Document ID: EPA-HQ-OPP-2003-0401-0004
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-12-12T05:00Z

1
UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
WASHINGTON,
D.
C.
20460
OFFICE
OF
PREVENTION,
PESTICIDES
AND
TOXIC
SUBSTANCES
TXR
No.
0051925
June
6,
2003
MEMORANDUM
SUBJECT:
OXADIAZON.
Response
to
the
60­
day
Comments
on
the
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED).
PC
Code:
109001,
Case
#
819425,
Submission
No.
S635115,
DP
Barcode
D290005
FROM:
Nancy
E.
McCarroll,
Toxicologist/
Risk
Assessor
Toxicology
Branch
Health
Effects
Division
(
7509C)

THRU:
Alberto
Protzel,
Ph.
D.,
Branch
Senior
Scientist
Toxicology
Branch
Health
Effects
Division
(
7509C)

TO:
Mark
Seaton,
Chemical
Review
Manager
Reregistration
Branch
II
Special
Review
and
Reregistration
Division
(
7508W)

Comments
received
from
the
registrant,
Bayer
Environmental
Science
(
formerly,
Aventis
Environmental
Science)
on
the
Human
Health
Risk
Assessment
for
the
reregistration
of
Oxadiazon
have
been
addressed
in
the
revised
HED
Chapter
of
the
RED.
The
revised
document
is
attached
and
the
revisions
are
as
follows:

cc:
Susan
Makris,
HED
Margaret
Rice,
SRRD
1
S.
C.
Price
(
1991).
Studies
on
Morphological
and
Biochemical
Changes
in
the
Livers
of
Rats
Treated
for
14
Days
with
Oxadiazon.
Robens
Institute
of
Health
and
Safety,
Surrey,
England;
Study
No.
R190/
0312;
Report
dated
January
9,

1991(
Unpublished)
MRID
No.
42310001.

2
Richert,
L.,
Price,
S.,
Chesne,
C.,
Maita,
K.
Carmichael,
N.
(
1996).
Comparison
of
the
induction
of
hepatic
peroxisome
proliferation
by
the
herbicide
oxadiazon
in
vivo
in
rats,
mice,
and
dogs
and
in
vitro
in
rat
and
human
hepatocytes.
Toxicol.
Appl.
Pharmacol
141:
35­
43.

3
HED
Memorandum,
Assessment
of
Mode
of
Action
on
Liver
Carcinogenicity,
February
28,
2001.
TXR
No.
0050506
2
Actions
in
Response
to
Bayer's
60­
Day
Comments
(
Report
dated
April
17,
2003)

I
GENERAL
COMMENTS
Global
Change
Throughout
the
Document
RESPONSE:
At
the
request
of
the
registrant,
the
names
"
Aventis
Enviromental
Science"
and
"
Aventis"
have
been
changed
throughout
the
Toxicology,
Occupational
and
Residential
Exposure
and
Chemistry
chapters
and
Health
Effects
Division's
(
HED's)
Risk
Assessment
Chapter
of
the
Reregistration
Eligibility
Decision
(
RED)
document
on
Oxidazion
and
now
read
"
Bayer
Enviromental
Science"
or
"
Bayer",
respectively.

II
COMMENTS
ON
TOXICOLOGY
ISSUES
a.
Lack
of
Agreement
with
the
Carcinogenicity
Peer
Review
Committee's
(
CARC)
classification
of
Oxadiazon
as
"
Likely
to
be
Carcinogenic
to
Humans"
because
Oxadiazon
is
a
peroxisome
proliferator.

Bayer
disagrees
with
the
CARC's
classification
of
Oxadiazon
as
a
"
Likely
to
be
Carcinogenic
to
Humans"
because
the
registrant
believes
that
"
the
available
evidence
indicates
that
Oxadiazon
belongs
to
the
peroxisome
proliferator
class
of
compounds.

RESPONSE:
Based
on
the
weight­
of­
the­
evidence,
the
HED's
Mechanism
of
Toxicity
Assessment
Review
Committee
(
MTARC),
which
convened
on
Feburary
8,
2001,
concluded
that
Oxadiazon
was
not
genotoxic.
Based
on
the
findings
from
a
14­
day
oral
mechanistic
study
in
rats
(
MRID
No.
42310001)
1
and
data
from
a
journal
article
(
Richert
et
al.,
1996)
2
that
was
found
and
extracted
by
our
reviewers,
MTARC
concluded
that
owing
to
shortcomings
in
the
database,
the
above
additional
pieces
of
information
do
not
convincingly
support
peroxisome
proliferation
as
the
non­
genotoxic
mode
of
action
for
Oxadiazon.
The
reasons
for
this
decision
were
outlined
in
the
Memorandum
of
Feburary
28,
20013
and
are
listed
below:
4
Shirasu,
Y.
(
1987).
Oxadiazon­
23
Month
Oral
Chronic
Toxicity
and
Oncogenicity
Study
in
Mice,
Institute
of
Environmental
Toxicology,
Mitsukaido
Laboratories,
Tokyo,
Japan,
Report
dated
February,
1987
(
Unpublished).
MRID
No.
40993301.

5
HED
Memorandum:
Lactofen:
Report
of
the
Mechanism
of
Toxicity
Assessment
Review
Committee,
dated
March
12,
2001.

6
HED
Memorandum:
Mechanism
of
Toxicity
SARC
Report:
Acifluorfen
(
PC
Code
114402),
dated
May
14,
2003.

3
1.
MTARC
follows
the
guidance
and
criteria
established
by
the
International
Life
Science
Institute
(
ILSI)
for
evaluating
peroxisome
proliferation
as
a
proposed
mode
of
action
for
non­
genotoxic,
tumorigenic
pesticides.
In
the
case
of
Oxadiazon,
there
is
ample
evidence
of
increased
liver
weights
in
both
sexes
of
several
rat
strains,
two
mouse
strains
and
Beagle
dogs
throughout
the
database.
However,
there
are
no
accompanying
studies
on
cell
proliferation
such
as
the
effect,
if
any,
of
Oxadiazon
on
replicative
or
scheduled
DNA
synthesis
(
SDS)
in
the
liver.
Positive
in
vivo
data
on
SDS
are
necessary
to
demonstrate
that
increased
liver
weight
is
associated
with
mitogenic
activity
and
not
with
cytotoxicity.
Additionally,
since
cell
proliferation
is
linked
directly
to
tumor
formation,
data
on
SDS
can
provide
a
sensitive
endpoint
for
a
possible
bench
mark
dose
analysis.

2.
MTARC
has
concerns
regarding
the
lack
of
concordance
between
the
dose
response
for
peroxisomal
enzymatic
activity
and
tumor
formation.
As
stated
in
the
MTARC
report,
Oxadiazon
induced
a
significant
increase
in
tumors
at
the
lowest
dose
tested
(
e.
g,
10.6
mg/
kg/
day)
in
the
submitted
mouse
chronic
toxicity
and
carcinogenicity
study
(
MRID
No.
40993301)
4
while
Richert
et
al.,
1996
reported
only
marginal
and
nonsignificant
activity
for
peroxisomal
palmitoyl
CoA
oxidase
(
PPCO)
after
mice
were
treated
for
14
days
with
a
higher
dose
(
20
mg/
kg/
day).
Similar
results
were
reported
in
mice
for
acetyl
carnitine
transferase
(
ACT).
Additionally,
only
a
slight
increase
in
the
number
of
peroxisomes
was
seen
by
Richert
et
al.,
1996
at
20
mg/
kg/
day.
These
findings
are
of
concern
because
changes
such
as
increased
peroxisomal
enzymes
or
increased
number
and
size
of
perixosomes
are
necessary
steps
in
tumors
formation.
Without
unambiguous
data,
the
Agency
is
reluctant
to
depart
from
satisfying
all
of
ILSI
criteria
for
peroxisome
proliferation.
Based
on
MTARC's
experience
with
peroxisome
proliferators,
it
was
further
stated,
that
increased
peroxisome
enzyme
activity
generally
occurs
(
regardless
of
the
time
interval)
at
doses
near
or
lower
than
the
tumorigenic
doses.
This
claim
is
supported
by
the
findings
from
mechanistic
studies
with
two
peroxisomal
proliferating
pesticides,
Lactofen5
and
Acifluorfen6
but
not
with
Oxadiazon.

3.
MTARC
continues
to
have
concerns
related
to
the
significance
of
decreased
catalase
activity
reported
in
the
14­
day
rat
study
(
MRID
No.
42310001).
Since
catalase
activity
is
a
marker
enzyme
for
the
peroxisome
organelle,
it
is
expected
to
7
Cattley,
R.
C.,
DeLuca,
J.,
Elcombe,
C.,
Fenner­
Crisp,
P.,
Lake,
B.
G.,
Marsman,
D.
S.,
Pastoor,
T.
A.,
Popp,
J.
A.,
Robinson,
D.
E.,
Schwetz,
B.,
Tugwood,
J.,
Wahli,
W.
(
1998).
Do
peroxisome
proliferating
compounds
pose
a
hepatocarcinogenic
hazard
to
humans?
Reg
Toxicol
and
Pharm
27:
47­
60.

4
increase
2­
fold
in
the
presence
of
a
peroxisome
proliferator7.
This
issue
was
not
addressed
in
the
14­
day
rat
study
or
in
the
60­
day
comment
document
prepared
by
the
Registrant.

4.
MTARC
also
believes
that
studies
in
mice
satisfying
all
of
ILSI's
criteria
are
necessary
before
the
Committee
will
reconvene
to
make
a
determination
on
Oxadiazon
b.
Lack
of
Agreement
with
the
Carcinogenicity
Peer
Review
Committee's
(
CARC)
classification
of
Oxadiazon
as
"
Likely
to
be
Carcinogenic
to
Humans"
because
humans
are
not
responsive
to
this
class
of
compounds.

