Document ID: EPA-HQ-OPP-2006-0165-0004
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-08-23T04:00Z

1
of
30
UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
WASHINGTON,
D.
C.
20460
OFFICE
OF
PREVENTION,
PESTICIDES
AND
TOXIC
SUBSTANCES
MEMORANDUM
Date:
June
20,
2006
SUBJECT:
Dimethenamid­
p
Human
Health
Risk
Assessment
for
Proposed
Uses
on
Onion,
Green;
Leek;
Onion,
Welsh;
and
Shallot,
Fresh
Leaves.
PC
Code:
129051,
Petition
No:
4E6844,
DP
Num:
316723.

Regulatory
Action:
Section
3
FROM:
Shaja
Brothers,
EPS
Risk
Integration
Minor
Use
and
Emergency
Response
Branch
Registration
Division
(
7505P)

THROUGH:
William
Cutchin,
Chemist
ARIA/
Technical
Review
Branch
Registration
Division,
(
7505P)

Christina
Swartz,
Chemist
Registration
Action
Branch
2
Health
Effects
Division
(
7509P)

TO:
D.
Rosenblatt/
B.
Madden
PM­
5
Risk
Integration
Minor
Use
and
Emergency
Response
Branch
Registration
Division
(
7505P)
2
of
30
TABLE
OF
CONTENTS
1.0
Executive
Summary
......................................................................................................
4
2.0
Ingredient
Profile
..........................................................................................................
6
2.1
Summary
of
Registered/
Proposed
Uses
....................................................................
6
2.2
Structure
and
Nomenclature.....................................................................................
6
2.3
Physical
and
Chemical
Properties
............................................................................
7
3.0
Hazard
Characterization/
Assessment
..........................................................................
7
3.1
Hazard
and
Dose­
Response
Characterization..........................................................
7
3.2
Adsorption,
Distribution,
Metabolism,
Excretion
(
ADME).....................................
8
3.3
Safety
Factor
for
Infants
and
Children
...................................................................
9
3.3.1
Adequacy
of
the
Exposure
Data
Base
.............................................................
10
3.4
Hazard
Identification
and
Toxicity
Endpoint
Selection.........................................
11
3.4.1
Acute
Reference
Dose
(
aRfD)
­
Females
age
13­
49.........................................
11
3.4.2
Acute
Reference
Dose
(
aRfD)
­
General
Population.......................................
11
3.4.3
Chronic
Reference
Dose
(
cRfD)
......................................................................
11
3.4.4
Incidental
Oral
Exposure
(
Short­
term
/
1­
30
days,
and
Intermediate­
term
/
1­
6
months)
.........................................................................................................................
12
3.4.5
Dermal
Absorption
..........................................................................................
12
3.4.6
Dermal
Exposure
(
Short­
term
/
1­
30
days).....................................................
12
3.4.7
Dermal
Exposure
(
Intermediate­
term
/
1­
6
months,
and
Long­
term
/
>
6
months)
12
3.4.8
Inhalation
Exposure,
(
Short­
Term
/
1­
30
days)
­
Females
13­
49
...................
13
3.4.9
Inhalation
Exposure:
(
Intermediate­
term
/
1­
6
months,
and
Long­
term
>
6
months)
13
3.4.10
Level
of
Concern
for
Margin
of
Exposure
......................................................
14
3.4.11
Classification
of
Carcinogenic
Potential
.........................................................
14
3.4.12
Summary
of
Toxicological
Doses
and
Endpoints
for
[
S]­
Dimethenamid­
p
for
Use
in
Human
Risk
Assessments
....................................................................................
14
3.6
Endocrine
disruption...............................................................................................
17
4.0
Public
Health
and
Pesticide
Epidemiology
Data........................................................
17
4.1
Incident
Reports
......................................................................................................
17
5.0
Dietary
Exposure/
Risk
Characterization
...................................................................
17
5.1
Pesticide
Metabolism
and
Environmental
Degradation.........................................
17
5.1.1
Metabolism
in
Primary
Crops.........................................................................
18
5.1.2
Metabolism
in
Animals
....................................................................................
18
5.1.3
Metabolism
in
Rotational
Crops
.....................................................................
19
5.1.4
Metabolism
in
Livestock..................................................................................
19
5.1.5
Analytical
Methodology...................................................................................
20
5.1.6
Environmental
Degradation............................................................................
20
5.1.7
Comparative
Metabolic
Profile
.......................................................................
20
5.1.8
Toxicity
Profile
of
Major
Metabolites
and
Degradates
..................................
21
5.1.9
Drinking
Water
Residue
Profile......................................................................
21
5.1.10
Food
Residue
Profile........................................................................................
22
5.2.11
International
Residue
Limits...........................................................................
24
3
of
30
5.3Dietary
Exposure
and
Risk............................................................................................
24
6.0
Residential
(
Non­
Occupational)
Exposure/
Risk
Characterization............................
25
6.1
Other
(
Spray
Drift,
etc.)
..........................................................................................
26
7.0
Aggregate
Risk
Assessments
and
Risk
Characterization...........................................
26
8.0
Cumulative
Risk
Characterization/
Assessment
.........................................................
27
9.0
Occupational
Exposure/
Risk
Pathway
.......................................................................
27
9.1
Short/
Intermediate­
term
Handler
Risk..................................................................
27
9.2
Short/
Intermediate­
term
Postapplication
Risk
......................................................
29
10.0
Data
Needs
and
Label
Requirements
.........................................................................
30
10.1
Occupational
and
Residential
Exposure.................................................................
30
References:
..............................................................................................................................
30
4
of
30
1.0
Executive
Summary
Dimethenamid
and
dimethenamid­
p
are
selective,
preemergence,
chloroacetamide
herbicides
with
existing
tolerances
for
residues
in
bean,
dry,
seed;
beet,
garden,
roots;
beet,
garden,
tops;
beet,
sugar,
dried
pulp;
beet,
sugar,
molasses;
beet,
sugar,
roots;
beet,
sugar,
tops;
corn,
field,
forage;
corn,
field,
grain;
corn,
field,
stover;
corn,
pop,
forage;
corn,
pop,
grain;
corn,
pop,
stover;
corn,
sweet,
forage;
corn,
sweet,
kernal
plus
cob
with
husk
removed;
corn,
sweet,
stover;
garlic;
horseradish;
onion,
dry
bulb;
peanut,
hay;
peanut,
nutmeat;
shallot,
bulb;
sorghum,
grain;
sorghum,
grain,
forage;
sorghum,
grain,
stover;
soybean,
seed;
and
tuberous
and
corm
vegetables.
Tolerances
are
established
for
residues
of
dimethenamid,
(
RS)­
2­
chloro­
N­[(
1­
methyl­
2­
methoxy)
ethyl]­
N­(
2,4­
dimethylthien­
3­
yl)
acetamide
under
40
CFR
§
180.464(
a).
As
the
tolerance
expression
includes
both
the
R
and
S
isomers,
these
tolerances
also
cover
the
registered
uses
of
dimethenamid­
p.
The
current
tolerances
for
all
plant
commodities
are
set
at
0.01
ppm.

IR­
4
has
received
a
request
for
the
minor
use
of
dimethenamid­
p
on
green
onion
for
control
of
annual
grasses,
broadleaf
weeds,
and
yellow
nutsedge.
Residue
data
have
been
generated
to
establish
tolerances
for
dimethenamid­
p
residues
in/
on
treated
green
onion
in
support
of
its
US
EPA
registration.
Pesticide
tolerance
petition
4E6844
is
currently
pending
for
the
uses
of
onion,
green;
leek;
onion,
welsh;
and
shallot,
fresh
leaves.

OUTLOOK
 
Herbicide
(
EPA
Reg.
No.
7969­
156)
is
an
emulsifiable
concentrate
(
EC)
formulation
containing
6.0
lb
ai/
gal
of
dimethenamid­
p.
The
Outlook
proposed
use
directions
for
bulb
vegetables
commodities
(
onion,
green;
leek;
onion,
welsh;
and
shallot,
fresh
leaves)
are
to
apply
at
post­
emergence,
at
a
maximum
rate
of
0.98
lb
ai/
A,
per
application
and
season,
using
ground
equipment.
This
product
contains
a
chloroacetamide
herbicide
and
is
active
against
annual
grasses,
broadleaf
weeds,
and
sedges.
It
is
currently
being
developed
by
BASF
Corporation
for
agricultural
use,
and
is
marketed
under
the
trade
names
Frontier,
Outlook,
Optill,
and
Guardsman.
Formulations
can
be
applied
as
banded
or
broadcast
pre­
plant,
preemergence
or
as
a
postemergence
application
using
ground
or
aerial
equipment.

The
toxicology
database
is
adequate
to
characterize
the
toxicity
of
dimethenamid­
p
and
to
assess
risk.
The
lethal
dose
(
LD)
50
study
with
[
S]­
dimethenamid­
p
shows
a
category
II
for
acute
oral
toxicity,
but
category
III
for
acute
dermal,
and
category
IV
for
inhalation.
It
is
a
mild
eye
and
skin
irritant,
and
causes
slight
skin
sensitization.
Pre­
and
postnatal
studies
showed
no
increased
offspring
susceptibility.
In
the
21­
day
dermal
rabbit
study,
serum
inorganic
phosphorus
decreases
were
noted
in
males
and
females
at
the
mid­
dose
and
male
body
weight
decrement
at
the
top
dose,
but
only
mild
skin
irritation
was
noted.
Chronic
studies
in
the
rat,
mouse
and
dog
with
[
RS]­
dimethenamid­
p
showed
body
weight
decrement
and
food
efficiency
decrement
at
the
lowest
effect
level
and
at
higher
dose
levels
liver
pathology,
stomach
hyperplasia,
and
some
indication
of
kidney
effects.
In
some
of
the
studies
liver
enzymes
and
cholesterol
levels
were
increased
at
doses
resulting
in
liver
pathology.
5
of
30
Peer
Reviews
classified
[
RS]­
dimethenamid­
p
as
a
group
"
C"
(
possible
human
carcinogen),
and
recommended
that
for
human
risk
assessment
the
reference
dose
(
RfD)
approach
should
be
used.
A
battery
of
mutagenicity
studies
with
[
S]­
dimethenamid­
p
were
universally
negative
for
genetic
mutations
including
unscheduled
DNA
synthesis.
Bridging
studies
to
the
[
RS]­
dimethenamid­
p
toxicity
data
are
complete.
Bridging
studies
with
[
S]­
dimethenamid­
p
consist
of
the
6
acute
studies,
a
subchronic
study
in
rats,
a
developmental
toxicity
study
in
rats
and
a
battery
of
mutagenicity
studies.

Metabolism
studies
with
[
RS]­
dimethenamid­
p
showed
extensive
metabolism
(>
30
metabolites).
In
the
rat,
dimethenamid­
p
parent
was
extensively
metabolized,
being
essentially
complete
within
3
days
and
over
90%
excreted
in
the
urine,
feces
and
bile
within
7
days.
The
developmental
toxicity
seen
in
the
rat
is
similar
for
the
two
technical
products.
However,
dose
related
maternal
toxicity
is
equal
to,
or
greater
than
25
mg/
kg/
day
with
the
[
S]
product
while
the
[
RS]
product
shows
similar
maternal
toxicity
at
equal
to,
or
greater
than
215
mg/
kg/
day.

Product
chemistry
data,
residue
chemistry
data
relevant
to
food
use,
and
environmental
fate
data
relevant
to
drinking
water
are
adequate
to
assess
human
exposure
to
dimethenamid­
p
and
its
metabolites.
Green
onion
crop
field
trial
residues
were
consistently
below
the
limit
of
detection
(
LOD;
0.003
ppm)
in
all
crops.
Finite
residues
are
not
expected
in
dimethenamid­
p
livestock
treated
feed
commodities
from
the
proposed
use
on
green
onion.

