UNITED STATES 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 

Special Review 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 Chlorflurenol ME. The risk assessment has been conducted in 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, shade trees, woody shrubs and vines, and to produce planting material for pineapple production. An 

evaluation of environmental risk to aquatic and terrestrial organisms as a result of the use of 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 reduce uncertainty, the registrant is requested to 

conduct: 

1 ) 16 1 - 1 Hydrolysis 

2) 16 1-2 Aqueous photolysis 

3) 1 6 1-3 Soil photolysis 

4) 162- 1 Aerobic soil metabolism 

Text Searchable Document
5) 162-2 Anaerobic soil metabolism 

6) 162-3 Anaerobic aquatic metabolism 

7) 163- 1 Adsorption/desorption 

8) 164-1 Terrestrial field dissipation 

9) 165-4 Fish bioaccumulation 

1 0) 20 1-1 Droplet Size Spectrum 

1 1 ) 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 order to 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: 

The registrant 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. The hydrolysis 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 of the 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 studies EFED 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. 

This product is highly toxic 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 is present 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: 

Do not discharge effluent containing this product into lakes, streams, ponds, estuaries, oceans, 

or other waters unless in accordance with the requirements of a National Pollutant Discharge 

Elimination System (NPDES) permit and the permitting authority has been notified in writing 

prior to discharge. Do not discharge effluent containing this product to 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 

16 1-3 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- 1 Leaching 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 

P AIRA 

TGAI or 

PAIRA 

TGAI or 

P AIRA 

TEP 

TEP 

20 1-1 Droplet Size 

Spectrum 

202-1 Drift Field 

Evaluation 

Bibliographic 

Citation 

43496201 

TGAI or 

Yes 

Waived 

3 

10 

3, 10, 1 1 

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, 11 
I. 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 # 

7 1 - 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 

TG A1 

TEP 

TGAl 

No Data Submitted - Data Gap 

120852100047 185 

140979 

45 137401 

45242602 

4524260 1 

45 137402 

90289 

1 1992511 20889 

120870 

45 137403 

45242603 

Invalid 

Invalid 

Invalid 
Table 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 

14 1 - 1 

141-2 

81-1 

83- I b 

83-3a 

Effects Data Requirements for Chlorflurenol ME. 

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 

TG Al 

TGAI 

TGAI 

43355402 

00082863 

45 19090 1 
UNI'I'EI) STti'IES ENVIRONMEN'I'AL, PRO'TECTION AGENCY 

,+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 Chlorflurenol Methyl Ester Reregistration 

Prepared by: 

Jennifer Leyhe, M.S. 

Larry Liu, Ph.D. 

Reviewed by: 

Karen Whitby, Ph.D. 

United States Environmental Protection Agency 

Office of Pesticide Programs 

Environmental Fate and Effects Division 

Environmental Risk Branch V 

1200 Pennsylvania 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 at Risk ...................................................................................................................... 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 . Risk to 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 at Risk ............................................................................. 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 Gaps Related to Exposure 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 planting material for 

pineapples . It is formulated as an emulsifiable concentrate. which is applied as a spray; or as a 

granule. which is broadcast with a spreader . Chlorflurenol ME penetrates 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 of three components. The major component is methyl 2-chloro-9- 

hydroxyfluorene-9-carboxylate (PC code 09880 1). 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 similar to 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 synthesized in a relatively constant 

ratio. For example, the ratio among PC code 098801, PC code 098802, and PC code 098803 on 

the label EPA Reg. No. 6936 1-1 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, although many 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 

on these limited data, chlorflurenol ME 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 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 of this 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 

of biological organization. 

Acute and chronic risk to all aquatic invertebrates, fish, and terrestrial invertebrates, and 

chronic risk to birds cannot be precluded because data are not available. In addition, data 

are unavailable for aquatic and terrestrial plants; however, since chlorflurenol ME is used 

as an herbicidelplant growth regulator, risk to aquatic vascular and non-vascular plants 

and non-target terrestrial and semi-aquatic plants is expected. 

nd Estuarinelmarine Fish and 
C. 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 supplemental or 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 due to 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 species that 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, fruitslpodsllarge insects, and seeds). Chlorflurenol ME 

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 suggest that 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 maternal NOAEL was 250 mg/kg bwlday. The 

maternal LOAEL is 750 mglkg bwlday based on body weight gain decrement and nominally 

decreased food efficiency. The developmental NOAEL is 250 mglkg bwlday. 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 characterize risks 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 chlorflurenol ME 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 synopsis of 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 including pH 7 is required) 

Guideline 16 1-2 Aqueous photolysis 

Guideline 16 1-3 Soil photolysis 

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 aquatic metabolism 

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 165-4 Fish 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 denied by EPA on 3/2/05) 

2. Ecological Effects 

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: There are no avian reproduction studies available; therefore risk could 

not be assessed. 

Guideline 123-1, 123-2: Terrestrial Plant 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 chlorflurenol ME is used as an herbicide and 

growth regulator, toxicity data on non-target plants are necessary to estimate risk. 

Available literature suggests that chlorflurenol causes reproductive 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 studies in 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 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 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 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 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 

- 6 
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) 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 of Endangered 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 LDso values 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 currently registered for use on turf, fencerows, hedgerows, 

rights-of-ways, forests, industrial areas, recreational areas, and pineapples as ground or aerial 

sprays. The rates of application range from 0.25 to 3.0 lb a.i./acre with no maximum number of 

applications/season and no set interval between applications specified on the 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 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 similar to 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 synthesized in a relatively constant ratio. 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, although many 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. 

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 R 1 

0 
No 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: Chlorflurenol ME 

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 (temperature unknown): 2.5 x 10-5 torr 

Water Solubility (temperature and pH unknown): 21.8 ppm 

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 

on these limited data, chlorflurenol ME 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 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. Efforts were 

made; however, no chemicals which have similar chemical structures as chlorflurenol ME were 

found. 

Chlorflurenol ME degraded by hydrolysis with a half-life of 161.2 days and 0.2 days at pHs 6 and 

9, respectively. The most environmentally relevant pH of 7 for aquatic systems was 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 transformation product 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 completely degraded by 26 days (study termination). 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, chlorflurenol ME 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 consists of 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 of the major component (11) and the former (111) is obtained as a byproduct during the 

manufacture of the latter compound (I). This chemical readily penetrates into herbaceous plants 

(via foliage andlor roots). It 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 as a 

result of chlorflurenol ME usage. EFED could not find information on the mode of action for this 

chemical. 

4. Overview of Pesticide Usage 

There are no data on the actual usage of chlorflurenol ME. 

