Document ID: EPA-HQ-OPP-2006-0179-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-04-12T04:00Z

FILE
NAME:
company.
wpt
(
7/
1/
2005)
(
xml)
Template
Number
P25
ATTENTION:

All
commodity
terms
must
comply
with
the
Food
and
Feed
Commodity
Vocabulary
database
(
http://
www.
epa.
gov/
pesticides/
foodfeed/).

All
text
in
blue
font
(
instructions
for
preparing
the
document),
should
be
removed
prior
to
sending
the
document
to
the
Federal
Register
Staff.
Instructional
text
and
prompts
in
green
font
should
also
be
removed.

COMPANY
FEDERAL
REGISTER
DOCUMENT
SUBMISSION
TEMPLATE
(
1/
1/
2005)

EPA
Registration
Division
contact:
[
insert
name
and
telephone
number
with
area
code]

INSTRUCTIONS:
Please
utilize
this
outline
in
preparing
tolerance
petition
documents.
In
cases
where
the
outline
element
does
not
apply
please
insert
A
NA­
Remove
@

and
maintain
the
outline.
The
comment
notes
that
appear
on
the
left
margin
represent
hidden
typesetting
codes
designed
to
expedite
the
processing
of
the
Federal
Register
document.
Please
do
not
remove
or
alter
these
comment
notes
or
change
the
margins,
font,
or
format
in
your
document.
Simply
replace
the
instructions
that
appear
in
italics
and
brackets,
i.
e.,

A
[
insert
company
name],@
with
the
information
specific
to
your
action.

TEMPLATE:

[
Interregional
Research
Project
No.
4]

[
Insert
petition
number]

EPA
has
received
a
pesticide
petition
([
insert
petition
number])
from
[
Interregional
Research
Project
No.
4
(
IR­
4)],
[
681
U.
S.
Highway
#
1
South,
North
Brunswick,
NJ
08902­
3390]
proposing,
pursuant
to
section
408(
d)
of
the
Federal
Food,
Drug,
and
Cosmetic
Act
(
FFDCA),
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
part
180.

Options
(
pick
one)

1.
by
establishing
a
tolerance
for
residues
of
2.
to
establish
an
exemption
from
the
requirement
of
a
tolerance
for
[
tebuconazole,
2
alpha­[
2­(
4­
Chlorophenyl)
ethyl]­
alpha­(
1,1­
dimethylethyl)­
1H­
1,2,4­
triazole­
1­
ethanol]
in
or
on
the
raw
agricultural
commodity
[
asparagus]
at
[
0.02]
parts
per
million
(
ppm).
EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
[[
The
nature
of
the
residue
in
plants
and
animals
is
adequately
understood.
The
residue
of
concern
is
the
parent
compound
only,
as
specified
in
40
CFR
180.474.]

2.
Analytical
method.
[
An
enforcement
method
for
plant
commodities
has
been
validated
on
various
commodities.
It
has
undergone
successful
EPA
validation
and
has
been
submitted
for
inclusion
in
PAM
II.
The
animal
method
has
also
been
approved
as
an
adequate
enforcement
method.]

3.
Magnitude
of
residues.
[
IR­
4
received
requests
from
the
states
of
Michigan
and
Washington
for
the
use
of
Tebuconazole
on
asparagus.
To
support
this
request,
magnitude
of
residue
data
were
collected
from
California,
Michigan,
New
Jersey,
and
Washington.
In
each
trial,
3
foliar
applications
of
the
test
substance
12
to
16
days
apart
were
made
to
the
treated
plots.
The
application
rates
ranged
from
0.168
to
0.181
lb
a.
i./
A
per
application
for
a
total
rate
range
of
0.512
to
524
lb
ai/
A
per
season.
All
applications
were
made
using
appropriate
spray
equipment,
and
the
spray
volume
was
sufficient
to
provide
adequate
dispersal
of
the
test
substance.
All
applications
were
made
to
the
ferns
in
the
fall.
The
ferns
were
mowed
after
senescing
prior
to
the
emergence
of
new
spears
in
the
spring.
The
new
spears
were
harvested
in
the
spring
as
done
commercially.
Samples
were
analyzed
using
gas
chromatography.
No
detectable
residues
of
Tebuconazole
were
found
in
any
of
the
treated
or
untreated
samples
at
the
lowest
level
of
method
validation
(
0.02
ppm).
These
data
support
the
proposed
0.02
ppm
tolerance.]

