Document ID: EPA-HQ-OPP-2006-0874-0011
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-11-01T05:00Z

SEQ CHAPTER \h \r 1 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON, D.C. 20460

OFFICE OF PREVENTION, 

PESTICIDES, AND TOXIC SUBSTANCES

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

  TOC \o "1-6" \h \z \u    HYPERLINK \l "_Toc140465908"  I.	Executive
Summary	  PAGEREF _Toc140465908 \h  3  

  HYPERLINK \l "_Toc140465909"  A.	Nature of Chemical Stressor	  PAGEREF
_Toc140465909 \h  3  

  HYPERLINK \l "_Toc140465910"  B.	Potential Risks to Non-target
Organisms	  PAGEREF _Toc140465910 \h  4  

  HYPERLINK \l "_Toc140465911"  C.	Conclusions - Exposure
Characterization	  PAGEREF _Toc140465911 \h  5  

  HYPERLINK \l "_Toc140465912"  D.	Conclusions - Effects
Characterization	  PAGEREF _Toc140465912 \h  5  

  HYPERLINK \l "_Toc140465913"  E.	Data Gaps and Uncertainties	  PAGEREF
_Toc140465913 \h  5  

  HYPERLINK \l "_Toc140465914"  1.	Environmental Fate	  PAGEREF
_Toc140465914 \h  6  

  HYPERLINK \l "_Toc140465915"  2.	Ecological Effects	  PAGEREF
_Toc140465915 \h  6  

  HYPERLINK \l "_Toc140465916"  F.	Summary of Endangered Species	 
PAGEREF _Toc140465916 \h  7  

  HYPERLINK \l "_Toc140465917"  II.	Problem Formulation	  PAGEREF
_Toc140465917 \h  8  

  HYPERLINK \l "_Toc140465918"  A.	Stressor Source and Distribution	 
PAGEREF _Toc140465918 \h  8  

  HYPERLINK \l "_Toc140465919"  1.	Source and Intensity	  PAGEREF
_Toc140465919 \h  8  

  HYPERLINK \l "_Toc140465920"  2.	Physicochemical, Fate, and Transport
Properties	  PAGEREF _Toc140465920 \h  8  

  HYPERLINK \l "_Toc140465921"  3.	Pesticide Type, Class, and Mode of
Action	  PAGEREF _Toc140465921 \h  10  

  HYPERLINK \l "_Toc140465922"  4.	Overview of Pesticide Usage	  PAGEREF
_Toc140465922 \h  10  

  HYPERLINK \l "_Toc140465923"  B.	Receptors	  PAGEREF _Toc140465923 \h 
10  

  HYPERLINK \l "_Toc140465924"  1.	Ecological Effects	  PAGEREF
_Toc140465924 \h  10  

  HYPERLINK \l "_Toc140465925"  a.	Aquatic Effects	  PAGEREF
_Toc140465925 \h  10  

  HYPERLINK \l "_Toc140465926"  b.	Terrestrial Effects	  PAGEREF
_Toc140465926 \h  10  

  HYPERLINK \l "_Toc140465927"  2.	Ecosystems at Risk	  PAGEREF
_Toc140465927 \h  10  

  HYPERLINK \l "_Toc140465928"  C.	Assessment Endpoints	  PAGEREF
_Toc140465928 \h  11  

  HYPERLINK \l "_Toc140465929"  D.	Conceptual Model	  PAGEREF
_Toc140465929 \h  12  

  HYPERLINK \l "_Toc140465930"  1.	Risk Hypotheses	  PAGEREF
_Toc140465930 \h  12  

  HYPERLINK \l "_Toc140465931"  2.	Diagram	  PAGEREF _Toc140465931 \h 
12  

  HYPERLINK \l "_Toc140465932"  E.	Analysis Plan	  PAGEREF _Toc140465932
\h  13  

  HYPERLINK \l "_Toc140465933"  1.	Methods for Conducting Ecological
Risk Assessment and Identification of Data Gaps	  PAGEREF _Toc140465933
\h  13  

  HYPERLINK \l "_Toc140465934"  2.	Measures to Evaluate Risk Hypotheses
and Conceptual Model	  PAGEREF _Toc140465934 \h  15  

  HYPERLINK \l "_Toc140465935"  a.	Measures of Exposure	  PAGEREF
_Toc140465935 \h  15  

  HYPERLINK \l "_Toc140465936"  b.	Measures of Effect	  PAGEREF
_Toc140465936 \h  15  

  HYPERLINK \l "_Toc140465937"  c.	Measures of Ecosystem and Receptor
Characteristics	  PAGEREF _Toc140465937 \h  16  

  HYPERLINK \l "_Toc140465938"  III.	Analysis	  PAGEREF _Toc140465938 \h
 16  

  HYPERLINK \l "_Toc140465939"  A.	Use Characterization	  PAGEREF
_Toc140465939 \h  16  

  HYPERLINK \l "_Toc140465940"  B.	Exposure Characterization	  PAGEREF
_Toc140465940 \h  17  

  HYPERLINK \l "_Toc140465941"  1.	Environmental Fate and Transport
Characterization	  PAGEREF _Toc140465941 \h  17  

  HYPERLINK \l "_Toc140465942"  2.	Measures of Aquatic Exposure	 
PAGEREF _Toc140465942 \h  17  

  HYPERLINK \l "_Toc140465943"  a.	Aquatic Exposure Modeling	  PAGEREF
_Toc140465943 \h  18  

  HYPERLINK \l "_Toc140465944"  b.	Aquatic Exposure Monitoring (Field
Data)	  PAGEREF _Toc140465944 \h  18  

  HYPERLINK \l "_Toc140465945"  3.	Terrestrial Exposure Assessment	 
PAGEREF _Toc140465945 \h  18  

  HYPERLINK \l "_Toc140465946"  a.	Terrestrial Animal Exposure Modeling	
 PAGEREF _Toc140465946 \h  18  

  HYPERLINK \l "_Toc140465947"  b.	Terrestrial Exposure Monitoring
(Field Data)	  PAGEREF _Toc140465947 \h  20  

  HYPERLINK \l "_Toc140465948"  4.	Non-Target Plant Exposure Assessment	
 PAGEREF _Toc140465948 \h  20  

  HYPERLINK \l "_Toc140465949"  C.	Ecological Effects Characterization	 
PAGEREF _Toc140465949 \h  20  

  HYPERLINK \l "_Toc140465950"  1.	Aquatic Effects: Animals and Plants	 
PAGEREF _Toc140465950 \h  20  