B. Receptors 

1. Ecological Effects 

Each assessment endpoint requires one or more measures of ecological effect, which are defined 

as changes in the attributes of an assessment endpoint itself or changes in a surrogate entity or 

attribute in response to exposure to a pesticide. Ecological measures of effect for this screeninglevel risk assessment are based on a suite of registrant-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 available for 

freshwater fish and invertebrates, estuarinelmarine fish and invertebrates, algae, and vascular 

plants. No studies on chlorflurenol ME are available for acute or chronic exposure for 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-submitted laboratory studies on chlorflurenol ME formulations are available for acute 

exposure of birds and mammals. In addition chronic studies have been submitted for mammals 

but not for birds. No toxicity studies on the effects of chlorflurenol ME on terrestrial plants or 

honeybees were submitted. Details of all registrant and open literature studies are provided in 

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

2. Ecosystems at Risk 

Ecosystems potentially at risk are expressed in terms of the selected assessment measures of 

effect. The typical assessment measures of effect for screening-level pesticide ecological risk 
assessments are reduced survival and reproductive and growth impairment for both aquatic and 

terrestrial animal species. Aquatic animal species of potential 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 as reported by HED 

(Appendix B) to estimate exposure concentrations as a result of the use of chlorflurenol ME. 

This assessment is not intended to represent a site or time-specific analysis. Likewise, the most 

sensitive toxicity endpoints are used from surrogate test species to estimate treatment-related 

direct effects on acute mortality and chronic reproductive, growth and survival assessment 

endpoints. Surrogate aquatic organisms include freshwater and saltwater fish and invertebrates. 

In the absence of toxicity data on amphibians, it is assumed that aquatic-phase amphibians are 

approximately as sensitive as fish to potential effects of a pesticide. Surrogate terrestrial animal 

species include birds and mammals. The risk assessment also assumes that reptiles and 

terrestrial-phase amphibians are approximately as sensitive to 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 from basic laboratory tests to applied 

field studies. 

For plants in terrestrial and semi-aquatic environments, the screening assessment endpoint is the 

perpetuation of populations of non-target species (crops and non-crop plant species). Endpoints 

assessed include emergence of seedlings and vegetative vigor. Although it is recognized that the 

endpoints of seedling emergence and 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 survivorship have important implications for both population rates of increase and 

habitat carrying capacity. 

The ecological relevance of selecting the above-mentioned assessment endpoints is as follows: 1) 

complete exposure pathways 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 potentially inhabit areas where pesticides are applied, or areas where runoff 

andlor spray drift may impact the sites because suitable habitat is available. 

The toxicity studies are used to evaluate the potential of chlorflurenol ME to cause adverse 

effects, to determine whether further testing is required, and to determine the need for 

precautionary label statements to minimize the potential adverse effects to non-target animals and 

plants (40 CFR $158.202,2002). A summary of the assessment endpoints and measures of effect 

selected to characterize potential ecological risks associated with exposure to chlorflurenol ME is 

provided in Table 3. 
D. Conceptual Model 

Table 3. Summary of Assessment Endpoints and Measurn of 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 chlorflurenol ME spray to the environment. The following 

risk hypothesis is presumed for this screening-level assessment: 

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. Laboratory rat acute oral LDSo. 

2b. Rat developmental NOAEL 

3a. Rainbow trout 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. Estuarineimarine fish acute: data gap 

4b. Estuarinelmarine invertebrate acute: data gap 

4c. Estuarine/marine fish chronic: data gap 

4d. Estuarinelmarine invertebrate chronic: data gap 

5a. Honeybee acute contact LDSo: data gap 

Non-target aquatic and terrestrial plants and animals may 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 of non-target terrestrial and aquatic 

animals and plants. 

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 chlorflurenol ME 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 chlorflurenol ME 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. Diagram 
Based on the preliminary iterative process of examining fate and effects data, the conceptual 

model or the risk hypothesis model for spray application to 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/exposure pathways 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) -., . ii .(Parent) ] ] (Parent + Deg) f ................................. ........ ....................... "".. ,.. ...... " . . ............................ ,. ................. 

St ressor 

Source1 

Exposure 

Media 

Chlorflurenol applied as groundlaerial spray 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 Individual Animals j 

1 population ; Reduced survival ] 

j growth I Reduced growth % .............................................. 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 of Data 

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 comparing 
measures of exposure to measures of effect. A commonly used measure of exposure is the 

estimated exposure concentration (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'able 3. The resulting RQ is then compared to a specified level of concern 

(LOC), which represents a point of departure for concern; if the 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 the policy 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 reasonable upper bound for terrestrial risk. The spatial extent is defined by the use 

area, and the areas downstream and areas potentially affected by spray drift. 

Generation of robust RQs is dependent on the quality of data from both fate and toxicological 

studies. The adequacy of the submitted data was evaluated relative to Agency guidelines. The 

following identified 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 of the fate and transport data 

requirements for chlorflurenol ME. The adequacy of the submitted data was evaluated relative to 

Agency guidelines. Data gaps identified for fate and transport include 

Guideline 16 1 - 1 Hydrolysis 

Guideline 16 1 -2 Aqueous photolysis 

Guideline 16 1-3 Soil photolysis 

Guideline 162-1 Aerobic soil metabolism 

Guideline 162-2 Anaerobic soil metabolism 

Guideline 162-3 Anaerobic aquatic metabolism 

Guideline 163-1 Adsorptioddesorption 

Guideline 164-1 Terrestrial field dissipation 

Guideline 165-4 Fish bioaccumulation 

Guideline 201 -1 Droplet Size Spectrum 

Guideline 202-1 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 

associated uncertainties: 

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 (a, b), 123-2: Terrestrial plant 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 chlorflurenol ME is used as an herbicide and 

growth regulator, toxicity data on non-target plants are necessary to estimate risk. 

Guideline 14 1-1 : 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 acute oral toxicity studies in mammals 

failed to establish definitive acute LDSo/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 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 studies EFED used these data. Therefore, the RQs may not accurately 

portray chronic risk to mammals. Risk may be under- or over-estimated. 

2. Measures to Evaluate Risk 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 

maximum proposed 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 empirically determined observations of pesticide residues on various terrestrial food items. 

The Kenaga nomogram, as modified by Fletcher et al., (Hoerger and Kenaga, 1972; Fletcher et 

al., 1994) is used to relate pesticide application rates to residues on terrestrial food items. The 

surface residue concentration (ppm) is estimated by multiplying the application rate (pounds 

active ingredient (a.i.) per acre) by a value specific to each food item. For multiple applications of 

a given use, the exposure model incorporates a first-order decay rate dependent on the foliar 

dissipation half-life of the chemical. In the absence of data, a default foliar dissipation half-life of 

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 assess risk to 

terrestrial organisms. EFED used the HED data to maintain consistency between EFED and 

HED. The conceptual approach 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)(For more 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 

representative of the most sensitive species but rather were selected based on their ability to 

thve under laboratory conditions. Measures of effect are based on deleterious changes in a 

receptor as a result of chemical exposure. Functionally, measures of effect typically used 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 assessments is due to 

- 15 
their clear relationship to 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 

relationship between these effects and higher-order processes is tenuous at best. Commonly used 

laboratory-derived toxicity values include estimates of acute mortality (e.g., LD50, LC50, or 

EC50) and estimates of 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. 

