Document ID: EPA-HQ-OPP-2006-0166-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-04-21T04:00Z

EPA
Registration
Division
contact:
Barbara
Madden,
703­
305­
6463
Interregional
Research
Project
Number
4
(
IR­
4)

PP#
1E6323
EPA
has
received
a
pesticide
petition
1E6323
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
180.242
by
establishing
a
tolerance
for
residues
of
thiabendazole,
(
2­(
4­
thiazolyl)
benzimidazole)
in
or
on
the
raw
agricultural
commodity
pea,
dry
at
0.05
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
qualitative
nature
of
the
residues
in
plants
is
adequately
understood
based
on
soybean,
sugar
beet,
and
wheat
metabolism
studies.
The
residues
of
concern
in
plants
include
thiabendazole
and
benzimidazole,
free
and
conjugated.

2.
Analytical
method.
Adequate
analytical
methodology
is
available
for
data
collection
enforcing
of
thiabendazole
residues.
The
Pesticide
Analytical
Manual
(
PAM)
Vol.
II
lists
four
spectrophotofluorometric
methods
(
Methods
I,
A,
B
and
C)
for
determining
residues
of
thiabendazole
per
se
in
or
on
plant
commodities,
and
one
spectrophotofluorometric
method
(
Method
D)
for
determining
residues
of
thiabendazole
and
5­
hydroxy­
thiabendazole
in
milk.

3.
Magnitude
of
residues.
A
total
of
five
field
residue
trials
were
conducted
by
IR­
4
on
dry
peas
at
different
locations
in
region
11,
three
in
Washington
and
two
in
Idaho.
No
quantitative
residues
(>
0.05
ppm)
of
thiabendazole
were
observed
in
the
samples.
Results
from
these
studies
support
the
proposed
tolerance
of
0.05
ppm
in
or
on
peas
(
dry).

B.
Toxicological
Profile
1.
Acute
toxicity.
Thiabendazole
has
low
acute
toxicity
via
oral
and
dermal
(
Category
III).
Thiabendazole
is
neither
irritating
to
the
eyes
or
skin
(
Category
IV)
nor
a
dermal
sensitizer.
In
primary
eye
and
primary
skin
irritation
studies,
thiabendazole
was
found
to
be
non­
toxic.
2
2.
Genotoxicity.
The
available
genetic
toxicology
studies
on
thiabendazole
indicate
that
the
compound
is
not
mutagenic
in
bacteria
or
clastogenic
in
vitro
in
mammalian
cells.
Thiabendazole
did
not
cause
DNA
strand
breaks
in
cultured
rat
hepatocytes
and
was
negative
for
structural
chromosome
aberrations
in
rats.

3.
Reproductive
and
developmental
toxicity.
In
the
rat
development
study,
the
observed
maternal
and
developmental
LOAEL/
NOAEL
of
40/
10
mg/
kg/
day
was
based
on
decrease
in
body
weight
and
food
consumption.

In
the
mouse
prenatal
development
toxicity
study,
there
were
reductions
in
maternal
body
weight
at
mid
(
100
mg//
kg/
day)
and
high
dose
(
299
mg/
kg/
day)
treatment
groups.
There
were
accompanying
reductions
in
feed
consumption
in
the
HDT
group.
The
mouse
maternal
and
developmental
LOAEL/
NOEAL
were
100/
25
mg/
kg/
day,
respectively.

In
a
rabbit
developmental
study,
decreased
maternal
body
weight
gains
and
decreased
food
consumption
were
seen
at
HDT
(
600
mg/
kg/
day).
There
was
also
decreased
fetal
body
weight
and
increased
resorptions
at
600
mg/
kg.
The
rabbit
maternal
and
developmental
LOAEL/
NOAEL
were
600/
150
mg/
kg,
respectively.
In
a
2­
generation
reproduction
study
in
the
rat,
the
parental
systemic
LOAEL
was
based
on
decreased
body
weight
gain
and
food
consumption
seen
at
30
mg/
kg.
The
NOEAL
was
10
mg/
kg.
The
offspring
LOAEL
was
based
on
decreased
body
weight
gain
in
offspring
during
lactation
seen
at
30
mg/
kg.
The
reproductive
LOAEL
was
>
90
mg/
kg.
The
effects
in
the
offspring
were
observed
at
higher
dosages
(
90
mg/
kg)
than
dosages
(
30
mg/
kg)
causing
parental
toxicity.
Therefore,
there
was
no
increased
susceptibility
4.
Subchronic
toxicity.
In
a
21
day
dermal
toxicity
study
in
the
rabbit,
thiabendazole
was
administered
dermally
to
rabbits.
No
systemic
or
dermal
toxicities
were
noted
at
doses
up
to
1000
mg/
kg/
day.
The
systemic
and
dermal
NOEL
was
1000
mg/
kg.