The
Hazard
Identification
Assessment
Review
Committee
(
HIARC)
has
concluded
that
sufficient
toxicological
information
is
available
on
dimethenamid­
p
for
selecting
the
doses
needed
to
assess
it's
occupational
risks
when
used
as
a
pesticide.
The
dose
picked
for
short­
term
dermal
and
short­
term
inhalation
exposures
is
the
lowest
observed
adverse
effect
level
(
LOAEL)
of
25
mg/
kg/
day,
from
a
developmental
oral
study
in
rats.
Lacking
a
clear
cut
no
observed
adverse
effect
level
(
NOAEL)
needed
for
risk
assessment,
a
8
mg/
kg/
day
dose
was
derived
from
the
LOAEL
using
an
uncertainty
factor
(
UF)
of
3.
For
intermediate­
term
dermal
and
intermediate­
term
inhalation
exposures,
a
NOAEL
of
6.8
mg/
kg/
day
was
selected
from
a
chronic
feeding
study
in
rats.
There
were
no
data
available
on
dermal
toxicity
and
dermal
absorption
on
dimethenamid­
p;
therefore,
a
dermal
absorption
rate
of
30%
was
extrapolated
from
the
developmental
oral
study.
An
absorption
rate
of
100%
was
assumed
for
inhalation.

There
are
no
residential,
or
other
non­
agricultural
uses
of
dimethenamid­
p.
Aggregate
risk
is
based
on
tolerance­
level
residues
and
an
assumption
of
100%
crop
treatment
for
the
food
uses,
and
on
Tier
II
estimates
for
the
drinking
water
contamination
that
may
be
associated
with
crop
uses.
The
upper­
bound
acute
population
adjusted
dose
(
aPAD)
risk
estimate
for
child­
bearing
females
is
less
than
1%
of
the
aPAD.
The
upper­
bound
chronic
population
adjusted
dose
(
cPAD)
risk
estimates
for
the
general
US
and
specific
population
sub­
groups
are
1%
or
less
of
the
cPAD.
A
determination
of
safety
can
be
made
for
aggregate
dietary
(
food
and
water)
exposure.

Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
EPA
has
not
made
a
common
mechanism
of
toxicity
finding
as
to
dimethenamid­
p
and
any
other
substances.
Also,
dimethenamid­
p
does
not
appear
to
produce
6
of
30
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
this
tolerance
action,
therefore,
EPA
has
not
assumed
that
dimethenamid­
p
has
a
common
mechanism
of
toxicity
with
other
substances.

ARIA
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
the
U.
S.
Population,
including
infants
and
children,
from
acute,
short­
and
intermediate­
term,
and
chronic
aggregate
exposure
to
dimethenamid­
p
residues.
ARIA
recommends
for
tolerances
for
the
residues
of
dimethenamid­
p
on
onion,
green;
leek;
onion,
Welsh;
and
shallot,
fresh
leaves
at
0.1
ppm.

2.0
Ingredient
Profile
OUTLOOK
 
Herbicide
(
EPA
Reg.
No.
7969­
156)
is
an
emulsifiable
concentrate
(
EC)
formulation
containing
6.0
lb
ai/
gal
of
dimethenamid­
p.
This
product
contains
a
chloroacetamide
herbicide
and
is
active
against
annual
grasses,
broadleaf
weeds,
and
sedges.
The
Outlook
proposed
use
directions
for
bulb
vegetables
commodities
(
onion,
green;
leek;
onion,
welsh;
and
shallot,
fresh
leaves)
are
to
apply
at
post­
emergence,
at
a
maximum
rate
of
0.98
lb
ai/
A,
per
application
and
season,
using
ground
equipment.

2.1
Summary
of
Registered/
Proposed
Uses
TABLE
2.1
Summary
of
Directions
for
Use
of
Dimethenamid­
p
Applic.
Timing,
Type,
and
Equip.
Formulation
[
EPA
Reg.
No.]
Applic.
Rate
(
lb
ai/
A)
Max.
No.
Applic.
per
Season
Max.
Seasonal
Applic.
Rate
(
lb
ai/
A)
PHI
(
days)
Use
Directions
and
Limitations
Green
Onion
Broadcast,
Foliar
Outlook
7969­
156
0.98
1
0.98
28­
32
12
hour
REI
2.2
Structure
and
Nomenclature
TABLE
2.2
Test
Compound
Nomenclature
Compound
Chemical
Structure
S
C
H
3
N
Cl
H
C
H
3
O
CH
3
CH
3
O
Common
name
Dimethenamid­
P
(
or
S­
dimethenamid)

Company
experimental
name
BAS
656
H;
SAN
1289
7
of
30
IUPAC
name
S­
2­
chloro­
N­(
2,4­
dimethyl­
3­
thienyl)­
N­(
2­
methoxy­
1­
methylethyl)­
acetamide
CAS
name
S­
2­
chloro­
N­[(
1­
methyl­
2­
methoxy)
ethyl]­
N­(
2,4­
dimethyl­
thien­
3­
yl)
acetamide
CAS
#
163515­
14­
8
End­
use
product/(
EP)
OUTLOOK
 
Herbicide
2.3
Physical
and
Chemical
Properties
TABLE
2.3
Physicochemical
Properties
of
the
Technical
Grade
Test
Compound
Parameter
Value
Referencea
Melting
point/
range
<­
50
°
C
1999/
10167
pH
3.3
(
in
1%
aqueous
emulsion)
1997/
5178
Density
1.195
g/
cm3
1999/
10167
Water
solubility
(
25
°
C)
1449
±
17
mg/
L
(
pH
6.16)
b
1996/
5411
Solvent
solubility
(
mg/
L
at
25
°
C)
20.8g/
100mL
in
hexane;
soluble
in
all
proportions
in
tetrahydrofuran,
isopropyl
alcohol,
acetone,
ACN,
DMSO,
DCM,
toluene,
and
n­
octanol
1997/
5196
Vapour
pressure
at
25
°
C
1.88
(
±
0.29)
x
10­
5
mm
Hg
1996/
5418
Dissociation
constant
(
pKa)
No
dissociation
(
pH
1
to
11;
25
°
C)
88/
11352
Octanol/
water
partition
coefficient
Log(
KOW)
77.6
and
1.89
(
Pow
and
log
Pow)
1998/
5071
UV/
visible
absorption
spectrumc
 
=
7560;
33nm
1998/
5123
a
BASF
Registration
Document
Number.
b
There
is
no
dissociation
in
water;
therefore,
pH
dependence
on
solubility
is
not
applicable.
c
The
molar
absorption
coefficient
(
g)
and
bandwidth
for
dimethenamid­
p
for
the
236
nm
absorbance
maximum.

3.0
Hazard
Characterization/
Assessment
3.1
Hazard
and
Dose­
Response
Characterization
The
acute
oral
toxicity
LD50
study
with
[
S]­
dimethenamid­
p
shows
a
category
II.
It
is
category
III
for
acute
dermal
and
inhalation,
a
mild
eye
and
skin
irritant,
and
causes
slight
skin
sensitization.
The
acute
oral
toxicity
LD50
with
[
RS]­
dimethenamid
is
category
III
and
the
remaining
categories
are
the
same
as
[
S]­
dimethenamid­
p.

Pre­
and
postnatal
studies
showed
no
increased
offspring
susceptibility.
The
developmental
toxicity
studies
show
increased
post­
implantation
loss
and
minor
skeletal
variations
in
the
rat
and
late
resorptions
and
minor
skeletal
variations
in
the
rabbit
at
the
highest
dose
tested
(
HDT),
but
no
increased
quantitative
sensitivity
in
the
conceptus.
In
the
rabbit,
the
developmental
effects
8
of
30
occurred
at
the
same
dose
as
maternal
toxicity
whereas
in
the
rat,
the
developmental
toxicity
occurred
at
much
higher
doses
than
in
the
maternal
animals.
The
reproduction
study
showed
pup
weight
decrements
and
parental
weight
decrements
at
the
same
dose
levels.
The
only
other
effects
noted
were
liver
weight
increases
in
both
parental
sexes.

In
the
21­
day
dermal
rabbit
study,
serum
inorganic
phosphorus
decreases
were
noted
in
males
and
females
at
the
mid­
dose
and
male
body
weight
decrement
at
the
top
dose,
but
only
mild
skin
irritation
was
noted.
Chronic
studies
in
the
rat,
mouse
and
dog
with
[
RS]­
dimethenamid
showed
body
weight
decrement
and
food
efficiency
decrement
at
the
lowest
effect
level
and
at
higher
dose
levels
liver
pathology,
stomach
hyperplasia,
and
some
indication
of
(
unconfirmed)
kidney
effects.
In
some
of
the
studies
liver
enzymes
and
cholesterol
levels
were
increased
at
doses
resulting
in
liver
pathology.
Longer
studies
show
toxicity
at
lower
doses.
The
rat
was
the
most
sensitive
species
to
the
toxic
effects
of
[
RS]­
dimethenamid.

Peer
Reviews
classified
[
RS]­
dimethenamid
as
a
group
"
C"(
possible
human
carcinogen),
and
recommended
that
for
human
risk
assessment
the
reference
dose
(
PAD)
approach
should
be
used.
An
increasing
trend
for
liver
adenomas
was
seen
in
males
in
the
rat
chronic
study.
No
dose­
related
tumors
were
seen
in
the
mouse
carcinogenicity
study.

A
battery
of
mutagenicity
studies
with
[
S]­
dimethenamid­
p
were
universally
negative
for
genetic
mutations
including
unscheduled
DNA
synthesis.
However,
mutagenicity
studies
with
[
RS]­
dimethenamid
showed
positive
results
for
unscheduled
DNA
synthesis
and
there
were
equivocal
results
in
two
dominant
lethal
studies.
It
is
noted
that
late
resorptions
contributed
mostly
to
the
positive
dominant
lethal
effects;
claimed
not
to
be
characteristic
of
a
dominant
lethal
effect.
In
some
of
the
studies
with
[
RS]­
dimethenamid,
the
studies
were
considered
positive,
but
should
have
been
repeated
because
of
equivocal
results,
such
as
precipitation
and
positive
responses
not
related
to
dose.

The
toxicity
data
base
for
the
[
RS]
mixture
is
complete
and
the
bridging
studies
to
the
[
RS]­
dimethenamid
toxicity
data
are
complete;
these
bridging
studies
consist
of
the
6
acute
studies,
a
subchronic
study
in
rats,
a
developmental
toxicity
study
in
rats
and
a
battery
of
mutagenicity
studies.
There
are
minor
inconsistencies
between
the
two
sets
of
data.
In
the
developmental
toxicity
studies
in
the
rat
with
[
S]­
dimethenamid­
p,
maternal
weight
decrement
was
shown
at
1/
8
the
LOAEL
for
mothers
dosed
with
[
RS]­
dimethenamid.
Since
the
toxicity
in
90­
day
feeding
studies
in
rats
with
[
S]­
dimethenamid­
p
and
[
RS]­
dimethenamid
were
very
similar,
the
finding
of
increased
toxicity
in
pregnant
dams
may
suggest
that
[
S]­
dimethenamid­
p
is
more
toxic
to
pregnant
rats.
This
difference
in
doses
resulting
in
body
weight
decrement
may
be
due
to
strain
drift
in
the
Sprague
Dawley
rats
used,
since
the
studies
were
conducted
9
years
apart.

3.2
Adsorption,
Distribution,
Metabolism,
Excretion
(
ADME)

Metabolism
studies
with
[
RS]­
dimethenamid­
p
showed
extensive
metabolism
(>
30
metabolites).
Thirty­
one
metabolites
were
identified
and
quantified.
The
initial
metabolite
formed
was
the
glutathione
conjugate
of
the
parent
at
the
active
chlorine
"
to
the
carbonyl
group,
with
subsequent
metabolism
at
the
glutathione
residue.
The
parent
was
extensively
metabolized,
9
of
30
being
essentially
complete
within
3
days
and
over
90%
being
excreted
in
the
urine,
feces
and
bile
within
7
days.
Excretion
products
with
highest
total
concentration
as
a
percent
(%)
of
administered
multiple
doses
of
10
mg/
kg
to
males
and
females,
respectively,
were
parent­
1.4%
and
1.2%,
M1­
3.3
&
7.2%,
M2­
3.6%
&
9.8%,
M3­
0.6%
&
0.4%,
M14­
2.8%
&
3.3%,
M16­
5.1%
&
3.3%,
M17­
0.6%
&
3.3%,
M19­
1.1%
&
1.4%.
Total
excretion
products
in
the
urine,
feces
or
bile
were
less
than
5%
of
the
administered
single
(
oral/
intravenous)
dose
of
10
mg/
kg
to
males
or
females,
except
for
M2
via
the
oral
dose
(
total
female,­
6.4%)
and
M1
via
the
intravenous
dose
(
total
female,­
6.1%).
Most
were
less
than
1%
of
the
administered
dose.
No
significant
differences
in
metabolism/
excretion
were
seen
between
males
and
females
including
biliary
excretion.
Up
to
45
putative
metabolites
were
reported
in
the
urine
and
up
to
50
were
reported
in
the
feces.
Of
the
unidentified
metabolites
none
exceeded
3%
and
most
were
less
than
1%
of
the
administered
dose.
Saturation
of
the
metabolic
system
was
seen
at
the
1,000
mg/
kg
dose.