  HYPERLINK \l "_Toc140465951"  2.	Terrestrial Effects	  PAGEREF
_Toc140465951 \h  20  

  HYPERLINK \l "_Toc140465952"  a.	Terrestrial Animals	  PAGEREF
_Toc140465952 \h  21  

  HYPERLINK \l "_Toc140465953"  b.	Terrestrial Plants	  PAGEREF
_Toc140465953 \h  22  

  HYPERLINK \l "_Toc140465954"  IV.	Risk Characterization	  PAGEREF
_Toc140465954 \h  22  

  HYPERLINK \l "_Toc140465955"  A.	Risk Estimation - Integration of
Exposure and Effects Data	  PAGEREF _Toc140465955 \h  22  

  HYPERLINK \l "_Toc140465956"  1.	Non-target Aquatic Animals and Plants
  PAGEREF _Toc140465956 \h  22  

  HYPERLINK \l "_Toc140465957"  a.	Acute and Chronic Risk to Animals	 
PAGEREF _Toc140465957 \h  22  

  HYPERLINK \l "_Toc140465958"  b.	Aquatic Plants	  PAGEREF
_Toc140465958 \h  22  

  HYPERLINK \l "_Toc140465959"  2.	Non-target Terrestrial Animals	 
PAGEREF _Toc140465959 \h  23  

  HYPERLINK \l "_Toc140465960"  a.	Acute Risk to Birds and Mammals	 
PAGEREF _Toc140465960 \h  23  

  HYPERLINK \l "_Toc140465961"  b.	Chronic Risk to Birds and Mammals	 
PAGEREF _Toc140465961 \h  23  

  HYPERLINK \l "_Toc140465962"  c.	Risk to Terrestrial Invertebrates	 
PAGEREF _Toc140465962 \h  24  

  HYPERLINK \l "_Toc140465963"  3.	Non-target Terrestrial and
Semi-Aquatic Plants	  PAGEREF _Toc140465963 \h  24  

  HYPERLINK \l "_Toc140465964"  B.	Risk Description - Interpretation of
Direct Effects	  PAGEREF _Toc140465964 \h  24  

  HYPERLINK \l "_Toc140465965"  1.	Risks to Aquatic Organisms	  PAGEREF
_Toc140465965 \h  24  

  HYPERLINK \l "_Toc140465966"  2.	Risks to Terrestrial Organisms	 
PAGEREF _Toc140465966 \h  25  

  HYPERLINK \l "_Toc140465967"  a.	Acute Risk to Birds and Mammals	 
PAGEREF _Toc140465967 \h  25  

  HYPERLINK \l "_Toc140465968"  b.	Chronic Risk to Birds and Mammals	 
PAGEREF _Toc140465968 \h  25  

  HYPERLINK \l "_Toc140465969"  c.	Non-target Terrestrial Invertebrates	
 PAGEREF _Toc140465969 \h  26  

  HYPERLINK \l "_Toc140465970"  d.	Terrestrial Plants	  PAGEREF
_Toc140465970 \h  26  

  HYPERLINK \l "_Toc140465971"  3.	Review of Incident Data	  PAGEREF
_Toc140465971 \h  26  

  HYPERLINK \l "_Toc140465972"  4.	Endocrine Effects	  PAGEREF
_Toc140465972 \h  27  

  HYPERLINK \l "_Toc140465973"  5.	Threatened and Endangered Species
Concerns	  PAGEREF _Toc140465973 \h  27  

  HYPERLINK \l "_Toc140465974"  a.	Action Area	  PAGEREF _Toc140465974
\h  27  

  HYPERLINK \l "_Toc140465975"  b.	Taxonomic Groups Potentially at Risk	
 PAGEREF _Toc140465975 \h  28  

  HYPERLINK \l "_Toc140465976"  i.	Discussion of Risk Quotients	 
PAGEREF _Toc140465976 \h  28  

  HYPERLINK \l "_Toc140465977"  ii.	Probit Dose Response Relationship	 
PAGEREF _Toc140465977 \h  29  

  HYPERLINK \l "_Toc140465978"  c.	Indirect Effects Analysis	  PAGEREF
_Toc140465978 \h  30  

  HYPERLINK \l "_Toc140465979"  d.	Critical Habitat	  PAGEREF
_Toc140465979 \h  31  

  HYPERLINK \l "_Toc140465980"  e.	Co-occurrence Analysis	  PAGEREF
_Toc140465980 \h  32  

  HYPERLINK \l "_Toc140465981"  C.	Description of Assumptions,
Limitations, Uncertainties, Strengths and Data Gaps	  PAGEREF
_Toc140465981 \h  33  

  HYPERLINK \l "_Toc140465982"  1.	Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps Related to Exposure For All Taxa	
 PAGEREF _Toc140465982 \h  33  

  HYPERLINK \l "_Toc140465983"  2.	Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps Related to Exposure For Aquatic
Species	  PAGEREF _Toc140465983 \h  33  

  HYPERLINK \l "_Toc140465984"  3.	Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps Related to Exposure For
Terrestrial Species	  PAGEREF _Toc140465984 \h  34  

  HYPERLINK \l "_Toc140465985"  a.	Location of Wildlife Species	 
PAGEREF _Toc140465985 \h  34  

  HYPERLINK \l "_Toc140465986"  b.	Routes of Exposure	  PAGEREF
_Toc140465986 \h  34  

  HYPERLINK \l "_Toc140465987"  c.	Incidental Pesticide Releases
Associated with Use	  PAGEREF _Toc140465987 \h  35  

  HYPERLINK \l "_Toc140465988"  d.	Residue Levels Selection	  PAGEREF
_Toc140465988 \h  35  

  HYPERLINK \l "_Toc140465989"  e.	Dietary Intake - The Differences
Between Laboratory and Field Conditions	  PAGEREF _Toc140465989 \h  36  

  HYPERLINK \l "_Toc140465990"  4.	Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps  Related to Effects Assessment	 
PAGEREF _Toc140465990 \h  36  

  HYPERLINK \l "_Toc140465991"  a.	Age Class and Sensitivity of Effects
Thresholds	  PAGEREF _Toc140465991 \h  37  

  HYPERLINK \l "_Toc140465992"  b.	Lack of Effects Data for Amphibians
and Reptiles	  PAGEREF _Toc140465992 \h  37  

  HYPERLINK \l "_Toc140465993"  c.	Use of the Most Sensitive Species
Tested	  PAGEREF _Toc140465993 \h  38  

  HYPERLINK \l "_Toc140465994"  5.	Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps Related to the Acute and Chronic
LOCs	  PAGEREF _Toc140465994 \h  38  

  HYPERLINK \l "_Toc140465995"  V.	Literature Cited	  PAGEREF
_Toc140465995 \h  39  

 

  SEQ CHAPTER \h \r 1 Executive Summary

Nature of Chemical Stressor   tc "A.  Nature of Chemical Stressor  " \l
2 

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 and/or
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 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 example, 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-carboxylate (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.