In
a
subchronic
toxicity
study,
thiabendazole
was
administered
to
rats
in
the
diet.
The
NOEL
of
10
mg/
kg
was
based
on
reduced
body
weight
gains
and
histopathological
changes
in
the
bone
marrow,
liver
and
thyroid.

In
another
subchronic
toxicity
study,
thiabendazole
was
administered
to
rats
by
gavage
at
doses
of
0,
25,
100,
or
400
mg/
kg/
day
for
14
weeks.
The
LOAEL
for
this
study
was
100
mg/
kg/
day.
The
NOEL
of
25
mg/
kg
was
based
on
histopathological
changes
of
the
liver,
thyroid,
kidneys,
and
spleen.

In
a
subchronic
toxicity
study
in
dogs,
thiabendazole
was
administered
orally
in
capsules
to
four
beagle
dogs
at
dose
levels
of
0,
35,
75,
or
150
mg/
kg/
day
for
14
weeks.
The
NOEL
was150
mg/
kg
based
on
the
increase
of
gallbladder
epithelial
cytoplasmic
vacuolation.
3
5.
Chronic
toxicity.
In
a
chronic
toxicity
study,
thiabendazole
was
administered
orally
in
capsules
to
four
beagle
dogs
at
dose
levels
of
0,
10,
40,
or
160
mg/
kg/
day
for
52
weeks.
The
LOAEL
for
this
study
was
40
mg/
kg
based
on
increased
liver
weight,
splenic
erythropoiesis
and
hemosiderosis
in
both
sexes.
The
LOAEL
was
10
mg/
kg.

In
a
chronic
toxicity
and
carcinogenicity
study,
thiabendazole
was
administered
to
rats
in
the
diet
at
dose
levels
of
0,
10,
30,
or
90
mg/
kg/
day
for104
weeks.
The
systemic
LOAEL
was
30
mg/
kg
based
on
increase
in
incidence
of
benign
thyroid
follicular
cell
adenoma.
The
NOAEL
was
10
mg/
kg.

In
a
carcinogenicity
study,
thiabendazole
was
administered
to
50
mice
for
105
weeks.
There
was
an
increase
in
mortality
in
all
dose
groups.
Body
weight
gains
were
significantly
lower
in
high
dose
female
and
male.
However,
no
treatment­
related
increase
in
tumor
incidence
above
background
level
was
observed.

6.
Animal
metabolism.
The
rat,
goat
and
hen
metabolism
studies
indicate
that
the
qualitative
nature
of
the
residues
in
animals
is
adequately
understood.
The
residue
of
concern
in
eggs,
milk,
and
poultry
and
livestock
tissue
is
thiabendazole
and
5­
hydroxy­
thiabendazole
(
free
and
conjugated)
and
benzimidazole.

In
a
rat
metabolism
study,
radio­
labeled
thiabendazole
was
administered
to
rats
by
gavage.
Thiabendazole
was
readily
absorbed
by
male
and
female
rats
following
oral
dosing.
Within
168
hours
of
dosing
,
over
89%
of
the
dose
was
excreted
in
urine
and
feces.
The
majority
of
the
administered
dose
was
recovered
in
the
urine
identified
as
the
glucuronide
conjugate
of
5­
hydroxythiabendazole
and
the
sulfate
conjugate
of
5­
hydroxy
thiabendazole.
The
data
indicate
that
the
renal
excretion
is
the
primary
pathway
for
the
elimination
of
thiabendazole
from
rats.
At
the
low
dose
level,
it
was
shown
that
thiabendazole
oxidizes
to
form
5­
hydroxythiabendazole,
followed
by
conjugation
to
form
glucuronide
and
sufate
conjugates
of
5­
hydroxythiabendazole.