3.3
Safety
Factor
for
Infants
and
Children
The
toxicity
database
is
adequate
for
an
FQPA
based
hazard
assessment
of
[
RS]­
dimethenamid
and
[
S]­
dimethenamid­
p.
The
bridging
studies
from
the
studies
with
[
RS]
dimethenamid
mixture
to
the
purified
[
S]­
dimethenamid­
p
enantiomer
have
been
conducted
as
required
and
are
considered
acceptable.
The
required
studies
with
the
[
S]
enantiomer
were;
(
1)
subchronic
feeding
study
in
rats,
(
2)
developmental
toxicity
in
rats,
(
3)
six
acute
studies,
and
(
4)
a
battery
of
mutagenicity
studies.

There
was
no
increased
quantitative
developmental
susceptibility
in
the
rat
studies
with
[
RS]
or
the
[
S]
technical
products
or
the
rabbit
study
with
the
[
RS]
technical
product.
There
was
no
indication
of
increased
susceptibility
in
the
rat
reproduction
study.
However,
it
is
noted
that
the
developmental
toxicity
study
in
rats
with
[
S]­
dimethenamid­
p
showed
no
maternal
NOAEL/
LOAEL
(
none/
25
mg/
kg/
day),
whereas
a
similar
study
in
rats
with
[
RS]­
dimenthenamid
showed
a
maternal
NOAEL/
LOAEL
of
50/
215
mg/
kg/
day.
This
would
suggest
that
either
the
[
S]
enantiomer
is
more
toxic
to
the
pregnant
female
rat
than
the
[
RS]
mixture,
or
that
there
was
strain
drift
in
the
two
studies
conducted
9
years
apart.
Both
studies
were
conducted
in
the
same
rat
strain
with
0.5%
CMC,
10
ml/
kg,
and
in
the
same
laboratory
with
very
similar
protocols.

The
only
evidence
of
neurotoxicity
was
decreased
motor
activity
and
ptosis
in
mothers
at
the
HDT
in
the
developmental
toxicity
study
in
rats
with
dimethenamid­
p
[
S].
There
is
no
evidence
of
similar
effects
in
the
study
in
rats
with
[
RS]­
dimethenamid.
With
regard
to
observations
suggesting
possible
neurotoxicity
in
the
rat
developmental
study,
these
observations
were
made
375
times
on
the
25
rats
in
the
highest
dose
group
during
the
study
with
[
S]­
dimethenamid­
p.
In
these
observations,
decreased
motor
activity
was
noted
8
times
in
6
rats
and
ptosis
(
droopy
eye
lids)
was
noted
4
times
in
4
rats.
These
clinical
observations
were
not
seen
in
control
animals
or
in
the
developmental
study
in
rats
dosed
with
[
RS]­
dimethenamid.

No
neurotoxicity
or
CNS
developmental
toxicity
was
seen
in
the
developmental
toxicity
studies.
Dams
in
the
developmental
toxicity
study
with
[
S]­
dimethenaimd­
p
showing
decreased
motor
activity
and
ptosis
at
the
HDT
were
neither
seen
in
most
animals
nor
persistent.
Both
findings
10
of
30
were
at
low
frequency
and
considered
to
be
related
to
general
toxicity
caused
by
the
excess
toxicity
at
the
comparatively
toxic
dose
levels
administered.
A
DNT
is
not
required.

No
offspring
pre­
or
postnatal
susceptibility
to
either
[
RS]­
dimethenamid
or
[
S]­
dimethenamid­
p
was
seen
in
a
rabbit
or
two
rat
developmental
studies
and
reproduction
study.
There
is
low
concern
for
pre­
or
postnatal
toxicity
since
the
developmental
effects
from
the
[
S]
and
[
RS]
mixture
are
similar
and
occur
at
similar
doses.
There
is
some
concern
about
lower
LOAEL
for
maternal
toxicity
seen
in
the
developmental
toxicity
study
in
rats
with
[
S]­
dimethenamid­
p
than
with
[
RS]­
dimethenamid.
This
concern
involves
a
lower
LOAEL
in
pregnant
rats
dosed
with
the
[
S]
enantiomer
than
with
[
RS]
mixture
and
whether
this
toxicity
represents
a
difference
between
the
[
S]
and
the
[
RS]
products
or
whether
it
is
due
to
strain
drift
over
the
two
studies
conducted
9
years
apart.
This
lower
maternal
toxicity
endpoint
with
an
extra
3X
uncertainty
factor
(
for
no
NOAEL)
in
the
developmental
toxicity
study
with
the
[
S]­
dimethenamid­
p
is
used
for
short­
term
dermal
and
inhalation
occupational
exposure.
Since
the
maternal
LOAEL
of
25
mg/
kg/
day
was
close
to
a
NOAEL,
an
extra
3X
uncertainty
factor
was
considered
adequate
protection
from
the
slight
maternal
weight
decrement
seen
at
25
mg/
kg/
day.
The
total
uncertainty
factor
associated
with
the
25
mg/
kg/
day
endpoint
is
300X.

3.3.1
Adequacy
of
the
Exposure
Data
Base
Based
on
the
hazard
data,
HED
recommended
the
special
FQPA
SF
be
reduced
to
1X
because
there
are
low
concerns,
and
no
residual
uncertainties
with
regard
to
pre­
and/
or
postnatal
toxicity.
Additionally,
based
on
the
quality
of
the
exposure
data,
the
dimethenamid
risk
assessment
team
recommended
that
the
special
FQPA
SF
be
reduced
to
1X.
The
recommendation
is
based
on
the
following:

 
The
dietary
food
exposure
assessment
utilizes
proposed
tolerance
level
residues
and
100%
CT
information
for
all
commodities.
By
using
these
screening­
level
assessments,
acute
and
chronic
exposure
will
not
be
underestimated.

 
The
dietary
drinking
water
assessment
(
Tier
2
estimates)
utilizes
values
generated
by
model
and
associated
modeling
parameters
which
are
designed
to
provide
health
protective,
high­
end
estimates
of
water
concentrations.

3.3.2
Toxicology
Conclusion
There
is
a
complete
toxicity
database
for
dimethenamid­
p
and
exposure
data
are
complete
or
are
estimated
based
on
data
that
reasonably
accounts
for
potential
exposures.
There
is
no
evidence
of
susceptibility
following
in
utero
and/
or
postnatal
exposure
in
the
developmental
toxicity
studies
in
rats
or
rabbits,
and
in
the
2­
generation
rat
reproduction
study.
There
are
no
residual
uncertainties
concerning
pre­
and
postnatal
toxicity
and
no
neurotoxicity
concerns.
The
acute
and
chronic
dietary
food
exposure
assessments
utilize
tolerance­
level
residues
and
an
assumption
of
100%
crop
treatment
for
food
uses,
and
Tier
II
estimates
for
drinking
water.
There
is
no
potential
for
drinking
water
exposure.
There
is
no
potential
for
residential
exposure.
Based
on
these
data
and
conclusions,
the
FQPA
Safety
Factor
can
be
reduced
to
1X.
11
of
30
Literature
Sources:
No
literature
reports
on
the
toxicity
of
[
S]­
dimethenamid­
P
were
found.
Structural
analogues
are
acetochlor
[
Group
B2
carcinogen],
metolachlor
[
Group
C
carcinogen],
propachlor
[
evidence
of
thyroid
tumors
and
ovarian
tumors]
and
alachlor
[
evidence
of
nasal,
stomach
and
thyroid
tumors].
All
are
chloroacetanilide
pesticides
and
cause
glutathione
depletion.
All
analogues
can
form
the
reactive
quinone
imine.
Due
to
the
thiophene
ring,
[
S]­
dimethenamid­
p
cannot.

3.4
Hazard
Identification
and
Toxicity
Endpoint
Selection
3.4.1
Acute
Reference
Dose
(
aRfD)
­
Females
age
13­
49
Selected
Study:
Developmental
toxicity
in
rabbits
(
MRID#
41706809).

 
Dose
and
Endpoint
for
Establishing
an
aRfD:
NOAEL
is
75
mg/
kg/
day.
LOAEL
is
150
mg/
kg/
day
based
on
developmental
effects
of
increased
resorptions,
implantation
loss
and
angulated
hyoid
alae.

 
Uncertainty
Factor
(
UF):
100
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation.

 
Comments
about
the
Study/
Endpoint/
Uncertainty
Factor:
The
resorptions
and
post
implantation
loss
are
presumed
to
be
single
dose
effects.
The
developmental
endpoint
is
appropriate
for
females
13­
49
and
is
of
the
appropriate
duration.
The
endpoint
is
supported
by
a
range­
finding
study
in
rats
with
[
S]­
dimethenamid­
p,
which
showed
increased
resorptions
at
400
mg/
kg/
day.

3.4.2
Acute
Reference
Dose
(
aRfD)
­
General
Population
An
appropriate
acute
endpoint
attributable
to
a
single
dose
was
not
available
in
the
toxicity
database
including
the
developmental
toxicity
studies.

3.4.3
Chronic
Reference
Dose
(
cRfD)

Selected
Study:
Chronic/
carcinogenicity
study
in
rats
(
MRID#'
s
41706808
/
42030102).

 
Dose
and
Endpoint
for
Establishing
an
cRfD:
NOAEL
is
5.1/
6.8
mg/
kg/
day
for
male/
female.
The
LOAEL
is
36/
49
mg/
kg/
day
for
male/
female
based
on
decreased
body
weight
and
body
weight
gain
from
week
1­
10
and
week
10­
104
in
both
sexes,
and
at
termination
increased
microscopic
hepatic
lesions
in
both
sexes.

 
Uncertainty
Factor
(
UF):
100
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation.

 
Comments
about
the
Study/
Endpoint/
uncertainty
Factor:
The
study
is
the
right
duration.
12
of
30
3.4.4
Incidental
Oral
Exposure
(
Short­
term
/
1­
30
days,
and
Intermediate­
term
/
1­
6
months)

This
endpoint
is
not
required
due
to
the
absence
of
residential
exposure.

3.4.5
Dermal
Absorption
No
dermal
absorption
studies
are
available.
Estimation
of
dermal
absorption
from
the
ratio
of
the
LOAEL
form
a
21­
day
dermal
study
in
rabbits
and
the
rabbit
developmental
toxicity
study
show
maximal
dermal
absorption
of
about
30%,
i.
e.,
[(
500
mg/
kg/
day
based
on
body
weight
change
from
the
21­
day
dermal
rabbit
study)/(
150
mg/
kg/
day
based
on
body
weight
change
from
the
developmental
toxicity
rabbit
study)]
X
100
=
30%.
Note:
The
LOAEL
for
the
21­
day
dermal
study
for
weight
decrement
in
males
was
used
for
comparison
to
the
body
weight
decrement
in
the
developmental
study
in
rabbits.

3.4.6
Dermal
Exposure
(
Short­
term
/
1­
30
days)

Selected
Study:
Developmental
Toxicity
Study
in
Rats
(
MRID#
44332243).

 
Dose
and
Endpoint
for
Risk
Assessment:
LOAEL
is
25
mg/
kg/
day
based
on
maternal
body
weight
decrement
gestational
days
13­
19
and
body
weight
gain
decrement
gestational
days
6­
16
and
decreased
food
consumption
gestational
day
6­
9.
There
was
no
NOAEL.