Bayer
commented
that
since
Oxadiazon
is
a
peroxisome
proliferator
and
thus
a
rodent
carcinogen
with
a
threshold,
it
is
not
likely
to
present
a
risk
to
humans.

RESPONSE:
None
of
the
U.
S.
regulatory
agencies,
including
EPA
have
developed
a
policy
on
whether
pesticides
that
are
shown
to
be
rodent
peroxisome
proliferators
have
any
relevant
impact
on
human
health
and
risk
assessments.
The
Agency
is
working
closely
with
ILSI
on
this
issue
but
can
not
depart
from
established
policy
until
ILSI
has
released
its
final
report
on
peroxisome
proliferators.
Until
that
time,
the
Agency
can
not
rule
out
the
possibility
that
exposure
to
peroxisome
proliferators
negates
a
human
cancer
risk.
Nevertheless,
with
compelling
data
showing
that
Oxadizon
is
a
peroxisome
proliferator
(
see
Response
Section
II,
a)
combined
with
a
credible
dose
response
from
a
sensitive
endpoint,
the
Q
1
*
may
be
removed
and
the
risk
unit
may
be
expressed
based
on
a
benchmark
dose
analysis.
From
the
above
considerations
and
in
light
of
the
absence
of
new
data,
the
original
conclusion
rendered
by
the
MTARC
has
not
changed
and
is
reiterated
below:

"
The
Committee
concluded,
therefore,
that
peroxisome
proliferation
may
be
a
possible
mode
of
action
for
Oxadiazon­
induced
liver
tumors
in
rats
and
mice.
However,
because
of
shortcomings
in
the
data
base,
the
available
information
do
not
support
this
proposed
nongenotoxic
mode
of
action
for
Oxadiazon
at
this
time."

c.
Data
wavier
for
the
28­
day
inhalation
study
Bayer
requested
that
the
28­
day
inhalation
toxicity
data
requirement
be
waived
because
the
fine
aerosol
particles
used
in
guideline
inhalation
studies
(
MMAD
of
1­
4

m)
have
no
relevance
to
aerial
spraying
with
nozzles
that
produce
droplets
with
a
volume
median
diameter
(
VMD)
ranging
from
125­
250

m.
8
Technical
Committee
of
the
Inhalation
Specialty
Section,
Society
of
Toxicology.
Recommendations
for
the
Conduct
of
Acute
Inhalation
Limit
Tests.
Fundamental
and
Applied
Toxicology.
Volume
18.
1992.
Pages
321­
327.

9
John
E.
Whalan
and
John
C.
Redden.
Interim
Policy
for
Particle
Size
and
Limit
Concentration
Issues
in
Inhalation
Toxicity
Studies.
Health
Effects
Division.
February
1,
1994.
Docket
control
number
OPP­
00394.

5
RESPONSE:
It
is
a
common
misconception
that
the
small
particle
size
used
in
a
rodent
study
(
MMAD
of
1­
3
µ
m
in
acute
studies,
1­
4
µ
m
in
multiple
exposure
studies)
has
no
relevance
to
the
large
droplet
size
that
comes
from
medium
to
coarse
nozzles
during
spraying.
This
reasoning,
however,
cannot
be
used
to
justify
granting
a
waiver.

The
sprayed
VDM
to
which
humans
are
exposed
is
far
smaller
than
the
nozzle
VDM.
Pesticides
are
typically
mixed
with
large
quantities
of
water
before
spraying.
When
the
aqueous
mix
is
aerially
sprayed,
droplets
rapidly
shrink
as
they
fall
due
to
water
evaporation.
The
degree
of
shrinkage
depends
on
temperature,
relative
humidity,
particle
size,
and
the
length
of
time
that
the
droplets
are
suspended
in
the
air.
A
droplet
that
is
125­
250
µ
m
in
diameter
(
e.
g.,
VMD
for
Ronstar
®
)
when
it
leaves
the
nozzle
may
be
considerably
smaller
when
it
reaches
the
ground
(
perhaps
2­
15
µ
m).
Since
humans
are
capable
of
inhaling
particles
>
100
µ
m,
it
is
reasonable
to
expect
a
significant
portion
of
these
particles
to
be
inhaled.
While
most
large
particles
are
captured
in
the
nose,
some
are
capable
of
reaching
the
lungs.
Large
particles
have
the
potential
to
do
considerable
local
damage
if
they
are
absorbed
because
of
the
volume
of
material
they
contain.
HED's
waiver
criteria
state
that
a
product
formulation
or
application
method
can
be
considered
essentially
noninhalable
provided

99%
of
the
particles
are
>
100
µ
m
in
diameter.

Furthermore,
rats
have
tortuous
nasal
turbinates
that
are
extremely
efficient
at
removing
particles
from
inhaled
air,
hence
most
particles
larger
than
1­
2
µ
m
are
captured
in
the
rodent
nose.
By
contrast,
human
noses
are
far
less
efficient
at
removing
particles.
Rats
are
also
obligate
nose
breathers
while
humans
are
not,
so
whatever
protection
the
nose
provides
is
bypassed
when
humans
breathe
through
their
mouths.

The
OPPTS
Guidelines
require
an
MMAD
of
1­
3
µ
m
in
inhalation
toxicity
studies
of
aerosols
so
that
a
portion
of
the
test
article
will
reach
the
lungs.
If
rats
are
exposed
to
larger
particles,
the
lungs
will
be
virtually
unexposed.
While
lung
exposure
is
important,
inhalation
exposure
can
involve
the
entire
respiratory
tract.
Depending
on
the
physical
and
chemical
properties
of
the
active
ingredient,
absorption
and
portal­
of­
entry
effects
(
e.
g.
irritation,
edema,
cellular
damage,
etc.)
can
occur
anywhere
from
the
nose
to
the
alveoli.

These
issues
were
brought
to
HED's
attention
in
1991
when
the
Technical
Committee
of
the
Inhalation
Specialty
Section
of
the
Society
of
Toxicology
challenged
HED's
acute
inhalation
limit
test
and
particle
size
criteria.
8
These
issues
were
presented
to
the
Science
Advisory
Panel
on
December
15,
1993.
The
Interim
Policy
for
Particle
Size
and
Limit
Concentration
Issues
in
Inhalation
Toxicity
Studies9
summarizes
the
history
and
the
science
behind
these
issues
and
provides
the
policy
that
is
still
in
use
today.
It
describes
why
using
an
MMAD
of
1­
4
µ
m
in
acute
studies
and
1­
3
µ
m
in
multiple
exposure
studies
is
relevant
to
real
world
exposure
in
humans.
10
EFED
Memorandum:
Tier
II
Estimated
Drinking
Water
Concentrations
(
EDWCs)
for
Human
Health
Risk
for
Oxadiazon
on
Florida
Golf
Course,
DP
Code:
D281176,
dated
April
15,
2002.

6
Based
on
the
above
considerations,
granting
a
waiver
for
sprayed
products
based
on
the
disparity
between
laboratory
and
"
real­
world"
particle
sizes
would
go
against
HED
policy.

d.
Typographical
error
(
page
18)

RESPONSE:
The
typographical
error
noted
by
the
Registrant
("
For
the
long­
term
dermal
exposure,
an
oral
endpoint
was
also
selected
using
a
NOAEL
of
0.036
mg/
kg/
day....")
has
been
corrected
to
read:

"...
using
a
NOAEL
of
0.36
mg/
kg/
day...."

III.
COMMENTS
ON
WATER
ISSUES
a.
Estimated
drinking
water
concentration
from
surface
water
of
246

g/
L
(
acute
peak
value)/
Table
11a
Bayer
claimed
that
the
acute
surface
water
concentration
of
246

g/
L,
calculated
with
the
model
FIRST
was
an
overestimation
of
the
likely
exposure
and
also
cited
Table
11a.

RESPONSE:
A
Tier
II
estimated
drinking
water
concentration
(
EDWCs)
assessment
performed
by
the
Environmental
Fate
and
Effects
Division
(
EFED)
10
was
completed
in
April
2002
but
was
not
available
at
the
time
the
preliminary
Human
Health
Risk
Assessment
or
the
revised
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED)
were
released.
The
HED
chapter
has
now
been
revised
to
reflect
the
use
of
the
PRZM/
EXAMS
modeling
and
basing
the
EDWCs
for
Oxadiazon
on
the
proposed
maximum
application
rate
of
8.0
lbs
a.
i./
A
and
3
applications
to
a
golf
course
(
constituting
the
major
use
of
the
pesticide).
Accordingly,
the
acute
surface
water
concentration
of
246

g/
L,
calculated
with
the
model
FIRST
has
been
reduced
to
181

g/
L.
The
refined
value
has
been
incorporated
into
the
HED
Human
Health
Risk
Assessment
(
pp.
6,
21,
and
41
and
Table
11a)
and
the
EFED
chapter.

b.
Table
11b,
Chronic
DWLOC
Calculations
/
EDWC
from
surface
water
of
100

g/
L
is
an
overestimate
The
Registrant
claimed
that
the
chronic
surface
water
concentration
of
100

g/
L,
calculated
with
the
model
FIRST
was
an
overestimation
of
the
likely
chronic
exposure
and
also
cited
Table
11b.

