Document ID: EPA-HQ-OPP-2005-0542-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-03-22T05:00Z

Interregional
Research
Project
No.
4
3E6543,
3E6561,
3E6760,
3E6738,
5E6920,
5E6921,
5E6922,
5E6923
EPA
has
received
the
following
pesticide
petitions
(
3E6543,
3E6561,
3E6760,
3E6738,
5E6920,
5E6921,
5E6922,
5E6923)
from
[
Interregional
Research
Project
No.
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
180.472,
by
establishing
a
tolerance
for
residues
of
[
imidacloprid,
1­[(
6­
chloro­
3­
pyridinyl)
methyl]­
N­
nitro­
2­
imidazolidinimine]
in
or
on
the
following
raw
agricultural
commodities:

1.
PP
5E6920
establishing
tolerances
for
imidacloprid
residues
on
tree
nut,
group
14
at
0.01
parts
per
million;
almond
hulls
at
2.5
parts
per
million
(
ppm);
and
pistachio
at
0.01
ppm.

2.
PP
5E6923
establishing
tolerances
for
imidacloprid
residues
on
herbs,
subgroup
19­
A
fresh
at
6.0
ppm
and
dried
at
62
ppm
3.
PP
5E6921
establishing
a
tolerance
for
imidacloprid
residues
on
pomegranates
at
0.7
ppm
4.
PP
5E6922
establishing
a
tolerance
for
imidacloprid
residues
on
banana
at
0.6
ppm
5.
PP
3E6561
establishing
a
tolerance
for
imidacloprid
residues
on
coffee
at
0.6
ppm
6.
PP
3E6738
establishing
tolerances
for
imidacloprid
residues
on
rapeseed,
seed
at
0.05
ppm;
Indian
rapeseed,
seed
at
0.05
ppm;
Indian
mustard,
seed
at
0.05
ppm;
field
mustard,
seed
at
0.05
ppm;
black
mustard,
seed
at
0.05
ppm;
flax,
seed
at
0.05
ppm;
safflower,
seed
at
0.05
ppm;
crambe,
seed
at
0.05
ppm;
borage,
seed
at
0.05
ppm;
and
sunflower,
seed
at
0.05
ppm.

7.
PP
3E6543
establishing
a
tolerance
with
regional
registrations,
as
defined
in
40
CFR
180.1,
for
imidacloprid
residues
on
caneberry
subgroup
13­
A
at
0.05
ppm.

8.
PP
3E6760
establishing
tolerances
for
imidacloprid
residues
on
sugar
apple
at
0.2
ppm;
cherimoya
at
0.2
ppm;
atemoya
at
0.2
ppm;
custard
apple
at
0.2
ppm;
ilama
at
0.2
ppm;
soursop
at
0.2
ppm;
and
biriba
at
0.2
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
and
large
animal
metabolism.
[
The
nature
of
the
imidacloprid
residue
in
plants
and
livestock
is
adequately
understood.
The
residues
of
concern
are
combined
residues
of
imidacloprid
and
it
metabolites
containing
the
6
chloropyridinyl
moiety,
all
calculated
as
imidacloprid.]

2.
Analytical
method.
[
The
analytical
method
is
a
common
moiety
method
for
imidacloprid
and
its
metabolites
containing
the
6
chloropyridinyl
moiety
using
a
permanganate
oxidation,
silyl
derivatization,
and
capillary
GC
MS
selective
ion
monitoring.
This
method
has
successfully
passed
a
petition
method
validation
in
EPA
labs.
There
is
a
confirmatory
method
specifically
for
imidacloprid
and
several
metabolites
utilizing
GC/
MS
and
HPLC
UV
which
has
been
validated
by
the
EPA
as
well.
Imidacloprid
and
its
metabolites
are
stable
for
at
least
24
months
in
the
commodities
when
frozen.]

