UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
WASHINGTON,
D.
C.
20460
OFFICE
OF
PREVENTION,
PESTICIDES
AND
TOXIC
SUBSTANCES
March
13,
2002
MEMORANDUM
SUBJECT:
DIURON:
The
REVISED
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED).
PC
Code:
035505.
Case
0046.
DP
Barcode
D281396.

FROM:
Diana
Locke
Ph
D.
and
Carol
Christensen
Risk
Assessors
Reregistration
Branch
II
Health
Effects
Division
(
7509C)

THRU:
Alan
Nielsen,
Branch
Senior
Scientist
Reregistration
Branch
II
Health
Effects
Division
(
7509C)

TO:
Margaret
Rice,
Chief
and
Richard
Dumas,
Team
Leader
Reregistration
Branch
II
Special
Review
and
Reregistration
Division
(
7508W)

The
attached
REVISED
Human
Health
Assessment
for
the
3­(
3,4­
dichlorophenyl)­
1,1­
dimethylurea
(
diuron)
RED
document
was
generated
as
part
of
Phase
2
of
the
Interim
Public
Participation
Process.
Comments
received
from
the
Registrant
during
the
Phase
I
Error­
Only
review
period
have
been
incorporated
in
this
version
of
the
HED
Human
Health
Assessment
for
Diuron.
The
Health
Effects
Division's
(
HED)
chapter
reflects
the
Agency's
current
guidelines
concerning
the
retention
of
the
Food
Quality
Protection
Act
(
FQPA)
factor
and
risk
assessment.
This
chapter
includes
a
summary
of
the
product
chemistry
from
Ken
Dockter,
residue
chemistry
and
dietary
risk
assessment
from
John
Punzi,
toxicology
review
from
Yung
Yang,
occupational
and
residential
exposure
from
Renee
Sandvig
and
Christina
Jarvis,
incidence
review
from
Ruth
Allen,
drinking
water
exposures
from
Ibrahim
Abdel­
Saheb
[
Environmental
Fate
and
Effects
Division
(
EFED)],
as
well
as
risk
assessment
and
characterization
from
Diana
Locke.
Carol
Christensen
incorporated
the
changes
to
the
risk
assessment
in
response
to
error­
only
comments.
The
Environmental
Fate
and
Effects
Division
(
EFED)
revised
the
drinking
water
exposure
assessment
based
upon
Registrant
comments.
The
new
memorandum
entitled
"
Drinking
Water
Reassessment
for
Diuron
and
its
Degradates"
dated
March
11,
2002
has
been
incorporated
into
the
Revised
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED)
as
appropriate.
TABLE
OF
CONTENTS
1.0
EXECUTIVE
SUMMARY
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1
2.0
PHYSICAL/
CHEMICAL
PROPERTIES
CHARACTERIZATION
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7
3.0
HAZARD
CHARACTERIZATION
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8
3.1
Hazard
Profile
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8
3.2
FQPA
Considerations
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12
3.3
Dose
Response
Assessment
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12
3.3.1
Acute
RfD
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13
3.3.2
Chronic
RfD
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13
3.3.3
Short­
term
(
1­
30
days)
Incidental
Oral
Exposure
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14
3.3.4
Intermediate­
term
(
1­
6
months)
Incidental
Oral
Exposure
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15
3.3.5
Dermal
Absorption
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15
3.3.6
Short­
(
1­
30
days)
and
Intermediate­
term
(
1­
6
months)
Dermal
Exposure
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15
3.3.7
Long­
term
(
6
months
to
life­
time)
Dermal
Exposure
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15
3.3.8
Inhalation
Exposure
(
All
Durations)
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16
3.3.9
Carcinogenic
Potential
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16
3.3.9.1
Combined
Chronic
Toxicity/
Carcinogenicity
Study
in
Rats
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16
3.3.9.2
Carcinogenicity
Study
in
Mice
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17
3.3.9.3
Classification
of
Carcinogenic
Potential
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17
3.3.10
Mutagenicity
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17
3.3.11
Mechanism
of
Carcinogenicity
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18
3.4
Endocrine
Disruption
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21
3.5
Potential
Tetrachloroazobenzene
Contamination
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22
4.0
EXPOSURE
ASSESSMENT
AND
CHARACTERIZATION
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22
4.1
Summary
of
Registered
Uses
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22
4.2
Dietary
Exposure/
Risk
Pathway
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24
4.2.1
Residue
Profile
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26
4.2.2
Acute
Dietary
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27
4.2.3
Chronic
Dietary
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27
4.2.4
Cancer
Dietary
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28
4.3
Water
Exposure/
Risk
Pathway
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28
4.4
Residential
Exposure/
Risk
Pathway
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32
4.4.1
Home
Uses
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32
4.4.1.1
Handler
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35
4.4.1.2
Postapplication
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36
4.4.2
Recreational
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37
4.4.3
Other
(
Spray
Drift;
Farm
Worker
Children,
etc.)
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37
5.0
AGGREGATE
RISK
ASSESSMENTS
AND
RISK
CHARACTERIZATIONS
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40
5.1
Acute
Risk
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41
5.2
Short­
term
Risk
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42
5.2.1
Aggregate
Short­
term
Risk
Assessment
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42
5.2.2
Short­
term
DWLOC
Calculations
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42
5.4
Chronic
Risk
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44
5.4.1
Chronic
Aggregate
Risk
Assessment
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44
5.4.2
Chronic
DWLOC
Calculations
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44
5.5
Cancer
Risk
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46
5.5.1
Aggregate
Cancer
Risk
Assessment
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46
5.5.2
Cancer
DWLOC
Calculations
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46
5.5.3
Additional
Cancer
Risks
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46
6.0
CUMULATIVE
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48
7.0
OCCUPATIONAL
EXPOSURE
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49
7.1
Agricultural
and
Non­
crop/
Utility
Uses
.
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50
7.1.1
Handler
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50
7.1.1.1
Noncancer
Exposure
and
Risk
Estimates
.
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52
7.1.1.2
Cancer
Exposure
and
Risk
Estimates
.
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53
7.1.2
Postapplication
Exposures
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53
7.1.2.1
Noncancer
Postapplication
Exposure
and
Risk
Estimates
.
.
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.
55
7.1.2.2
Postapplication
Exposure
and
Risk
Estimates
for
Cancer
.
.
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.
56
7.1.2.2.1
Private
Growers
(
10
Days
Exposure
Per
Year)
.
.
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.
56
7.1.2.2.2
Commercial
Farm
Workers
(
30
Days
Exposure
Per
Year)
.
.
.
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.
.
56
7.2
Mildewcide
in
Paints,
Solvents,
Adhesives,
and
Coatings
.
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56
7.2.1
Occupational
Handler
Exposures/
Risks
.
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56
7.2.1.1
Noncancer
Risks
.
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58
7.2.1.1
Cancer
Risks
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58
7.2.2
Postapplication
Exposures
to
Paint
Containing
Diuron
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58
7.3
Algaecide
in
Commercial
Fish
Production
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59
7.3.1
Handlers
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59
7.3.1.1
Noncancer
Exposures/
Risks
for
Pond
Uses
.
.
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59
7.3.1.2
Cancer
Exposures/
Risks
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59
7.3.2
Occupational
Postapplication
Exposures
to
Commercial
Fish
Ponds
.
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60
7.4
Incident
Data
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60
8.0
DATA
NEEDS/
LABEL
REQUIREMENTS
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60
ATTACHMENTS
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62
1
DIURON
1.0
EXECUTIVE
SUMMARY
Diuron
[
3­(
3,4­
Dichlorophenyl)­
1,1­
dimethylurea]
is
a
pre­
and
post­
emergent
herbicide
that
controls
a
wide
variety
of
annual
and
perennial
broad
leafed
and
grassy
weeds
on
both
crop
and
noncrop
sites.
The
mechanism
of
herbicidal
action
is
the
inhibition
of
photosynthesis.
Products
containing
diuron
are
intended
for
both
occupational
and
residential
uses.
Occupational
uses
include
agricultural
food
and
non­
food
crops;
ornamental
trees,
flowers,
and
shrubs;
paints
and
coatings;
ornamental
fish
and
catfish
production;
rights­
of­
way
and
industrial
sites.
Residential
uses
include
ponds,
aquariums,
and
paints.
Diuron
is
formulated
as
a
technical
product
and
formulation
intermediate,
granular,
pellet/
tablet,
wettable
powder,
dry
flowable,
emulsifiable
concentrate,
flowable
concentrate,
soluble
concentrate,
and
ready­
to­
use
solution.
Diuron
is
applied
using
the
following
equipment:
groundboom
sprayer,
aerial
equipment,
chemigation,
rights­
of­
way
sprayer,
high­
pressure
handwand,
low­
pressure
handwand,
tractor­
drawn
spreader,
granular
backpack
spreader,
push­
type
spreader,
airless
sprayer,
paintbrush,
shaker­
type
applicator,
backpack
sprayer,
belly
grinder,
and
by
hand.
Products
intended
for
residential
use
may
be
applied
using
a
spoon,
by
hand,
by
airless
sprayer,
or
by
paintbrush/
roller.
Application
rates
range
from
0.8
lbs
active
ingredient
(
ai)/
acre
for
corn
to
87.1
lbs
ai/
acre
for
non­
crop
areas.

Diuron
has
low
acute
toxicity
(
Toxicity
Category
3­
4)
by
the
oral,
dermal,
or
inhalation
exposure
routes.
Diuron
is
not
an
eye
or
skin
irritant,
and
not
a
skin
sensitizer.
The
primary
target
organs
are
the
hematopoietic
system,
the
bladder,
and
renal
pelvis.
Erythrocyte
damage
resulted
in
hemolytic
anemia
and
compensatory
hematopoiesis,
which
were
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
erythrocytic
regeneration
were
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
edema
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
in
both
sexes.
The
available
data
did
not
reveal
any
developmental
or
reproductive
toxicity.
The
HED
Carcinogenicity
Peer
Review
Committee
(
CPRC)
characterized
diuron
as
a
"
known/
likely"
human
carcinogen
based
on
urinary
bladder
carcinomas
in
both
sexes
of
the
Wistar
rat,
kidney
carcinomas
in
the
male
rat,
and
mammary
gland
carcinomas
in
the
female
NMRI
mouse.
The
CPRC
also
recommended
a
low
dose
linear
extrapolation
model
with
a
Q1
*
of
1.91
x
10­
2
(
mg/
kg/
day)­
1
be
applied
to
the
animal
data
for
the
quantification
of
human
risk,
based
on
the
urinary
bladder
carcinomas
in
the
rat.
Diuron
was
not
mutagenic
in
bacteria
or
in
cultured
mammalian
cells
and
no
indication
of
DNA
damage
in
primary
rat
hepatocytes
was
observed.
There
were
marginal
statistically
significant
increases
in
cells
with
structural
aberrations
in
a
Sprague
Dawley
rat
in
vivo
bone
marrow
chromosomal
aberration
assay.
However,
the
levels
of
aberrations
were
within
historical
2
control
range
and
assessed
negative.

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.
Also,
no
systemic
toxicity
was
observed
following
repeated
dermal
dosing
up
to
1200
mg/
kg/
d.
Therefore,
no
short­
or
intermediate­
term
dermal
endpoints
were
chosen
either.
The
short­
term
incidental
oral
and
the
inhalation
endpoints
are
based
on
decreased
maternal
body
weight
and
food
consumption
observed
in
a
rabbit
developmental
toxicity
study
[
No
Observable
Adverse
Effect
Level
(
NOAEL)
=
10
mg/
kg/
d].
The
intermediate­
term
incidental
oral
and
intermediate­
term
inhalation
endpoints
are
based
on
hematological
effects
observed
at
10
mg/
kg
at
6
months
in
the
chronic
rat
study.
The
NOAEL
is
1
mg/
kg/
d.
The
chronic
dietary,
and
long­
term
dermal
and
inhalation
endpoints
are
based
on
hemolytic
anemia
and
compensatory
hematopoiesis
[
Lowest
Observable
Adverse
Effect
Level
(
LOAEL)
=
1.0
mg/
kg/
d].
Since
the
dose
and
endpoint
for
establishing
the
chronic
dietary
reference
Dose
(
RfD)
is
a
LOAEL
and
a
NOAEL
was
not
established,
a
total
uncertainty
factor
(
UF)
of
300
was
applied
(
UF
of
100
to
account
for
both
interspecies
extrapolation
and
intra­
species
variability,
an
additional
UF
of
3
to
account
for
the
lack
of
a
NOAEL).
The
FQPA
Safety
Factor
Committee
recommended
that
the
FQPA
safety
factor
be
reduced
to
1x
since
there
is
no
indication
of
quantitative
or
qualitative
increased
susceptibility
of
rats
or
rabbits
to
in
utero
or
postnatal
exposure.

Estimated
chronic
dietary
(
food)
risk
estimates
associated
with
the
use
of
diuron
do
not
exceed
the
Agency's
level
of
concern
for
any
population
subgroup
including
the
most
highly
exposed
subgroup,
children
ages
1­
6
years.
The
chronic
dietary
risk
for
children
1­
6
years
of
age
is
approximately
7%
of
the
chronic
Population
Adjusted
Dose
(
cPAD
=
0.003
mg/
kg/
d)
and
approximately
3%
for
the
general
U.
S.
population.
The
chronic
exposure
analysis
utilized
field
trial
data
which
include
residues
of
the
parent
diuron
and
its
metabolites
that
are
hydrolyzable
to
3,4­
dichloroaniline
(
3,4­
DCA);
3,4­
dichlorophenylurea
and
3­(
3,4­
dichlorophenyl)­
1­
methylurea.
The
analysis
also
included
processing
data,
where
applicable,
and
percent
crop
treated
information.
Approximately
40%
of
the
exposure
to
diuron
from
food
is
from
orange
juice
and
orange
juice
concentrate.
The
estimated
cancer
dietary
risk
associated
with
the
use
of
diuron
indicates
a
borderline
exceedance
above
1
x
10­
6
and
shows
a
lifetime
risk
estimate
of
1.68
x
10
­
6
for
the
general
population
but,
is
not
of
concern.
Though
this
is
the
most
refined
assessment
achievable
based
on
the
available
data/
information,
it
may
also
be
considered
conservative
since
the
exposure
analysis
used
data
from
field
trials
conducted
at
the
highest
application
rates
and
some
processing
data
are
still
outstanding.

The
Agency
has
determined
that
there
are
potential
occupational
exposures
to
mixers,
loaders,
applicators
and
other
handlers
during
the
usual
use­
patterns
associated
with
diuron.
Based
on
the
agricultural
and
non­
crop
use
patterns,
31
major
occupational
exposure
scenarios
were
identified
and
are
expected
to
be
of
short­
(
1­
30
days)
and
intermediate­
(
1­
6
months)
term
duration.
For
these
durations,
the
Level
of
Concern
(
LOC)
or
target
Margin
of
Exposure
(
MOE)
for
occupational
workers
is
100.
MOEs
>
100
are
not
considered
to
be
of
concern.
Calculations
of
occupational
noncancer
3
risk
based
on
inhalation
exposures
during
agricultural
and
non­
crop
uses
indicate
that
the
inhalation
MOEs
are
more
than
100
at
the
highest
possible
level
of
mitigation
for
all
of
the
short­
term
occupational
exposure
scenarios,
except
applying
sprays
with
a
high
pressure
handwand.
Sixteen
of
the
31occupational
scenarios
were
identified
as
having
intermediate­
term
durations
of
exposure.
Of
these,
none
have
a
non­
cancer
risk
of
concern
for
intermediate­
term
inhalation
exposure
at
the
highest
level
of
mitigation
Potential
occupational
cancer
risks
from
diuron
use
were
assessed.
Both
the
potential
inhalation
and
dermal
exposures
were
included
in
the
cancer
risk
assessment
and
a
4%
dermal
absorption
factor
(
upper
bound
estimate)
was
applied
to
dermal
exposures.
In
general,
the
Agency
is
concerned
when
occupational
cancer
risk
estimates
exceed
1
x
10­
4.
The
Agency
will
seek
ways
to
mitigate
the
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
1
x
10­
6
or
less.
Out
of
a
total
of
31occupational
handler
scenarios,
five
have
cancer
risks
greater
than
1
x
10­
4
at
the
highest
feasible
level
of
mitigation
and
are
of
concern.
Twenty­
six
of
the
occupational
handler
scenarios
have
cancer
risks
between
1
x
10­
4
and
1
x
10­
6
at
the
highest
feasible
level
of
mitigation.
Both
occupational
and
residential
(
see
below)
cancer
risk
assessments
are
considered
protective
based
on
conservative
exposure
assumptions
and
a
high­
end
dermal
absorption
factor.
The
Agency
has
determined
that
there
are
potential
postapplication
exposures
to
workers
during
the
agricultural
and
non­
crop
uses
associated
with
diuron.
However,
a
noncancer
postapplication
assessment
was
not
conducted,
since
only
dermal
exposures
are
expected
and
no
dermal
toxicity
is
expected
from
short
or
intermediate­
term
exposures.
For
the
postapplication
cancer
assessment,
only
the
crops
whose
foliage
can
be
sprayed
without
damage
were
assessed
for
postapplication
exposure
to
foliage.
The
crops
that
can
be
sprayed
without
foliage
damage
are
oats,
wheat,
birdsfoot
trefoil,
clover,
grass
grown
for
seed,
alfalfa,
asparagus,
pineapple,
and
sugarcane.
Postapplication
cancer
risks
for
private
growers
(
10
days
of
exposure
per
year)
were
calculated
at
both
the
typical
application
rate
and
the
maximum
application
rates.
All
potential
cancer
risks
to
private
growers
were
estimated
to
be
less
than
1
x
10­
4
on
the
day
of
treatment.
Postapplication
cancer
risks
for
commercial
applicators
(
30
days
per
year)
were
calculated
at
the
typical
application
rate
only.
All
potential
cancer
risks
to
commercial
applicators
were
less
than
1
x
10­
4
on
the
day
of
treatment.
Since
diuron
is
applied
directly
to
the
soil,
there
may
also
be
significant
postapplication
exposure
to
diuron
resulting
from
contact
with
treated
soil
when
planting
seedlings,
moving
irrigation
lines,
or
other
soil
related
activities.

Occupational
risk
assessments
were
conducted
for
the
use
of
diuron
as
a
mildewcide
in
paint.
Four
occupational
handler
scenarios
were
identified
for
the
use
of
diuron
in
paint
and
are
expected
to
be
of
short­
and
intermediate­
term
exposure
duration.
The
calculations
of
short­
and
intermediate­
term
inhalation
risk
from
the
use
of
diuron
in
paint
indicate
that
MOEs
are
more
than
100
at
the
assessed
level
of
mitigation
for
all
the
exposure
scenarios,
except
applying
paints
with
an
airless
sprayer
(
indoors).
At
the
assessed
level
of
mitigation,
all
four
scenarios
have
potential
cancer
risks
between
1
x
10­
4
and
1
x
10­
6.
However,
it
is
likely
that
risks
are
even
lower
since
the
cancer
assessment
incorporated
a
number
of
conservative
assumptions,
such
as
maximum
application
rate
and
an
upper
bound
dermal
absorption
factor.
Occupational
postapplication
exposures
to
paint
containing
diuron
may
occur
in
industrial
settings
around
open
vats
used
in
paint
processing.
Inhalation
and
dermal
exposures
may
also
occur
while
maintaining
industrial
equipment.
No
postapplication
exposure
data
4
have
been
submitted
to
determine
the
extent
of
postapplication
exposures
in
the
industrial
settings.
Nonetheless,
inhalation
exposures
are
expected
to
be
minimal
because
of
the
low
vapor
pressure
of
diuron
(
2
x
10­
7
mm
Hg
at
30
E
C)
and
aerosol
formation
is
not
expected.
Dermal
postapplication
exposures
are
expected
to
be
lower
than
when
handling/
loading
the
formulated
product.
Therefore,
postapplication
exposures
in
the
industrial
settings
are
expected
to
be
minimal
and
not
of
concern.

Occupational
risk
assessments
were
also
conducted
for
the
use
of
diuron
as
an
algaecide
in
commercial
fish
ponds.
Four
short­
term
occupational
handler
scenarios
were
identified
for
the
use
of
diuron
in
commercial
fish
production
and
the
inhalation
MOEs
from
all
four
of
the
commercial
fish
production
scenarios
were
greater
than
100
at
the
baseline
level
of
mitigation
and
are
not
of
concern.
With
maximum
mitigation
measures
(
engineering
control
level),
all
four
scenarios
have
estimated
cancer
risks
of
less
than
1
x
10­
6
and
are
not
of
concern.
Occupational
postapplication
exposure
to
diuron
in
treated
fish
production
ponds
is
not
likely
to
result
in
a
risk
of
concern
based
on
the
extremely
high
dilution
rate.

The
Agency
has
determined
that
there
are
potential
exposures
to
residential
mixers,
loaders,
and
applicators
during
1)
loading
ready­
to­
use
liquids,
2)
applying
paints/
stains
with
a
paintbrush,
and
3)
applying
paints
with
an
airless
sprayer
(
outdoor
applications
only).
Residential
exposures
to
diuron
are
expected
to
be
short­
term.
For
residential
handlers,
calculations
of
noncancer
risk
indicate
that
the
inhalation
MOEs
are
more
than
100
for
all
of
the
exposure
scenarios
and
are
not
of
concern.
For
residential
populations,
cancer
risks
less
than
1
x
10­
6
are
not
considered
to
be
of
concern.
All
residential
handler
scenarios
have
a
potential
cancer
risk
greater
than
1
x
10­
6
and
are
of
concern,
except
for
the
loading
ready­
to­
use
liquids
for
ponds
and
aquariums
scenario,
which
is
not
of
concern.
The
Agency
notes
that
cancer
risk
estimates
to
residential
handlers
of
diuron
treated
paint
are
based
on
two
exposures
per
year,
which
is
considered
a
high­
end
assumption.

Postapplication
inhalation
or
dermal
exposure
resulting
from
the
indoor
use
of
diuron
in
paints
is
also
expected
to
be
minimal
because
of
the
low
vapor
pressure
of
diuron,
and
because
diuron­
treated
paint
is
only
likely
to
be
used
in
rooms
where
high
humidity
is
expected
(
i.
e.
a
bathroom),
and
would
rarely
be
used
in
the
entire
house.
Postapplication
inhalation
and
dermal
exposure
resulting
from
the
use
of
diuron
in
residential
ponds
and
aquariums
is
also
expected
to
be
minimal
based
on
the
extremely
high
dilution
rate.

When
potential
food
and
residential
inhalation
exposures
were
combined
for
short­
term
aggregate
risk
estimates,
they
resulted
in
aggregate
short­
term
MOEs
=
1043
and
1045
for
adult
males
and
females,
respectively.
Based
on
the
lack
of
systemic
toxicity
expected
by
the
dermal
route,
it
was
not
appropriate
to
combine
residential
dermal
and
inhalation
exposure
estimates
for
risk
assessment
purposes.
Based
on
labeled
uses,
no
intermediate­
or
long­
term
residential
handler,
or
postapplication
exposures
of
any
duration,
are
expected.
Based
on
supported
uses,
no
incidental
oral
exposures
are
expected.
Aggregate
short­
term
risk
estimates
for
diuron
and
its
metabolites
hydrolyzable
to
3,4­
DCA
would
combine
exposures
from
food
(
average),
water,
and
inhalation.
Since
measured
drinking
water
5
data
(
monitoring
data)
are
limited
and
cannot
be
quantitatively
included
in
the
risk
assessment,
estimates
of
allowable
levels
of
drinking
water
were
calculated
instead.
The
Agency
determined
that
it
was
unlikely
that
more
than
one
of
the
residential
handler
activities
would
occur
concurrently
during
a
shortterm
time
period.
Therefore,
the
Agency
took
the
protective
approach
of
including
the
exposures
from
the
activity
which
could
potentially
result
in
the
most
exposure
to
the
homeowner,
applying
paint
with
an
airless
sprayer,
in
the
aggregate
assessment.
The
Agency
can
conclude
with
reasonable
certainty
that
residues
of
diuron
plus
its
metabolites
hydrolyzable
to
3,4­
DCA,
resulting
from
applications
of
diuron,
in
drinking
water
would
not
likely
result
in
a
short­
term
aggregate
risk
to
male
and
female
adult
homeowners
above
the
Agency's
level
of
concern.

Aggregate
chronic
(
noncancer)
risk
estimates
include
the
contribution
of
risk
from
dietary
sources
(
food
+
water)
and
residential
sources.
However,
based
on
the
labeled
uses,
no
long­
term
or
chronic
residential
exposures
are
expected.
Chronic
risk
estimates
from
exposures
to
food
alone,
do
not
exceed
the
Agency's
level
of
concern.
However,
the
Agency
cannot
conclude
with
reasonable
certainty
that
residues
of
diuron,
plus
its
metabolites
hydrolyzable
to
3,4­
DCA,
in
drinking
water
would
not
likely
result
in
an
aggregate
chronic
risk
to
infants,
children,
or
adults
above
the
Agency's
level
of
concern.
The
Agency
based
this
determination
on
a
comparison
of
estimated
concentrations
of
diuron
and
its
metabolites
in
surface
waters
to
back­
calculated
"
drinking
water
levels
of
comparison"
(
DWLOCs)
for
diuron
plus
its
metabolites.
The
estimated
ground
water
concentrations
are
not
expected
to
exceed
the
DWLOCs.

Estimated
exposure
to
food
alone
results
in
a
cancer
risk
for
the
U.
S.
general
population
that
is
not
of
concern.
However,
residential
exposures
to
applicators
applying
paint
with
a
paintbrush
or
airless
sprayer
may
result
in
potential
cancer
risks
that
are
of
concern.
Since
potential
cancer
risks
from
exposures
during
residential
activities,
alone,
are
of
concern,
no
aggregate
cancer
risk
and
no
DWLOCs
were
calculated.
Any
potential
additional
exposure
to
residues
in
water
are
of
concern.

The
Metabolism
Assessment
Review
Committee
(
MARC)
recommended
that
a
separate
dietary
cancer
assessment
be
conducted
for
N'­(
3­
chlorophenyl)­
N,
N­
dimethyl
urea
(
MCPDMU),
a
potential
residue
of
concern
in
drinking
water,
but
not
found
in
food
(
in
plant
or
animal
metabolism
studies).
The
MARC
raised
concerns
for
MCPDMU
based
on
an
analogous
compound,
N'­(
4­
chlorophenyl)­
N,
N­
dimethyl
urea
(
monuron).
With
the
exception
of
the
position
of
the
chlorine,
the
structures
are
identical.
There
are
cancer
concerns
for
monuron
but
the
target
organs
are
different
than
those
affected
by
diuron.
In
the
absence
of
the
data
needed
for
a
more
comprehensive
evaluation
of
MCPDMU,
the
carcinogenic
risk
assessment
was
conducted
using
the
Q1
*
of
monuron
[
1.52
x
10­
2
(
mg/
kg/
day)­
1]
that
is
based
on
male
rat
liver
neoplastic
nodule
and/
or
carcinoma
combined
tumor
rates.
The
calculated
potential
cancer
risk
to
the
U.
S.
general
population
from
exposure
to
MCPDMU
in
catfish
is
1.02
x
10­
7
and
is
not
of
concern.
However,
the
estimated
concentration
of
MCPDMU
in
surface
water
exceeds
the
DWLOC
and
is
of
concern.

In
summary,
diuron
has
low
acute
toxicity
and
no
systemic
toxicity
was
observed
following
6
repeated
dermal
dosing.
!
The
potential
dietary
risks,
based
on
food
alone,
are
not
of
concern.
However,
the
estimated
chronic
surface
water
concentrations
exceed
the
DWLOCs.
!
The
aggregate
short­
term
risk
(
food
+
water
+
residential)
is
not
of
concern.
!
Occupational
noncancer
risks
based
on
inhalation
exposures
during
agricultural
and
non­
crop
uses
are
not
of
concern
at
the
highest
possible
level
of
mitigation
for
all
of
the
short­
term
occupational
exposure
scenarios,
except
applying
sprays
with
a
high
pressure
handwand.
Intermediate­
term
handler
risks
from
agricultural
and
non­
crop
uses
are
not
of
concern
at
the
highest
possible
level
of
mitigation
for
all
assessed
exposure
scenarios.
Out
of
a
total
of
31
agricultural
and
non­
crop
occupational
handler
scenarios,
five
have
potential
cancer
risks
greater
than
1
x
10­
4
at
the
highest
feasible
level
of
mitigation
and
are
of
concern,
and
26
have
cancer
risks
between
1
x
10­
4
and
1
x
10­
6
at
the
highest
feasible
level
of
mitigation.
Though
there
are
potential
postapplication
exposures
to
workers
during
the
agricultural
and
non­
crop
uses
associated
with
diuron,
a
noncancer
postapplication
assessment
was
not
conducted,
since
no
dermal
toxicity
is
expected
from
short
or
intermediate­
term
exposures.
All
potential
postapplication
cancer
risks
to
private
growers
and
commercial
applicators
were
estimated
to
be
less
than
1
x
10­
4
on
the
day
of
treatment.
!
Occupational
risk
assessments
were
also
conducted
for
the
use
of
diuron
as
a
mildewcide
in
paint.
With
mitigation,
there
are
no
concerns
for
noncancer
risks
to
occupational
handlers
exposed
to
paints
containing
diuron,
except
for
intermediate­
term
inhalation
risks
from
applying
paints
with
an
airless
sprayer
(
indoors).
With
mitigation,
all
occupational
mildewcide
scenarios
have
potential
cancer
risks
between
1
x
10­
4
and
1
x
10­
6.
Postapplication
exposures
are
expected
to
be
minimal.
!
The
occupational
handler
scenarios
identified
for
the
use
of
diuron
in
commercial
fish
production
have
estimated
noncancer
risks
that
are
not
of
concern
at
the
baseline
level
of
mitigation.
With
maximum
mitigation
measures,
all
the
fish
production
scenarios
have
estimated
cancer
risks
of
less
than
1
x
10­
6
and
are
not
of
concern.
Postapplication
exposures
to
diuron
in
treated
fish
production
ponds
is
minimal
and
not
of
concern.
!
For
residential
handlers
exposed
during
paint
and,
pond
and
aquarium
uses,
the
noncancer
risks
are
not
of
concern
but,
potential
cancer
risks
are
greater
than
1
x
10­
6
and
are
of
concern,
except
for
the
loading
ready­
to­
use
liquids
for
ponds
and
aquariums
scenario,
which
is
not
of
concern.
Postapplication
inhalation
and
dermal
exposure
resulting
from
the
use
of
diuron
in
ponds
and
aquariums,
and
from
the
indoor
use
of
diuron
in
paints,
is
expected
to
be
minimal.
7
2.0
PHYSICAL/
CHEMICAL
PROPERTIES
CHARACTERIZATION
Diuron
[
3­(
3,4­
dichlorophenyl)­
1,1­
dimethylurea]

Empirical
formula:
C9H10Cl
2N2O
Molecular
weight:
233.1
CAS
Registry
No.:
330­
54­
1
PC
Code:
035505
NH
N
CH
3
CH3
O
Cl
Cl
The
product
chemistry
data
base
is
not
complete;
new
confidential
statement
of
formula
(
CSF)
data
are
required
which
reflect
preliminary
analyses
of
current
products
together
with
discussions
of
formation
of
impurities.
Trace
amounts
of
a
manufacturing
impurity,
tetrachloro­
azobenzene
(
TCAB),
that
are
of
toxicological
concern,
may
be
present
(
see
Section
3.5).
The
available
Generic
Series
830
physical
and
chemical
properties
of
diuron
are
given
below
(
Diuron.
List
A
Reregistration
Case
0046.
PC
Code
035505.
Product
Chemistry
Chapter
for
the
Reregistration
Eligibility
Decision
[
RED]
Document.
DP
Barcode
D274489.
Ken
Dockter.
June
26,
2001).