  SEQ CHAPTER \h \r 1 Potential Risks to Non-target Organisms

  SEQ CHAPTER \h \r 1 This is the Environmental Fate and Effects
Division’s (EFED) national screening-level ecological risk assessment
for the proposed re-registration of chlorflurenol ME.    HYPERLINK  \l
"Table1"  Table 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.   SEQ CHAPTER \h \r 1 
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   SEQ CHAPTER \h \r 1 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 herbicide/plant growth regulator, risk to
aquatic vascular and non-vascular plants and non-target terrestrial and
semi-aquatic plants is expected.

  SEQ CHAPTER \h \r 1 Table 1.  Summary of Environmental Risk
Conclusions for Aquatic and Terrestrial Organisms and Plants exposed to
Chlorflurenol ME.

  SEQ CHAPTER \h \r 1 Acute and Chronic Risk to Freshwater and
Estuarine/marine Fish and Invertebrates	  SEQ CHAPTER \h \r 1 Risk could
not be precluded due to lack of data.

  SEQ CHAPTER \h \r 1 Risk to Aquatic Vascular and Non-Vascular Plants	 
SEQ CHAPTER \h \r 1 Risk could not be precluded due to lack of data.

  SEQ CHAPTER \h \r 1 Acute Risk to Birds	  SEQ CHAPTER \h \r 1
Definitive acute dose-based RQ values for avian receptors could not be
derived because there are no definitive LD50 values.  

  SEQ CHAPTER \h \r 1 Chronic Risk to Birds	  SEQ CHAPTER \h \r 1 Risk
could not be precluded due to lack of data.

  SEQ CHAPTER \h \r 1 Acute Risk to Mammals	  SEQ CHAPTER \h \r 1
Definitive acute dose-based RQ values for mammalian receptors could not
be derived because there are no definitive LD50 values.  

  SEQ CHAPTER \h \r 1 Chronic Risk to Mammals	The reported RQ values are
above the chronic LOC (1.0) for species that feed on short grass, tall
grass, and broadleaf plants/small insects (RQ range = 0.02 to 2.90).

  SEQ CHAPTER \h \r 1 Terrestrial Plants	  SEQ CHAPTER \h \r 1 Risk
could not be precluded due to lack of data.

  SEQ CHAPTER \h \r 1 Non-target Invertebrates	  SEQ CHAPTER \h \r 1
Risk could not be precluded due to lack of data.

  SEQ CHAPTER \h \r 1 Conclusions - Exposure Characterization

The registrant has submitted three studies to fulfill 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.

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 plants/small insects,
fruits/pods/large 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.

  SEQ CHAPTER \h \r 1 Conclusions - Effects Characterization

  SEQ CHAPTER \h \r 1 Results of acute toxicity studies on birds suggest
that chlorflurenol ME is practically nontoxic on an acute oral basis
(LD50 >10,000 mg a.i./kg body weight) and practically nontoxic on an
acute dietary basis (LC50 >5,000 mg a.i./kg diet).  Mammalian data
suggest that chlorflurenol ME is practically nontoxic (LD50  >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 bw/day.  The maternal LOAEL is 750 mg/kg bw/day based on body
weight gain decrement and nominally decreased food efficiency.  The
developmental NOAEL is 250 mg/kg bw/day. The developmental LOAEL is 750
mg/kg bw/day, based on treatment-related delayed ossification in skull
bones (nasal and frontal) in fetuses and litters.

  SEQ CHAPTER \h \r 1 No quantitative data are available to characterize
risks from exposure of chlorflurenol ME to freshwater and
estuarine/marine 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.

Data Gaps and Uncertainties

  SEQ CHAPTER \h \r 1 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).    SEQ CHAPTER \h \r 1 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.

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 161-2 Aqueous photolysis

Guideline 161-3 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 Adsorption/desorption (the submitted study
(MRID43496202) was determined to be supplemental and the
adsorption/desorption 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 201-1 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)

Ecological Effects  tc "	1. Environmental Fate " \l 3 

  SEQ CHAPTER \h \r 1 Guidelines 72-1, 72-2, 72-3, 72-4: Acute and   SEQ
CHAPTER \h \r 1 chronic data for freshwater and estuarine/marine fish
and invertebrates are not available; therefore risk could not be
assessed.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Guideline 141-1: Honey Bee Acute Contact Toxicity;
no data are available; therefore risk could not be assessed.

  SEQ CHAPTER \h \r 1 Acute oral and dietary toxicity studies in birds
and acute oral toxicity to mammals failed to establish definitive acute
LD50/LC50 values (i.e., the LC50 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 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 crop/weed 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.

Summary of Endangered Species

  HYPERLINK  \l "Table2"  Table 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.

  

Table 2.  Listed species risks associated with direct or indirect
effects due to applications of chlorflurenol for turf use.

Listed Taxon	Direct Effects	Indirect Effects

Terrestrial and semi-aquatic plants - monocots	Yes a	Yes

Terrestrial and semi-aquatic plants – dicots	Yes a	Yes

Insects	Yes a	Yes

Birds	Acute – Yes c; Chronic –  Yes a	Yes

Terrestrial phase amphibians	Yes a	Yes

Reptiles	Acute – Yes c; Chronic –  Yes a	Yes

Mammals	Acute –  Yes c; Chronic – Yes b	Yes

Aquatic vascular plants	Yes a	Yes

Freshwater fish	Yes a	Yes

Aquatic phase amphibians	Yes a	Yes

Freshwater crustaceans	Yes a	Yes

Mollusks	Yes a	Yes

Marine/estuarine fish	Yes a	Yes

Marine/estuarine crustaceans	Yes a	Yes

a We cannot preclude risk due to lack of data.

b The reported RQ values are above the chronic LOC (1.0) for species
that feed on short grass, tall grass, and broadleaf plants/small insects
(RQ range = 0.02 to 2.90).

c RQs could potentially exceed acute listed species LOCs unless the
actual LD50 values are established in laboratory studies to be greater
than ~16,715 mg a.i./kg body weight or if the amount available in the
environment was lowered below 500 ppm

Problem Formulation

Stressor Source and Distribution

Source and Intensity  tc "1.  Source and Intensity " \l 3 

  SEQ CHAPTER \h \r 1 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.    SEQ CHAPTER \h \r 1 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.  