RESPONSE:
A
Tier
II
estimated
drinking
water
concentration
(
EDWCs)
assessment
performed
by
11
Ibid
12
Ibid
7
the
Environmental
Fate
and
Effects
Division
(
EFED)
11
was
completed
in
April
2002
but
was
not
available
at
the
time
the
preliminary
Human
Health
Risk
Assessment
or
the
revised
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED)
were
released.
The
HED
chapter
has
now
been
revised
to
reflect
the
use
of
the
PRZM/
EXAMS
modeling
and
basing
the
EDWCs
for
Oxadiazon
on
the
proposed
maximum
application
rate
of
8.0
lbs
a.
i./
A
and
3
applications
to
a
golf
course
(
constituting
the
major
use
of
the
pesticide).
Accordingly,
the
chronic
surface
water
concentration
of
100

g/
L,
calculated
with
the
model
FIRST
has
been
reduced
to
65

g/
L
using
PRZM/
EXAM
modeling.
Despite
this
refinement,
the
chronic
DWLOCs
for
infants
and
children
(
36

g/
mL)
are
still
lower
than
the
refined
value
(
65

g/
L).
Therefore,
HED's
conclusion,
that
there
are
concerns
for
children
chronically
exposed
to
Oxadiazon
in
drinking
water
derived
from
surface
waters,
has
not
changed.
The
refined
values
and
appropriate
text
have
been
incorporated
into
the
HED
Human
Health
Risk
Assessment
(
pp.
6,
and
42
and
Table
11b)
and
the
EFED
chapter.

c.
Table
11c,
Chronic
Cancer
DWLOC
Calculations
/
EDWC
from
surface
water
of
100

g/
L
is
an
overestimate
The
Registrant
claimed
that
the
chronic
cancer
surface
water
concentration
of
100

g/
L,
calculated
with
the
model
FIRST
was
an
overestimation
of
the
likely
chronic
exposure
and
also
cited
Table
11c.

RESPONSE:
A
Tier
II
estimated
drinking
water
concentration
(
EDWCs)
assessment
performed
by
the
Environmental
Fate
and
Effects
Division
(
EFED)
12
was
completed
in
April
2002
but
was
not
available
at
the
time
the
preliminary
Human
Health
Risk
Assessment
or
the
revised
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED)
were
released.
The
HED
chapter
has
now
been
revised
to
reflect
the
use
of
the
PRZM/
EXAMS
modeling
and
basing
the
EDWCs
for
Oxadiazon
on
the
proposed
maximum
application
rate
of
8.0
lbs
a.
i./
A
and
3
applications
to
a
golf
course
(
constituting
the
major
use
of
the
pesticide).
Accordingly,
the
chronic
cancer
surface
water
concentration
of
100

g/
L,
calculated
with
the
model
FIRST
has
been
reduced
to
56

g/
L
using
PRZM/
EXAM
modeling.
Despite
this
refinement,
the
surface
water
cancer
DWLOC
for
the
U.
S.
population
(
0.49

g/
L)
remains
lower
than
the
refined
value
(
56

g/
L).
Therefore,
HED's
conclusion,
that
there
is
a
concern
for
lifetime
exposure
to
Oxadiazon
in
surface
and
ground
water,
remains
unchanged.
The
refined
values
and
appropriate
text
have
been
incorporated
into
the
HED
Human
Health
Risk
Assessment
(
p.
42,
Table
11c)
and
the
EFED
chapter.

IV.
COMMENTS
ON
EXPOSURE
ISSUES
a.
Harmonization
within
and
between
documents
Bayer
notes
that
page
5
of
the
Occupational
and
Residential
Exposure
(
ORE)
document
provides
a
8
use
figure
on
golf
courses
of
77%
while
the
Environmental
Fate
and
Effects
Division
(
EFED)
Risk
Assessment
uses
77%
or
65%.
The
use
figures
should
be
harmonized
within
and
between
the
different
documents.

RESPONSE:
This
error
has
been
corrected
in
the
revised
ORE
document.

Bayer
also
notes
that
page
8
of
the
ORE
document
provides
a
use
figure
on
golf
courses
of
71%
while
the
EFED
Risk
Assessment
uses
77%
or
65%.
The
use
figures
should
be
harmonized
within
and
between
the
different
documents.

RESPONSE:
This
error
has
been
corrected
to
77%
in
the
revised
ORE
document.

b.
Unacceptability
of
Transferable
Turf
Residue
(
TTR)
studies
(
MRID
44995501
and
­
02)

Bayer
finds
the
statement
and
the
conclusion
on
page
27
of
the
ORE
document,
to
be
confusing.
The
two
TTR
studies
(
MRID#
449955­
01
and
449955­
02)
were
apparently
not
accepted
by
EPA
because
they
used
the
modified
California
Roller
sampling
device
and
not
the
ORETF
device.
Bayer
refers
the
Agency
to
the
ORETF
submission
"
Evaluation
of
Transferable
Turf
Residue
Techniques
"(
MRID#
4497203)"
which
recommends
the
California
roller
as
the
ORETF
technique
for
conducting
TTR
studies.
Therefore,
why
were
the
studies
not
accepted
when
the
modified
California
Roller
technique
and
the
ORETF
Technique
are
identical
?

Bayer
is
also
concerned
about
the
statement
that
HED
does
not
considered
TTR
values
less
than
1%
of
the
application
rate
to
be
acceptable.
Granular
formulation
have
consistently
been
demonstrate
to
have
TTR
values
less
than
1%
of
the
application
rate.
This
statement
appears
to
relate
to
the
relationship
between
the
generic
residential
SOP
transfer
coefficients
of
14,500
cm2/
hr
and
8200
cm2/
hr
for
children
and
TTRs
less
than
1%
of
the
application
rate
(
HED
policy
12,
revised
22
February
2001).
Policy
12
states
that
the
revised
transfer
coefficients
should
not
be
used
with
TTRs
of
less
than
1%
of
the
application
rate.
Based
on
policy
12,
transfer
coefficients
of
43000
cm2/
hr
for
adults
and
8700
cm2/
hr
for
children
are
to
be
used
when
the
TTR
values
are
less
than
1%.
Therefore,
the
Oxadiazon
TTR
studies
not
considered
to
be
acceptable
should
be
reevaluated
and
used
with
higher
transfer
coefficients
if
the
TTRs
are
less
than
1%.

RESPONSE:
HED
agrees
that
the
California
roller
technique
is
the
most
efficient
of
all
the
measuring
techniques
to
collect
TTR
data.
However,
a
transfer
coefficient
(
TC)
measurement
should
be
taken
concurrently
with
the
TTR
measurement.
In
the
absence
of
a
concurrent
TC
measurement,
HED's
Expo
SAC
Policy
12
indicates
that
the
default
TC
values
and
5%
of
application
rate
for
TTR
should
be
used
to
estimate
short­
term
exposure.

In
the
submitted
Bayer
study,
the
TTR
values
measured
were
0.07%
of
application
rate
for
granular
and
0.15%
of
application
rate
for
liquid.
HED
Exposure
SAC
and
the
Oxadiazon
ORE
RED
chapter
clearly
address
this
policy
issue.
That
is,
if
either
condition
applies:
9
1)
TTR
collected
via
California
roller
technique
in
absence
of
concurrent
TC
values,
and/
or
2)
TTR
values<
0.5%
of
application
rate
for
granular
and
<
1%
for
liquid
applications
then,
HED
uses
default
values
as
per
residential
SOP
(
Policy
12,
revised
22
February
2001)
for
conducting
exposure
assessment.

The
use
of
low
TTRs
with
the
current
transfer
coefficients
may
underestimate
dermal
exposure.
HED
further
reviewed
Science
Advisory
Council
Exposure
Policy
12
(
February
22,
2001)
and
concluded
that
transfer
coefficients
of
43000
cm2/
hr
for
adults
or
8700
cm2/
hr
for
children
have
been
changed
to
14,500
cm2/
hr
for
adults
and
5,200
cm2/
hr
for
children
(
1­
6
yrs)
in
the
current
revised
SOP
(
February
22,
2001).
Based
on
these
considerations,
the
Agency
does
not
change
its
position
on
the
default
values
or
the
TCs
used
in
this
risk
assessment.

c.
Default
values
Bayer
contends
that
the
golf
course
TCs
developed
concurrent
TTR
monitoring
using
the
modified
California
method.
Therefore,
the
TTRs
obtained
from
the
submitted
Ronstar
WP
study
should
be
used
in
lieu
of
the
default
5%
value.

RESPONSE:
The
submitted
study
(
MRID#
43517801)
measured
the
exposure
associated
with
Jazzercise
on
turf.
Jazzercise
actions
are
significantly
different
from
golfing
actions,
therefore,
it
is
not
appropriate
to
use
the
TTR
values
obtained
from
this
study
as
surrogate
data.
HED
used
the
standard
default
value
from
the
SOP.

Bayer
further
contends
that
the
TTR
values
on
p.
35
of
the
ORE
document
should
be
based
on
the
result
of
the
Ronstar
WP
study
and
not
the
default
values
of
5%.
Defaults
stated
in
the
residential
SOPs
are
to
be
used
only
in
the
absence
of
chemical­
specific
data.