Table
1.
Generic
Series
830
Physical
and
Chemical
Properties
GLN
MRID
Data
6302
Color
1
White
6303
Physical
state
1
Crystal
6304
Odor
1
None
7200
MP
1
158o
C
7840
Water
solubility
1
42
ppm
@
25o
C
7950
vp
1
2
x
10­
7
mm
Hg
@
30o
C
7550
Log
Pow
2
2.68
6320
Corrosion
characteristics
43842201
Not
corrosive
8
6313
Stability
to
normal
and
elevated
temperatures,
metals,
and
metal
ions
43842201
Stable
for
2
yrs.
in
double
polyethylene
bag
inside
a
fiber
drum
under
warehouse
conditions.
Metals
and
metal
ion
data
not
given.

7050
UV/
Visible
absorption
NG
NG:
Not
Given.

1
Diuron.
CASRN:
330­
54­
1.
http://
toxnet.
nlm.
nih.
gov/
egi­
bin/
sis/
search.

2
Reddy,
K.
N.
and
M.
A.
Locke.
1996.
Molecular
Properties
as
Descriptors
of
Octanol­
Water
Partition
Coefficients
of
Herbicides.
Water,
Air
and
Soil
Pollution
Vol.
86:
pp
389­
405.

3.0
HAZARD
CHARACTERIZATION
3.1
Hazard
Profile
Diuron
is
a
substituted
urea
herbicide
for
the
control
of
a
wide
variety
of
annual
and
perennial
broad
leaved
and
grassy
weeds
on
both
crop
and
non­
crop
sites.
The
mechanism
of
herbicidal
action
is
the
inhibition
of
photosynthesis.
Diuron
has
a
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
(
Diuron
­
Toxicology
Disciplinary
Chapter
for
the
Reregistration
Eligibility
Decision.
Yung
Yang.
0ctober
2,
2001).

The
primary
diuron
target
organs
are
the
hematopoietic
system,
bladder,
and
renal
pelvis.
Erythrocyte
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
edema
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
in
both
sexes.
9
Although
the
developmental
toxicity
study
in
rats
is
classified
as
unacceptable,
the
data
base
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.

The
HED
Carcinogenicity
Peer
Review
Committee
(
CPRC)
characterized
diuron
as
a
"
known/
likely"
human
carcinogen,
based
on
urinary
bladder
carcinomas
in
both
sexes
of
the
Wistar
rat,
kidney
carcinomas
in
the
male
rat
(
a
rare
tumor),
and
mammary
gland
carcinomas
in
the
female
NMRI
mouse.
The
CPRC
also
recommended
a
low
dose
linear
extrapolation
model
with
a
Q1
*
of
1.91
x
10­
2
(
mg/
kg/
day)­
1
be
applied
to
the
animal
data
for
the
quantification
of
human
risk,
based
on
the
urinary
bladder
carcinomas
in
the
rat.
Diuron
was
not
mutagenic
in
bacteria
or
in
cultured
mammalian
cells
and
no
indication
of
DNA
damage
in
primary
rat
hepatocytes
was
observed.
There
were
marginal
statistically
significant
increases
in
cells
with
structural
aberrations
in
a
Sprague
Dawley
rat
in
vivo
bone
marrow
chromosomal
aberration
assay.
However,
the
levels
of
aberrations
were
within
the
historical
control
range
and
assessed
negative.

The
Hazard
Identification
Assessment
Review
Committee
(
HIARC)
determined
that
a
28­
day
inhalation
study
is
required
to
address
the
concern
for
inhalation
exposure
potential
based
on
the
use
pattern.
The
registrant
can
follow
the
90­
day
inhalation
study
protocol
but
cease
exposure
at
28
days.
The
HIARC
also
determined
that
a
repeated
chronic
dog
study
is
not
required;
a
new
study
would
not
provide
additional
data
since
the
observed
effects
are
similar
in
the
rat
and
the
rat
is
the
more
sensitive
species
for
this
chemical.

Table
2.
Acute
Toxicity
of
Diuron
Guideline
No.
Study
Type
MRID
#
Results
Toxicity
Category
870.1100
Acute
Oral
00146144
LD50
=
4721
mg/
kg
(
M)
>
5000
mg/
kg
(
F)
III
870.1200
Acute
Dermal
00146146
LD50
>
2000
mg/
kg
III
870.1300
Acute
Inhalation
40228803
LC50
>
7.1
mg/
L
IV
870.2400
Primary
Eye
Irritation
00146147
At
48
hrs,
all
irritation
had
cleared.
III
870.2500
Primary
Skin
Irritation
00146148
All
irritation
had
cleared
by
72
hrs.
IV
870.2600
Dermal
Sensitization
00146149
Nonsensitizer
N/
A
870.6200
Acute
Neurotoxicity
N/
A
Not
available
N/
A
10
Table
3.
Subchronic,
Chronic
and
Other
Toxicity
Guideline
#/
Study
Type
MRID
#
(
year)/
Classification/
Doses
Results
870.3100
90­
Day
oral
toxicity
in
rats
MRID
40886502
(
1988)
Acceptable/
Nonguideline
0,
4,
10,
or
25
ppm
(
0,
0.3,
0.7,
or
1.6
mg/
kg/
day
for
males
and
0,
0.3,
0.8,
1.8
mg/
kg/
day
for
females)
The
NOAEL
can
not
be
determined
based
on
equivocal
findings
in
the
urinary
bladder
including
blood
vessel
dilation,
reduced
transparency,
and
increased
firmness.

870.3200
21/
28­
Day
dermal
toxicity
in
rabbits
MRID
42718301
(
1992)
Acceptable/
Guideline
0,
50,
500,
or
1200
mg/
kg/
day
Systemic
toxicity
NOAEL
=
1200
mg/
kg/
day
(
HDT)

870.3465
90­
Day
inhalation
toxicity
Not
available
Not
available
870.3700a
Prenatal
developmental
toxicity
in
rats
MRID
40228801
(
1986)
Unacceptable/
Guideline
0,
16,
80,
or
400
mg/
kg/
day
Maternal
toxicity
NOAEL
=
16
mg/
kg/
day.
Maternal
toxicity
LOAEL
=
80
mg/
kg/
day,
based
on
decreased
body
weight
gain
and
food
consumption.

Developmental
toxicity
NOAEL=
80
mg/
kg/
day.
Developmental
toxicity
LOAEL
=
400
mg/
kg/
day,
based
on
whole
litter
resorption,
reduced
fetal
body
weights,
and
delayed
ossification
of
the
vertebrae
and
sternebrae.

870.3700b
Prenatal
developmental
toxicity
in
rabbits
MRID
40228802
(
1986)
Acceptable/
Guideline
0,
2,
10,
or
50
mg/
kg/
day
Maternal
toxicity
NOAEL
=
10
mg/
kg/
day.
Maternal
toxicity
LOAEL
=
50
mg/
kg/
day,
based
on
decreased
body
weight
and
food
consumption.

Developmental
toxicity
NOAEL
=
50
mg/
kg/
day
(
HDT).

870.3800
Reproduction
and
fertility
effects
in
rats
MRID
41957301
(
1990)
Acceptable/
Guideline
0,
10,
250,
or
1750
ppm.
(
0,
0.58,
14.8,
or
101
mg/
kg/
day
for
males
and
0,
0.71,
18.6,
or
132
mg/
kg/
day
for
females,
respectively.
Parental
NOAEL
=
250
ppm
(
18.6
mg/
kg/
day).
Parental
LOAEL
=
1750
ppm
(
132
mg/
kg/
day)
based
on
decreased
body
weight,
body
weight
gain,
food
consumption
and
food
efficiency
in
both
generations.

Reproductive
NOAEL
=
1750
ppm
(
HDT).

Offspring
NOAEL
=
250
ppm
(
18.6
mg/
kg/
day).
Offspring
LOAEL
=
1750
ppm
(
132
mg/
kg/
day)
based
on
decreased
body
weight
of
the
F1
and
F2
pups
during
lactation.

870.4200b
Chronic
toxicity
in
dogs
MRID
00091192
(
1964)
Unacceptable/
Guideline
0,
25,
125,
250,
or
2500/
1250
ppm
(
0,
1.8,
9.4,
18.8,
or
93.8
mg/
kg/
day
by
conversion
factor
of
0.075)
for
24
months.
NOAEL
=
125
ppm
(
9.4
mg/
kg/
day)
in
males
and
250
ppm
(
18.8
mg/
kg/
day)
for
females.
LOAEL
=
250
ppm
(
18.8
mg/
kg/
day)
for
males
and
1250
ppm
(
93.8
mg/
kg/
day)
for
females
based
on
anemia
and
body
weight
losses.
Guideline
#/
Study
Type
MRID
#
(
year)/
Classification/
Doses
Results
11
870.4300
Combined
Chronic/
Carcinogenicity
in
rats
MRID
40886501,43871901,
43804501,
44302003
(
1986)
Acceptable/
Guideline
0,
25,
250,
2500
ppm
(
0,
1.0,
10,
or
111
mg/
kg/
day
for
males
and
0,
1.7,
17,
or
203
mg/
kg/
day
for
females)
for
24
months.
NOAEL
=
Not
established.
LOAEL
=
25
ppm
(
1.0
mg/
kg/
day
for
males
and
1.7
mg/
kg/
day
for
females)
based
on
evidence
of
hemolysis
and
compensatory
hematopoiesis
(
decreased
erythrocyte
counts,
increased
reticulocyte
counts,
increased
spleen
weight
and
bone
marrow
activation).

Dosing
was
considered
adequate.

870.4300
Carcinogenicity
in
mice
MRID
42159501
(
1983)
Acceptable/
Guideline
0,
25,
250,
or
2500
ppm
(
0,
5.4,
50.8,
or
640.13
mg/
kg/
day
for
males
and
0,
7.5,
77.5,
or
867.0
mg/
kg/
day
for
females)
for
24
months
NOAEL
=
250
ppm
(
50.8
and
77.5
mg/
kg/
day)
for
males
and
females.
LOAEL
=
2500
ppm
(
640.1
and
867.0
mg/
kg/
day)
for
males
and
females
based
on
hemolytic
anemia
and
liver
toxicity
in
both
sexes
and
urinary
bladder
toxicity
in
females.

Dosing
was
considered
adequate.

870.5100
Gene
mutation
Salmonella
typhimurium
reverse
gene
mutation
MRID
00146608
(
1985),
40228805
(
1991)
Acceptable/
Guideline
Independent
trials
were
negative
in
S.
typhimurium
strains
TA1535,
TA97,
TA98
and
TA100
up
to
the
highest
doses
tested
(
10
µ
g/
plate
­
S9;
250
µ
g/
plate
+
S9);
higher
concentrations
(
$
50
µ
g/
plate
­
S9;
500
µ
g/
plate
+
S9)
were
cytotoxic.

870.5300
Gene
mutation
Chinese
hamster
ovary
(
CHO)/
HGPRT
cell
forward
gene
mutation
assay
MRID
00146609
(
1985)
Acceptable/
Guideline
Independent
tests
were
negative
up
to
cytotoxic
doses
without
S9
activation
(
1.250
mM,
.
291
µ
g/
mL)
and
with
S9
activation
(
0.5
mM
.
117
µ
g/
mL).

870.5375
Chromosomal
aberration
in
vivo
rat
bone
marrow
cytogenetic
assay
MRID00146611
(
1985)
MRID
44350301
(
1997)
(
revised)
Acceptable/
Guideline
The
test
was
negative
in
Sprague
Dawley
rats
up
to
cytotoxic
doses.
A
significant
(
p<
0.05)
increase
in
the
percentage
of
abnormal
cells
and
the
average
number
of
aberrations
per
cell
was
seen
but
only
when
the
data
were
combined
for
the
high­
and
mid­
dose
males
and
females
at
the
48­
hour
sampling
time.
A
significant
positive
linear
trend
was
also
recorded
for
the
combined
(
by
sex)
aberrations
per
cell
and
percentage
abnormal
cells.
Nevertheless,
the
values
fell
well
within
the
range
of
historical
control
ranges.

870.5375
Mouse
Bone
Marrow
Micronucleus
MRID
45494502
(
1995)
80%
ai,
45494503
(
1995)
42.4%
ai,
45494504
(
1996)
80%
ai,
45494505
(
1998)
98.1%
ai
Acceptable/
Guideline
Preliminary
review
indicates
no
evidence
of
cytogenetic
effect
in
mice
administered
either
technical
grade
or
formulated
diuron.

870.5550
Unscheduled
DNA
Synthesis
MRID
00146610
(
1985)
Acceptable/
Guideline
The
test
was
negative
up
to
cytotoxic
doses
(
$
0.33
mM,
equivalent
to
.
76
F
g/
mL).
Guideline
#/
Study
Type
MRID
#
(
year)/
Classification/
Doses
Results
12
870.7485
Metabolism
and
pharmacokinetics
MRID
42010501
(
1996)
Acceptable/
Guideline
Diuron
was
rapidly
absorbed,
metabolized
and
excreted.
Urine
was
the
major
route
of
excretion.
Metabolism
of
diuron
involved
Noxidation
ring
hydroxylation,
demethylation,
dechlorination,
and
conjugation
to
sulfate
and
glucuronic
acid.

870.7600
Dermal
penetration
Not
available
for
diuron.
Not
available.

3.2
FQPA
Considerations
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
HIARC
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.
The
HIARC
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.

No
acute
or
subchronic
neurotoxicity
study
is
available.
However,
there
are
no
neurotoxic
signs
in
any
of
the
submitted
subchronic
or
chronic
studies
and
a
literature
search
did
not
reveal
any
studies
relevant
for
assessing
the
potential
neurotoxicity
of
diuron.

The
FQPA
Safety
Factor
Committee
concluded
that
the
safety
factor
could
be
removed
(
1x)
for
diuron
because
(
DIURON
­
Report
of
the
FQPA
Safety
Factor
Committee.
Brenda
Tarplee.
August
7,
2001):

g)
There
is
no
indication
of
quantitative
or
qualitative
increased
susceptibility
of
rats
or
rabbits
to
in
utero
or
postnatal
exposure;
h)
A
DNT
study
with
diuron
is
not
required;
and
i)
The
dietary
(
food
and
drinking
water)
and
non­
dietary
(
residential)
exposure
assessments
will
not
underestimate
the
potential
exposures
for
infants
and
children.

3.3
Dose
Response
Assessment
13
Diuron
has
low
acute
toxicity
and
no
developmental
or
neurotoxic
concerns.
Since
no
adverse
effects
attributable
to
a
single
exposure
were
identified
in
available
studies,
no
acute
dietary
endpoint
was
chosen.
Also,
no
systemic
toxicity
was
observed
following
repeated
dermal
dosing
up
to
1200
mg/
kg/
d.
Therefore,
no
short­
or
intermediate­
term
dermal
endpoints
were
chosen
either.
The
shortterm
incidental
oral
and
the
inhalation
endpoints
are
based
on
maternal
decreased
body
weight
and
food
consumption
observed
in
a
rabbit
developmental
toxicity
study.
The
chronic
dietary,
intermediate­
term
inhalation,
and
long­
term
dermal
and
inhalation
endpoints
are
based
on
hemolytic
anemia
and
compensatory
hematopoiesis
(
DIURON:
2nd
Report
of
the
Hazard
Identification
Assessment
Review
Committee.
Yung
Yang.
August
28,
2001).

3.3.1
Acute
RfD
None
selected.
No
adverse
effects
attributed
to
a
single
exposure
(
dose)
were
identified
including
in
the
rat
or
rabbit
developmental
toxicity
studies.

3.3.2
Chronic
RfD
The
study
selected
was
an
acceptable/
guideline
chronic
toxicity/
oncogenicity
study
(
MRID
40886501;
supplemental
MRIDs
43871901,
43804501,
and
44302003),
in
which
diuron
(
98.7%
a.
i)
was
administered
to
groups
of
60
male
and
60
female
Wistar
rats
at
dietary
concentrations
of
0,
25,
250,
or
2500
ppm
(
0,
1.0,
10,
or
111
mg/
kg/
d,
respectively,
for
males
and
0,
1.7,
17,
or
203
mg/
kg/
d
for
females,
respectively)
for
up
to
24
months.
At
12
months,
10
animals/
sex/
group
were
sacrificed
for
interim
evaluation.
Treatment
with
diuron
did
not
affect
the
survival
of
rats.
The
only
reported
treatment­
related
clinical
sign
was
reddish
discolored
or
bloody
urine
in
some
high­
dose
males.
A
significant
decrease
in
body
weight
and
body
weight
gain
was
seen
in
both
sexes
of
high­
dose
rats
throughout
the
study.

Diuron
affected
the
hematopoietic
system
resulting
in
hemolytic
anemia
and
compensatory
hematopoiesis,
which
were
manifested
as
significantly
decreased
erythrocyte
counts,
hemoglobin
levels,
and
hematocrit
and
increased
MCV,
MCH,
abnormal
erythrocyte
forms,
reticulocyte
counts,
and
leukocyte
counts.
See
Diuron
­
Toxicology
Disciplinary
Chapter
for
the
Reregistration
Eligibility
Decision.
Yung
Yang.
October
2,
2001.
Gross
pathology
showed
that
the
incidence
of
urinary
bladder
wall
thickening
was
elevated
at
24
months
for
low­
and
high­
dose
males
and
high­
dose
females
(
p<
0.05
or
0.01).
Microscopic
evaluation
showed
that
epithelial
focal
hyperplasia
of
the
urinary
tract
and
renal
pelvis
increased
in
severity
in
both
sexes
at
12
and/
or
24
months,
and
increased
in
incidence
in
highdose
males
at
12
months
and
in
high­
dose
females
at
12
and/
or
24
months
with
mid­
dose
females
showing
an
increased
incidence
at
24
months.
Some
gross
and/
or
microscopic
changes
were
also
seen
in
the
liver
(
increased
weight,
swelling,
discoloration,
vacuolar
cell
degeneration,
round
cell
infiltration,
hyperemia),
although
these
effects
were
not
clearly
primary
effects
of
treatment.

The
dose
and
endpoint
for
establishing
the
chronic
RfD
is
the
LOAEL
=
1.0
mg/
kg/
day
based
on
14
Chronic
RfD
=
1.0
(
LOAEL)
mg/
kg/
day
=
0.003
mg/
kg/
day
300
(
UF)
evidence
of
hemolytic
anemia
and
compensatory
hematopoiesis
(
decreased
erythrocyte
count,
increased
reticulocyte
counts,
increased
spleen
weight
and
bone
marrow
activation).
A
NOAEL
was
not
established.
A
total
UF
of
300
was
applied
(
UF
of
100
to
account
for
both
interspecies
extrapolation
and
intra­
species
variability,
an
additional
UF
of
3
to
account
for
the
lack
of
a
NOAEL).

3.3.3
Short­
term
(
1­
30
days)
Incidental
Oral
Exposure
The
study
selected
was
an
acceptable/
guideline
developmental
toxicity
study
in
rabbits
(
MRID#
40228802).
In
the
developmental
toxicity
study,
24­
25
artificially
inseminated
New
Zealand
white
rabbits
per
group
were
administered
0,
2,
10,
or
50
mg/
kg/
day
of
Diuron
(
99%
a.
i.)
by
gavage
on
gestation
days
(
GD)
7­
19,
inclusive.
On
GD
29,
all
surviving
does
were
sacrificed
and
examined
grossly.
One
control
animal
died
on
GD
0
due
to
an
anaphylactic
shock
reaction
during
insemination
and
one
high­
dose
doe
aborted
and
was
killed
on
GD
26.
These
deaths
were
considered
unrelated
to
treatment.
All
remaining
animals
survived
to
scheduled
termination.
No
treatment­
related
clinical
signs
of
toxicity
were
observed
in
any
animal.
Maternal
liver
weights
were
comparable
between
the
treated
and
control
groups
and
gross
necropsy
was
unremarkable.

Maternal
body
weights,
body
weight
gains,
and
food
consumption
for
the
low­
and
mid­
dose
groups
were
similar
to
the
control
levels
throughout
the
study.
Absolute
body
weights
of
the
high­
dose
does
were
significantly
less
than
the
controls
on
GD
20.
Mean
body
weight
gains
by
the
high­
dose
group
were
significantly
reduced
as
compared
with
the
controls
during
the
intervals
of
GD
10­
13,
13­
16,
and
7­
20
(
weight
loss).
Weight
gain
by
the
high­
dose
group
was
significantly
greater
than
the
controls
during
the
post­
dosing
interval.
Food
consumption
by
the
high­
dose
group
was
significantly
less
than
the
controls
during
the
GD
13­
16,
16­
20
and
7­
20
intervals.
The
maternal
toxicity
LOAEL
was
established
at
50
mg/
kg/
day
based
on
decreased
body
weights
and
food
consumption
during
the
dosing
interval.
The
maternal
toxicity
NOAEL
was
established
at
10
mg/
kg/
day.

At
cesarean
section,
the
pregnancy
rates,
numbers
of
corpora
lutea,
implantation
sites,
resorptions,
and
live
fetuses,
and
fetal
body
weights
were
similar
between
the
treated
and
control
groups.
No
doseor
treatment­
related
external,
visceral,
or
skeletal
malformations/
variations
were
observed
in
any
fetus.
Therefore,
the
developmental
toxicity
NOAEL
is
$
50
mg/
kg/
day
and
the
developmental
toxicity
LOAEL
is
not
identified.

The
dose
and
endpoint
selected
for
risk
assessment
is
10
mg/
kg/
day
(
NOAEL)
based
on
maternal
toxicity
(
decreased
body
weights
and
food
consumption
during
the
dosing
interval)
at
50
mg/
kg/
day
(
LOAEL).
An
UF
of
100
to
account
for
both
interspecies
extrapolation
and
intra­
species
variability
was
applied
and,
since
the
FQPA
safety
factor
was
reduced
to
1x,
the
LOC
is
100
and
the
calculated
15
MOEs
must
be
100
or
above.

NOTE:
This
study
was
previously
classified
as
unacceptable/
upgradable
based
on
deficiencies
in
analytical
data
of
sample
analysis.
However,
the
HIARC
determined
that
this
study
is
acceptable
because
the
low
nominal
level
of
sample
concentration
was
observed
at
the
low
dose
only
and
the
NOAEL
was
established
at
the
mid­
dose
with
the
LOAEL
at
the
high­
dose.
Therefore,
the
deficiencies
in
the
analytical
data
did
not
affect
the
results
of
the
study.
The
systemic
toxicity
(
expressed
as
maternal
toxicity)
is
relevant
for
the
populations
(
infants
and
children)
and
duration
(
1­
30
days)
of
concern.

Short­
term
incidental
oral
LOC
=
100
3.3.4
Intermediate­
term
(
1­
6
months)
Incidental
Oral
Exposure
The
study
selected
was
the
chronic
toxicity/
carcinogenicity
study
in
rats
(
MRID#
40886501,
43871901,
43804501,
44302003).
See
Chronic
RfD,
section
3.3.2.
The
dose
and
endpoint
for
risk
assessment
was
a
NOAEL
of
1.0
mg/
kg/
day
based
on
hematological
effects
observed
at
10
mg/
kg/
day
(
LOAEL)
at
the
6th
month
observation.
It
is
noted
that
this
NOAEL/
LOAEL
is
different
from
the
24th
month
observation
where
the
NOAEL
is
not
established
(
LOAEL=
1.0
mg/
kg/
day).
The
endpoint
observed
at
the
6th
month
observation
period
is
appropriate
for
this
exposure
duration
and
is
relevant
for
the
population
of
concern.

A
UF
of
100
and
the
FQPA
safety
factor
of
1x
were
applied
to
the
risk
assessment;
therefore
the
LOC
=
100
and
the
calculated
MOEs
must
be
100
or
above.

Intermediate­
term
incidental
oral
LOC
=
100
3.3.5
Dermal
Absorption
No
dermal
absorption
study
is
available.
An
upper­
bound
estimation
of
dermal
absorption
of
4%
was
extrapolated
using
the
maternal
LOAEL
of
50
mg/
kg/
day
from
the
oral
developmental
toxicity
study
in
the
rabbit
and
the
NOAEL
of
1200
mg/
kg/
day
(
HDT)
from
the
21­
day
dermal
toxicity
study
in
the
rabbit:
the
ratio
is
50/
1200
or
4%.

Dermal
absorption
factor
=
4%

3.3.6
Short­
(
1­
30
days)
and
Intermediate­
term
(
1­
6
months)
Dermal
Exposure
None
selected.
No
systemic
toxicity
was
seen
following
repeated
dermal
dosing
at
1200
mg/
kg/
day
in
the
rabbit
dermal
toxicity
study.
Also,
there
is
no
developmental
toxicity
concern.
No
hazard
was
identified
and
no
quantitative
assessment
is
required.
16
3.3.7
Long­
term
(
6
months
to
life­
time)
Dermal
Exposure
The
study
selected
was
the
chronic
toxicity/
carcinogenicity
study
in
rats
(
MRID#
40886501,
43871901,
43804501,
44302003).
See
Chronic
RfD,
section
3.3.2.
The
dose
and
endpoint
selected
for
risk
assessment
was
1.0
mg/
kg/
day
(
LOAEL)
based
on
evidence
of
hemolytic
anemia
and
compensatory
hematopoiesis
(
decreased
erythrocyte
count,
increased
reticulocyte
counts,
increased
spleen
weight
and
bone
marrow
activation).
A
NOAEL
was
not
established.
An
additional
UF
of
3
is
applied
to
account
for
the
lack
of
a
NOAEL
in
this
study.
Therefore,
the
LOC
=
300.
An
MOE
<
300
with
a
dermal
absorption
factor
of
4%,
is
potentially
of
concern.

3.3.8
Inhalation
Exposure
(
All
Durations)

Except
for
an
acute
inhalation
study,
for
which
diuron
was
placed
in
Toxicity
Category
4
(
LC
50
>
7.1
mg/
L),
no
other
studies
are
available
via
this
route.
Therefore,
the
HIARC
selected
the
NOAELs
from
oral
studies
for
risk
assessment.
Since
the
doses
identified
for
inhalation
risk
assessment
are
from
oral
studies,
route­
to­
route
extrapolation
should
be
as
follows:

The
inhalation
exposure
component
(
i.
e.,
F
g
a.
i./
day)
using
a
100%
(
default)
absorption
rate
and
application
rate
should
be
converted
to
an
equivalent
oral
dose
(
mg/
kg/
day).
Then,
the
oral
equivalent
doses
should
be
compared
to
the
following
NOAELs/
LOAEL
to
calculate
the
MOEs.

Short­
term
NOAEL=
10
mg/
kg/
day
(
developmental
rabbit
study)
Intermediate­
term
NOAEL=
1.0
mg/
kg/
day
(
chronic
rat
study
at
6
month)
Long­
term
LOAEL=
1.0
mg/
kg/
day
(
chronic
rat
study)

A
UF
of
100
for
short­
and
intermediate­
term
exposures
and
a
UF
of
300
(
additional
3
is
applied
to
account
for
the
lack
of
a
NOAEL
in
the
study)
for
long­
term
exposures,
and
the
FQPA
safety
factor
of
1x,
were
applied
to
the
risk
assessment;
therefore
the
LOCs
=
100,
100,
and
300,
respectively.

Short­
term
inhalation
LOC
=
100
Intermediate­
term
inhalation
LOC
=
100
Long­
term
inhalation
LOC
=
300
3.3.9
Carcinogenic
Potential
3.3.9.1
Combined
Chronic
Toxicity/
Carcinogenicity
Study
in
Rats
An
acceptable/
guideline
combined
chronic
toxicity/
carcinogenicity
study
in
rats
was
submitted
(
MRID#
40886501,
43871901,
43804501,
44302003).
This
study
showed
conclusive
evidence
for
the
carcinogenicity
of
diuron
in
male
and
female
rats.
The
incidence
of
urinary
bladder
carcinoma
was
increased
at
2500
ppm
in
both
sexes
(
males:
33/
49
vs.
1/
50
for
controls;
females:
11/
50
vs.
0/
48
for
17
controls;
p<
0.01).
The
malignancies
were
usually
characterized
as
transitional
epithelial
carcinomas.
The
slight
increase
(
not
statistically
significant)
in
the
incidence
of
urinary
bladder
papillomas
and
the
3
neoplasms
in
the
renal
pelvis
in
high­
dose
males
(
one
papilloma
and
two
carcinomas)
were
also
considered
treatment­
related.
Dosing
was
adequate
based
on
numerous
toxic
effects
(
hematological,
microscopic,
etc.)
observed
in
the
animals
at
all
tested
doses.

3.3.9.2
Carcinogenicity
Study
in
Mice
An
acceptable/
guideline
carcinogenicity
study
in
mice
was
submitted
(
MRID#
42159501,
43349301).
Treatment
of
up
to
102
weeks
with
2500
ppm
diuron
resulted
in
a
significant
increase
in
the
incidences
of
mammary
adenocarcinomas
(
control,
4%;
2500
ppm,
12%,
p
#
0.05)
and
ovarian
luteomas
(
control,
6%;
2500
ppm,
14%,
p
#
0.01)
in
female
NMRI
(
SPF
HAN)
mice
under
the
conditions
of
this
study.
However,
the
incidence
of
mammary
adenocarcinoma
in
high­
dose
females
was
at
or
near
the
high
range
of
incidences
seen
in
historic
controls.
Dosing
was
adequate
based
on
observations
at
the
highest
dose
tested,
including
decreased
body
weight
of
both
sexes,
increased
spleen
and
liver
weights
in
males
and
increased
incidence
of
urinary
bladder
edema
and
epithelial
hyperplasia,
thickened
mucosa
and
enlarged
uterine
horn
in
females.

3.3.9.3
Classification
of
Carcinogenic
Potential
The
HED
Carcinogenicity
Peer
Review
Committee
(
CPRC)
met
on
December
18,
1996
and
classified
diuron
as
a
"
known/
likely"
human
carcinogen,
based
on
urinary
bladder
carcinomas
in
both
sexes
of
the
Wistar
rat,
kidney
carcinomas
in
the
male
rat
(
a
rare
tumor),
and
mammary
gland
carcinomas
in
the
female
NMRI
mouse
(
Carcinogenicity
Peer
Review
of
Diuron.
Linda
Taylor
and
Esther
Rinde.
May
8,
1997).
The
CPRC
also
recommended
a
low
dose
linear
extrapolation
model
with
a
Q1
*
of
1.91
x
10­
2
(
mg/
kg/
day)­
1
be
applied
to
the
animal
data
for
the
quantification
of
human
risk,
based
on
the
urinary
bladder
carcinomas
in
the
rat
(
Diuron
­
Revised
Q1*,
(
3/
4'
s
Interspecies
Scaling
Factor),
1985
Wistar
Rat
2
Year
Dietary
Study.
PC
035505.
Bernice
Fisher.
September
23,
1998).

3.3.10
Mutagenicity
Acceptable
genetic
toxicology
studies
with
diuron
have
been
submitted
to
the
Agency.
Findings
from
these
studies
indicated
the
following:

Gene
Mutations
1)
Salmonella
typhimurium
reverse
gene
mutation
assay
(
MRID#
00146608/
40228805):
Independent
trials
were
negative.
2)
Chinese
Hamster
Ovary
(
CHO)/
HGPRT)
cell
forward
gene
mutation
assay
(
MRID#
00146609):
Independent
tests
were
negative
up
to
cytotoxic
doses
with/
without
S9
activation.

