to characterize honey bee acute contact toxicity values (EPA, 2004): 

### Toxicity of Test Substance (purity) TGAl(98.77%)

TGAI (96%)

TGAI (99.1%) 

### chlorflurenol 

### ME to mammals. Toxicity Value and Affected Endpoints LDjo> 5000 mglkg Reversible hunched posture, lethargy and diarrhea was seen In 8/10 rats. NOAEL = 30.6129.9 mglkglday for maleslfemales. LOAEL = 94.0194.4 mglkglday for maleifemales based on decreased erythrocytes, hemoglobin and hematocrit by week 4 in males and females, supported by hemosiderin deposits in llver and incidence of gastritis and possible decreased body weight in males and femalesby month 13 of the study, but not in females by study termination at 24 months. Transient alkaline phos. and elevated SGPT was seen at the HDT. Maternal: NOAEL = 250 mglkglday LOAEL = 750 mglkglday based on statistically significant and treatment related reduced body weight gain during the treatment period, GD 6- 16. Devel: NOAEL = 250 mgikglday LOAEL = 750 mglkglday based on treatment-related increase in incompletely ossified anterior skull bones [nasal and frontal bones about doubled that of controls]. In addition a cleft palate was seen in each of two litters and one diaphragmatic hernia at 1000 mglkglday and one cleft palate at 750 mglkglday [cleft palate is rare In rats, historical incidence not given]. Identification Number (Author,Year) 43355402 (Wnorowski, 1994) 00082863 (Frohberg, H.; Metallinos, A,; Pies, H.; et al. ,975)

45 190901 (Muller, W. 2000) Study Classification Acceptable

Acceptable

AcceptableNo acute toxicity data are available to quantitatively assess risk of chlorflurenol ME exposure to terrestrial invertebrates. LD50 ( pg a.i./bee) <2 2-< 1 1 >I I

e. Terrestrial Insects: Chronic Studies Toxicity Category Highly toxic Moderately toxic Practically nontoxic

No chronic toxicity data are available to quantitatively assess risk of chlorflurenol 

### ME exposure to terrestrial invertebrates. 111. Toxicity to Freshwater Aquatic Animals
a. Freshwater Fish, Acute Two freshwater fish toxicity studies using the TGAI are required to establish the acute toxicity of chlorflurenol 

### ME to fish. The preferred test species are bluegill sunfish (a warmwater fish) and rainbow trout (a coldwater fish). In general, categories of acute toxicity for aquatic organisms can be classified according to the toxicity reference value (LC5()) given by a study (EPA 2001):

Currently, there are no adequate acute freshwater fish data available for chlorflurenol 

### ME. Therefore, the guideline (572-1) is not fulfilled. LC,, (PP~) <0. 1 0.1-1 >I-10 >lo-100

> 100

>

b. Freshwater Fish, Chronic Toxicity Category Very highly toxic Highly toxic Moderately toxic Slightly toxic Practically nontoxic

A freshwater fish early life-stage test using the TGAI is required for chlorflurenol 

### ME because the end-use product may be transported to the aquatic environment from the intended site use via drift or runoff events. Currently, there are no adequate chronic freshwater fish data available for chlorflurenol 

### ME. Therefore, the guideline ($72-4a) is not fulfilled.
c. Freshwater Invertebrates, Acute A freshwater aquatic invertebrate toxicity test using the TGAI is required to establish the toxicity of chlorflurenol 

### ME to aquatic invertebrates. Thepreferred test species is Daphnia 

### magna. Currently, there are no adequate acute freshwater invertebrate data available for chlorflurenol ME. Therefore, the guideline ($72-2)is not fulfilled.

### d. Freshwater Invertebrate, Chronic A freshwater aquatic invertebrate life-cycletest using the TGAI is required for chlorflurenol ME because the end-use product may be transported to this environment from the intended siteuse via drift or runoff events. Currently, there are no adequate chronic freshwater invertebrate data available for chlorflurenol ME. Therefore,the guideline ($72-4b) is not fulfilled. 

### IV. Toxicity to Estuarine and Marine Animals
a. Estuarine and 

### Marine Fish, Acute Acute toxicity testing with estuarinelmarine fish using the TGAI is required for chlorflurenol ME because the end-use product may reach the estuarinelmarine environment based on its use in coastal states. The preferred test species is sheepshead minnow (Cyprinodon variegatus). Currently, there are no adequate acute estuarinelrnarine fish data available for chlorflurenol ME. Therefore, the guideline ($72-3d) is not fulfilled. 