7.
Metabolite
toxicology.
The
nature
of
residues
in
plants
and
animals
is
adequately
understood.
Residues
of
concern
in
plants
include
thiabendazole
and
its
metabolite
benzimidazole,
free
and
conjugated.
The
residue
of
concern
in
animal
commodities
are
thiabendazole
and
5­
hydroxythiabendazole
(
free
and
conjugated)
and
benzimidazole.
No
additional
additional
toxicologically
significant
metabolites
were
detected
in
any
of
the
plant
or
animal
metabolism
studies.

8.
Endocrine
disruption.
Thiabendazole
does
not
belong
to
a
class
of
chemicals
known
or
suspected
of
having
adverse
effects
on
the
endocrine
system.
Developmental
toxicity
studies
in
rats
and
rabbits
and
a
reproduction
study
in
rats
gave
no
indication
that
thiabendazole
might
have
any
effects
on
endocrine
function
related
to
development
and
reproduction.

C.
Aggregate
Exposure
1.
Dietary
Exposure.
Tier
III/
IV
acute
and
chronic
dietary
exposure
evaluations
were
made
for
thiabendazole
using
the
Dietary
Exposure
Evaluation
Model
software
with
the
Food
Commodity
Intake
4
Database
(
DEEM­
FCIDTM,
version
2.03)
from
Exponent.
These
exposure
assessments
included
all
registered
uses
(
apple,
avocado,
banana,
dry
bean,
cantaloupe,
carrot,
citrus
fruit,
mango,
mushroom,
papaya,
pear,
potato,
soybean,
strawberry,
sweet
potato
and
wheat)
and
a
proposed
use
on
dry
peas.
USDA­
PDP
monitoring
data
(
1994
 
2002,
not
decomposited)
was
used
for
all
crops
except
avocados,
mangos,
papayas,
dry
peas
and
dry
beans.
The
residue
values
for
avocados,
mangos
and
papayas
were
from
field
trials
where
the
fruit
was
treated
post­
harvest
at
a
rate
selected
to
support
the
maximum
use
pattern
specified
on
thiabendazole
product
labels.
The
residue
values
for
dry
peas
were
from
field
trials
where
thiabendazole
was
applied
as
a
seed
treatment
at
the
maximum
intended
proposed
use
rate.
The
proposed
tolerance
value
was
used
for
dry
beans,
as
no
residue
data
was
available
for
seed
treatment
use.
Since
PDP
data,
field
trial
data
and
current
tolerance
values
reflect
analysis
for
thiabendazole
only,
a
correction
factor
was
applied
to
wheat,
soybean,
dry
bean,
dry
pea,
sweet
potato,
cantaloupe
and
strawberry
residue
values
to
account
for
anticipated
residues
of
benzimidazole
which
is
a
metabolite
of
thiabendazole.
Benzimidazole
conversion
factors,
crop
processing
factors,
secondary
residues
in
animal
commodities
and
percent
of
crop
treated
values
were
taken
from
the
EPA's
September
7,
2000
dietary
exposure
assessment
on
thiabendazole
(
DP
Barcode
No.
D267542).
All
consumption
data
for
these
assessments
were
taken
from
the
USDA's
Continuing
Survey
of
Food
Intake
by
individuals
(
CSFII)
with
the
1994­
96
consumption
database
and
the
Supplemental
CSFII
children's
survey
(
1998)
consumption
database.

i.
Food.

Acute
Risk.
The
acute
dietary
risk
assessment
was
performed
for
all
population
subgroups
with
an
acute
reference
dose
of
0.1
mg/
kg­
bw/
day
based
on
an
acute
no
observable
adverse
effect
level
(
NOAEL)
of
10
mg/
kg­
bw/
day
from
a
rat
developmental
toxicity
study
and
an
uncertainly
factor
of
100X.
The
100X
safety
factor
includes
intra­
and
inter­
species
variations.
No
additional
FQPA
safety
factor
was
applied.
For
the
purpose
of
the
aggregate
risk
assessment,
the
exposure
value
was
expressed
in
terms
of
margin
of
exposure
(
MOE),
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
In
addition,
exposure
was
expressed
as
a
percent
of
the
acute
reference
dose
(%
aRfD).
Acute
exposure
to
the
U.
S.
population
resulted
in
a
MOE
of
494
(
20.2%
of
the
acute
RfD
of
0.1
mg/
kg­
bw/
day).
Acute
exposure
to
the
most
sensitive
subpopulation
(
children
1
to
2
years
old)
resulted
in
a
MOE
of
212
(
47.2%
of
the
acute
RfD
of
0.1
mg/
kg­
bw/
day).
Since
the
benchmark
MOE
for
this
assessment
is
100
and
since
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
acute
dietary
(
food)
exposure
to
residues
arising
from
the
current
and
proposed
uses
for
thiabendazole.