 
Uncertainty
Factor
(
UF):
300
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation
and
additional
3X
for
the
lack
of
a
clear
NOAEL.
Since
the
LOAEL
of
25
mg/
kg/
day
was
close
to
a
NOAEL,
an
extra
3X
uncertainty
factor
was
considered
adequate
protection
from
the
slight
body
weight
change
decrement
seen
in
the
pregnant
rat
at
the
LOAEL.

 
Comments
about
the
Study/
Endpoint/
uncertainty
Factor:
The
endpoint
is
appropriate
for
short­
term
exposure
(
1­
30
days)
and
it
protects
the
potentially
pregnant
female
and
developing
conceptus.
The
endpoint
from
21­
day
dermal
study
was
not
used
because
it
would
not
adequately
protect
for
the
effects
seen
in
the
pregnant
rat.
A
correction
factor
for
dermal
absorption
must
be
applied
to
the
oral
study.

 
Note:
An
endpoint
is
not
required
for
short­
term
/
1­
30
days
for
infant
and
children
due
to
the
absence
of
residential
exposure.

3.4.7
Dermal
Exposure
(
Intermediate­
term
/
1­
6
months,
and
Long­
term
/
>
6
months)

Selected
Study:
Chronic
feeding
study
in
rats
(
MRID#'
s
41706808
/
42030102).

 
Dose
and
Endpoint
for
Risk
assessment:
NOAEL
is
5.1/
6.8
mg/
kg/
day
for
male/
female.
The
LOAEL
is
36/
49
mg/
kg/
day
for
male/
female
based
on
decreased
body
weight
and
body
13
of
30
weight
gain
from
week
1­
10
and
week
10­
104
in
both
sexes,
and
at
termination
increased
microscopic
hepatic
lesions
in
both
sexes.

 
Uncertainty
Factor
(
UF):
100
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation.

 
Comments
about
the
Study/
Endpoint/
uncertainty
Factor:
The
study
showed
the
same
NOAEL
at
10
weeks
as
at
termination
and
thus,
is
of
the
correct
time
frame
for
both
intermediate
and
long­
term
exposure.
Since
an
oral
study
was
used,
the
endpoint
must
be
corrected
for
dermal
absorption.
A
correction
factor
for
dermal
absorption
must
be
applied
to
the
oral
study.

3.4.8
Inhalation
Exposure,
(
Short­
Term
/
1­
30
days)
­
Females
13­
49
Selected
Study:
Developmental
Toxicity
study
in
Rats
(
MRID#
44332243).

 
Dose
and
Endpoint
for
Risk
Assessment:
LOAEL
is
25
mg/
kg/
day
based
on
maternal
body
weight
decrement
gestational
days
13­
19
and
body
weight
gain
decrement
gestational
days
6­
16
and
decreased
food
consumption
gestational
day
6­
9.
There
was
no
NOAEL.

 
Uncertainty
Factor
(
UF):
300
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation
and
additional
3X
for
the
lack
of
a
clear
NOAEL.
Since
the
LOAEL
of
25
mg/
kg/
day
was
close
to
a
NOAEL,
an
extra
3X
uncertainty
factor
was
considered
adequate
protection
from
the
slight
body
weight
change
decrement
seen
in
the
pregnant
rat
at
the
LOAEL.

 
Comments
about
the
Study/
Endpoint/
uncertainty
Factor:
The
endpoint
is
appropriate
for
short­
term
exposure
(
1­
30
days)
and
it
protects
the
potentially
pregnant
female
and
developing
conceptus.
Assume
100%
absorption
should
be
applied
to
the
oral
study.

3.4.9
Inhalation
Exposure:
(
Intermediate­
term
/
1­
6
months,
and
Long­
term
>
6
months)

Selected
Study:
Chronic/
carcinogenicity
study
in
rats
(
MRID#'
s
41706808
/
42030102).

 
Dose
and
Endpoint
for
Risk
Assessment:
NOAEL
is
5.1/
6.8
mg/
kg/
day
for
male/
female.
The
LOAEL
is
36/
49
mg/
kg/
day
for
male/
female
based
on
decreased
body
weight
and
body
weight
gain
from
week
1­
10
and
week
10­
104
in
both
sexes,
and
at
termination
increased
microscopic
hepatic
lesions
in
both
sexes.

 
Uncertainty
Factor
(
UF):
100
This
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation.

 
Comments
about
the
Study/
Endpoint/
uncertainty
Factor:
The
endpoint
is
appropriate
for
intermediate
and
long­
term
occupational
exposure
because
the
same
NOAEL
was
seen
at
10
weeks
as
at
termination.
Assume
100%
absorption.
14
of
30
3.4.10
Level
of
Concern
for
Margin
of
Exposure
Table
3.4.10
Summary
of
Levels
of
Concern
for
Risk
Assessment.

Route
Short­
Term
(
1­
30
Days)
Intermediate­
Term
(
1
­
6
Months)
Long­
Term
(>
6
Months)

Occupational
(
Worker)
Exposure
Dermal
300
100
100
Inhalation
300
100
100
3.4.11
Classification
of
Carcinogenic
Potential
The
Carcinogenicity
Peer
Review
of
dimethenamid
of
3/
23/
95
(
TXR#
012143)
and
6/
15/
92
(
TXR#
012831)
stated
that
the
weight
of
evidence
classification
was
Group
C
­
possible
human
carcinogen
and
recommended
that
for
the
purpose
of
risk
characterization
the
reference
dose
(
PAD)
approach
should
be
used
for
quantification
of
human
risk.
This
decision
was
based
on
a
statistically
significant
increasing
trend
for
liver
cell
tumors
(
benign
and
malignant
combined)
in
male
rats
and
statistically
significant
increasing
trend,
and
did
not
show
significance
by
pair
wise
comparison.
Dimethenamid­
p
has
shown
positive
results
in
some
genotoxicity
tests
and
is
structurally
related
to
other
carcinogens.
An
acceptable
study
in
mice
showed
no
dose
related
tumors.

3.4.12
Summary
of
Toxicological
Doses
and
Endpoints
for
[
S]­
Dimethenamid­
p
for
Use
in
Human
Risk
Assessments
3.4.12
Summary
of
Toxicological
Doses
and
Endpoints
for
[
S]­
DIMETHENAMID­
p
for
Use
in
Human
Risk
Assessments
Exposure/
Scenario
Dose
Used
in
Risk
Assessment,
Interspecies,
Intraspecies,
and
any
Traditional
UF
Special
FQPA
SF
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
15
of
30
3.4.12
Summary
of
Toxicological
Doses
and
Endpoints
for
[
S]­
DIMETHENAMID­
p
for
Use
in
Human
Risk
Assessments
Exposure/
Scenario
Dose
Used
in
Risk
Assessment,
Interspecies,
Intraspecies,
and
any
Traditional
UF
Special
FQPA
SF
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Acute
Dietary
(
Females
13­
49
years
of
age)

Based
on
[
RS]
data
NOAEL
=
75
mg/
kg/
day
UF
=
100
Acute
RfD
=
0.75
mg/
kg/
day
FQPA
SF
=
1X
aPAD
=
acute
RfD
FQPA
SF
=
0.75
mg/
kg/
day
Developmental
Toxicity
in
rabbits
Maternal;
LOAEL
=
150
mg/
kg/
day
based
on
abortions
and
decreased
body
weight
gain
and
food
consumption.
Developmental;
LOAEL
=
150
mg/
kg/
day
based
on
post­
implantation
loss
Acute
Dietary
(
General
population
including
infants
and
children)
Not
Applicable
No
studies
identify
an
acute
hazard
(
dose
and
endpoint)
based
on
a
single
oral
exposure
(
dose)

Chronic
Dietary
(
All
populations)

Based
on
[
RS]
data
NOAEL=
5
mg/
kg/
day
UF
=
100
Chronic
RfD
=
0.05
mg/
kg/
day
FQPA
SF
=
1X
cPAD
=
chronic
RfD
FQPA
SF
=
0.05
mg/
kg/
day
Chronic/
carcinogenicity
rats
LOAEL
=
M/
F;
36/
49
mg/
kg/
day
based
on
decreased
body
weight
and
body
weight
gain
in
both
sexes,
increased
food
conversion
ratios
in
females,
and
increased
microscopic
hepatic
lesions
in
both
sexes.

Dermal
Absorption
Based
on
[
RS]
data
30%
No
studies
are
available.
Value
estimated
from
the
ratio
of
the
LOAEL
for
maternal
weight
decrement
in
developmental
study
to
LOAEL
for
male
weight
decrement
in
the
21­
day
dermal
study.
Ratio
of
[(
Developmental
rabbit
maternal
LOAEL,
body
weight)/(
21­
day
Dermal
rabbit
LOAEL
for
systemic
toxicity,
body
weight)]
X
100
=
(
150/
500)
x
100
=
30%
16
of
30
3.4.12
Summary
of
Toxicological
Doses
and
Endpoints
for
[
S]­
DIMETHENAMID­
p
for
Use
in
Human
Risk
Assessments
Exposure/
Scenario
Dose
Used
in
Risk
Assessment,
Interspecies,
Intraspecies,
and
any
Traditional
UF
Special
FQPA
SF
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Dermal
Short­
Term
(
1­
30
days)
LOAEL
=
25
mg/
kg/
day
Dermal
Absorption
=
30%
MOE
=
300
Developmental
toxicity
study
in
rats
(
MRID
44332243).
LOAEL
=
25
mg/
kg/
day
was
based
on
maternal
body
weight
decrement,
body
weight
gain
decrement
and
decreased
food
consumption.

Dermal
Intermediate­
Term,
(
1­
6
months)
NOAEL
=
6.8
mg/
kg/
day
(
F)
Dermal
Absorption
=
30%
UF
=
1
MOE
=
100
Chronic
feeding
study
in
rats
(
MRID
41706808
&
42030102).
LOAEL
=
36/
49
mg/
kg/
day
(
M/
F)
based
on
decreased
body
weight
and
body
weight
gain
and
at
termination
increased
microscopic
hepatic
lesions.
NOAEL
=
5.1/
6.8
mg/
kg/
day
for
(
M/
F)

Inhalation,
Short­
Term
(
1­
30
days)
LOAEL
=
25
mg/
kg/
day
(
F)
Inhalation
Absorption
=
100%
UF
=
3
2
MOE
=
300
same
as
Dermal,
short
­
term
Inhalation
Intermediate
­
Term
(
1­
6
months)
NOAEL
=
6.8
mg/
kg/
day
(
F)
Inhalation
Absorption
=
100%
UF
=
1
MOE
=
100
same
as
Dermal
intermediate­
term
Cancer
Classified
as
"
C";
a
possible
human
carcinogen;
however,
no
Q1*
was
has
been
established
for
an
assessment
of
cancer
risk.

UF
=
uncertainty
factor,
FQPA
SF
=
Special
FQPA
safety
factor,
NOAEL
=
no
observed
adverse
effect
level,
LOAEL
=
lowest
observed
adverse
effect
level,
PAD
=
population
adjusted
dose
(
a
=
acute,
c
=
chronic)
RfD
=
reference
dose,
MOE
=
margin
of
exposure,
LOC
=
level
of
concern,
NA
=
Not
Applicable
17
of
30
3.6
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
recommendations
of
its
Endocrine
Disruptor
and
Testing
Advisory
Committee
(
EDSTAC),
EPA
determined
that
there
was
a
scientific
basis
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).

In
the
available
toxicity
studies
with
the
technical
grade
of
the[
RS]
and
[
S]
dimethenamid
products,
no
effects
related
to
endocrine
disruption
were
noted.

4.0
Public
Health
and
Pesticide
Epidemiology
Data
4.1
Incident
Reports
Available
sources
of
incident
data
in
humans
were
reviewed
for
dimethenamid­
p.
These
sources
included
the
Incident
Data
System
consisting
of
reports
submitted
to
EPA
by
registrants
and
the
public
since
1992,
California
Pesticide
Illness
Surveillance
Program
which
has
reports
(
primarily
occupational)
since
1982,
seven
states
funded
by
NIOSH
provided
data
on
occupational
cases
for
1998­
2002,
reports
to
the
nation's
Poison
Control
Centers
for
1993­
2001,
and
reports
in
the
scientific
literature
reported
on
Medline.
Among
the
above
databases
only
one
had
a
single
report
of
a
spray
drift
victim
who
developed
a
rash,
eye
irritation,
and
other
symptoms.
The
dermal
and
eye
effects
were
considered
consistent
with
the
toxicity
profile
of
dimethenamid­
p,
but
the
systemic
effects
were
not.
No
conclusions
can
be
drawn
from
this
one
incident,
and
no
recommendations
are
warranted.

