Interregional
Research
Project
Number
4
(
IR­
4)

2E6438
EPA
has
received
a
pesticide
petition
([
2E6438])
from
[
Interregional
Research
Project
Number
4
(
IR­
4),
Rutgers,
The
State
University
of
New
Jersey,
681
U.
S.
Highway
No.
1
South,
North
New
Brunswick,
NJ
08902,
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
by
establishing
a
tolerance
for
residues
of
diuron,
(
3­(
3,4­
dichlorophenyl)­
1,1­
dimethylurea)
in
or
on
the
raw
agricultural
commodities
mint
at
2.0
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.
The
metabolism
of
diuron
in
plants
and
animals
from
the
results
of
wheat,
corn,
orange,
ruminant,
and
poultry
studies
together
with
the
environmental
fate
studies
conducted
in
soil
and
water
and
has
identified
the
following
14C­
containing
residues
in
plants:
diuron,
3,4­
dichlorophenylurea
(
DCPU),
and
3­(
3,4­
dichlorophenyl)­
1­
methylurea
(
DCPMU).
No
other
dichloroaniline­
containing
metabolites
were
identified.
The
majority
of
radioactivity
in
the
aqueous/
organic
fractions
was
characterized
as
polar
unknowns.
Radiovalidation
of
a
GC/
ECD
data
collection
method,
which
is
similar
to
the
enforcement
method,
suggested
that
a
good
portion
of
these
polar
metabolites
can
be
converted
to
3,4­
DCA.

2.
Analytical
method.
An
analytical
method
is
available,
a
modified
form
of
DuPont
Agricultural
Products
method
#
5470.
The
principle
of
the
determination
is
the
hydrolysis
of
diuron
and
its
metabolites
by
alkaline
reflux
to
3,4­
dichloroanaline
(
3,4­
DCA),
followed
by
a
distillation
of
the
aniline
into
an
acid
solution.
The
acid
distillate
is
made
alkaline
with
concentrated
base
and
subsequently
extracted
into
an
organic
solvent
(
hexane)
and
analyzed
by
gas
chromatography.
With
the
modified
method,
recoveries
exceeded
70%
and
the
limit
of
quantitation
(
LOQ)
is
0.01
<
greek­
m>
g/
g.

3.
Magnitude
of
residues.
One
field
trial
was
conducted
on
a
9
½
year
oil
mint
field
with
a
loam
soil
type.
Treatments
were
made
on
April
7,
1993
using
a
CO2
backpack
sprayer
equipped
with
6
Flat
Fan
8003
nozzles.
Treatments
consisted
of
a
1x
rate
of
2.4
lb
active,
1.5x
rate
of
3.6
lb
active,
and
a
2x
rate
of
4.8
lb
active.
Control
plots
were
located
800
feet
away
from
treated
plots
in
the
same
field.
The
mint
was
cut
on
August
9
and
allowed
to
dry
in
the
field
until
August
11
or
12
for
collection.
Control
plants
were
collected
on
August
11
and
a
portion
of
the
samples
were
distilled
into
oil
on
the
same
day.
Plants
from
plots
treated
with
the
3.6
lb
active
rate
of
diruon
were
collected
on
August
12
and
distilled
into
oil
on
the
same
day.
The
protocol
specified
to
collect
samples
from
the
highest
rate
that
did
not
result
in
excessive
herbicide
injury
to
the
mint
plants.
Samples
were
processed
into
oil
within
4
hours
of
collection.
All
samples
were
placed
in
frozen
storage
at
0
F
until
being
shipped
by
ACDS
freezer
truck
on
August
20,
1993.
All
samples
were
received
frozen
at
the
laboratory
and
retained
in
frozen
storage.
Bulk
forage
samples
were
ground
with
dry
ice
and
returned
to
frozen
storage.
One
freezer
failure
was
reported,
however,
the
maximum
temperature
recorded
was
­
13
C.
The
maximum
period
from
harvest
to
analysis
was
641
days.
The
method
used
for
analysis
was:
Morse
Laboratories,
Inc.
SOP#
Meth­
65,
Revision
#
3,
"
Determination
of
Substituted
Urea
Herbicides,
Linuron,
Diuron,
and
their
metabolites
in
Soil
and
Agricultural
Products",
August
1993.
Method
validation
recoveries
at
0.05,
0.5,
and
5.0
ppm,
ranged
from
64
to
73%
(
averaging
70%
n=
11)
on
hay
and
ranged
from
77
to
90%
(
averaging
81%
n=
9)
on
mint
oil.
Two
recovery
samples
were
extracted
and
analyzed
concurrently
with
the
field
treated
samples,
concurrent
recovery
for
hay
samples
were
71
to
73%
for
0.05
and
5.0,
respectively
and
81
and
77%
at
0.05
and
0.5
ppm,
respectively,
for
oil
samples.
No
diuron
residues
were
recovered
at
or
above
the
reliable
limit
of
quantitation
of
0.05
ppm,
from
any
of
the
control
forage
or
oil
samples.
Residue
in
the
treated
forage
samples
ranged
from
0.143
to
0.212
ppm
and
from
0.0605
to
0.0619
ppm
in
the
oil
samples.
Therefore,
diuron
residues
did
not
concentrate
when
the
mint
samples
were
distilled
into
oil.
The
nature
of
the
residues
is
adequately
understood
and
an
adequate
analytical
method
is
available
for
enforcement
purposed.
Based
on
the
above
information,
retaining
this
tolerance
would
protect
the
public
health
and
would
not
expose
man
or
the
environment
to
unreasonable
adverse
effects.