  SEQ CHAPTER \h \r 1 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-carboxylate (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,
10-15% methyl-2,7-dichloro-9-hydroxyfluorene-9-carboxylate and 15-20%
methyl-9-hydroxyfluorene-9-carboxylate.

	

	Methyl-2-chloro-9-hydroxyfluorene-9-carboxylate; R1 = Cl; R2 = H; R3 =
CH3.

Methyl-2,7-dichloro-9-hydroxyfluorene-9-carboxylate; R1 = R2 = Cl; R3 =
CH3.

Methyl-9-hydroxyfluorene-9-carboxylate; R1 = R2 = H; R3 = CH3.

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.:					2536-31-4

	PC Code:					098801

	Molecular Formula: 				C15H11ClO3

	Molecular Weight:				274.7 g/mol			

	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.

In laboratory mobility studies, chlorflurenol ME was highly to very
highly mobile in a sandy loam soil from Germany.

  SEQ CHAPTER \h \r 1 Pesticide Type, Class, and Mode of Action

Chlorflurenol 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 (II).  The minor components are
methyl 2,7-dichloro-9-hydroxyfluorene-9-carboxylate (III) and methyl
9-hydroxyfluorene-9-carboxylate (I).  The latter (I) is used as the
starting material for the production of the major component (II) and the
former (III) is obtained as a byproduct during the manufacture of the
latter compound (I).  This chemical readily penetrates into herbaceous
plants (via foliage and/or 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. 

  SEQ CHAPTER \h \r 1 Overview of Pesticide Usage

There are no data on the actual usage of chlorflurenol ME.    SEQ
CHAPTER \h \r 1  

Receptors

Ecological Effects  tc "1.  Ecological Effects " \l 3 

  SEQ CHAPTER \h \r 1 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 screening-level 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.  

  SEQ CHAPTER \h \r 1 Aquatic Effects

  SEQ CHAPTER \h \r 1 Toxicity data sufficient for use in a risk
assessment for chlorflurenol ME are not available for freshwater fish
and invertebrates, estuarine/marine 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.

  SEQ CHAPTER \h \r 1 Terrestrial Effects

  SEQ CHAPTER \h \r 1 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.    SEQ CHAPTER \h \r 1 No toxicity studies on
the effects of chlorflurenol ME on terrestrial plants or honeybees were
submitted.    SEQ CHAPTER \h \r 1 Details of all registrant and open
literature studies are provided in Appendix D.  Where data are lacking,
risk could not be precluded.

  SEQ CHAPTER \h \r 1 Ecosystems at Risk

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Assessment Endpoints

  SEQ CHAPTER \h \r 1 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.    SEQ CHAPTER \h \r 1 For
aquatic plants, the assessment endpoint is the maintenance and growth of
standing crop or biomass.  

  SEQ CHAPTER \h \r 1 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 and/or 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  
HYPERLINK  \l "Table3"  Table 3 .

Table 3.   SEQ CHAPTER \h \r 1 Summary of Assessment Endpoints and
Measures of Effect for Chlorflurenol ME.

Assessment Endpoint	Measure of Effect

  SEQ CHAPTER \h \r 1 1.  Abundance (i.e., survival, reproduction, and
growth) of individuals and populations of birds.	  SEQ CHAPTER \h \r 1
1a.  Bobwhite quail acute oral LD50 (guideline-recommended species).

1b.  Bobwhite quail subacute dietary LC50 (guideline-recommended
species).

1c.  Avian chronic/reproduction: data gap

  SEQ CHAPTER \h \r 1 2.  Abundance (i.e., survival, reproduction, and
growth) of individuals and populations of mammals.	  SEQ CHAPTER \h \r 1
2a.  Laboratory rat acute oral LD50.

2b.  Rat developmental NOAEL 

  SEQ CHAPTER \h \r 1 3.  Survival and reproduction of individuals and
communities of freshwater fish and invertebrates.	  SEQ CHAPTER \h \r 1
3a.  Rainbow trout and bluegill sunfish acute LC50 : data gap

3b.  Water flea acute LC50: data gap

3c.  Freshwater fish chronic: data gap

3d.  Freshwater invertebrate chronic: data gap

  SEQ CHAPTER \h \r 1 4.  Survival and reproduction of individuals and
communities of estuarine/marine fish and invertebrates.	  SEQ CHAPTER \h
\r 1 4a. Estuarine/marine fish acute: data gap

4b. Estuarine/marine invertebrate acute: data gap

4c. Estuarine/marine fish chronic: data gap

4d. Estuarine/marine invertebrate chronic: data gap

  SEQ CHAPTER \h \r 1 5.    SEQ CHAPTER \h \r 1 Survival of terrestrial
invertebrate populations (beneficial insects and earthworms).	  SEQ
CHAPTER \h \r 1 5a.   SEQ CHAPTER \h \r 1 Honeybee acute contact LD50:
data gap

  SEQ CHAPTER \h \r 1 LD50 = Lethal dose to 50% of the test population.

LC50 (EC50) = Lethal (effective) concentration to 50% of the test
population.

Conceptual Model

Risk Hypotheses  tc "1.  Risk Hypotheses " \l 3 

  SEQ CHAPTER \h \r 1 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:

  SEQ CHAPTER \h \r 1 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 unwanted
plants.  Based on available information regarding the persistence, mode
of action, direct and indirect toxicity, chlorflurenol ME may have the
potential to compromise growth, reproduction, and/or survival of
non-target terrestrial and aquatic animals and plants.

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 runoff/erosion 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.

  SEQ CHAPTER \h \r 1 Diagram

  SEQ CHAPTER \h \r 1 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   HYPERLINK  \l
"Figure1"  Figure 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.  

 

Analysis Plan

Methods for Conducting Ecological Risk Assessment and Identification of
Data Gaps

  SEQ CHAPTER \h \r 1 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 LD50 or NOAEC.  Assessment endpoints and
their respective measures of effect are listed in   HYPERLINK  \l
"Table3"  Table 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.

