Document ID: EPA-HQ-OPP-2005-0145-0004
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-02-08T05:00Z

FILE
NAME:
company.
wpt
(
1/
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:
[
Tony
Kish,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.
Washington,
DC
20460 
0001;
Telephone
number:
(
703)
308 
9943;
e­
mail
address:
giles­
parker.
cynthia@
epa.
gov.]

INSTRUCTIONS:
Please
utilize
this
outline
in
preparing
tolerance
petition
documents.
In
cases
where
the
outline
element
does
not
apply
please
insert
"
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.,
"[
insert
company
name],"
with
the
information
specific
to
your
action.

TEMPLATE:

[
BASF
Corporation]

[
Insert
petition
number]

EPA
has
received
a
pesticide
petition
([
insert
petition
number])
from
[
BASF
Corporation],
[
Research
Triangle
Park,
NC
27709]
proposing,
pursuant
to
section
408(
d)
of
2
the
Federal
Food,
Drug,
and
Cosmetic
Act
(
FFDCA),
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
part
180
by
establishing
a
tolerance
for
residues
of
[
Boscalid
(
BAS
510F);
[
3­
pyridinecarboxamide,
2­
chloro­
N­(
4'­
chloro(
1,1'­
biphenyl)­
2­
yl]]
in
or
on
the
raw
agricultural
commodity
for
increasing
the
tolerance
for
[
strawberry]
at
[
4.0]
parts
per
million
(
ppm)
and
for
increasing
the
tolerance
for
[
Berries,
crop
group
13,]
to
[
8.0]
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.
[
Nature
of
the
residue
studies
(
OPPTS
Harmonized
Guideline
860.1300)
were
conducted
in
grapes,
lettuce
and
beans
as
representative
crops
in
order
to
characterize
the
fate
of
boscalid
(
BAS
510F)
in
all
crop
matrices.
In
all
three
crops
the
boscalid
(
BAS
510F)
Residues
of
Concern
(
ROC)
were
characterized
as
parent
boscalid
(
BAS
510F).
A
confined
rotational
crop
study
also
determined
that
parent
was
the
residue
of
concern
in
the
representative
crops
of
radish,
lettuce
and
wheat.]

2.
Analytical
method.
[
In
plants
the
parent
residue
is
extracted
using
an
aqueous
organic
solvent
mixture
followed
by
liquid/
liquid
partitioning
and
a
column
clean
up.
Quantitation
is
by
gas
chromatography
using
mass
spectrometry
(
GC/
MS).
In
livestock
the
residues
are
extracted
with
methanol.
The
extract
is
treated
with
enzymes
in
order
to
release
the
conjugated
glucuronic
acid
metabolite.
The
residues
are
then
isolated
by
liquid/
liquid
partition
followed
by
column
chromatography.
The
hydroxylated
metabolite
is
acetylated
followed
by
a
column
clean­
up.
The
parent
and
acetylated
metabolite
are
quantitated
by
gas
chromatography
with
electron
capture
detection.]

3.
Magnitude
of
residues.
[
Residue
levels
of
boscalid
(
BAS
510F)
were
determined
in
Stone
Fruits
(
peach,
cherry,
and
plum)
and
Pome
Fruits
(
apples
and
pears)
samples
treated
post­
harvest
with
one
application
of
BAS
516F
(
a
mixture
of
BAS
500F
and
BAS
510F).
Field
trials
were
carried
out
in
order
to
determine
the
magnitude
of
the
residue
in/
on
Belgian
Endives.
Field
trials
were
conducted
in
the
United
States
in
the
required
regions
for
Belgian
Endives.
The
number
and
locations
of
field
trials
and
post­
harvest
treatments
are
in
accordance
with
OPPTS
Guideline
860.1500.

Field
trials
and
post­
harvest
treatments
were
carried
out
using
the
maximum
label
rate,
the
maximum
number
of
applications,
and
the
minimum
pre­
harvest
interval
for
each
crop
or
crop
group.]

B.
Toxicological
Profile
3
1.
Acute
toxicity.
[
Based
on
available
acute
toxicity
data
BAS
510F
and
its
formulated
products
do
not
pose
acute
toxicity
risks.
The
acute
toxicity
studies
place
technical
Boscalid
(
BAS
510F)
in
toxicity
category
IV
for
acute
oral;
category
III
for
acute
dermal
and
category
IV
for
acute
inhalation.
BAS
510F
is
category
IV
for
both
eye
and
skin
irritation,
and
it
is
not
a
dermal
sensitizer.
For
Belgian
Endives,
the
formulated
end
use
product
proposed
is
as
follows:
a
water
dispersible
granule
(
WG)
termed
Pristine
®
(
BAS
516
02/
04F)
containing
a
2:
1
mixture
of
boscalid
(
BAS
510F)
and
pyraclostrobin
(
BAS
500F).
BAS
516
02F
has
an
acute
oral
toxicity
category
of
III,
acute
dermal
of
category
III,
acute
inhalation
of
category
IV,
eye
irritation
of
category
III,
skin
irritation
of
category
IV,
and
is
not
a
dermal
sensitizer.