### b. Estuarine and Marine Fish, Chronic An estuarineimarine fish early life-stage toxicity test using the TGAI is required for chlorflurenol ME because the end-use product may be transported to this environment from the intended site use via drift or runoff events. The preferred test species is sheepshead minnow (Cyprinodon variegatus). Currently, there are no adequate chronic estuarinelmarine fish data available for chlorflurenol ME. Therefore, the guideline ($72-4a) is not fulfilled. 

### c. Estuarine and Marine Invertebrate, Acute An estuarineimarine invertebrate acute toxicity test using the TGAI is required for chlorflurenol 

### ME because the end-use product may be transported to this environment from the intended site use via drift or runoff events. Currently, there are no adequate acute estuarinelmarine invertebrate data available for chlorflurenol ME. Therefore,the guideline ($72-4a) is not fulfilled. 

### d. Estuarine and Marine Invertebrate, Chronic An estuarinelmarine invertebrate chronic test using the TGAI is required for chlorflurenol ME because the end-use product may be transported to the aquatic environment from the intended site use via drift or runoff events. Currently, there are no adequate chronic estuarinelmarine invertebrate data available for chlorflurenol 

### ME. Therefore, the guideline ($72-4b) is not fulfilled. VI. 

### Toxicity to Aquatic and Terrestrial Plants
a. Aquatic Plants Aquatic plant testing is required for any pesticide that has outdoor non-residential terrestrial uses and that may move off-site by runoff orby drift from aerial applications or ground spray. Testing on a vascular plant, Duck weed (Lemna gibba), and the nonvascular Pseudokirchneriellasuhcapitutu, Anabaena,flos-aquae, Navicula pelliculosa and Skeletonema costatum are required for Tier 11. Currently, there are no adequate data available for chlorflurenol 

### ME. Therefore, the guideline 

### (5123-2) is not fulfilled. 

### b. Terrestrial Plants Tier I1 terrestrial plant tests (seedling gemination/seedling emergence and vegetative vigor) evaluating the effects of the maximum exposure level of the typical end-use product are required for all herbicides with outdoor uses and unknown phytotoxicity. For seedling emergence and vegetative vigor testing, the following plant species and groups should be tested: (1) six species of at least four dicotyledonous families, one species of which is soybean (Glycine max) and the second crop is a root crop; and (2) four species of at least two monocotyledonous families, one of which is corn (Zeu mays). Currently, there are no adequate data available for chlorflurenol 

### ME. Therefore, the guideline 

### (5123-1) is not fulfilled.

### APPENDIX 

### E. The Risk Quotient Method and Levels of Concern The risks to terrestrial and aquatic organisms are determined based on a method by which risk quotients (RQs) are compared with levels of concern (LOCs). This method provides an indication of a chemical's potential to cause an effect in the field from effects observed in laboratoly studies, when the chemical is used as directed. Risk quotients are expressed as the ratio of the estimated environmental concentration (EEC) to the species-specific toxicity reference value (TRV): 

### EEC RQ= - 

### TRV Units for EEC and TRV should be the same (e.g., pg/L or ppb). The RQ is compared to the LOC as part of a risk characterization. Acute and chronic LOCs for terrestrial and aquatic organisms are given in recent Agency guidance (EPA, 2004) and summarized in Table E-1 below.

Acute Riska Acute Restricted Usee Acute Endangered speciesf Chronic Risk

Acutc Risk Acute Restricted Use Acute Endangered Species Chronic Risk

Acute Risk Acutc Endangered Species Mammals and Birds EEC~ILC~~ or LDjo/sqftC or ~~~~ida~~ EEC/LCSo or LDjo/sqft or LDSOiday (or LD,, <SO mgikg) EECiLCsoor LDjoisqft or LDjo/day EECiNOAEC Aquatic Animals EECVLCjoor ECjo EEC/LCjoor ECjo EEC/LCjoor ECjo EECINOAEC Terrestrial and Semi-aquatic Plants EEC/EC2j EEC/ECojor NOAEC

### Table 

### El. Level of concern (LOC)

### by risk presumption category 

### (EPA, 2004). Risk Presumption RQ LOC Aquatic Plants Acute Risk EEC~IEC~~ 1 Acutc Endangered Species EECVECo or NOAEC 1 potential for acute toxicity for receptor species if RQ -, LOC (EPA,2004). "~stimated environtnental concentration (ppm) on avian/tnamtnalian food items '~n~/fi' ''mg oftoxicant consumed per day 'Potential for acute toxicity for receptor species, even considering restricted use classification, if RQ > LOC (EPA,2004) 'Potential for acute toxicity for endangered species of receptor species if RQ > LOC (EPA, 2004). 'EEC = ppb or pptn in water "EEC = Ibs a.i./A EECs used to assess acute and chronic risk to avian and mammalian species to chlorflurenol 