  SEQ CHAPTER \h \r 1 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 161-1 Hydrolysis

Guideline 161-2 Aqueous photolysis

Guideline 161-3 Soil photolysis

Guideline 162-1 Aerobic soil metabolism

Guideline 162-2 Anaerobic soil metabolism

Guideline 162-3 Anaerobic aquatic metabolism

Guideline 163-1 Adsorption/desorption

Guideline 164-1 Terrestrial field dissipation

Guideline 165-4 Fish bioaccumulation

Guideline 201-1 Droplet Size Spectrum 

Guideline 202-1 Drift Field Evaluation

  SEQ CHAPTER \h \r 1 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:

  SEQ CHAPTER \h \r 1 Guidelines 72-1, 72-2, 72-3, 72-4: Acute and   SEQ
CHAPTER \h \r 1 chronic data for freshwater and estuarine/marine fish
and invertebrates are not available; therefore risk could not be
assessed.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Guideline 141-1: Data for honey bee acute contact
toxicity are not available; therefore risk could not be assessed.

  SEQ CHAPTER \h \r 1 Acute oral and dietary toxicity studies in birds
and acute oral toxicity studies in mammals failed to establish
definitive acute LD50/LC50 values (i.e., the LD50/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.

Measures to Evaluate Risk Hypotheses and Conceptual Model

 tc "1.  Methods for Conducting Ecological Risk Assessment and
Identification of Data Gaps " \l 3 

Measures of Exposure  tc "a.  Measures of Exposure " \l 4 

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.

  SEQ CHAPTER \h \r 1 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.    SEQ CHAPTER \h \r 1 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 chlorflurenol ME turf use with the maximum
proposed application rate (3.0 lb 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).

  SEQ CHAPTER \h \r 1 Measures of Effect

  SEQ CHAPTER \h \r 1 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 thrive 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 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.   
SEQ CHAPTER \h \r 1 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.  

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 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).

  SEQ CHAPTER \h \r 1 Measures of Ecosystem and Receptor Characteristics

  SEQ CHAPTER \h \r 1 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   HYPERLINK  \l "Table3"  Table 3 .    SEQ CHAPTER \h \r 1 For
aquatic assessments, generally fish and aquatic invertebrates in both
freshwater and estuarine/marine 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 plants/small insects,
fruits/pods/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 plants/small insects, and
fruits/pods/seeds/large insects).    SEQ CHAPTER \h \r 1 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.

Analysis

  SEQ CHAPTER \h \r 1 Use Characterization

Chlorflurenol ME [(RS)-2-chloro-9-hydroxyfluorene-9-carboxylic acid
methyl ester; CF 125, 12.5% a.i.] is an herbicide/plant 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./A 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.

Exposure Characterization

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 chlorflurenol ME that was quantified
was 2-chloro-9-fluorenone (Compound IV; fluorenone). 
2-Chloro-9-hydroxyfluorene-9-carboxylic acid (Compound II) 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.  

Measures of Aquatic Exposure  tc "1.  Environmental Fate and Transport
Characterization " \l 3 

Aquatic Exposure Modeling  tc "a.  Aquatic Exposure Modeling " \l 4 

Since there are limited fate data for chlorflurenol ME no aquatic
modeling was conducted.

  SEQ CHAPTER \h \r 1 Aquatic Exposure Monitoring (Field Data)

There are no aquatic exposure monitoring data.

  SEQ CHAPTER \h \r 1 Terrestrial Exposure Assessment

  SEQ CHAPTER \h \r 1 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.  

  SEQ CHAPTER \h \r 1 Terrestrial Animal Exposure Modeling

  SEQ CHAPTER \h \r 1 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  
HYPERLINK  \l "Table4"  Table 4 .

  SEQ CHAPTER \h \r 1 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

Maximum application rate	3.0 lb a.i./A	Product Label

Likely # of applications per year	8	HED a

Likely application interval	28 days	HED a

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 crop/weed 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.

  SEQ CHAPTER \h \r 1 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 half-life, 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, and/or 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 crop/weed 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.

  SEQ CHAPTER \h \r 1 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   HYPERLINK  \l "Table5"  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.

  SEQ CHAPTER \h \r 1 Table 5.  Upper-bound and mean terrestrial EECs
estimated for the chlorflurenol ME spray application scenario using
Kenaga values.

Forage Type

	Upper-bound Residues

(ppm)	Mean Residues (ppm)

short grass	1671.50	591.99

tall grass	766.10	250.72

broadleaf plants and small insects	940.22	313.41

fruits/pods/large insects	104.22	48.75

  SEQ CHAPTER \h \r 1 Terrestrial Exposure Monitoring (Field Data)

  SEQ CHAPTER \h \r 1 No data were identified to provide information on
terrestrial monitoring.

  SEQ CHAPTER \h \r 1 Non-Target Plant Exposure Assessment

  SEQ CHAPTER \h \r 1 No toxicity data were identified to provide
information on terrestrial plants.

  SEQ CHAPTER \h \r 1 Ecological Effects Characterization

  SEQ CHAPTER \h \r 1 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.  Estuarine/marine 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.

  SEQ CHAPTER \h \r 1 In general, categories of acute toxicity ranging
from “practically nontoxic” to “very highly toxic” have been
established for aquatic organisms (based on LC50 and EC50 values or
limit of solubility), mammals (based on LD50 values), avian species
(based on LD50 and LC50 values), and non-target insects (based on LD50
values for honey bees) (U.S. EPA 2001).  These categories are presented
in Appendix D.

  SEQ CHAPTER \h \r 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.  SEQ CHAPTER \h \r 1 

  SEQ CHAPTER \h \r 1 Terrestrial Effects

  SEQ CHAPTER \h \r 1 The toxicity endpoints used to characterize risks
of chlorflurenol ME exposure to birds and mammals are summarized in  
HYPERLINK  \l "Table6"  Table 6 .  Results of all studies in terrestrial
organisms are summarized in Appendix D, Tables D1 to D3.

  SEQ CHAPTER \h \r 1 Table 6.  Chlorflurenol ME Toxicity Reference
Values for Terrestrial Organisms.