Since preliminary review of the available ecological effects data suggests that chlorflurenol ME is 

practically nontoxic to birds and mammals on an acute exposure basis, acute effects to 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 available for 

aquatic species, terrestrial plants, and insects. However, there are literature studies that show 

reproductive effects on terrestrial plants. 

A search of the open literature using EPA's Ecotoxicology database, ECOTOX, was conducted to 

identify studies to fill the data gap for acute and chronic exposure of chlorflurenol ME to aquatic 

fish and invertebrates, terrestrial invertebrates; search of the ECOTOX database did not identify 

studies to 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 1 terrestrial animal assessment, 

are intended to be generally representative of any aquatic or terrestrial ecosystem associated with 

areas where chlorflurenol ME is used. The receptors addressed by the aquatic and terrestrial risk 

assessments are summarized in 'l'able 3. For aquatic assessments, generally fish and aquatic 

invertebrates in both freshwater and estuarinelmarine environments are represented, when 

available. For terrestrial assessments, mammals are represented by three different size classes 

and five potential foraging categories (short grass, tall grass, broadleaf plantslsmall insects, 

fruitslpods/seeds/large insects, 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/large insects). For terrestrial plants, generally both dicots and monocots are 

represented. Detailed information regarding the data available for these various classes of 

aquatic and terrestrial receptors is provided in Appendix D. 

111. Analysis 

A. Use Characterization 

Chlorflurenol ME [(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, shade trees, 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 shade trees (due to lack of information, EFED is unable to convert it to lb 

ai/A), woody shrubs and vines, forest conifers and junipers, recreational areas and industrial areas 
(outdoors); and 1.0875 lb a.i./A for pineapples. The labels indicate that for optimum results, 

chlorflurenol ME can be used in conjunction with other traditional herbicides. 

B. Exposure Characterization 

1. Environmental Fate and Transport Characterization 

Environmental Persistence 

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. 

However, based on these limited data, chlorflurenol ME 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 requirements was determined to be unacceptable because 

the study was conducted outdoor. 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. 

The primary route of dissipation could not be determined. Photodegradation may 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 considered by EFED as a small-scale quasi field dissipation study), chlorflurenol ME 

degraded with a half-life of 1.3 days in a sandy loam soil from Germany. However, these 

experimental plots were outdoors under 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 because no studies were 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 chlorflurenol ME could not be evaluated because no studies were 

submitted. 

Environmental Metabolites 

The major transformation product of chlodurenol ME that was quantified was 2-chloro-9- 

fluorenone (Compound IV; fluorenone). 2-Chloro-9-hydroxyfluorene-9-carboxylic acid 

(Compound 11) was also identified as a major transformation product of hydrolysis, but was not 

quantified. 

The transformation pathway 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 exposure monitoring data. 

3. Terrestrial Exposure Assessment 

Terrestrial wildlife exposure estimates are typically calculated for birds and mammals, 

emphasizing a dietary exposure route for uptake of pesticide active ingredients. These exposures 

are considered as surrogates for terrestrial-phase amphibians as well 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 single pesticide 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 application through oral or dietary exposure to vegetative plant material or insects when 

foraging in the treated fields for nesting material or food. Therefore estimation of pesticide 

concentrations in wildlife food items focuses on quantifying possible dietary ingestion of residues 

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 application and foliar 

dissipation half-life data are required to run the model. The model provides estimates of exposure 

concentrations and 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 sources of exposure to avian, mammalian, reptilian, or 

terrestrial-phase amphibian receptors. 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 of the methodology implemented by T-REX, are presented in Appendix C (T-REX 

Model). 

For multiple applications, the EEC is determined by adding the mass on the surface immediately 

following the application to 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 values used for estimating avian and mammalian exposure risks to 

chlorflurenol ME are summarized in 'Table 4. 

Table 4. Input parameters used in T-REX v1.2.3 to determine terrestrial EECs for the maximum 

ehlorflurenol ME spray application scenario. 

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 a 
Table 4. Input parameters used in T-REX v1.2.3 to determine terrestrial EECs for the maximum 

chlorflurenol ME spray application scenario. 

Input Variable 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 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. 

In addition, 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 

rate, frequency of application, andlor number of applications are higher than the input parameters 

used for the exposure scenario that 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 (derived by HED, see 

Appendix B), to assess risk to terrestrial organisms. 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. 

By comparing estimated exposure concentrations to acute and chronic toxicity reference values, 

RQs are calculated. The EECs on food items may be compared directly with dietary toxicity data 

or converted to an oral dose, as is done for small mammals. For mammals, the residue 

concentration is converted to daily oral dose based on the fraction of body 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 of the 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 are presented in Table 5. 

For the maximum chlorflurenol ME application scenario, acute concentrations for different forage 

types ranged from 104.22 to 1671.50 ppm for upper-bound residues and 48.75 to 591.99 ppm for 

mean residues. Chlorflurenol ME concentrations were highest on the surfaces of short grass and 

lowest on the surfaces of fruits, pods, and large insects. 

Table 5. Upper-bound and mean terrestrial EECs estimated for the chlorflurenol ME spray application 

scenario using Kenaga vahes. 

Forage Type Upper-bound Residues Mean Residues 

(PPW @P@ 

short grass 1671 .SO 59 1.99 
tall grass 

broadleaf plants and small insects 

fruitsipodsilarge insects 104.22 48.75 

b. Terrestrial Exposure 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 information on terrestrial plants. 

C. Ecological Effects Characterization 

In screening-level ecological risk assessments, effects characterization describes the types of 

effects a pesticide can produce in an aquatic or terrestrial organism. This characterization is 

based on registrant-submitted studies that describe acute and chronic effects toxicity information 

for various aquatic and terrestrial animals and plants. Appendix D summarizes the results of the 

registrant-submitted toxicity studies used to characterize effects for this risk assessment. Toxicity 

testing reported in this section does not represent all species of birds, mammals, or aquatic 

organisms. Only a few surrogate species for both freshwater fish and birds are used to represent 

all freshwater fish (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 assessment assumes that avian and reptilian toxicities are similar. The same assumption 

is used for fish and aquatic amphibians. 