3.
Magnitude
of
residues.
Residue
trials
have
been
conducted
to
support
the
requested
tolerances
on
the
above
crops.
­
[
Tree
nut
crop
group
14]:
IR­
4
has
received
requests
from
California
for
tree
nuts.
Ten
field
trials
(
five
almond
and
five
pecan)
were
performed
on
tree
nuts
to
support
the
proposed
tolerance
of
0.01
ppm
on
tree
nuts,
group
14
and
pistachio
as
well
as
a
tolerance
of
2.5
ppm
on
almond
hulls.
­
[
Herb
subgroup]:
Seven
field
trials
were
conducted
throughout
the
USA
to
support
the
proposed
tolerance
of
6
ppm
for
fresh
herbs
and
62
ppm
for
dried
herbs.
­
[
Pomegranates]:
Three
field
trials
were
conducted
on
pomegranates
to
support
the
proposed
tolerance
of
0.7
ppm
for
pomegranates.
­
[
Bananas]:
Five
trials
were
conducted
on
bananas
to
support
the
proposed
tolerance
of
0.6
ppm
on
bananas.
­
[
Coffee]:
Five
field
trials
were
conducted
in
coffee
to
support
the
proposed
tolerance
of
0.6
ppm
on
coffee.
­
[
Sunflower]:
Six
field
trials
were
conducted
in
sunflower
to
support
the
proposed
tolerance
of
0.05
ppm
on
rapeseed,
Indian
rapeseed,
Indian
mustard,
field
mustard,
black
mustard,
flax,
safflower,
crambe,
borage
and
sunflower
seed.
­
[
Raspberry]:
Two
trials
were
conducted
in
raspberries
to
support
the
proposed
tolerance
of
0.05
ppm
in
the
caneberry
subgroup,
13­
A
as
well
as
juneberry,
lingonberry
and
salal.
­
[
Sugar
Apple]:
Three
trials
were
conducted
in
sugar
apples
to
support
the
proposed
tolerance
of
0.2
ppm
in
tropical
fruit
(
sugar
apple,
cherimoya,
atemoya,
custard
apple,
ilama,
soursop
and
biriba).

B.
Toxicological
Profile
1.
Acute
toxicity.
Imidacloprid
has
low
acute
toxicity
via
the
dermal
and
inhalation
routes
and
moderate
acute
toxicity
via
the
oral
route.
The
acute
oral
LD50
value
for
imidacloprid
technical
was
found
to
be
424
mg/
kg
for
male
rats
and
>
450
mg/
kg
for
female
rats.
The
acute
dermal
LD50
is
>
5000
mg/
kg
and
the
4
hour
rat
inhalation
LC50
is
>
5.33
mg/
L
in
the
rat.
Imidacloprid
is
not
irritating
to
rabbit
skin
or
eyes.
Imidacloprid
did
not
cause
skin
sensitization
in
guinea
pigs.
2.
Genotoxicty.
Imidacloprid
has
been
evaluated
for
genotoxicity
using
in
vivo
and
in
vitro
tests,
including
mammalian
cell
gene
mutation
tests,
chromosomal
aberration
tests,
unscheduled
DNA
synthesis
tests,
bacterial
DNA
repair
tests
and
other
mutagenicity
studies.
The
weight
of
evidence
shows
that
imidacloprid
is
not
mutagenic.

3.
Reproductive
and
developmental
toxicity.
In
a
developmental
toxicity
study
with
Sprague
Dawley
rats,
pregnant
animals
received
an
oral
administration
of
imidacloprid
at
0,
10,
30,
or
100
mg/
kg/
day
during
gestation.
The
maternal
NOAEL
was
10
mg/
kg/
day
based
on
decreased
body
weight
gain
and
the
fetal
NOAEL
was
30
mg/
kg/
day
based
on
a
slight
increase
in
the
incidence
of
wavy
ribs
in
the
presence
of
maternal
toxicity.

In
a
developmental
toxicity
study
with
rabbits,
pregnant
animals
were
given
oral
doses
of
imidacloprid
at
0,
8,
24,
or
72
mg/
kg
bwt/
day
during
gestation.
For
maternal
toxicity,
the
NOAEL
was
24
mg/
kg
/
day
and
the
LOEL
was
72
mg/
kg/
day
based
on
mortality,
decreased
body
weight
gain,
and
decreased
food
consumption.
For
developmental
toxicity,
the
NOAEL
was
24
mg/
kg
bwt/
day
and
the
LOAEL
was
72
mg/
kg
bwt/
day
based
on
decreased
fetal
body
weight
and
increased
resorptions.