RESPONSE:
The
tables
on
pages
37
(
Table
8),
38
(
Table
9)
and
39
(
Table
10)
of
the
revised
Human
Health
Risk
Assessment
use
the
TTR
values
from
study
(
MRID#
43517801).
The
tables
also
show
the
risk
if
the
standard
default
value
is
used.
HED
typically
provides
a
range
of
risk
estimates
based
on
defaults
and
chemical
specific
data
to
SRRD,
if
required.
However,
risk
managers
base
their
final
decision
on
all
of
the
data
shown
for
these
scenarios.

d.
Table
verification
The
Registrant
believes
that
the
information
on
Table
10,
p.
39
should
be
verified.
Bayer
does
not
understand
how
the
percent
values
for
the
hand­
to­
mouth
activities
were
derived,
and
why
the
TTR
values
are
higher
for
the
exposure
from
irrigated
grass
than
the
one
for
the
non­
irrigated
grass,
while
the
TTR
based
on
study
MRID
43517801
indicates
the
reverse
situation.
Values
presented
in
Table
10,
MRID
43517801
are
different
from
the
values
presented
in
the
revised
Occupational
and
Residential
Exposure
Assessment
document
page
28
provides
the
following
TTR
values
for
non­
10
irrigated
and
the
irrigated
plots:
"
on
day
0,
the
highest
average
turf­
transferable
residues
(
TTR)
for
non­
irrigated
plots
was
1.22

g
per
cm2
and
0.694

g
per
cm2
on
irrigated
plot.".

RESPONSE:
The
turf­
transferable
residues
(
TTR)
values
indicated
on
page
28
of
the
ORE
document
were
obtained
from
the
study
MRID
43517801.
This
study
was
conducted
with
3.0
lb
ai/
A.
In
Tables
8,
9
and
10
the
TTR
values
have
been
adjusted
to
reflect
the
label
rate
of
4.0
lb
ai/
A.
A
correction
has
been
made
to
Table
10
in
the
revised
Human
Health
Risk
Assessment
and
in
the
ORE
document
to
present
the
correct
TTR
values
for
irrigated
grass
versus
non­
irrigated
grass.
HUMAN
HEALTH
RISK
ASSESSMENT
FOR
OXADIAZON
PC
Code
No.
109001
U.
S.
Environmental
Protection
Agency
Office
of
Pesticide
Programs
Health
Effects
Division
(
7509C)

Nancy
McCarroll,
Risk
Assessor
1
OXADIAZON
RISK
ASSESSMENT
TABLE
OF
CONTENTS
1.0
Executive
Summary
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
.
.
3
2.0
Physical/
Chemical
Properties
Characterization
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
8
3.0
Hazard
Characterization
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
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.
.
.
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.
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.
.
.
.
.
.
.
.
.
.
9
3.1
Hazard
Profile
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
9
3.2
FQPA
Considerations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
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.
.
.
.
.
.
.
12
3.3
Dose
Response
Assessment
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
17
4.0
Exposure
Assessment
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
20
4.1
Summary
of
Registered
Uses
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
20
4.2
Dietary
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
21
4.2.1
Food
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
21
4.2.2
Water
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
21
4.2.2.1
Surface
Water
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
21
4.2.2.2
Ground
Water
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
21
4.3
Occupational
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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22
4.3.1
Handler
.
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22
4.3.1.1
Noncancer
Handler
Exposures/
Risks
.
.
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23
4.3.1.2
Cancer
Handler
Exposures/
Risks
.
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26
4.3.2
Occupational
Postapplication
.
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31
4.3.2.1
Data
Sources
and
Assumptions
for
Scenarios
Considered
.
.
.
.
.
31
4.3.2.2
Postapplication
Exposure
Risk
Estimates
.
.
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.
32
4.3.3
Non­
Occupational
Postapplication
Exposures
with
Risk
.
.
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.
32
4.3.3.1
Non­
occupational
Postapplication
Dermal
Exposure
(
Adults
and
Toddlers)
.
.
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35
4.3.3.1.1
Data
Sources
and
Assumptions
for
Scenarios
Considered
.
.
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.
35
4.3.3.1.2
Non­
occupational
Postapplication
Dermal
Exposure
Risk
Estimates
.
.
.
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35
4.3.3.2
Incidental
Oral
Exposure
for
Toddlers
.
.
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36
4.3.4
Incident
Data
.
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40
5.0
Aggregate
Risk
Assessments
and
Risk
Characterization
.
.
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41
5.1
DWLOCs
for
Acute
Exposure
.
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41
5.2
DWLOCs
for
Chronic
Exposure
.
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41
5.3
DWLOCs
for
Cancer
.
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42
5.4
Aggregate
Risk
Assessment
.
.
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44
2
6.0
Cumulative
Risk
.
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44
7.0
Endocrine
Disruption
.
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45
8.0
Data
Needs/
Label
Requirements
.
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45
8.1
Toxicology
.
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45
8.2
Product
and
Residue
Chemistry
.
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46
8.3
Occupational
and
Residential
Exposure
.
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46
9.0
Attachments.
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..........................................................................
47
13
No
Observable
Adverse
Effect
Level
3
1.0
EXECUTIVE
SUMMARY
The
Agency
has
conducted
a
human
health
risk
assessment
for
the
active
ingredient
oxadiazon,
[
2­
tert­
butyl­
4­(
2,4­
dichloro­
5­
isopropoxyphenyl)­
delta
2­
1,3,4­
oxadiazolin­
5­
one],
for
the
purpose
of
making
a
reregistration
eligibility
decision.
Oxadiazon
is
a
selective
pre­
emergent
and
early
post
emergence
herbicide
registered
to
control
annual
grasses
and
broadleaf
weeds.
The
trade
name
for
oxadiazon
in
the
U.
S.
is
Ronstar
®
.
The
Registrant,
Bayer
Environmental
Science
is
supporting
use
of
oxadiazon
on
turf
(
e.
g.,
golf
courses,
apartment/
condo
lawns,
athletic
fields,
parks,
playgrounds
and
cemeteries)
and
ornamentals
(
Gorrell,
2001).
Like
other
oxadiazoles,
it
displays
light­
dependent
phytotoxicity
through
the
inhibition
of
protoporphyrinogen
oxidase,
an
enzyme
critical
in
the
biosynthesis
of
chlorophyl
and
heme.
Accumulation
of
protoporphyrin
IX
following
exposure
to
oxadiazon
has
been
demonstrated
in
plants,
yeast
and
mouse
liver
mitochondria.
Bayer
is
not
supporting
any
tolerances
for
oxadizon
in
the
United
States
(
Gorrell,
2001).
There
is
also
no
CODEX
(
Canadian
or
Mexican
tolerances)
for
oxadiazon
(
Piper,
2001a).
The
request
for
revocation
of
tolerances
for
residues
of
oxadiazon
on
food
and
feed
has
been
granted
and
tolerances
will
be
revoked
(
Piper,
2001b).
Since
only
the
non­
food
uses
of
oxadiazon
on
turf
and
ornamentals
will
be
retained,
it
has
been
determined
that
a
Food
Quality
Protection
Act
(
FQPA)
assessment
was
not
required.
Based
on
the
current
and
anticipated
use
patterns,
dietary
risk
assessments
are
also
not
required.

Oxadiazon
is
applied
via
hand
held
sprayers,
manual
spreaders
and
tractor­
drawn
equipment.
Aerial
application
was
voluntarily
canceled
by
the
Registrant.
This
pesticide
can
be
applied
at
a
frequency
of
1
to
3
applications
per
season
and
at
an
application
rate
of
2.0
to
4.0
pounds
ai/
acre.
Use
sites
include
golf
courses,
roadsides
and
nurseries.
In
addition,
oxadiazon
may
be
applied
by
commercial
operators
to
landscapes
(
which
could
include
residential
landscapes
such
as
apartment/
condo
lawns,
parks,
playing
fields
and
cemeteries),
and
these
use
patterns
indicate
a
potential
non­
occupational
exposure
for
adults
and
children.
Two
formulations
are
available:
wettable
powder
and
granular.

Oral
toxicity
is
well
characterized
for
oxadiazon
but
dermal
and
inhalation
toxicity
are
not.
Accordingly,
the
short
and
intermediate­
term
toxicological
endpoints
selected
for
the
dermal
and
inhalation
risk
assessments
were
based
on
an
oral
endpoint
from
a
rat
developmental
study.
In
this
study,
a
NOAEL13
of
12
mg/
kg/
day
was
selected
based
on
an
increased
incidence
of
fetal
loss.
A
dermal
absorption
rate
of
9%
was
applied
to
the
dermal
risk
assessments
and
a
100%
absorption
rate
was
applied
to
the
inhalation
risk
assessments.

In
both
subchronic
and
chronic
studies,
the
major
target
organ
of
oxadiazon
is
the
liver.
Effects
were
consistent
among
the
species
tested
(
rat,
dog,
mouse)
and
typically
included
enlarged
livers
along
with
increases
in
serum
clinical
chemistry
parameters
associated
with
hepatotoxicity.
The
hematopoietic
system
also
appeared
to
be
a
target
of
oxadiazon
in
all
three
species,
based
on
mild
14
Metabolism
Assessment
Review
Committee
15
Health
Effects
Division
16
Margin
of
Exposure
17
Personal
Protective
Equipment
4
anemia
(
reductions
in
RBC,
hematocrit
and/
or
hemoglobin).
This
is
consistent
with
its
ability
to
inhibit
protoporphyrinogen
oxidase.
In
a
rat
metabolism/
pharmacokinetic
study,
oxadiazon
was
extensively
metabolized,
primarily
via
hydroxylation
and
glucuronide
conjugation.
The
MARC14
concluded,
however,
that
the
only
residue
of
concern
is
the
parent
compound,
oxadiazon
because
major
degradates
would
only
be
minor
components
in
the
enviroment
and
are
not
likely
to
be
significantly
more
toxic
than
the
parent
(
Piper,
2001b).

The
Office
of
Pesticide
Programs
(
OPP)
Carcinogenicity
Peer
Review
Committee
(
CARC)
has
classified
oxadiazon
as
"
likely
to
be
carcinogenic
to
humans"
based
on
the
combined
incidence
of
male
mouse
liver
adenoma
and/
or
carcinoma
rates
in
the
ICR­
JCL
mouse
strain.
A
quantitative
risk
(
Q1*)
of
7.11
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents
was
used
for
the
human
health
risk
assessments.