In general, categories of acute toxicity ranging from "practically nontoxic" to "very highly toxic" 

have been established for aquatic organisms (based on LC50 and ECso values or limit of 

solubility), mammals (based on LD50 values), avian species (based on LDso and 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. Terrestrial Effects 

The toxicity endpoints used to characterize risks of chlorflurenol ME exposure to birds and 

mammals are summarized in Table 6. Results of all studies in terrestrial organisms are 

summarized in Appendix D, Tables Dl to D3. 

, Table 6. GhloPaurenol ME Todcity Reference Values for Terr~eat Organisms. 

Speege SeSelIentifIc ToxteIty Effeets Refemnet! 

Name Rdemnce [Clmsifledltion) 
a. Terrestrial Animals 

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 laboratory rats (MRID 43355402; Acceptable) show 

that the LD50 for chlorflurenol ME is >5,000 mg a.i./kg body weight; therefore, chlorflurenol ME 

is categorized as practically nontoxic to mammalian species on an acute oral basis. EFED will 

use the acute oral LD50 of >5,000 mg a.i.1kg body 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 Sprague Dawley 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 1000 mglkg 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.1kg body weight; therefore, chlorflurenol 

ME is categorized as practically nontoxic 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 19090 1 

(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 diet 
the 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 chlorflurenol ME and the likelihood of effects on aquatic life, 

wildlife, and plants based on varying pesticide-use scenarios. The risk 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 - Integration of Exposure and Effects Data 

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 chlorflurenol ME 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-target Aquatic Animals and Plants 

a. Acute and Chronic Risk 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 Terrestrial Animals 

a. Acute Risk to Birds and Mammals 

Mammalian S~ecies 

Definitive acute dose-based RQ 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 categorized as practically non-toxic to mammals on an acute oral 

basis. 

Avian S~ecies 

Definitive acute dose- and dietary-based RQ 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./kg bodyweight 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 chronic RQs for mammals using the chronic toxicity value for the 

rat (MRID 45 190901). Dose- and dietary-based chronic RQs for mammals are summarized in 

'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-g and 35-g mammals that forage on short grass, tall grass, and 

broadleaf plantslsmall insects (RQ range = 1.14 to 2.90) and for 1000-g mammals that forage on 

short grass (RQ = 1.33). Dietary-based RQs do not exceed chronic risk (LOC 1) to mammalian 

species (RQ range = 0.02 to 0.33). These RQs were calculated using upper-bound residues. 

Table 7. Dose- and Dietary-based Chronic RQs for Mammals Exposed to Chlorflurenol ME 

Based on Umer Bound Residues as Calculated by T-REX 

Crop Use 

(Application 

Rate) 

Body 

Weight 

(g) 

Dose-based Chronic Mammalian RQs a 

Mammalian Risk Quotients 

Turf 

(3.0 lb a.i./A) 

Short 

Grass 

15 

3 5 

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 

0.6 1 

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- and Dietary-based Chronic RQs for Mammals Exposed to Chlorflurenol ME 

Based on Uauer Bound Residues as Calculated by T-REX. 

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

to birds. Risk cannot be precluded. 

Crop Use 

(Application 

Rate) 

c. Risk to Terrestrial Invertebrates 

No toxicity data are available to quantitatively assess risk of chlorflurenol ME 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 Terrestrial and Semi-Aquatic Plants 

No toxicity data are available to quantitatively assess risk of chlorflurenol ME exposure to 

terrestrial However, since chlorflurenol ME is used as an herbicide and as a growth 

regulator, risk to non-target plants may occur. 

Mammalian Risk Quotients 

B. Risk Description - Interpretation of Direct 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 contiguous United 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 

Insects 
which do not occur throughout the U.S. In addition, this does not account for chlorflurenol ME 

moving to aquatic systems via 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 chlorflurenol ME enters water systems, non-target aquatic 

organisms may be at risk. 

2. Risks to Terrestrial Organisms 

a. Acute Risk to Birds and Mammals 

Based on the submitted acute oral toxicity studies on birds and mammals, chlorflurenol ME is 

categorized as practically non-toxic to birds and mammals on an acute oral and/or dietary (birds 

only) basis (LDSo > 10000 mg 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 lowered below 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 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. 

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 chronic risk to listed and non-listed mammals. As shown in 

Table 7, some dose-based RQs for chronic risk to mammalian species are above the chronic risk 

LOC (1) for the maximum spray application scenario considered 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 = 1.33 to 2.90), tall grass (RQ range = 0.61 to 1.33), and 

broadleaf plants/small insects (RQ range = 0.75 to 1.63). The chronic LOC is not exceeded for 

mammals of any size feeding on fruits/pods/large insects (RQ range = 0.08 to 0.18) or seeds (RQ 

range = 0.02 to 0.04). Chronic dietary-based RQs do not exceed the chronic LOC 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 addition to upper-bound values were calculated (See 

Table F-5;Appendix F). Using the non-conservative mean residue values, implying that higher 

predicted residue values are expected half the time, only the RQ for 15g mammals that feed on 

short grass (RQ = 1.02) exceeds the chronic LOC. 

These 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 studies EFED used these data. 

Therefore, the RQs may not accurately portray 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 chlorflurenol ME to 

terrestrial invertebrates. Since chlorflurenol ME 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 available to characterize risks from application of 

chlorflurenol ME to terrestrial plants. However, since chlorflurenol ME is used as an herbicide 

and growth regulator, risk to terrestrial plants is assumed. 

Chlorflurenol ME has been shown to induce parthenocarpy in cucumbers (Robinson et al. 1971) 

and interrupt ovule development in muskmelons (Snyder et al. 1983). Robinson et al. (1971) 

stated that at lower concentrations (1 0 -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 chlorflurenol ME may also suffer from 

increased parthenocarpy, severely limiting their ability to reproduce. 

3. Review of Incident Data 

Incident reports submitted to EPA since approximately 1994 have 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 

- 2 6 
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 there has 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 amended by 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 similar to an effect produced by a naturally-occurring estrogen, or other such 

endocrine effects as the Administrator may designate." Following the recommendations of its 

Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC), EPA determined 

that there was scientific basis for including, as part of the program, the androgen- and thyroid 

hormone systems, in addition to the estrogen hormone system. EPA also adopted EDSTAC's 

recommendation that the Program include evaluations of potential effects in wildlife. For 

pesticide chemicals, EPA will use FIFRA, to the extent that effects in wildlife may help 

determine whether 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, screening of 

additional hormone systems may be added to the Endocrine Disruptor Screening Program 

(EDSP). When the appropriate screening and or testing protocols being considered under the 

Agency's Endocrine Disruptor Screening Program have been developed, chlorflurenol ME may 

be subjected to additional screening and or testing to better characterize effects related to 

endocrine disruption. 