5.0
Dietary
Exposure/
Risk
Characterization
5.1
Pesticide
Metabolism
and
Environmental
Degradation
The
metabolism,
or
degradation
of
dimethenamid­
p,
has
been
adequately
studied
in
the
rat,
in
plants,
in
ruminants
and
poultry,
and
in
the
environment.
Metabolism
data
for
ruminants
and
poultry
livestock
is
presented
essentially
for
qualitative
purposes
since
the
Agency
does
not
expect
finite
dimethenamid­
p
residue
to
occur
in
livestock
commodities
even
though
dimethenamid­
p
may
be
used
on
animal
feed
stuff
such
as
field
corn
and
sugar
beets.
Finite
residues
of
dimethenamid­
p
are
not
expected
in
livestock
commodities
due
to
the
very
low
(
less
than
detection)
levels
of
dimethenamid­
p
seen
in
residue
field
trial
studies
on
these
feed
items.
18
of
30
Based
on
an
analysis
of
the
structural
relationship
of
metabolites
to
parent
dimethenamid­
p,
the
toxicity
of
metabolites
is
not
expected
to
exceed
the
parent
compound.

5.1.1
Metabolism
in
Primary
Crops
The
nature
of
the
residue
in
plants
is
adequately
understood.
Soybean
and
corn
metabolism
studies
are
available
and
have
been
reviewed
by
the
HED
Metabolism
Committee
(
M.
Flood,
11/
10/
92;
and
M.
Bradley,
12/
8/
93).
The
metabolism
of
dimethenamid­
p
in
plants
involves
conjugation
with
glutathione,
with
subsequent
transformation
of
the
glutathione
moiety
to
yield
a
variety
of
metabolites.
The
residue
of
concern
for
purposes
of
the
tolerance
expression
(
and
risk
assessment)
was
determined
to
be
dimethenamid
per
se.

In
addition,
a
sugar
beet
metabolism
study
was
recently
reviewed
(
D.
Dotson,
4/
14/
04)
in
conjunction
with
various
root,
tuber,
corm
and
bulb
vegetables.
Following
three
early
season
foliar
applications
of
[
3­
14C­
thienyl]
dimethenamid
to
sugar
beets
at
a
total
rate
of
1.2
lb
ai/
A,
total
radioactive
residues
(
TRR)
were
0.078
and
0.284
ppm
in/
on
sugar
beet
roots
and
tops
harvested
126
days
after
the
last
treatment.
The
metabolite
profile
was
similar
for
roots
and
tops,
and
dimethenamid­
p
was
not
detected
in/
on
either
commodity.
For
both
roots
and
tops,
the
majority
of
14C­
residues
were
characterized
as
minor
unknowns
each
present
at
#
8%
of
the
TRR.
One
unknown
polar
fraction
accounted
for
>
10%
of
the
TRR
in
roots,
but
was
present
at
<
0.01
ppm.
The
metabolic
pathway
for
[
14C]
dimethenamid
in
sugar
beets
is
complex,
but
proceeds
via
a
pathway
similar
to
that
observed
in
corn
and
soybeans.
However,
two
metabolites
not
identified
in
corn
or
in
soybean
were
found
in
sugar
beets.
These
are
the
sulfoxide
of
the
cysteine
conjugate
and
the
N­
malonyl
conjugate
of
the
cysteine
conjugate,
and
together
accounted
for
<
6
%
of
the
TRR
in
sugar
beets.

5.1.2
Metabolism
in
Animals
The
rat
metabolism
study
indicates
that
dimethenamid­
p,
at
single
low
and
high
doses,
is
extensively
metabolized
to
approximately
31
identified
metabolites,
and
is
essentially
completely
(
90%)
excreted
in
the
urine,
feces,
and
bile
within
7
days.
Excretion
products
were
qualitatively
independent
of
sex,
but
minor
quantitative
differences
were
seen
between
males
and
females.
In
the
urine,
females
excreted
about
47%
to
63%
and
males
about
31%
to
35%
at
low
and
high
oral
doses,
i.
v
doses
and
multiple
doses.
In
feces,
females
excreted
26%
to
48%
and
males
30%
to
62%
at
low
and
high
oral
doses,
i.
v.
doses
and
multiple
doses.

The
primary
route
of
metabolism
is
the
liver
with
less
than
2.5%
of
the
dose
being
recovered
as
parent.
None
of
the
metabolites
were
more
than
10%
with
most
being
less
than
2%
as
free
or
conjugate.
On
the
basis
of
the
metabolites
identified
in
the
urine
and
feces,
the
primary
metabolic
pathways
for
dimethenamid­
p
involve
glutathione
conjugation
via
displacement
of
the
chlorine
atom
followed
by
(
1)
breakdown
of
the
glutathione
to
mercapturic
acid,
or
(
2)
hydrolysis
of
the
thio
bond
of
mercaptan,
which
is
then
methylated
and
oxidized
to
the
methylsufoxide
and
methylsulfone.
Additional
major
metabolic
reactions
include
Omethylation
of
the
2­
methoxyl­
1­
methylethyl
moiety
to
form
a
2­
hydroxylated
product
and
oxidation
of
the
2­
methyl
group
on
the
thiophene
ring
to
produce
a
hydroxymethyl.
Dimerization,
cyclization,
and
hydroxylation
at
the
thiol
also
occur
following
hydrolysis
of
the
19
of
30
glutathione
conjugate.
Other
minor
pathways
for
dimethenamid­
p
involve
direct
biotransformation
reactions
such
as
reductive
chlorination,
oxidation
of
the
sulfur
on
the
thiophene
ring
to
form
a
sulfoxide,
oxidation
of
the
2­
or
4­
methyl
group
on
the
thiophene
ring,
and
cyclization
and
hydroxylation
of
the
thiol.
Saturation
of
glutathione
pathway
may
have
occurred
at
the
higher
dose.

There
are
no
rat
metabolism
studies
with
[
S]­
dimethenamid­
p,
however,
consideration
of
the
potential
differences
in
metabolism
of
the
[
R]
and
[
S]
enantiomer
of
dimethenamid
indicates
that
few
of
the
products
are
likely
to
be
affected
by
the
orientation
of
the
asymmetric
carbon,
since
most
metabolism
occurs
at
least
2
carbons
and
a
nitrogen
removed
from
the
asymmetric
center.
However,
products
including
a
nitrogen
containing
ring
structure
may
be
preferentially
formed
depending
on
possible
steric
hindrance
in
the
ring.

5.1.3
Metabolism
in
Rotational
Crops
The
requirements
for
confined
accumulation
in
rotational
crops
are
satisfied.
An
adequate
confined
rotational
crop
study
was
reviewed
by
the
Agency.
The
study
includes
data
on
winter
wheat
planted
141
days
after
treatment
(
DAT),
lettuce
planted
322
DAT,
and
carrots
planted
332
DAT.
The
maximum
concentration
of
any
metabolite/
degradate
in
harvested
wheat
was
0.01
ppm
for
the
sulfoxide
of
thiolactic
acid
conjugate.
Based
on
these
data,
HED
concluded
that
a
4­
month
rotational
interval
is
adequate
for
fall­
seeded
cereal
grains
and
other
crops
may
be
planted
the
following
spring.
The
current
use
directions
specify
that
treated
areas
may
be
replanted
at
any
time
with
crops
which
have
dimethenamid­
p
tolerances.

5.1.4
Metabolism
in
Livestock
Ruminant:
In
the
ruminant
metabolism
study,
a
dairy
goat
was
dosed
orally
for
4
days
with
[
14C]
dimethenamid
at
levels
equivalent
to
223
ppm
(>
10,000x
MTDB
of
0.019
ppm.
Total
radioactive
residues
were
16.6
ppm
in
liver,
9.9
ppm
in
kidneys,
0.97
ppm
in
muscle
and
fat,
and
0.98
ppm
in
milk.
[
14C]
Dimethenamid
was
extensively
metabolized
and
identification
of
metabolites
was
limited.
The
principle
metabolites
identified
in
milk
and
tissues
included:
M17
in
kidney
(
9%
TRR),
liver
(
2.7%
TRR),
muscle
(
11.4%
TRR),
fat
(
5.4%
TRR),
and
milk
(
5.2%
TRR);
the
cysteine
conjugate
of
parent
in
kidney
(
1%
TRR),
liver
(
7.2%
TRR),
muscle
(
14.2%
TRR),
and
milk
(
11.2%
TRR);
and
the
glutathione
conjugate
of
parent
in
kidney
(
5%
TRR),
liver
(
2.2%
TRR),
muscle
(
8.3%
TRR),
fat
(
2.1%
TRR),
and
milk
(
7.9%
TRR).
Metabolite
M7
was
also
identified
as
a
major
component
in
kidneys
(
24.1%
TRR)
and
milk
(
24.2%
TRR),
and
metabolite
M22
was
identified
in
liver
(
6.1%
TRR).
None
of
the
remaining
unknown
components
were
present
at
more
than
10%
of
the
TRR
in
milk
or
any
tissue.

Poultry:
In
the
poultry
metabolism
study,
three
hens
were
dosed
orally
for
4
days
with
[
14C]
dimethenamid
at
levels
equivalent
to
167
ppm
(­
17,000x
MTDB
of
0.01
ppm).
Total
radioactive
residues
were
8.33
ppm
in
liver,
0.58
ppm
in
muscle,
0.29
ppm
in
fat,
0.30
ppm
in
egg
whites
and
0.62
ppm
in
egg
yolks.
The
metabolism
of
[
14C]
dimethenamid
in
hens
was
extensive,
with
parent
only
being
identified
in
fat
(
34.9%
TRR).
Other
than
parent
in
fat,
no
one
compound
appears
to
account
for
more
than
10%
of
the
TRR
in
any
given
tissue.
Although
only
limited
identification
of
14C­
residues
was
achieved,
the
poultry
metabolism
study
was
deemed
20
of
30
adequate
because
the
dosing
level
was
highly
exaggerated
compared
to
the
MTDB
and
the
extensive
metabolism
of
dimethenamid­
p
resulted
in
numerous
minor
metabolites
(<
10%
TRR).

Note
that
after
considering
the
extensive
metabolism
of
dimethenamid­
p
in
animals,
the
exaggerated
dosing
levels
used
in
the
animal
metabolism
studies,
and
the
expected
low
level
of
dietary
exposure
of
livestock
to
dimethenamid­
p,
the
HED
Metabolism
Assessment
Review
Committee
(
MARC)
concluded
that
tolerances
(
and
risk
assessment)
are
not
required
for
animal
commodities
(
M.
Flood,
11/
10/
92).

5.1.5
Analytical
Methodology
An
adequate
enforcement
method
is
available
for
determining
dimethenamid­
p
residues
in
plants
and
soil.
The
GC/
NPD
method
(
AM­
0884­
0193­
1)
has
been
validated
by
the
Agency
and
submitted
for
publication
in
FDA's
Pesticide
Analytical
Manual,
Volume
II.
The
method
does
not
separate
the
R
and
S
isomers
of
dimethenamid
and
the
limit
of
quantitation
(
LOQ)
is
0.01.
As
tolerances
are
not
required
for
animal
commodities,
no
analytical
methods
for
animal
commodities
are
required.

5.1.6
Environmental
Degradation
Dimethenamid­
p
is
mobile
(
Kd
=
1.4
to
3.0)
and
moderately
persistent
in
the
environment.
Dimethenamid­
p
is
moderately
susceptible
to
aerobic
biodegradation
(
mean
half­
life
=
37
days
at
the
90%
confidence
interval),
and
stable
to
hydrolysis.
Photodegradation
in
aqueous
media
is
expected
to
be
a
minor
route
of
dissipation.
Dimethenamid­
p
is
likely
to
leach
to
ground
water,
and
has
the
potential
to
contaminate
drinking
water.