For
Pome
Fruits
(
Crop
Group
11)
and
Stone
Fruits
(
Crop
Group
12),
the
product
proposed
is
BAS
516F
510F
containing
boscalid
(
BAS
510F)
and
pyraclostrobin
(
BAS
500F).
BAS
516F
has
an
acute
oral
toxicity
category
of
III,
acute
dermal
of
category
III,
acute
inhalation
of
category
IV,
eye
irritation
of
category
III,
skin
irritation
of
category
IV,
and
is
not
a
dermal
sensitizer.]

2.
Genotoxicty.
[
Ames
Test
(
1
Study;
gene
point
mutation):
Negative;
In
Vitro
CHO/
HGPRT
Locus
Mammalian
Cell
Mutation
Assay
(
1
Study;
point
gene
mutation):
Negative;
In
Vitro
V79
Cell
Cytogenetic
Assay
(
1
Study;
Chromosome
Damage):
Negative;
In
Vivo
Mouse
Micronucleus
(
1
Study;
Chromosome
Damage):
Negative;
In
Vitro
Rat
Hepatocyte
(
1
Study;
DNA
damage
and
repair):
Negative.
BAS
510F
has
been
tested
in
a
total
of
5
genetic
toxicology
assays
consisting
of
in
vitro
and
in
vivo
studies.
It
can
be
stated
that
BAS
510F
did
not
show
any
mutagenic,
clastogenic
or
other
genotoxic
activity
when
tested
under
the
conditions
of
the
studies
mentioned
above.
Therefore,
BAS
510F
does
not
pose
a
genotoxic
hazard
to
humans.]

3.
Reproductive
and
developmental
toxicity.
[
The
reproductive
and
developmental
toxicity
of
BAS
510F
was
investigated
in
a
two­
generation
rat
reproduction
study
as
well
as
in
rat
and
rabbit
teratology
studies.
There
were
no
adverse
effects
on
reproduction
in
the
two­
generation
study
at
any
dose
tested.
The
reproductive
NOAEL
is
10,000
ppm
(
1165
and
1181
for
males
and
females,
respectively),
the
highest
dose
tested.
Pup
effects
were
observed,
at
the
highest
dose
tested
only.
In
males
of
the
F1
generation,
reduced
body
weight
and
reduced
body
weight
gain
were
observed
at
10,000
ppm.
Additionally,
hepatocyte
degeneration
was
observed
in
males
in
animals
of
both
the
F0
and
F1
generations
at
10,000
ppm.
The
parental
systemic
NOAEL
is
1000
and
10,000
(
113
and
1181
mg/
kg
b.
w./
day)
for
males
and
females,
respectively.
Toxicity
to
the
offspring
was
seen
at
1,000
ppm
in
the
form
of
decreased
pup
weights
in
the
F2
males,
and
at
10,000
ppm
in
the
form
of
decreased
pup
weights
for
both
males
and
females
of
both
the
F1
and
F2
generations.
The
offspring
NOAEL
is
100
and
1000
ppm
(
12
and
116
mg/
kg
b.
w./
day)
for
males
and
females,
respectively.
4
The
Agency
concluded
that
there
are
no
residual
uncertainties
for
pre­
and
postnatal
toxicity
as
the
degree
of
concern
is
low
for
the
susceptibility
seen
in
the
above
studies,
and
the
dose
and
endpoints
selected
for
the
overall
risk
assessments
will
address
the
concerns
for
the
body
weight
effects
seen
in
the
offspring.
Although
the
dose
selected
for
overall
risk
assessments
(
21.8
mg/
kg
b.
w./
day)
is
higher
than
the
NOAELs
in
the
2­
generation
reproduction
study
(
10.1
mg/
kg
b.
w./
day)
and
the
developmental
neurotoxicity
study
(
14
mg/
kg
b.
w./
day),
these
differences
are
considered
to
be
an
artifact
of
the
dose
selection
process
in
these
studies.
For
example,
there
is
a
10­
fold
difference
between
the
LOAEL.
(
106.8
mg/
kg
b.
w./
day)
and
the
NOAEL
(
10.1
mg/
kg
b.
w./
day)
in
the
two
generation
reproduction
study.
A
similar
pattern
was
seen
with
regard
to
the
developmental
neurotoxicity
study,
where
there
is
also
a
10­
fold
difference
between
the
LOAEL
(
147
mg/
kg
b.
w./
day)
and
the
NOAEL
(
14
mg/
kg
b.
w./
day).
There
is
only
a
2­
3­
fold
difference
between
the
LOAEL
(
57
mg/
kg
b.
w./
day)
and
the
NOAEL
(
21.8
mg/
kg
b.
w./
day)
in
the
critical
study
used
for
risk
assessment.
Because
the
gap
between
the
NOAEL
and
LOAEL
in
the
2­
generation
reproduction
and
developmental
neurotoxicity
studies
was
large
and
the
effects
at
the
LOAELs
were
minimal,
the
true
no­
observedadverse
effect­
level
was
probably
considerably
higher.
Therefore,
the
selection
of
the
NOAEL
of
21.8
mg/
kg
b.
w./
day
from
the
1­
year
dog
study
is
conservative
and
appropriate
for
the
overall
risk
assessments.
In
addition,
the
endpoints
for
risk
assessment
are
based
on
thyroid
effects
seen
in
multiple
species
(
mice,
rats
and
dogs)
and
after
various
exposure
durations
(
subchronic
and
chronic
exposures)
which
were
not
observed
at
the
LOAELs
in
either
the
2­
generation
reproduction
or
the
developmental
neurotoxicity
studies.
Based
on
these
data,
the
Agency
concluded
that
there
are
no
residual
uncertainties
for
pre­
and
post­
natal
toxicity.