Results of the submitted developmental study in mammals show exposure to chlorflurenol ME 

produces adverse effects on reproductive parameters. Observed effects in the submitted 

mammalian study include maternal 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/or testing to better characterize effects related to endocrine 

disruption. 

Chronic exposure studies on the effects of chlorflurenol have not been conducted in aquatic 

organisms or birds. Therefore, EFED must consider the 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 indirectly by 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 pesticide treatment 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 assumes that 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 distance from the treatment area. 

Section III(A) of this risk assessment presents the pesticide use sites that 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 are below the 

listed species LOCs, a "no effect" conclusion is 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 indicate no 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 assumptions lead to RQs in excess of the listed species LOCs for a 

given taxonomic group, a potential for a "may affect" conclusion exists and may be associated 

with direct effects on listed species belonging to that taxonomic group or may extend to indirect 

effects upon listed species that depend upon that taxonomic group as a resource. In such cases, 

additional information on the 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 species uses 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 screening is a listing of pesticide use sites and taxonomic 

groups for which RQ calculations reveal 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 (also used as a surrogate for 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 (freshwater and 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 Invertebrates 
Risk quotients for acute and chronic effects to freshwater and estuarinelmarine fish and 

invertebrates could not be calculated because there are no acceptable toxicity studies. 

Aquatic Plants and Algae 

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 LCs0 values. 

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 LD50 or 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 exposure via 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 LCso or LDSo has not been established for a particular taxonomic group, an individual effects 

probability is not estimated. 

Freshwater and EstuarineIMarine Fish and Invertebrates 

No toxicity data are available to quantitatively assess individual risk of chlorflurenol ME 

exposure to 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 acknowledges that pesticides have the potential to exert indirect effects upon the 

listed organisms by, for example, perturbing forage or 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 taxonomic group are used to make inferences concerning the potential 

for indirect effects upon listed species that rely upon non-listed organisms in these taxonomic 

groups as resources critical to their life cycle. Species-specific concerns for chlorflurenol ME 

indirect effects to listed organisms will require a determination of the coincidence of 

chlorflurenol ME use with locations of listed species and the biologically based resources upon 

which they depend. 

The Agency uses the dose response relationship from 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 information on 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 ascertain if a "not likely to adversely 

affect" determination can be made. The degree to whlch additional analyses are performed 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 for potential indirect effects for listed species dependant 

upon that taxa, and therefore, the more intensive the 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 chlorflurenol ME proposed usage, EFED's screening level analysis shows that there is 

a concern for indirect effects to listed species that may depend upon other taxonomic group for 

their survival (e.g., invertebrates as a food source for listed fish, etc.). Screening-level RQs 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 determine if a rationale for a "not likely to adversely 

affect" determination is possible. Using our best professional judgment, EFED concludes that 

due to the lack of toxicity data for fish, aquatic invertebrates, aquatic plants, birds (chronic), and 

terrestrial plants, risk cannot be precluded and there may be a potential concern for indirect 

effects to the following groups of organisms in the action area: 

Terrestrial plants 

Aquatic plants 

Birds 

Mammals 

Reptiles 

Aquatic Invertebrates 

Fish 
Amphibians 

Terrestrial Insects 

For listed species that may potentially be indirectly affected by 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 critical habitat 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 considerations or 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 are used 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 of the 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 are potentially impacted indirectly or critical 

habitats that is potentially impacted directly by 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, if they 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. 

monocots 
e. Co-occurrence Analysis 

The goal of the analysis for co-location is to determine whether sites of pesticide use are 

geographically associated with known locations of listed species. At the screening level, this 

analysis is accomplished using the LOCATES database. The database uses location information 

for listed species at the county level and compares it to agricultural census data for crop 

production at the same county level of resolution. The product is a listing of federally listed 

species that are located within counties known to produce the crop upon which the pesticide will 

be used. Because the Level I screening assessment 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 screening risk 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 endangeredlthreatened species 

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 15 mg 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 LOCATES run 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 federally listed birds, fish, mammals, 

amphibians, crustaceans, reptiles, arachnids, insects, plants, snails, and clams to the chlorflurenol 

ME use sites. This requirement may be satisfied in one of three ways: 1) having membership in 

the FIFRA Endangered Species Task 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 information will be 

used by the OPP Endangered Species Protection Program to develop recommendations to avoid 

adverse effects to listed species. 

C. Description of Assumptions, Limitations, Uncertainties, Strengths and 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 considered in 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 uncertainty in the aquatic and terrestrial risk assessments. There 

are no valid toxicity data for any aquatic species, birds (chronic only), terrestrial invertebrates, 

and plants. The toxicity assessment for terrestrial animals is limited by the number of species 

tested in the available toxicity studies. Use of toxicity 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 

The registrant 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 16 1-1 : 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. The 

hydrolysis 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 * 1 OC. 

This study was determined to be unacceptable. The aerobic soil metabolism data requirements 

have not been fulfilled. A new study using 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 specify that four different soil types should be used. This study 
was 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 available to support the terrestrial exposure assessment for chlorflurenol ME is 

substantially incomplete. Application interval, number of applications per year, and a foliar 

dissipation study, which are input variables for modeling of risks to birds and mammals (i.e., TREX), are lacking. The terrestrial modeling 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 of Willis and McDowell(1987), was used. 

Therefore, if these values are lower or higher terrestrial EECs may be overestimated or 

underestimated. 

a. Location of Wildlife Species 

For screening terrestrial risk assessments, a generic bird or mammal is assumed to occupy either 

the treated field or adjacent areas receiving the pesticide at a rate commensurate with the 

treatment rate on the target field. This assumption may lead to an overestimation of exposure to 

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 of pesticides consider dietary exposure 

alone, and assume that 100% of the 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 assumption of 100% diet from a treated area may be realistic 

for acute exposures, but long-term exposures modeled as single food types composed entirely of 

material from a treated field is uncertain. Other routes of exposure, not considered in this 

assessment, are discussed below. 

Incidental Soil Investion Ex~osure 

This risk assessment does not consider incidental soil ingestion. Available data suggest that up to 

15% of the diet can consist of incidentally ingested soil depending on the species and feeding 

strategy (Beyer et al. 1994). A simple first approximation of soil concentration of pesticide from 

spray application shows that ingestion of soil at an incidental rate of up to 15% of the diet would 

not increase dietary exposure. 

Inhalation Ex~osure 

The screening risk assessment does not consider inhalation exposure. Such exposure may occur 

through three potential sources: (1) spray material in droplet form at the time of application (2) 

vapor phase pesticide volatilizing from treated surfaces, and (3) airborne particulate (soil, 

vegetative material, and pesticide dusts). 
Available data suggest that inhalation exposure at 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 (particles reaching the lung) is limited to a maximum diameter of 2 to 5 

microns. Theoretically, inhalation of pesticide active ingredient in the vapor phase may be 

another source of exposure for some pesticides under some exposure situations. 