B.
Toxicological
Profile
1.
Acute
toxicity.
[
Tebuconazole
exhibits
moderate
toxicity.
The
rat
acute
oral
LD50
=
3,933
milligram/
kilogram
(
mg/
kg)
(
category
III);
the
rabbit
acute
dermal
LD50
>
5,000
mg/
kg
(
category
IV);
and
the
rat
acute
inhalation
LC50
>
0.371
milligram/
Liter
(
mg/
L)
(
category
II).
3
Technical
tebuconazole
was
slightly
irritating
to
the
eye
(
category
III)
and
was
not
a
skin
irritant
(
category
IV)
in
rabbits.
Tebuconazole
was
not
a
dermal
sensitizer.]

2.
Genotoxicty.
[
An
Ames
test
with
Salmonella
sp.,
a
mouse
micronucleus
assay,
a
sister
chromatid
exchange
assay
with
Chinese
hamster
ovary
cells,
and
an
unscheduled
DNA
synthesis
assay
with
rat
hepatocytes
provided
no
evidence
of
mutagenicity.]

3.
Reproductive
and
developmental
toxicity.
[
a.
In
a
developmental
toxicity
study,
pregnant
female
rats
were
gavaged
with
technical
tebuconazole
at
levels
of
0,
30,
60,
or
120
mg/
kg/
day
between
days
6
and
15
of
gestation.
The
maternal
NOAEL
was
30
mg/
kg/
day
and
the
maternal
LOAEL
was
60
mg/
kg/
day
based
on
increased
absolute
and
relative
liver
weights.
The
developmental
NOAEL
was
30
mg/
kg/
day
and
the
developmental
LOAEL
was
60
mg/
kg/
day
based
on
delayed
ossification
of
thoracic,
cervical
and
sacral
vertebrae,
sternum
and
limbs
plus
an
increase
in
supernumerary
ribs.
b.
In
a
developmental
toxicity
study,
pregnant
female
rabbits
were
gavaged
with
technical
tebuconazole
at
levels
of
0,
10,
30,
or
100
mg/
kg/
day
between
days
6
and
18
of
gestation.
The
maternal
NOAEL
was
30
mg/
kg/
day
and
the
maternal
LOAEL
was
100
mg/
kg/
day
based
on
minimal
depression
of
body
weight
gains
and
food
consumption.
The
developmental
NOAEL
was
30
mg/
kg/
day
and
the
developmental
LOAEL
was
100
mg/
kg/
day
based
on
increased
postimplantation
losses,
malformations
in
8
fetuses
out
of
5
litters
(
including
peromelia
in
5
fetuses/
4
litters;
palatoschisis
in
1
fetus/
1
litter),
hydrocephalus
and
delayed
ossification.
c.
In
a
developmental
toxicity
study,
pregnant
female
mice
were
gavaged
with
technical
tebuconazole
at
levels
of
0,
10,
30,
or
100
mg/
kg/
day
between
days
6
and
15
of
gestation
(
part
1
of
study)
or
at
levels
of
0,
10,
20,
30,
or
100
mg/
kg/
day
between
days
6
and
15
of
gestation
(
part
2
of
study).
The
maternal
NOAEL
was
10
mg/
kg/
day
and
the
maternal
LOAEL
was
20
mg/
kg/
day.
Maternal
toxicity
(
hepatocellular
vacuolation
and
elevations
in
AST,
ALP
and
alkaline
phosphatase)
occurred
at
all
dose
levels
but
was
minimal
at
10
mg/
kg/
day.
Reduction
in
mean
corpuscular
volume
in
parallel
with
reduced
hematocrit
occurred
at
doses
greater
than
or
equal
to
20
mg/
kg/
day.
The
liver
was
the
target
organ.
The
developomental
NOAEL
was
10
mg/
kg/
day
and
the
developmental
LOAEL
was
30
mg/
kg/
day
based
on
an
increase
in
the
number
of
runts.
d.
In
a
developmental
toxicity
study,
pregnant
female
mice
were
administered
dermal
doses
of
technical
tebuconazole
applied
at
levels
of
0,
100,
300,
or
1,000
mg/
kg/
day
between
days
6
and
15
of
gestation.
Equivocal
maternal
toxicity
was
observed
1,000
mg/
kg/
day.
The
maternal
NOAEL
was
<
nearly­
eq>
1,000
mg/
kg/
day.
The
developmental
NOAEL
was
1,000
mg/
kg/
day.
e.
In
a
2­
generation
reproduction
study,
rats
were
fed
technical
tebuconazole
at
levels
of
0,
100,
300,
or
1,000
ppm,
(
0,
5,
15,
or
50
mg/
kg/
day,
males
and
females).
The
parental
maternal
NOAEL
was
15
mg/
kg/
day
and
the
parental
LOAEL
was
50
mg/
kg/
day
based
on
4
depressed
body
weights,
increased
spleen
hemosiderosis
and
decreased
liver
and
kidney
weights.
The
reproductive
NOAEL
was
15
mg/
kg/
day
and
the
reproductive
LOAEL
of
50
mg/
kg/
day
based
on
decreased
pup
body
weights
from
birth
through
3
­
4
weeks.
f.
In
a
developmental
neurotoxicity
study,
pregnant
female
rats
were
fed
a
nominal
concentration
of
0,
100,
300
or
1000
ppm
of
tebuconazole
in
the
diet.
The
NOAEL
for
maternal
toxicity
in
this
study
was
300
ppm
(
based
on
mortality,
body
weight
and
feed
consumption
reductions,
and
prolonged
gestation
in
the1000
ppm
dosage
group).
The
1000
ppm
dose
level
was
considered
to
be
excessively
toxic
for
the
F1
offspring,
based
on
mortality,
marked
reductions
in
pup
body
weight
and
body
weight
gain,
reduction
in
pup
absolute
brain
weight
(
at
postpartum
day
(
PD)
12
and
adult),
a
developmental
delay
in
vaginal
patency,
and
decreased
cerebellar
thickness.
The
effects
on
brain
weight
and
morphology
are
considered
to
represent
incomplete
compensation
for
the
marked
decrease
in
body
weight
gain
during
development.
By
approximately
day
80
postpartum,
the
body
weight
had
completely
recovered
in
the
females
but
was
still
reduced
(
89%
of
the
control
group
value)
in
the
males.
The
brain
weights
had
shown
an
incomplete
recovery
(
90%
to
93%
of
the
control
group
values)
in
both
sexes.
The
EPA
has
determined
that
the
LOAEL
for
offspring
toxicity
in
this
study
is
100
ppm..
Technical
grade
tebuconazole
did
not
cause
any
specific
neurobehavioral
effects
in
the
offspring
when
administered
to
the
dams
during
gestation
and
lactation
at
dietary
concentrations
up
to
and
including
1000
ppm.]