Chromosome
Aberrations
18
3)
In
vivo
bone
marrow
cytogenetic
assay
in
male
Sprague
Dawley
rats
administered
0,
50,
500
or
5000
mg/
kg/
day
by
single
oral
gavage
(
MRID#
00146611
and
44350301):
The
test
was
negative.
Signs
of
overt
toxicity
(
mortality,
body
weight
loss,
ocular
discharge,
depression,
labored
respiration,
diarrhea,
and
tremors)
were
noted
at
5000
mg/
kg.
Cytotoxicity
to
the
target
organ
as
indicated
by
the
significantly
decreased
(
p
#
0.01)
mitotic
indices
at
24
and
48
hours
for
high­
dose
males;
data
combined
for
both
sexes
were
also
significantly
decreased
at
24
hours.
A
significant
positive
linear
trend
was
also
recorded
for
the
combined
(
by
sex)
aberrations
per
cell
and
the
percentage
of
abnormal
cells.
Nevertheless,
the
values
fell
well
within
the
range
of
historical
controls.

4)
Mouse
bone
marrow
micronucleus
assays
(
MRIDs
45494502­
05):
Preliminary
review
indicates
no
evidence
of
cytogenetic
effect
in
mice
administered
either
technical
grade
or
formulated
diuron.

Other
Mutagenic
Mechanisms
5)
Unscheduled
DNA
synthesis
(
UDS)
in
primary
rat
hepatocytes
assay
(
MRID#
00146610):
The
test
was
negative
up
to
cytotoxic
doses.

Diuron
was
not
mutagenic
in
bacteria
or
in
cultured
mammalian
cells
and
no
indication
of
DNA
damage
in
primary
rat
hepatocytes
was
observed.
There
were
marginal
statistically
significant
increases
in
cells
with
structural
aberrations
in
a
Sprague
Dawley
rat
in
vivo
bone
marrow
chromosomal
aberration
assay.
However,
the
levels
of
aberrations
were
within
the
historical
control
range
and
assessed
negative.

3.3.11
Mechanism
of
Carcinogenicity
In
1996,
the
HED
CPRC
classified
diuron
as
a
"
known/
likely"
human
carcinogen,
based
on
urinary
bladder
carcinoma
in
both
sexes
of
the
Wistar
rat,
kidney
carcinomas
in
the
male
rat
(
a
rare
tumor),
and
mammary
gland
carcinomas
in
the
female
NMRI
mouse
[
Diuron
(
PC
035505):
Assessment
of
Mode
of
Action
on
Bladder
Carcinogenicity.
Yung
Yang.
September
20,
2001].
The
CPRC
also
recommended
a
low
dose
linear
extrapolation
model
with
Q1
*
of
1.91x10­
2
(
mg/
kg/
day)­
1
be
applied
to
the
animal
data
for
the
quantification
of
human
risk,
based
on
the
urinary
bladder
carcinomas
in
the
rat.

The
registrant
has
argued
that
this
assessment
needed
reconsideration
for
the
following
reasons
(
MRID
45494501):
1)
there
is
no
history
of
human
carcinogenesis
as
a
result
of
diuron
exposure,
2)
there
is
a
plausible
mode
of
action
that
discounts
the
relevance
of
the
rat
bladder
carcinomas
to
humans,
3)
the
mouse
historical
data
were
not
considered
in
their
entirety
and
should
be
considered
`
spontaneous,"
4)
the
structure
activity
relationships
actually
decrease
the
weight­
of­
the­
evidence
of
diuron
carcinogenicity
rather
than
increase
the
weight,
and
5)
new
guidelines
are
in
place
that
separate
the
`
known'
from
`
likely'
category.

The
Agency's
CPRC
and
Mechanism
of
Toxicity
Assessment
Review
Committee
(
MTARC)
have
reviewed
the
submitted
information/
data
[
Cancer
Classification
and
Mechanism
of
Action
(
MRID
19
45494501)
and
mutagenicity
studies
(
MRIDs
45494502­
05)],
considered
the
registrant's
proposed
mechanism
of
action
and
determined
that
diuron
will
not
be
re­
classified
at
this
time
(
DIURON:
Cancer
Classification
and
Mechanism
of
Action.
Yung
Yang.
October
10,
2001).
The
Agency
based
its
decision
on:
1)
the
registrant
did
not
submit
any
data
or
information
to
support
its
claim
that
there
is
no
evidence
of
human
carcinogenesis,
2)
the
submitted
information
is
insufficient
to
support
a
mode
of
action
on
bladder
carcinogenicity
for
diuron,
3)
the
mouse
historical
data
have
been
reviewed
and
included
in
the
updated
DER
(
MRIDs
42159501
and
43349301)
and
the
Agency
concluded
that
a
positive
oncogenic
response
was
seen
in
high­
dose
female
mice
compared
to
the
control
group,
4)
there
is
insufficient
evidence
to
support
the
notion
that
the
structure
activity
relationships
actually
decrease
the
weight­
of­
the­
evidence
of
diuron
carcinogenicity
rather
than
increase
the
weight,
and
5)
preliminary
reviews
have
been
conducted
on
newly
submitted
in
vivo
cytogenetic
mutagenicity
studies
[
Mouse
bone
marrow
micronucleus
assays
(
MRIDs
45494502­
05)]
and
no
evidence
of
cytogenetic
effect
was
seen
in
mice
administered
either
technical
grade
or
formulated
diuron;
however,
these
studies
provide
little
additional
information
since
the
CPRC
has
already
concluded
that
there
is
little
or
no
concern
for
the
mutagenic
activity
of
diuron.
20
Table
4.
Summary
of
Toxicology
Endpoint
Selection
EXPOSURE
SCENARIO
DOSE
(
mg/
kg/
day)
ENDPOINT
STUDY
Acute
Dietary
No
appropriate
endpoint
attributed
to
a
single
dose
was
identified.
Therefore,
an
acute
RfD
was
not
established.

Chronic
Dietary
LOAEL
=
1.0
UF
=
300
FQPA
SF
=
1*
Evidence
of
hemolytic
anemia
and
compensatory
hematopoiesis
(
significantly
decreased
erythrocyte
counts,
hemoglobin
levels,
and
hematocrit,
and
increased
MCV,
MCH,
abnormal
erythrocyte
forms,
reticulocyte
counts,
and
leukocyte
count)
Combined
chronic
toxicity/
carcinogenicity
study
in
rats
MRID
40886501,
43871901,
43804501,
44302003
Chronic
RfD
=
0.003
mg/
kg/
day
cPAD
=
0.003
mg/
kg/
day
Incidental
Oral,
short­
term
(
1­
30
days)
NOAEL=
10
UF
=
100
FQPA
SF
=
1*
Decreased
body
weight
and
food
consumption
at
maternal
LOAEL
of
50
mg/
kg/
day.
Developmental
toxicity
study
in
rabbits
MRID
40228802
LOC
for
residential
MOE
=
100
Incidental
Oral,
Intermediate­
Term
(
1­
6
months)
NOAEL
=
1.0
UF
=
100
FQPA
SF
=
1*
Altered
hematological
parameters
at
LOAEL
of
10
mg/
kg/
day,
observed
at
6
months.
Chronic
toxicity/
carcinogenicity
study
in
rats
MRID
40886501,
43871901,
43804501,
44302003
LOC
for
residential
MOE
=
100
Dermal,
Short­
Intermediate­
Term
No
systemic
toxicity
was
seen
following
repeated
dermal
dosing
at
1200
mg/
kg/
day
in
the
rabbit
dermal
toxicity
study.
Also,
there
is
no
developmental
concern.
No
hazard
was
identified
and
no
quantitative
assessment
is
required.

Dermal,
Long­
Term
(
6
months
to
lifetime

Absorption
factor
of
4%
used
for
conversion
from
oral
to
dermal
route
LOAEL
=
1.0
UF
=
300
FQPA
SF
=
1*
Evidence
of
hemolytic
anemia
and
compensatory
hematopoiesis
(
significantly
decreased
erythrocyte
counts,
hemoglobin
levels,
and
hematocrit,
and
increased
MCV,
MCH,
abnormal
erythrocyte
forms,
reticulocyte
counts,
and
leukocyte
count).
Chronic
toxicity/
carcinogenicity
study
in
rats
MRID
40886501,
43871901,
43804501,
44302003
LOC
for
occupational/
residential
MOE
=
300
Inhalation,
Short­
Term
(
1­
30
days)**
NOAEL
=
10
UF
=
100
FQPA
SF
=
1*
Decreased
body
weight
and
food
consumption
at
maternal
LOAEL
of
50
mg/
kg/
day.
Developmental
toxicity
study
in
rabbits
MRID
40228802
LOC
for
occupational/
residential
MOE
=
100
21
Inhalation,
Intermediate­
Term
(
1­
6
months)**
NOAEL
=
1.0
UF
=
100
FQPA
SF
=
1*
Altered
hematological
parameters
at
LOAEL
of
10
mg/
kg/
day,
observed
at
6
months.
Chronic
toxicity/
carcinogenicity
study
in
rats
MRID
40886501,
43871901,
43804501,
44302003
LOC
for
occupational/
residential
MOE
=
100
Inhalation,
Long­
Term
(
6
months
to
life­
time)**
LOAEL
=
1.0
UF
=
300
FQPA
SF
=
1*
Evidence
of
hemolytic
anemia
and
compensatory
hematopoiesis
(
significantly
decreased
erythrocyte
counts,
hemoglobin
levels,
and
hematocrit,
and
increased
MCV,
MCH,
abnormal
erythrocyte
forms,
reticulocyte
counts,
and
leukocyte
count).
Chronic
toxicity/
carcinogenicity
study
in
rats
MRID
40886501,
43871901,
43804501,
44302003
LOC
for
occupational/
residential
MOE
=
300
Cancer
Known/
likely
human
carcinogen
Urinary
bladder
carcinoma
in
both
sexes
of
the
Wistar
rat,
kidney
carcinomas
in
the
male
rat
(
a
rare
tumor),
and
mammary
gland
carcinomas
in
the
female
NMRI
mouse
Carcinogenicity
study
in
rats
and
mice
MRID
40886501,
43871901,
43804501,
44302003
and
42159501,
43349301
Q1*
=
1.91
x
10­
2
(
mg/
kg/
day)­
1
*
FQPA
SF
only
applied
to
residential
and
other
non­
occupational
exposures
**
An
oral
endpoint
was
used
for
inhalation
exposure:
inhalation
exposure
assumed
equivalent
to
oral
exposure.

3.4
Endocrine
Disruption
EPA
is
required
under
the
FFDCA,
as
amended
by
FQPA,
to
develop
a
screening
program
to
determine
whether
certain
substances
(
including
all
pesticide
active
and
other
ingredients)
"
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen,
or
other
such
endocrine
effects
as
the
Administrator
may
designate."
Following
the
recommendations
of
its
Endocrine
Disruptor
Screening
and
Testing
Advisory
Committee
(
EDSTAC),
EPA
determined
that
there
was
scientific
bases
for
including,
as
part
of
the
program,
the
androgen
and
thyroid
hormone
systems,
in
addition
to
the
estrogen
hormone
system.
EPA
also
adopted
EDSTAC's
recommendation
that
the
Program
include
evaluations
of
potential
effects
in
wildlife.
For
pesticide
chemicals,
EPA
will
use
FIFRA
and,
to
the
extent
that
effects
in
wildlife
may
help
determine
whether
a
substance
may
have
an
effect
in
humans,
FFDCA
authority
to
require
the
wildlife
evaluations.
As
the
science
develops
and
resources
allow,
screening
of
additional
hormone
systems
may
be
added
to
the
Endocrine
Disruptor
Screening
Program
(
EDSP).

When
the
appropriate
screening
and/
or
testing
protocols
being
considered
under
the
Agency's
EDSP
have
been
developed,
diuron
may
be
subjected
to
additional
screening
and/
or
testing
to
better
22
characterize
effects
related
to
endocrine
disruption.

At
this
time,
neither
the
available
submitted
studies
on
diuron
nor
the
literature
show
any
indication
of
endocrine
disruption
effects.

3.5
Potential
Tetrachloroazobenzene
Contamination
Diuron
has
been
reported
to
contain
trace
amounts
of
a
manufacturing
impurity,
3,3',
4,4'­
tetrachloroazobenzene,
a.
k.
a.
TCAB,
which
has
been
shown
to
be
a
cytochrome
P450
enzyme
inducer.
A
summary
of
short­
term
bioassays
compiled
by
the
National
Toxicology
Program
states
that
(
TOX­
65,
1998),

"
3,3',
4,4'­
tetrachloroazobenzene
caused
typical
dioxin­
like
effects,
such
as
thymic
atrophy,
an
increase
in
liver
weights,
induction
of
hepatic
cytochrome
P4501A,
and
decreased
mean
body
weight
gains.
Furthermore,
in
the
13­
week
studies,
a
sharp
decrease
in
circulating
thyroxine
concentrations
was
observed
even
at
the
lowest
dose
(
0.1
mg/
kg)
tested
in
rats.
Other
effects
included
a
decrease
in
epididymal
spermatozoal
concentration
in
mice,
major
effects
on
the
hematopoietic
system,
and
increased
incidences
of
hyperplasia
of
the
forestomach
in
3
and
30
mg/
kg
males
and
30
mg/
kg
females.
A
no­
observable­
adverse­
effect­
level
(
NOAEL)
was
not
reached
in
rats.
The
NOAEL
in
mice
was
0.1
mg/
kg.
Comparison
of
various
dioxin­
like
effects
in
these
studies
with
those
reported
in
the
literature
indicate
that
3,3',
4,4'­
tetrachloroazobenzene
is
six
to
two
orders
of
magnitude
less
potent
than
2,3,7,8­
tetrachlorodibenzo­
p­
dioxin."

Chronic
toxicity/
carcinogenicity
studies
are
not
available
for
TCAB.
The
specific
endpoint(
s)
and
related
dose
levels
that
may
be
observed
in
chronic
toxicity
studies,
or
the
specific
carcinogenic
potential
of
this
compound
is
not
known.
However,
since
it
is
assumed
that
TCAB
may
have
been
present
in
all
diuron
toxicological
test
materials,
including
the
test
material
for
the
chronic
toxicity/
carcinogenicity
studies,
the
Agency
believes
that
the
risks
from
exposure
to
diuron
(
including
carcinogenic
potential)
have
not
been
underestimated.

4.0
EXPOSURE
ASSESSMENT
AND
CHARACTERIZATION
4.1
Summary
of
Registered
Uses
Diuron
is
an
herbicide
currently
registered
for
use
on
a
variety
of
fruit,
vegetable,
nut,
and
field
crops.
At
this
time,
products
containing
diuron
are
intended
for
both
occupational
and
non­
occupational
(
residential)
uses.
Occupational
uses
include
agricultural
food
and
non­
food
crops;
fruit
and
nut
crops;
ornamental
trees,
flowers,
and
shrubs;
paints
and
coatings;
ornamental
fish
and
catfish
production;
and
non­
crop
areas
such
as
rights­
of­
way
and
industrial
sites.
Non­
occupational
uses
include
residential
ponds,
aquariums,
and
paints.
23
Diuron
is
a
pre­
and
post­
emergent
herbicide
that
controls
a
wide
variety
of
annual
and
perennial
broad
leafed
and
grassy
weeds
on
both
crop
and
non­
crop
sites.
Examples
of
the
types
of
weeds
that
diuron
is
used
to
control
include
(
but
are
not
limited
to)
the
following:
button
weed,
pigweed,
carpetweed,
poison
ivy,
milkweed,
vines,
chickweed,
ragweed,
aster,
thistle,
dandelion,
morning
glory,
mustard,
wild
turnip,
pepper
weed,
wild
oat,
Bermuda
grass,
orchard
grass,
crabgrass,
love
grass,
fescue,
velvet
grass,
rye
grass,
witch
grass,
and
blue
grass.
Diuron
is
also
used
as
a
mildewcide
in
paints
and
an
algaecide
in
ponds.

Diuron
is
formulated
as
a
technical
product
and
formulation
intermediate
(
98.8
to
80
%
ai),
granular
(
0.2
%
to
20
%
ai),
pellet/
tablet
(
0.51
%
to
19
%
ai),
wettable
powder
(
25
%
to
80
%
ai),
dry
flowable
(
water
dispersible
granules;
40
%
to
80
%
ai),
emulsifiable
concentrate
(
2
%
to
80
%
ai),
flowable
concentrate
(
19
%
to
47.5
%
ai),
soluble
concentrate
(
5.1
%
to
40
%
ai),
and
ready­
to­
use
solution
(
0.67
%
to
19
%
ai).
Application
rates
range
from
0.8
to
87.1
lbs
ai/
acre.

Equipment
for
commercial
use
includes
groundboom
sprayer,
aerial
equipment,
chemigation,
rightsof
way
sprayer,
high­
pressure
handwand,
low­
pressure
handwand,
tractor­
drawn
spreader,
push­
type
spreader,
airless
sprayer,
paintbrush,
shaker­
type
applicator,
backpack
sprayer,
backpack
granular
spreader,
belly
grinder,
and
by
hand.
Products
intended
for
residential
use
may
be
applied
using
a
spoon,
by
hand,
by
airless
sprayer,
or
by
paintbrush/
roller.

Diuron
is
generally
applied
to
the
soil
prior
to
germination
of
weed
seeds
or
when
weeds
are
in
an
active
growth
stage.
Diuron
may
also
be
applied
as
a
post­
emergent
herbicide,
either
as
a
directed
spray
or
over
the
top
of
resistant
foliage.
It
may
be
applied
one
to
two
times
per
season,
with
the
exception
of
sugarcane
(
three
times
per
season)
to
control
a
wide
range
of
broad
leafed
and
grassy
weeds.

Occupational­
Use
Sites
The
occupational
crop
use
sites
in
this
assessment
have
been
grouped
as
follows:

Vegetables
and
Field
Crops:
alfalfa
(
forage),
artichokes,
asparagus,
barley,
blackberries,
boysenberries,
blueberries,
cane
berries,
corn
(
field
corn
only),
cotton,
currants,
dewberries,
elderberries,
gooseberries,
grapes,
huckleberries,
loganberries,
mint,
oats,
olives,
peas
(
field
or
southern),
pineapples,
raspberries,
sorghum,
sugarcane,
and
wheat.

Fruit
and
Nut
Trees
(
orchard
crops),
including
apples,
bananas,
citrus,
filberts
(
hazelnuts),
macadamia
nuts,
pecans,
peaches,
pears,
papayas,
plantains,
and
walnuts.

Ornamental
Trees,
Flowers,
and
Shrubs,
including
shade
trees,
citrus
trees
(
non­
bearing
and
nursery
stock),
tree
plantings
(
including
ash,
cedar,
elm,
oak,
pine,
poplar,
and
fir),
Easter
lilies,
gladiolus,
iris,
lilies,
narcissus,
and
ornamental
grasses.
24
Cotton
Defoliant
(
state
labels
only)

Non­
crop
Areas,
including
rights­
of­
way;
industrial
sites;
drainage
systems;
irrigation
systems;
lakes,
ponds,
holding
basins,
and
other
similar
sites
that
have
been
drained;
airports
and
landing
fields;
fire
plugs;
cable
closures;
and
warehouses.

Paints,
Solvents,
Adhesives,
and
Coatings
Ornamental
Fish
and
Catfish
Ponds
Residential
Use
Sites
Residential
Ponds
and
Aquariums
Paints,
Solvents,
Adhesives,
and
Coatings
4.2
Dietary
Exposure/
Risk
Pathway
Tolerances
range
from
0.05
ppm
(
meats,
milk)
to
7
ppm
in/
on
asparagus
(
Residue
Chemistry
Chapter
for
the
Diuron
Reregistration
Eligibility
Decision
Document.
John
Punzi.
July
29,
2001).
Diuron
is
applied
1
or
2
times
per
season
using
single
application
rates
of
approximately
1
pound
per
acre.
Usage
data
concerning
domestic
percent
crop
treated
data
from
the
Biological
and
Economic
Assessment
Division
(
BEAD)
indicate
that
~
50%
of
citrus,
25%
of
berries,
15%
of
nuts,
10%
of
cotton,
grapes,
peaches,
or
pome
fruit,
and
1%
of
field
crops
are
treated
with
diuron.
Nearly
10
million
pounds
of
diuron
are
used
annually
in
the
United
States.

Tolerances
for
residues
of
diuron
in/
on
plant
and
animal
commodities
are
established
under
40
CFR
§
180.106.
Diuron
tolerances
are
currently
expressed
as
diuron
per
se.
The
Agency
is
recommending
that
the
tolerance
expression
for
diuron
be
revised
to
include
metabolites
hydrolyzable
to
3,4­
dichloroaniline
(
3,4­
DCA).
This
determination
is
based
on
the
results
of
the
reviewed
plant
and
animal
metabolism
studies.
Adequate
analytical
methods
exist
for
data
collection
and
tolerance
enforcement
in
plants.
Independent
laboratory
validation
of
the
enforcement
method
is
required
for
livestock
methods
prior
to
Agency
validation.
Label
revisions
are
required
for
many
crops
in
order
to
reflect
the
parameters
of
use
patterns
for
which
residue
data
are
available.
Many
of
the
revisions
concern
retreatment
intervals,
preharvest
intervals
(
PHI's)
and
rotational
crop
restrictions.

The
Metabolism
Assessment
Review
Committee
(
MARC)
met
on
July
3,
2001
to
discuss
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
(
Diuron
Metabolism
Committee
Briefing
Memo.
John
Punzi.
August,
27,
2001).
25
NH
N
O
Cl
Cl
CH
3
CH
3
NH
NH
O
Cl
Cl
CH
3
NH
NH
2
O
Cl
Cl
The
14C­
containing
residues
that
were
identified
in
plants
(
Table
5):
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.

Table
5.
Parent
and
Major
Metabolites
Diuron:
3­(
3,4­
dichlorophenyl)­
1,1­
dimethylurea
DCPMU;
IN­
15654:
3­(
3,4­
dichlorophenyl)­
1­
methylurea
DCPU;
IN­
R915:
3,4­
dichlorophenylurea
In
animals,
the
principal
residue
identified
was
DCPU.
The
parent
and
other
dichloroanilinecontaining
metabolites
(
i.
e.,
3,4­
DCA
and
DCPMU)
that
can
be
determined
by
the
current
enforcement
methods
were
detected
in
much
smaller
quantities.
Four
minor
hydroxylated
metabolites
(
2­
OH­
DCA;
2­
OH­
DCPU;
2­
OH­
DCPMU;
and
N­
acetyl­
2­
OH­
DCA)
were
also
detected;
these
metabolites
were
not
observed
in
plants
and
would
not
be
determined
by
the
current
enforcement
method.

The
major
portion
of
radioactive
residues
in
milk
(
in
lactating
goats)
was
comprised
of
several
conjugated
polar
components
which
collectively
accounted
for
56%
of
total
radioactive
residue
(
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.
Although
these
polar
components
were
not
wholly
identified,
the
registrant
noted
that
the
results
from
a
radiovalidation
study
suggest
that
a
large
portion
of
these
polar
components
are
hydrolyzable
to
3,4­
DCA
and
would
be
quantified
using
the
residue
enforcement
method.

The
environmental
data
base
indicates
that
diuron
has
potential
for
leaching
to
ground
and
surface
water.
The
environmental
metabolism
studies,
conducted
under
a
variety
of
conditions,
demonstrate
that
monochlorinated
methylphenyl
urea
(
MCMPU)
and
monochlorinated
dimethylphenyl
urea
(
MCDMPU)
can
be
formed
under
some
conditions
and
that
MCDMPU
is
a
major
degradate
in
aquatic
aerobic
and
anaerobic
studies.
DCPMU
was
also
identified
as
a
major
environmental
degradate
in
several
studies
and
3,4­
DCA,
DCMU,
PDMU
were
identified
as
minor
metabolites.

The
MARC
concluded
that
for
tolerance
expression
and
risk
assessment
purposes,
the
residues
of
26
concern
in/
on
plants
and
animals
are
diuron
and
its
metabolites
that
are
hydrolyzable
to
3,4­
DCA
[
Diuron.
Results
of
the
Health
Effects
Division
(
HED)
Metabolism
Assessment
Review
Committee(
MARC)
Meeting
Held
on
03­
JULY­
2001.
John
Punzi.
August
10,
2001].
This
decision
was
based
on:
1)
the
assumption
that
the
metabolites
would
not
be
any
more
toxic
than
the
parent
and
2)
the
consideration
that
the
analytical
methods
used
to
collect
the
field
trial
data
are
not
capable
of
measuring
each
metabolite
individually.
To
account
for
the
poor
recovery
of
hydroxylated
metabolites
from
milk,
it
was
determined
that
the
levels
of
diuron
residues
in
milk
identified
in
the
ruminant
feeding
study
would
be
multiplied
by
10
(
The
Metabolism
Committee
Meetings
for
Diuron
Held
on
October
21
and
November
5,
1993.
Randy
Perfetti.
November
17,
1993)
to
account
for
all
of
the
exposure
to
diuron­
related
residues
in
the
risk
assessment.

The
MARC
also
concluded
that
for
risk
assessment
purposes,
the
residues
of
concern
in
drinking
water
are
parent,
and
metabolites
that
are
hydrolyzable
to
3,4­
DCA,
and
MCPDMU.
The
MARC
raised
concerns
for
MCPDMU
based
on
an
analogous
compound,
monuron.
With
the
exception
of
the
position
of
the
chlorine,
the
structures
are
identical.
There
are
cancer
concerns
for
monuron
but
the
target
organs
are
different
than
those
affected
by
diuron.
The
MARC
recommended
that
a
separate
cancer
assessment
be
conducted
for
MCPDMU.

4.2.1
Residue
Profile
Diuron
is
used
on
a
wide
variety
of
food
and
feed
crops.
Residue
levels
from
United
States
Department
of
Agriculture
(
USDA)
and
Food
and
Drug
Administration
(
FDA)
monitoring
programs
do
not
include
all
the
residues
of
concern
needed
for
the
Agency's
diuron
risk
assessment
(
diuron
and
metabolites
convertible
to
3,4­
DCA)
and
would
be
inappropriate
for
this
analysis.
Anticipated
residues
(
ARs)
from
field
trial
data
were
utilized
to
estimate
the
dietary
exposure
to
diuron
from
the
diets
of
the
U.
S.
population
as
well
as
certain
population
subgroups.
These
ARs
were
developed
previously
(
D250038,
Rick
Loranger.
October
8,
1998
and
D169227,
Christina
Swartz.
April
27,
2001).
The
field
trials
were
conducted
at
the
highest
application
rates
for
the
crop
tested
and
therefore,
the
residues
from
these
trials
are
considered
high
end.
Available
processing
data
for
apple,
citrus
and
grapes
were
available
and
indicated
that
there
was
no
concentration,
nor
reduction,
in
residue
values
for
these
processed
commodities
(
i.
e.
juice,
dried
fruit).
The
sugarcane
processing
study
showed
a
reduction
of
residues
in
refined
sugar
but
a
concentration
of
residues
in
molasses.
With
the
exception
of
residue
data
from
the
processing
of
sugarcane
into
refined
sugar
and
molasses,
the
only
additional
refinements
to
the
residue
data
are
the
use
of
averaged
percent
crop
treated
(%
CT)
information
(
Quantitative
Usage
Analysis
for
Diuron.
Alan
Halvorson.
March
20,
2001
and
Updated
QUA.
Alan
Halvorson.
April
27,
2001).

The
registrants
have
committed
to
label
changes
which
would
restrict
the
application
of
diuron
to
asparagus
plantings
prior
to
the
appearance
of
spears.
Residues
of
diuron
in/
on
asparagus
are
reduced
by
approximately
one
order
of
magnitude
(
from
2.8
to
0.26
ppm)
by
this
proposed
use.
To
examine
the
effect
of
the
differing
residue
values
for
asparagus
on
the
dietary
risk,
calculations
were
performed
using
27
residue
levels
reflecting
treatment
of
asparagus
crops
before
and
after
spears
appear.
There
were
minimal
changes
in
the
chronic
exposure
estimates
using
data
from
pre­
emergence
or
post­
emergence
applications
of
diuron
to
asparagus.

4.2.2
Acute
Dietary
Diuron
is
not
acutely
toxic.
No
adverse
effects
attributed
to
a
single
exposure
were
identified
in
any
available
study.
Therefore,
no
acute
dietary
risk
assessment
was
conducted.

4.2.3
Chronic
Dietary
A
chronic
exposure
analysis
for
diuron
and
its
metabolites
that
are
hydrolyzable
to
3,4­
DCA
was
performed
utilizing
the
Dietary
Exposure
Evaluation
Model
(
DEEMTM)
software
Version
7.73,
which
incorporates
USDA's
Continuing
Surveys
of
Food
Intake
by
Individuals
(
CSFII),
1989­
1992.
The
1989­
1992
data
are
based
on
the
reported
consumption
patterns
of
more
than
10,000
individuals
over
three
consecutive
days,
and
therefore
represent
more
than
30,000
unique
"
person
days"
of
data.
Foods
"
as
consumed"
(
e.
g.
apple
pie)
are
linked
to
raw
agricultural
commodities
and
their
food
forms
(
e.
g.
apples
cooked/
canned
or
wheat
flour)
by
proprietary
recipe
translation
files
within
DEEM.
Consumption
data
are
averaged
for
the
entire
U.
S.
population
and
within
population
subgroups
for
chronic
exposure
assessment.
For
chronic
exposure
and
risk
assessment,
an
estimate
of
the
residue
level
in
each
food
or
food
form
(
e.
g.
orange
or
orange
juice)
on
the
commodity
residue
list
is
multiplied
by
the
average
daily
consumption
estimate
for
that
food/
food
form.
The
resulting
residue
consumption
estimate
for
each
food/
food
form
is
summed
with
the
residue
consumption
estimates
for
all
other
food/
food
forms
on
the
commodity
residue
list
to
arrive
at
the
total
estimated
exposure.
The
calculated
chronic
exposure
(
residue
x
consumption)
was
compared
to
a
cPAD
of
0.003
mg/
kg/
day,
which
reflects
an
FQPA
factor
of
1x.
Noncancer
dietary
exposure
estimates
are
expressed
in
mg/
kg
bw/
d
and
as
a
percent
of
the
cPAD
(
Diuron
­
Chronic
Dietary
Exposure
Assessment
(
PC
Code
035505);
DP
Barcode
D276683;
Case
0046.
John
Punzi.
September
10,
2001).

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
(
Table
6).
Approximately
40%
of
the
exposure
to
diuron
from
food
is
from
orange
juice
and
orange
juice
concentrate.

Table
6:
Chronic
Dietary
Risk
Estimates
Population
Exposure
mg/
kg/
day
%
Chronic
PAD
U.
S.
Population
0.000088
3
All
Infants
(<
1
year)
0.000077
3
Population
Exposure
mg/
kg/
day
%
Chronic
PAD
28
Children
1­
6
years
0.00020
7
Children
7­
12
years
0.000118
4
Females
13­
50
years
0.000069
2
Males
13­
19
years
0.000098
3
Males
20+
years
0.000066
2
Seniors
55+
years
0.000083
3
4.2.4
Cancer
Dietary
The
estimated
cancer
dietary
risk
associated
with
the
use
of
diuron
indicates
a
borderline
exceedance
above
1
x
10­
6
and
shows
a
lifetime
risk
estimate
of
1.68
x
10
­
6
for
the
general
population
but,
is
not
of
concern
(
Table
7).
As
discussed
earlier,
the
residues
used
in
the
calculations
are
from
field
trials
conducted
at
the
highest
application
rates
and
some
processing
data
are
still
outstanding.
Therefore,
the
exposure
calculation
is
a
conservative
estimate.
Again,
the
Agency
assumed
that
exposure
was
to
diuron
and
its
metabolites
that
are
hydrolyzable
to
3,4­
DCA.
For
the
cancer
risk
assessment,
the
calculated
chronic
exposure
(
residue
x
consumption)
was
calculated
with
a
Q1*
of
1.91
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents.