B.
Toxicological
Profile
1.
Acute
toxicity.
Diuron
has
low
acute
toxicity
(
Toxicity
Category
3
or
4)
by
the
oral,
dermal,
or
inhalation
exposure
routes.
Diuron
is
not
an
eye
or
skin
irritant,
and
not
a
skin
sensitizer.
A
rat
metabolism
study
indicated
that
diuron
is
rapidly
absorbed
and
metabolized
within
24
hours
post­
dose
at
the
low
dose
and
within
48
hours
post­
dose
at
the
high
dose.
The
urine
is
the
major
route
of
excretion
in
both
sexes.
A
small
amount
of
diuron
is
detected
in
the
feces.
The
highest
tissue
residue
levels
were
found
in
the
liver
and
kidneys
4
days
post
14C­
diuron
dose.
The
metabolism
of
diuron
involved
N­
oxidation,
some
ring
hydroxylation,
demethylation,
dechlorination,
and
conjugation
to
sulfate
and
glucuronic
acid.

2.
Genotoxicty.

i.
Salmonella
typhimurium
reverse
gene
mutation
assay
(
MRID#
00146608/
40228805):
Independent
trials
were
negative.

ii.
Chinese
Hamster
Ovary
(
CHO)/
HGPRT)
cell
forward
gene
mutation
assay
(
MRID#
00146609):
Independent
tests
were
negative
up
to
cytotoxic
doses
with/
without
S9
activation.
3.
Reproductive
and
developmental
toxicity.
There
is
an
acceptable
developmental
toxicity
study
in
rabbits
and
an
acceptable
two­
generation
reproduction
study
in
rats.
A
developmental
toxicity
study
in
rats
was
classified
as
unacceptable
due
to
deficiencies
in
analytical
data
on
the
sample
analysis;
however,
the
Agency
considered
the
developmental
toxicity
study
in
rats
adequate
for
the
FQPA
susceptibility
assessment
based
on
the
observation
that
the
developmental
toxicity
NOAEL
was
higher
than
the
maternal
NOAEL
and
concluded
that
a
developmental
neurotoxicity
(
DNT)
study
is
not
required.
There
is
no
indication
of
increased
susceptibility
to
young
exposed
to
diuron
in
the
available
studies.
In
the
developmental
toxicity
study
in
rabbits,
there
were
no
developmental
effects
at
the
highest
dose
tested.
In
the
developmental
toxicity
study
in
rabbits
and
in
the
2­
generation
rat
reproduction
study,
developmental/
offspring
effects
were
observed
only
at
maternally/
parentally
toxic
dose
levels.