In
a
2
generation
reproductive
toxicity
study,
imidacloprid
was
administered
to
rats
at
dietary
levels
of
0,
100,
250,
or
700
ppm.
For
parental/
systemic
toxicity,
the
NOAEL
was
250
ppm
(
16.5
mg/
kg/
day)
and
the
LOAEL
was
700
ppm
based
on
decreased
body
weight
in
both
sexes.
The
reproductive
NOAEL
was
the
highest
dose
tested,
700
ppm.

4.
Subchronic
toxicity.
In
a
dermal
toxicity
study,
groups
of
5
male
and
5
female
New
Zealand
White
rabbits
received
repeated
dermal
applications
of
imidacloprid
at
1,000
mg/
kg
body
weight/
day
,
6
hours/
day,
5
days/
week
for
3
weeks.
No
dermal
or
systemic
toxicity
was
seen.
For
systemic
and
dermal
toxicity,
the
no
observable
adverse
effect
level
(
NOAEL)
was
>
1,000
mg/
kg/
day.

5.
Chronic
toxicity.
A
chronic
toxicity/
carcinogenicity
study
was
performed
with
imidacloprid
administered
to
male
and
female
rats
for
two
years
at
dietary
levels
of
100,
300,
900
or
1800
ppm.
There
was
no
evidence
of
carcinogenicity.
At
300
ppm,
there
was
an
increased
incidence
of
mineralized
particles
in
thyroid
colloid
of
male
rats.
The
NOAEL
was
100
ppm
(
5.7
mg/
kg/
day
for
males
and
7.6
mg/
kg/
day
for
females).

The
oncogenic
potential
of
imidacloprid
was
investigated
in
B6C3F1
mice.
Dietary
doses
were
0,
100,
330,
1000
or
2000
ppm.
Decreased
body
weights,
decreased
food
consumption
and
hepatocellular
hypertrophy
were
seen
at
the
highest
dose
level.
There
was
no
evidence
of
carcinogenicity.
The
NOAEL
was
2000
ppm
(
208
mg/
kg
for
males
and
274
for
females).

6.
Animal
metabolism.
[
The
metabolism
of
NTN
33893
(
imidacloprid)
in
rats
was
reported
in
seven
studies.
These
data
show
that
imidacloprid
was
rapidly
absorbed
and
eliminated
in
the
excreta
(
90%
of
the
dose
within
24
hours),
demonstrating
no
biologically
significant
differences
between
sexes,
dose
levels,
or
route
of
administration.
Elimination
was
mainly
renal
(
70
80%
of
the
dose)
and
fecal
(
17
25%).
The
major
part
of
the
fecal
activity
originated
in
the
bile.
Total
body
accumulation
after
48
hours
consisted
of
0.5%
of
the
radioactivity
with
the
liver,
kidney,
lung,
skin
and
plasma
being
the
major
sites
of
accumulation.
Therefore,
bioaccumulation
of
imidacloprid
is
low
in
rats.
Maximum
plasma
concentration
was
reached
between
1.1
and
2.5
hours.
Two
major
routes
of
biotransformation
were
proposed
for
imidacloprid.
The
first
route
included
an
oxidative
cleavage
of
the
parent
compound
rendering
6
chloronicotinic
acid
and
its
glycine
conjugate.
Dechlorination
of
this
metabolite
formed
the
6
hydroxynicotinic
acid
and
its
mercapturic
acid
derivative.
The
second
route
included
the
hydroxylation
followed
by
elimination
of
water
of
the
parent
compound
rendering
NTN
35884.
A
comparison
between
[
methylene
14C]
imidacloprid
and
[
imidazolidine
4,5
14C]
imidacloprid
showed
that
while
the
rate
of
excretion
was
similar,
the
renal
portion
was
higher
with
the
imidazolidine
labeled
compound.
In
addition,
accumulation
in
tissues
was
higher
with
the
imidazolidine
labeled
compound
(
approximately
1%
of
the
recovered
radioactivity).