Findings
from
reproduction
and
developmental
toxicity
studies
indicate
that
there
is
no
quantitative
evidence
of
increased
susceptibility
of
rats
or
rabbits
following
in
utero
or
postnatal
exposure
to
oxadiazon.
Similarly,
there
is
no
evidence
of
neurobehavioral
alterations,
neuropathological
effects
or
neurodevelopmental
potential
in
any
of
the
available
toxicity
studies.

HED15
has
determined
that
there
are
potential
exposures
to
occupational
mixers,
loaders,
applicators,
or
other
occupational
handlers
during
standard
use­
patterns
associated
with
oxadiazon.
Fourteen
major
exposure
scenarios
were
identified
for
occupational
exposure
of
handlers.
These
scenarios
include
mixing,
loading
and
applying
through
the
use
of
ground
spray,
granular
and
lawn
application
methods.
The
exposure
scenarios
are
of
short­
term
(
1­
7
days)
and
intermediate­
term
(
1
week
to
several
weeks);
use
patterns
do
not
indicate
any
long­
term
use.
The
target
MOE16
of
100
for
occupational
exposure
scenarios
was
selected
based
on
the
uncertainty
factors
of
10x
for
intraspecies
variation
and
a
10x
for
interspecies
extrapolation.
Since
the
effects
from
dermal
and
inhalation
exposure
are
based
on
the
same
oral
study
(
i.
e.,
rat
developmental
study),
the
doses
for
these
routes
and
durations
were
aggregated.

Calculation
of
non­
cancer
occupational
risk
based
on
combined
dermal
and
inhalation
exposure
indicates
that
with
the
exception
of
one
scenario
[
i.
e.,
low
pressure
handwand
­
wettable
powder
formulations
(
with
the
feasible
level
of
mitigation)],
all
other
potential
exposure
scenarios
provide
at
least
one
application
rate
with
total
MOEs

100
at
baseline
or
with
PPE17
or
engineering
controls.
Dermal
exposure,
rather
than
inhalation
exposure,
appears
to
be
the
main
contributor
to
the
total
MOE
for
the
low
pressure
handwand
­
wettable
powder
formulation
scenario
as
well
as
the
majority
of
occupational
exposures.
18
Turf
Transferable
Residue
5
Cancer
risks
for
occupational
dermal
and
inhalation
exposures
range
from
1.65E­
2
to
4.66E­
7
at
baseline,
1.05E­
3
to
1.38E­
7
with
PPE
or
4.92E­
5
to
1.10E­
8
with
engineering
controls.
Overall,
these
data
suggest
that
none
of
the
evaluated
scenarios
have
cancer
risks
that
exceed
1.00E­
4
(
the
Agency's
level
of
concern
for
occupational
cancer
risk
begins
at

1.00E­
4
with
all
attempts
to
mitigate
risks
to

1.00E­
6,
when
possible).

Postapplication
contact
of
workers
with
oxadiazon
is
generally
minimal
because
of
the
use
sites
(
turf,
conifer
nurseries,
sod
farms,
landscape­
industrial
sites
or
herbaceous
ornamental
crops
early
in
the
season,
either
pre­
plant
or
before
weeds)
and
the
mechanization
(
machine
harvesting
and
mowing)
utilized
in
cultivating
these
crops
reduces
the
postapplication
contact
of
workers
with
oxadiazon.
Nevertheless,
the
Agency
has
ascertained
that
there
are
potential
postapplication
exposures
to
individuals
re­
entering
treated
areas
associated
with
the
following
scenarios:
mowing
roadsides,
Bermuda
grass
right­
of­
ways,
sod
farms
and
golf
courses
as
well
as
harvesting
sod
farms.
Since
oxadiazon
is
not
volatile
(
has
a
low
vapor
pressure
of
1.0x10­
6
mm
Hg)
and
is
used
outdoors,
the
inhalation
component
of
postapplication
exposure
is
anticipated
to
be
negligible.
Hence,
the
dermal
route
is
the
route
of
consequence.
For
short
and
intermediate­
term
occupational
non­
cancer
risks,
transplanting
and/
or
harvesting
weeds
either
manually
or
mechanically,
had
MOEs
(
30)
that
failed
to
meet
the
target
MOE
of
100.
All
other
occupational
postapplication
activities
had
MOEs
of
1000.
Cancer
risks
for
occupational
postapplication
scenarios
were
estimated
not
to
exceed
HED's
level
of
concern
(
i.
e.,

1.00E­
4).

The
oxadiazon
labels
indicate
that
use
of
this
pesticide
is
limited
to
licensed
operators
and
the
product
is
not
available
to
homeowners.
However,
there
are
potential
postapplication
dermal
exposures
to
adults
and
toddlers
entering
oxadiazon­
treated
lawns
and
potential
postapplication
risks
to
toddlers
from
incidental
ingestion
of
turfgrass
and/
or
"
hand­
to­
mouth"
exposure
when
entering
lawns
treated
with
the
granular
and
wettable
powder
formulations.
For
these
assessments,
the
duration
of
postapplication
dermal
exposure
is
expected
to
be
either
short­
term
or
intermediate­
term,
based
on
oxadiazon
turf
residue
dissipation
data.
The
short­
term
and
intermediate­
term
MOEs
for
dermal
exposures
were
calculated
using
a
NOAEL
of
12
mg/
kg/
day;
this
value
was
derived
from
the
same
developmental
rat
study
used
for
the
occupational
handler
noncancer
exposures.
For
the
cancer
risk
estimates,
the
Q1*
of
7.11
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents
was
used.

Results
show
that
all
non­
cancer
dermal
scenarios
developed
for
adults
and
toddlers
had
short­
term
and
intermediate­
term
dermal
MOEs
greater
than
100.
The
cancer
risks
for
all
adult
residential
dermal
postapplication
exposures
fell
between
1.59x
10­
5
to
7.51
x
10­
7.

Estimated
incidental
oral
exposure
("
hand­
to­
mouth")
for
toddlers
had
an
MOE
of
100
using
the
TTR18
default
values
from
the
residential
SOP.
When
the
TTR
data
from
the
submitted
oxadiazon
study
were
used,
however,
the
MOEs
were
90
to
240.
The
former
MOE
does
not
exceed
the
target
19
Estimated
Drinking
Water
Concentrations
20
Drinking
Water
Levels
of
Concern
6
value
of
100;
nonetheless,
the
TTR
data
from
the
submitted
study
were
for
the
wettable
powder
formulation
and
the
major
use
of
oxadiazon
is
with
the
granular
formulation.
It
is
probable,
therefore,
that
the
risk
indicated
when
the
TTR
data
from
the
submitted
study
were
applied,
is
an
overestimate
and
not
likely
to
be
a
cause
for
concern.
MOEs
were
not
calculated
for
the
incidental
ingestion
of
oxadiazon
granules
because
an
acute
RfD
was
not
selected
for
this
non­
food
use
pesticide.
Additionally,
there
is
no
indication
from
the
studies
in
the
guideline
database
that
a
single
oral
exposure
to
oxadiazon
presents
a
hazard.
This
statement
is
also
supported
by
the
high
rat
acute
oral
LD50
for
oxadiazon
(>
5,000
mg/
kg).
It
is
thought,
therefore,
that
the
incidental
ingestion
of
granules
is
not
likely
to
be
a
cause
for
concern.

Monitoring
data
for
oxadiazon
residues
in
surface
and
ground
water
were
not
available.
Consequently,
potential
exposures
and
risks
from
oxadiazon
residues
in
unfinished
drinking
water
were
assessed
using
Tier
II
PRZM/
EXAM
(
surface
waters)
and
SCI­
GROW
(
ground
water)
modeling
estimates.
For
risk
assessment
purposes,
surface
water
EDWCs19
of
oxadiazon
were
an
acute
(
peak)
value
of
181
ppb
(

g/
L)
basing
the
EDWCs
for
Oxadiazon
on
the
proposed
maximum
application
rate
of
8.0
lbs
a.
i./
A
and
3
applications
to
a
golf
course
(
constituting
the
major
use
of
the
pesticide).
Ground
water
EDWCs
were
average
annual
value
of
100
ppb
(

g/
L).
These
values
generally
depict
worst­
case
scenarios,
and
represent
the
upper­
bound
estimates
of
the
concentration
that
might
be
found
in
surface
water
and
ground
water
due
to
the
use
of
oxadiazon
on
turf.
These
model
estimates
were
compared
to
DWLOCs20,
the
theoretical
concentration
of
pesticide
in
drinking
water
that
would
be
an
acceptable
upper
limit
in
light
of
the
aggregate
exposure
to
the
pesticide
from
other
sources.
Results
for
acute
DWLOC
calculations
show
that
acute
exposure
of
each
population
(
U.
S.
population,
females
13­
50
years,
children
1­
6
years
and
infants)
to
residues
of
oxadiazon
in
surface
and
ground
water
are
of
no
concern.
For
chronic
DWLOCs,
the
U.
S.
population
as
a
whole
had
a
DWLOC
value
that
exceeded
the
surface
and
ground
water
targets.
The
chronic
DWLOC
values
derived
for
infants
and
children
exceeded
the
EDWCs
for
ground
water
but
not
for
surface
water.
Despite
the
PRZM/
EXAM
modeling
for
surface
waters,
the
chronic
DWLOCs
for
infants
and
children
(
36