4.
Subchronic
toxicity.
[
a.
In
a
90­
day
oral
feeding
study,
rats
were
administered
technical
tebuconazole
at
levels
of
0,
100,
400,
or
1,600
ppm
(
0,
8,
34.8,
or
171.7
mg/
kg/
day
for
males
or
0,
10.8,
46.5,
or
235.2
mg/
kg/
day
for
females).
In
males,
the
no
observed
adverse
effect
level
(
NOAEL)
was
34.8
mg/
kg/
day
and
the
lowest
observed
adverse
effect
level
(
LOAEL)
was
171.7
mg/
kg/
day
based
on
decreased
body
weight
and
decreased
body
weight
gain,
adrenal
vacuolation
and
spleen
hemosiderosis.
In
females,
the
NOAEL
was
10.8
mg/
kg/
day
and
the
LOAEL
of
46.5
mg/
kg/
day
was
based
on
adrenal
vacuolation.
b.
In
a
90­
day
oral
feeding
study,
Beagle
dogs
were
administered
technical
tebuconazole
at
levels
of
0,
200,
1,000,
or
5,000
ppm
(
0,
74,
368,
or
1,749
mg/
kg/
day
for
males
or
0,
73,
352,
or
1,725
mg/
kg/
day
for
females).
In
females,
the
NOAEL
was
73
mg/
kg/
day
and
the
LOAEL
was
352
mg/
kg/
day
based
on
decreased
body
weight
and
decreased
body
weight
gain,
decreased
food
consumption
and
increased
liver
N­
demethylase
activity.
At
the
highest
dose
tested
(
HDT),
lens
opacity
was
seen
in
all
males
and
in
one
female
and
cataracts
were
seen
in
three
females.
c.
In
a
21­
day
dermal
toxicity
study,
rabbits
were
exposed
dermally
to
technical
tebuconazole
5
days
a
week
at
doses
of
0,
50,
250,
or
1,000
mg/
kg/
day.
No
significant
systemic
effects
were
seen.
The
systemic
NOAEL
>
1,000
mg/
kg/
day.
d.
In
a
21­
day
inhalation
toxicity
study,
rats
were
exposed
to
technical
tebuconazole
(
15
exposures
­
6
hours/
day
for
3
weeks)
at
airborne
concentrations
of
0,
0.0012,
0.0106,
or
0.1558
mg/
L/
day.
The
NOAEL
was
0.0106
mg/
L/
day
and
the
LOAEL
was
0.1558
mg/
L/
day
based
on
piloerection
and
induction
of
liver
N­
demethylase.]
5
5.
Chronic
toxicity.
[
a.
In
a
2­
year
combined
chronic
feeding/
carcinogenicity
study,
rats
were
administered
technical
tebuconazole
at
levels
of
0,
100,
300,
or
1,000
ppm
(
0,
5.3,
15.9,
or
55
mg/
kg/
day
for
males
or
0,
7.4,
22.8,
or
86.3
mg/
kg/
day
for
females).
In
males,
the
NOAEL
was
5.3
mg/
kg/
day
and
the
LOAEL
was
15.9
mg/
kg/
day
based
on
C­
cell
hyperplasia
in
the
thyroid
gland.
In
females,
the
NOAEL
was
7.4
mg/
kg/
day
and
the
LOAEL
was
22.8
mg/
kg/
day
based
on
body
weight
depression,
decreased
hemoglobin,
hematocrit,
mean
corpuscular
volume
and
mean
corpuscular
hemoglobin
concentration
and
increased
liver
microsomal
enzymes.
No
evidence
of
carcinogenicity
was
found
at
the
levels
tested.
b.
In
a
1­
year
chronic
feeding
study,
Beagle
dogs
were
administered
technical
tebuconazole
at
levels
of
0,
40,
200,
or
1,000
(
weeks
1­
39)
and
2,000
ppm
(
weeks
40­
52)
(
0,
1,
5
or
25/
50
mg/
kg/
day
for
males
and
females).
The
NOAEL
was
1
mg/
kg/
day
and
the
LOAEL
was
5
mg/
kg/
day
based
on
ocular
lesions
(
lenticular
and
corneal
opacity)
and
hepatic
toxicity
(
changes
in
the
appearance
of
the
liver
and
increased