### ME were calculated using the model T-REX. Currently the Agency does not perform assessments for chronic risk to plants or acutelchronic risks to non-target terrestrial invertebrates. TheAgency has developed an Endangered Species Protection Program to identify pesticides whose use may cause adverse impacts on endangered and threatened species, and to implement mitigation measures that will eliminate the adverse impacts. At present, the program is being implemented on an interim basis as described in a Federal Register notice (54 FR 27984-28008, July 3, 1989),and isproviding information to pesticide users to help them protect these species on a voluntary basis. As currentlyplanned, the final program will call for label modifications referring to required limitations on pesticide uses, typically as depicted in county-specific bulletins or by other site-specific mechanisms as specified by statepartners. A final program, which may be altered from the interim program, will be described in 

### a future Federal Register notice. The Agency is not imposing label modifications at this time. Rather, any requirements for product use modifications will occur in the future under the Endangered Species Protection Program. Limitations in the use of chlorflurenol 

### ME may be required to protect endangered and threatened species, but these limitations have not been defined and may be formulation specific. The Agency will notify the registrants if any label modifications are necessary. Such modifications would most likely consist of the generic label statement referring pesticide users to use limitations contained in county Bulletins. Literature Cited U.S. EPA. 1989. U.S. Environmental Protection Agency. Endangered Species Program. Washington, DC. Federal Register: 27984-28008, July 

### 3. U.S. EPA. 2004. U.S. Environmental Protection Agency. Overview of the Ecological Risk Assessment Process in the Office of Pesticide Programs, U.S. Environmental Protection Agency: Endangered and Threatened Species Effects Determinations. Office of Prevention, Pesticide, and Toxic Substances. January 23.

### APPENDIX F: Detailed Risk Quotients This appendix presents detailed risk quotient (RQ) calculations for birds and mammals. Exposure for terrestrial animals was estimated using EECs generated by the model T-REX. Toxicity values used to derive RQs were evaluated and taken from both registrant-submitted and open-literature studies. Risk quotient values that exceed LOCs are discussed in the Risk Characterization section of the main report. Table F1. Dose- and Dietary-based ChronicRQs for MammalsExposed to Chlorfluenol ME Based on Upper Bound Residues as Calculatedby T-REX. Crop Use (Application Rate) Body Weight (g)

Dose-based Chronic Mammalian RQs a Mammalian Risk Quotients

Turf (30 Ib a I A)

I Seeds

15 3 5 1,000 Fruits/Pods/ Large Insects Short Grass

Dietarv-based Chronic Mammalian RQs 2.90 

### ' 2.48 

### ' 1.33 

### '

Turf (3.0 Ib a.i./A) Tall Grass Broadleaf PlantsfSmall Insects

1.33 

### ' 1.14 

### ' 0.61

0.33 Chron~c dose-based RQ = EECINOAEL, where EEC values areupper bound res~dues expressed as equ~valent dose (mg a I /kgbody we~ght) gcne~ated from T-REX and the tox~c~ty value IS the chronic dose-based NOAEL = 250 mg a I ikgiday In the rat I' Ch~on~c d~etary-based RQ = EECMOAEC, where EEC values aleuppel bound res~dues expressed as d~etaly concentratlons (mg a.1/kg dlet)genetated from T-REX and the tox~c~ty value 1sthe chron~c d~eta~y-based NOAEC = 5000 mg a I /kg d~et In rats (converted from the rat o~al dose study) 'RQ5 are above the LOC for chron~c nsk (LOC 1)

Table F2. Dose- and Dietary-based ChronicRQs for Mammals Exposed to ChlorflurenolMEBased on Mean Residues as Calculated by T-REX. 