g/
L)
are
still
lower
than
the
refined
value
(
65

g/
L).
Hence,
the
Agency
has
concerns
for
children
chronically
exposed
to
oxadiazon
in
drinking
water
derived
from
surface
waters.
In
addition,
EDWCs
for
both
surface
and
ground
water
were
higher
than
the
cancer
DWLOC;
therefore,
the
cancer
risk
exceeds
HED's
level
of
concern
for
lifetime
exposure
to
oxadiazon
in
surface
and
ground
water.
It
should
be
noted,
however,
that
EDWC
values
derived
from
the
PRZM/
EXAM
and
SCI­
GROW
models
represent
the
compounding
of
several
worst
case
scenarios.
Similarly,
the
SCI­
GROW
model
used
for
the
ground
water
analysis,
is
based
on
high
concentrations
observed
in
shallow
ground
water
after
agricultural
treatment
of
permeable
soils.
Since
this
combination
of
conditions
is
encountered
in
only
1%
of
the
agricultural
use
area
in
the
U.
S.,
it
is
not
likely
that
oxadiazon
would
pose
a
potential
cancer
concern
for
exposure
to
oxadiazon
in
ground
water
(
Barrett,
1998).
21
Risk
Assessment
Committee
22
National
Pesticide
Telecommunication
Network
7
The
RARC21
recommended
that
an
aggregate
risk
assessment
not
be
conducted
on
oxadiazon
because
the
DWLOC
values
are
based
on
conservative
default
values
since
no
monitoring
data
were
available
on
oxadiazon
and
the
refined
model
for
turf
analysis
is
not
completed
at
this
time.
In
addition,
data
used
to
develop
residential
exposure
estimates
(
dermal
exposure
values)
were
also
conservative
because
the
highest
mean
postapplication
TTR
residue
value
from
the
submitted
study
along
with
the
data
from
the
wettable
powder
formulation
were
used
.
Thus,
any
aggregation
of
a
conservative
water
number
with
a
conservative
residential
exposure
estimate
would
result
in
an
even
more
conservative
expression
of
aggregate
risk.
The
RARC
also
noted
that
guidance
from
management
on
this
issue
is
forthcoming.

Oxadiazon
has
not
been
reported
to
cause
life­
threatening
illness
or
death
in
humans.
Most
of
the
cases
appear
to
be
related
to
irritation
to
the
skin,
eyes
and
mucous
membranes.
Some
cases
may
be
related
to
an
allergic
reaction.
On
the
list
of
the
top
200
chemicals
for
which
NPTN22
received
calls
from
1984­
1991
inclusively,
oxadiazon
was
ranked
192nd
with
12
incidents
in
humans
reported
and
5
incidents
in
animals
(
mostly
pets).

In
summary,
the
potential
risks
from
occupational
exposure
to
oxadiazon
are
generally
below
HED's
level
of
concern.
However,
even
with
the
feasible
level
of
mitigation,
there
is
one
occupational
exposure
scenario
(
i.
e.,
low
pressure
handwand­
wettable
powder
formulations)
and
there
are
postapplication
occupational
exposures
associated
with
transplanting
and/
or
harvesting
weeds
manually
or
mechanically
that
are
of
concern.
HED
also
had
concerns
for
chronic
and
lifetime
exposure
to
oxadiazon
in
drinking
water
derived
from
surface
and/
or
ground
water.
8
2.0
PHYSICAL/
CHEMICAL
PROPERTIES
CHARACTERIZATION
Oxadiazon
[
2­
tert­
butyl­
4­(
2,4­
dichloro­
5­
isopropoxyphenyl)­
delta­
2­
1,3,4­
oxadiazolin­
5­
one]
is
a
preemergence,
early
postemergence
herbicide
registered
to
control
annual
grasses
and
broadleaf
weeds.

Oxadiazon
Empirical
formula:
C15H18Cl
2N2O
3
Molecular
weight:
345.2
CAS
Registry
No.:
19666­
30­
9
PC
Code:
109001
Oxadiazon
is
an
odorless
white
crystalline
powder
with
a
melting
point
of
90

C,
a
density
of
1.3
gm/
mL
and
it
has
a
low
solubility
in
water
(
0.0007
g/
L
at
20

C).
It
is
stable
at
normal
and
elevated
temperatures
(
at
55

C),
stable
in
the
presence
of
metals
(
aluminum,
iron
and
tin)
and
metal
ions
(
ferric
chloride),
and
has
a
low
vapor
pressure
(
1.0x10­
6
mm
Hg).
A
single
manufacturing
use
product
(
MP)
registered
under
the
PC
Code
109001
was
identified
as
Bayer
Environmental
Science
USA
LP
94%
technical
(
T);
only
this
Bayer
94%
T
is
subject
to
the
RED
(
Dockter,
2001;
Piper,
2001).
The
Registrant
lists
oxadiazon
as
not
leaching
and
persistent
in
soil
(
Dockter,
2001).
Both
the
Product
Chemistry
and
the
Residue
Chemistry
databases
for
oxadiazon
are
complete.
9
3.0
HAZARD
CHARACTERIZATION
3.1
Hazard
Profile
Oxadiazon
is
a
selective
pre­
emergent
herbicide
of
the
oxadiazole
class.
Like
other
oxadiazoles,
it
displays
light­
dependent
phytotoxicity
through
the
inhibition
of
protoporphyrinogen
oxidase.
Accumulation
of
protoporphyrin
IX
following
exposure
to
oxadiazon
has
been
demonstrated
in
plants,
yeast
and
mouse
liver
mitochondria.

Details
of
the
hazard
assessment
of
oxadiazon
can
be
found
in
the
HED's
Toxicology
Disciplinary
Chapter
(
Hansen
and
McCarroll,
2001);
major
features
of
the
toxicology
profile
are
presented
below.
In
acute
studies,
oxadiazon
is
only
slightly
toxic
(
Toxicity
Categories
III
or
IV)
with
an
oral
LD
50
>
5000
mg/
kg,
a
dermal
LD
50
>
2000
mg/
kg
and
an
inhalation
LC
50
>
1.94
mg/
L.
Oxadiazon
is
mildly
irritating
to
ocular
tissue
and
negligibly
irritating
to
the
skin
(
both
Toxicity
Category
III)
and
is
not
a
dermal
sensitizer
(
Table
1).

Table
1.
Acute
Toxicity
Data
on
Oxadiazon
Guideline
No./
Study
Type
MRID
No.
Results
Toxicity
Category
870.1100
Acute
oral
toxicity
(
rat)
41866501
(
97.5%
a.
i.)
LD50
>
5000
mg/
kg

,

combined
IV
870.1200
Acute
dermal
toxicity
(
rabbit)
41866502
(
97.5%
a.
i.)
LD50
>
2000
mg/
kg,

,

combined
III
870.1300
Acute
inhalation
toxicity
(
rat)
41866503
(
93.7%
a.
i.)
LC50
>
1.94
mg/
L

,

combined
III
870.2400
Acute
eye
irritation
(
rabbit)
41866504
(
97.5%
a.
i.)
Mild
irritant
to
ocular
tissues
III
870.2500
Acute
dermal
irritation
(
rabbit)
41866505
(
97.5%
a.
i.)
Negligibly
irritating
to
skin
III
870.2600
Skin
sensitization
(
guinea
pig)
41230401
(
93.7%
a.
i.)
Not
a
dermal
sensitizer
(
Buehler
test)
­­

870.6200a
Acute
neurotoxicity
screening
battery
(
rat)
ND
­­
­­

ND
No
data
­
not
required
for
oxadiazon.

The
major
target
organ
of
oxadiazon
is
the
liver.
Effects
were
consistent
among
the
species
tested
(
rat,
dog,
mouse)
in
both
subchronic
and
chronic
studies
and
typically
included
enlarged
livers
along
with
increases
in
serum
clinical
chemistry
parameters
associated
with
hepatotoxicity
such
as
alkaline
phosphatase
and
serum
aspartate
or
alanine
aminotransferase.
Findings
in
rats
and
mice
23
Cancer
Assessment
Review
Committee
10
included
fatty
changes,
pigmented
Kupffer
cells
and
bile
canaliculi
and
bile
duct
proliferation,
periacinar
swelling
and
pallor,
increased
acidophilic
cells,
hyperplasia
and
hepatocellular
necrosis.
No
treatment­
related
microscopic
lesions
were
observed
in
the
subchronic
dog
study
and
findings
in
the
chronic
study
were
only
observed
at
the
highest
dose
tested
(
200
mg/
kg/
day),
where
only
two
animals/
sex
were
assigned
and
one
female
was
sacrificed
in
moribund
condition.
These
findings
included
increased
liver
weight
and
hepatocellular
histopathology
(
centriacinar
vacuolation,
periacinar
apoptosis
and
inflammation).
The
hematopoietic
system
also
appeared
to
be
a
target
of
oxadiazon
in
all
three
species,
based
on
mild
anemia
[
reductions
in
red
blood
cells
(
RBC),
hematocrit
and/
or
hemoglobin].
This
is
consistent
with
its
its
ability
to
inhibit
protopotphyrinogen
oxidase,
an
enzyme
involved
in
the
synthesis
of
both
heme
and
chlorophyll.
In
addition
to
effects
on
the
liver,
increased
pigmentation
in
the
kidney
was
observed
in
rats,
along
with
increased
blood
urea
nitrogen
(
BUN)
and
kidney
weights.
Although
a
dose­
dependent
increase
in
thyroid
weight
was
observed
in
the
dog
subchronic
oral
toxicity
study
and
at
the
highest
dose
tested
of
the
chronic
dog
studies,
treatment­
related
changes
in
thyroid
weights
or
gross/
microscopic
observations
were
not
observed
in
other
studies
(
thyroid
hormones
were
not
evaluated).
In
general,
males
appeared
to
be
slightly
more
sensitive
to
oxadiazon
than
females.