Based
on
an
aerobic
soil
metabolism
study
conducted
on
both
[
RS]
and
[
S]­
only
dimethenamid,
three
minor
degradates,
M23
(
oxalamide),
M31
(
STGA),
and
M27
(
sulfonate
sodium
salt)
were
recovered
at
maximums
of
less
than
or
equal
to
8%
of
the
applied
radioactivity.
Three
other
degradates
M30
(
STLA),
M32
(
TGA)
and
M11
(
based
on
HPLC
analysis)
were
present
at
3.8%
of
the
applied
radioactivity
from
0
to
182
days
post­
treatment.
[
14C]
Residues
associated
with
the
fulvic
acid,
humic
acid
and
humin
fractions
were
maximums
of
8.6­
8.9%
(
56
days),
23.0­
25.1%
(
84
days)
and
9.6­
10.4%
(
182
days)
of
the
applied
radioactivity,
respectively.
Evolved
14CO2
accounted
for
28.5­
29.2%
of
the
applied
radioactivity
at
182
days
post­
treatment.

5.1.7
Comparative
Metabolic
Profile
Dimethenamid­
p
is
readily
absorbed
through
the
rat
gastro­
intestinal
tract
and
is
primarily
excreted
in
the
urine,
with
most
of
a
dose
being
excreted
in
24
hours
for
low
doses
and
48
hours
for
higher
doses.
Biliary
excretion
is
significant
but
is
a
minor
route.
The
tissue
burden
is
low,
with
up
to
only
3.3%
of
the
dose
remaining
in
the
tissues.
A
total
of
10
fractions
(
nine
metabolites
and
one
isomer)
were
noted
in
the
urine
and
5
fractions
in
the
feces.
The
major
urinary
metabolites
in
these
fractions
were
sulfate
and
glucuronide
conjugates
and
the
major
fecal
metabolite
was
a
p­
hydroxy
derivative
of
dimethenamid­
p.
The
sulfate
and
glucuronide
conjugates
and
p­
hydroxy
derivative
of
dimethenamid­
p
were
recognized
as
the
biliary
21
of
30
metabolites.
Dimethenamid
per
se,
was
detected
only
in
small
amounts
in
the
urine
and
feces.
Minor
quantitative
differences
related
to
gender
were
identified.

Metabolism
of
dimethenamid­
p
in
other
animals
(
poultry
and
ruminants)
appears
to
be
similar
to
its
metabolism
in
rats.
The
metabolism
seems
to
proceed
by
de­
chlorination
of
the
pyridazinone
ring
to
yield
a
dechlorinated
dimethenamid­
p
or
by
hydroxylation
of
the
phenyl
ring
to
yield
a
hydroxylated
dimethenamid­
p.
The
hydroxylated
dimethenamid­
p
may
further
degrade
to
form
a
sulfate
conjugate
of
p­
hydroxy
dimethenamid­
p.

The
major
residues
found
in
plants
include
parent
dimethenamid­
p,
dephenylated
dimethenamidp
and
conjugates
of
each.
Residues
of
parent
dimethenamid­
p
tend
to
predominate
after
postemergent
treatment
of
sugar
beets,
while
residues
of
desphenyl
dimethenamid­
p
or
its
conjugates
predominate
after
pre­
emergent
treatment.
Residues
of
desphenyl
dimethenamid­
p
or
its
conjugates
also
predominate
in
rotational
crops.
Since
the
most
significant
route
of
soil
degradation
of
dimethenamid­
p
is
microbial
formation
of
desphenyl
dimethenamid­
p,
this
pattern
seems
to
suggest
that
the
desphenyl
metabolites
are
more
predominantly
the
result
of
soil
metabolism
and
subsequent
uptake
by
plants
than
of
plant
metabolism
itself.

5.1.8
Toxicity
Profile
of
Major
Metabolites
and
Degradates
Little
information
is
available
on
the
toxicity
of
the
major
dimethenamid­
p
metabolites.
The
hydroxy
dimethenamid­
p
metabolite
formed
in
food
animals
appears
to
be
also
formed
in
the
rat,
and
is,
therefore,
part
of
the
total
toxic
exposure
for
these
animals.
It
is
unlikely
to
be
more
toxic
than
the
parent.

The
desphenyl
metabolite
is
also
unlikely
to
be
more
toxic
than
the
parent.
It
is
difficult
to
know,
however,
what
effect
the
removal
of
the
entire
benzene
ring
will
have
on
the
toxicology.
This
metabolite
is
not
formed
in
rats
and,
therefore,
is
not
a
part
of
the
toxic
profile
to
which
the
rat
is
exposed
when
dosed
with
the
parent.
After
correction
for
molecular
weight
differences,
the
LD50
of
the
parent
and
of
the
desphenyl
metabolite
are
similar.

5.1.9
Drinking
Water
Residue
Profile
Data
relevant
to
dimethenamid­
p
residue
in
drinking
water
have
been
evaluated
by
EFED,
and
Estimated
Environmental
Concentrations
(
EEC)
were
provided
in
a
risk
assessment
(
D285455,
L.
Shanaman,
4/
22/
03).
Drinking
water
concentrations
have
been
predicted
using
a
standard
Georgia
onion
scenario
as
a
surrogate
for
use
on
all
crops,
using
acceptable
environmental
fate
and
transport
data
submitted
to
the
Agency.
The
maximum
proposed
seasonal
application
rate
is
1.5
lb
ai/
acre
(
maximum
of
1.5
lb
ai/
acre
for
individual
applications),
which
can
be
divided
into
2
applications
per
year,
made
at
14­
day
intervals.

Dimethenamide­
p
is
mobile
(
Kd
=
1.4
to
3.0),
moderately
persistent
in
the
environment,
moderately
susceptible
to
aerobic
biodegradation
(
mean
half­
life
=
37
days
at
the
90%
confidence
interval),
and
stable
to
hydrolysis.
Photodegradation
in
aqueous
media
is
expected
to
be
a
minor
route
of
dissipation.
Dimethenamide­
p
is
likely
to
leach
to
ground,
and
has
the
potential
to
contaminate
drinking
water.
In
most
cases,
data
for
both
the
racemic
mixture
and
the
22
of
30
resolved
isomer
were
used
to
generate
model
input
values.
Submitted
aerobic
soil
metabolism
half­
lives
were
not
significantly
different,
and
therefore
not
distinguishable,
between
the
resolved
and
the
mixed
isomers.

Tier
II
surface
water
concentrations
are
predicted
by
the
PRZM/
EXAMS
model
at
49
ug/
L
for
acute
exposure,
7.9
ug/
L
for
non­
cancer
chronic
exposure,
and
5.1
ug/
L
for
overall
chronic
exposure.
Ground
water
concentrations
of
0.42
ug/
L
were
predicted
by
the
Tier
I
model,
SCIGROW.
This
assessment
is
for
parent
compound
only.

Table
5.1.9
Summary
of
Estimated
Surface
and
Ground
Water
Concentrations
for
Dimethenamidp

Dimethenamid­
p
Surface
Water
EEC
ppb
Ground
Water
EEC
ppb
Acute
49
0.42
Chronic
(
non­
cancer)
7.9
0.42
Chronic
(
cancer)
5.1
0.42
5.1.10
Food
Residue
Profile
Dimethenamid
and
dimethenamid­
p
are
selective,
preemergence,
chloroacetamide
herbicides
with
existing
tolerances
for
bean,
dry,
seed;
beet,
garden,
roots;
beet,
garden,
tops;
beet,
sugar,
dried
pulp;
beet,
sugar,
molasses;
beet,
sugar,
roots;
beet,
sugar,
tops;
corn,
field,
forage;
corn,
field,
grain;
corn,
field,
stover;
corn,
pop,
forage;
corn,
pop,
grain;
corn,
pop,
stover;
corn,
sweet,
forage;
corn,
sweet,
kernal
plus
cob
with
husk
removed;
corn,
sweet,
stover;
garlic;
horseradish;
onion,
dry
bulb;
peanut,
hay;
peanut,
nutmeat;
shallot,
bulb;
sorghum,
grain;
sorghum,
grain,
forage;
sorghum,
grain,
stover;
soybean,
seed;
and
tuberous
and
corm
vegetables.
Tolerances
are
established
at
0.01
ppm
for
residues
of
dimethenamid,
(
RS)­
2­
chloro­
N­[(
1­
methyl­
2­
methoxy)
ethyl]­
N­(
2,4­
dimethylthien­
3­
yl)
acetamide
under
40
CFR
§
180.464(
a).
A
pesticide
tolerance
petition
(
4E6844)
is
currently
pending
for
dimethenamid­
p
on
onion,
green;
leek;
onion,
welsh;
and
shallot,
fresh
leaves.
The
residue
data
are
summarized
below.
The
maximum
seasonal
rate
for
use
on
the
above
crops
is
1
lb
ai/
A,
except
potatoes
can
be
treated
at
the
maximum
rate
of
1.25
lb
ai/
A,
and
dry
bulb
onions
at
the
maximum
seasonal
rate
of
1.5
lb
ai/
A.

 
Residue
in
Processed
Commodities.
The
requirements
for
magnitude
of
the
residue
in
processed
food/
feed
are
satisfied
for
corn,
peanut,
potato,
soybean,
and
sugar
beet.
The
available
data
indicate
that
residues
of
dimethenamid­
p
do
not
concentrate
in
processed
commodities
of
corn
grain,
peanuts,
potatoes,
soybean
seeds,
or
sugar
beets.

 
Residue
in
Rotational
Crops.
The
requirements
for
confined
accumulation
in
rotational
crops
are
satisfied.
An
adequate
confined
rotational
crop
study
was
reviewed
by
the
Agency
on11/
24/
92.
The
study
includes
data
on
winter
wheat
planted
141
DAT,
lettuce
planted
322
DAT
and
carrots
planted
332
DAT.
The
maximum
concentration
of
any
metabolite/
degradate
in
harvested
wheat
was
0.01
ppm
for
the
sulfoxide
of
thiolactic
acid
conjugate.
Based
on
these
data,
HED
concluded
that
a
4­
month
rotational
interval
is
23
of
30
adequate
for
fall­
seeded
cereal
grains
and
other
crops
may
be
planted
the
following
Spring.
The
current
use
directions
specify
that
treated
areas
may
be
replanted
at
any
time
with
crops
which
have
dimethenamid­
p
tolerances.

 
Residue
in
Crops.
Dietary
risk
assessment
is
based,
in
part,
on
the
following
field
trial
data
that
describe
the
level
of
dimethenamid
­
p
residue
in
treated
foods.
Field
trial
data
(
with
the
50:
50
R:
S)
are
adequate
for
dry
beans,
corn
(
field,
pop,
and
sweet),
onions
(
dry
bulb),
peanuts,
potatoes,
grain
sorghum,
soybean,
and
sugar
beets,
and
are
based
on
trials
conducted
at
the
maximum
labeled
use
rates.

 
Field
corn:
Trials
were
conducted
with
a
single
application
of
dimethenamid­
p
EC
at
1.5
lb
ai/
A
(
1x)
as
preplant
incorporated,
preemergence,
or
early
post­
emergence.
Dimethenamid­
p
residues
in
these
tests
were
<
0.01
ppm
(
less
than
the
limit
of
detection;
LOD)
in/
on
all
samples
of
forage,
silage,
grain,
and
fodder.
In
addition,
data
on
residues
of
the
sulfonate
conjugate
of
dimethenamid­
p
in
corn
were
provided
in
conjunction
with
re­
analyses
of
corn
raw
agricultural
commodities
(
RACs).
Analyses
of
corn
forage
samples
from
these
tests
indicate
that
residues
of
the
sulfonate
conjugate
are
<
0.05
ppm.

 
Soybean:
Trials
were
conducted
with
a
single
application
of
dimethenamid
EC
at
1.5
lb
ai/
A
(
1x)
as
preplant
incorporated,
preemergence,
or
early
post­
emergence.
Dimethenamid­
p
residues
in
these
tests
were
<
0.01
ppm
in/
on
all
samples
of
hay,
seeds,
and
straw.
Residues
were
also
<
0.01
ppm
in/
on
forage
samples,
with
the
exception
of
two
forage
samples
from
the
1992
tests,
which
had
residues
of
0.011
ppm.
Another
8
tests
were
conducted
on
soybeans
in
1993
to
support
use
of
a
later
post­
emergence
application
(
up
to
3rd
trifoliate)
at
1.5
lb
ai/
A.
In
these
tests,
dimethenamid­
p
residues
were
<
0.01
ppm
in/
on
all
samples
of
grain,
hay,
and
straw
and
were
<
0.01­
0.171
ppm
in/
on
forage
(
dimethenamid
labels
prohibit
the
feeding
of
treated
soybean
forage,
hay,
or
straw
to
livestock).