# - 1.63 1.39 

### ' 0.75

0.15

Crop Use (Application Rate) 0.18 0.15 0.08

0.19

Body Weight (g) 0.04 0.03 0.02

Dose-based Chronic Mammalian RQs a 0.02

Mammalian Risk Quotients

Turf (3 O Ib a i /A) NA

Short Grass

15 3 5 1,000 Tall Grass

Dietarv-based Chronic Mammalian RQs 1.02 

### ' 0.88 0.46
Turf(3.0 Ib a i /A) Broadleaf PlantslSmall Insects

0.43 0 37 0.20

" Ch~on~c dose-based RQ = EECINOAEL, where EEC values are mean res~dues expressed as equ~valent dose (mg a I /kg body welght) genelated t~om T-REX and the tox~c~ty value ISthe chron~c dose-based NOAEL =250 mg a I kgtday In the rat I' Chron~c d~etary-based RQ = EECINOAEC, where EEC values are mean ~es~dues expressed as d~etary concentratlons (mga I /kg d~et) generated fromT-REX and the tox~c~ty value ISthe chron~c d~eta~y-based NOAEC = 5000 mg a I /kgd~et In lats (converted from the rat oral dosc ~tudy)

RQs are above the LOC fo~ chron~c nsk (LOC I) 0.123 FruitdPodsI Large Insects Seeds

0.54 0.47 0.24

0 05 0.08 0.07 0.04

0.06 0.02 0.02 0.01

0.01 NA

### APPENDIX 

### G. Summary of EndangerediThreatened Species 

## Species Occurrence in Selected States and Selected Taxa
No species were excluded All Medium Types Reported 

### Mammal, Marine mml, Bird,Amphibian, Reptile, Fish, Crustacean, Bivalve, Gastropod, Arachnid, Insect, Dicot, Monocot, Ferns, Confiycds,Lichen Alabama, Alaska, Arizona, Arkansas, California,Colorado, Connecticut, Delaware, District of Columbia, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Maine, Maryland, Massachusetts,Michigan, Minnesota, Mississippi, Missouri, Montana, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Carolina, North Dakota, Ohio, Oklahoma, Oregon, Pennsylvania, Puerto Rico, Rhode Island, South Carolina, SouthDakota, Tennessee, Texas, Utah, Vermont, Virginia, Washington, West Virginia, Wisconsin, Wyoming 

### Alabama ( 87) species 

### Alaska ( 5) species 

### Arizona ( 59) species 

### Arkansas ( 23) species 

### California ( 295) species 

### Colorado ( 26) species 

### Connecticut ( I 1) species 

### Delaware ( 8)species 

### District of Columbia( 2)species 

### Florida ( 105) species 

### Georgia ( 61) species 

### Hawaii ( 345) species 

### Idaho ( 23) species 

### lllin0is ( 26) species 

### Indiana ( 24) species 

### 10 

### wa ( 15) species 

### Kansas ( 13) species 

### Kentucky ( 49) species 

### Louisiana ( 23) species 

### Maine ( 10) species 

### Maryland ( 17) species 

### Massachusetts ( 15) species

### Michigan ( 21) species 

### Minnesota ( 12) species 

### Mississippi ( 32) species 

### Missouri ( 30) species 

### Montana ( 14) species 

### Nebraska ( I 1) species 

### Nevada ( 38) species 

### New Hampshire ( 6) species 

### New Jersey ( 12) species 

### New Mexico ( 47) species 

### New York ( 16) species 

### North Carolina ( 58) species 

### North Dakota ( 6)species 

### Ohio ( 23) species 

### Oklahoma ( 19) species 

### Oregon ( 47) species 

### Pennsylvania ( 9) species 

### Puerto Rico ( 70) species 

### Rhode Island ( 7) species 

### South Carolina ( 40) species 

### South Dakota ( 9) species 

### Tennessee ( 87) species 

### Texas ( 88) species 

### Utah ( 38) species 

### Vermont ( 5) species 

### Virginia ( 62) species 

### Washington ( 36) species 

### West Virginia ( 18) species 

### Wisconsin ( 16) species 

### Wyoming ( 10) species 

### No species were selected for exclusion. Dispersed species included in report.

## APPENDIX 

## H. Data Requirement Tables Table 

### HI. Environmental Fate Data Requirements. Date: Case No: n/a Chemical No: 098801 Data Require~nents CHLORFLURENOLME DATA REQUIREMENTS FOR THE ENVIRONMENTAL FATE AND EFFECTS DIVISION

161-1 Hydrolysis 1 6 1-2 Photolysis in Water 161-3Photolysis in Soil Metabolism Studies - Lab:

162-1 Aerobic Soil Metabolism 162-2 Anaerobic Soil Metabolism 162-3Anaerobic Aquatic ~o~n~osition'