The impact from exposure to dusts contaminated with the pesticide cannot 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 consider dermal exposure, except as it is indirectly included in 

calculations of RQs based on lethal doses per unit of pesticide treated area. Dermal exposure 

may occur through three potential sources: (1) direct application of 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 pursuing modeling techniques to account for dermal exposure 

via direct application of spray and by incidental contact with vegetation. 

drink in^ Water Ex~osure 

Drinking water exposure to a pesticide active ingredient may be the result of consumption of 

surface water or consumption of the pesticide in dew or other water on the surfaces of treated 

vegetation. For pesticide active ingredients with a potential to dissolve in runoff, puddles on the 

treated field may contain the chemical. 

c. Incidental Pesticide Releases Associated with Use 

This risk assessment is based on the assumption that the entire treatment area is subject to 

chlorflurenol ME application at the rates specified on the label. In reality, there is the potential 

for uneven application of chlorflurenol ME through such plausible 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 application equipment used (e.g., 

increased application at turnabouts when using older ground application equipment). 

d. Residue Levels Selection 

As discussed earlier in the exposure section of this document, the Agency relies on the work of 

Hoerger and Kenaga (1 972) and Fletcher et al. (1 994) for setting the assumed pesticide residues 

in wildlife dietary items. The Agency believes that these residue assumptions reflect 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 estimates of exposure involve highly 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. Depending upon 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 LCs0 or 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 estimate would result in an underestimation 

of field exposure by food consumption by 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 assimilation ranges from 41 - 85% (US. Environmental 

Protection Agency, 1993). If it is assumed that laboratory chow 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, exposure may 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 or below 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 (1 983) has suggested that an upper-bound limit to this 

behavior might be the typical intake rate multiplied by 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 avoid plant 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: Terrestrial plant 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 chlorflurenol ME is used as an herbicide and 

growth regulator, toxicity data on non-target plants are necessary to 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 in birds and acute oral toxicity studies in mammals 

failed to establish definitive acute LD50/LCs0 values (i.e., the LCs0 was 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 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 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 applications per year were used as derived by HED 

(Appendix B). HED used information provided 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 Sensitivity of Effects Thresholds 

It is generally recognized that test organism age may have a significant impact on the observed 

sensitivity to a toxicant. The screening risk assessment acute toxicity data for fish are collected 

on juvenile 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 

also performed on juveniles, with mallard being 5-10 days old and quail at 10-14 days 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 Effects Data 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 to 
be reflective of or protective (more sensitive) of herpetofauna. Amphibians are characterized by 

a permeable skin. The most important route of exposure for aquatic amphibians would likely be 

the dermal route. Using freshwater fish 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 demands would likely be similar. 

For terrestrial species, however, the difference between amphibians and birds and reptiles and 

birds is quite large. Terrestrial amphibians and reptiles are both ectothermic while birds are 

endothermic; birds have a higher basal metabolic rate required to maintain constant body 

temperature. The higher metabolic demands of birds may be predispose birds to higher relative 

exposures. However, this does not address any potential differences in toxicity. To date, there 

are few controlled studies on reptile species that could be 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 assumed that the use of surrogate effects data is sufficiently 

conservative to apply the broad of species within taxonomic groups. If other species are more or 

less sensitive to chlorflurenol ME than the surrogates, risks may be under- or overestimated, 

respectively. The Agency is not limited to a base set of surrogate toxicity information in 

establishing risk assessment conclusions. The Agency also considers toxicity data on nonstandard test species when available. Further research is required to determine whether, in 

general, reptiles and terrestrial-phase amphibians are suitably represented by bird species in 

assessing risks for chlorflurenol ME. 

c. Use of the Most Sensitive Species Tested 

Although the screening risk assessment relies on a selected toxicity endpoint from the most 

sensitive species tested, it does not necessarily mean that the selected toxicity endpoints reflect 

sensitivity of the 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 relationship between the 

sensitivity of the most sensitive tested species versus wild species (including listed species) is 

unknown and a source of significant uncertainty. 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 species has historically been driven by availability and ease of 

maintenance. A widespread comparison of species is 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 Chronic LOCs 

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 doselresponse relationship 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. Predictions based on low probability events are by 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 species within a taxon. Calculating the 

probability of individual effects at the lower and upper bounds of the slope is designed to address 
this source of uncertainty but the extent to which this captures the variability within a taxon is 

unknown. In some cases, a probit dose-response relationship cannot be calculated. In these 

instances, event probabilities are calculated based on a default slope assumption of 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 

study performed by CELAMERCK. Gmbh & Co. KG, Rhein, Germany, 

compiled and submitted by SRS International Corporation, Washington, 

DC, an agent for Nita Industries, Inc. Study No. CFM-NITA-1611. 

MRID 43496202b Doebbler, G.F. 198 1. Soil adsorption/desorption of chlorflurenol MEmethyl ester. Unpublished study performed by Union Carbide Corporation 

Environmental Services, Tarrytown, NY; sponsored by EM Industries, 

Inc., Elrnsford, NY; and submitted by Nita Industries, Inc., (location not 

reported). Study Number CFM-NITA-1631. UCCES Project No. 1 1507- 

86. EPA Case Number 2095. Active Ingredient Number 98801. 

MRID 43496202a Schliiter, H. 198 1. Leaching of '4~-chlorflurenol ME-methyl. 

Unpublished study performed by Celamerck GmbH & Co. KG, 

IngelheirnMein, Germany and submitted by Nita Industries, Inc., 

(location not reported). Study Number CFM-NITA-163 1. CM Document 

No. 109AA-922-003. EPA Case Number 2095. Active Ingredient Number 

98801. 

MRID 43595403 Sieper, H. 1969. Aerobic soil metabolism study. Unpublished study 

performed by E. MERCK AG, Darmstadt, Germany, compiled and 

submitted by SRS International Corporation, Washington, DC, an agent for 

Nita Industries, Inc. Study No. CFM-NITA-162 1. 

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 study received Apr 25, 1978 

under 21 137-EX-3; prepared by E. Merck, West Germany, submitted by 

EM Laboratories, Inc., Elms- ford, N.Y.; CDL:097056-A) 

MRID 43355402 Wnorowski, G. 1994. Acute Oral Toxicity Limit Test: (Chlorflurenol ME 

Methyl): Lab Project Number: 3 1 70. Unpublished study prepared by 

Product Safety Labs. 16 p. 