Table
7.
Summary
of
Dietary
Exposure
and
Risk
for
Diuron
Population
Acute
Dietary
Chronic
Dietary
Cancer
Dietary
NA
Exposure
(
mg/
kg/
day)
Risk
(%
cPAD)
Exposure
(
mg/
kg/
day)
Lifetime
Risk
(
Q1*=
0.0191)

U.
S.
Population
0.000088
3
0.000088
1.68
x
10­
6
All
Infants
<
1
year
0.000077
3
Not
Applicable
Children
1­
6
years
0.000200
7
Children
7­
12
years
0.000118
4
Females
13­
50
years
0.000069
2
4.3
Water
Exposure/
Risk
Pathway
The
diuron
drinking
water
exposure
assessment
was
based
primarily
on
1)
submitted
environmental
fate
studies,
2)
limited
but
targeted
monitoring
data
for
diuron
and
its
degradates,
and
3)
monitoring
data
for
the
parent
only.
Although
monitoring
data
for
the
parent
and
its
degradates
were
not
extensive,
the
29
available
measured
data
were
revealing.
For
example,
monitoring
of
32
lakes
in
Texas
showed
that
diuron
was
the
predominant
contaminate
detected.
Surface
and
ground
water
conclusions
from
these
sources
were
compared
with
simulation
model
predictions.
Monitoring
sources
included
United
States
Geological
Survey
(
USGS)
and
published
literature
(
Drinking
Water
Assessment
for
diuron
and
its
degradates.
Ibrahim
Abdel­
Saheb.
March
11,
2001).
There
is
no
Maximum
Contaminant
Level
Goal
(
MCLG)
or
Maximum
Contaminant
Level
(
MCL)
established
by
the
Agency's
Office
of
Water
for
diuron.

Diuron
has
the
potential
to
leach
to
ground
water
and
to
contaminate
surface
waters
through
run­
off.
Environmental
fate
data
analyzed
by
EFED
show
that
diuron
is
persistent.
Diuron
is
stable
to
hydrolysis
at
pH's
5,
7,
and
9.
The
calculated
half­
lives
in
aqueous
and
soil
photolysis
studies
were
43
and
173
days,
respectively.
The
half­
lives
in
aerobic
and
anaerobic
soil
metabolism
studies
were
372
and
1000
days,
respectively.
However,
in
viable
laboratory
aquatic
systems,
degradation
appeared
to
be
accelerated
with
half­
lives
of
33
and
5
days
in
aerobic
and
anaerobic
systems,
respectively.
The
predominant
degradate
formed
in
both
the
soil
photolysis
and
aerobic
soil
metabolism
studies
was
DCPMU.
The
only
significant
(>
10
%
of
applied)
degradate
in
the
aerobic
and
anaerobic
aquatic
metabolism
studies
was
MCDMPU.
Diuron
dissipated
from
bare
ground
plots
with
half­
lives
ranging
from
73
to
133
days,
and
the
major
degradate
(
MCDMPU)
dissipated
from
the
same
plots
with
half­
lives
ranging
from
217
to
1733
days.
Diuron
and
MCDMPU
residues
were
detected
mainly
at
the
upper
15­
30
cm
depths
at
all
sites
and
sporadically
detected
below
this
depth.
An
upgradable
adsorption/
desorption/
leaching
study
(
MRID#
44490501)
showed
that
diuron
has
a
low­
medium
Koc
(
468­
1666).
In
addition,
diuron
has
low
water
solubility
(
42
ppm).

The
degradate
3,4­
DCA
is
an
environmental
degradate
common
to
diuron,
linuron,
and
propanil.
EFED
does
not
have
sufficient
fate
and
transport
data
on
3,4­
DCA.
In
an
aerobic
soil
metabolism
study
with
the
compound
propanil,
3,4­
DCA
had
a
half­
life
of
30
days
(
MRID#
41537801),
and
in
a
water
paddy
the
half­
life
ranged
from
2­
3
days
(
MRID#
42200401,
42200501).
Even
though
these
studies
suggest
that
3,4­
DCA
will
not
persist
in
soil
or
water,
3,4­
DCA
has
been
detected
often
in
surface
water.
Thus,
more
data
are
needed
to
understand
the
fate
of
this
degradate
in
soil
and
water.
TCAB,
also
a
compound
of
concern
for
human
health
(
see
Section
3.5),
was
identified
as
having
a
minor
presence
in
a
diuron
soil
photolysis
study
(
MRID#
41719302)
with
a
maximum
concentration
of
0.038
ppm.

Surface
Water
Exposure:
EFED
has
targeted,
but,
limited
monitoring
data
on
the
concentrations
of
diuron
and
its
degradates
in
surface
water.

A
study
on
the
occurrence
of
cotton
herbicides
and
insecticides
in
the
Playa
lakes
of
the
high
plains
of
western
Texas
concluded
that
diuron
was
the
major
pesticide
detected
in
water
samples
collected
from
32
lakes
with
a
mean
concentration
of
2.7
ppb.
Diuron
metabolites
(
DCPMU,
DCPU,
and
3,4­
DCA)
were
found
in
71%
of
the
samples
analyzed.
The
mean
concentrations
of
these
metabolites
were
0.45
ppb
for
DCPMU,
0.31
ppb
for
3,4­
DCA,
and
0.2
ppb
for
DCPU.
In
this
study,
water
samples
30
were
taken
within
two
days
after
diuron
application
to
cotton
in
the
region.
Diuron
usage
on
cotton
in
this
part
of
the
state
reached
an
average
of
$
1.379
lb
ai/
mile/
yr.
Even
though,
the
monitoring
of
diuron
concentrations
from
use
on
cotton
in
this
part
of
the
state
is
an
example
of
a
targeted
study,
the
frequency
of
surface
water
sampling
and
the
length
of
the
sampling
period
were
insufficient
to
satisfy
the
temporal
and
spatial
requirements
for
regulatory
purposes.
This
study
has
limited
use
in
a
national
assessment
because
EFED
does
not
expect
western
Texas
to
be
one
of
the
most
vulnerable
use
areas
for
runoff.
However,
because
the
samples
were
taken
within
two
days
after
application,
the
results
may
represent
a
lower
bound
of
possible
peak
concentrations
that
could
occur
in
drinking
water
in
that
area.

The
USGS
National
Water
Quality
Assessment
Program
(
NAWQA)
collected
1420
surface
water
samples
from
62
agricultural
stream
sites
during
the
period
from
1992­
1998.
Sampling
was
for
the
parent
only.
One
to
two
samples
were
collected
each
month
throughout
the
year
during
periods
when
pesticide
transport
in
the
streams
was
expected
to
be
low.
At
most
sites,
the
sampling
frequency
was
increased
to
1
to
3
samples
per
week
during
periods
when
elevated
levels
of
pesticides
were
expected
in
the
streams.
Diuron
was
detected
in
7.32%
of
the
samples
(
detection
limit
=
0.05
ppb)
with
an
average
concentration
of
0.13
ppb
in
95%
of
samples.
The
maximum
concentration
of
diuron
was
13
ppb
(
estimated
concentration).

The
monitoring
data,
though
useful
in
a
limited
capacity,
are
either
not
nationally
representative
or
did
not
monitor
for
any
of
the
degradates
and
would
underestimate
potential
drinking
water
exposures.
Therefore,
EFED
calculated
estimated
exposure
concentrations
(
EEC)
in
surface
waters
employing
Tier
II
surface
water
modeling
using
the
Index
Reservoir
(
IR)
and
Percent
Crop
Area
(
PCA)
modifications
to
PRZM
and
EXAMS.
The
IR
represents
a
potential
vulnerable
drinking
water
source
from
a
specific
area
(
Illinois)
with
specific
cropping
patterns,
weather,
soils,
and
other
factors.
The
PCA
is
a
generic
watershed­
based
adjustment
factor
which
represents
the
portion
of
a
watershed
planted
to
a
crop
or
crops
and
will
be
applied
to
pesticide
concentrations
estimated
for
the
surface
water
component
of
the
drinking
water
exposure
assessment.
The
IR­
PCA
PRZM/
EXAMS
model
was
used
to
determine
estimated
surface
water
concentrations
of
diuron
and
its
degradates
DCPMU,
DCPU,
3,4­
DCA,
and
N'­(
3­
chlorophenyl)­
N­
N­
dimethylurea
(
MCPDMU).
Modeling
results
are
shown
in
Table
9.
The
modeled
concentrations
are
higher
(
9­
100
times)
than
the
levels
found
in
existing
surface
water
monitoring
data
targeted
to
pesticide
use
areas.

Ground
Water
Exposure:
EFED
has
limited
targeted
monitoring
data
on
the
concentrations
of
diuron
and
its
degradates
in
groundwater.
Table
8
shows
validated
monitoring
data
for
diuron
that
were
collected
for
the
states
of
California
(
CA),
Florida
(
FL),
Georgia
(
GA),
and
Texas
(
TX)
from
1971­
1991.

Table
8.
Groundwater
monitoring
data
for
diuron
(
USEPA
1992).
Number
of
wells
sampled
(
number
of
wells
with
residues).

State
number
of
well
(
detections)
range
of
conc.
(
ppb)
31
CA
2010
(
82)
0.05
­
3.95
FL
15385
(
9)
1.18
­
5.37
GA
70
(
67)
1.00
­
5.00
TX
31
(
2)
0.01
­
0.02
According
to
the
Ground
Water
Protection
Section
of
the
Florida
Department
of
Environmental
Protection,
ground
water
samples
collected
from
wells
between
May/
1990
and
November/
1997,
showed
diuron
detections
ranging
from
0.94
­
12
ppb
(
detection
limit
=
0.48
ppb).
The
arithmetic
mean
concentration
was
2.44
ppb.
Well
water
samples
were
collected
from
the
following
counties:
Highlands,
Jackson,
Lake,
Orange,
and
Polk.
With
the
exception
of
the
12
ppb
sample
in
Orange
County,
the
majority
of
the
detections
were
in
Highlands
County
where
citrus
is
grown.
Diuron
concentrations
in
Highlands
County
decreased
with
time
to
about
1
ppb
but
were
detected
every
year.
In
Polk
County,
diuron
concentrations
showed
a
seasonal
pattern,
with
the
highest
concentrations
in
the
spring
and
lowest
concentrations
in
the
fall,
but
it
was
not
detected
in
all
years.

The
USGS
NAWQA
analyzed
pesticide
occurrence
and
concentrations
for
major
aquifers
and
shallow
ground
water
in
agricultural
areas
(
detection
limit
=
0.05
ppb).
Analysis
of
2608
samples
(
major
aquifers
study)
showed
diuron
in
71%
of
the
samples
analyzed
with
a
maximum
concentration
of
0.34
ppb.
The
maximum
diuron
concentration
in
897
samples
from
shallow
groundwater
sites
was
2.0
ppb,
with
diuron
detected
in
only
1.23%
of
samples
analyzed
(
USGS,
1998).
A
major
component
of
the
sampling
design
in
the
NAWQA
study
was
to
target
specific
watersheds
and
shallow
ground
water
areas
that
are
influenced
primarily
by
a
single
dominant
land
use(
agricultural
or
urban)
that
is
important
in
the
particular
area.
The
ground
water
data
were
primarily
collected
from
a
combination
of
production
and
monitoring
wells.

Even
though
the
ground
water
monitoring
data
collected
by
NAWQA
are
from
sites
considered
typical
for
use
areas,
the
frequency
of
sampling
and
the
length
of
sampling
period
were
not
sufficient
to
represent
the
temporal
and
spatial
requirements
for
regulatory
purposes.
In
addition,
USGS
studies
only
monitored
for
the
parent.
Therefore,
the
Screening
Concentration
in
Groundwater
(
SCI­
GROW)
model
was
used
to
estimate
potential
ground
water
concentrations
for
diuron
and
its
degradates.
Modeling
results
are
shown
in
Table
9.
32
Table
9.
Estimated
environmental
concentrations
in
surface
and
ground
water
for
diuron
and
its
degradates
from
diuron
use
on
citrus.

model
EECs
(
F
g/
L)
use(
s)
modeled
PCA
Diuron
DCPM
U
DCPU
3,4­
DCA
MCPDMU
one
application
of
diuron
on
citrus
@
9.6
lb
ai/
acre,
ground
application
Default
(
0.87)
Surface
water/
peak
613
130
5.80
0.08
136
Surface
water/
1­
10­
year
average
128
27.0
1.20
0.02
36.4
Surface
water/
mean
of
annual
values
85.0
18.0
0.80
0.01
25.5
Groundwater/
(
peak
and
long­
term
average)
6.5
2.50
0.1
2X10­
4
1.38
The
IR­
PCA
modeling
results
indicate
that
diuron
and
its
degradates
have
the
potential
to
contaminate
surface
waters
by
runoff
in
areas
with
large
amounts
of
annual
rainfall.
Modeling
results
(
EECs)
were
several
orders
of
magnitude
(
ranging
from
9­
100
times)
higher
than
diuron
surface
water
monitoring
data
from
known
pesticide
use
areas.
Though
environmental
metabolism
studies
indicate
that
MCPDMU
is
an
environmental
degradate
of
diuron,
it
either
was
not
detected
in
any
of
the
monitoring
studies
or
the
researchers
did
not
look
for
it.
Since
EFED
lacks
complete
environmental
fate
data
(
such
as
the
aerobic
aquatic
and
anaerobic
aquatic
studies)
on
any
of
the
degradates,
the
EECs
for
surface
and
ground
water
were
based
on
half­
lives
that
were
calculated
on
cumulative
residues
(
Drinking
Water
Assessment
for
diuron
and
its
degradates.
Ibrahim
Abdel­
Saheb.
March
11,
2001).

4.4
Residential
Exposure/
Risk
Pathway
4.4.1
Home
Uses
There
are
potential
residential
exposures
from
activities
associated
with:
1)
pond
and
aquarium
use
and
2)
paint
use.
Though
there
are
existing
labels
for
applications
of
granular
formulations
of
diuron
to
turf,
most
are
limited
to
industrial
and
non­
crop
uses.
Others
(
reg.
#
33560­
46
and
#
802­
352)
are
either
pending
cancellation
by
the
registrant
or
the
registrant
has
agreed
to
place
language
specifically
restricting
residential
uses
on
the
label.
Therefore,
with
these
actions
by
the
registrants
of
the
labels
mentioned
above,
no
residential
turf
uses
exist
for
diuron
and
a
residential
assessment
for
turf
was
not
conducted
(
Occupational
and
Residential
Exposure
Assessment
and
Recommendations
for
the
Reregistration
Eligibility
Decision
Document
for
Diuron.
Renee
Sandvig
and
Christina
Jarvis.
October
16,
2001).

Pond
and
Aquarium
Use
Three
diuron
products
are
designed
for
residential
use
as
algaecide
in
ponds
and
aquariums
and
are
being
supported
for
reregistration.
They
are
Pond
Block
(
0.51%
ai,
reg.
#
33034­
1)
and
No
More
33
Algae
(
0.67%
ai,
reg.
#
33034­
2),
which
are
both
in
tablet/
block
form,
and
No
More
Algae
(
0.67%
ai,
reg.
#
33034­
3),
which
is
in
ready
to
use
liquid
form.
No
exposure
data
exist
for
the
use
of
the
algaecide
tablets/
blocks.
Since
the
products
are
formulated
as
tablets/
blocks
and
dissolve
in
less
than
5
minutes,
minimal
exposure
is
expected
and
was
not
quantified.
Furthermore,
exposure
from
the
block/
tablet
forms
of
diuron
are
expected
to
be
less
than
exposure
from
the
liquid
formulation,
since
spillage
may
occur
from
measuring
and
pouring
liquid
diuron.

The
No
More
Algae
liquid
is
used
at
a
rate
of
one
teaspoon
(
5
ml)
for
every
10
gallons
of
aquarium
or
pond
water.
Treatment
should
be
repeated
once
a
month
or
when
algae
growth
reappears.
Residential
exposure
may
result
from
measuring
the
liquid
and
pouring
the
liquid
into
the
aquarium
or
pond.
Unit
exposure
data
from
the
Pesticide
Handlers
Exposure
Database
(
PHED)
for
the
mixing/
loading
of
liquids
will
be
used
to
assess
this
exposure.
Dermal
exposure
for
noncancer
risk
estimates
was
not
calculated,
since
no
toxicity
by
the
dermal
route
is
expected
for
this
duration.
Exposure
is
expected
to
be
short­
term
(
1
to
30
days).

Paint
Use
Antimicrobial
exposures
to
handlers
are
defined
by
the
Antimicrobial
Division
(
OPP/
EPA)
as
"
primary"
and
"
secondary"
handlers.
The
primary
handlers
are
defined
as
those
individuals
exposed
to
the
formulated
product
(
adding
the
diuron
product
into
vats
of
paint
during
its
manufacturing),
while
the
secondary
handlers
are
those
individuals
exposed
to
the
active
ingredient
as
a
direct
result
of
its
incorporation
into
an
end
use
product
(
individuals
using
the
caulk
or
paint
that
in
itself
is
not
a
registered
pesticidal
product).
HED
has
identified
and
assessed
the
primary
handlers
as
those
individuals
who
mix
and
load
diuron
formulation
at
the
manufacturing
facility
for
use
as
a
mildewcide
in
adhesives,
caulks,
sealants,
and
paints.
The
secondary
handlers
are
commercial
and
residential
applicators
who
apply
adhesives,
caulks,
sealants,
and
paints.
Since
diuron
is
only
added
during
the
manufacturing
process,
only
the
secondary
handler
use
(
application
of
the
products
containing
diuron)
was
assessed
in
the
residential
assessment.

No
handler
exposure
data
have
been
submitted
to
determine
the
extent
of
these
exposures.
Secondary
residential
handlers
were
assessed
using
an
airless
sprayer
and
a
paint
brush.
Unit
exposure
data
used
to
assess
the
exposure
resulting
from
applying
paint
containing
diuron
with
an
airless
sprayer
and
a
paintbrush
were
taken
from
a
previous
chlorothalonil
assessment
(
Revised
Occupational
and
Residential
Exposure
Assessment
for
the
Chlorothalonil
Reregistration
Eligibility
Decision
(
RED).
Jeff
Evans.
January
22,
1997).
This
assessment
used
data
from
a
proprietary
worker
exposure
study
conducted
on
the
use
of
chlorothalonil
in
paint.
These
data
were
merged
with
data
contained
in
PHED
to
increase
the
number
of
replicates
and
the
quality
of
the
unit
exposure
data.
The
surrogate
chlorothalonil
study
data
are
assumed
to
be
representative
of
the
exposure
from
the
use
of
diuron
using
the
same
equipment,
since
the
two
chemicals
are
formulated
together
in
three
out
of
the
four
currently
registered
diuron
paint
products.
The
clothing
and
personal
protective
equipment
(
PPE)
scenarios
for
each
type
of
exposure
reflect
the
clothing
and
PPE
worn
in
the
study
from
which
the
unit
exposure
values
were
derived.
The
clothing
worn
in
the
chlorothalonil
assessment
were
long
pants
and
long
34
sleeved
shirt,
which
are
different
from
the
short
sleeved
and
short
pants
clothing
normally
considered
possible
for
residential
exposures.
Therefore,
for
comparison,
data
representing
both
clothing
scenarios
(
long
sleeves
and
long
pants,
as
well
as
short
sleeves
and
short
pants)
were
also
included
in
the
assessment
for
the
application
of
paint
with
an
airless
sprayer
and
a
paint
brush/
roller.

Although
there
is
potential
exposure
during
the
application
of
the
other
treated
materials
(
e.
g.,
caulks
and
sealants),
they
were
not
included
in
this
assessment
because
no
data
are
available
to
assess
these
uses.
There
is
also
a
potential
for
exposure
from
applying
paint
with
a
roller.
It
is
HED's
professional
judgement
that
the
airless
sprayer
and
paintbrush
scenarios
represent
the
high
end
exposures
for
diuron
antimicrobial
secondary
uses
and
therefore,
would
likely
be
protective
of
the
exposures
from
caulk
and
sealant
uses
and
painting
with
a
roller.

No
data
are
available
to
determine
whether
or
not
diuron
contained
in
paint
products
would
be
more
or
less
readily
absorbed
through
the
skin.
35
4.4.1.1
Handler
The
Agency
has
determined
that
there
are
potential
exposures
to
residential
mixers,
loaders,
and
applicators
during
the
usual
use­
patterns
associated
with
diuron.
Based
on
the
use
patterns,
five
major
residential
exposure
scenarios
were
identified
for
diuron:
(
1)
Loading
ready­
to­
use
liquids;
(
2)
Applying
paints/
stains
with
a
paintbrush;
(
3)
Applying
paints/
stains
with
a
paintbrush
(
study
data);
(
4)
Applying
paints
with
an
airless
sprayer;
and
(
5)
Applying
paints
with
an
airless
sprayer
(
study
data).

In
addition
to
diuron's
mildewcide
use
in
paints
and
stains,
it
is
also
used
in
plaster,
stuccos,
sealants,
caulking,
and
fillers.
Unit
exposure
data
only
exists
for
the
use
of
paints/
stains
with
airless
sprayer
and
paintbrush.
These
exposure
scenarios
are
assumed
to
have
a
higher
exposure
than
the
use
of
diuron
in
plaster,
stucco,
sealants,
caulking
and
fillers,
since
less
material
would
be
applied
in
a
day.
Therefore,
the
paint/
stain
assessment
is
considered
protective
for
exposure
resulting
from
the
use
of
diuron
in
plaster,
stucco,
sealants,
caulking,
and
fillers.

The
exposures
to
residential
secondary
handlers
are
expected
to
be
of
a
short­
term
duration
(
less
than
30
days).
For
homeowners,
the
airless
sprayer
is
assumed
to
be
used
for
outdoor
applications
only.
Homeowner
use
of
diuron
treated
paint
indoors
is
restricted
to
small
rooms
such
as
bathrooms,
laundry
rooms,
etc.
where
the
use
of
an
airless
sprayer
is
unlikely
to
occur.
For
the
cancer
risk
assessment,
homeowners
applying
diuron
treated
paint
are
assumed
to
be
exposed
two
days
per
year,
which
is
considered
a
high­
end
assumption.

Short­
term
Exposure/
Risk
Table
10
presents
the
short
term
(
1­
30
days)
dermal
and
inhalation
exposures
at
baseline
as
well
as
the
risk
assessments
for
the
inhalation
exposures.
No
systemic
toxicity
was
seen
following
repeated
dermal
dosing
in
the
dermal
toxicity
study
therefore,
no
quantitative
assessment
of
risk
by
the
dermal
route
is
required.
No
PPE
or
engineering
controls
are
assumed
for
residential
exposures.
Residential
handlers
are
assumed
to
be
wearing
short­
sleeved
shirts
and
short
pants.

The
short­
term
risk
assessment
incorporated
a
NOAEL
of
10
mg/
kg/
day
for
noncancer
inhalation
exposures
and
had
an
LOC
or
target
MOE
of
100,
including
the
1x
FQPA
factor.
The
calculations
of
short­
term
inhalation
risk
indicate
that
the
inhalation
MOEs
are
more
than
100
at
the
baseline
level
for
the
all
the
assessed
exposure
scenarios
and
are
not
considered
risks
of
concern.

Cancer
Exposure/
Risk
To
assess
cancer
risk,
an
average
daily
dose,
a
lifetime
daily
dose
and
a
total
cancer
risk
are
calculated.
For
the
cancer
assessment,
potential
dermal
exposure
was
included
with
a
high­
end
dermal
absorption
factor
(
measured
from
a
submitted
study)
of
4%.
Assumptions
included
in
the
calculations
were
an
average
adult
lifetime
of
70
years
and
an
exposure
duration
of
50
years.
The
number
of
exposures
per
year
for
the
pond
and
aquarium
uses
are
based
on
the
label
recommendations.
The
"
No
More
Algae"
liquid
label
states
that
"
For
regular
maintenance,
use
once
a
month
or
as
algae
starts
to
36
reappear."
Therefore,
12
exposures
per
year
were
assumed.
Homeowners
applying
diuron
treated
paint
are
exposed
two
days
per
year.
Since
it
would
be
unusual
for
a
homeowner
to
paint
their
house
every
year
with
diuron
treated
paint,
this
is
considered
a
high­
end
estimate.

Cancer
risks
equal
to
or
less
than
1
x
10­
6
are
not
considered
to
be
of
concern.
Risks
greater
than
1
x
10­
6
for
the
general
population
are
considered
to
be
of
concern.
The
residential
cancer
risk
assessment
was
conducted
using
the
diuron
Q1*
of
1.91
x
10­
2
and
is
summarized
in
Table
11.

The
following
scenarios
have
cancer
risks
greater
than
1
x
10­
6
at
the
baseline
level
of
exposure
(
bracketed
numbers
can
be
matched
to
the
exposure
scenarios
in
the
tables):

(
2)
Applying
paints/
stains
with
a
paint
brush;

(
3)
Applying
paints/
stains
with
a
paint
brush
(
study
data)
for
stains;

(
4)
Applying
paint
with
an
airless
sprayer;
and
(
5)
Applying
paint
with
an
airless
sprayer
(
study
data).

The
following
scenarios
have
cancer
risks
less
than
1
x
10­
6
at
the
baseline
level
of
exposure:

(
1)
Loading
ready
to
use
liquids
for
ponds
and
aquariums
All
scenarios
were
assessed
at
the
maximum
rate
of
application.
Average
application
rate
for
the
paint
use
is
unknown
and
is
requested
to
refine
this
risk.
The
residential
cancer
risk
is
considered
conservative
since
an
upper
bound
dermal
absorption
rate
was
used
(
no
dermal
penetration
study
was
submitted),
coupled
with
maximum
application
rates.

4.4.1.2
Postapplication
Postapplication
inhalation
and
dermal
exposure
resulting
from
the
use
of
diuron
in
ponds
and
aquariums
is
expected
to
be
minimal.
Diuron
is
applied
to
ponds/
aquariums
in
the
form
of
a
liquid
and
an
effervescent
tablet.
Due
to
the
high
dilution
rate
of
the
liquid
in
pond
and
aquarium
water
(
0.0000074
lb
ai
per
gallon
of
water),
and
the
effervescent
nature
of
the
tablet
(
expected
to
dissolve
in
less
than
five
minutes),
postapplication
exposure
to
diuron
in
pond
and
aquarium
water
is
expected
to
be
minimal.
Furthermore,
postapplication
activities
in
and
around
ponds/
aquariums
treated
with
diuron
are
assumed
to
be
infrequent.

Postapplication
inhalation
and
dermal
exposure
resulting
from
the
indoor
use
of
diuron
in
paints
is
also
expected
to
be
minimal.
The
Agency
has
conducted
a
screening­
level
inhalation
assessment
using
the
Multi­
Chamber
Concentration
and
Exposure
Model
(
MCCEM).
MCCEM
uses
air
infiltration
and
37
interzonal
air
flow
rates,
together
with
user
inputs
for
emission
rates,
decay
rates,
and
outdoor
concentrations
to
calculate
time­
varying
indoor
concentrations
and
associated
indoor
inhalation
exposure
due
to
product
or
material
emissions
in
several
zones
or
chambers
within
a
residence.
The
results
of
this
model,
coupled
with
diuron's
low
vapor
pressure
(
2
x
10­
7
mm
Hg
at
30
E
C),
show
minimal
postapplication
inhalation
exposure.
Furthermore,
diuron­
treated
paint
is
only
likely
to
be
used
in
rooms
where
high
humidity
is
expected
(
i.
e.
a
bathroom),
and
would
rarely
be
used
in
the
entire
house.
It
is
unlikely
that
a
homeowner
would
receive
a
significant
amount
of
postapplication
inhalation
exposure
from
diuron­
treated
paint,
as
the
very
nature
of
its
use
is
as
a
mildewcide,
and
any
substantial
loss
of
the
active
ingredient
from
the
paint
would
render
the
product
ineffective.