Chronic
Risk.
The
chronic
assessment
was
run
using
DEEM­
FCID
 
software
using
the
tolerance
value
for
dry
beans,
the
average
field
trial
residue
value
for
dry
peas
and
the
average
USDAPDP
residue
values
for
all
other
registered
crops
that
are
currently
supported
by
the
product
labels.
The
residue
values
for
wheat,
legume
vegetables,
sweet
potatoes,
cantaloupes
and
strawberries
were
adjusted
to
account
for
residues
of
benzimidazole.
Exposure
from
drinking
water
was
input
directly
into
the
DEEM­
FCID
 
software
as
the
chronic
surface
water
EDWC
of
0.5
ppm,
which
was
obtained
from
the
EPA's
2002
RED
document.
5
The
chronic
dietary
risk
assessment
was
performed
for
all
population
subgroups
with
a
chronic
reference
dose
of
0.1
mg/
kg­
bw/
day
based
on
a
2
year
feeding/
chronic/
carcinogenicity
study
in
rats
with
a
NOAEL
of
10
mg/
kg­
bw/
day
and
an
uncertainly
factor
of
100X.
The
100­
fold
safety
factor
includes
intra­
and
interspecies
variations.
No
additional
FQPA
safety
factor
was
applied.
For
the
purpose
of
the
aggregate
risk
assessment,
the
exposure
values
were
expressed
in
terms
of
margin
of
exposure
(
MOE),
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
In
addition,
exposure
was
expressed
as
a
percent
of
the
reference
dose
(%
RfD).
Chronic
(
non­
cancer)
exposure
to
the
U.
S.
population
resulted
in
a
MOE
of
23,579
(
0.4%
of
the
chronic
RfD
of
0.1
mg/
kg­
bw/
day).
Chronic
exposure
to
the
most
exposed
sub­
population
(
children
1
to
2
years
old)
resulted
in
a
MOE
of
6,785
(
1.5%
of
the
chronic
RfD
of
0.1
mg/
kg­
bw/
day).
Since
the
benchmark
MOE
for
this
assessment
is
100
and
since
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
chronic
dietary
(
food
+
water)
exposure
to
residues
arising
from
the
current
and
proposed
uses
for
thiabendazole.

Cancer
Risk.
The
chronic
(
cancer)
assessment
was
run
using
DEEM­
FCID
 
software
using
the
tolerance
value
for
dry
beans,
the
average
field
trial
residue
value
for
dry
peas
and
the
average
USDA­
PDP
residue
values
for
all
other
registered
crops
that
are
currently
supported
by
the
product
labels.
The
residue
values
for
wheat,
legume
vegetables,
sweet
potatoes,
cantaloupes
and
strawberries
were
adjusted
to
account
for
residues
of
benzimidazole.
Exposure
from
drinking
water
was
input
directly
into
the
DEEM­
FCID
 
software
as
the
chronic
surface
water
EDWC
of
0.5
ppm,
which
was
obtained
from
the
EPA's
2002
RED
document.

In
accordance
with
the
Cancer
Assessment
Review
Committee,
the
Margin
of
Exposure
(
MOE)
approach
was
used
to
assess
chronic
cancer
dietary
risk
for
thiabendazole
based
on
a
Point
of
Departure
(
POD)
of
10
mg/
kg/
day.
The
results
of
the
chronic
(
cancer)
dietary
(
food
+
water)
assessment
indicated
a
MOE
of
23,579
for
the
general
U.
S.
population.
For
thiabendazole,
a
chronic
cancer
MOE
of
greater
than
100
is
below
the
level
of
concern
for
the
EPA
therefore
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
chronic
(
cancer)
dietary
(
food
+
water)
exposure
to
residues
arising
from
the
current
and
proposed
uses
for
thiabendazole.