Metabolism 

# 1 PAIRA 

### ' 158.290ENVIRONMENTAL FATE Degradation Studies - Lab:

PAIRA TGAI or PAIRA TGAI or PAIRA

TGAl or PAIRA TGAl or PAIRA TGAI or

163- 1 Leaching and adsorption/desorption

1 Use pattern2

TGAI or

Mobilitv Studies: 

### I 10

I 

# 1 1 3, 10, 11 3, 10

10

3, 10, 11 3 

# I yes

Dissipation Studies 

### - Field: 164-1 Terrestrial Field TGAI or PAIRA Bibliographic Citation

Supplemental (pH 7 was not Yes (a study should be conducted at 43496201

3, 10, 11

Yes Waived Dissipation 

## I TEP 

## 1 3,ll 

## I

Prospective Groundwater Study ' 158.440 SPAY DRIFT 20 1-1 Droplet Size Spectrum 202- 1Drift Field Evaluation Study Classification

164-3 Forestry 

## 1 TEP Additional Data Required Under FIFRA?

used)

43496202

10 Accumulation Studies:

TEP PH 7) Yes Yes

165-4 Fish Bioaccumulation 165-5 Aquatic Non-Target Organisms Yes (a study should be conducted under the controlled environment) Yes 43595403

Supplemental (one German soil was used)

3, 11 3, 11 3, 11 Unacceptable (an open study system

was used)

Yes (three additional soils should be used)

Ground Water Monitoring Studies: 166-1 Small Scale TGAI or PAIRA TEP

Reserved
Yes yes 3, 10

10 Yes No1. Composition: TGAI = Technical grade of the active ingredient; PA1 = Pure active ingredient; PARA

= Pure active ingredient, radiolabeled; TEP =Typical end-use product. 

### 2. Use Patterns: 1 = TerrestrialIFood; 2 = TerrestrialIFeed; 3 = Terrestrial Non-Food; 4 = Aquatic Food; 5 = Aquatic Non-Food (Outdoor); 6 = Aquatic Non-Food (Industrial); 7 = Aquatic Non-Food (Residential); 8 = Greenhouse Food; 9 = Greenhouse Non-Food; 10 =Forestry; 1 1 =Residential Outdoor; 12 = Indoor Food; 13 = Indoor Non-Food; 14 = Indoor Medical; 15 = Indoor Residential.
Table H2.

Guideline#

71-1

71-2

7 1-4

72-1

72-2
72-3(a)
72-3(b)
72-3(c)
72-4(a)Ecological Effects Data Requirementsfor ChlorflurenolME. Data Requirement

Avian Oral LDjo Avian Dietary LCjo Test Substance

TGAl

TGAl MRID # or Citation

43595401 43623601 43623602 Avian Reproduction

Freshwater Fish LCjo

Freshwater Invertebrate Acute LCio
EstuarineIManne Fish LC50 EstuarineIMarine

Mollusk ECSo EstuarmelMarine

Shrimp EC,o Freshwater Fish Early Life-Stage Study Classification

Acceptable Acceptable Are additional data needed for ecological risk

assessment? No

No

Yes

Yes

No

Yes

Yes

Yes

Yes

Yes No Data Submitted - Data Gap

TGAI

TEP

TGAl

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Subm~tted - Data Gap

No Data Submitted - Data Gap 1208521000471 85 140979 45137401 45242602 45242601 45 137402

90289 1 1992511 20889 120870 45137403 45242603 Invalid

Invalid

InvalidTable HZ.
Guideline#

72-4(b, 72-4(c)

72-5
123-l (a)
123-l(b)

123-2

141-1

141-2
81-1

83-1b 83-3a Ecological Effects Data Data Requirement

Aquat~c Invertebrate Life-Cycle (freshwater)

Aquatic Invertebrate L~fe-Cycle (marine) Fish Full L~fe-Cycle Seedling Emergence (Tier 11) Vegetative Vigor (T~er 11) Aquatic Plant Growth (Tier 11) Honey Bee Acute

Contact LDSo Honey Bee Res~due on Foliage Acute Oral Toxicity to Rat Dog Chronic Study Prenatal Developmental

Toxic~ty Study - Rat Requirements for Chlorflurenol ME.
Test Substance MRID # or Citation

Yes

Yes
Yes
Yes

Yes

Yes

Yes

Waived

Yes
Yes
Yes Study Classification

No Data Submitted

- Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap

No Data Submitted - Data Gap Are additional data neededfor ecological risk

assessment?

TGAI

TGAI TGAl 43355402

00082863 45190901 Acceptable Acceptable Acceptable

### APPENDIX I. Incident Reports There areno incidentsreported for chlorflurenol

### ME.