No
teratogenic
effects
were
noted
in
either
the
rat
or
rabbit
developmental
studies.
In
the
rat
study,
evidence
of
maternal
or
developmental
toxicity
was
not
observed
at
any
dose
(
highest
dose
tested
of
1,000
mg/
kg
b.
w./
day).
Neither
a
maternal
nor
developmental
LOAEL
were
found
since
the
highest
dose
tested
was
the
NOAEL
in
both
studies.
In
the
rabbit
teratology
study,
maternal
toxicity
observed
at
the
mid
dose
of
300
milligrams/
kilogram
of
body
weight
(
mg/
kg
b.
w./
day)
consisted
of
discolored/
reduced
feces
in
one
dam
and
an
abortion
in
one
dam.
This
finding
is
not
necessarily
indicative
of
a
definitive
test
substance
related
adverse
effect.
The
dam
which
displayed
the
fecal
alterations
and
abortion
also
displayed
decreased
body
weight
and
body
weight
gain
­
compared
to
the
group
mean­
during
gestation.
These
decreases
occurred
even
prior
to
compound
administration.
Food
consumption
was
also
dramatically
decreased
in
this
dam
compared
to
the
other
animals
in
the
group.
Every
day
from
gestation
day
(
GD)
1 
12,
this
dam
had
food
consumption
values
which
were
less
than
half
the
mean
for
the
group
(
compound
administration
began
on
GD
7).
From
GD
13
to
26
(
when
the
animal
aborted
and
was
sacrificed)
this
dam
ate
essentially
nothing
(
food
consumption
during
this
time
period
was
less
than
or
equal
to
1.5
grams
food/
day).
These
decreases
in
body
weight,
body
weight
gain,
and
food
consumption,
prior
to
compound
administration,
all
5
indicate
an
animal
in
poor
health
and
this
poor
state
of
health,
rather
than
compound
exposure,
was
likely
the
reason
for
the
fecal
alterations
and
abortion.

At
the
high
dose
of
1,000
mg/
kg
b.
w./
day
a
maternal
body
weight
gain
decrease
compared
to
controls
of
81%
was
observed
during
the
treatment
period.
Reduced
food
consumption,
reduced
body
weight
and
abortions
in
three
dams,
were
also
seen
at
1,000
mg/
kg
b.
w./
day.
Evidence
of
developmental
toxicity
was
not
seen
at
any
dose
tested.