MRID 43595401 Estop, C. and R. Teske. 1969. Acute Oral Toxicity of Chlorflurenol ME 

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 Chlorflurenol ME 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 Chlorflurenol ME Methyl in Mallard Ducklings: Lab Project Number: 

152-002-02. Unpublished study prepared by Bio-Life Associates, Inc. 46 p. 

MRID 45190901 Muller, W. 2000. Chlorflurenol ME-Methyl, Technical Oral (Gavage) 

Teratogenicity Study in the Rat: Lab Project Number: 926-460-028: 460- 

028. Unpublished study prepared by Hazleton Laboratories Deutschland 

GmbH. 222 p. 

Open Literature and Government Reports 

Beyer, W. N.; Connor, E; Gerould, S. 1994. Survey of soil ingestion by wildlife. Journal of 

Wildlife Management 58:375-382. 

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 on plants. 

Environ. Tox. And Chem. 13(9):1383-1391. 

Hoerger, F. and E.E. Kenaga. 1972. Pesticide residues on plants: correlation of representative 

data as a basis for estimation of their magnitude in 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. The relationship 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 parthenocarpy in 

the cucumber. Science 171 : 125 1-1252. 

Snyder, J. C., C. Carter, and D. E. Knavel. 1983. Chlorflurenol ME interrupts ovule 

development of muskmelon. HortScience 18:345-347. 

T-REX. 2005. Terrestrial Residue Exposure Model (T-REX), Version 1.2.3. August 8,2005. 

Environmental Fate and Effects Division, Office of Pesticide Programs, U.S. Environmental 

Protection Agency, Washington, D.C. 

U.S. EPA. 1993. U. S. Environmental Protection Agency. 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 Protection Agency, Ecological Fate and Effects Division. Draft 

Version, August 2001. 

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. 

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): The hydrolysis of non-radiolabeled chlorflurenol ME applied at a rate of 1.8 

or 18 mg a.i./L (ppm) was studied in the dark at 25OC in sterile pH 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. 1 1 1.1 % of the applied 

at time 0, to ca. 55.6% at 4.5 hours (0.19 days; study termination); applied at a rate of 1.8 ppm, 

chlorflurenol ME decreased from ca. 116.7% of the applied at time 0, to ca. 41.7% at 7 hours 

(0.2 9 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-carboxylic acid 

(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 1 I I~L distilled water (equivalent to 0.52 hdcm rain) 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% of the 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% of the 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% of the 

applied radioactivity was detected in the leachate in the other three soils. 

In the aged column leaching portion of the 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 1 1.5% and 1.8% of the applied, respectively. 

Following 45 days of leaching, an average of 18.0% of the 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% of the applied in the aged soil and 1.9% in the soil segments (0-20 
cm); 2-chloro-9-fluorene totaled 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 if the German soil used was comparable to soils 

found in a typical chlorflurenol ME 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 Products in 

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"d application 

Apply anytime weeds actively 

3.0 lb ailacre 

1.0 lb 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: 

for plant 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. 

(RE1 48 hours) 

A 2"d application 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"d application 

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. The results 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 as the batch code models FATE and TERREEC that calculate 

terrestrial exposure concentration estimates on plant surfaces following pesticide application. 

However, T-REX performs 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: The type of use (e.g., turf, residential, crop, foliar, right-of-way, etc.) 

applicable, also provide crop name. 

Product name and form: The name of the 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, if the 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 100 in the % A.I. cell above; otherwise, enter your application rate 

in lbs formulatiodA here 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 available magnitude of residue (1 71-4), 

the reduction of residue (1 71 -5) and the foliar dissipation (132-1) 

studies submitted by the registrant to HED for determining 
pesticide 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 evaluate the effect of 

alternative assumptions of residue half life assumption on the 

outcome of the terrestrial wildlife risk assessment and include 

this evaluation in the discussion of risk assessment uncertainties. 

Application interval*^: The minimutn interval (days) between multiple applications (if any). 

Note: This version of the 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 explore possible mitigation effort effects on risk 

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 species be 

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 of the 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. See the 

progratn author for assistance if needed. 

1. Avian Endpoints 

The following avian toxicity endpoints may be entered into T-REX : 

LDSU LDso for 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 LDSOshould be calculated for all species and 

the lowest value should be used. 

The risk assessor should note that this version of the model assumes a set body weight for tested 

bobwhite quail (1 78 g) and mallard duck (1 580 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 alternate body 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 of the 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 express the endpoint BOTH as NOAEC 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 of these values should be used over the 

estimated values calculated by 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. 

The risk 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 extrapolating test 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 (1 993) 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 as presented by Hoerger and Kenaga 

(1 972) and modified by Fletcher et al. (1 994). These concentrations are determined using 

nomograms that relate application rate of a pesticide to residues remaining on dietary items of 

terrestrial organisms. The results of the 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 are to be 

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 the 
estimated 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 of Dietary Concentrations on Selected Food 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 of the 365 days is returned as the EEC used 

to estimate potential risk to birds and mammals as described 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, 1 10 for 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 of the chemical still present on the surfaces on the 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. 

The use of the 35-day half-life is based on the highest reported value (36.9 days), 

as reported 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 so that 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 (1 14% of its 

body weight), a 100-gram bird would consume 65 grams of food daily (65% of its body weight 

daily), and 1000-gram bird 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 100 mgtkg-diet (ppm) x 1.14 kg dietlkg bw (1 14%) would 

result in an equivalent dose-based EEC of 1 14 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 consumed for 3 weight classes of mammals. 

T-REX calculates food intake based 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. Calculating Adjusted 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 of the 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 

Percent Body Weight Consumed (day 

-1) a 

95 121 

66 / 15 

1513 
estimation. 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; 1580g mallard; 

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 of risk quotients are calculated by T-REX based on the 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 estimated to be on 

selected food items. These risk 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 incorporate the 

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. Pesticide Application 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 or Dietary 

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 scenario that 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) 1 adjusted LD,, 

(mgikg-bw) 

Kenaga EEC (mgkg-food item) 1 LC5, (mglkg-diet) 

EEC (mglkg-food item) 1 NOAEC (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 applications per year 8 HED 

Minimutn Application Interval 28 days HED 

Foliar hali-life 35 days T-REX Default Value 

" Representative exposure scenario for turf use. 
B. Avian and Mammalian Endpoints 

Discussion of the available endpoints and those used for determination of risk 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 terrestrial EECs estimated for the maximum 

chlorflurenol ME spray application scenario using Kenaga values. 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 

fruitsipodsllarge insects 104.22 48.75 

'' EEC equivalent dose = Upper-bound Kenaga value * (%BW consu1nd100). %BW consumed = 1 14%. 65%, and 29% for small, medium. 

and large birds, respectively. 

V1. References 

Dunning, J.B. 1984. Body weights of 686 species of North 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 on plants. 