Oxadiazon
is
not
readily
absorbed
by
the
skin.
In
a
rat
dermal
absorption
study,
up
to

9%
of
the
applied
dose
of
technical
oxadiazon
was
absorbed
after
10
hours
of
exposure,
this
includes
2.65%
absorbed
and
6.07%
which
could
be
potentially
absorbed.
The
21­
day
rabbit
dermal
toxicity
study
supports
low
dermal
absorption:
no
toxicity
was
observed
at
the
limit
dose
of
1000
mg/
kg/
day.

Following
long­
term
dietary
administration,
oxadiazon
caused
an
increased
incidence
of
hepatocellular
adenoma
and
carcinoma
in
rats
and
mice.
Consistent
findings
were
reported
in
a
total
of
four
acceptable
studies
in
two
species
(
2
mouse
and
2
rat
studies).
A
third
mouse
study
was
unacceptable,
although
increased
hepatocellular
tumors
were
also
observed
in
mice
of
both
sexes.
In
CD­
1
mice,
statistically
significant
increases
of
hepatocellular
adenoma
and
combined
adenoma/
adenocarcinoma
were
observed
at
all
dose
levels
tested
(

100
ppm)
in
both
males
and
females.
The
incidence
of
hepatocellular
carcinoma
was
increased
at
all
doses
in
males
but
only
at
the
two
highest
doses
in
females.
The
highest
dose
tested
exceeded
the
maximum
tolerated
dose
(
MTD)
for
males,
based
on
excessive
mortality.
In
ICR­
JCL
mice,
adenomas,
carcinomas
and
combined
adenomas/
carcinomas
were
increased
in
males
at
the
two
highest
doses
but
only
at
the
highest
dose
in
females.
In
SPF
Wistar
rats,
the
incidence
of
hepatocellular
adenomas,
carcinomas
and
combined
adenomas/
carcinomas
was
increased
in
males
only.
A
second
study
in
F344
rats
showed
a
treatment­
related
increase
in
the
incidence
of
hepatocellular
carcinoma
and
combined
adenoma/
carcinoma
only
in
males.
A
classification
of
"
likely
to
be
carcinogenic
to
humans"
was
assigned
by
the
CARC23
using
the
EPA
Draft
Guidelines
for
Carcinogen
Risk
Assessment
of
July
1999
(
Diwan,
2001).
A
quantitative
risk
(
Q1*)
of
7.11
x
10­
2
(
mg/
kg/
day)­
1
was
calculated
as
the
most
potent
unit
risk,
based
on
the
incidence
of
male
mouse
liver
adenoma
and/
or
carcinoma
combined
tumor
rates
in
the
ICR­
JCL
mouse
(
Brunsman,
2001).
24
Mechanism
of
Toxicity
Assessment
Review
Committee
25
Hazard
Identification
Assessment
Review
Committee
11
In
a
special
submitted
mechanistic
study
in
rats
and
a
published
study
in
rats,
mice
and
dogs,
oxadiazon
induced
peroxisomal
proliferation
(
based
on
liver
enlargement,
peroxisomal
enzyme
induction
and
electron
microscopy)
after
a
14­
day
dietary
administration.
Some
peroxisomal
proliferator
compounds
are
known
to
be
liver
carcinogens,
but
the
HED
MTARC24
determined
that
there
are
insufficient
data
available
to
support
this
as
a
mechanism
of
carcinogenicity
for
oxadiazon
due
to
insufficient
data
showing
hepatocellular
proliferation,
lack
of
concordance
between
the
enzyme
induction
dose­
response
and
tumor
formation
and
an
unexplained
decrease
in
catalase,
which
is
normally
significantly
increased
by
peroxisomal
proliferator
compounds
(
McCarroll,
2001a).

Oxadiazon
did
not
show
mutagenic
potential
in
any
in
vitro
assays
with
bacteria
(
S.
typhimurium
and
E.
coli)
or
mammalian
cells
(
TK
+/­
mouse
lymphoma
cells),
did
not
show
clastogenic
potential
in
the
in
vitro
Chinese
hamster
ovary
cell
chromosomal
aberration
assays
and
did
not
induce
unscheduled
DNA
synthesis
in
cultured
primary
rat
hepatocytes.
However,
a
dose­
related
increase
in
transformation
frequencies
was
observed
in
an
in
vitro
Syrian
hamster
kidney
BHK21
C13/
HRC1
cell
transformation
assay.

Significant
fetal
toxicity
(
fetal
loss
due
to
resorptions
and
post­
implantation
loss,
decreased
fetal
weight,
skeletal
variations)
was
observed
in
developmental
toxicity
studies
in
both
rats
and
rabbits.
These
fetal
effects
occurred
at
the
same
dose
levels
at
which
slight
maternal
toxicity
(
decreased
weight
gain/
weight
loss)
were
observed.
Offspring
survival
effects
were
also
observed
in
the
rat
two­
generation
reproduction
study.
No
toxicity
was
reported
at
the
lowest
dose
tested;
however,
in
the
range­
finding
phase
of
the
reproduction
study
at
higher
dose
levels,
fetal
and
neonatal
survival
were
also
sharply
reduced.
The
decreased
neonatal
survival
was
due
at
least
in
part
to
effects
on
lactation,
based
on
findings
of
inactive
mammary
glands
in
the
dams
at
necropsy.
It
is
likely
that
neonatal
loss
may
have
resulted
from
starvation
and
would,
therefore,
be
an
effect
of
direct
maternal
toxicity.
Inactivity
of
the
mammary
tissue
as
a
possible
effect
of
endocrine
disruption
was
considered
by
the
HIARC25
but
was
not
found
to
be
likely
since
there
was
no
evidence
from
any
other
study
in
the
database
suggesting
endocrine
disruption
(
McCarroll,
2001
b).
No
fetal
malformations
were
observed
in
the
rat
or
rabbit
developmental
toxicity
studies;
however,
some
skeletal
variations
(
delayed
ossification,
asymmetric
pelvis)
were
reported.
The
above
findings
indicate
that
there
is
no
quantitative
evidence
of
increased
susceptibility
of
rats
or
rabbits
following
in
utero
or
postnatal
exposure
to
oxadiazon.

Neurotoxicity
studies
are
not
required
for
oxadiazon
because
no
clinical
signs
of
toxicity
suggestive
of
neurobehavioral
alterations
nor
evidence
of
neuropathological
effects
were
observed
in
any
of
the
available
toxicity
studies.
There
was
no
evidence
for
neurodevelopmental
potential
of
oxadiazon
in
the
rat
and
rabbit
developmental
toxicity
studies,
nor
in
the
rat
two­
generation
reproductive
toxicity
study.
12
In
a
rat
metabolism/
pharmacokinetic
study,
oxadiazon
was
extensively
metabolized,
primarily
via
hydroxylation
and
glucuronide
conjugation.
Eighteen
(
18)
metabolites
were
identified
in
the
urine
and
feces,
of
which
4
urinary
and
5
fecal
metabolites
were
present
at
levels
greater
than
1%
of
the
dose.
After
7
days,

83%
of
the
administered
dose
was
excreted
in
the
urine
and
feces
(
total
recovery

94%)
for
all
dose
groups.
Females
excreted
more
radioactivity
in
the
urine
than
males.
The
excretion
of
radioactivity
into
the
urine
and
the
feces
was
sex
dependent
and
the
tissue
residues
were
very
low
in
all
tissues
except
liver
and
fat.
Low
doses
(
5
mg/
kg,
single
or
multiple)
of
oxadiazon
were
completely
absorbed,
metabolized
and
excreted
in
the
urine
and
feces
and
virtually
no
free
oxadiazon
was
found
in
the
urine.
At
this
dose,
the
rates
and
routes
of
excretion
of
radioactivity
were
similar.
At
high
dose
(
500
mg/
kg),
the
rate
of
excretion
was
affected
but
the
route
was
not.
Intact
oxadiazon
was
present
in
feces
only
and
was
dose­
related:
at
the
high
dose,
more
than
53%
of
the
administered
radioactivity
was
intact
oxadiazon
in
the
feces;
at
5
mg/
kg,
not
more
than
4.8%
of
the
dose
was
intact
oxadiazon
in
the
feces.
Based
on
the
available
data,
the
MARC
concluded
that
the
only
residue
of
concern
is
the
parent
compound,
oxadiazon
because
major
degradates
would
only
be
minor
components
in
the
enviroment
and
are
not
likely
to
be
significantly
more
toxic
than
the
parent
(
Piper
2001b).
Subchronic,
chronic
and
other
types
of
toxicity
studies
are
summarized
in
Table
2.

The
only
data
gap
that
has
been
identified
at
this
time
is
a
28­
day
inhalation
study
(
OPPTS
No.
870.3465).
This
study
is
not
a
guideline
requirement
for
oxadiazon,
but
has
been
requested
by
the
Agency
because
some
currently
registered
products
of
oxadiazon
include
spray
formulations
(
McCarroll,
2001
b)
which
could
result
in
exposure
via
the
inhalation
route.