Developmental
neurotoxicity
was
not
observed
at
any
dose
in
the
developmental
neurotoxicity
study.
No
maternal
toxic
effects
were
noted
at
any
dose
in
this
study.
No
developmental
toxicity
was
seen
at
the
low
dose
of
12
mg/
kg
b.
w./
day
(
100
ppm).
Reduced
body
weights
and
body
weight
gains
were
seen
at
118
mg/
kg
b.
w./
day
(
1,000
ppm)
during
post
natal
day
(
PND)
1 
4.
Reduced
body
weights
and
body
weight
gains
were
seen
at
1,183
mg/
kg
b.
w./
day
(
10,000
ppm)
as
well
as
decreased
absolute
pup
brain
weight
at
day
PND
11
(
both
sexes)
and
decreased
brain
length
(
males
only)
at
PND.
The
reduced
pup
brain
weights
and
decreased
brain
length
go
hand­
in­
hand
and
both
are
due
to
the
decreased
pup
weights
seen
at
this
dose.
In
this
respect,
it
should
be
noted
that
pup
brain
weights
relative
to
body
weight
at
PND
11
were
not
significantly
different
from
controls
at
this
dose.
Though
no
maternal
toxicity
was
seen
in
this
study,
other
studies
using
similar
doses
of
BAS
510F
resulted
in
maternal
toxicity.
A
dose
of
118
mg/
kg
b.
w./
day
in
female
rats
of
the
same
strain
in
the
multigeneration
study,
resulted
in
an
increased
incidence
of
hepatic
centrilobular
hypertrophy
­
a
parameter
which
could
not
have
been
detected
in
the
developmental
neurotoxicity
(
DNT)
study
as
liver
histopathology
on
parental
animals
was
not
performed
in
the
DNT
study
.]

4.
Subchronic
toxicity.
[
The
subchronic
toxicity
of
BAS
510F
was
investigated
in
a
90 
day
feeding
studies
with
rats,
mice
and
dogs,
and
in
a
28 
day
dermal
administration
study
in
rats.
Additonally
a
90 
day
neurotoxicity
study
in
rats
was
performed.
Generally,
mild
toxicity
was
observed.
At
high
dose
levels
(
doses
above
the
LOAELs)
in
feeding
studies,
all
three
species
displayed
alterations
in
various
clinical
chemistry
parameters.
These
clinical
chemistry
alterations
were
likely
secondary
to
general
toxicity.
Statistically
significant
increased
absolute
and
relative
thyroid
weights
were
observed
in
male
rats
only
at
doses
at
and
above
the
LOAEL.
Increased
absolute
and
relative
liver
weights
were
observed
in
both
sexes
at
doses
above
the
LOAEL
in
rats
and
dogs.
Increased
absolute
and
relative
liver
weights
were
seen
in
both
sexes
of
the
mouse
at
lower
doses.
However,
the
increases
in
liver
weights
at
these
lower
doses
in
the
mouse
were
not
deemed
to
be
compound
related
due
to
the
unusually
low
concurrent
control
liver
weight
values.
At
doses
above
the
LOAELs,
liver
weight
increases
were
supported
by
histopathology
alterations
in
the
rat
and
mouse,
but
not
in
the
dog.
Overall,
only
mild
toxicity
was
observed
in
oral
subchronic
testing.

In
the
28 
day
repeat
dose
dermal
study,
no
systemic
effects
were
noted
up
to
the
highest
dose
tested
of
1,000
mg/
kg
b.
w./
day.
6
In
a
90 
day
rat
neurotoxicity
study,
there
was
no
mortality,
signs
of
clinical
toxicity,
or
adverse
effects
on
food
consumption
or
body
weight
at
any
dose
level
in
either
sex.
No
signs
of
neurotoxicity
were
observed
during
clinical
observations,
functional
observation
batteries,
motor
activity
measurements
of
neuropathology.
Therefore,
there
were
no
selective
neurotoxic
effects.
Adverse
effects
were
not
seen
even
at
the
highest
dose
level
tested.
A
LOAEL
was
not
found
and
the
NOAEL
is
the
highest
tested
of
15,000
ppm
(
1,050
mg/
kg
b.
w./
day
in
males;
1,272
mg/
kg
b.
w./
day
in
females).]

5.
Chronic
toxicity.
[
Based
on
review
of
the
available
data,
the
Reference
Dose
(
RfD)
for
BAS
510F
will
be
based
on
a
1­
year
feeding
study
in
dogs
with
a
NOAEL
of
21.8
mg/
kg
b.
w./
day.
Using
an
uncertainty
factor
of
100,
the
RfD
is
calculated
to
be
0.218
mg/
kg
b.
w./
day.
The
following
are
summaries
of
chronic
toxicity
studies
submitted
to
EPA.