4.
Subchronic
toxicity.
The
primary
diuron
target
sites
are
blood,
bladder,
and
kidney.
Erythrocyte
(
red
blood
cell)
damage
resulted
in
hemolytic
anemia
and
compensatory
hematopoiesis,
which
are
manifested
as
significantly
decreased
erythrocyte
counts,
hemoglobin
levels,
and
hematocrit,
and
increased
mean
corpuscular
volume
(
MCV),
mean
corpuscular
hemoglobin
(
MCH),
abnormal
erythrocyte
forms,
reticulocyte
counts,
and
leukocyte
count.
Consistent
observations
of
erythocytic
regeneration
are
seen
in
chronic
toxicity
studies
in
rats,
mice
and
dogs.
Gross
pathology
findings
in
chronic
rat
and
mouse
studies
showed
increased
incidences
of
urinary
bladder
swelling
and
wall
thickening
at
high
doses.
Microscopic
evaluation
showed
dose­
related
increases
in
the
severity
of
epithelial
focal
hyperplasia
of
the
urinary
bladder
and
renal
pelvis
(
kidney)
in
both
sexes.
Although
the
developmental
toxicity
study
in
rats
is
classified
as
unacceptable,
the
database
as
a
whole
is
adequate
for
pre­
and
post­
natal
toxicity
evaluation
and
did
not
reveal
developmental
or
reproductive
toxicity.
The
NOAELs
for
maternal/
parental
toxicity
were
either
less
than
or
equal
to
the
NOAELs
for
fetal
or
reproductive
toxicity.
A
complete
summary
of
the
toxicity
database
is
discussed
in
the
document
titled
"
Diuron
­
Phase
2:
Revised
Toxicology
Disciplinary
Chapter
for
the
Reregistration
Eligibility
Decision,"
dated
March
6,
2002.

5.
Chronic
toxicity.

EPA
has
established
the
RfD
for
diuron
at
0.003
mg/
kg/
day.
This
RfD
is
based
on
a
2
year
chronic
feeding/
oncogenicity
study
in
the
rat
with
a
LOAEL
of
1.02
mg/
kg/
day
and
an
uncertainty
factor
(
UF)
of
300
(
additional
UP
of
3
for
the
use
of
a
LOAEL)
based
on
decreased
erythrocyte
count
in
females,
increased
hemodiderin
in
the
spleen,
increased
spleen
weight,
bone
marrow
activation,
increased
hematopoietic
marrow,
decreased
fat
marrow
(%
surface
area
of
fat
marrow
in
bone
marrow)
and
thickened
urinary
bladder
wall
in
males.

6.
Animal
metabolism.
Livestock
Commodities:
The
14C­
containing
residues
that
were
identified
in
lactating
goats
were
as
follows.
The
principal
residue
identified
was
DCPU
which
comprised
10%
of
TRR
in
milk,
27%
of
TRR
in
fat,
35%
of
TRR
in
kidney,
23%
of
TRR
in
liver,
and
22%
of
TRR
in
muscle.
The
parent
and
other
dichloroaniline­
containing
metabolites
(
i.
e.,
3,4­
DCA
and
DCPMU)
were
detected
in
trace
quantities
(
0.01
ppm
each)
except
in
liver
(
0.12
ppm).
Four
minor
(
each
6%
of
TRR)
hydroxylated
metabolites
(
2­
OH­
DCA;
2­
OH­
DCPU;
2­
OHDCPMU;
and
N­
acetyl­
2­
OH­
DCA)
were
also
detected;
these
metabolites
were
not
observed
in
plants
and
would
not
be
determined
by
the
enforcement
method.
The
major
portion
of
radioactive
residues
in
milk
was
comprised
of
several
conjugated
polar
components
which
collectively
accounted
for
56%
of
TRR.
These
polar
components
also
accounted
for
substantial
portions
of
the
total
radioactivity
in
liver
(
collectively
25%
of
TRR)
and
kidney
(
collectively
23%
of
TRR).
Attempts
to
further
elucidate
the
nature
of
these
polar
materials
using
various
techniques
(
e.
g.,
enzyme
digestions,
heat
treatment)
were
not
successful.

Poultry:
The
14C­
containing
residues
that
were
identified
in
laying
hens
were
as
follows.
DCPU,
which
comprised
45%
of
TRR
in
liver,
67­
75%
of
TRR
in
muscle,
47%
of
TRR
in
skin
with
fat,
57%
of
TRR
in
egg
yolk,
and
54%
of
TRR
in
egg
white.
The
parent,
other
dichloroaniline­
containing
metabolites
(
i.
e.,
DCPMU),
and
hydroxylated
metabolites
(
2­
OH­
diuron,
2­
OH­
DCA,
2­
OH­
DCPU,
2­
OHDCPMU,
and
N­
acetyl­
2­
OH­
DCA)
were
identified
only
in
trace
quantities
(
mostly
at
0.01
ppm
each).
Adequate
radiovalidation
data
were
submitted
for
the
proposed
enforcement
method
for
animal
commodities.
The
GC
method
recovered
86
to
>
100%
of
the
TRR
in
liver,
kidney,
and
muscle;
however,
the
method
recovered
only
10%
of
the
TRR
in
milk
and
25%
of
the
TRR
in
fat.
The
low
recovery
in
milk
was
previously
addressed
(
DP
Barcodes
D195058
and
D195068,
11/
30/
93,
R.
Perfetti).
It
was
concluded
that
because
the
major
portion
of
radioactive
residues
in
milk
appear
to
be
hydroxy
metabolites,
which
cannot
be
converted
to
DCA
and
do
need
not
be
quantitated,
a
new
method
would
not
be
required
for
milk.
Instead,
it
was
determined
that
the
levels
of
diuron
residues
in
milk
identified
in
the
ruminant
feeding
study
would
be
multiplied
by
10
to
account
for
all
of
the
exposure
in
the
risk
assessment.
The
low
recovery
in
fat
was
most
likely
due
to
the
low
residue
levels
present
in
fat.
In
a
separate
radiovalidation
study,
the
GC
method
recovered
62
to
77%
of
the
TRR
in
poultry
liver
and
muscle,
and
58
to
65%
of
the
TRR
in
egg
whites
and
yolks.