4.4.2
Recreational
There
are
no
recreational
use
sites
for
diuron.

4.4.3
Other
(
Spray
Drift;
Farm
Worker
Children,
etc.)

Spray
drift
is
always
a
potential
source
of
exposure
to
residents
nearby
to
spraying
operations.
This
is
particularly
the
case
with
aerial
application,
but,
to
a
lesser
extent,
could
also
be
a
potential
source
of
exposure
from
groundboom
application
methods.
The
Agency
has
been
working
with
the
Spray
Drift
Task
Force,
EPA
regional
offices
and
state
lead
agencies
for
pesticide
regulation
and
other
parties
to
develop
the
best
spray
drift
management
practices.
The
Agency
is
now
requiring
interim
mitigation
measures
for
aerial
applications
that
must
be
placed
on
product
labels/
labeling.
The
Agency
has
completed
its
evaluation
of
the
new
data
base
submitted
by
the
Spray
Drift
Task
Force,
of
which
U.
S.
pesticide
registrants
are
members,
and
is
developing
a
policy
on
how
to
appropriately
apply
the
data
and
the
AgDRIFT
computer
model
to
its
risk
assessments
for
pesticides
applied
by
air,
orchard
airblast
and
ground
hydraulic
methods.
After
the
policy
is
in
place,
the
Agency
may
impose
further
refinements
in
spray
drift
management
practices
to
reduce
off­
target
drift
and
risks
associated
with
aerial
as
well
as
other
application
types,
where
appropriate.
38
Table
10:
Residential
Short­
Term
Baseline
Table
Exposure
Scenario
(
Scenario
#)
Dermal
Unit
Exposure
(
mg/
lb
ai)
a
Inhalatio
n
Unit
Exposure
(
F
g/
lb
ai)
b
Data
Source
Site/
Use
Application
Ratec
Amount
Treatedd
Dermal
Dosee
Inhalation
Dose
(
mg/
kg/
day)
f
Inhalation
MOEg
Mixer/
Loader
Loading
Ready
to
Use
Liquids
(
1)
2.9
1.2
PHED
V1.1
Pond
0.0000074
lb
ai
per
gallon
3000
Gallons
per
day
0.00092
0.00000038
26,000,000
PHED
V1.1
Pond
0.0000074
lb
ai
per
gallon
1000
Gallons
per
day
0.00031
0.00000013
79,000,000
PHED
V1.1
Aquarium
0.0000074
lb
ai
per
gallon
50
Gallons
per
day
0.000015
0.0000000063
1,600,000,000
Applicator
Applying
Paint/
Stains
with
Paintbrush
(
2)
230
280
PHED
V1.1
Paint
0.0532
lb
ai
per
gallon
2
Gallons
per
day
0.35
0.00043
23,000
PHED
V1.1
Stain
0.0532
lb
ai
per
gallon
5
Gallons
per
day
0.87
0.0011
9,400
Applying
Paint/
Stains
with
Paintbrush
(
study
data)
(
3)
290
507
Chlorothalonil
Study/
PHED
Paint
0.0532
lb
ai
per
gallon
2
Gallons
per
day
0.44
0.00077
13,000
Chlorothalonil
Study/
PHED
Stain
0.0532
lb
ai
per
gallon
5
Gallons
per
day
1.1
0.0019
5,200
Applying
Paint
with
Airless
Sprayer
(
4)
79
830
PHED
V1.1
Paint
0.0532
lb
ai
per
gallon
15
Gallons
per
day
0.90
0.0095
1,100
Applying
Paint
with
Airless
Sprayer
(
study
data)
(
5)
33.33
433
Chlorothalonil
Study/
PHED
Paint
0.0532
lb
ai
per
gallon
15
Gallons
per
day
0.38
0.0049
2,000
Footnotes:
a
Baseline
dermal
exposure
represents
short
pants,
short
sleeves
and
no
gloves,
except
for
the
chlorothalonil
study,
MRID
43600102,
which
represent
long
pants,
long
sleeved
shirts
and
no
gloves.
b
Baseline
inhalation
unit
exposure
represents
no
respirator.
c
Application
rates
are
based
on
the
maximum
application
rates
listed
on
the
"
No
More
Algae"
liquid
label
and
paint
labels.
d
Amount
treated
per
day
are
from
EPA
estimates
of
average
aquarium
and
pond
size
and
the
maximum
pond
size
listed
on
the
label.
Paint/
stain
assumptions
are
from
Expo
SAC
39
policy
#
12.15
e
Daily
Dermal
Dose
(
mg/
kg/
day)
=
(
Dermal
Unit
Exposure
(
mg/
lb
ai)
x
Application
Rates
(
lb
ai/
A
and
lb
ai/
sq.
ft.)
x
Area
Treated
per
day
(
acres
and
square
feet))/
body
weight
(
70
kg).
f
Daily
Inhalation
dose
(
mg/
kg/
day)
=
(
Inhalation
Unit
Exposure
(
F
g/
lb
ai)
x
(
1mg/
1000
F
g)
Conversion
Factor
x
Application
Rate
(
lb
ai/
gallon)
x
Amount
Treated
per
day
(
gallons/
day))/
body
weight
(
70
kg).
g
Short­
term
Inhalation
MOE
=
Inhalation
NOAEL
(
10
mg/
kg/
day)
/
Daily
Inhalation
Dose
(
mg/
kg/
day).
40
Table
11:
Residential
Cancer
(
Q*)
Risk
Table
Exposure
Scenario
(
Scenario
#)
Use
site
Application
Rate
Amount
Treated
Total
Daily
Dosea
Baseline
Daily
LADDb,
c
Baseline
Riskd
Mixer/
Loader
(
12
days/
year)

Loading
Ready
to
Use
Liquids
(
1)
pond
0.0000074
lb
ai
per
gallon
3000
Gallons
per
day
0.000037
8.7
E­
7
1.7
E­
8
pond
0.0000074
lb
ai
per
gallon
1000
Gallons
per
day
0.000012
2.9
E­
7
5.5
E­
9
aquarium
0.0000074
lb
ai
per
gallon
50
Gallons
per
day
0.00000062
1.5
E­
8
3.0
E­
10
Applicator
(
2
days/
year)

Applying
Paint/
Stains
with
Paintbrush
(
2)
Paint
0.0532
lb
ai
per
gallon
2
Gallons
per
day
0.014
5.5
E­
5
1.1
E­
6
Stains
0.0532
lb
ai
per
gallon
5
Gallons
per
day
0.036
1.4
E­
4
2.7
E­
6
Applying
Paint/
Stains
with
Paintbrush
(
study
data)
(
3)
Paint
0.0532
lb
ai
per
gallon
2
Gallons
per
day
0.018
5.0
E­
5
9.5
E­
7
Stains
0.0532
lb
ai
per
gallon
5
Gallons
per
day
0.046
1.3
E­
4
2.4
E­
6
Applying
Paint
with
Airless
Sprayer
(
4)
Paint
0.0532
lb
ai
per
gallon
15
Gallons
per
day
0.045
1.8
E­
4
3.4
E­
6
Applying
Paint
with
Airless
Sprayer
(
study
data)
(
5)
Paint
0.0532
lb
ai
per
gallon
15
Gallons
per
day
0.020
5.5
E­
5
1.1
E­
6
Footnotes:
a
Total
Daily
Dose
(
mg/
kg/
day)
=
Daily
Dermal
Dose
(
mg/
kg/
day)
*
Dermal
Absorption
(
4%)
+
Daily
Inhalation
Dose
(
mg/
kg/
day).
See
Table
10
for
daily
dermal
and
inhalation
doses.
b
The
number
of
exposures
per
year
are
based
on
the
label
recommendations.
The
No
More
Algae
Liquid
label
states
that
"
For
regular
maintenance,
use
once
a
month
or
as
algae
starts
to
reappear."
Therefore,
12
exposures
per
year
were
assumed.
Two
exposures
per
year
assumed
for
residential
person
painting
their
home.
15
c
Lifetime
average
daily
dose
(
LADD)
(
mg/
kg/
day)
=
Total
Daily
Dose
(
mg/
kg/
day)
*
(
number
of
days
of
exposure
per
year
/
365
days/
year)
*
(
50
years
exposed
/
70
years
in
a
lifetime).
d
Cancer
risk
=
LADD
(
mg/
kg/
day)
*
Q1
(
1.91E­
2
mg/
kg/
day1).
41
5.0
AGGREGATE
RISK
ASSESSMENTS
AND
RISK
CHARACTERIZATIONS
Risk
is
a
function
of
exposure
multiplied
by
hazard
(
Risk
=
Exposure
x
Hazard).
Exposure
may
be
measured
or
modeled,
depending
on
the
available
data.
Ideally
the
exposure
data
would
be
chemical
specific
occupational
or
residential
monitoring
data,
at­
the­
tap
drinking
water
data,
and
close­
to­
theplate
food
residue
data
on
all
crops.
In
the
absence
of
an
ideal
data
set,
surrogate
data,
and
other
factors
are
incorporated
into
the
exposure
assessments
(
dietary
and
non­
dietary)
to
present
a
reasonable
exposure
picture
based
on
the
best
available
data.
The
hazard
portion
of
the
risk
equation
has
several
layers
of
safety
built
into
it
to
provide
a
cushion
between
exposure
and
the
dose
at
which
adverse
effects
were
seen
in
an
animal
study.
Generally,
endpoints
are
based
on
the
dose
at
which
no
observable
adverse
effect
is
seen
in
an
animal
study.
This
is
the
No
Observable
Adverse
Effect
Level
(
NOAEL).
The
Lowest
Observable
Adverse
Effect
Level
(
LOAEL)
is
the
next
highest
dose
in
an
animal
study,
up
from
the
NOAEL,
at
which
the
adverse
effect
of
concern
is
seen.
Since
the
toxicity
studies
used
for
endpoint
selection
are
conducted
in
animals,
and
there
are
differences
between
individual
humans,
additional
uncertainty
factors
for
inter­
and
intra­
species
variability
are
integrated
into
the
hazard
portion
of
the
risk
equation.
Since
the
passage
of
the
FQPA,
an
additional
layer
of
protection
is
factored
in
(
when
appropriate)
to
provide
an
even
greater
safety
cushion
between
exposure
and
toxic
effects
for
particularly
sensitive
populations.
It
is
in
this
light
that
expressions
of
risk
(
risk
numbers)
should
be
viewed
with
an
understanding
that
they
are
not
portrayals
of
imminent
toxic
effects
to
humans
but
as
a
measure
of
the
distance
between
potential
exposure
and
possible
toxic
effects.

In
accordance
with
current
HED
policy
(
effective
03/
11/
99)
the
acute
and
chronic
dietary
endpoints
are
expressed
as
acute
Population
Adjusted
Dose
(
aPAD)
and
chronic
PAD
(
cPAD),
and
no
longer
as
an
adjusted
Reference
Dose
(
RfD).

RfD
=
acute
or
chronic
NOAEL
Uncertainty
Factor
(
UF)

Generally,
an
UF
of
100
is
applied
for
intra­
and
inter­
species
differences.

PAD
=
acute
or
chronic
RfD
FQPA
factor
The
use
of
the
PAD
will
apply
whether
the
FQPA
factor
is
retained
(
10x
or
3x)
or
not
(
1x).
When
a
PAD
is
used,
such
as
in
the
dietary
assessment,
the
risk
is
expressed
as
a
percentage
of
the
PAD
which
is
equal
to
the
measured
exposure
divided
by
the
PAD
and
then
multiplied
by
100
or:

Risk
(%
PAD)
=
Exposure
x
100
PAD
Occupational,
residential
(
when
applicable),
and
the
aggregate
risk
(
when
appropriate)
will
still
be
42
expressed
as
the
Margin
of
Exposure
(
MOE).

MOE
=
NOAEL
(
mg/
kg/
d
Exposure
(
mg/
kg/
d)

Current
HED
policy
requires
that
FQPA
safety
factors
be
retained
for
dietary
and
non­
occupational
exposures,
when
appropriate,
not
occupational
exposures
(
Memorandum,
Special
Report
of
the
FQPA
Safety
Factor
Committee,
B.
Tarplee
and
J.
Rowland,
April
15,
1998).
Therefore,
an
MOE
of
>
100
is
generally
needed
in
the
occupational
exposure
risk
assessment.
For
diuron,
if
there
were
long­
term
occupational
exposures
(
none
are
expected)
an
MOE
of
>
300
would
be
needed
since
a
3x
was
factored
in
because
a
LOAEL
was
selected
for
the
endpoint.
Since
the
FQPA
factor
is
1x,
for
residential
uses,
MOEs
>
100/
300
are
also
needed
for
short­
and
intermediate­
term,
and
long­
term
exposures,
respectively.

Generally,
the
Agency
calculates
Drinking
Water
Levels
of
Comparison
(
DWLOC)
for
comparison
to
measured
or
modeled
drinking
water
concentrations
for
the
risk
analysis.
The
DWLOC
is
the
concentration
in
drinking
water,
as
part
of
the
aggregate
exposure,
that
occupies
no
more
than
100%
of
the
PAD.
The
dietary
exposure
from
food
and
DWLOC
together,
cannot
be
greater
than
100%
of
the
PAD.
Any
measured
or
modeled
drinking
water
estimates
that
are
less
than
the
DWLOC
are
not
of
concern.

The
Agency
has
calculated
DWLOCs
for
chronic
(
noncancer)
and
short­
term
exposure
to
diuron
and
its
degradates
(
metabolites
hydrolyzable
to
3,4­
DCA)
in
surface
and
ground
water
for
the
population
subgroups;
children
1­
6
years
(
most
highly
exposed
population),
infants
<
1
year,
females
13­
50
years,
and
the
general
U.
S.
population.
No
adverse
effects
attributed
to
a
single
exposure
to
diuron
were
identified
in
any
available
studies.
Therefore,
no
acute
dietary
risk
assessment
was
conducted
and
hence,
no
acute
DWLOC
(
DWLOCacute)
was
calculated.
The
DWLOCcancer
is
the
concentration
in
drinking
water
as
a
part
of
the
aggregate
chronic
exposure
that
results
in
a
negligible
cancer
risk
(
10­
6).
Residential
exposures
to
adult
handlers
would
be
factored
into
the
DWLOCcancer;
however,
the
estimated
residential
risks
alone
are
above
the
Agency's
level
of
concern,
therefore,
DWLOCcancer
=
0.

Since
no
systemic
toxicity
was
seen
in
the
dermal
toxicity
study,
no
short­
or
intermediate­
term
occupational
or
residential
risk
assessment
by
the
dermal
route
was
needed.
The
exception
was
for
the
cancer
assessment,
for
which
the
oral
study
and
a
dermal
absorption
factor
(
measured
from
a
submitted
study)
were
used.
Based
on
the
labeled
uses,
no
incidental
oral
exposures
are
expected.
Due
to
the
lack
of
availability/
submission
of
acceptable/
guideline
inhalation
studies
using
diuron,
occupational
and
residential
risk
assessments
were
conducted
using
endpoints
selected
from
oral
studies.
To
fully
characterize
the
hazard
and
subsequent
potential
risk
from
exposures
to
diuron
and
its
metabolites
a
28­
day
inhalation
study
in
rats
is
needed.
43
5.1
Acute
Risk
No
adverse
effects
attributed
to
a
single
exposure
to
diuron
were
identified
in
any
available
studies.
Therefore,
no
acute
dietary
risk
assessment
was
conducted,
no
DWLOCacute
was
calculated,
and
hence,
no
acute
aggregate
risk
was
conducted.

5.2
Short­
term
Risk
5.2.1
Aggregate
Short­
term
Risk
Assessment
When
potential
food
and
residential
inhalation
exposures
are
combined
they
result
in
aggregate
short­
term
MOEs
=
1043
and
1045
for
adult
males
and
females,
respectively,
which
are
not
of
concern.
Based
on
labeled
uses,
no
intermediate­
or
long­
term
residential
handler,
or
postapplication
exposures
of
any
duration,
are
expected.

Aggregate
short­
term
risk
estimates
for
diuron
and
its
metabolites
hydrolyzable
to
3,4­
DCA
would
combine
exposures
from
food
(
average),
water,
and
inhalation.
Since
measured
drinking
water
data
(
monitoring
data)
are
limited
and
cannot
be
quantitatively
included
in
the
risk
assessment,
estimates
of
allowable
levels
of
drinking
water
were
calculated
(
see
DWLOCs
below)
instead.
The
Agency
determined
that
it
was
unlikely
that
more
than
one
of
the
residential
handler
activities
would
occur
concurrently
during
a
short­
term
time
period.
Therefore,
the
Agency
took
the
protective
approach
of
including
the
exposures
from
the
activity
which
could
potentially
result
in
the
most
exposure
to
the
homeowner,
applying
paint
with
an
airless
sprayer,
in
the
aggregate
assessment.
It
should
be
noted
that
residential
exposures
are
calculated
at
baseline
(
no
personal
protective
equipment,
no
engineering
controls).

The
"
MOE
approach"
was
used
to
calculate
the
short­
term
aggregate
risk,
combining
food
and
inhalation
exposures,
and
using
a
NOAEL
of
10
mg/
kg/
day.
A
UF
of
100
(
10x
for
interspecies
extrapolation,
10x
for
intraspecies
variability)
and
the
1x
FQPA
safety
factor
for
diuron
were
applied
to
the
assessment;
therefore,
an
MOE
of
greater
than
100
is
not
of
concern.

5.2.2
Short­
term
DWLOC
Calculations
Though
some
limited
chemical­
specific
water
monitoring
data
are
available,
they
are
not
nationally
representative
and
not
at­
the­
tap
data.
Though
they
may
be
indicative
of
surface
water
and
ground
water
levels
of
diuron
and
its
metabolites,
under
very
limited
conditions,
the
Agency
believes
that
they
are
unsuitable
to
be
quantitatively
included
in
aggregate
risk
assessment.
Therefore,
estimated
environmental
concentrations
(
EECs)
were
calculated
by
EFED
to
estimate
the
potential
contribution
to
the
averaged
(
chronic)
exposure
from
drinking
water,
and
the
EECs
were
compared
to
the
short­
term
DWLOCs.
44
The
current
Agency
default
body
weight
and
consumption
values
are
10
kg
and
1
liter/
day,
respectively,
for
all
infants
and
children,
70
kg
and
2
liters/
day
for
adult
males,
and
60
kg
and
2
liters/
day
for
adult
females.
These
default
values
and
others
are
presently
under
review
in
the
Agency
(
Office
of
Research
and
Development).
If
at
a
future
time,
the
Agency
decides
to
change
the
default
assumptions
used,
the
impact
of
the
changes
on
the
diuron
risk
assessment
will
be
considered.

The
DWLOCshort­
term
is
the
concentration
in
drinking
water,
as
part
of
the
aggregate
exposure,
that
combined
with
average
food
exposures
and
residential
exposures
and
divided
into
the
short­
term
NOAEL,
results
in
an
MOE
that
is
greater
than
the
LOC
or
target
MOE.
Any
measured
or
modeled
drinking
water
estimates
that
are
less
than
the
DWLOC
are
not
of
concern.
As
part
of
the
aggregate
risk
assessment
for
diuron,
the
short­
term
assessment
was
handled
using
the
reciprocal
MOE
equation
("
1/
MOE
approach")
for
calculating
the
aggregate
MOE
and
solving
for
the
term
MOEwater.
The
reciprocal
MOE
equation
is
only
used
when
the
toxic
effects
on
which
the
endpoints
are
selected
are
the
same
and
when
the
LOCs
are
identical
for
all
MOEs
in
the
calculation.

Based
on
the
supported
uses
of
diuron,
no
incidental
oral
(
hand­
to­
mouth)
exposures
are
expected
and
therefore,
were
not
factored
into
the
aggregate
and
DWLOC
calculations,
i.
e.
no
exposures
to
children
are
expected.
Also,
no
systemic
toxicity
following
repeated
dermal
dosing
was
observed
in
submitted
studies
therefore,
dermal
exposures
were
not
factored
into
the
equation
either.

Taking
into
account
the
uses
proposed
in
this
action,
the
Agency
can
conclude
with
reasonable
certainty
that
residues
of
diuron
plus
its
metabolites
hydrolyzable
to
3,4­
DCA,
resulting
from
applications
of
diuron,
in
drinking
water
would
not
likely
result
in
an
aggregate
short­
term
risk
to
male
and
female
adult
homeowners
above
the
Agency's
level
of
concern.
The
Agency
based
this
determination
on
a
comparison
of
estimated
concentrations
of
diuron
and
its
metabolites
(
DCPMU,
DCPU,
3,4­
DCA)
in
surface
and
ground
waters
to
back­
calculated
"
levels
of
comparison"
for
diuron
plus
its
metabolites
in
drinking
water.
The
EECs
in
surface
and
ground
waters
were
derived
from
water
quality
models
that
used
conservative
assumptions
(
health­
protective)
regarding
the
pesticide
transport
from
the
point
of
application
to
surface
or
ground
water,
and
were
supplemented
with
limited
monitoring
data.

Modeled
Tier
2
(
PRZM/
EXAMS)
estimates
of
concentrations
of
diuron
plus
its
metabolites
in
surface
water
were
below
the
short­
term
DWLOCs
for
male
and
female
adults
and
are
not
of
concern.
The
EECs
calculated
by
EFED
were
based
on
the
highest
labeled
rate
of
application
for
citrus.
Modeled
Tier
1
SCI­
GROW
estimates
of
ground
water
concentrations
of
diuron
plus
its
metabolites
were
below
the
short­
term
DWLOCs
and
are
not
of
concern.
45
Table
12.
Aggregate
Short­
Term
Risk
and
DWLOC
Calculations
(
Inhalation/
Oral
Endpoints
and
NOAELs
the
Same)

Population
Short
­
Term
Scenario
NOAEL
mg/
kg/
d
LOC1
Max
Exposure2
mg/
kg/
d
Average
Food
Exposure
mg/
kg/
d
Residential
Exposure3
mg/
kg/
d
Aggregate
MOE
(
food
and
residential)
4
Max
Water
Exposure5
mg/
kg/
d
Surface
Water
EEC6
(
F
g/
L)
Ground
Water
EEC6
(
F
g/
L)
Short­
Term
DWLOC7
(
F
g/
L)

Adult
Male
10
100
0.1
0.000088
0.0095
1043
0.09
104
9.1
3153
Adult
Female
10
100
0.1
0.000069
0.0095
1045
0.09
104
9.1
2700
1
LOC
(
Target
MOE)
includes
safety
factors
totaling
100
for
inter­
species
extrapolation
(
10x)
and
intra­
species
variability
(
10x).
2
Maximum
Exposure
(
mg/
kg/
day)
=
NOAEL/
LOC
3
Residential
Exposure
=
Inhalation
Exposure
4
Aggregate
MOE
=
[
NOAEL
÷
(
Avg
Food
Exposure
+
Residential
Exposure)]
5
Maximum
Water
Exposure
(
mg/
kg/
day)
=
Target
Maximum
Exposure
­
(
Food
Exposure
+
Residential
Exposure)
6
The
crop
producing
the
highest
level
was
used
to
assess
exposure
to
diuron,
DCPMU,
DCPU,
3,4­
DCA,
total.
7
DWLOC(
F
g/
L)
=
[
maximum
water
exposure
(
mg/
kg/
day)
x
body
weight
(
kg)]
[
water
consumption
(
L)
x
10­
3
mg/
F
g]

5.4
Chronic
Risk
5.4.1
Chronic
Aggregate
Risk
Assessment
Aggregate
chronic
(
noncancer)
risk
estimates
include
the
contribution
of
risk
from
dietary
sources
(
food
+
water)
and
residential
sources.
However,
based
on
the
labeled
uses,
no
long­
term
or
chronic
residential
exposures
are
expected.
Chronic
risk
estimates
from
exposures
to
food,
associated
with
the
use
of
diuron
do
not
exceed
the
Agency's
level
of
concern
for
the
most
highly
exposed
population
subgroup,
children
ages
1­
6
years
of
age.
The
chronic
dietary
(
food
only)
risk
estimate
for
children
ages
1­
6
years
of
age
was
<
7%
of
the
chronic
PAD.

As
mentioned
above,
though
some
limited
chemical­
specific
water
monitoring
data
are
available,
they
are
not
nationally
representative
and
not
at­
the­
tap
data.
Therefore,
EECs
were
calculated
by
EFED
to
estimate
the
potential
contribution
to
the
chronic
exposure
from
drinking
water,
and
the
EECs
were
compared
to
the
chronic
DWLOCs.

5.4.2
Chronic
DWLOC
Calculations
To
calculate
the
DWLOC
for
chronic
(
noncancer)
exposure
relative
to
a
chronic
toxicity
endpoint,
the
dietary
food
exposure
(
from
DEEM
 
)
was
subtracted
from
the
PAD
to
obtain
the
exposure
to
46
diuron
and
its
3,4­
DCA­
containing
metabolites
in
drinking
water
that
would
not
be
of
concern.

A
chronic
DWLOC
(
DWLOCchronic)
was
calculated
using
the
following
formulae:

DWLOCchronic
(
µ
g/
L)
=
chronic
water
exposure
(
mg/
kg/
d)
x
body
weight
(
kg)
consumption
(
L/
d)
x
10­
3
mg/
µ
g
chronic
water
exposure
(
mg/
kg/
d)
=
[
cPAD
­
(
chronic
food
+
residential(
ADD)(
mg/
kg/
d))]

Where
ADD
=
average
daily
dose
Residential
exposures
were
not
factored
into
the
DWLOCchronic
since
no
long­
term
residential
exposures
(
handler
or
postapplication)
are
expected.

Taking
into
account
the
uses
proposed
in
this
action,
the
Agency
cannot
conclude
with
reasonable
certainty
that
residues
of
diuron
plus
its
metabolites
hydrolyzable
to
3,4­
DCA,
resulting
from
applications
of
diuron,
in
drinking
water
would
not
likely
result
in
a
chronic
dietary
risk
to
infants,
children,
and
adults
above
the
Agency's
level
of
concern.
The
Agency
based
this
determination
on
a
comparison
of
estimated
concentrations
of
diuron
and
its
metabolites
in
surface
waters
to
backcalculated
"
levels
of
comparison"
for
diuron
plus
its
metabolites
in
drinking
water.

Modeled
Tier
2
(
PRZM/
EXAMS)
estimates
of
concentrations
of
diuron
plus
its
metabolites
(
DCPMU,
DCPU,
3,4­
DCA)
in
surface
water
were
above
the
chronic
DWLOCs
for
all
population
subgroups
and
are
of
concern
(
Table
13).
The
EECs
calculated
by
EFED
were
based
on
the
highest
labeled
rate
of
application
for
citrus.
Modeled
Tier
1
SCI­
GROW
estimates
of
ground
water
concentrations
of
diuron
plus
its
metabolites
(
DCPMU,
DCPU,
3,4­
DCA)
were
below
the
chronic
DWLOCs
and
are
not
of
concern.

Table
13
Summary
of
Chronic
DWLOC
Calculations
Population
Subgroups
cPAD
mg/
kg/
d
Food
Exposure
mg/
kg/
d
Maximum
Water
Exposure
mg/
kg/
d
PRZM/
EXAMS
(
ppb)
surface
water
(
total
EECs)
SCI­
GROW
(
ppb)
ground
water
(
total
EECs)
DWLOCchronic
(
ppb)

U.
S.
Population
0.003
0.000088
0.0029
104
9.1
102
Females
13­
50
yrs
0.003
0.000069
0.0029
104
9.1
88
Infants
<
1
yr
0.003
0.000077
0.0029
104
9.1
29
47
Children
1­
6
yrs
0.003
0.00020
0.0028
104
9.1
28
5.5
Cancer
Risk
5.5.1
Aggregate
Cancer
Risk
Assessment
Though
estimated
exposure
to
food
alone
results
in
a
cancer
risk
(
1.68
x
10­
6)
for
the
U.
S.
general
population,
it
is
not
of
concern.
The
estimates
of
exposures
from
food
are
based
on
a
refined
analysis
(%
CT
and
some
processing
data),
but
used
data
from
field
trails
conducted
at
the
maximum
application
rates
and
cannot
be
further
refined
without
additional
data
(
processing
data,
monitoring
data
that
includes
the
parent
and
its
metabolites
that
are
hydrolyzable
to
3,4­
DCA).
Residential
exposures
to
applicators
(
adults)
applying
paint
with
a
paintbrush
or
airless
sprayer
result
in
potential
cancer
risks
that
are
of
concern
(
range
1.9
x
10­
6
to
6.8
x
10­
6).
This
is
a
conservative
assessment
based
on
Residential
SOPs
and
includes
an
estimate
of
dermal
exposure
and
an
upper
bound
dermal
absorption
factor.
Residential
exposures
to
homeowners
loading
ready­
to­
use
liquids
do
not
result
in
potential
cancer
risks
that
are
of
concern.

5.5.2
Cancer
DWLOC
Calculations
For
the
cancer
(
Q1*)
exposure
calculations,
the
Agency
uses
a
multi­
year
mean
water
concentration
values.
The
DWLOCcancer
is
the
concentration
in
drinking
water
as
a
part
of
the
aggregate
chronic
exposure
that
results
in
a
negligible
cancer
risk
(
10­
6).
Residential
exposures
to
adult
handlers
would
be
factored
into
the
DWLOCcancer
however,
since
the
potential
cancer
risks
from
exposures
during
residential
activities,
alone,
are
of
concern,
no
DWLOCs
were
calculated
and
allowable
exposures
to
water
are
essentially
"
0."

5.5.3
Additional
Cancer
Risks
The
MARC
recommended
that
a
separate
dietary
cancer
assessment
be
conducted
for
MCPDMU,
a
potential
residue
of
concern
in
water,
but
not
found
in
plant
or
animal
residue
studies.
The
MARC
raised
concerns
for
N'­(
3­
chlorophenyl)­
N,
N­
dimethyl
urea
(
MCPDMU)
based
on
an
analogous
compound,
N'­(
4­
chlorophenyl)­
N,
N­
dimethyl
urea
(
monuron).
With
the
exception
of
the
position
of
the
chlorine,
the
structures
are
identical.
There
are
cancer
concerns
for
monuron
but
the
target
organs
are
different
than
those
affected
by
diuron.
Monuron
produces
kidney
and
liver
tumors
in
male
rats
(
NTP
technical
Report
266,
1988).
The
most
potent
unit
risk,
Q1
*
of
those
calculated
for
monuron
is
that
for
male
rat
liver
neoplastic
nodule
and/
or
carcinoma
combined
tumor
rates
at
1.52
x
10­
2
(
mg/
kg/
day)­
1,
in
human
equivalents
(
MONURON:
Quantitative
Risk
Assessment
(
Q1
*)
Based
On
F344/
N
Rat
Dietary
Study
With
3/
4'
s
Interspecies
Scaling
Factor.
PC
Code
035501.
Lori
L.
Brunsman.
July
5,
2001).
48
Since
there
is
potential
for
MCPDMU
to
occur
in
water,
the
Agency
considered
possible
exposures
to
MCPDMU
from
ingestion
of
catfish,
as
well
as
from
drinking
water.
The
AR
of
MCPDMU
in
catfish
was
calculated
using
the
following
inputs:

2
ppm
tolerance
for
catfish
x
0.251
x
0.352
=
anticipated
residue
Where:
1
The
fraction
of
applied
radioactive
diuron
converted
to
MCPDMU
in
an
aerobic
aquatic
metabolism
study
(
see
EFED
chapter).
The
data
were
obtained
from
a
sample
taken
30
days
after
initiation
of
the
study
and
was
the
highest
residue
value
found.
The
study
indicated
an
approximately
linear
correlation
of
MCPDMU
vs
time
and
the
30
day
sample
was
the
longest
interval
provided.
2
%
CT
for
catfish.

Using
the
Q1*
for
monuron,
the
calculated
cancer
risk
to
the
U.
S.
general
population
from
potential
exposure
to
MCPDMU
in
catfish
alone
is
1.02
x
10­
7
and
is
not
of
concern.

A
DWLOCcancer
for
MCPDMU
was
calculated
to
determine
whether
potential
exposures
to
MCPDMU
only
(
Drinking
Water
Assessment
for
diuron
and
its
degradates.
Ibrahim
Abdel­
Saheb.
March
11,
2001)
in
drinking
water
from
surface
or
ground
water
sources
is
of
concern.
As
illustrated
below,
the
EEC
of
MCPDMU
from
surface
water
(
PRZM/
EXAMS)
exceeds
the
DWLOCcancer
and
is
of
concern.

Summary
of
Cancer
DWLOC
Calculations
for
MCPDMU
Population
Subgroup
Negligible
Risk
Q1*
(
mg/
kg/
d)­
1
Chronic
Food
Exposure
PRZM/
EXAMS
(
ppb)
SCIGROW
(
ppb)
DWLOCcancer
(
ppb)

U.
S.
Population
0.000001
0.0152
0.000007
26
1.4
2.0
There
are
several
issues
to
consider
when
characterizing
the
magnitude
of
the
potential
cancer
risk
from
exposure
to
MCPDMU,
and
the
appropriateness
of
the
analogy
to
monuron
(
Personal
communication.
Alberto
Protzel.
October
4,
2001):

°
There
is
no
proven
mechanism
for
the
carcinogenic
effect
of
monuron
in
rats,
to
allow
for
the
satisfactory
evaluation
of
the
effect
on
carcinogenicity
of
going
from
the
4­
chloro
isomer
in
monuron
to
the
3­
chloro
isomer
in
the
water
metabolite.

°
There
are
no
toxicity
data
on
the
3­
chloro
isomer
to
comfortably
rule
it
out
as
a
carcinogen.

In
the
absence
of
the
data
needed
for
a
more
comprehensive
evaluation,
the
carcinogenic
risk
assessment
was
conducted
using
the
Q1
*
of
monuron.
It
is
possible
to
speculate
that
the
actual
risk
for
49
the
3­
chlorophenyl
isomer
might
be
lower
(
how
much
lower
cannot
be
established)
than
the
calculations
indicate
based
on
the
following
observations:

°
Both
monuron
and
its
metabolic
product
p­
chloroaniline
(
a.
k.
a.
4­
chloroaniline)
have
been
shown
to
be
carcinogens.
Monuron
produced
tumors
of
the
kidney
and
liver
in
male
rats
(
NTP
technical
Report
266,
1988).
PCA
produced
tumors
of
the
liver
and
spleen
in
male
mice
(
NTP
Technical
Report
351,
1989).
In
contrast,
the
pesticide
chlorpropham
(
isopropyl­
m­
chlorcarbanilate),
which
releases
3­
chloroaniline
(
excreted
in
urine
as
1­
2%
of
the
dose
and
is
a
moiety
associated
with
the
3­
chloro
water
metabolite
of
diuron),
is
currently
classified
by
the
Agency
as
an
E­
carcinogen.
Although
3­
chloroaniline
produced
a
statistically
significant
increase
in
testicular
interstitial
cell
adenomas
in
rats,
well
above
historical
controls,
the
significant
increase
occurred
at
1000
mg/
kg/
day,
a
dose
considered
by
the
Agency
to
be
excessive.