The
chronic
toxicity/
oncogenicity
studies
with
BAS
510F
include
a
12 
month
feeding
study
with
Beagle
dogs,
an
18 
month
B63CF1
mouse
feeding
study,
a
24 
month
Wistar
rat
chronic
feeding
study
and
a
24 
month
Wistar
rat
oncogenicity
study.

At
the
highest
dose
tested
in
dogs,
effects
observed
consisted
primarily
of
increased
liver
and
thyroid
weights
and
some
serum
clinical
chemistry
changes.
The
NOAEL
was
800
ppm
(
21.8
mg/
kg
b.
w./
day
males;
22.1
mg/
kg
b.
w./
day
females).

Decreased
body
weights
were
seen
in
males
in
the
mouse
chronic
study
at
doses
of
8000
ppm
(
1804
mg/
kg
b.
w./
day)
and
above.
Decreased
female
body
weight
was
seen
at
doses
of
2,000
ppm
(
331
mg/
kg
b.
w./
day)
and
above.
The
target
organ
in
this
study
was
the
liver.
The
NOAEL
was
65
and
443
mg/
kg
b.
w./
day
(
8000
and
2000
ppm)
for
male
and
female
mice,
respectively.
In
both
the
rat
chronic
and
oncogenicity
studies,
the
highest
dose
tested
of
15,000
ppm
exceeded
a
maximum
tolerated
dose
(
MTD)
and
was
discontinued
after
17
months.
Effects
observed
at
the
next
highest
dose
of
2,500
ppm
primarily
centered
around
the
thyroid
and
liver.
The
NOAEL
was
23
and
30
mg/
kg
b.
w./
day
(
2500
ppm)
for
male
and
female
rats,
respectively.

Overall,
mild
toxicity
was
observed
with
chronic
exposure
to
BAS
510F.
No
evidence
of
treatment­
induced
oncogenicity
was
observed
in
the
mouse
or
dog
studies.
A
slight
increase
in
thyroid
follicular
cell
adenomas
was
seen
in
both
sexes
at
the
high
dose
when
the
data
from
both
rat
bioassays
are
combined.

A
mode
of
action
(
MOA)
for
the
thyroid
follicular
cell
adenomas
has
been
proposed.
This
MOA
is
based
on
the
EPA
publication
``
Assessment
of
Thyroid
Follicular
Cell
Tumors,"
March
1998,
EPA/
630/
R 
97/
002.
This
document
describes
the
criteria
which
must
be
met
in
order
for
a
compound
to
be
considered
under
the
MOA
described
in
that
publication.
BASF
Corporation
believes
that
BAS
510F
has
met
the
cited
criteria.
7
Threshold
effects.
Based
on
a
review
of
the
available
chronic
toxicity
data,
BASF
believes
EPA
will
establish
the
RfD
for
BAS
510F
at
0.281
mg/
kg
b.
w./
day.
This
RfD
for
BAS
510F
is
based
on
the
2 
year
chronic
and
2 
year
oncogenicity
studies
in
rats
and
the
1
year
dog
study
with
a
the
lowest
threshold
NOAEL
of
21.8
mg/
kg
b.
w./
day
for
males.
Using
an
uncertainty
factor
of
100,
the
RfD
is
calculated
to
be
0.218
mg/
kg
b.
w./
day.
Based
on
the
acute
toxicity
data,
BASF
believes
that
BAS
510F
does
not
pose
any
acute
dietary
risks.

BAS
510F
was
shown
to
be
noncarcinogenic
in
mice
and
dogs.
There
was
a
slight
increase
in
thyroid
follicular
cell
ademonas
at
the
high
dose
in
both
sexes
in
the
rat.
A
threshold
based
MOA
for
these
tumors
based
on
the
EPA
publication
``
Assessment
of
Thyroid
Follicular
Cell
Tumors''
(
EPA/
630/
R 
97/
002,
March,
1998),
has
been
proposed.
BASF
believes
the
data
to
support
this
proposed
mode
of
action
are
strong,
and
that
the
thyroid
tumors
seen
in
the
rat
following
BAS
510F
exposure
have
a
threshold.
In
addition,
a
battery
of
genotoxicity
studies
demonstrated
that
BAS
510F
has
no
genotoxic
or
clastogenic
potential.
Therefore,
BASF
believes
that
the
threshold
approach
to
regulating
BAS
510F
is
appropriate.
Also,
it
should
be
noted
that,
while
the
Agency
has
in
the
past
considered
tumors
of
this
type
to
be
potential
human
carcinogens,
the
European
Union
has
published
a
policy
which
considers
these
tumor
types,
when
they
occur
at
low
incidence
rates
in
the
rat,
to
not
be
relevant
to
man.
(
The
publication:
European
Commission,
European
Chemicals
Bureau,
ECBI/
49/
99
 
Add.
1
Rev.
2;
``
Draft
Summary
Record,
Commission
Group
of
Specialized
Experts
in
the
fields
of
Carcinogenicity,
Mutagenicity
and
Reprotoxicity''
Meeting
at
Arona,
1 
2
September
1999).
Therefore,
BASF
believes
that
these
tumors
are
not
likely
relevant
to
humans
and,
if
these
tumors
are
to
be
considered
relevant
to
humans,
the
threshold
approach
to
cancer
risk
assessment
is
appropriate.]