siderosis).
c.
In
a
1­
year
chronic
feeding
study,
Beagle
dogs
were
administered
technical
tebuconazole
at
levels
of
0,
100,
or
150
ppm
(
0,
3.0,
or
4.4
mg/
kg/
day
for
males
or
0,
3.0
or
4.5
mg/
kg/
day
for
females).
The
NOAEL
was
3.0
mg/
kg/
day
and
the
LOAEL
was
4.4
mg/
kg/
day
based
on
adrenal
affects
in
both
sexes.
In
males
there
was
hypertrophy
of
adrenal
zona
fasciculata
cells
amounting
to
4/
4
at
150
ppm
and
to
0/
4
at
100
ppm
and
in
controls.
Other
adrenal
findings
in
males
included
fatty
changes
in
the
zona
glomerulosa
(
3/
4)
and
lipid
hyperplasia
in
the
cortex
(
2/
4)
at
150
ppm
vs.
(
1/
4)
for
both
effects
at
100
ppm
and
control
dogs.
In
females
there
was
hypertrophy
of
zona
fasciculata
cells
of
the
adrenal
amounting
to
4/
4
at
150
ppm
and
to
0/
4
at
100
ppm
and
1/
4
in
controls.
Fatty
changes
in
the
zona
glomerulosa
of
the
female
adrenal
amounted
to
2/
4
at
150
ppm
and
to
1/
4
at
100
ppm
and
in
controls.
d.
In
a
91­
week
carcinogenicity
study,
mice
were
administered
technical
tebuconazole
at
levels
of
0,
500,
or
1,500
ppm
(
0,
84.9,
or
279
mg/
kg/
day
for
males
or
0,
103.1,
or
365.5
mg/
kg/
day
for
females).
Neoplastic
histopathology
consisted
of
statistically
significant
increased
incidences
of
hepatocellular
neoplasms;
adenomas
(
35.4%)
and
carcinomas
(
20.8%)
at
1,500
ppm
in
males
and
carcinomas
(
26.1%)
at
1,500
ppm
in
females.
Statistically
significant
decreased
body
weights
and
increased
food
consumption
were
reported
that
were
consistent
with
decreased
food
efficiency
at
500
and
1,500
ppm
in
males
and
at
1,500
ppm
in
females.
Clinical
chemistry
values
(
dose­
dependent
increases
in
plasma
GOT,
GPT
and
Alkaline
Phosphatase)
for
both
sexes
were
consistent
with
hepatotoxic
effects
at
both
500
and
1,500
ppm.
Relative
liver
weight
increases
reached
statistical
significance
at
both
500
and
1,500
ppm
in
males
and
at
1,500
ppm
in
females.
Non­
neoplastic
histopathology
included
dose­
dependent
increases
in
hepatic
pancinar
fine
fatty
vacuolation,
statistically
significant
at
500
and
1,500
ppm
in
males
and
at
1,500
ppm
in
females.
Other
histopathology
included
significant
oval
cell
proliferation
in
both
sexes
and
dose­
dependent
ovarian
atrophy
that
was
statistically
significant
at
500
and
1,500
ppm.
The
Maximum
Tolerated
Dose
(
MTD)
was
achieved
at
or
around
500
ppm.]
6
6.
Animal
metabolism.
[
Rats
were
gavaged
with
1
or
20
mg/
kg
radio­
labeled
technical
tebuconazole.
98.1
%
of
the
oral
dose
was
absorbed.
Within
72
hours
of
dosing,
over
87%
of
the
dose
was
excreted
in
urine
and
feces.
At
sacrifice
(
72
hours
post
dosing),
total
residue
(­
GI
tract)
amounted
to
0.63%
of
the
dose.
A
total
of
10
compounds
were
identified
in
the
excreta.
A
large
fraction
of
the
identified
metabolites
corresponded
to
successive
oxidations
steps
of
a
methyl
group
of
the
test
material.
At
20
mg/
kg,
changes
in
detoxication
patterns
may
be
occurring.]