°
Sabbioni
and
Neuman
(
Carcinogenesis
11:
111­
115,1990)
studied
the
in­
vivo
binding
of
arylamines
to
a
cellular
macromolecule
(
hemoglobin).
3­
Chloroaniline
(
administered
to
rats
pure
or
as
chlorpropham)
produced
1/
10
or
less
the
amount
of
hemoglobin
adducts
that
was
produced
by
4­
chloroaniline
(
administered
to
rats
pure
or
as
monuron).
This
observation
might
suggest
less
avidity
of
3­
chloroaniline
than
4­
chloroaniline
for
cellular
macromolecules.

6.0
CUMULATIVE
The
Agency
does
not
currently
have
data
available
to
determine
with
certainty
whether
diuron
has
a
common
mechanism
of
toxicity
with
any
other
substances.
For
purposes
of
this
human
health
risk
assessment,
the
Agency
has
assumed
that
diuron
does
not
have
a
common
mechanism
of
toxicity
with
any
other
pesticides.
Additional
weight­
of­
the­
evidence
supports
this
approach
as
is
discussed
below.

In
May
1999,
the
Agency
performed
a
Section
18
risk
assessment
for
diuron
use
in
catfish
ponds
(
ID#
99MS0001.
SECTION
18
EXEMPTION
FOR
THE
USE
OF
DIURON
80W
IN
CATFISH
PONDS
IN
MISSISSIPPI.
DP
Barcode:
D255462.
Pamela
Hurley,
Richard
Loranger,
Steven
Weiss.
May
13,
1999).
At
that
time,
the
estimated
residues
of
propanil
and
linuron
were
added
to
those
of
diuron
and
the
risk
assessment
was
performed
using
the
noncancer
endpoints
selected
for
diuron.
All
three
chemicals
contain
within
their
structures,
3,4­
DCA.
However,
linuron
and
diuron
are
ureas,
while
propanil
is
not.
Though
propanil
readily
metabolizes
to
3,4­
DCA,
neither
diuron
nor
linuron
metabolize
to
3,4
 
DCA
in
plant
or
animal
metabolism
studies.

Since
1999,
the
Agency
has
received
and
evaluated
new
information,
performed
a
more
comprehensive
assessment
of
propanil
and
linuron,
and
re­
evaluated
its
approach
to
the
assessment
of
diuron.
The
MARC
does
not
recommend
aggregating
residues
of
3,4­
DCA
for
the
propanil
and
diuron
risk
assessments
[
Personal
communication.
Christine
Olinger
(
MARC
Chair)
to
Sherrie
Kinard.
September
19,
2001].
3,4­
DCA
is
a
significant
residue
of
concern
for
propanil,
but
is
not
a
residue
of
50
concern
per
se
for
diuron.
The
analytical
method
for
quantifying
residues
of
concern
from
applications
of
diuron
converts
all
residues
to
3,4­
DCA
as
a
technical
convenience.
However,
3,4­
DCA
is
not
a
significant
residue
in
diuron
plant
and
animal
metabolism
or
hydrolysis
studies.
Therefore,
the
MARC
recommended
that
all
residues
hydrolyzable
to
3,4­
DCA
would
be
included
in
the
tolerance
expression
for
diuron,
because
no
validated
enforcement
method
is
available
for
quantification
for
the
actual
residues
of
concern
for
diuron
[
Diuron.
Results
of
the
Health
Effects
Division
(
HED)
Metabolism
Assessment
Review
Committee
(
MARC)
Meeting
Held
on
03­
JULY­
2001.
John
Punzi.
August
10,
2001].
Additionally,
propanil
and
its
metabolite
3,4­
DCA
were
found
to
induce
methemoglobinemia,
the
endpoint
of
concern
for
propanil.
Diuron
has
not
been
shown
to
cause
this
effect.
Diuron
induces
hemolytic
anemia
and
compensatory
hematopoiesis,
which
are
mechanistically
different
from
methemoglobinemia.

Linuron
and
diuron
metabolism
studies
show
that
both
chemicals
metabolize
to
DCPU
and
DCPMU.
However,
for
reasons
that
are
yet
unknown,
these
chemicals
do
not
induce
the
same
toxic
effects
in
mammals.
Submitted
data
indicate
that
diuron
is
primarily
(
though
not
exclusively)
metabolized
by
the
hydroxylation
of
the
urea
group
in
either
the
methyl
or
the
amino
position
and
conjugated.
Linuron,
on
the
other
hand,
appears
to
be
primarily
ring­
hydroxylated
and
conjugated.
The
methoxy
group
is
removed,
followed
by
the
methyl
group,
with
ring
hydroxylation.
Unlike
linuron,
hydroxylation
of
the
phenyl
ring
is
not
a
major
metabolite
pathway
of
diuron
and,
both
methyl
groups
are
lost.
Methemoglobinemia
is
the
dominant
toxic
effect
of
concern
for
linuron.
As
mentioned
above,
diuron
does
not
induce
methemoglobinemia.
Mechanistic
and
reproductive
studies
show
that
linuron,
and
to
some
extent
propanil,
is
an
androgen
receptor
antagonist
and
that
linuron
induces
testicular
abnormalities
in
rodents.
Studies
with
diuron
showed
no
indications
of
any
endocrine
effects
and
no
developmental
or
reproductive
effects.
Though
the
mechanisms
of
action
for
the
differing
effects
induced
by
the
two
ureas,
diuron
and
linuron,
are
not
entirely
known,
there
is
sufficient
cause
to
believe
that
exposures
from
the
two
compounds
should
not
be
cumulated.

In
addition,
in
1999
the
estimated
dietary
cancer
risk
for
diuron
did
not
include
residues
from
linuron
and
propanil
since
it
was
recognized
that
the
target
organs
for
tumor
induction
for
diuron
are
different
from
those
for
linuron
and
propanil,
and
data
were
available
which
indicated
that
the
mechanism
of
action
may
be
different
for
diuron.
Currently
available
data
support
that
decision.

In
conclusion,
the
Agency
has
assumed
that
diuron
does
not
have
a
common
mechanism
of
toxicity
with
any
other
pesticides.
For
purposes
of
this
human
health
risk
assessment,
a
cumulative
risk
assessment
is
not
warranted.

7.0
OCCUPATIONAL
EXPOSURE
The
Agency
has
determined
that
there
are
potential
exposures
to
mixers,
loaders,
applicators
and
other
handlers
during
the
usual
use­
patterns
associated
with
diuron.
Based
on
the
use
patterns,
31
51
major
occupational
exposure
scenarios
were
identified
for
diuron.
Calculations
of
noncancer
risk
based
on
inhalation
exposure
indicate
that
the
inhalation
margins
of
exposure
(
MOEs)
are
more
than
100
at
the
highest
possible
level
of
mitigation
for
all
of
the
short­
term
occupational
exposure
scenarios
except
applying
sprays
with
a
high
pressure
handwand.
Sixteen
of
the
31
occupational
scenarios
were
identified
as
having
intermediate­
term
durations
of
exposure.
Of
these,
none
have
a
non­
cancer
risk
of
concern
for
intermediate­
term
inhalation
exposure
at
the
highest
possible
level
of
mitigation.
A
noncancer
postapplication
risk
assessment
was
not
conducted,
since
no
systemic
toxicity
by
the
dermal
route
is
expected
for
the
short­
or
intermediate­
term
durations.
Postapplication
cancer
risks
for
private
growers
were
calculated
at
both
the
typical
application
rate
and
the
maximum
application
rate
for
each
crop
grouping.
All
cancer
risks
to
private
growers
were
less
than
1
x
10­
4
on
the
day
of
treatment.
Postapplication
cancer
risks
for
commercial
applicators
were
calculated
at
the
typical
application
rate
for
each
crop
grouping.
All
potential
cancer
risks
to
commercial
applicators
were
less
than
1
x
10­
4
on
the
day
of
treatment.

Occupational
risk
assessments
were
conducted
for
the
use
of
diuron
as
a
mildewcide
in
paint.
Four
occupational
handler
scenarios
were
identified
for
the
use
of
diuron
in
paint
and
are
expected
to
be
of
short­
and
intermediate­
term
exposure
duration.
The
calculations
of
short­
and
intermediate­
term
inhalation
risk
from
the
use
of
diuron
in
paint
indicate
that
MOEs
are
more
than
100
at
the
assessed
level
of
mitigation
for
all
the
exposure
scenarios,
except
applying
paints
with
an
airless
sprayer
(
indoors).
At
the
assessed
level
of
mitigation,
all
four
scenarios
have
potential
cancer
risks
between
1
x
10­
4
and
1
x
10­
6.
Occupational
postapplication
exposures
to
paint
containing
diuron
may
occur
in
industrial
settings
around
open
vats
used
in
paint
processing.
Inhalation
and
dermal
exposures
may
also
occur
while
maintaining
industrial
equipment.
No
postapplication
exposure
data
have
been
submitted
to
determine
the
extent
of
postapplication
exposures
in
the
industrial
settings.
Nonetheless,
inhalation
exposures
are
expected
to
be
minimal
because
of
the
low
vapor
pressure
of
diuron
(
2
x
10­
7
mm
Hg
at
30
E
C)
and
aerosol
formation
is
not
expected.
Dermal
postapplication
exposures
are
expected
to
be
lower
than
when
handling/
loading
the
formulated
product.
Therefore,
postapplication
exposures
in
the
industrial
settings
are
expected
to
be
minimal
and
not
of
concern.

Occupational
risk
assessments
were
also
conducted
for
the
use
of
diuron
as
an
algaecide
in
commercial
fish
ponds.
Four
short­
term
occupational
handler
scenarios
were
identified
for
the
use
of
diuron
in
commercial
fish
production
and
the
inhalation
MOEs
from
all
four
of
the
commercial
fish
production
scenarios
were
greater
than
100
at
the
baseline
level
of
mitigation
and
are
not
of
concern.
With
maximum
mitigation
measures
(
engineering
control
level),
all
four
scenarios
have
estimated
cancer
risks
of
less
than
1
x
10­
6
and
are
not
of
concern.
Occupational
postapplication
exposure
to
diuron
in
treated
fish
production
ponds
is
not
likely
to
result
in
a
risk
of
concern
based
on
the
extremely
high
dilution
rate.

7.1
Agricultural
and
Non­
crop/
Utility
Uses
7.1.1
Handler
52
The
EPA
has
determined
that
there
are
potential
exposures
to
mixers,
loaders,
applicators,
and
other
handlers
during
usual
use­
patterns
associated
with
diuron.
Based
on
the
use
patterns,
31
major
occupational
exposure
scenarios
were
identified
for
diuron:
(
1a)
mixing/
loading
liquid
formulations
for
aerial
application;
(
1b)
mixing/
loading
liquid
formulations
for
chemigation;
(
1c)
mixing/
loading
liquid
formulations
for
groundboom
application;
(
1d)
mixing/
loading
liquid
formulations
for
rights­
of­
way
sprayers;
(
1e)
mixing/
loading
liquid
formulations
for
high­
pressure
hand
wand;
(
2a)
mixing/
loading
dry
flowables
for
aerial
application;
(
2b)
mixing/
loading
dry
flowables
for
chemigation;
(
2c)
mixing/
loading
dry
flowables
for
groundboom
application;
(
2d)
mixing/
loading
dry
flowables
for
rights­
of­
way
spray
application;
(
2e)
mixing/
loading
dry
flowables
for
high­
pressure
hand
wand;
(
3a)
mixing/
loading
wettable
powders
for
aerial
application;
(
3b)
mixing/
loading
wettable
powders
for
chemigation;
(
3c)
mixing/
loading
wettable
powders
for
groundboom
application;
(
3d)
mixing/
loading
wettable
powders
for
rights­
of­
way
spray
application;
(
3e)
mixing/
loading
wettable
powders
for
high­
pressure
hand
wand;
(
4)
loading
granulars
for
tractor­
drawn
spreaders;
(
5)
applying
sprays
for
aerial
application;
(
6)
applying
sprays
for
groundboom
application;
(
7)
applying
sprays
with
a
rights­
of­
way
sprayer;
(
8)
applying
sprays
with
a
high­
pressure
hand
wand;
(
9)
applying
granulars
for
a
tractor­
drawn
spreader;
(
10)
applying
granulars
with
a
spoon;
(
11)
applying
granulars
for
hand
application;
(
12)
flagging
aerial
spray
applications;
(
13)
mixing/
loading/
applying
liquids
with
a
low­
pressure
hand
wand;
(
14)
mixing/
loading/
applying
liquids
with
a
backpack
sprayer;
(
15)
mixing/
loading/
applying
wettable
powders
with
a
low­
pressure
hand
wand;
(
16)
loading/
applying
granulars
with
a
pump
feed
backpack
spreader;
(
17)
loading/
applying
gravity
feed
backpack
spreader;
(
18)
loading/
applying
granulars
for
a
belly
grinder
application;
and
(
19)
loading/
applying
granulars
with
a
push­
type
spreader.
Since
granulars
are
only
used
on
non­
crop/
utility
areas,
aerial
application
of
granulars
and
flaggers
supporting
aerial
operations
were
not
assessed.

Current
diuron
labels
have
PPE
requirements
ranging
from
no
PPE
listed
to
long­
sleeved
shirt
and
long
pants,
waterproof
gloves,
shoes,
socks,
protective
eye
wear,
chemical
resistant
headgear,
and
a
dust/
mist
filtering
respirator.
Mixer
and
loaders
must
also
wear
a
chemical
resistant
apron.

Table
3
in
the
attached
document,
Occupational
and
Residential
Exposure
Assessment
and
Recommendations
for
the
Reregistration
Eligibility
Decision
Document
for
Diuron.
Renee
Sandvig
and
Christina
Jarvis.
October
16,
2001,
summarizes
the
caveats
and
parameters
specific
to
the
surrogate
data
used
for
each
handler
scenario
and
the
corresponding
exposure/
risk
assessment.
These
caveats
include
the
source
of
the
data
and
an
assessment
of
the
overall
quality
of
the
data.
The
assessment
of
data
quality
is
based
solely
on
the
number
of
observations
and
the
available
quality
control
data.
The
quality
control
data
are
based
on
a
grading
criteria
established
by
the
PHED
Task
Force.
The
PHED
Task
Force
is
comprised
of
representatives
from
the
U.
S.
EPA,
Health
Canada,
the
California
Department
of
Pesticide
regulation,
and
member
companies
of
the
American
Crop
Protection
Association.
The
sources
of
the
surrogate
include:

!
Pesticide
Handlers
Exposure
Database
(
PHED).
53
!
Outdoor
Residential
Exposure
Task
Force
(
ORETF).
The
task
force
recently
submitted
proprietary
data
to
the
Agency
on
hose­
end
sprayers,
push­
type
granular
spreaders,
and
handgun
sprayers
(
MRID
#
44972201).
The
ORETF
data
were
used
in
this
assessment
in
place
of
PHED
data
for
the
"
loading/
applying
granulars
using
a
push­
type
spreader"
scenario.

!
Worker
Exposure
Study
During
Application
In
Banana
Plantation
With
Temik
10G
(
MRID
#
451672­
01).
The
Agency
has
used
data
from
the
aldicarb
(
Temik)
study
to
assess
exposures
and
risks
to
handlers
applying
granulars
with
a
pump
feed
backpack
sprayer.

!
Worker
Exposure
Study
During
Application
of
Regent
20GR
In
Banana
Plantation
(
MRID
#
452507­
02).
The
Agency
has
used
data
from
the
fipronil
(
Regent
20
GR)
study
to
assess
exposures
and
risks
to
handlers
loading
and
applying
granulars
with
a
gravity
feed
backpack
sprayer.
In
addition,
the
Agency
has
also
used
data
from
the
fipronil
study
to
assess
exposures
and
risks
to
occupational
handlers
loading
and
applying
granulars
using
a
scoop
and
bucket.

Calculations
for
the
handler
risk
assessment
were
completed
for
a
range
of
maximum
application
rates
for
specific
crops
recommended
by
the
available
diuron
labels
and
the
LUIS
report.
These
rates
were
assessed
in
order
to
bracket
risk
levels
associated
with
the
various
use
patterns.

7.1.1.1
Noncancer
Exposure
and
Risk
Estimates
Noncancer
handler
exposure
assessments
were
completed
using
a
baseline
exposure
scenario
and,
if
required,
increasing
levels
of
risk
mitigation
(
PPE
and
engineering
controls)
in
an
attempt
to
achieve
an
appropriate
margin
of
exposure.
The
baseline
scenario
generally
represents
a
handler
wearing
long
pants,
a
long­
sleeved
shirt,
no
respirator,
and
no
chemical­
resistant
gloves
(
there
are
exceptions
pertaining
to
the
use
of
gloves,
and
these
are
noted).
Noncancer
dermal
risks
from
the
use
of
diuron
were
not
calculated.
No
systemic
toxicity
following
repeated
dermal
dosing
at
1200
mg/
kg/
day
was
seen
in
the
rabbit
dermal
toxicity
study;
therefore,
a
quantitative
noncancer
dermal
risk
assessment
(
short­
and
intermediate­
term)
is
not
required.
However,
calculations
of
daily
dermal
exposure
and
daily
dermal
dose
were
included
for
purposes
of
the
cancer
risk
assessment.

Handler
exposures
to
diuron
are
expected
to
be
mainly
of
short­
term
duration
(
one
day
to
one
month).
Intermediate­
term
exposure
(
one
month
to
several
months)
for
handlers
is
possible
for
large
field
crops,
including
corn,
wheat,
oats
and
cotton,
because
of
their
long
planting
seasons.
Rights­
ofway
sprayer
scenarios
for
utility
and
industrial
areas
are
assumed
to
be
of
intermediate­
term
duration,
because
utility
workers
could
possibly
treat
rights­
of­
way
areas
(
roadsides,
railroads,
etc)
all
summer
long.
The
short­
term
inhalation
MOEs
were
calculated
using
the
NOAEL
of
10
mg/
kg/
day,
from
the
developmental
toxicity
study
in
rabbits.
The
intermediate­
term
MOEs
were
calculated
using
the
NOAEL
of
1.0
mg/
kg/
day,
from
the
chronic
toxicity
study
in
rats.
An
LOC
or
target
MOE
of
100
has
been
identified
as
the
target
risk
level
for
short­
and
intermediate­
term
occupational
exposure
scenarios.
Tables14
and
15
show
a
summary
of
the
short­
and
intermediate­
term
exposures
and
MOEs.
54
Of
the
31
identified
occupational
handler
exposure
scenarios,
all
short­
and
intermediate­
term
exposure
scenarios
resulted
in
MOEs
greater
than
100
with
PPE
and
Engineering
Control
mitigation
for
all
scenarios
for
which
engineering
controls
are
feasible.
The
only
scenario
for
which
the
estimated
risks
(
MOEs)
were
calculated
to
be
less
than
100,
and
therefore
of
concern
to
the
Agency,
is
Applying
Sprays
for
High­
Pressure
Handwand
Application
at
the
maximum
application
rate
of
0.96
lb
ai
per
gallon,
at
both
minimum
and
maximum
levels
of
PPE
protection
(
MOEs
range
from
46
to
92).
Engineering
Controls
are
not
feasible
for
this
scenario.

7.1.1.2
Cancer
Exposure
and
Risk
Estimates
The
cancer
handler
exposure
scenarios
are
identical
to
those
assessed
in
the
noncancer
handler
assessment.
To
assess
cancer
risk,
a
total
daily
dose,
a
lifetime
daily
dose
and
a
total
cancer
risk
are
calculated.
The
total
daily
dose
is
calculated
to
include
both
dermal
and
inhalation
exposure
(
dermal
dose
includes
dermal
absorption
since
an
oral
cancer
endpoint
was
used)
and
used
a
Q1*=
1.91
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents.

The
assessment
assumed
that
the
average
lifetime
is
70
years,
exposure
duration
is
35
years,
and
that
the
exposures
per
year
are:
10
days
per
year
for
the
private
grower
and
30
days
per
year
for
a
commercial
applicator.
Maximum
application
rates
were
used
in
the
private
grower
assessment.
Typical
application
rates
were
used
in
both
the
private
grower
and
commercial
applicator
assessments.
It
was
assumed
that
as
the
frequency
of
exposure
increased,
the
probability
of
being
exposed
to
a
maximum
application
rate
would
decrease.
Therefore,
maximum
application
rates
were
not
assessed
for
the
commercial
applicator.
Table
16
summarizes
the
cancer
risks
associated
with
the
handling
of
diuron
for
the
baseline,
maximum
PPE
and
engineering
control
level
of
mitigation.
In
general,
the
Agency
is
concerned
when
occupational
cancer
risk
estimates
exceed
1
x
10­
4.
The
Agency
will
seek
ways
to
mitigate
the
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
1
x
10­
6
or
less.

Five
of
the
assessed
scenarios
have
cancer
risks
greater
than
1
x
10­
4
at
the
highest
feasible
level
of
mitigation
(
private
farmer/
commercial
applicator,
typical/
max
rate)
and
are
of
concern
(
See
Occupational
and
Residential
Exposure
Assessment
and
Recommendations
for
the
Reregistration
Eligibility
Decision
Document
for
Diuron.
Renee
Sandvig
and
Christina
Jarvis.
October
16,
2001).
Twenty­
six
of
the
scenarios
have
cancer
risks
between
1
x
10­
4
and
1
x
10­
6
at
the
highest
feasible
level
of
mitigation
(
private
farmer/
commercial
applicator,
typical/
max
rate).

7.1.2
Postapplication
Exposures
EPA
has
determined
that
there
are
potential
postapplication
exposures
to
individuals
entering
treated
fields.
The
current
diuron
labels
have
a
restricted
entry
interval
(
REI)
requirement
of
12
hours
with
the
following
early
entry
PPE
required:
coveralls
over
long
sleeved
shirt
and
long
pants,
waterproof
gloves,
chemical
resistant
footwear
plus
socks,
protective
eye
wear
and
chemical
resistant
headgear
for
55
overhead
exposures.

Many
of
the
applications
of
diuron
are
soil
directed
or
pre­
plant,
since
the
application
of
diuron
to
most
of
the
registered
crops
would
result
in
plant
damage.
Only
the
crops
whose
foliage
can
be
sprayed
without
damage
were
assessed
for
postapplication
exposure
to
foliage.
The
crops
that
can
be
sprayed
without
foliage
damage
are
oats,
wheat,
birdsfoot
treefoil,
clover,
grass
grown
for
seed,
alfalfa,
asparagus,
pineapple,
and
sugarcane.

Significant
exposure
to
diuron
may
result
from
contact
with
treated
soil
when
planting
seedlings,
moving
irrigation
lines,
or
other
soil
related
activities
since
diuron
is
applied
directly
to
the
soil.
At
this
time,
no
transfer
coefficients
exist
for
activities
resulting
in
contact
with
treated
soil.
There
are
also
no
data
on
the
soil
residue
dissipation
of
diuron.
A
worker
exposure
study
and
a
diuron
soil
residue
dissipation
study
would
be
needed
to
assess
this
risk.
Transfer
coefficients
do
not
exist
for
the
mechanical
harvesting
of
alfalfa
and
asparagus
and
these
activities
are
considered
of
special
concern
according
to
the
Agriculture
Transfer
Coefficient
Exposure
SAC
policy
3.1.
Significant
worker
exposure
is
possible
from
mechanical
harvesting
of
these
crops.

Since
diuron
can
be
applied
as
a
defoliant
soon
before
harvest,
exposure
to
cotton
harvesters
is
of
special
concern
for
this
chemical.
Data
recently
submitted
to
the
Agency
show
that
there
is
exposure
during
the
mechanical
harvesting
of
cotton.
Exposure
can
result
from
the
following
occupational
job
functions:
picker
operator,
module
builder,
tramper,
and
raker.
A
picker
operator
is
the
individual
that
drives
the
harvesting
machine,
usually
with
an
enclosed
cab.
A
module
builder
operator
is
the
individual
that
operates
the
controls
of
the
module
builder
into
which
the
picker
loads
the
cotton.
The
module
builder
is
used
to
receive
the
cotton
and
then
compact
it
into
modules
or
bales.
A
tramper
is
the
individual
who
stands
on
top
of
the
module
builder
and
helps
direct
the
cotton
out
of
the
picker
and
into
the
module
builder.
The
tramper
than
jumps
into
the
module
builder
and
redistributes
the
cotton
within
the
module
builder.
A
raker
is
the
individual
who
rakes
up
the
spilled
cotton
and
puts
it
back
into
the
module
builder.
The
models
presently
used
to
assess
occupational
postapplication
exposure
cannot
be
used
since
the
foliage
has
dropped
off
of
the
cotton
plants
by
the
time
of
harvest.
There
are
no
standard
default
transfer
coefficients
for
these
activities
at
this
time.
Data
on
these
exposure
potentials
are
requested.
Diuron
labels
with
the
cotton
defoliant
use
should
specify
that
cotton
can
only
be
harvested
mechanically.

Chemical­
specific
postapplication
exposure
and/
or
environmental
fate
data
have
not
yet
been
submitted
by
the
registrant
in
support
of
reregistration
of
diuron.
In
lieu
of
these
data,
a
surrogate
postapplication
assessment
was
conducted
to
determine
potential
human
risks
incurred
from
applying
diuron
to
the
foliage
of
the
crops
that
can
be
sprayed
without
damage
to
the
leaves.
The
surrogate
assessment
in
Table
17
is
based
on
both
the
typical
and
maximum
application
rates
that
a
private
farmer/
grower
may
reasonably
be
expected
to
be
exposed
to
for
a
short
duration
(
10
days).
The
surrogate
assessment
in
Table
18
is
based
on
the
typical
application
rates
that
a
commercial
applicator
may
be
reasonably
expected
to
be
exposed
to
for
a
more
extended
duration
(
30
days).
The
maximum
56
application
rates
are
not
included
in
the
postapplication
assessment
for
the
commercial
applicator,
as
it
is
unlikely
that
a
commercial
applicator
would
be
exposed
at
the
maximum
application
rate
for
30
days
a
year,
i.
e.
it
was
assumed
that
as
the
frequency
of
the
exposure
increased,
the
probability
of
being
exposed
to
a
maximum
application
rate
would
decrease.

7.1.2.1
Noncancer
Postapplication
Exposure
and
Risk
Estimates
A
noncancer
postapplication
risk
assessment
was
not
conducted,
since
no
systemic
toxicity
by
the
dermal
route
is
expected
for
the
short­
or
intermediate­
term
durations.
57
7.1.2.2
Postapplication
Exposure
and
Risk
Estimates
for
Cancer
In
general,
the
Agency
is
concerned
when
postapplication
occupational
cancer
risk
estimates
exceed
1
x10­
4.
This
diuron
postapplication
cancer
assessment
assumes
that
a
worker
would
contact
day
zero
residues
(
residues
on
the
day
of
application)
for
ten
or
thirty
days
a
year,
every
year
for
35
years.
Since
it
is
unlikely
that
a
postapplication
worker
would
contact
the
highest
possible
residue
value
for
that
length
of
time,
this
assessment
is
considered
very
conservative.

7.1.2.2.1
Private
Growers
(
10
Days
Exposure
Per
Year)

Postapplication
cancer
risks
for
private
growers
were
calculated
at
both
the
typical
application
rate
and
the
maximum
application
rate
for
each
crop
grouping.
All
cancer
risks
to
private
growers
were
less
than
1
x
10­
4
on
the
day
of
treatment
(
Table
17).

7.1.2.2.2
Commercial
Farm
Workers
(
30
Days
Exposure
Per
Year)

Postapplication
cancer
risks
for
commercial
farm
workers
were
calculated
at
the
typical
application
rate
for
each
crop
grouping.
All
potential
cancer
risks
to
commercial
farm
workers
were
less
than
1
x
10­
4
on
the
day
of
treatment
(
Table
18).

Historically,
setting
REIs
on
cancer
endpoints
has
been
difficult
because
of
the
need
for
lifetime
use
assumptions.
To
estimate
the
LADD
(
Life­
time
Average
Daily
Dose),
the
typical
application
rate,
the
number
of
days
worked
per
year,
and
the
number
of
years
one
would
be
exposed
during
a
working
lifetime
are
needed.
Each
one
of
these
variables
is
dependent
upon
many
factors.
For
example,
the
number
of
days
worked
per
year
must
correspond
to
the
days
worked
when
the
pesticide
of
concern
has
been
applied.
Additionally,
the
residue
dissipation
over
the
work
interval
should
be
estimated.
Without
an
estimate
for
residue
dissipation
one
needs
to
assume
(
conservatively)
that
the
worker
travels
from
one
treated
field
to
another
so
that
the
highest
residue
value
is
always
contacted.
In
the
case
of
diuron,
a
screening
estimate
was
developed
because
lifetime
use
data
are
not
available.

7.2
Mildewcide
in
Paints,
Solvents,
Adhesives,
and
Coatings
7.2.1
Occupational
Handler
Exposures/
Risks
Diuron
is
used
as
a
mildewcide
in
paints,
solvents,
adhesives,
stains,
polymer
latices,
plaster,
stuccos,
sealants,
caulking,
fillers,
and
coatings.
For
these
uses,
four
labels
exist:
EPA
Reg.
Nos.
67071­
15,
67071­
2,
67071­
17,
and
5383­
101.
These
products
are
formulated
as
a
flowable
concentrate,
a
tablet,
an
emulsifiable
concentrate,
and
a
paste
form,
respectively.
Traditionally,
OPP's
Antimicrobial
Division
assesses
antimicrobial
uses
of
pesticides.
However,
in
the
case
of
diuron,
the
antimicrobial
uses
were
assessed
by
HED.
These
pesticide
products
are
incorporated
into
paint
at
0.20
to
2.5
%
during
the
initial
phase
of
the
manufacturing
process.
HED
has
identified
and
assessed
the
58
primary
handlers
as
those
individuals
who
mix
and
load
diuron
formulation
at
the
manufacturing
facility
for
use
as
a
mildewcide
in
adhesives,
caulks,
sealants,
and
paints
(
see
discussion
of
primary
vs.
secondary
handlers
in
section
4.4.1
Home
Uses).
The
secondary
handlers
are
commercial
applicators
who
apply
adhesives,
caulks,
sealants,
and
paints.

No
handler
exposure
data
have
been
submitted
to
determine
the
extent
of
these
exposures.
The
Agency
assessed
the
risks
to
the
primary
handlers
using
the
dermal
and
inhalation
exposure
data
for
loading
liquids
and
tablet
formulations
from
the
proprietary
Chemical
Manufacturers
Association
(
CMA)
antimicrobial
exposure
study
(
MRID
42587501).
No
unit
exposure
data
exist
to
assess
the
mixing
and
loading
of
the
paste
formulation
into
paint.
It
is
assumed
that
this
exposure
would
be
similar
to
mixing
and
loading
liquids
into
paint
products.
Two
primary
handler
exposure
scenarios
have
been
identified
and
include:
1)
Mixing/
Loading
liquids
and
2)
Loading
tablets.

In
addition
to
the
primary
handlers,
secondary
handlers
are
assessed
using
an
airless
sprayer
and
a
paint
brush.
Unit
exposure
data
used
to
assess
the
exposure
resulting
from
applying
paint
containing
diuron
with
an
airless
sprayer
and
a
paintbrush
were
taken
from
a
previous
chlorothalonil
assessment
(
again,
see
discussion
in
section
4.4.1
Home
Uses).
The
clothing
and
PPE
scenarios
for
each
type
of
exposure
reflect
the
clothing
and
PPE
worn
in
the
study
from
which
the
unit
exposure
values
were
derived.
Although
there
is
potential
exposure
during
the
application
of
the
other
treated
materials
(
e.
g.,
caulks
and
sealants),
they
are
not
included
because
no
data
are
available
to
assess
the
uses.
There
is
also
potential
for
exposure
from
applying
paint
with
a
roller.
It
is
HED's
professional
judgement
that
the
airless
sprayer
and
paintbrush
scenarios
represent
the
high
end
exposures
for
diuron
antimicrobial
secondary
uses.
Two
secondary
handler
exposure
scenarios
have
been
identified
and
include:
3)
Applying
paints
with
an
airless
sprayer,
and
4)
Applying
paints
with
a
paint
brush.