6.
Animal
metabolism.
[
In
the
rat,
the
predominant
route
of
excretion
of
BAS
510F
is
fecal
with
urinary
excretion
being
minor.
The
half­
life
of
BAS
510F
is
less
than
24
hours.
Saturation
of
absorption
appears
to
be
occurring
at
the
high
dose
level.
BAS
510F
is
rapidly
and
intensively
metabolized
to
a
large
number
of
biotransformation
products.
The
hydroxylation
of
the
diphenyl
moiety
was
the
quantitatively
most
important
pathway.
Second
most
important
was
the
substitution
of
the
Cl
of
the
2­
chloropyridine
part
against
SH
by
conjugation
with
glutathione.
No
major
differences
were
observed.
In
hens
and
goats
the
residues
of
concern
were
determined
to
be
parent,
the
hydroxylated
metabolite
M510
F01
(
2­
chloro­
N­(
4'
chloro­
5­
hydroxy­
biphenyl­
2­
yl)
nicotinamide),
and
the
glucuronic
acid
of
the
metabolite
M510
F02.]

7.
Metabolite
toxicology.
[
No
additional
studies
were
required
for
metabolite
toxicology.]

8.
Endocrine
disruption.
[
No
specific
tests
have
been
conducted
with
BAS
510F
to
8
determine
whether
the
chemical
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen
or
other
endocrine
effects.
However,
there
were
no
significant
findings
in
other
relevant
toxicity
studies
(
i.
e.,
subchronic
and
chronic
toxicity,
teratology
and
multi­
generation
reproductive
studies)
which
would
suggest
that
BAS
510F
produces
endocrine
related
effects.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
An
assessment
was
conducted
to
evaluate
the
potential
risk
due
to
chronic
dietary
exposure
of
the
U.
S.
population
and
sub­
populations
to
residues
of
Boscalid.
Tolerance
values
for
boscalid
(
BAS
510F)
have
previously
been
established
and
are
listed
in
U.
S.
40
CFR
§
180.589.

This
analysis
included
all
crops
with
established
boscalid
tolerance
values,
crops
pending
tolerance
assignment
(
vegetable,
leafy
group
4
at
50
ppm;
almond
hulls
15
ppm;
banana
pulp
0.05;
Belgian
Endive
12
ppm);
and
an
increase
in
tolerance
for
post
harvest
stone
fruit,
crop
group
12
at
9.0
ppm
and
post
harvest
pome
fruit,
crop
group
11
at
8.0
ppm,
strawberry
at
4.0
and
berries,
crop
group
13
at
8.0.]

i.
Food.
[
Acute
Dietary
Exposure
Assessment
An
acute
assessment
was
not
needed
since
the
U.
S.
EPA
Toxicological
Endpoint
Selection
(
TES)
Committees
had
previously
evaluated
the
Boscalid
toxicity
data
and
determined
there
were
no
toxic
effects
attributable
to
a
single
dose.
Therefore,
a
quantitative
acute
dietary
exposure
and
risk
assessment
were
not
required.
Chronic
Dietary
Exposure
Assessment
A
Tier
1
chronic
dietary
exposure
assessment
was
conducted
assuming
tolerance
level
residues,
default
processing
factors,
100%
crop
treated
factors
for
all
crops
and
consumption
data
from
the
USDA
Continuing
Survey
of
Food
Intake
by
Individuals
(
CSFII
1994
­
1996,
1998)
and
the
EPA
Food
Commodity
Ingredient
Database
(
FCID)
using
Exponent's
Dietary
Exposure
Evaluation
Module
(
DEEM­
FCID)
software.
Residues
in
animal
commodities
(
i.
e.
meat,
meat
byproducts,
fat,
milk,
eggs)
were
included
at
the
tolerance
levels
currently
established
and
listed
in
U.
S.
40
CFR
§
180.589.
Water
consumption
(
direct
and
indirect)
was
also
included
in
the
assessment
using
a
chronic
drinking
water
concentration
of
26
ug/
L
(
ppb).