7.
Metabolite
toxicology.
A
rat
metabolism
study
indicated
that
diuron
is
rapidly
absorbed
and
metabolized
within
24
hours
post­
dose
at
low
dose
and
within
48
hours
post­
dose
at
high
dose.
The
urine
is
the
major
route
of
excretion
in
both
sexes.
A
small
amount
of
diuron
is
detected
in
the
feces.
No
apparent
difference
was
observed
between
single
and
multiple
low
oral
doses.
There
was
no
apparent
sex­
related
difference
in
either
absorption
or
elimination.
Metabolism
of
diuron
involved
Noxidation
ring
hydroxylation,
demethylation,
dechlorination,
and
conjugation
to
sulfate
and
glucuronic
acid.
The
major
urine
metabolite
was
IN­
R915
(
3,4­
dichlorophenylurea),
which
accounted
for
>
20%
of
the
total
administered
dose.
Other
metabolites
were
glucuronide
conjugates,
sulfate
conjugates
and
free
metabolites.

8.
Endocrine
disruption.
At
this
time,
neither
the
available
submitted
studies
on
diuron
nor
the
literature
show
any
indication
of
endocrine
disruption
effects.
C.
Aggregate
Exposure
1.
Dietary
exposure.
There
are
no
adverse
effects
attributed
to
a
single
exposure
identified
in
any
available
studies.
In
addition,
diuron
has
low
acute
toxicity
and
no
developmental
or
neurotoxic
concerns.
Therefore,
no
acute
dietary
endpoint
was
chosen
and
no
acute
dietary
risk
assessment
was
conducted.
Diuron
is
a
preplant,
pre­
or
post­
emergent
herbicide,
used
on
a
variety
of
fruits,
vegetables,
nuts
and
field
crops.
Tolerances
are
established
for
residues
of
diuron
in
or
on
food
commodities
at
levels
ranging
from
0.1
ppm
to
7
ppm
(
40
CFR
180.106).

i.
Food.
Estimated
chronic
dietary
(
food)
risk
estimates
associated
with
the
use
of
diuron
do
not
exceed
the
Agency's
level
of
concern
(>
100%
cPAD)
for
any
population
subgroup
including
the
most
highly
exposed
population
subgroup,
children
ages
1­
6
years.
The
chronic
dietary
risk
for
children
ages
1­
6
years
is
7%
of
the
chronic
PAD
and
3%
for
the
general
U.
S.
population.
Orange
juice
and
orange
juice
concentrate
are
the
largest
contributors
to
dietary
exposure
from
diuron.
The
estimated
cancer
dietary
risk
associated
with
the
use
of
diuron
indicates
a
borderline
exceedance
above
1
x
10­
6
(
i.
e.,
probability
greater
than
one
in
one
million)
and
shows
a
lifetime
risk
estimate
of
1.68
x
10­
6
for
the
general
population
but
is
not
of
concern.
There
are
no
adverse
effects
attributed
to
a
single
exposure
identified
in
any
available
studies.
In
addition,
diuron
has
low
acute
toxicity
and
no
developmental
or
neurotoxic
concerns.
Therefore,
no
acute
dietary
endpoint
was
chosen
and
no
acute
dietary
risk
assessment
was
conducted.