  SEQ CHAPTER \h \r 1 Exposure Scenario	  SEQ CHAPTER \h \r 1 Species	 
SEQ CHAPTER \h \r 1 Scientific Name	  SEQ CHAPTER \h \r 1 Exposure
Duration	  SEQ CHAPTER \h \r 1 Toxicity Reference Value	Effects	  SEQ
CHAPTER \h \r 1 Reference

(Classification)

  SEQ CHAPTER \h \r 1 Mammals

  SEQ CHAPTER \h \r 1 Acute	Rat	Rattus norvegicus	Acute Oral	LD50 > 5000
mg/kg body weight	

Mortality	43355402

(Acceptable)

  SEQ CHAPTER \h \r 1 Chronic	Rat	Rattus norvegicus	Days 6-15 of
gestation	Maternal NOAEL = 250 mg/kg/day	body weight gain decrement and
nominally decreased food efficiency	  SEQ CHAPTER \h \r 1 45190901

(Acceptable)

Developmental NOAEL = 250 mg/kg/day	delayed ossification in skull bones

	  SEQ CHAPTER \h \r 1 Birds

Acute   SEQ CHAPTER \h \r 1 (Dose-based)	Bobwhite Quail 	Colinus
virginianus	Single Oral Dose	LD50 >10,000 mg a.i./kg body weight	

Mortality	43595401

(Acceptable)

Acute   SEQ CHAPTER \h \r 1 (Dietary-based)	Bobwhite Quail 

Mallard Duck	Colinus virginianus

Anas Platyrhynchos	8 days	

LC50 > 5,000 mg a.i./kg diet

	Mortality	43623601

(Acceptable)

43623602

(Acceptable)

  SEQ CHAPTER \h \r 1 Chronic	Data gap

  SEQ CHAPTER \h \r 1 Plants

Acute	Data gap

  SEQ CHAPTER \h \r 1 Chronic	Data gap

  SEQ CHAPTER \h \r 1 Terrestrial Animals

Mammalian Species

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./kg body weight to
evaluate acute dose-based risk to mammalian species.

In a developmental toxicity study (MRID 45190901), chlorfurenol-methyl
ester was administered to pregnant Sprague Dawley rats by gavage.  The
maternal NOAEL was 250 mg/kg bw/day.  The maternal LOAEL is 750 mg/kg
bw/day based on body weight gain decrement and nominally decreased food
efficiency.  The developmental NOAEL is 250 mg/kg bw/day. The
developmental LOAEL is 750 mg/kg bw/day, 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 mg/kg bw/day and one cleft palate at
750 mg/kg bw/day (cleft palate is rare in rats).   

  SEQ CHAPTER \h \r 1 Avian Species

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./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 LD50 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 LC50 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 LC50 value of >5,000 mg a.i./kg diet to assess the
risk of acute dietary exposure of birds to chlorflurenol ME.

  SEQ CHAPTER \h \r 1 Non-target Insects

No data are available for non-target insects.

  SEQ CHAPTER \h \r 1 Terrestrial Plants

No data are available for terrestrial plants.

Risk Characterization

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Risk Estimation - Integration of Exposure and
Effects Data

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Non-target Aquatic Animals and Plants

  SEQ CHAPTER \h \r 1 Acute and Chronic Risk to Animals

Acute and   SEQ CHAPTER \h \r 1 chronic risk to fish and invertebrates
cannot be evaluated at this time because no toxicity data are available.
 Risk cannot be precluded.

  SEQ CHAPTER \h \r 1 Aquatic Plants

  SEQ CHAPTER \h \r 1 Risk to aquatic plants cannot be evaluated at this
time because no toxicity data are available.  Risk cannot be precluded.

  SEQ CHAPTER \h \r 1 Non-target Terrestrial Animals

  SEQ CHAPTER \h \r 1 Acute Risk to Birds and Mammals

  SEQ CHAPTER \h \r 1 Mammalian Species

  SEQ CHAPTER \h \r 1 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 LD50 was >5000 mg a.i./kg body weight).  Based on
these results, chlorflurenol ME TGAI is categorized as practically
non-toxic to mammals on an acute oral basis.   

  SEQ CHAPTER \h \r 1 Avian Species

  SEQ CHAPTER \h \r 1 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 (LD50
>10,000 mg a.i./kg bodyweight and LC50 > 5,000 mg a.i./kg diet).  

Chronic Risk to Birds and Mammals

Mammalian Species

T-REX was used to calculate chronic RQs for mammals using the chronic
toxicity value for the rat (  SEQ CHAPTER \h \r 1 MRID 45190901).    SEQ
CHAPTER \h \r 1 Dose- and dietary-based chronic RQs for mammals are
summarized in   HYPERLINK  \l "Table7"  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 plants/small insects (RQ range = 1.14 to 2.90)
and for 1000-g mammals that forage on short grass (RQ = 1.33).    SEQ
CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Table 7.  Dose- and Dietary-based Chronic RQs for
Mammals Exposed to Chlorflurenol ME Based on Upper Bound Residues as
Calculated by T-REX.

  SEQ CHAPTER \h \r 1 Crop Use

(Application Rate)	Body 

Weight (g)	Mammalian Risk Quotients

Short Grass	Tall Grass	Broadleaf Plants/Small Insects	Fruits/Pods/Large
Insects	Seeds

Dose-based Chronic Mammalian RQs  a

Turf

(3.0 lb a.i./A)	15	2.90  c	1.33 c	1.63 c	0.18	0.04

	35	2.48 c	1.14 c	1.39 c	0.15	0.03

	1,000	1.33 c	0.61	0.75	0.08	0.02

Dietary-based Chronic Mammalian RQs  b

Turf (3.0 lb a.i./A)	0.33	0.15	0.19	0.02	NA

a  Chronic dose-based RQ = EEC/NOAEL, 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.

b  Chronic dietary-based RQ = EEC/NOAEC, 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).

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

  SEQ CHAPTER \h \r 1 Avian Species

  SEQ CHAPTER \h \r 1 No toxicity data are available to quantitatively
assess chronic risk of chlorflurenol ME exposure to birds.  Risk cannot
be precluded.

Risk to Terrestrial Invertebrates

  SEQ CHAPTER \h \r 1 No toxicity data are available to quantitatively
assess risk of chlorflurenol ME exposure to terrestrial invertebrates. 
Risk cannot be precluded.

Non-target Terrestrial and Semi-Aquatic Plants

  SEQ CHAPTER \h \r 1 No toxicity data are available to quantitatively
assess risk of chlorflurenol ME exposure to terrestrial plants. 
However, since chlorflurenol ME is used as an herbicide and as a growth
regulator, risk to non-target plants may occur.

  SEQ CHAPTER \h \r 1 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 IV.C).
 In most instances RQs could not be calculated due to data gaps.

  SEQ CHAPTER \h \r 1 Risks to Aquatic Organisms

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 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.  