 
Dry
beans,
grain
sorghum,
peanuts,
and
sweet
corn:
A
total
of
28
tests
were
conducted
for
each
crop
in
1994
reflecting
preemergence
and
post­
emergence
application.
Dimethenamid­
p
EC
was
applied
in
each
test
at
a
rate
of
1.5
lb
ai/
A
(
1x
the
maximum
labeled
rate),
and
RACs
for
each
crop
were
harvested
at
the
appropriate
intervals.
Dimethenamid­
p
residues
were
<
0.01
ppm
in/
on
all
samples
of
dry
bean
seeds,
hay,
and
straw,
and
were
<
0.01­
0.07
ppm
in/
on
bean
forage
(
the
current
labels
prohibit
the
feeding
of
treated
bean
forage
to
livestock).
For
grain
sorghum,
dimethenamid
residues
were
<
0.01
ppm
in/
on
all
samples
of
forage,
fodder
and
grain.
For
sweet
corn,
dimethenamid­
p
residues
were
<
0.01
ppm
in/
on
all
samples
of
sweet
corn
ears
and
fodder.
For
peanuts,
dimethenamid­
p
residues
were
<
0.01
ppm
in/
on
all
samples
of
peanut
forage,
hay,
nutmeats,
and
hulls.
24
of
30
 
Dry
bulb
onions:
Dimethenamid­
p
(
6
lb/
gal
EC)
was
applied
at
1.5
lb
ai/
A
(
1x)
to
onions
as
a
single
post­
emergence
application
at
the
2nd
true
leaf
stage.
Duplicate
treated
samples
of
dry
bulb
onions
were
harvested
from
each
test
at
30
and
45
days
post­
treatment.
Residues
of
dimethenamid­
p
were
<
0.01
ppm
in/
on
all
onion
samples
harvested
at
either
post­
treatment
interval.
 
Potatoes:
Dimethenamid­
p
(
6
lb/
gal
EC)
was
applied
as
(
i)
a
preplant
incorporated
(
PPI)
application
at
0.80­
0.87
lb
ai/
A
(
0.9x),
(
ii)
a
preemergence
(
PRE)
application
at
0.80­
0.87
lb
ai/
A
(
0.9x),
or
(
iii)
a
lay­
by
application
at
1.21­
1.29
lb
ai/
A
(
1.3x).
Residues
of
dimethenamid­
p
were
<
0.01
ppm
in/
on
all
samples
of
mature
potatoes
from
the
PPI
and
PRE
applications.
Residues
were
also
<
0.01
ppm
in/
on
all
samples
harvested
40
days
following
the
lay­
by
application,
and
from
all
samples
in
the
residue
decline
tests.
 
Sugar
beets:
Dimethenamid­
p
(
6
lb/
gal
EC)
was
applied
at
1.0
lb
ai/
A
(
1x)
to
sugar
beets
as
a
single
post­
emergence
broadcast
application
at
the
8th
leaf
stage.
Residues
of
dimethenamid­
p
were
<
0.01
ppm
in/
on
all
samples
of
roots
harvested
60­
118
days
post­
treatment
and
#
0.01
ppm
in/
on
all
samples
of
tops
harvested
36­
110
days
post­
treatment.

 
Green
onions:
In
six
supervised
crop
field
trials
conducted
in
Florida
(
FL),
Georgia
(
GA),
and
Texas
(
TX)
and
in
British
Columbia
(
BC),
Ontario
(
ON),
and
Quebec,
Canada
(
QC),
dimethenamid­
p
6
pounds
per
gallon
EC
(
6
lb/
gal
EC)
was
applied
once
foliarly
to
green
onions
at
0.92­
1.06
lb
ai/
A/
season
(
1.03­
1.19
kg
ai/
ha/
season).
Green
onion
samples
were
harvested
at
pre­
harvest
intervals
(
PHI)
of
28­
32
days.
A
twelve
hour
restricted
entry
interval
is
required.

5.2.11
International
Residue
Limits
There
are
no
established
Codex,
Mexican,
or
Canadian
maximum
residue
limits
for
dimethenamid­
p
in/
on
onion.

5.3Dietary
Exposure
and
Risk
Aggregate
dietary
risk
for
dimethenamid­
p
is
assessed
by
comparing
acute
and
chronic
dietary
(
food
and
drinking
water)
exposure
estimates
to
their
respective
aPAD
and
cPAD,
with
risk
expressed
as
a
percent
of
the
PAD.
The
dimethenamid
aPAD
is
0.75
mg/
kg/
day
(
child­
bearing
females13­
49)
and
the
cPAD
is
0.05
mg/
kg/
day
(
general
US
population,
and
specific
population
subgroups).
Exposure
estimates
that
are
less
than
100%
of
the
aPAD/
cPAD
indicate
a
determination
of
safety
can
be
concluded.

Consumption
Data/
DEEM
Software:
The
acute
and
chronic
aggregate
(
food
and
drinking
water)
exposure
assessment
was
conducted
using
the
Dietary
Exposure
Evaluation
Model
software
with
the
Food
Commodity
Intake
Database
(
DEEM­
FCID
 
,
Version
1.3)
which
incorporates
consumption
data
from
the
USDA
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII),
1994­
1996
and
1998.
The
1994­
96,
98
data
are
25
of
30
based
on
the
reported
consumption
of
more
than
20,000
individuals
over
two
nonconsecutive
survey
days.
Consumption
data
are
averaged
for
the
entire
U.
S.
population
and
within
population
subgroups
for
chronic
exposure
assessment,
but
are
retained
as
individual
consumption
"
events"
for
acute
exposure
assessment.
Exposure
estimates
are
expressed
in
mg/
kg
body
weight/
day
and
risk
as
a
percent
of
the
aPAD/
cPAD.

An
upper­
bound
(
Tier
I)
acute
and
chronic
aggregate
risk
assessment
was
conducted
for
dimethenamid­
p
food
commodities
and
drinking
water
combined.
The
residue
estimate
for
each
food
commodity
is
based
on
the
tolerance
for
that
crop
(
0.01
ppm)
and
each
crop
is
assessed
as
if
100%
of
the
crop
has
been
treated
with
dimethenamid­
p.
The
EEC
inputs
(
acute/
chronic)
for
drinking
water
are
described
as
"
Tier
II",
but
are
considered
upper­
bound
estimates
for
finished
drinking
water.
It
should
also
be
noted
that,
like
the
tolerance
level
inputs
for
foods,
the
residue
inputs
for
drinking
water
are
point
estimates
rather
than
a
residue
distribution
(
as
seen
in
probabilistic
assessments).

The
estimated
acute
(
one
day)
aggregate
dietary
risk
exposure
for
females
13­
49
years
is
less
than
1%
of
the
dimethenamid­
p
aPAD,
and
the
estimated
chronic
aggregate
dietary
risk
exposure
for
all
population
subgroups
are
1%
or
less
of
the
dimethenamid­
p
cPAD
(
0.05
mg/
kg/
day).

Table
5.3
Results
of
Acute
and
Chronic
Dietary
Exposure
and
Risk
Estimates
for
Dimethenamid­
p.

Population
Subgroup
PAD,
mg/
kg/
day
Exposure,
mg/
kg/
day
%
PAD
Acute
Dietary
Estimates
(
95th
Percentile
of
Exposure)

Females
13­
49
yrs
0.75
0.002417
<
1
Chronic
Dietary
Estimates
DEEM­
FCID
Population
Subgroups
PAD,
mg/
kg/
day
Exposure,
mg/
kg/
day
%
PAD
U.
S.
Population
0.05
0.000205
<
1
All
infants
(<
1
yr)
0.05
0.000605
1
Children
1­
2
yrs
0.05
0.000329
<
1
Children
3­
5
yrs
0.05
0.000316
<
1
Children
6­
12
yrs
0.05
0.000221
<
1
Youth
13­
19
yrs
0.05
0.000163
<
1
Adults
20­
49
yrs
0.05
0.000187
<
1
Females
13­
49
yrs
old
0.05
0.000185
<
1
Adults
50+
yrs
0.05
0.000187
<
1
6.0
Residential
(
Non­
Occupational)
Exposure/
Risk
Characterization
26
of
30
There
are
no
non­
agricultural
(
or
residential)
uses
of
dimethenamid­
p.
Therefore,
potential
risk
from
such
uses
is
not
considered
at
this
time.

6.1
Other
(
Spray
Drift,
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
the
ground
application
method
employed
for
dimethenamid­
p.
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.
On
a
chemical
by
chemical
basis,
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,
a
membership
of
U.
S.
pesticide
registrants,
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
with
specific
products
with
significant
risks
associated
with
drift.

7.0
Aggregate
Risk
Assessments
and
Risk
Characterization
In
accordance
with
the
FQPA,
HED
must
consider
and
aggregate
pesticide
exposures
and
risks
from
three
major
sources:
food,
drinking
water,
and
residential
exposures.
In
an
aggregate
assessment,
exposures
from
relevant
sources
are
added
together
and
compared
to
quantitative
estimates
of
hazard
(
e.
g.,
a
NOAEL
or
PAD),
or
the
risks
themselves
can
be
aggregated.
When
aggregating
exposures
and
risks
from
various
sources,
HED
considers
both
the
route
and
duration
of
exposure.

Tier
II
surface
water
concentrations
are
predicted
by
the
PRZM/
EXAMS
model
at
49
ug/
L
for
acute
exposure,
7.9
ug/
L
for
non­
cancer
chronic
exposure,
and
5.1
ug/
L
for
overall
chronic
exposure.
Ground
water
concentrations
of
0.42
ug/
L
were
predicted
by
the
Tier
I
model,
SCIGROW.
This
assessment
is
for
parent
compound
only.

Aggregate
dietary
risk
for
dimethenamid­
p
is
assessed
by
comparing
acute
and
chronic
dietary
(
food
and
drinking
water)
exposure
estimates
to
their
respective
aPAD
and
cPAD,
with
risk
expressed
as
a
percent
of
the
PAD.
There
are
no
residential,
or
other
nonagricultural
uses
of
dimethenamid­
p.
An
aggregate
cancer
risk
analysis
was
not
performed.
Aggregate
risk
is
based
on
tolerance­
level
residues
and
an
assumption
of
100%
crop
treatment
for
the
food
uses,
and
on
Tier
II
estimates
for
the
drinking
water
contamination
that
may
be
associated
with
crop
uses.
Exposure
estimates
that
are
less
than
100%
of
the
aPAD/
cPAD
are
not
of
concern.
The
dimethenamid
aPAD
is
0.75
mg/
kg/
day
(
child­
bearing
females13­
49)
and
the
cPAD
is
0.05
mg/
kg/
day
(
general
US
population,
and
specific
population
subgroups).
The
upper­
bound
dietary
aPAD
risk
estimate
for
child­
bearing
females
is
less
than
1%
of
the
aPAD.
The
upper­
bound
dietary
27
of
30
cPAD
risk
estimates
for
the
general
US
and
specific
population
sub­
groups
are
1%
or
less
of
the
cPAD.
Since
there
are
no
residential
uses
of
exposure
for
dimethenamid­
p,
and
water
and
food
are
both
included
in
the
dietary
exposure
estimate,
no
further
calculations
are
necessary.
Exposure
estimates
are
less
than
100%
of
the
aPAD/
cPAD;
therefore,
are
not
of
concern.