ii.
Drinking
water.
Environmental
laboratory
studies
have
shown
that
in
drinking
water
only,
diuron
partially
degrades
to
another
chemical
referred
to
as
MCPDMU
(
N'­(
3­
chlorophenyl)­
N,
Ndimethyl
urea).
However,
the
environmental
fate
and
persistence
of
MCPDMU
are
uncertain.
MCPDMU
is
structurally
similar
to
monuron
[
N'­(
4­
chlorophenyl)­
N,
N­
dimethyl
urea],
a
pesticide
no
longer
registered
in
the
United
States.
Monuron
produces
tumors
in
the
kidney
and
liver
in
male
rats
and
has
a
Q1*
of
1.52
x
10­
2.
Due
to
the
structural
similarity
between
MCPDMU
and
monuron,
the
Agency
believes
it
is
prudent
to
evaluate
the
carcinogenic
risk
associated
with
MCPDMU
based
upon
the
hazard
information
concerning
the
chemical
monuron.
The
Agency
believes
MCPDMU
is
likely
less
toxic
than
monuron,
but
is
unable
to
quantify
this
difference
without
further
information.
The
approach
used
in
this
assessment
yields
a
high­
end
estimate.
Absent
information
specifically
about
the
carcinogenic
potential
of
MCPDMU,
the
Agency
has
taken
this
conservative,
health
protective
approach
in
its
assessment.
The
Agency
is
addressing
this
uncertainty
by
requiring
additional
information
about
the
behavior
and
fate
of
diuron
and
its
drinking
water
degradate,
MCPDMU.
Two
separate
cancer
risk
assessments
were
completed
for
diuron
and
MCPDMU
(
N'­(
3­
chlorophenyl)­
N,
N­
dimethyl
urea),
a
degradate
of
diuron
in
water
only.
Because
the
cancer
effects
(
i.
e.,
target
organs)
for
the
two
compounds
differ,
the
risks
from
diuron
and
MCPDMU
are
not
combined.
Based
on
a
Q1*
of
a
similar
compound,
monuron,
the
estimated
dietary
risk
for
MCPDMU
is
1.02
x
10­
7,
which
includes
catfish
consumption
only.
The
anticipated
residue
of
MCPDMU
in
catfish
was
calculated
using
the
2
ppm
tolerance
for
catfish,
the
fraction
of
applied
radioactive
diuron
converted
to
MCPDMU
in
an
aerobic
aquatic
metabolism
study
and
the
percent
crop
treated
for
catfish.
Neither
diuron
nor
monuron
are
regulated
under
the
Safe
Drinking
Water
Act.
As
a
result,
neither
Maximum
Contaminant
Levels
(
MCLs)
nor
drinking
water
health
advisories
(
HAs)
for
these
chemicals
have
been
established
by
the
EPA
Office
of
Water.
However,
diuron
was
placed
on
a
list
of
contaminants
to
be
monitored
during
2001
and
2002.
This
information
will
be
used
to
support
EPA
decisions
concerning
whether
or
not
to
regulate
and
establish
standards
for
diuron
in
drinking
water.]

2.
Non­
dietary
exposure.
Because
of
the
low
percent
of
paint
containing
diuron,
exposure
to
home
applicators
is
not
likely
to
be
a
significant
contributor
to
aggregate
risk.
Calculated
diuron
potential
cancer
risks
from
food
and
residential
applicator
exposure
(
paints
and
stains)
show
a
slight
exceedance
of
the
Agency's
level
of
concern,
1
x
10­
6.
Both
assessments
include
conservative
exposure
assumptions.
In
both
cases
additional
data
will
allow
for
refinement
of
the
exposure
portion
of
the
assessment.]

D.
Cumulative
Effects
EPA
did
not
perform
a
cumulative
risk
assessment
of
diuron
because
the
Agency
has
not
determined
that
there
are
any
other
chemical
substances
that
have
a
mechanism
of
toxicity
common
with
that
of
diuron.