  SEQ CHAPTER \h \r 1 Risks to Terrestrial Organisms  

  SEQ CHAPTER \h \r 1 Acute Risk to Birds and Mammals

  SEQ CHAPTER \h \r 1 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 (LD50 > 10000 mg a.i./kg body weight for birds; LC50 > 5000
mg a.i./kg diet for birds; LD50 > 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
LD50 values are established in laboratory studies to be greater than
~16,715 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 LD50 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.

 	  SEQ CHAPTER \h \r 1 

  SEQ CHAPTER \h \r 1 Chronic Risk to Birds and Mammals

  SEQ CHAPTER \h \r 1 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.    SEQ
CHAPTER \h \r 1 As shown in   HYPERLINK  \l "Table7"  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).  

  SEQ CHAPTER \h \r 1 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.  

  SEQ CHAPTER \h \r 1 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.  While the dietary-based estimates may
suggest greater “realism,” they too suffer from some uncertainties. 
Primarily, the dietary-based 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.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Terrestrial Plants

  SEQ CHAPTER \h \r 1 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 (10 -20 ppm), parthenocarpy was induced when cucumber
plants were treated in the flowering stage; however, at a higher
concentration (40 ppm) parthenocarpy was induced two week prior to the
flowering stage.  In muskmelons, ovule development was halted when
chlorflurenol was applied 10 – 12 days before anthesis (Snyder et al.
1983).  Since parthenocarpic plants produce fruits with no seeds, sexual
reproduction cannot occur.  Nontarget plants that come in contact with
chlorflurenol ME may also suffer from increased parthenocarpy, severely
limiting their ability to reproduce. 

Review of Incident Data

  SEQ CHAPTER \h \r 1 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 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.

  SEQ CHAPTER \h \r 1 No incident reports involving aquatic or
terrestrial exposure to chlorflurenol ME have been reported.

Endocrine Effects

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 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. 
  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Chronic exposure studies on the effects of
chlorflurenol have not been conducted in aquatic organisms or birds.
Therefore, EFED must consider the possibility that chlorflurenol ME may
have detrimental effects on the endocrine system in these taxa.

Threatened and Endangered Species Concerns

Action Area  tc "a.  Action Area " \l 4 

  SEQ CHAPTER \h \r 1 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 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 subsequent 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.

  SEQ CHAPTER \h \r 1 Taxonomic Groups Potentially at Risk

  SEQ CHAPTER \h \r 1 The Level I screening assessment process for
listed species uses the generic taxonomic group-based 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

Estuarine/marine fish 

Estuarine/marine invertebrates

Terrestrial plants

Algae and aquatic plants

  SEQ CHAPTER \h \r 1 Discussion of Risk Quotients

  SEQ CHAPTER \h \r 1 Should estimated exposure levels occur in
proximity to listed resources, the available screening-level information
suggests a potential concern for direct effects to listed fish
(freshwater and estuarine/marine), aquatic invertebrate (freshwater and
estuarine/marine), 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

  SEQ CHAPTER \h \r 1 Risk quotients for acute and chronic effects to
freshwater and estuarine/marine fish and invertebrates could not be
calculated because there are no acceptable toxicity studies.

  SEQ CHAPTER \h \r 1 Aquatic Plants and Algae

  SEQ CHAPTER \h \r 1 Risk quotients for aquatic plants and algae could
not be calculated because there are no acceptable toxicity studies.

  SEQ CHAPTER \h \r 1 Birds

  SEQ CHAPTER \h \r 1 Definitive acute dose- or dietary-based RQ values
for avian receptors could not be derived because there are no definitive
LD50 or LC50 values.  

  SEQ CHAPTER \h \r 1 Risk quotients for chronic effects to birds could
not be calculated because there are no acceptable toxicity studies.

  SEQ CHAPTER \h \r 1 Mammals

Definitive acute dose- or dietary-based RQ values for mammalian
receptors could not be derived because there are no definitive LD50 or
LC50 values.  

The   SEQ CHAPTER \h \r 1 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 plants/small insects.  

  SEQ CHAPTER \h \r 1 Terrestrial Plants

  SEQ CHAPTER \h \r 1 Risk quotients for terrestrial plants could not be
calculated because there are no acceptable toxicity studies.

  SEQ CHAPTER \h \r 1 Probit Dose Response Relationship

  SEQ CHAPTER \h \r 1 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
IECv1.1.xls, developed by Ed Odenkirchen (6/22/04).  It is important to
note that the IEC model output can go as low as 1 x 10-16 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 LD50 or LC50 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).  In
instances where an LC50 or LD50 has not been established for a
particular taxonomic group, an individual effects probability is not
estimated.

  SEQ CHAPTER \h \r 1 Freshwater and Estuarine/Marine Fish and
Invertebrates

  SEQ CHAPTER \h \r 1 No toxicity data are available to quantitatively
assess individual risk of chlorflurenol ME exposure to aquatic
organisms.

  SEQ CHAPTER \h \r 1 Mammals and Birds

  SEQ CHAPTER \h \r 1 Definitive LC50/LD50s are not available to
quantitatively assess individual risk of chlorflurenol ME exposure to
terrestrial organisms.

  SEQ CHAPTER \h \r 1 Indirect Effects Analysis

  SEQ CHAPTER \h \r 1 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 which 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).

  SEQ CHAPTER \h \r 1 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, Services-provided “species profiles,” and further
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:

  SEQ CHAPTER \h \r 1 Terrestrial plants

Aquatic plants

Birds

Mammals

Reptiles  

Aquatic Invertebrates

Fish

Amphibians

Terrestrial Insects

  SEQ CHAPTER \h \r 1 For listed species that may potentially be
indirectly affected by the Federal action, see Appendix G (Locates run).

  SEQ CHAPTER \h \r 1 Critical Habitat

  SEQ CHAPTER \h \r 1 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.

  HYPERLINK  \l "Table8"  Table 8  provides a list of the taxa that may
be directly or indirectly affected.

Table 8.  Listed species risks associated with direct or indirect
effects due to applications of chlorflurenol for turf use.