ii.
Drinking
Water.
Another
potential
source
of
exposure
of
the
general
population
to
residues
of
thiabendazole
are
residues
in
drinking
water.
Drinking
water
concentration
estimates
are
made
by
reliance
on
simulation
or
modeling
taking
into
account
data
on
the
physical
characteristics
of
thiabendazole.
The
Agency
uses
the
First
Index
Reservoir
Screening
Tool
(
FIRST)
or
the
Pesticide
Root
Zone/
Exposure
Analysis
Modeling
System
(
PRZM/
EXAMS)
to
produce
estimates
of
pesticide
concentrations
in
an
index
reservoir.
The
Screening
Concentration
in
Ground
Water
(
SCI­
GROW)
model
is
used
to
predict
pesticide
concentrations
in
shallow
groundwater.
For
a
screening
level
assessment
for
surface
water
EPA
will
generally
use
FIRST
(
a
Tier
I
model)
before
using
PRZM/
EXAMS
(
a
Tier
II
model).
The
FIRST
model
is
a
subset
of
the
PRZM/
EXAMS
model
that
uses
a
specific
high­
end
runoff
scenario
for
pesticides.
While
both
FIRST
and
PRZM/
EXAMS
incorporate
6
an
index
reservoir
environment,
the
PRZM/
EXAMS
model
includes
a
percent
crop
area
factor
as
an
adjustment
to
account
for
the
maximum
percent
crop
coverage
within
a
watershed
or
drainage
basin.

Acute
Exposure
from
Drinking
Water.
The
acute
estimated
drinking
water
concentration
(
EDWC)
of
thiabendazole
was
compared
to
the
acute
Drinking
Water
Levels
of
Comparison
(
DWLOC).
The
DWLOC
for
thiabendazole
was
calculated
to
be
528
ppb
based
on
an
acute
Population
Adjusted
Dose
(
aPAD)
of
0.1
mg/
kg/
day
for
the
most
sensitive
population
subgroup
(
children
1­
2
years
old).
In
the
2002
EPA
RED
document,
the
acute
EDWCs
of
thiabendazole
were
estimated
to
be
2
ppb
for
surface
water
based
on
the
GENEEC
model
and
0.01
ppb
for
ground
water
based
on
the
SCI­
GROW
model.
Since
the
acute
DWLOC
of
528
ppb
is
considerably
higher
than
the
acute
EDWC
of
2
ppb,
the
EPA
should
not
have
a
concern
for
acute
risk
from
either
surface
or
ground
water.

Chronic
Exposure
from
Drinking
Water.
Chronic
(
non­
cancer)
dietary
exposure
to
thiabendazole
from
food
plus
drinking
water
was
calculated
using
the
DEEM­
FCID
 
software
for
all
population
subgroups.
In
the
2002
EPA
RED
document,
the
chronic
EDWCs
of
thiabendazole
were
estimated
to
be
0.5
ppb
for
surface
water
based
on
the
GENEEC
model
and
0.01
ppb
for
ground
water
based
on
the
SCI­
GROW
model.
The
EDWC
for
surface
water
was
conservatively
entered
directly
into
the
DEEM­
FCID
 
software
as
water
(
direct
and
indirect,
all
sources).
For
the
most
exposed
subpopulation
(
children
1
to
2
years
old),
the
chronic
(
non­
cancer)
dietary
exposure
from
food
plus
water
resulted
in
a
MOE
of
6,785.
Since
this
value
is
higher
than
the
benchmark
MOE
of
100,
the
EPA
should
not
have
a
concern
for
chronic
(
non­
cancer)
risk
from
exposure
to
thiabendazole
from
either
surface
or
ground
water.

Chronic
(
cancer)
dietary
exposure
to
thiabendazole
from
food
plus
drinking
water
was
calculated
using
the
DEEM­
FCID
 
software
for
the
U.
S.
population.
The
EDWC
for
surface
water
(
0.5
ppb,
from
the
2002
EPA
RED
document)
was
conservatively
entered
into
the
DEEM­
FCID
 
software
for
water
(
direct
and
indirect,
all
sources).
For
the
U.
S.
population,
the
chronic
cancer
dietary
exposure
from
food
plus
water
resulted
in
a
MOE
of
23,579.
Since
this
value
is
higher
than
the
benchmark
MOE
of
100,
the
EPA
should
not
have
a
concern
for
chronic
cancer
risk
from
exposure
to
thiabendazole
from
either
surface
or
ground
water.