E.
Safety
Determination
1.
U.
S.
population.
In
its
July,
2002
TRED,
EPA
determined
that
the
established
uses
for
diuron,
with
amendments
and
changes
as
specified
in
that
document,
met
the
safety
standard
under
the
FQPA
amendments
to
section
408(
b)(
2)(
D)
of
the
FFDCA,
that
there
is
a
reasonable
certainty
of
no
harm
for
the
general
population.
In
reaching
this
determination,
EPA
considered
all
available
information
on
the
toxicity,
use
practices,
and
scenarios,
and
the
environmental
behavior
of
diuron.
An
acute
dietary
risk
assessment
was
not
performed
because
no
adverse
effects
attributed
to
a
single
exposure
were
identified
in
any
available
study.
For
chronic
(
non­
cancer)
risk
from
food
alone,
the
risks
from
diuron
are
not
of
concern.
The
estimated
cancer
dietary
risk
associated
with
the
use
of
diuron
indicates
a
slight
exceedance
above
1
x
10­
6
and
shows
a
lifetime
risk
estimate
of
1.68
x
10­
6
for
the
general
population.
However,
the
Agency
has
determined
that
potential
dietary
cancer
risk
is
not
of
concern
because
the
residues
used
in
the
calculations
are
from
field
trials
conducted
at
the
highest
application
rates
and
some
residue
processing
data
are
still
outstanding.
Therefore,
the
exposure
calculation
is
a
conservative
estimate.
Acute
risks
from
drinking
water
exposures
are
not
of
concern.
For
chronic
drinking
water
risk,
drinking
water
monitoring
data
from
Florida,
California,
and
the
U.
S.
Geological
Survey
National
Water
Quality
Assessment
(
NAWQA)
Program
were
used
to
determine
the
estimated
environmental
concentrations
(
EECs)
in
surface
water.
These
monitoring
data
confirm
that
actual
concentrations
of
diuron
are
substantially
less
than
previous
model
estimates.
Although
modeled
estimates
showed
only
a
marginal
exceedance
of
the
WLOC,
monitoring
data
show
84
concentrations
substantially
below
the
chronic
DWLOC.
Short­
term
residential
exposures
to
diuron
are
not
of
concern.
The
Agency
has
concluded
that
the
potential
cancer
risk
from
residential
use
is
negligible
because
of
the
low
volume
of
diuron
used
in
paint
and
the
sporadic,
short­
term
duration
of
homeowner
exposures.

2.
Infants
and
children.
In
its
July
2002
TRED,
EPA
determined
that
the
established
tolerances
for
diuron,
meet
the
safety
standards
under
the
FQPA
amendments
to
section
408(
b)(
2)(
C)
of
the
FFDCA,
that
there
is
a
reasonable
certainty
of
no
harm
for
infants
and
children.
The
safety
determination
for
infants
and
children
considered
the
factors
noted
above
for
the
general
population,
but
also
takes
into
account
the
possibility
of
increased
dietary
exposure
due
to
the
specific
consumption
patterns
of
infants
and
children,
as
well
as
the
possibility
of
increased
susceptibility
to
the
toxic
effects
of
diuron
residues
in
this
population
subgroup.
In
determining
whether
or
not
infants
and
children
are
particularly
susceptible
to
toxic
effects
from
diuron
residues,
EPA
considered
the
completeness
of
the
database
for
developmental
and
reproductive
effects,
the
nature
of
the
effects
observed,
and
other
information.
The
FQPA
Safety
Factor
has
been
removed
(
i.
e.,
reduced
to
1x)
for
diuron
because:
1)
there
is
no
indication
of
quantitative
or
qualitative
increased
susceptibility
of
rats
or
rabbits
to
in
utero
or
postnatal
exposure;
2)
a
DNT
study
with
diuron
is
not
required;
and
3)
the
dietary
(
food
and
drinking
water)
and
non­
dietary
(
residential)
exposure
assessments
will
not
underestimate
the
potential
exposures
for
infants
and
children.]

F.
International
Tolerances
[
The
Codex
Alimentarius
Commission
has
not
established
or
proposed
Codex
MRLs
for
residues
of
diuron;
therefore,
there
are
no
issues
pertaining
to
harmonization
of
U.
S.
tolerance
with
Codex
MRLs.

Canadian
tolerances
(
from
PMRA
web
site)
include
the
following:
7
ppm
in/
on
asparagus
1
ppm
in/
on
citrus,
corn,
grapes,
pineapple,
potatoes
and
wheat.

Mexican
tolerances
(
from
1992
Diuron
Residue
Chemistry
Registration
Standard
Update)
are
established
for
diuron
as
follows:

7
ppm
in/
on
asparagus
4
ppm
in/
on
dry
citrus
pulp
2
ppm
in/
on
alfalfa,
corn
(
forage),
sorghum
(
forage),
wheat
(
straw,
forage)
1ppm
in/
on
artichoke,
cottonseed,
sugarcane,
citrus
fruit,
apple,
corn
grain,
peaches,
potatoes,
pears,
pineapple,
sorghum
(
grain),
wheat
(
grain
and
straw)
and
grapes.
0.5
ppm
in/
on
papaya
0.1
ppm
in/
on
nuts.]