Listed Taxon	Direct Effects	Indirect Effects

Terrestrial and semi-aquatic plants - monocots	Yes a	Yes

Terrestrial and semi-aquatic plants – dicots	Yes a	Yes

Insects	Yes a	Yes

Birds	Acute – Yes c; Chronic –  Yes a	Yes

Terrestrial phase amphibians	Yes a	Yes

Reptiles	Acute – Yes c; Chronic –  Yes a	Yes

Mammals	Acute –  Yes c; Chronic – Yes b	Yes

Aquatic vascular plants	Yes a	Yes

Freshwater fish	Yes a	Yes

Aquatic phase amphibians	Yes a	Yes

Freshwater crustaceans	Yes a	Yes

Mollusks	Yes a	Yes

Marine/estuarine fish	Yes a	Yes

Marine/estuarine crustaceans	Yes a	Yes

a We cannot preclude risk due to lack of data.

b The reported RQ values are above the chronic LOC (1.0) for species
that feed on short grass, tall grass, and broadleaf plants/small insects
(RQ range = 0.02 to 2.90).

c RQs could potentially exceed acute listed species LOCs unless the
actual LD50 values are established in laboratory studies to be greater
than ~16,715 mg a.i./kg body weight or if the amount available in the
environment was lowered below 500 ppm

  SEQ CHAPTER \h \r 1 Co-occurrence Analysis

  SEQ CHAPTER \h \r 1 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 endangered/threatened
species 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.  

  SEQ CHAPTER \h \r 1 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 endangered/threatened
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.

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

This risk assessment relies on best available estimates of environmental
fate and physicochemical 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.

Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related
to Exposure For All Taxa  tc "1.  Assumptions, Limitations,
Uncertainties, Strengths and Data Gaps Related to Exposure For All Taxa
" \l 3 

  SEQ CHAPTER \h \r 1 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.    SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Assumptions, Limitations, Uncertainties, Strengths
and Data 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. 

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1   SEQ CHAPTER \h \r 1 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°C.  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.  SEQ CHAPTER \h \r 1 

  SEQ CHAPTER \h \r 1 Assumptions, Limitations, Uncertainties, Strengths
and Data Gaps Related to Exposure For Terrestrial Species

  SEQ CHAPTER \h \r 1 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., T-REX), 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.

  SEQ CHAPTER \h \r 1 Location of Wildlife Species

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Routes of Exposure

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Incidental Soil Ingestion Exposure	

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Inhalation Exposure

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Dermal Exposure

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Drinking Water Exposure

  SEQ CHAPTER \h \r 1 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.   SEQ CHAPTER \h \r 1  For pesticide active
ingredients with a potential to dissolve in runoff, puddles on the
treated field may contain the chemical.

  SEQ CHAPTER \h \r 1 Incidental Pesticide Releases Associated with Use

  SEQ CHAPTER \h \r 1 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).

  SEQ CHAPTER \h \r 1 Residue Levels Selection

  SEQ CHAPTER \h \r 1 As discussed earlier in the exposure section of
this document, the Agency relies on the work of Hoerger and Kenaga
(1972) and Fletcher et al. (1994) for setting the assumed pesticide
residues in wildlife dietary items. The Agency 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.

Dietary Intake - The Differences Between Laboratory and Field Conditions

  SEQ CHAPTER \h \r 1 The acute and chronic characterization of risk
rely on comparisons of wildlife dietary residues with LC50 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% (U.S.
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 (1983) 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.

  SEQ CHAPTER \h \r 1 Assumptions, Limitations, Uncertainties, Strengths
and Data Gaps  Related to Effects Assessment

  SEQ CHAPTER \h \r 1 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:

  SEQ CHAPTER \h \r 1 Guidelines 72-1, 72-2, 72-3, 72-4: Acute and   SEQ
CHAPTER \h \r 1 chronic data for freshwater and estuarine/marine fish
and invertebrates are not available; therefore, risk could not be
assessed.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Guideline 141-1: Data for honey bee acute contact
toxicity are not available; therefore, risk could not be assessed.

  SEQ CHAPTER \h \r 1 Acute oral and dietary toxicity studies in birds
and acute oral toxicity studies in mammals failed to establish
definitive acute LD50/LC50 values (i.e., the LC50 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 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 crop/weed 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.

  SEQ CHAPTER \h \r 1 Age Class and Sensitivity of Effects Thresholds

  SEQ CHAPTER \h \r 1 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 older/adult 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.

Lack of Effects Data for Amphibians and Reptiles

  SEQ CHAPTER \h \r 1 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
non-standard 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.   

  SEQ CHAPTER \h \r 1 Use of the Most Sensitive Species Tested

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Assumptions, Limitations, Uncertainties, Strengths
and Data Gaps Related to the Acute and Chronic LOCs

  SEQ CHAPTER \h \r 1 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 dose/response 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).

Literature Cited

Environmental Fate   SEQ CHAPTER \h \r 1 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.  1981.  Soil adsorption/desorption of
chlorflurenol ME-methyl ester.  Unpublished study performed by Union
Carbide Corporation Environmental Services, Tarrytown, NY; sponsored by
EM Industries, Inc., Elmsford, NY; and submitted by Nita Industries,
Inc., (location not reported).  Study Number CFM-NITA-1631.  UCCES
Project No. 11507-86.  EPA Case Number 2095.  Active Ingredient Number
98801.

MRID 43496202a 	Schlüter, H.  1981.  Leaching of 14C-chlorflurenol
ME-methyl.  Unpublished study performed by Celamerck GmbH & Co. KG,
Ingelheim/Rhein, Germany and submitted by Nita Industries, Inc.,
(location not reported).  Study Number CFM-NITA-1631.  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-1621.

Ecological   SEQ CHAPTER \h \r 1 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 21137-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: 3170. 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.

  SEQ CHAPTER \h \r 1 Open Literature and Government Reports

  SEQ CHAPTER \h \r 1 Beyer, W. N.; Connor, E; Gerould, S. 1994. Survey
of soil ingestion by wildlife. Journal of Wildlife Management
58:375-382.

  SEQ CHAPTER \h \r 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.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 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:
1251-1252.

Snyder, J. C., C. Carter, and D. E. Knavel.  1983.  Chlorflurenol ME
interrupts ovule development of muskmelon.  HortScience 18:345-347.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 U.S. EPA.  1993.  U. S. Environmental Protection
Agency. Wildlife Exposure Factors Handbook. Volume I of II. 
EPA/600/R-93/187a. Office of Research and Development, Washington, D. C.
20460.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 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.

  SEQ CHAPTER \h \r 1 Urban, D.J. and N.J. Cook.  1986. Hazard
Evaluation Division Standard Evaluation Procedure Ecological Risk
Assessment.  EPA 540/9-85-001. U.S. Environmental Protection Agency,
Office of Pesticide Programs, Washington, DC.

  SEQ CHAPTER \h \r 1 Willis and McDowell. 1987. Pesticide persistence
on foliage. Environ. Contam. Toxicol.  100:23-73.

 PAGE   

 PAGE   3