8.0
Cumulative
Risk
Characterization/
Assessment
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
EPA
has
not
made
a
common
mechanism
of
toxicity
finding
as
to
dimethenamid­
p
and
any
other
substances.
Also,
dimethenamid­
p
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
this
tolerance
action,
therefore,
EPA
has
not
assumed
that
dimethenami­
p
has
a
common
mechanism
of
toxicity
with
other
substances.
For
information
regarding
EPA's
efforts
to
determine
which
chemicals
have
a
common
mechanism
of
toxicity
and
to
evaluate
the
cumulative
effects
of
such
chemicals,
see
the
policy
statements
released
by
EPA's
Office
of
Pesticide
Programs
concerning
common
mechanism
determinations
and
procedures
for
cumulating
effects
from
substances
found
to
have
a
common
mechanism
on
EPA's
website
at
http://
www.
epa.
gov/
pesticides/
cumulative/.

9.0
Occupational
Exposure/
Risk
Pathway
An
occupational
risk
assessment
was
completed
for
a
Section
3
registration
of
dimethenamid­
p
for
its
use
on
onion,
green;
leek;
onion,
welsh;
and
shallot,
fresh
leaves
(
D316723;
S.
Oonnithan;
February
1,
2006).

For
this
submission,
the
label
specifies
one
application
of
the
product
per
season.
Under
this
scenario,
two
types
of
occupational
exposures
are
encountered:
(
a)
exposure
to
handlers
consisting
mixers/
loaders,
applicators
and
flaggers
and
(
b)
postapplication
exposure
to
agricultural
workers
when
they
enter
the
treated
field
to
perform
weeding,
thinning,
irrigation,
scouting,
etc.
The
handler
exposure
is
further
segmented
to
include
(
i)
mixers/
loaders
who
transfer
and
mix
the
pesticide
formulation
with
the
diluent
and
load
the
diluted
product
into
the
spray
equipment,
(
ii)
applicators
who
operate
the
ground
and/
or
aerial
application
equipment
and
(
iii)
flaggers
who
assist
the
aerial
applicator
in
locating
sprayed
area
while
using
aerial
equipment.
The
post­
application
exposure
occurs
when
laborers
enter
the
treated
field
to
do
various
types
of
activities.
Occupational
exposures
to
mixers/
loaders,
applicators
and
agricultural
workers
are
addressed
here;
exposure
to
flaggers
is
not
applicable,
because
the
use
directions
calls
for
using
only
ground
application
equipment.

To
reduce
the
exposure
to
pesticide
residues
by
handlers
and
workers,
the
product
labels
specify
use
of
various
PPE
consistent
with
the
toxicity
of
the
active
ingredient
and/
or
formulation
and
the
equipment
used
to
apply
the
formulation.

9.1
Short/
Intermediate­
term
Handler
Risk
28
of
30
The
petitioner
did
not
submit
any
chemical­
specific
exposure
data
for
estimating
the
occupational
exposures
to
handlers
and
workers.
Therefore,
the
Agency
used
surrogate
exposure
data
from
the
PHED
(
ver
1.1)
and
default
values
established
by
HED's
ExpoSAC
for
the
calculation
of
exposures
to
handlers
and
workers.

Based
on
the
proposed
use
of
Outlook
Herbicide
on
green
bulb
vegetables,
following
assumptions
and
parameters
are
considered
for
estimating
the
exposure
levels
and
risks
to
handlers
and
farm
workers:

 
handlers
and
workers
would
be
exposed
to
the
pesticide
only
for
a
short­
term
(
1
to
30
days)
and
an
intermediate­
term
(
1­
6
months)
per
year.
 
the
handlers
and
workers
wear
label
recommended
PPE
(
baseline
PPE
includes
long
sleeved
shirt,
long
pants,
shoes
with
socks
and
no
respirator).
 
the
maximum
single/
seasonal
application
rate
is
taken
as
0.98
lb
ai/
A.
 
the
dermal
and
inhalation
exposure
values
are
for
baseline
PPE,
EC
formulation
and
ground
application
equipment.
 
the
area
treated/
day
is
taken
as
80
acres,
which
is
the
Agency's
estimate
of
acreage
that
could
be
treated
in
a
single
day
for
the
formulation
and
application
equipment
 
the
dermal
and
inhalation
absorption
rates
taken
are
30%
and
100%,
respectively.
 
the
average
body
weight
of
handlers
was
taken
as
70
kg.
The
70
kg
body
weight
was
taken
because
the
NOAEL
was
based
on
female
test
animals.

Applying
these
assumptions
and
parameters,
the
short­
and
intermediate­
term
risks
to
mixers/
loaders
and
applicators
were
estimated
and
presented
in
Table
9.1.

Table
9.1
Short
and
Intermediate­
term
Exposure
Estimates
for
Mixers/
Loaders/
Applicators
Applying
Outlook
Herbicide
on
Green
BulbVegetables
Using
Ground
Equipment1
Exposure
Scenario
Mitigation
Level
2
Dermal
Unit
Exposure
(
mg/
lb
ai)
3
Inhalation
Unit
Exposure
(
µ
g/
lb
ai)
3
Dermal
Daily
Dose
(
mg/
kg/
day)
4
Inhalation
Daily
Dose
(
mg/
kg/
day)
5
Short­
term
Combined
MOE
6
Inter.
term
Combined
MOE
7
Baseline
2.9
1.2
1.137
0.002
7
6
Mixers/
Loaders
Minimal
0.023
1.2
0.009
0.002
785
642
Applicators
Baseline
0.014
0.74
0.005
0.001
1,288
1,053
1
The
application
equipment
is
assumed
to
be
a
ground
boom
sprayer.
2
Baseline
mitigation
consists
of
long­
sleeve
shirt,
long
pants,
shoes,
and
socks
and
no
respirator.
Minimal
mitigation
consists
of
baseline
mitigation
plus
chemical
resistant
gloves.
3
Dermal
and
inhalation
unit
exposure
values
are
for
baseline
and
minimal
PPEs
from
PHED..
4
Daily
dermal
dose
=
(
dermal
unit
exposure
*
dermal
absorption
factor
[
30%]
*
application
rate
[
0.98
lb
ai/
A]
*
area
treated/
day
[
80
A])
/
body
weight
[
60
kg].
5
Daily
inhalation
dose
=
(
inhalation
unit
exposure
*
conversion
factor
[
1mg/
1000

g]
*
inhalation
absorption
factor
[
100%]
*
application
rate
[
0.98
lb
ai/
A]
*
area
treated/
day
[
80
A])
/
body
weight
[
60
kg].
6
Short­
term
combined
MOE
=
LOAEL
short­
term
(
25
mg/
kg/
day)/
Dermal
daily
dose
[
mg/
kg/
day]
+
inhalation
daily
dose
[
mg/
kg/
day]).
29
of
30
7
Intermediate­
term
combined
MOE
=
NOAEL
intermediate­
term
(
6.8
mg/
kg/
day)/
Dermal
daily
dose
[
mg/
kg/
day]
inhalation
daily
dose
[
mg/
kg/
day]).

The
MOEs
for
the
mixers/
loaders
and
applicators
resulting
from
the
proposed
uses
of
Outlook
®
Herbicide
on
green
bulb
vegetables
are
summarized
in
Table
9.1.
The
data
indicate
that
the
combined
short­
and
intermediate­
term
MOEs
range
from
6
to
7
with
the
baseline
PPE
(
long­
sleeve
shirt,
long
pants,
shoes
with
socks
and
no
respirator).
This
level
of
risk
is
higher
than
the
Agency's
level
of
concern
(
target
MOEs
of
300
and
100
for
short­
and
intermediate­
term
exposure
periods,
respectively.
If
the
mixers/
loaders
wore
chemical­
resistant
gloves
in
addition
to
the
baseline
PPE,
the
combined
exposures
for
short­
and
intermediate­
term
are
drastically
reduced
raising
the
MOEs
to
>
600;
thereby
attaining
an
acceptable
level
of
concern.
For
applicators,
the
combined
dermal
and
inhalation
routes
of
exposure
is
not
a
concern
(
MOE
=
>
1200)
even
with
the
baseline
PPE.
The
petitioner
already
prescribes
under
PPE
section
on
the
label,
use
of
chemicalresistant
gloves
by
the
handlers
and
applicators;
therefore,
no
additional
mitigation
statement
is
required
on
the
label.

The
short­
and
intermediate­
term
risks
to
handlers,
calculated
in
this
assessment
are
based
on
a
central
tendency
estimate
of
unit
exposures
and
an
upper­
percentile
assumption
for
the
application
rate,
and
are
assumed
to
be
representative
of
high­
end
exposures.
The
uncertainties
associated
with
this
assessment
stem
from
the
use
of
surrogate
exposure
data
(
e.
g.,
differences
in
use
scenario
and
data
confidence),
and
assumptions
regarding
the
amount
of
chemical
handled.
The
estimated
exposures
are
believed
to
be
reasonable
high­
end
estimates
based
on
observations
from
field
studies
and
professional
judgement.

9.2
Short/
Intermediate­
term
Postapplication
Risk
Postapplication
exposure
to
pesticides
is
a
concern
when
farm
workers
enter
the
treated
field
to
do
hand­
weeding,
thinning,
irrigation,
scouting
and
other
agricultural
activities.
At
this
time,
a
postapplication
exposure
assessment
was
not
performed
because
the
risk
to
workers
who
may
enter
the
treated
field
is
expected
to
be
negligible,
because
of
the
following
reasons:
(
i)
Outlook
®

Herbicide
formulation
is
used
as
a
pre­
emergence
herbicide
and
is
applied
without
the
need
for
any
soil
incorporation,
(
ii)
the
active
ingredient
in
the
formulation,
dimethenamid­
p,
has
a
low
acute
toxicity
profile
(
Toxicity
Category
III
for
acute
dermal,
acute
inhalation,
and
acute
eye
irritation;
and
Category
IV
for
acute
dermal
irritation,
and
(
iii)
the
product
has
a
12
hour
re­
entry
interval
(
REI)
and
the
label
specifies
adequate
PPE
in
the
Agricultural
Use
Requirements
box
of
the
label
for
protecting
the
workers
who
may
enter
the
treated
field
after
the
REI
period.
Based
on
the
acute
toxicity
categories,
the12­
hour
REI
is
appropriate.

An
occupational
risk
assessment
for
cancer
effects
to
handlers
and
agricultural
workers
from
the
use
dimethenamid­
p
on
green
bulb
vegetables
was
not
performed
here,
as
no
Q1*
was
established
by
HIARC.
30
of
30
10.0
Data
Needs
and
Label
Requirements
Toxicological
Profile
­
None
Residue
Chemistry
­
None
Occupational
Residential
Exposure
­
None
10.1
Occupational
and
Residential
Exposure
The
Outlook
Herbicide
formulation
is
a
skin
sensitizer;
but,
the
appropriate
warning
statement
is
missing
on
the
label.
Therefore,
HED
recommends
adding
the
following
language
to
the
Precautionary
Statements
section
of
the
label
"
Prolonged
or
frequently
repeated
skin
contact
may
cause
allergic
reaction
in
some
individuals."

References:

DP
Num:
316723;
S.
Oonnithan;
February
1,
2006;
Occupational
Exposure
Assessment
for
the
Proposed
Use
of
Outlook
Herbicide
(
EPA
Reg.
No.
7969­
156)
on
Green
Onion,
Leek,
Spring
Onion
or
Scallions,
Japanese
Bunching
Onion,
Green
Shallots,
or
Green
Eschalots.

DP
Num:
316226;
Christina
Swartz:
January
24,
2006;
Dimethenamid­
p:
Acute
and
Chronic
Dietary
Exposure
Assessment
for
Section
18
Emergency
Exemption
Request
for
the
use
of
Winter
Squash
in
Oregon.

PP#
4E6844;
DP
Num:
318282;
Shaja
Brothers,
in
process;
Dimethenamid­
p
Acute
and
Chronic
Dietary
Exposure
Assessments
for
the
Section
3
Registration
Action.

DP
Num:
304790;
Rich
Griffin;
August
12,
2004;
Dimethenamid/
Dimethenamid­
p:
Human
Health
Risk
Assessment.

DP
Num:
285455;
L.
Shanaman;
April
22,
2003;
IR­
4
Tolerance
Petition
for
Dimethenamide­
p
(
Outlook
and
Frontier
®
6.0)
Use
on:
Onion
(
Dry
Bulb),
Garlic,
Shallots
(
Dry
Bulb),
Tuberous
and
Corm
Vegetables,
Sugar
Beet,
Garden
Beet
and