These
four
exposure
scenarios
were
used
to
assess
the
handler
risks
to
diuron's
antimicrobial
uses.
The
noncancer
and
cancer
risk
equations
and
assumptions
stated
previously
in
this
assessment
were
also
used
to
calculate
exposure
from
diuron's
antimicrobial
uses.
The
industrial
and
commercial
painter
exposure
scenarios
are
believed
to
have
a
short
(
one
to
30
days)
and
intermediate­
term
(
one
month
to
180
days)
exposure
duration.
It
is
assumed
that
diuron
would
only
be
mixed
into
paint
every
other
week,
five
days
a
week.
This
type
of
intermittent
exposure
frequency
is
not
considered
a
chronic
exposure
scenario
(
greater
then
180
days)
because
diuron
is
not
believed
to
be
used
continuously
for
at
least
180
days
and
the
rat
metabolism
study
(
MRID
440196­
01)
indicates
that
urinary
and
fecal
excretion
of
diuron
is
nearly
complete
within
24
hours
in
the
low­
dose
groups
(
10
mg/
kg/
day)
and
within
48
hours
in
high­
dose
groups
(
400
mg/
kg/
day).
For
the
cancer
risk
assessment,
workers
handling
diuron
in
the
industrial
setting
(
mixing
diuron
into
paints)
are
assumed
to
be
exposed
to
diuron
in
paints
125
days
per
year
(
50
weeks
worked/
year
x
0.5
"
every
other
week"
x
5
days/
week)
and
commercial
painters
applying
diuron
treated
paint
are
assumed
to
be
exposed
50
days
per
year
(
only
in
paints
needing
mildewcide
and
not
all
paint
is
treated
with
diuron).
59
7.2.1.1
Noncancer
Risks
The
short­
term
inhalation
NOAEL
of
10
mg/
kg/
day
and
the
intermediate­
term
inhalation
NOAEL
of
1.0
mg/
kg/
day
were
used
for
all
noncancer
exposures
and
have
a
target
MOE
of
100.
The
calculations
of
short­
term
inhalation
risk
indicate
that
inhalation
MOEs
are
more
than
100
at
the
assessed
level
of
mitigation
for
the
all
the
exposure
scenarios
and
therefore,
not
of
concern.
The
calculations
of
intermediate­
term
inhalation
risk
indicate
that
inhalation
MOEs
are
more
than
100
at
the
assessed
level
of
mitigation
for
the
all
the
exposure
scenarios
except
the
following
(
Table
19):

!
Applying
paints
with
an
airless
sprayer
indoors.

7.2.1.1
Cancer
Risks
In
general,
the
Agency
is
concerned
when
occupational
cancer
risk
estimates
exceed
1
x
10­
4.
The
Agency
will
seek
ways
to
mitigate
the
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
1
x
10­
6
or
less.

The
following
scenarios
have
cancer
risks
between
1
x
10­
4
and
1
x
10­
6
at
the
assessed
level
of
mitigation
(
Table
20):

!
(
1)
Mixing/
loading
of
liquids
into
paint
products;

!
(
2)
Loading
of
tablets
into
paint
products;

!
(
3)
Applying
paints
with
an
airless
sprayer;
and
!
(
4)
Applying
paints
with
a
paint
brush.

All
scenarios
were
assessed
at
the
maximum
rate
of
application.
Average
application
rate
for
the
paint
use
is
unknown
and
is
requested
to
refine
this
risk.

7.2.2
Postapplication
Exposures
to
Paint
Containing
Diuron
Postapplication
exposures
may
occur
in
industrial
settings
around
open
vats
used
in
paint
processing.
Inhalation
and
dermal
exposures
may
also
occur
while
maintaining
industrial
equipment.
No
postapplication
exposure
data
have
been
submitted
to
determine
the
extent
of
postapplication
exposures
in
the
industrial
settings.
Nonetheless,
inhalation
exposures
are
expected
to
be
minimal
because
of
the
low
vapor
pressure
of
diuron
(
2
x
10­
7
mmHg
at
30
E
C)
and
aerosol
formation
is
not
expected.
Dermal
postapplication
exposures
are
expected
to
be
lower
than
when
handling/
loading
the
formulated
product.
Therefore,
postapplication
exposures
in
the
industrial
settings
are
expected
to
be
minimal
and
not
of
concern.
60
7.3
Algaecide
in
Commercial
Fish
Production
7.3.1
Handlers
Diuron
is
also
used
as
an
algaecide
in
the
commercial
production
of
ornamental
fish,
bait
fish,
and
catfish.
For
these
uses,
there
are
two
state
labels
(
FL99000200
and
AR99000800),
a
section
18,
and
several
other
Griffin
labels
pending
approval.
Based
on
the
use
patterns
of
diuron
as
an
algaecide,
four
occupational
exposure
scenarios
were
identified:
(
1a)
Mixing/
loading
dry
flowables
for
catfish
production;
(
1b)
Mixing/
loading
dry
flowables
for
ornamental
fish
production;
(
2a)
Mixing/
loading
wettable
powders
for
catfish
production;
and
(
2b)
Mixing/
loading
wettable
powders
for
ornamental
fish
production.
All
handler
exposures
are
expected
to
be
short­
term
in
duration.
An
occupational
assessment
on
the
use
of
diuron
in
commercial
catfish
production
has
already
been
conducted
by
the
Agency
(
ID
#
99MS0001.
Section
18
Exemption
for
the
Use
of
Diuron
80W
in
Catfish
Ponds
in
Mississippi.
Pam
Hurley,
Rick
Loranger,
and
Steven
Weiss.
May
13,
1999).
All
assumptions
used
to
calculate
exposure
are
based
on
this
assessment.
Since
no
other
data
exist
at
this
time,
the
assumptions
used
for
catfish
production
in
this
assessment
are
assumed
to
be
applicable
to
ornamental
fish
production
as
well.
The
noncancer
and
cancer
risk
equations
and
assumptions
stated
previously
in
this
assessment
were
also
used
to
calculate
exposure
from
commercial
fish
production.
HED
assumed
an
average
pond
size
of
15
acres,
4
feet
deep,
with
20
ponds
per
farm
(
no
more
than
25%
would
be
expected
to
be
treated
per
day).
The
assumptions
on
pond
size
and
numbers
of
ponds
per
farm
are
based
on
telephone
conversations
between
HED
staff
(
Pilot
Interdisciplinary
Risk
Assessment
Team)
and
contacts
at
Auburn
and
Mississippi
State
Universities
in
1996.

7.3.1.1
Noncancer
Exposures/
Risks
for
Pond
Uses
The
LOC
or
target
MOE
for
short­
term
inhalation
exposures
is
100.
The
inhalation
MOEs
from
all
four
of
the
commercial
fish
production
scenarios
were
greater
than
100
at
the
baseline
level,
without
mitigation,
and
are
not
considered
a
risk
of
concern
(
Table
21).

7.3.1.2
Cancer
Exposures/
Risks
In
general,
the
Agency
is
concerned
when
occupational
cancer
risk
estimates
exceed
1
x
10­
4.
The
Agency
will
seek
ways
to
mitigate
the
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
1
x
10­
6
or
less.
All
four
exposure
scenarios
have
cancer
risks
between
1
x
10­
4
and
1
x
10­
6
at
the
baseline
level
of
mitigation.
When
additional
PPE
was
added
as
a
mitigation
measure,
exposures
from
mixing/
loading
dry
flowables
for
catfish
ponds
and
mixing/
loading
wettable
powders
resulted
in
potential
cancer
risks
of
less
than
1
x
10­
6
and
not
of
concern.
When
additional
PPE
was
added
to
the
mixing/
loading
dry
flowables
for
ornamental
fish
ponds
scenario,
the
potential
cancer
risk
was
calculated
to
be
between
1
x
10­
4
and
1
x
10­
6.
All
four
exposure
scenarios
have
cancer
risks
of
less
than
1
x
10­
6
with
maximum
feasible
mitigation,
including
engineering
controls
(
Table
22).
61
7.3.2
Occupational
Postapplication
Exposures
to
Commercial
Fish
Ponds
Occupational
postapplication
exposure
to
diuron
in
treated
fish
production
ponds
is
not
likely
to
result
in
a
risk
of
concern
based
on
the
extremely
high
dilution
rate
(
maximum
application
rate
is
0.00000838
lb
ai/
gallon
of
pond
water),
low
frequency
of
postapplication
activities,
and
a
low
dermal
absorption
value
(
4%).

7.4
Incident
Data
The
Agency
searched
several
databases
for
reports
of
incidents
occurring
resulting
from
exposures
to
diuron.
The
databases
searched
were
the
Incident
Data
System
(
IDS),
American
Association
of
Poison
Control
Centers
(
AAPCC),
California
Pesticide
Illness
Surveillance
Program,
and
National
Pesticide
Telecommunication
Network
(
NPTN).
There
were
incidents
reported
involving
both
adults
and
children.
Most
were
treated
on
an
outpatient
basis
but
a
few
required
hospitalization
and
one
death
occurred.
A
direct
connection
between
exposure
to
diuron
as
the
cause
and
the
reported
death
has
not
been
made
as
of
this
writing.
Some
incident
reports
described
symptoms
such
as
eye
irritation,
rash,
dizziness,
respiratory
irritation
and
headaches
for
both
agricultural
and
nonagricultural
exposures.
Specific
details
may
be
found
in
Review
of
Diuron
Poisoning
Incident
Data.
Chemical:
#
035505.
Ruth
Allen.
October
11,
2001.

The
incident
data
show
that
the
number
of
poisoning
incidents
for
diuron
alone
is
relatively
small
in
any
one
surveillance
system.
Also,
the
incidents
are
scattered
in
time
and
location,
and
many
of
the
incidents
involve
diuron
use
in
mixtures.
Therefore,
few
conclusions
can
be
drawn.
However,
the
1995
Louisiana
elementary
school
incident
in
which
diuron
was
associated
with
the
illnesses
of
23
children
and
9
adults,
remains
unexplained.
There
are
no
known
recreational
or
school
building
registered
uses
of
diuron.
The
Agency
has
an
independent
initiative
to
reduce
the
use
of
pesticides
in
and
around
schools.
If
diuron
is
associated
with
other
illnesses
in
schools,
consideration
should
be
given
to
label
language
modifications
that
would
specifically
prohibit
use
in
and
around
schools.

8.0
DATA
NEEDS/
LABEL
REQUIREMENTS
Product
Chemistry
1.
The
product
chemistry
data
base
is
not
complete;
new
confidential
statements
of
formula
(
CSFs)
are
required
which
reflect
preliminary
analyses
of
current
products
together
with
discussions
of
formation
of
impurities.

2.
UV/
Visible
absorption
data/
spectra
are
required
(
830.7050).

Residue
Chemistry
62
Refer
to
Table
B
on
page
52
of
the
Residue
Chemistry
Chapter
for
the
Diuron
Reregistration
Eligibility
Decision
(
RED)
Document.
John
Punzi.
July
29,
2001
for
more
details
of
the
requirements,
listed
by
guideline.

3.
Label
revisions
are
required
for
many
crops
in
order
to
reflect
the
parameters
of
use
patterns
for
which
residue
data
are
available.
Many
of
the
revisions
concern
retreatment
intervals,
Preharvest
Intervals
(
PHI's)
and
rotational
crop
restrictions.

4.
Though
adequate
analytical
methods
exist
for
data
collection
and
tolerance
enforcement
in
plants,
independent
laboratory
validation
of
the
enforcement
method
is
required
for
livestock
methods
prior
to
Agency
validation.

5.
Multiresidue
methods
for
diuron
and
metabolites
of
toxic
concern
are
required
for
plants
and
livestock.

6.
Results
from
animal
feeding
studies
suggest
that
tolerances
are
necessary
for
poultry
or
egg
commodities
and
for
meats
and
milk.
Residue
data
are
not
available
for
several
potential
feed
items.
If
the
maximum
dietary
burden
does
not
increase
when
recalculated
from
all
potential
feed
items
after
acceptable
field
trial
data
are
submitted,
then
the
established
tolerances
for
residues
in
fat,
meat,
and
meat
byproducts
of
cattle,
goats,
hogs,
horses,
and
sheep
can
be
lowered.

7.
The
reregistration
requirements
for
magnitude
of
the
residue
in
plants
are
not
fulfilled
for:
alfalfa
forage;
globe
artichoke;
barley
hay;
cotton
gin
byproducts;
field
corn
aspirated
grain
fractions;
field
corn
forage
and
stover;
filbert;
grass
forage,
hay,
seed
screenings,
and
straw;
lemon;
pear;
oat
forage,
hay;
olive;
field
pea
vines
and
hay;
sorghum
aspirated
grain
fractions,
stover,
and
forage;
wheat
forage
and
hay.
Additional
crop
field
trial
data
are
required
for
these
commodities.

8.
The
reregistration
requirements
for
processing
data
are
not
fulfilled
for:
field
corn
and
olives.

9.
The
registrants
have
indicated
that
a
Section
3
tolerance
for
diuron
in/
on
catfish
is
desired.
Since
the
metabolism
committee
is
concerned
with
a
monochlorinated
diuron
metabolite
identified
in
water,
a
metabolism
study
of
diuron
in
fish
is
required.
The
registrants
are
directed
to
OPPTS
860.1400
for
study
guidelines
and
encouraged
to
submit
a
study
protocol
prior
to
initiating
the
study.

10.
Field
rotational
crop
trials
have
been
conducted
on
representative
crops
at
less
that
the
maximum
application
rates,
and
with
1
year
plant
back
intervals
(
PBI).
Some
labels
indicate
a
2
year
PBI.
The
Agency
recommends
that
the
registrants
provide
additional
data
to
support
the
higher
application
rate
and
believes
that
the
2­
yr
PBI
is
not
practical.
The
registrants
should
remove
the
2­
63
yr
PBI
from
the
registered
uses
and
provide
data
to
support
the
3.2
lb
ai/
A
application
rate
and
1­
yr
PBI.
Until
adequate
data
are
supplied,
labels
should
be
amended
to
restrict
rotational
crops
to
those
crops
which
currently
are
registered
as
primary
crops.

Toxicology
11.
A
28­
day
inhalation
study
is
required
to
address
the
concern
for
inhalation
exposure
potential
based
on
the
use
pattern.
The
registrant
can
follow
the
90­
day
inhalation
study
protocol
but
cease
exposure
at
28
days.

Occupational/
Residential
Exposures
12.
Data
are
needed
to
assess
the
following
occupational
handler
scenarios:
mixing/
loading/
applying
wettable
powders
or
dry
flowables
with
a
backpack
sprayer,
and
mixing/
loading/
applying
dry
flowables
with
a
low­
pressure
handwand.

13.
Average
application
rate
for
the
paint
use
is
unknown
and
is
requested
to
refine
the
cancer
risk
from
paint
use.

14.
No
transfer
coefficients
exist
for
activities
resulting
in
contact
with
treated
soil.
There
are
also
no
data
on
the
soil
residue
dissipation
of
diuron.
A
worker
exposure
study
and
a
diuron
soil
residue
dissipation
study
would
be
needed
to
assess
the
risk
from
postapplication
contact
with
treated
soil.

15.
Transfer
coefficients
do
not
exist
for
the
mechanical
harvesting
of
alfalfa
and
asparagus
and
these
activities
are
considered
of
special
concern
according
to
the
Agriculture
Transfer
Coefficient
Exposure
SAC
policy
3.1.

ATTACHMENTS
Carcinogenicity
Peer
Review
of
Diuron.
Linda
Taylor
and
Esther
Rinde.
May
8,
1997.

Diuron
(
PC
035505):
Assessment
of
Mode
of
Action
on
Bladder
Carcinogenicity.
Yung
Yang.
September
20,
2001.

DIURON:
Cancer
Classification
and
Mechanism
of
Action.
Yung
Yang.
October
10,
2001.

Diuron
­
Chronic
Dietary
Exposure
Assessment
(
PC
Code
035505);
DP
Barcode
D276683;
Case
0046.
John
Punzi.
September
10,
2001.

Diuron.
List
A
Reregistration
Case
0046.
PC
Code
035505.
Product
Chemistry
Chapter
for
the
64
Reregistration
Eligibility
Decision
[
RED]
Document.
DP
Barcode
D274489.
Ken
Dockter.
June
26,
2001.

Diuron
Metabolism
Committee
Briefing
Memo.
John
Punzi.
August
27,
2001.

DIURON
­
Report
of
the
FQPA
Safety
Factor
Committee.
Brenda
Tarplee.
August
7,
2001.

DIURON:
2nd
Report
of
the
Hazard
Identification
Assessment
Review
Committee.
Yung
Yang.
August
28,
2001.

Diuron.
Results
of
the
Health
Effects
Division
(
HED)
Metabolism
Assessment
Review
Committee
(
MARC)
Meeting
Held
on
03­
JULY­
2001.
John
Punzi.
August
10,
2001.

Diuron
­
Revised
Q1*,
(
3/
4'
s
Interspecies
Scaling
Factor),
1985
Wistar
Rat
2
Year
Dietary
Study.
PC
035505.
Bernice
Fisher.
September
23,
1998.

Diuron
­
Toxicology
Disciplinary
Chapter
for
the
Reregistration
Eligibility
Decision.
Yung
Yang.
0ctober
2,
2001.

Drinking
Water
Assessment
for
Diuron
and
its
Degradates.
Ibrahim
Abdel­
Saheb.
March
11,
2001.

MONURON:
Quantitative
Risk
Assessment
(
Q1
*)
Based
On
F344/
N
Rat
Dietary
Study
With
3/
4'
s
Interspecies
Scaling
Factor.
PC
Code
035501.
Lori
L.
Brunsman.
July
5,
2001.

Occupational
and
Residential
Exposure
Assessment
and
Recommendations
for
the
Reregistration
Eligibility
Decision
Document
for
Diuron.
Renee
Sandvig
and
Christina
Jarvis.
December
5,
2001.

Quantitative
Usage
Analysis
for
Diuron.
Alan
Halvorson.
March
20,
2001.

Residue
Chemistry
Chapter
for
the
Diuron
Reregistration
Eligibility
Decision
Document.
John
Punzi.
July
29,
2001.

Review
of
Diuron
Poisoning
Incident
Data.
Chemical:
#
035505.
Ruth
Allen.
October
11,
2001.

Updated
QUA.
Alan
Halvorson.
April
27,
2001.
65
Table
14:
Summary
of
Short­
Term
Exposure
Variables
and
MOEs
for
Agricultural
and
Non­
crop
Uses
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Short­
term
Inhalation
Eng.
Control
MOEd,
h
Mixer/
Loader
Mixing/
Loading
Liquids
for
Aerial
application
(
1a)
Sugarcane
6
lb
ai
per
acre
350
Acres
per
day
280
­
­
­

Alfalfa
3.2
lb
ai
per
acre
1200
Acres
per
day
150
­
­
­

Mixing/
Loading
Liquids
for
Chemigation
application
(
1b)
Sugarcane
6
lb
ai
per
acre
350
Acres
per
day
280
­
­
­

Mixing/
Loading
Liquids
for
Groundboom
application
(
1c)
Grapes
9.6
lb
ai
per
acre
80
Acres
per
day
760
­
­
­

Alfalfa
3.2
lb
ai
per
acre
200
Acres
per
day
910
­
­
­

Mixing/
Loading
Liquids
for
Rights­
of­
Way
Sprayer
application
(
1d)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
3,000
­
­
­

Utility/
industrial
areas
0.90
lb
ai
per
gallon
650
­
­
­

Mixing/
Loading
Liquids
for
High­
Pressure
Handwand
application
(
1e)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
3,000
­
­
­

Utility/
industrial
areas
0.90
lb
ai
per
gallon
650
­
­
­

Mixing/
Loading
Dry
Flowables
for
Aerial
application
(
2a)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
410
­
­
­

Alfalfa
3.2
lb
ai
per
acre
1200
Acres
per
day
240
­
­
­

Mixing/
Loading
Dry
Flowables
for
Chemigation
application
(
2b)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
410
­
­
­

Mixing/
Loading
Dry
Flowables
for
Groundboom
application
(
2c)
Grapes
9.6
lb
ai
per
acre
80
Acres
per
day
1,200
­
­
­
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Short­
term
Inhalation
Eng.
Control
MOEd,
h
66
Alfalfa
3.2
lb
ai
per
acre
1200
Acres
per
day
1,400
­
­
­

Mixing/
Loading
Dry
Flowables
for
Rights­
of­
Way
Sprayer
application
(
2d)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
4,700
­
­
­

Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
950
­
­
­

Mixing/
Loading
Dry
Flowables
for
High­
Pressure
handwand
application
(
2e)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
4,700
­
­
­

Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
950
­
­
­

Mixing/
Loading
Wettable
Powders
for
Aerial
application
(
3a)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
7.3
36
73
1,300
Alfalfa
3.2
lb
ai
per
acre
1200
Acres
per
day
4.2
21
42
760
Mixing/
Loading
Wettable
Powders
for
Chemigation
application
(
3b)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
7.3
36
73
1,300
Mixing/
Loading
Wettable
Powders
for
Groundboom
application
(
3c)
Grapes
9.6
lb
ai
per
acre
80
Acres
per
day
21
110
­
­

Alfalfa
3.2
lb
ai
per
acre
200
Acres
per
day
25
130
­
­

Mixing/
Loading
Wettable
Powders
for
Rights­
of­
Way
Sprayer
application
(
3d)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
85
420
­
­

Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
17
85
170
­

Mixing/
Loading
Wettable
Powders
for
High­
Pressure
handwand
application
(
3e)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
85
420
­
­
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Short­
term
Inhalation
Eng.
Control
MOEd,
h
67
Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
17
85
170
­

Loading
Granulars
for
Tractor­
Drawn
Spreaders
application
(
4)
Utility/
Industrial
Areas
87.1
lb
ai
per
acre
80
Acres
per
day
59
300
­
­

Applicator
Applying
Sprays
for
Aerial
application
(
5)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
see
eng.
controls
see
eng.
controls
see
eng.
controls
4,600
Alfalfa
3.2
lb
ai
per
acre
1200
Acres
per
day
see
eng.
controls
see
eng.
controls
see
eng.
controls
2,700
Applying
Sprays
for
Groundboom
application
(
6)
Grapes
9.6
lb
ai
per
acre
80
Acres
per
day
1200
­
­
­

Alfalfa
3.2
lb
ai
per
acre
200
Acres
per
day
1500
­
­
­

Applying
Sprays
for
Rightsof
Way
Sprayer
application
(
7)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
930
­
­
NF
Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
190
­
­
NF
Applying
Sprays
for
High­
Pressure
handwand
application
(
8)
Grapes
0.19
lb
ai
per
gallon
1000
Gallons
per
day
46
230
­
NF
Utility/
Industrial
Areas
0.96
lb
ai
per
gallon
9.2
46
92
NF
Applying
Granulars
for
Tractor­
Drawn
Spreaders
application
(
9)
Utility/
Industrial
Areas
87.1
lb
ai
per
acre
80
Acres
per
day
84
420
­
460
Applying
Granulars
with
a
spoon
(
10)
Industrial
Areas
87.1
lb
ai
per
acre
100
sq
ft
per
day
78,000
­
­
NF
Applying
Granulars
for
Hand
application
(
11)
Industrial
Areas
87.1
lb
ai
per
acre
100
sq
ft
per
day
740
­
­
NF
Flagger
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Short­
term
Inhalation
Eng.
Control
MOEd,
h
68
Flagging
for
Sprays
application
(
12)
Sugarcane
6.4
lb
ai
per
acre
350
Acres
per
day
890
­
­
­

Mixer/
Loader/
Applicator
Mixing/
Loading/
Applying
Liquids
for
Low
Pressure
Handwand
application
(
13)
Industrial
Areas
0.90
lb
ai
per
gallon
40
Gallons
per
day
650
­
­
NF
Mixing/
Loading/
Applying
Liquids
for
Backpack
sprayer
application
(
14)
Industrial
Areas
0.90
lb
ai
per
gallon
40
Gallons
per
day
650
­
­
NF
Mixing/
Loading/
Applying
Wettable
Powders
for
Low
Pressure
Handwand
application
(
15)
Industrial
Areas
0.96
lb
ai
per
gallon
40
Gallons
per
day
17
83
170
NF
Loading/
Applying
Granulars
with
a
pump
feed
granular
spreader
(
16)
Industrial
Areas
87.1
lb
ai
per
acre
5
Acres
per
day
380
­
­
NF
Loading/
Applying
Granulars
with
a
gravity
feed
granular
spreader
(
17)
Industrial
Areas
87.1
lb
ai
per
acre
5
Acres
per
day
36
180
­
NF
Loading/
Applying
Granulars
for
Belly
Grinder
application
(
18)
Industrial
Areas
87.1
lb
ai
per
acre
1
Acre
per
day
130
­
­
NF
Loading/
Applying
Granulars
for
Push­
type
spreader
(
ORETF)
application
(
19)
Industrial
Areas
87.1
lb
ai
per
acre
5
Acres
per
day
210
­
­
NF
Footnotes:
a
Crops
named
are
index
crops
which
are
chosen
to
represent
all
other
crops
at
or
near
that
application
rate
for
that
use.
See
the
application
rates
listing
in
the
use
summary
section
of
this
document
for
further
information
on
application
rates
used
in
this
assessment.
b
Application
Rates
are
based
on
the
maximum
application
rates
listed
on
the
diuron
labels.
c
Amount
handled
per
day
are
from
Science
Advisory
Council
on
Exposure's
Policy
#
9.1.9
d
Short­
term
MOE
=
Short­
term
NOAEL
(
mg/
kg/
day)/
Daily
Inhalation
Dose
(
mg/
kg/
day).
e
Baseline:
no
respirator.
f
Minimum
PPE:
dust
mist
respirator.
g
Maximum
PPE:
organic
vapor
respirator.
h
Engineering
controls:
closed
mixing/
loading,
enclosed
cab,
truck
or
cockpit.
See
the
appendix,
Tables
A,
B,
C
and
D
for
the
inputs
and
dermal
and
inhalation
dose
calculations.
69
­
Scenario's
calculated
MOE
exceeds
the
target
MOE
at
the
previous
level
of
mitigation.
(
MOE
>
100),
NF
=
Not
feasible
for
this
scenario
(
no
available
engineering
controls).
Bolded
MOE
values
show
a
risk
of
concern
at
the
highest
possible
level
of
mitigation
for
the
corresponding
scenario.
70
Table
15:
Summary
of
Intermediate­
Term
Exposure
Variables
and
MOEs
for
Agricultural
and
Non­
crop
Uses
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Inhalation
Eng.
Control
MOEd,
h
Mixer/
Loader
Mixing/
Loading
Liquids
for
Aerial
application
(
1a)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
76
380
­
­

1200
Acres
per
day
22
110
­
­

Mixing/
Loading
Liquids
for
Chemigation
application
(
1b)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
76
380
­
­

Mixing/
Loading
Liquids
for
Groundboom
application
(
1c)
cotton
2.2
lb
ai
per
acre
80
Acres
per
day
330
­
­
­

200
Acres
per
day
130
­
­
­

Mixing/
Loading
Liquids
for
Rights­
Of­
Way
Sprayer
(
1d)
utility/
industrial
areas
0.9
lb
ai
per
gallon
1000
gallons
per
day
65
320
­
­

Mixing/
Loading
Dry
Flowables
for
Aerial
application
(
2a)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
120
­
­
­

1200
Acres
per
day
34
180
­
­

Mixing/
Loading
Dry
Flowables
for
Chemigation
application
(
2b)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
120
­
­
­

Mixing/
Loading
Dry
Flowables
for
Groundboom
application
(
2c)
cotton
2.2
lb
ai
per
acre
80
Acres
per
day
520
­
­
­

1200
Acres
per
day
210
­
­
­

Mixing/
Loading
Dry
Flowables
for
Rights­
Of­
Way
Sprayer
(
2d)
utility/
industrial
areas
0.96
lb
ai
per
gallon
1000
gallons
per
day
95
490
­
­

Mixing/
Loading
Wettable
Powders
for
Aerial
application
(
3a)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
2.1
11
21
380
1200
Acres
per
day
0.62
3.1
6.2
110
Mixing/
Loading
Wettable
Powders
for
Chemigation
application
(
3b)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
2.1
11
21
380
Exposure
Scenario
(
Scenario
#)
Cropa
Application
ratesb
Area
Treatedc
Inhalation
Baseline
MOEd,
e
Inhalation
Min
PPE
MOEd,
f
Inhalation
Max
PPE
MOEd,
g
Inhalation
Eng.
Control
MOEd,
h
71
Mixing/
Loading
Wettable
Powders
for
Groundboom
application
(
3c)
cotton
2.2
lb
ai
per
acre
80
Acres
per
day
9.2
46
92
1,700
200
Acres
per
day
3.7
18
37
660
Mixing/
Loading
Wettable
Powders
for
Rights­
Of­
Way
Sprayer
(
3d)
utility/
industrial
areas
0.96
lb
ai
per
gallon
1000
gallons
per
day
1.7
8.5
17
300
Applicator
Applying
Sprays
for
Aerial
application
(
5)
cotton
2.2
lb
ai
per
acre
350
Acres
per
day
see
eng.
controls
see
eng.
controls
see
eng.
controls
1,300
1200
Acres
per
day
see
eng.
controls
see
eng.
controls
see
eng.
controls
390
Applying
Sprays
for
Groundboom
application
(
6)
cotton
2.2
lb
ai
per
acre
80
Acres
per
day
540
­
­
­

200
Acres
per
day
210
­
­
­

Applying
Sprays
for
Rights­
Of­
Way
(
7)
utility/
industrial
areas
0.96
lb
ai
per
gallon
1000
gallons
per
day
19
93
190
­

Flagger
Flagging
for
Sprays
application
(
12)
cotton
2.2
lb
ai
per
acre
350
Acres
per
Day
260
­
­
­