Environ. Tox. And Chem. 13(9):1383-1391. 

Hoerger, F. and E.E. Kenaga. 1972. Pesticide residues on plants: correlation of representative 

data as a basis for estimation of their 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 

The toxicity 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 in the U.S.), 

three species of freshwater fish (rainbow trout (Salrno gairdnevi), bluegill sunfish (Lepomis 

muci.oc/tii-us), and fathead minnow (Pimephales promelas)) are used to represent all freshwater 

fish species (over 900 in the U.S.), and one estuarinelmarine fish species (sheepshead minnow 

(Cypi-inodon variegutus)) 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 is usually the waterflea (Daphnia magna), and for 

estuarinelmarine invertebrates the surrogate species are mysid shnmp (Mysidopsis bahia) and 

eastern oyster (Crassostt-ea virginica). 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 aquatic plants. 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 fro111 Ecological Planning and Toxicology, Inc. 1996. 

11. Toxicity to Terrestrial Animals 

In general, categories of acute toxicity for avian species can be 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 

100 1-5000 

>5000 

I LD, (mg a.i./kg) I Toxicity Category I 

Toxicity Category 

Very highly toxic 

Highly toxic 

Moderately toxic 

Slightly toxic 

Practically nontoxic 
a. Birds, Acute and Subacute 

<I0 

1 0-50 

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 (Anas plutyrl~.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 10,000 mg a.i./kg 

bodyweight by oral gavage in corn oil. One bird 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 LDso for 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./kg body weight to 

evaluate acute dose-based risk to avian species. The guideline requirement [$71-11 is 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. The preferred test species are mallard duck (Anus platyrhynchos) 

(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 of the 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 of chlorflurenol ME to birds. 

Species 

Bobwhite 

Quail (Collntr~ 

l'~t~lt11flt11c~) 

Test 

Substance 

(purity) 

TGAl (96% 

a.i ) 

Toxicity 

Category 

Practically 

~~~~~~i~ 

Effects 

LDjo >I 0,000 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 

Acceptable 
b. Birds, Chronic 

Table D2. Acute dietary toxicity of chlorflurenol 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 (Anas platyrhynchos; a waterfowl). No studies were submitted to the USEPA; 

therefore this guideline requirement has not been filled. 

Species 

Mallard Duck 

04 rius 

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 LDjo for chlorflurenol ME is >5,000 mg a.i./kg body weight; therefore, chlorflurenol ME is 

categorized as practically nontoxic to mammalian species on an acute oral basis. EFED will use 

the acute oral LDjo of >5,000 mg a.i.1kg body 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 104 weeks. 

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 

Acceptable 
vs. 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 of the 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 decrease through 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 1000 ppm 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 1000 ppm 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 30.6129.9 mglkglday 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 13 of the study, but not in 

females by study termination at 24 months. 

In a developmental toxicity study (MRID 45 19090 1) with chlorfurenol-methyl ester was 

administered to 3 1 pregnant female, Crl:CD(SD):BR strain of Sprague Dawley ratslgroup by 

gavage at dose levels of 0,250,750 or 1000 mg a.i./kg bwlday 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 16 at 750 and 1000 mglkgtday, and at 1000 mglkgiday 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. The maternal 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 = 0.05291 at 1000 mglkg 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 

Classification 
d. Terrestrial Insects and Mites: Acute Contact and Foliar Residue Studies 

Table D3. 

SpecieslTest Type 

Laboratory Rat 

Acute 

Dolnestlc Dog 

Chron~c 

7 

Laboratory 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 the honey 

bee, Apis mellifei-a, is an acute contact, single-dose laboratory study designed to estimate the 

quantity of toxicant 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 females by 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 

Acceptable 
No 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. The preferred 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-cycle 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 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 or by drift from aerial applications or ground spray. Testing 

on a vascular plant, Duck weed (Lemna gibba), and the nonvascular Pseudokirchneriella 
suhcapitutu, 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 

(5 123-2) 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 

(5 123-1) 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= - 

TR V 

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) 

EECiLCso or LDjoisqft or LDjo/day 

EECiNOAEC 

Aquatic Animals 

EECVLCjo or ECjo 

EEC/LCjo or ECjo 

EEC/LCjo or ECjo 

EECINOAEC 

Terrestrial and Semi-aquatic Plants 

EEC/EC2j 

EEC/ECoj or 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 of toxicant 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. 

The Agency 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 is providing information to pesticide users to help them protect these species 

on a voluntary basis. As currently planned, 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 state partners. 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 Chronic RQs for Mammals Exposed to Chlorfluenol ME Based on 

Upper Bound Residues as Calculated by T-REX. 

Crop Use 

(Application 

Rate) 

Body 

Weight (g) 

Dose-based Chronic Mammalian RQs a 

Mammalian Risk Quotients 

Turf 

(3 0 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 are upper bound res~dues expressed as equ~valent dose (mg a I /kg body 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 ale uppel bound res~dues expressed as d~etaly concentratlons (mg a.1 /kg 

dlet) genetated from T-REX and the tox~c~ty value 1s the 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 Chronic RQs for Mammals Exposed to Chlorflurenol ME Based 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) 

N A 

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 IS the 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 (mg a I /kg d~et) 

generated from T-REX and the tox~c~ty value IS the chron~c d~eta~y-based NOAEC = 5000 mg a I /kg d~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 N A 
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, 

South 

Dakota, 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 

CHLORFLURENOL ME 

DATA REQUIREMENTS FOR THE 

ENVIRONMENTAL FATE AND EFFECTS DIVISION 

161-1 Hydrolysis 

1 6 1-2 Photolysis in Water 

16 1-3 Photolysis in Soil 

Metabolism Studies - Lab: 

162-1 Aerobic Soil 

Metabolism 

162-2 Anaerobic Soil 

Metabolism 

162-3 Anaerobic Aquatic 

~o~n~osition' 

Metabolism 1 PAIRA 

' 158.290 ENVIRONMENTAL 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- 1 Drift 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 

No 
1. 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 Requirements for Chlorflurenol ME. 

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 

4524260 1 

45 137402 

90289 

1 1992511 20889 

120870 

45 137403 

45242603 

Invalid 

Invalid 

Invalid 
Table HZ. 

Guideline # 

72-4( b, 

72-4(c) 

72-5 

123- l (a) 

123-l(b) 

123-2 

141-1 

141-2 

81-1 

83-1 b 

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 needed for 

ecological risk 

assessment? 

TGAI 

TGAI 

TGAl 

43355402 

00082863 

45 190901 

Acceptable 

Acceptable 

Acceptable 
APPENDIX I. Incident Reports 

There are no incidents reported for chlorflurenol ME.