2.
Non­
dietary
Exposure.
There
are
no
thiabendazole
pesticide
products
registered
for
use
by
homeowners.
Thiabendazole­
treated
carpets
and
paints,
can
however,
be
used
by
homeowners.
In
the
2002
EPA
RED
document,
the
Agency
indicated
that
homeowners
are
not
at
risk
from
exposure
to
thiabendazole­
treated
carpets
since
the
pesticide
is
applied
to
the
backing
of
carpets
during
the
manufacturing
process
and
estimates
are
extremely
conservative.
Due
to
thiabendazole's
use
profile,
the
Agency
concluded
that
there
is
a
low
potential
for
residential
exposure.
The
low
concentrations
of
thiabendazole
incorporated
in
paints,
adhesives,
paper
and
carpet
greatly
reduces
the
potential
for
exposure.
In
all
cases,
residential
exposure
is
not
expected
to
exceed
occupational
post­
application
exposure
and
therefore
would
not
be
expected
to
exceed
the
EPA's
level
of
concern.
7
D.
Cumulative
Effects
Cumulative
Exposure
to
Substances
With
a
Common
Mechanism
of
Toxicity.
Section
408(
b)(
2)(
D)(
v)
requires
that,
when
considering
whether
to
establish,
modify,
or
revoke
a
tolerance,
the
Agency
consider
"
available
information"
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
"
other
substances
that
have
a
common
mechanism
of
toxicity".
The
Agency
is
examining
whether
and
to
what
extent
benzimidazole
fungicidal
pesticides
share
a
common
mechanism
of
toxicity.
Current
information
on
the
common
mechanism
of
toxicity
for
benzimidazole
fungicides
is
limited
and
the
Agency's
understanding
of
this
relationship
needs
to
be
further
developed.
As
a
result,
the
Agency
has
not
determined
if
it
would
be
appropriate
to
include
them
in
a
cumulative
risk
assessment
with
other
benzimidazole
fungicides
or
carcinogenic
chemicals.
Therefore,
for
the
purposes
of
this
tolerance
action,
the
EPA
has
not
assumed
that
thiabendazole
has
a
common
mechanism
of
toxicity
with
other
benzimidazole
or
carcinogenic
chemicals.

E.
Safety
Determination
1.
U.
S.
Population.
Using
the
conservative
assumptions
described
above,
and
based
on
the
completeness
and
reliability
of
the
toxicity
data,
the
acute
aggregate
(
food
plus
water)
exposure
calculation
for
current
and
proposed
uses
of
thiabendazole
provided
a
MOE
of
493
for
the
U.
S.
population.
Since
the
acute
aggregate
MOE
of
493
exceeds
the
acute
aggregate
benchmark
MOE
of
100,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
occur
to
the
U.
S.
Population
from
acute
aggregate
exposures
arising
from
the
current
and
proposed
uses
for
thiabendazole.

2.
Infants
and
children.
Using
the
conservative
assumptions
described
in
the
exposure
section
above,
and
based
on
the
completeness
and
reliability
of
the
toxicity
data,
the
acute
aggregate
(
food
plus
water)
exposure
calculation
for
current
and
proposed
uses
of
thiabendazole
provided
a
MOE
of
203
for
children
1
­
2
years
old
(
the
most
sensitive
population
subgroup).
Since
the
acute
aggregate
MOE
of
203
exceeds
the
acute
aggregate
benchmark
MOE
of
100,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
occur
to
infants
and
children
from
acute
aggregate
exposures
arising
from
the
current
and
proposed
uses
for
thiabendazole.

F.
International
Tolerances
The
Codex
Alimentarius
Commission
has
established
maximum
residue
limits
(
MRLs)
for
thiabendazole
in/
on
various
fruit,
vegetable
and
animal
commodities.
Codex
MRLs
for
thiabendazole
are
currently
expressed
in
terms
of
the
parent
for
plant
commodities
and
in
terms
of
the
sum
of
parent
and
5­
hydroxythiabendazole
for
animal
commodities.
Once
the
tolerance
expressions
for
U.
S.
tolerances
are
modified
to
include
residues
of
benzimidazole,
the
U.
S.
tolerance
definition
will
no
longer
be
compatible
with
Codex.
The
MRLs
for
banana,
cereal
grain,
citrus
fruits
and
milk
are
the
only
MRLs
that
are
numerically
equivalent
to
the
reassessed
U.
S.
tolerances.

The
Codex
Alimentarius
Commission
has
established
maximum
residue
limits
(
MRLs)
for
thiabendazole
in/
or
various
fruit,
vegetable
and
animal
commodities.
8