Dietary
exposure
estimates
were
compared
against
the
established
Boscalid
chronic
Population
Adjusted
Dose
(
cPAD)
of
0.218
mg/
kg
b.
w./
day
for
all
populations.
Results
of
the
chronic
dietary
assessments
are
listed
in
the
table
below.
The
estimated
chronic
dietary
exposure
from
crops
and
animal
commodities
was
less
than
59
%
of
the
cPAD
for
all
subpopulations.
Additional
refinements
such
as
the
use
of
anticipated
residues
and
adjusted
crop
treated
factors
would
further
reduce
the
estimated
chronic
dietary
exposure.
The
results
in
Table
1
demonstrate
there
are
no
safety
concerns
for
any
9
subpopulation
based
on
established
and
new
uses,
and
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.]

Table
1.
Summary
of
Chronic
Dietary
Exposure
Assessment
Considering
Crops
with
Established
and
Proposed
Tolerances
for
Boscalid
and
Water
Consumption
(
direct
and
indirect)
Population
Subgroups
Exposure
Estimate
(
mg/
kg
b.
w./
day)
%
cPAD
U.
S.
Population
0.028363
13.01
All
Infants
0.089961
41.27
Children
1­
2
years
0.127038
58.27
Children
3­
5
years
0.083722
38.40
Children
6­
12
years
0.036814
16.89
Youth
13­
19
years
0.018289
8.39
Females
13­
49
years
0.018277
8.38
Adults
20­
49
years
0.020717
9.50
Adults
50+
years
0.018988
8.71
%
cPAD
=
percent
of
chronic
population
adjusted
dose
Exposure
estimates
based
on
tolerance
values,
default
processing
factors,
and
100%
CT
for
all
crops/
commodities.
Drinking
water
concentration
of
26
ppb
used
in
the
assessment.

ii.
Drinking
water.
[
Based
on
PRZM/
EXAMS
and
SCI­
GROW
models,
the
estimated
drinking
water
exposure
concentrations
of
boscalid
for
chronic
exposure
were
26
ppb
for
surface
water
and
0.63
ppb
for
ground
water.
These
drinking
water
concentrations
were
included
used
with
the
direct
and
indirect
water
consumption
and
included
in
the
food
exposure
shown
in
the
Table
1
above.

Acute
Aggregate
Exposure
and
Risk
(
Food
and
water)
Since
the
U.
S.
EPA
Toxicological
Endpoint
Selection
(
TES)
Committees
has
evaluated
the
Boscalid
toxicity
data
and
determined
there
was
no
toxicological
endpoints
for
acute
dietary
exposure,
the
determination
of
an
acute
aggregate
exposure
and
risk
evaluation
was
not
required.

Chronic
Aggregate
Exposure
and
Risk
(
food
and
water)
Using
the
exposure
assumptions
described
in
this
notice
of
filing,
BASF
has
concluded
that
exposure
from
food
and
water
will
utilize
13%
of
the
cPAD
for
the
U.
S.
population,
41%
of
the
cPAD
for
all
infants
(<
1
year
old),
and
58%
of
the
cPAD
for
children
1­
2
years
old.
The
results
demonstrate
that
there
are
no
safety
concerns
for
any
subpopulation
based
on
established
and
new
uses,
and
that
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.
10
In
summary,
we
can
conclude
with
reasonable
certainty
that
no
harm
will
occur
from
chronic
aggregate
exposure
of
Boscalid.

Short­
and
Intermediate
Term
Aggregate
Exposure
and
Risk
(
Food,
Water
and
Residential
Exposure)
Short­
and
intermediate­
term
aggregate
exposure
takes
into
account
residential
exposure
plus
chronic
exposure
from
food
and
water.
Residential
exposure
is
used
to
refer
to
nonoccupational
and
non­
dietary
exposure.
No
new
residential
uses
are
currently
being
registered
for
boscalid
that
would
increase
non­
dietary
exposure.
The
residential
exposure
value
used
in
this
risk
assessment
was
previously
determined
by
the
EPA
(
Federal
Register,
Volume
68,
No
146,
July
30,
2003)
and
considers
dermal
exposure
to
adults
from
the
golf
course
use.
The
exposure
calculated
is
considered
to
be
representative
for
youth
playing
golf
because
youth
and
adults
possess
similar
body
surface
area
to
weight
rations
and
because
the
dietary
exposure
for
youth
(
13­
19
years
old)
is
less
than
that
of
the
general
US
population.
The
calculated
exposure
from
golf
course
use
is
0.0008
mg/
kg
bw/
day.
The
aggregate
short­
and
intermediate
term
exposure
included
chronic
food
exposure,
chronic
water
exposure,
and
golf
course
use
exposure.
The
aggregate
exposure
was
0.029163
mg/
kg
bw/
day.
This
exposure
value
was
compared
the
cPAD
to
derived
a
%
cPAD
ultilization.
The
short­
and
intermediate
term
exposure
will
utilize
only
13.4
%
of
the
cPAD
for
the
U.
S.
population.
The
results
demonstrate
that
there
are
no
safety
concerns
for
any
subpopulation
based
on
established
and
new
uses,
and
that
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.
In
summary,
we
can
conclude
with
reasonable
certainty
that
no
harm
will
occur
from
short­
and
intermediate
term
aggregate
exposure
of
Boscalid.]