7.
Metabolite
toxicology.
[
NA­
Remove]

8.
Endocrine
disruption.
[
The
toxicology
database
for
imidacloprid
is
current
and
complete.
Studies
in
this
database
include
evaluation
of
the
potential
effects
on
reproduction
and
development,
and
an
evaluation
of
the
pathology
of
the
endocrine
organs
following
short­
or
long
term
exposure.
These
studies
revealed
no
primary
endocrine
effects
due
to
imidacloprid.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
Assessments
were
conducted
to
evaluate
potential
risks
due
to
chronic
and
acute
dietary
exposure
of
the
U.
S.
population
and
selected
population
subgroups
to
residues
of
imidacloprid.
These
analyses
cover
all
registered
and
pending
uses
for
imidacloprid
including
the
above
listed
crops
(
i.
e.,
tree
nuts,
pistachio,
herb
subgroup,
caneberry
subgroup,
pomegranate,
bananas,
coffee,
rapeseed,
Indian
rapeseed,
Indian
mustard,
field
mustard,
black
mustard,
flax,
safflower,
crambe,
borage,
sunflower,
sugar
apple,
cherimoya,
atemoya,
custard
apple,
ilama,
soursop
and
biriba.

Novigen
Sciences,
Inc.'
s
Dietary
Exposure
Evaluation
Model
(
DEEM­
FCID
 
)
,
which
is
licensed
to
Bayer,
was
used
to
estimate
the
chronic
and
acute
dietary
exposure.
This
software
uses
the
food
consumption
data
from
the
1994­
1998
USDA
Continuing
Surveys
of
Food
Intake
by
Individuals
(
CSFII
1994­
1998).

The
endpoint
for
acute
dietary
risk
assessments
is
based
on
neurotoxicity
characterized
by
decreases
in
motor
or
locomotor
activity
in
female
rats
at
42
mg/
kg
bwt/
day
(
LOEL)
from
an
acute
neurotoxicity
study.
Based
on
an
uncertainty
factor
of
10x
for
inter­
species,
10x
for
intra­
species
and
3x
for
use
of
a
LOAEL
rather
than
a
NOAEL,
EPA
has
established
an
acute
reference
dose
(
aRfD)
=
0.14
mg/
kg
bwt/
day.

For
chronic
dietary
analyses,
EPA
has
established
the
reference
dose
(
cRfD)
for
imidacloprid
at
0.057
mg/
kg/
day
based
on
a
NOAEL
of
5.7
mg/
kg
bwt/
day
from
a
rat
chronic
toxicity
carcinogenicity
study
and
uncertainty
factors
of
10x
for
inter­
species
and
10x
for
intra­
species.
Results
from
the
acute
and
chronic
dietary
exposure
analyses
described
below
demonstrate
a
reasonable
certainty
that
no
harm
to
the
overall
U.
S.
population
or
any
population
subgroup
will
result
from
the
use
of
imidacloprid
on
currently
registered
and
pending
uses.]

i.
Food.
[
Tier
3
acute
and
chronic
risk
assessments
were
conducted
using
PDP
data
or
the
results
of
field
trials
conducted
at
maximum
label
application
rates
and
the
shortest
pre­
harvest
intervals.
No
adjustments
were
made
to
account
for
dissipation
of
residues
during
storage,
transportation
from
the
field
to
the
consumer,
washing
or
peeling.
Therefore,
the
actual
dietary
exposure
will
be
less
than
that
presented
here.

For
the
chronic
analysis,
mean
field
trial
residues
were
calculated.
For
the
acute
Monte
Carlo
analysis,
the
entire
distribution
of
residue
field
trial
data
was
used
for
the
"
non­
blended"
and
"
partially
blended"
foods
as
determined
by
EPA's
HED
SOP
99.6.
For
the
foods
considered
as
"
blended"
by
EPA'S
HED
SOP
99.6,
mean
field
trial
residue
data
were
used.
As
allowed
in
EPA's
draft
guidance
for
submission
of
probabilistic
human
health
exposure
assessments
one
half
LOD/
LOQ
values
were
used
for
all
non­
detected
values
(
values
below
the
sensitivity
of
the
method).
The
acute
Monte
Carlo
dietary
exposure
assessment
estimated
the
percent
of
the
aPAD
and
corresponding
margins
of
exposure
(
MOE)
for
the
overall
U.
S.
population,
(
all
seasons),
and
various
subpopulations.
In
this
analysis,
the
exposure
for
the
total
U.
S.
population
was
equal
to
9.4%
of
the
aPAD
at
the
99.9th
percentile.
The
most
highly
exposed
population
subgroup,
children
(
1­
2
yrs),
had
an
exposure
equal
to
27.1%
of
the
aPAD
at
the
99.9th
percentile.
Therefore,
the
acute
dietary
exposure
estimates
are
below
EPA's
level
of
concern
for
the
overall
U.
S.
population
as
well
as
the
various
subpopulations.