7.
Metabolite
toxicology.
[
NA­
Remove]

8.
Endocrine
disruption.
[
No
special
studies
investigating
potential
estrogenic
or
endocrine
effects
of
tebuconazole
have
been
conducted.
However,
the
standard
battery
of
required
studies
has
been
completed.
These
studies
include
an
evaluation
of
the
potential
effects
on
reproduction
and
development,
and
an
evaluation
of
the
pathology
of
the
endocrine
organs
following
repeated
or
long­
term
exposure.
These
studies
are
generally
considered
to
be
sufficient
to
detect
any
endocrine
effects
but
no
such
effects
were
noted
in
any
of
the
studies
with
either
tebuconazole
or
its
metabolites.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
An
aggregate
risk
assessment
was
conducted
for
residues
of
tebuconazole
using
Exponent
Inc.=
s
Dietary
Exposure
Evaluation
Model
(
DEEMTM)
software.
Crops
included
in
this
risk
assessment
are
all
registered
uses
for
tebuconazole,
Section
18
uses,
and
all
pending
uses
which
include
barley,
wheat,
tree
nut
crop
group,
pistachio,
beans,
cotton,
pome
fruit,
asparagus,
coffee,
garlic,
onion,
corn,
soybean,
stone
fruit,
turnips,
hops,
cucurbits
crop
group,
mango,
sunflower,
okra,
and
lychee.
For
both
the
acute
and
chronic
assessments,
the
LOAEL
of
8.8
mg/
kg/
day
from
Bayer
=