2.
Non­
dietary
exposure.
[
No
new
residential
uses
are
currently
being
registered
for
boscalid
that
would
increase
non­
dietary
exposure.
A
non­
occupational
dermal
postapplication
exposure/
risk
assessment
for
individuals
golfing
and
harvesting
fruit
at
"
UPick
farms
and
orchards
was
previously
conducted
by
EPA
(
Federal
Register,
Volume
68,
No
146,
July
30,
2003).
Because
U­
Pick
is
a
one­
time
event
(
duration
<
1
day)
and
the
EPA
found
that
the
oral
studies
indicated
there
were
no
endpoints
appropriate
to
quantitate
acute
risk.
Therefore,
only
the
golfing
scenario
was
evaluated
with
respect
to
nonoccupational
non­
dietary
exposure.
The
dermal
MOE's
for
adults
playing
golf
were
27,000
 
74,000.
Although
specific
MOE's
were
not
calculated
for
youths
playing
golf,
the
adult
MOEs
are
considered
representative
since
the
body
surface
area
to
weight
ratios
for
adolescents
do
not
vary
significantly
from
those
of
adults.]

D.
Cumulative
Effects
[
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".
BAS
510F
is
a
foliar
fungicide
chemically
belonging
to
the
carboxin
class
of
fungicides.
BAS
510F
acts
in
the
fungal
cell
by
inhibiting
11
mitochondrial
respiration
through
inhibition
of
the
succinate­
ubiquinone
oxidase
reductase
system
in
Complex
II
of
the
mitochondrial
electron
transport
chain.
BAS
510F
shares
this
mode
of
action
with
only
one
other
currently
registered
U.
S.
pesticide
­
carboxin.

The
EPA
is
currently
developing
methodology
to
perform
cumulative
risk
assessments.
At
this
time,
there
is
no
available
data
to
determine
whether
BAS
510F
has
a
common
mechanism
of
toxicity
with
other
substances
or
how
to
include
this
pesticide
in
a
cumulative
risk
assessment.
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
BAS
510F
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.]

E.
Safety
Determination
1.
U.
S.
population.
[
Using
the
conservative
exposure
assumptions
described
above
and
based
on
the
completeness
and
the
reliability
of
the
toxicity
data,
BASF
has
estimated
that
dietary
exposure
(
food
and
water)
to
BAS
510F
will
utilize
13%
of
the
cPAD
for
the
U.
S.
population.
The
aggregate
exposure
including
food,
water,
and
residential
(
golf)
exposure
to
boscalid
will
utilize
13.4%
of
the
cPAD.
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
the
aggregate
exposure
to
residues
of
BAS
510F,
including
anticipated
dietary
and
drinking
water
exposures
and
golf
course
use
exposures.]

2.
Infants
and
children.
[
Using
the
conservative
exposure
assumptions
described
above
and
based
on
the
completeness
and
the
reliability
of
the
toxicity
data,
BASF
has
estimated
that
dietary
exposure
(
food
and
water)
to
BAS
510F
will
utilize
58
%
of
the
cPAD
for
children
subgroup
(
children
1­
2
years
of
age)
and
41%
of
the
cPAD
for
infants
(<
1
year
old).
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
to
infants
or
children
will
result
from
the
aggregate
exposure
to
residues
of
BAS
510F,
including
anticipated
dietary
and
drinking
water
exposures
and
non­
occupational
exposures.]

F.
International
Tolerances
[
A
maximum
residue
level
(
MRL)
has
not
been
established
for
Boscalid
(
BAS
510F)
in
any
crop
by
the
Codex
Alimentarius
Commission.]