The
chronic
dietary
exposure
estimated
the
percent
of
the
chronic
population
adjusted
dose
(
cPAD)
for
the
overall
US
population
(
all
seasons)
and
various
subpopulations.
In
this
analysis,
the
exposure
for
the
total
U.
S.
population
was
equal
to
1.2%
of
the
cPAD.
The
most
highly
exposed
population
subgroup,
children
(
1
2
yrs),
had
an
exposure
equal
to
2.5%
of
the
cPAD.
Therefore,
the
chronic
exposure
estimates
are
below
EPA's
level
of
concern
for
the
overall
U.
S.
population
as
well
as
the
various
subpopulations.]

ii.
Drinking
water.
[
EPA,
as
published
in
the
Federal
Register
(
68
FR
35303­
35315),
calculated
EECs
for
surface
water
(
acute
36.04
ppb
and
chronic
17.24
ppb)
and
ground
water
(
acute
and
chronic
both
2.09
ppb).
Since
the
maximum
application
rate
(
single
and
seasonal)
for
the
new
uses
do
not
exceed
previously
established
use
rates,
these
EECs
are
still
valid
for
the
new
uses.
The
current
exposure
assessment
calculated
acute
and
chronic
DWLOCs
at
1021
ppb
and
556
ppb,
respectively,
for
the
most
exposed
subpopulation
(
children
1­
2
yrs).
Since
the
DWLOCs
are
significantly
larger
than
the
EECs,
there
is
no
concern
with
dietary
exposure
to
residues
of
imidacloprid
for
even
the
most
exposed
subpopulation.]

2.
Non­
dietary
exposure.
[
Imidacloprid
is
currently
registered
for
use
on
the
following
residential
non­
dietary
sites:
Granular
products
for
application
to
lawns
and
ornamental
plants;
ready­
to­
use
spray
for
application
to
flowers,
shrubs
and
house
plants;
plant
spikes
for
application
to
indoor
and
outdoor
residential
potted
plants;
ready­
to­
use
potting
medium
for
indoor
and
outdoor
plant
containers;
liquid
concentrate
for
application
to
lawns,
trees,
shrubs
and
flowers;
and
ready­
to­
use
liquid
for
directed
spot
application
to
cats
and
dogs.
In
addition,
there
are
numerous
registered
products
intended
for
use
by
commercial
applicators
to
residential
sites.
These
include
gel
baits
for
cockroach
control;
products
intended
for
commercial
ornamental,
lawn
and
turf
pest
control;
products
for
ant
control;
and
products
used
as
preservatives
for
wood
products,
building
materials,
textiles
and
plastics.
The
non­
dietary
exposure
assessment
is
discussed
in
the
Final
Rule
on
Imidacloprid
Pesticide
Tolerance
published
in
Unit
III.
C.
3.
of
the
Federal
Register
of
June
13,
2003
(
68
FR
35303).]

D.
Cumulative
Effects
[
Imidacloprid
is
a
chloronicotinyl
insecticide.
At
this
time,
the
EPA
has
not
made
a
determination
that
imidacloprid
and
other
substances
that
may
have
a
common
mechanism
of
toxicity
would
have
cumulative
effects.
Therefore,
for
these
tolerance
petitions,
it
is
assumed
that
imidacloprid
does
not
have
a
common
mechanism
of
toxicity
with
other
substances
and
only
the
potential
risks
of
imidacloprid
in
its
aggregate
exposure
are
considered.]