s
rat
developmental
neurotoxicity
study
was
used.
The
populations
adjusted
doses
for
acute
dietary
(
aPAD)
and
chronic
dietary
(
cPAD)
were
determined
by
dividing
the
LOAEL
by
an
uncertainty
factor
of
1000
(
10X
for
interspecies
differences,
10X
for
intraspecies
variability,
and
10X
for
extrapolation
from
a
LOAEL
to
a
NOAEL):
aPAD
and
cPAD
=
8.8/
1000
=
0.0088
mg/
kg
bw/
day.]

I.
Food.
[
An
acute
and
chronic,
Tier
3
dietary
(
food)
risk
assessments
were
conducted
using
data
from
field
trials
and
data
from
PDP
where
appropriate.
The
acute
analysis
indicated
that
the
most
highly
exposed
population
subgroup
was
Children
(
1­
2
yrs)
with
an
exposure
equal
to
27.6%
of
the
aPAD.
The
U.
S.
total
population
had
an
exposure
equal
to
17.5%
of
the
aPAD.
The
chronic
analysis
also
showed
that
the
most
highly
exposed
population
subgroup
was
children
7
(
1­
2
yrs)
with
an
exposure
equal
to
1.1%
of
the
cPAD.
The
total
U.
S.
population
had
a
chronic
exposure
equal
to
0.4%
of
the
cPAD.
These
exposure
estimates
are
below
EPA
=

s
level
of
concern.]

ii.
Drinking
water.
[
No
monitoring
data
are
available
for
residues
of
tebuconazole
in
drinking
water
and
EPA
has
established
no
health
advisory
levels
or
maximum
contaminant
levels
for
residues
of
tebuconazole
in
drinking
water.
The
potential
concentrations
of
tebuconazole
in
drinking
water
were
determined
using
the
TIER
II
PRZM/
EXAMS
model
for
surface
water
and
the
SCI­
GROW
model
for
groundwater.
Since
the
estimated
groundwater
concentrations
were
considerably
lower
than
the
surface
water
concentrations,
the
more
conservative
surface
water
estimates
were
used
to
calculate
the
Drinking
Water
Estimated
Concentration
(
DWEC).
The
PRZM/
EXAMS
model
estimated
an
acute
DWEC
of
33.8
ppb
and
a
chronic
DWEC
of
19.2
ppm.

Bayer
has
calculated
an
acute
Drinking
Water
Level
of
Comparison
(
aDWLOC)
for
the
total
U.
S.
population
at
254
ppb
and
an
aDWLOC
for
the
most
highly
exposed
population
subgroup
(
children
(
1­
2
yrs))
at
64
ppb.
Chronic
DWLOCs
for
the
U.
S.
total
population
and
children
(
1­
2
yrs)
were
calculated
to
be
307
and
87,
respectively.
Since
these
DWLOCs
are
greater
than
their
respective
DWECs
determined
by
the
PRZM/
EXAMS
model,
tebuconazole
exposure
from
drinking
water
is
below
EPA
=

s
level
of
concern.]

2.
Non­
dietary
exposure.
[
Tebuconazole
is
currently
registered
for
use
on
the
following
residential
non­
food
sites:
residential
application
to
roses,
flowers,
trees
and
shrubs;
the
formulation
of
wood­
based
composite
products;
wood
products
for
in­
ground
contact;
plastics;
exterior
paints,
glues
and
adhesives.
Residential
exposure
to
homeowners
who
mix,
load
and
apply
tebuconazole
to
roses,
flowers,
trees
and
shrubs
as
well
as
post­
application
exposure
of
adults
and
youth
(
age
10­
12)
to
tebuconazole
residues
from
this
use
was
assessed.
(
Based
on
the
US
EPA
residential
exposure
SOPs,
the
use
pattern
precludes
likely
post­
application
exposure
to
younger
age
groups.)
Short­
term
and
intermediate­
term
margins
of
exposure
for
homeowners
mixing,
loading
and
applying
tebuconazole
using
pump
sprayers
and
hoseend
sprayers
were
3040
and
218,
respectively.
Chronic
margins­
of­
exposure
for
the
homeowner
mixer/
loader/
applicator
using
the
same
equipment
were
14,900
and
1070
ppm,
respectively.
Short­
term
and
intermediate­
term
margins
of
post­
application
exposure
for
adults
ranged
from
408
­
2120.
The
margins­
of
exposure
for
youth
ranged
from
712
to
3700.
Chronic
margins
of
post­
application
exposure
exceeded
4930
for
adults
and
youth.