Footnotes:
a
Crops
named
are
index
crops
which
are
chosen
to
represent
all
other
crops
at
or
near
that
application
rate
for
that
use.
See
the
application
rates
listing
in
the
use
summary
section
of
this
document
for
further
information
on
application
rates
used
in
this
assessment.
b
Application
Rates
are
based
on
the
maximum
application
rates
listed
on
the
diuron
labels.
c
Amount
handled
per
day
are
from
Science
Advisory
Council
on
Exposure's
Policy
#
9.1.9
d
Short­
term
MOE
=
Short­
term
NOAEL
(
mg/
kg/
day)/
Daily
Inhalation
Dose
(
mg/
kg/
day).
e
Baseline:
no
respirator.
f
Minimum
PPE:
dust
mist
respirator.
g
Maximum
PPE:
organic
vapor
respirator.
h
Engineering
controls:
Closed
mixing/
loading,
enclosed
cab,
truck
or
cockpit.
See
the
appendix,
Tables
E,
F,
G,
and
H
for
the
inputs
and
dermal
and
inhalation
dose
calculations.
­
Scenario's
calculated
MOE
exceeds
the
target
MOE
at
the
previous
level
of
mitigation.
(
MOE
>
100),
NF
=
Not
feasible
for
this
scenario
(
no
available
engineering
controls).
Bolded
MOE
values
show
a
risk
of
concern
at
the
highest
possible
level
of
mitigation
for
the
corresponding
scenario.
72
Table
16:
Cancer(
Q*)
Risk
Summary
for
Agricultural
and
Non­
crop
Uses
Exposure
Scenario
(
Scenario
#)
Baselinea
Maximum
PPEb
Engineering
Controlc
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typica
l
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Mixer/
Loader
Mixing/
Loading
Liquids
for
Aerial
application
(
1a)
9.2
E­
4
6.1
E­
4
1.8
E­
3
6.3
E­
6
4.2
E­
6
1.3
E­
5
3.4
E­
6
2.2
E­
6
6.7
E­
6
1.7
E­
3
1.3
E­
3
3.9
E­
3
1.2
E­
5
9.0
E­
6
2.7
E­
5
6.1
E­
6
4.8
E­
6
1.4
E­
5
Mixing/
Loading
Liquids
for
Chemigation
application
(
1b)
9.2
E­
4
6.1
E­
4
1.8
E­
3
6.3
E­
6
4.2
E­
6
1.3
E­
5
3.4
E­
6
2.2
E­
6
6.7
E­
6
Mixing/
Loading
Liquids
for
Groundboom
application
(
1c)
3.4
E­
4
1.4
E­
4
4.2
E­
4
2.3
E­
6
9.6
E­
7
2.9
E­
6
1.2
E­
6
5.1
E­
7
1.5
E­
6
2.8
E­
4
2.2
E­
4
6.6
E­
4
1.9
E­
6
1.5
E­
6
4.5
E­
6
1.0
E­
6
8.0
E­
7
2.4
E­
6
Mixing/
Loading
Liquids
for
Rights­
of­
Way
Sprayer
application
(
1d)
8.4
E­
5
2.8
E­
5
8.4
E­
5
5.7
E­
7
1.9
E­
7
5.7
E­
7
3.1
E­
7
1.0
E­
7
3.1
E­
7
3.9
E­
4
3.9
E­
4
1.2
E­
3
2.7
E­
6
2.7
E­
6
8.1
E­
6
1.4
E­
6
1.4
E­
6
4.3
E­
6
Mixing/
Loading
Liquids
for
High­
Pressure
handwand
application
(
1e)
8.4
E­
5
2.8
E­
5
8.4
E­
5
5.7
E­
7
1.9
E­
7
5.7
E­
7
3.1
E­
7
1.0
E­
7
3.1
E­
7
3.9
E­
4
3.9
E­
4
1.2
E­
3
2.7
E­
6
2.7
E­
6
8.1
E­
6
1.4
E­
6
1.4
E­
6
4.3
E­
6
Mixing/
Loading
Dry
Flowables
for
Aerial
application
(
2a)
2.9
E­
5
1.8
E­
5
5.4
E­
5
1.6
E­
5
1.0
E­
5
3.1
E­
5
5.6
E­
7
3.5
E­
7
1.1
E­
6
4.9
E­
5
3.8
E­
5
1.2
E­
4
2.8
E­
5
2.2
E­
5
6.6
E­
5
9.6
E­
7
7.5
E­
7
2.3
E­
6
Mixing/
Loading
Dry
Flowables
for
Chemigation
application
(
2b)
2.9
E­
5
1.8
E­
5
5.4
E­
5
1.6
E­
5
1.0
E­
5
3.1
E­
5
5.6
E­
7
3.5
E­
7
1.1
E­
6
Mixing/
Loading
Dry
Flowables
for
Groundboom
application
(
2c)
9.8
E­
6
4.1
E­
6
1.2
E­
5
5.6
E­
6
2.3
E­
6
7.0
E­
6
1.3
E­
7
8.0
E­
8
2.4
E­
7
8.2
E­
6
6.4
E­
6
1.9
E­
5
4.7
E­
6
3.7
E­
6
1.1
E­
5
1.9
E­
7
1.3
E­
7
3.8
E­
7
Exposure
Scenario
(
Scenario
#)
Baselinea
Maximum
PPEb
Engineering
Controlc
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typica
l
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
73
Mixing/
Loading
Dry
Flowables
for
Rights­
of­
Way
Sprayer
application
(
2d)
2.5
E­
6
8.2
E­
7
2.5
E­
6
1.4
E­
6
4.7
E­
7
1.4
E­
6
4.8
E­
8
1.6
E­
8
4.8
E­
8
1.2
E­
5
1.2
E­
5
3.7
E­
5
7.0
E­
6
7.0
E­
6
2.1
E­
5
2.4
E­
7
2.4
E­
7
7.2
E­
7
Mixing/
Loading
Dry
Flowables
for
High­
Pressure
handwand
application
(
2e)
2.5
E­
6
8.2
E­
7
2.5
E­
6
1.4
E­
6
4.7
E­
7
1.4
E­
6
4.8
E­
8
1.6
E­
8
4.8
E­
8
1.2
E­
5
1.2
E­
5
3.7
E­
5
7.0
E­
6
7.0
E­
6
2.1
E­
5
2.4
E­
7
2.4
E­
7
7.2
E­
7
Mixing/
Loading
Wettable
Powders
for
Aerial
application
(
3a)
1.6
E­
3
10.0
E­
4
3.0
E­
3
8.0
E­
5
5.0
E­
5
1.5
E­
4
5.3
E­
6
3.3
E­
6
9.9
E­
6
2.7
E­
3
2.1
E­
3
6.4
E­
3
1.4
E­
4
1.1
E­
4
3.2
E­
4
9.1
E­
6
7.1
E­
6
2.1
E­
5
Mixing/
Loading
Wettable
Powders
for
Chemigation
application
(
3b)
1.6
E­
3
10.0
E­
4
3.0
E­
3
8.0
E­
5
5.0
E­
5
1.5
E­
4
5.3
E­
6
3.3
E­
6
9.9
E­
6
Mixing/
Loading
Wettable
Powders
for
Groundboom
application
(
3c)
5.5
E­
4
2.3
E­
4
6.9
E­
4
2.7
E­
5
1.1
E­
5
3.4
E­
5
1.8
E­
6
7.6
E­
7
2.3
E­
6
4.6
E­
4
3.6
E­
4
1.1
E­
3
2.3
E­
5
1.8
E­
5
5.3
E­
5
1.5
E­
6
1.2
E­
6
3.5
E­
6
Mixing/
Loading
Wettable
Powders
for
Rights­
of­
Way
Sprayer
application
(
3d)
1.4
E­
4
4.6
E­
5
1.4
E­
4
6.8
E­
6
2.3
E­
6
6.8
E­
6
4.5
E­
7
1.5
E­
7
4.5
E­
7
6.9
E­
4
6.9
E­
4
2.1
E­
3
3.4
E­
5
3.4
E­
5
1.0
E­
4
2.3
E­
6
2.3
E­
6
6.8
E­
6
Mixing/
Loading
Wettable
Powders
for
High­
Pressure
handwand
application
(
3e)
1.4
E­
4
4.6
E­
5
1.4
E­
4
6.8
E­
6
2.3
E­
6
6.8
E­
6
4.5
E­
7
1.5
E­
7
4.5
E­
7
6.9
E­
4
6.9
E­
4
2.1
E­
3
3.4
E­
5
3.4
E­
5
1.0
E­
4
2.3
E­
6
2.3
E­
6
6.8
E­
6
Loading
Granulars
for
Tractor­
Drawn
Spreaders
application
(
4)
5.3
E­
5
5.3
E­
5
1.6
E­
4
8.0
E­
6
8.0
E­
6
2.4
E­
5
1.1
E­
6
1.1
E­
6
3.2
E­
6
Applicator
Exposure
Scenario
(
Scenario
#)
Baselinea
Maximum
PPEb
Engineering
Controlc
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typica
l
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
74
Applying
Sprays
for
Aerial
application
(
5)
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
2.2
E­
6
1.4
E­
6
4.2
E­
6
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
See
eng
controls
3.9
E­
6
3.0
E­
6
9.0
E­
6
Applying
Sprays
for
Groundboom
application
(
6)
3.7
E­
6
1.6
E­
6
4.7
E­
6
1.5
E­
6
6.2
E­
7
1.8
E­
6
7.0
E­
7
2.9
E­
7
8.7
E­
7
3.1
E­
6
2.4
E­
6
7.3
E­
6
1.2
E­
6
9.6
E­
7
2.9
E­
6
5.8
E­
7
4.5
E­
7
1.4
E­
6
Applying
Sprays
for
Rights­
of­
Way
Sprayer
application
(
7)
4.0
E­
5
1.3
E­
5
4.0
E­
5
8.6
E­
6
2.9
E­
6
8.6
E­
6
NF
NF
NF
2.0
E­
4
2.0
E­
4
6.0
E­
4
4.3
E­
5
4.3
E­
5
1.3
E­
4
NF
NF
NF
Applying
Sprays
for
High­
Pressure
handwand
application
(
8)
1.1
E­
4
3.6
E­
5
1.1
E­
4
1.6
E­
5
5.3
E­
6
1.6
E­
5
NF
NF
NF
5.2
E­
4
5.4
E­
4
1.6
E­
3
8.0
E­
5
8.0
E­
5
2.4
E­
4
NF
NF
NF
Applying
Granulars
for
Tractor­
Drawn
Spreaders
application
(
9)
4.2
E­
5
4.2
E­
5
1.3
E­
4
7.5
E­
6
7.5
E­
6
2.3
E­
5
7.9
E­
6
7.9
E­
6
2.4
E­
5
Applying
Granulars
with
a
Spoon
(
10)
9.3
E­
8
9.3
E­
8
2.8
E­
7
6.6
E­
8
6.6
E­
8
2.0
E­
7
NF
NF
NF
Applying
Granulars
for
Hand
application
(
11)
2.5
E­
5
2.5
E­
5
7.4
E­
5
1.2
E­
5
1.2
E­
5
3.7
E­
5
NF
NF
NF
Flagger
Flagging
for
Spray
application
(
12)
6.6
E­
6
4.1
E­
6
1.2
E­
5
3.6
E­
6
2.3
E­
6
6.8
E­
6
1.3
E­
7
8.3
E­
8
2.5
E­
7
Mixer/
Loader/
App
Mixing/
Loading/
Applyin
g
Liquids
for
Low
Pressure
Handwand
application
(
13)
5.4
E­
4
5.4
E­
4
1.6
E­
3
2.4
E­
6
2.4
E­
6
7.2
E­
6
NF
NF
NF
Exposure
Scenario
(
Scenario
#)
Baselinea
Maximum
PPEb
Engineering
Controlc
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typica
l
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
Private
Farmer/
10
days/
Maximu
m
Rate
Cancer
Riskd
Private
Farmer/
10
days/
Typical
Rate
Cancer
Riske
Commercial
applicator/
30
days/
Typical
Rate
Cancer
Riskf
75
Mixing/
Loading/
Applyin
g
Liquids
for
Backpack
sprayer
application
(
14)
1.8
E­
5
1.8
E­
5
5.3
E­
5
9.0
E­
6
9.0
E­
6
2.7
E­
5
NF
NF
NF
Mixing/
Loading/
Applyin
g
Wettable
Powders
for
Low
Pressure
Handwand
application
(
15)
2.1
E­
4
2.1
E­
4
6.2
E­
4
5.1
E­
5
5.1
E­
5
1.5
E­
4
NF
NF
NF
Loading/
Applying
Granulars
with
a
Pump
Feed
Backpack
Spreader
(
16)
1.4
E­
5
1.4
E­
5
4.0
E­
5
7.8
E­
6
7.8
E­
6
2.4
E­
5
Loading/
Applying
Granulars
with
a
Gravity
Feed
Backpack
Spreader
(
17)
1.1
E­
4
1.1
E­
4
3.3
E­
4
5.4
E­
5
5.4
E­
5
1.6
E­
4
Loading/
Applying
Granulars
for
Belly
Grinder
application
(
18)
1.5
E­
4
1.5
E­
4
4.5
E­
4
7.6
E­
5
7.6
E­
5
3.1
E­
4
NF
NF
NF
Loading/
Applying
Granulars
for
Push­
type
spreader
(
ORETF)
application
(
19)
3.5
E­
5
3.5
E­
5
1.1
E­
4
5.5
E­
6
5.5
E­
6
1.7
E­
5
NF
NF
NF
Footnotes:
a
Baseline
represents
long
pants,
long
sleeved
shirt,
no
gloves
(
except
scenarios
10,
11,
14,
15,
16
and
17
which
represent
gloves),
open
mixing/
loading,
open
cab/
tractor,
and
no
respirator.
b
Maximum
PPE
represents
long
sleeves,
long
pants,
coveralls,
chemical
resistant
gloves,
open
mixing/
loading,
open
cab
tractor
and
an
organic
vapor
respirator,
except
for
scenarios
10,
16
and
17,
which
represent
single
layer
of
clothing,
gloves
and
a
dust­
mist
respirator
(
minimum
PPE)
which
is
the
clothing
scenarios
from
the
proprietary
studies
(
EPA
MRIDs
451672­
01
and
452507­
02).
c
Engineering
controls:
closed
mixing/
loading,
enclosed
cab,
truck
or
cockpit.
Baseline
level
clothing.
Chemical
resistant
gloves
for
the
mixing/
loading
of
liquids.
d
Cancer
risk
assessed
using
the
maximum
label
application
rates
and
10
days
of
exposure
per
year
assumed
for
a
private
farmer.
e
Cancer
risk
assessed
using
the
typical
application
rates
given
to
EPA
by
Griffin,
sources
quoted
are
Doanes,
NCFAP,
USDA,
and
Griffin
Information.
Maximum
application
rates
were
used
for
the
non­
crop/
industrial
areas,
because
no
information
of
the
typical
rates
of
these
uses
is
available.
10
days
of
exposure
per
year
assumed
for
a
private
farmer.
f
Cancer
risk
assessed
using
the
typical
application
rates
given
to
EPA
by
Griffin,
sources
quoted
are
Doanes,
NCFAP,
USDA,
and
Griffin
Information.
Maximum
application
rates
were
used
for
the
non­
crop/
industrial
areas,
because
no
information
of
the
typical
rates
of
these
uses
is
available.
30
days
of
exposure
per
year
assumed
for
a
commercial
applicator.
Cancer
risk
=
LADD
(
mg/
kg/
day)
*
Q1
(
1.91
E­
2
mg/
kg/
day1).
See
appendix
Tables
I
,
J
,
and
K
for
the
inputs
and
calculations
of
total
daily
dose,
LADD
and
cancer
risk.
NF
=
Not
feasible
for
this
scenario
(
no
available
engineering
controls).
76
Bolded
cancer
risks
values
have
risks
less
than
1.0
E­
4
at
the
highest
possible
level
of
mitigation.
77
Table
17:
Cancer
Postapplication
for
Private
Growers
(
Shorter­
Term
Duration/
10
Days
Exposure
Per
Year)

Transfer
Coefficient
Crop
Groupinga
Diuron
Specific
Crops
b
Highest
Crop
Group
Application
Rate
(
lbs
ai/
acre)
c
Transfer
Coefficient
d
(
cm2/
hr)
Activitye
DATf
DFRg
(
F
g/
cm2)
LADDh
Cancer
Riski
Field/
row
crops,
low/
medium
Oats,
Wheat,
Birdsfoot
Trefoil,
Clover,
Grass
Grown
For
Seed,
and
Alfalfa.
2.5
(
typical)
100
(
low)
Irrigation,
scouting,
thinning
0
5.61
3.5e­
5
6.7e­
7
1500
(
medium)
Irrigation,
scouting
0
5.61
5.3e­
4
1.0e­
5
3.25
(
maximum)
100
(
low)
Irrigation,
scouting,
thinning
0
7.29
4.6e­
5
8.7e­
7
1500
(
medium)
Irrigation,
scouting
0
7.29
6.8e­
4
1.3e­
5
Sugarcane
Sugarcane
2.4
(
typical)
1000
(
medium)
Scouting
immature
plants
0
5.39
3.4e­
4
6.4e­
6
6.4
(
maximum)
1000
(
medium)
Scouting
immature
plants
0
14.36
9.0e­
4
1.7e­
5
Vegetable,
Stem./
Stalk
Asparagus
and
Pineapple.
4
(
typical)
300
(
low)
Irrigation,
scouting,
thinning
0
8.98
1.7e­
4
3.2e­
6
500
(
medium)
Irrigation
and
scouting
mature
plants
0
8.98
2.8e­
4
5.4e­
6
1000
(
high)
hand
harvesting
and
pruning
0
8.98
5.6e­
4
1.1e­
5
6.4
(
maximum)
300
(
low)
Irrigation,
scouting,
thinning
0
14.36
2.7e­
4
5.2e­
6
500
(
medium)
Irrigation
and
scouting
mature
plants
0
14.36
4.5e­
4
8.6e­
6
1000
(
high)
hand
harvesting
and
pruning
0
14.36
9.0e­
4
1.7e­
5
Footnotes:
a
Crops
were
grouped
according
to
the
transfer
coefficient
crop
groups
listed
in
Science
Advisory
Council
on
Exposure
Policy
3.1.14
b
Crops
within
the
transfer
coefficient
group
that
are
registered
for
diuron.
c
Highest
application
rate
for
all
of
the
diuron
specific
crops
within
the
transfer
coefficient
crop
group.
d
Transfer
Coefficients
from
Science
Advisory
Council
on
Exposure
Policy
3.1.14
e
Activities
from
Science
Advisory
Council
on
Exposure
Policy
3.1.14
Every
activity
listed
may
not
occur
for
every
crop
in
the
group.
f
DAT
is
"
days
after
treatment"
(
0
days
=
12
hours
after
application).
g
DFR
(
F
g/
cm2)
=
application
rate
*
correction
factor
*
fraction
of
ai
retained
on
foliage
(
20%)
*
(
1­
dissipation
rate
(
10%))
time(
hours).
78
h
Lifetime
average
daily
dose
(
LADD)
(
mg/
kg/
day)
=
Average
Daily
Dose
(
mg/
kg/
day)
*
(
10
days
of
exposure
per
year
/
365
days/
year)
*
(
35
years
exposed
/
70
years
in
a
lifetime).
i
Cancer
risk
=
LADD
(
mg/
kg/
day)
*
Q1
(
1.91
E­
2
mg/
kg/
day1).
79
Table
18:
Cancer
Postapplication
for
Commercial
Farm
Workers
(
Longer­
Term
Duration/
30
Days
Exposure
Per
Year)

Transfer
Coefficient
Crop
Groupinga
Diuron
Specific
Crops
b
Highest
Crop
Group
Application
Rate
(
lbs
ai/
acre)
c
Transfer
Coefficient
d
(
cm2/
hr)
Activitye
DATf
DFRg
(
F
g/
cm2)
LADDh
Cancer
Riski
Field/
row
crops,
low/
medium
Oats,
Wheat,
Birdsfoot
Trefoil,
Clover,
Grass
Grown
For
Seed,
and
Alfalfa.
2.5
(
typical)
100
(
low)
Irrigation,
scouting,
thinning,
weeding
immature/
low
foliage
plants
0
5.61
1.1e­
4
2.0e­
6
1500
(
medium)
Irrigation,
scouting,
weeding
mature/
high
foliage
plants
0
5.61
1.6e­
3
3.0e­
5
Sugarcane
Sugarcane
2.4
(
typical)
1000
(
medium)
Scouting
immature
plants
0
5.39
1.0e­
3
1.9e­
5
Vegetable,
Stem./
Stalk
Asparagus
and
Pineapple.
4
(
typical)
300
(
low)
Irrigation,
scouting,
thinning,
weeding
immature
plants
0
8.98
5.1e­
4
9.7e­
6
500
(
medium)
Irrigation
and
scouting
mature
plants
0
8.98
8.4e­
4
1.6e­
5
1000
(
high)
hand
harvesting
and
pruning
0
8.98
1.7e­
3
3.2e­
5
Footnotes:
a
Crops
were
grouped
according
to
the
transfer
coefficient
crop
groups
listed
in
Science
Advisory
Council
on
Exposure
Policy
3.1.14.
b
Crops
within
the
transfer
coefficient
group
that
are
registered
for
diuron.
c
Highest
application
rate
for
all
of
the
diuron
specific
crops
within
the
transfer
coefficient
crop
group.
d
Transfer
Coefficients
from
Science
Advisory
Council
on
Exposure
Policy
3.1.14
e
Activities
from
Science
Advisory
Council
on
Exposure
Policy
3.1.14
Every
activity
listed
may
not
occur
for
every
crop
in
the
group.
f
DAT
is
"
days
after
treatment"
(
0
days
=
12
hours
after
application).
g
DFR
(
F
g/
cm2)
=
application
rate
*
correction
factor
*
fraction
of
ai
retained
on
foliage
(
20%)
*
(
1­
dissipation
rate
(
10%))
time(
hours).
h
Lifetime
average
daily
dose
(
LADD)
(
mg/
kg/
day)
=
Average
Daily
Dose
(
mg/
kg/
day)
*
(
30
days
of
exposure
per
year
/
365
days/
year)
*
(
35
years
exposed
/
70
years
in
a
lifetime).
i
Cancer
risk
=
LADD
(
mg/
kg/
day)
*
Q1
(
1.91
E­
2
mg/
kg/
day1).
80
Table
19:
Short­
and
Intermediate­
term
Antimicrobial
Uses
of
Diuron
and
MOEs
Exposure
Scenario
(
Scenario
#)
Clothing
Attire
Dermal
Unit
Exposure
(
mg/
lb
ai)
a
Inhalation
Unit
Exposure
(
F
g/
lb
ai)
b
Max
Appl.
Ratec
(
lb
ai/
gal)
Amount
Treatedd
Dermal
Dose
(
mg/
kg/
day)
e
Inhalation
Dose
(
mg/
kg/
day)
f
Short­
term
Inhalation
MOEg
Int.­
term
Inhalation
MOEg
Primary
Handlers
Mixing/
loading
of
Liquids
into
Paint
Products
(
1)
Open
pour,
long
pants,
long­
sleeved
shirt,
chemical
resistant
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
0.184
1.7
0.0532
100
gal
0.014
0.00013
77,000
7,700
1,000
gal
0.14
0.0013
7,700
770
Loading
of
Tablets
into
Paint
Products
(
2)
0.412
11.8
0.0532
100
gallons
0.031
0.00090
11,000
1,100
1,000
gal
0.31
0.0090
1,100
110
Secondary
Handlers
Applying
Paints
with
an
Airless
Sprayer
(
3)
Indoor
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
36.22
470
0.0532
50
gallons
1.4
0.018
560
56
Long
pants,
long
sleeved
shirt,
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
12
470
0.46
0.018
560
56
Outdoor
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
33.33
86.6
0.0532
50
gallons
1.3
0.0033
3,000
300
Long
pants,
long
sleeved
shirt,
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
8.87
86.6
0.34
0.0033
3,000
300
Applying
Paints
with
a
Paint
Brush
(
4)
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
290
101
0.0532
5
gallons
1.1
0.00038
26,000
2,600
Footnotes:
a,
b
Dermal
and
inhalation
unit
exposures
are
from
CMA
and
Chlorothalonil
studies.
11,12
c
Application
rates
are
based
on
diuron
paint
labels
d
Amount
treated
is
based
on
assumptions
from
EPA's
Antimicrobial
Division
and
HED
Expo
SAC
Policy
#
9.1.9
e
Dermal
dose
(
mg/
kg/
day)
=
[(
unit
exposure
(
mg/
lb
ai)
*
Appl.
rate
(
lb
ai/
gallon)
*
gallons
handled)/
Body
weight
(
70
kg).
f
Inhalation
dose
(
mg/
kg/
day)
=
[
unit
exposure
(
F
g/
lb
ai)
*
0.001
mg/
F
g
unit
conversion
*
max
appl
rate
(
lb
ai/
gal)
*
gallons
handled]
/
Body
weight
(
70
kg).
g
MOE
=
NOAEL
(
mg/
kg/
day)
/
Daily
Dose
[
Intermediate­
term
inhalation
NOAEL
=
1.0
mg/
kg/
day].
Target
MOE
is
100
for
occupational/
commercial.
81
Table
20:
Diuron
Cancer
Assessment
for
Antimicrobial
Uses
Exposure
Scenario
(
Scenario
#)
Clothing
Attire
Dermal
Unit
Exposure
(
mg/
lb
ai)
a
Inhalation
Unit
Exposure
(
F
g/
lb
ai)
b
Maximum
Application
Ratec
(
lb
ai/
gal)
Amount
Treatedd
Total
Absorbed
Dose
(
mg/
kg/
day)
e
LADD
(
mg/
kg/
day)
f
Riskg
Primary
Handlers
(
125
day/
year)

Mixing/
loading
of
Liquids
into
Paint
Products
(
1)
Open
pour,
long
pants,
long­
sleeved
shirt,
chemical
resistant
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
0.184
1.7
0.0532
100
gal
6.9
E­
4
1.2
E­
4
2.3
E­
6
1,000
gal
6.9
E­
3
1.2
E­
3
2.3
E­
5
Loading
of
Tablets
into
Paint
Products
(
2)
0.412
11.8
0.0532
100
gallons
2.1
E­
3
3.7
E­
4
7.0
E­
6
1,000
gallons
2.1
E­
2
3.7
E­
3
7.0
E­
5
Secondary
Handlers
(
50
day/
year)

Applying
Paints
with
an
Airless
Sprayer
(
3)
Indoor
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
36.22
470
0.0532
50
gallons
7.3
E­
2
5.0
E­
3
9.5
E­
5
Long
pants,
long
sleeved
shirt,
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
12
470
3.6
E­
2
2.5
E­
3
4.7
E­
5
Outdoor
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
33.33
86.6
0.0532
50
gallons
5.4
E­
2
3.7
E­
3
7.1
E­
5
Long
pants,
long
sleeved
shirt,
gloves,
and
a
5­
fold
PF
dust/
mist
type
respirator
8.87
86.6
1.7
E­
2
1.1
E­
3
2.2
E­
5
Applying
Paints
with
a
Paint
Brush
(
4)
Long
pants,
long
sleeved
shirt,
and
a
5­
fold
PF
dust/
mist
type
respirator
290
101
0.0532
5
gallons
4.4
E­
2
3.0
E­
3
5.8
E­
5
Footnotes:
a,
b
Dermal
and
inhalation
unit
exposures
are
from
CMA
and
Chlorothalonil
studies.
11,12
c
Application
rates
are
based
on
diuron
paint
labels
d
Amount
treated
is
based
on
assumptions
from
EPA's
Antimicrobial
Division
and
HED
Expo
SAC
Policy
#
9.1.9
e
Total
daily
absorbed
dose
(
mg/
kg/
day)
=
[(
dermal
dose
(
mg/
lb
ai)
*
dermal
absorption
(
4%)+
inhalation
dose
(
mg/
lb
ai)].
See
Table
6
for
the
corresponding
dermal
dose
and
inhalation
dose.
f
LADD
(
Lifetime
average
daily
dose)
mg/
kg/
day
=
Total
daily
absorbed
dose
(
mg/
kg/
day)
*
(
days
worked
per
year/
365
days
per
year)
*
(
35
years
worked/
70
year
lifetime).
Days
worked
per
year
are
estimates.
g
Risk
=
LADD
(
mg/
kg/
day)
*
Q1
*
=
1.91e­
2
(
mg/
kg/
day)­
1.
82
83
Table
21:
Short­
Term
Baseline
Table
for
Algaecide
Use
in
Commercial
Fish
Production
Exposure
Scenario
(
Scenario
#)
Dermal
Unit
Exposure
(
mg/
lb
ai)
a
Inhalation
Unit
Exposure
(
F
g/
lb
ai)
b
Use
Application
Rate
c
Dermal
Dose
(
mg/
kg/
day)
d
Inhalation
Dose
(
mg/
kg/
day)
e
Inhalation
MOE
f
Mixer/
Loader
Mixing/
Loading
Dry
Flowables
(
1a)
0.066
0.77
Catfish
Production
7.5
lb
ai
per
day
0.0071
0.000083
120,000
Mixing/
Loading
Dry
Flowables
(
1b)
0.066
0.77
Ornamental
Fish
Production
819
lb
ai
per
day
0.77
0.0090
1,100
Mixing/
Loading
Wettable
Powders
(
2a)
3.7
43
Catfish
Production
7.5
lb
ai
per
day
0.40
0.0046
2,200
Mixing/
Loading
Wettable
Powders
(
2b)
3.7
43
Ornamental
Fish
Production
15.0
lb
ai
per
day
0.79
0.0092
1,100
Footnotes:
a
Baseline
dermal
exposure
represents
long
sleeves
and
long
pants.
b
Baseline
inhalation
unit
exposure
represents
no
respirator.
c
Application
Rates
are
based
on
the
diuron
commercial
fish
production
labels
and
EPA
estimates.
d
Daily
Dermal
Dose
(
mg/
kg/
day)
=
(
Dermal
Unit
Exposure
(
mg/
lb
ai)
x
Application
Rates
(
lb
ai/
A
and
lb
ai/
sq.
ft.)
x
Area
Treated
per
day
(
acres
and
square
feet))/
body
weight
(
70
kg).
e
Daily
Inhalation
dose
(
mg/
kg/
day)
=
(
Inhalation
Unit
Exposure
(
F
g/
lb
ai)
x
(
1mg/
1000
F
g)
Conversion
Factor
x
Application
Rate
(
lb
ai/
gallon)
x
Amount
Treated
per
day
(
gallons/
day))/
body
weight
(
70
kg).
f
Short­
term
Inhalation
MOE
=
Inhalation
NOAEL
(
10
mg/
kg/
day)
/
Daily
Inhalation
Dose
(
mg/
kg/
day).
84
Table
22:
Cancer(
Q*)
Risk
Table
for
Algaecide
Use
in
Commercial
Fish
Production
Exposure
Scenario
(
Scenario
#)
Use
Applicatio
n
Rate
a
Exposure
s
Per
Yeara
Baselin
e
Total
Daily
Doseb
Baselin
e
Daily
LADDc
Baselin
e
Riskd
Max
PPE
Total
Daily
Doseb
Max
PPE
LADDc
Max
PPE
Riskd
Eng
Cont
Total
Daily
Doseb
Eng
Cont
LADDc
Eng
Cont
Riskd
Mixer/
Loader
Mixing/
Loading
Dry
Flowables
(
1a)
Catfish
Production
7.5
lb
ai
per
day
9
0.00037
4.50E­
6
8.60E­
8
0.00021
2.59E­
6
4.94E­
8
0.000007
2
8.85E­
8
1.70E­
9
Mixing/
Loading
Dry
Flowables
(
1b)
Ornamental
Fish
Production
819
lb
ai
per
day
3
0.040
1.64E­
4
3.13E­
6
0.023
9.41E­
5
1.80E­
6
0.00078
9.66E­
6
1.85E­
7
Mixing/
Loading
Wettable
Powders
(
2a)
Catfish
Production
7.5
lb
ai
per
day
9
0.020
2.52E­
4
4.82E­
6
0.0010
1.25E­
5
2.40E­
7
0.000068
8.35E­
7
1.59E­
8
Mixing/
Loading
Wettable
Powders
(
2b)
Ornamental
Fish
Production
15.0
lb
ai
per
day
9
0.041
5.05E­
4
9.64E­
6
0.0020
2.51E­
5
4.79E­
7
0.00014
1.67E­
6
3.19E­
8
Footnotes:
a
Based
on
diuron
commercial
fish
production
labels
and
EPA
estimates.
b
Total
Daily
Dose
(
mg/
kg/
day)
=
Daily
Dermal
Dose
(
mg/
kg/
day)
+
Daily
Inhalation
Dose
(
mg/
kg/
day).
See
Table
8
for
daily
dermal
and
inhalation
doses.
c
Lifetime
average
daily
dose
(
LADD)
(
mg/
kg/
day)
=
Average
Daily
Dose
(
mg/
kg/
day)
*
(
number
of
days
of
exposure
per
year
/
365
days/
year)
*
(
35
years
exposed
/
70
years
in
a
lifetime).
d
Cancer
risk
=
LADD
(
mg/
kg/
day)
*
Q1
(
1.91E­
2
mg/
kg/
day1).