E.
Safety
Determination
1.
U.
S.
population.
[
Using
the
conservative
exposure
assumptions
described
above
and
based
on
the
completeness
of
the
toxicity
data,
it
can
be
concluded
that
aggregate
exposure
to
residues
of
imidacloprid
present
a
reasonable
certainty
of
no
harm.
Exposure
from
residues
in
crops
utilizes
9.4%
of
the
aPAD
and
1.2%
of
the
cPAD.
EPA
generally
has
no
concerns
for
exposures
below
100%
of
the
Population
Adjusted
Doses.
Drinking
water
levels
of
concern
are
well
above
the
estimated
drinking
water
concentrations
as
calculated
by
conservative
models.
An
aggregate
assessment
for
all
uses
for
imidacloprid
demonstrated
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
the
US
Population
from
uses
of
imidacloprid.]

2.
Infants
and
children.
[
EPA
has
considered
data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
2
generation
reproduction
study
in
the
rat.
These
studies
are
discussed
under
Section
B
(
Toxicology
Profile)
above.
The
developmental
toxicity
data
demonstrated
no
increased
sensitivity
of
rats
or
rabbits
to
in
utero
exposure
to
imidacloprid.
In
addition,
the
multi
generation
reproductive
toxicity
study
did
not
identify
any
increased
sensitivity
of
rats
to
in
utero
or
post
natal
exposure.
Parental
NOAELs
were
lower
or
equivalent
to
developmental
or
offspring
NOAELs.
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.

FFDCA
section
408
provides
that
EPA
shall
apply
an
additional
tenfold
margin
of
safety
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
pre
and
post
natal
toxicity
and
the
completeness
of
the
data
base
unless
EPA
determines
that
a
different
margin
of
safety
will
be
safe
for
infants
and
children.
EPA
has
determined
that
the
toxicological
database
is
complete
for
FQPA
purposes
and
that
there
are
no
residual
uncertainties
for
pre­/
post­
natal
toxicity
for
imidacloprid.
Based
on
the
available
toxicity
data
the
EPA
has
recommended
that
the
Special
FQPA
Safety
Factor
be
reduced
to
1x.

Based
on
the
exposure
assessments
described
above
and
on
the
completeness
and
reliability
of
the
toxicity
data,
it
can
be
concluded
that
the
dietary
exposure
from
all
label
and
pending
uses
of
imidacloprid
consumes
27.1%
of
the
aPAD
at
the
99.9th
percentile
and
2.5%
of
the
cPAD
for
the
most
sensitive
population
subgroup,
children
1­
2
years.
Thus,
it
can
be
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
imidacloprid
residues.]

F.
International
Tolerances
[
Imidacloprid
is
a
insecticide
used
throughout
the
world
to
control
insect
pests
in
crops,
trees,
ornamental
plants
and
turf.
An
evaluation
of
the
maximum
residue
limits
(
MRLs)
was
conducted
No
CODEX
Maximum
Residue
Levels
(
MRLs)
have
been
established
for
residues
of
imidacloprid
on
any
crops.]

Commodity
Proposed
Tolerance
(
USEPA)
(
PPM)
Current
MRL
(
CODEX)
(
PPM)

Tree
nut
crop
group
14
0.01
0.05
(
pecan)

Pistachio
0.01
­­

Herb
subgroup
19­
A
6.0
(
fresh)
­­

Herb
subgroup
19­
A
62
(
dried)
­­

Pomegranates
0.7
­­

Banana
0.6
0.05
Coffee
0.6
­­

Rapeseed,
seed
0.05
0.05
Indian
rapeseed,
seed
0.05
­­

Indian
mustard,
seed
0.05
­­

Field
mustard,
seed
0.05
­­

Black
mustard,
seed
0.05
­­

Flax,
seed
0.05
­­
Safflower,
seed
0.05
­­

Crambe,
seed
0.05
­­

Borage,
seed
0.05
­­

Sunflower,
seed
0.05
­­

Caneberry
subgroup
13­
A
0.05
­­

Juneberry
0.05
­­

Lingonberry
0.05
­­

Salal
0.05
­­

Sugar
apple
0.2
­­

Cherimoya
0.2
­­

Atemoya
0.2
­­

Custard
apple
0.2
­­

Ilama
0.2
­­

Soursop
0.2
­­

Biriba
0.2
­­