For
the
remaining
uses
(
wood
treatment,
plastics,
paints,
glues
and
adhesives)
EPA
has
determined
that
exposure
via
incidental
ingestion
(
by
children)
and
inhalation
is
not
a
concern
for
these
products
which
are
used
outdoors.
A
non­
dietary
assessment
of
exposure
to
tebuconazole
from
the
8
copper
tebuconazole­
treated
wood
showed
all
tebuconazole
MOEs
exceeding
10,000.
Therefore,
there
is
no
unacceptable
risk
associated
with
this
use
for
tebuconazole.]

D.
Cumulative
Effects
[
Tebuconazole
is
a
member
of
the
triazole
class
of
systemic
fungicides.
At
this
time,
the
EPA
has
not
made
a
determination
that
tebuconazole
and
other
substances
that
may
have
a
common
mechanism
of
toxicity
would
have
cumulative
effects.
Therefore,
for
this
tolerance
petition,
it
is
assumed
that
tebuconazole
does
not
have
a
common
mechanism
of
toxicity
with
other
substances
and
only
the
potential
risks
of
tebuconazole
in
its
aggregate
exposure
are
considered.
The
cumulative
effects
of
the
primary
common
metabolites
(
1,2,4­
triazole
and
its
TA
and
TAA
conjugates
are
being
addressed
by
the
US
Triazole
Task
Force.]

E.
Safety
Determination
1.
U.
S.
population.
[
Based
on
the
exposure
assessments
described
above
under
Aggregate
Exposure
and
on
the
completeness
and
reliability
of
the
toxicity
data,
it
can
be
concluded
that
aggregate
exposure
estimates
from
all
label
and
pending
uses
of
tebuconazole
are
17.5%
of
the
aPAD
and
0.4%
percent
of
the
cPAD
for
dietary
exposures.
Exposure
estimates
calculated
from
tebuconazole
in
drinking
water
are
below
the
EPA
=

s
level
on
concern.
In
addition,
no
unacceptable
risks
were
determined
for
non­
dietary
exposure.]

2.
Infants
and
children.
[
In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
tebuconazole,
data
from
developmental
toxicity
studies
in
mice,
rats,
rabbits
and
a
2­
generation
reproduction
study
in
the
rat
are
considered.
The
developmental
toxicity
studies
are
designed
to
evaluate
adverse
effects
on
the
developing
organism
resulting
from
maternal
pesticide
exposure
during
gestation.
Reproduction
studies
provide
information
relating
to
effects
from
exposure
to
the
pesticide
on
the
reproductive
capability
of
mating
animals
and
data
on
systemic
toxicity.

Using
the
conservative
exposure
assumptions
described
above
under
Aggregate
Exposure,
it
can
be
concluded
that
the
aggregate
dietary
exposure
estimates
from
the
proposed
uses
of
tebuconazole
would
not
exceed
27.6%
of
the
aPAD
and
1.1%
of
the
cPAD
for
the
most
sensitive
population
subgroup
children
(
1­
2
years).
Exposure
estimates
calculated
from
tebuconazole
in
drinking
water
are
below
the
EPA
=

s
level
on
concern.
In
addition,
no
unacceptable
risks
were
determined
for
non­
dietary
exposure.]

F.
International
Tolerances
[
MRLs
of
0.05
mg/
kg
have
been
established
in/
on
asparagus
in
France,
Italy
and
Japan.
No
CODEX
MRLs
have
been
established
for
tebuconazole
in/
on
asparagus.]
9