3.2
FQPA
Considerations
From
the
available
data,
it
was
concluded
that
there
is
no
quantitative
evidence
of
increased
susceptibility
of
rats
or
rabbits
following
in
utero
or
postnatal
exposure
to
oxadiazon.
However,
it
has
been
determined
that
an
FQPA
assessment
is
not
required
because
oxadiazon
has
no
food
or
feed
uses;
the
request
for
revocation
of
tolerances
for
residues
of
oxadiazon
on
food
and
feed
has
been
granted
and
tolerances
will
be
revoked
(
Piper,
2001b).
13
Table.
2
Subchronic,
Chronic
and
Other
Toxicity
Tables
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
SUBCHRONIC
TOXICITY
STUDIES
870.3100
90­
Day
oral
toxicity
(
CD
rat)
00111804
(
1970)
Acceptable/
guideline
0,
25,
100
or
1000
mg/
kg/
d
(
diet)
NOAEL
=
25
mg/
kg/
day
LOAEL
=
100
mg/
kg/
day
based
on
decreased
body
weight,
increased
liver
weight,
hematological
changes
and
clinical
chemistry
and
pathological
changes
associated
with
liver
damage.

870.3150
90­
Day
oral
toxicity
in
(
Beagle
dog)
00111805
(
1970)
Acceptable/
guideline
0,
25,
100
or
1000
mg/
kg/
d
(
capsule)
NOAEL
<
25
mg/
kg/
day
LOAEL

25
mg/
kg/
day
based
on
increased
thyroid
weights
in
males.

870.3200
21­
Day
dermal
toxicity
(
NZW
rabbit)
41863602
(
1991
)
Acceptable/
guideline
0,
100,
500
or
1000
mg/
kg/
day
NOAEL

1000
mg/
kg/
day.
LOAEL
>
1000
mg/
kg/
day.

DEVELOPMENTAL
AND
REPRODUCTIVE
TOXICITY
STUDIES
870.3700a
Prenatal
developmental
(
SD
rat)
40470202
(
1987)
Acceptable/
guideline
0,
3,
12
or
40
mg/
kg/
day
(
gavage)
Maternal
NOAEL
=
12
mg/
kg/
day.
LOAEL
=
40
mg/
kg/
day
based
on
decreased
body
weight/
weight
gain.
Developmental
NOAEL
=
12
mg/
kg/
day
LOAEL
=
40
mg/
kg/
day
based
on
increased
fetal
resorptions/
implantation
loss,
decreased
pup
weight
and
increased
incidence
of
incomplete
ossification.

870.3700b
Prenatal
developmental
(
NZW
rabbit)
40470201
(
1987)
Acceptable/
guideline
0,
20,
60
or
180
mg/
kg/
day
(
gavage)
Maternal
NOAEL
=
20
mg/
kg/
day
LOAEL
=
60
mg/
kg/
day
based
on
transient
weight
loss
during
the
first
week
of
treatment.
Developmental
NOAEL
=
60
mg/
kg/
day
LOAEL
=
180
mg/
kg/
day
based
on
increased
postimplantation
loss
and
late
resorptions,
decreased
fetal
weight
and
increased
bilateral
hind­
limb
flexure.

870.3800
Reproduction
and
fertility
effects
(
CD
rat)
41239801
(
1988)
Acceptable/
guideline
0,
20,
60
or
200
ppm
(
M/
F
0,
1.5/
1.84,
4.65/
5.63
or
15.50/
18.20
mg/
kg/
day,
premating)
Parental/
Systemic
NOAEL

15.5
mg/
kg/
day
LOAEL
>
15.5
mg/
kg/
day
(
decreased
gestational
weight
gain
in
RF
study
at
38
mg/
kg/
day).
Reproductive
NOAEL

15.5
mg/
kg/
day
LOAEL
>
15.5
mg/
kg/
day
(
inactive
mammary
tissue,
fetal/
neonatal
mortality
in
the
RF
study
at
38
mg/
kg/
day).
Offspring
NOAEL

15.5
mg/
kg/
day
LOAEL
>
15.5
mg/
kg/
day
(
fetal/
neonatal
mortality
in
the
RF
study
at
38
mg/
kg/
day).
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
14
CHRONIC
TOXICITY
AND
CARCINOGENICITY
STUDIES
870.4100a
Chronic
toxicity
(
rat)
See
870.4300,
Combined
chronic
toxicity/
carcinogenicity
870.4100b
Chronic
toxicity
(
Beagle
dog)
41326401(
1989)
Acceptable/
guideline
0,
5,
20
or
60
mg/
kg/
day
(
capsule)
NOAEL
=
5
mg/
kg/
day
LOAEL
=
20
mg/
kg/
day
based
on
increased
absolute
and
relative
female
liver
weight
accompanied
by
similar
changes
in
liver
weight
for
both
sexes
at
60
mg/
kg/
day.

870.4200
Carcinogenicity
(
CD­
1
mouse)
00044322
(
1980)
Unacceptable/
guideline
0,
300,
1000
or
2000
ppm
(
M/
F
0,
48/
62,
153/
201
or
319/
417
mg/
kg/
day),
in
diet
NOAEL
<
48
mg/
kg/
day
LOAEL

48
mg/
kg/
day
based
on
increased
liver
weight,
serum
enzymes
related
to
liver
damage
and
microscopic
pathology
in
the
liver
of
both
sexes.
Evidence
of
carcinogenicity­
increased
incidence
of
hepatocellular
carcinoma,
both
sexes
at

48/
62
mg/
kg/
day.

870.4200
Carcinogenicity
(
CD­
1
mouse)
00115733
(
1982)
Acceptable/
guideline
0,
100,
300,
1000
or
2000
ppm
(
M/
F
0,
12/
14,
37/
44,
122/
143
or
254/
296
mg/
kg/
day),
in
diet
NOAEL

12
mg/
kg/
day
LOAEL
<
12
mg/
kg/
day
based
on
clinical
signs,
increased
liver
weights
in
males
and
increased
microscopic
pathology
in
the
liver
of
both
sexes.
Evidence
of
carcinogenicity
­
increased
incidence
of
hepatocellular
neoplasms
(
adenoma,
combined
adenoma/
carcinoma)
in
both
sexes
at
all
doses
tested
(
carcinoma
alone
increased
in
all
male
groups
and
at

143
mg/
kg/
day
in
females).

870.4200
Carcinogenicity
(
ICR­
JCL
mouse)
40993301
(
1987)
Acceptable/
guideline
0,
3,
10,
100
or
1000
ppm
(
M/
F
0,
0.315/
0.278,
1.09/
0.92,
10.6/
9.3
or
113/
99
mg/
kg/
day),
in
diet
NOAEL
=
1.09
mg/
kg/
day
LOAEL
=
10.6
mg/
kg/
day
based
on
anemia
and
microscopic
lesions
in
the
liver
and
kidneys
(
all
in
males).
Evidence
of
carcinogenicity
­
increased
incidence
of
hepatocellular
neoplasms
(
adenomas,
carcinomas
and
combined
adenomas/
carcinomas
in
males
at

10.6
mg/
kg/
day
and
in
females
at
99
mg/
kg/
day).

870.4300
Combined
chronic
toxicity/
carcinogenicity
(
F344
rat)
00149003,
00157780
(
1982,
1986)
Acceptable/
guideline
0,
10,
100,
1000
or
3000
ppm
(
M/
F
0,
0.5/
0.6,
5.9/
4.8,
50.9/
60.9
or
163.1/
192.7
mg/
kg/
day,
in
diet
NOAEL
=
0.5
mg/
kg/
day
LOAEL
=
4.8
mg/
kg/
day
based
on
increased
liver
weights
in
both
sexes
and
increased
total
serum
protein
in
females.
Evidence
of
carcinogenicity
­
increased
incidence
of
hepatocellular
neoplasms
in
males
(
adenomas
and
combined
adenomas/
carcinomas
in
males
at

50.9
mg/
kg/
day).
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
15
870.4300
Combined
chronic
toxicity/
carcinogenicity
(
Wistar
rat)
40993401
(
1987)
Acceptable/
guideline
0,
3,
10,
100
or
1000
ppm
(
M/
F
0,
0.106/
0.131,
0.36/
0.44,
3.5/
4.2
or
39/
44
mg/
kg/
day)
NOAEL
=
0.36
mg/
kg/
day
LOAEL
=
3.5
mg/
kg/
day
based
on
increased
incidence
of
hepatocellular
centrilobular
swelling
in
males.
Evidence
of
carcinogenicity­
increased
incidence
of
hepatocellular
neoplasms
in
males
(
adenomas
and
combined
adenomas/
carcinomas
at

4.2
mg/
kg/
day
and
carcinomas
at
39
mg/
kg/
day).

MUTAGENICITY
AND
CELL
TRANSFORMATION
STUDIES
870.5100
Gene
Mutation
Bacterial
reverse
gene
mutation
assay
and
870.5500
Bacterial
DNA
Repair
Assay
00069893
(
1976)
Acceptable/
guideline
S.
typhimurium
and
E.
coli
100­
2500
and
10­
1000

g/
plate
w/
o
S9
and
10­
1000

g/
plate
w/
S9.
B.
subtilis
20­
2000

g/
plate
w/
o
S9.
Negative
in
S.
typhimurium
strains
TA1535,
TA1437,
TA1538,
TA98
and
TA100;
E.
coli
strain
WP2
hcr­
and
B.
subtilis
strains
H17
and
M45
(
cytotoxicity
not
observed
).

870.5100
Gene
Mutation
Bacterial
reverse
gene
mutation
assay
41871701
(
1991)
Acceptable/
guideline
50­
5000

g/
plate
w/
o
or
w/
S9.
Negative
in
S.
typhimurium
strains
TA1535,
TA1537,
TA1538,
TA98
and
TA100
(
cytotoxicity
observed
at

3330

g/
plate
w/
o
S9
but
not
w/
S9).
Insoluble
at

500

g/
plate.

870.5300
Gene
Mutation
In
vitro
mammalian
cell
forward
gene
mutation
assay
00115726
(
1982)
Acceptable/
guideline
15.6­
1000

g/
mL
(
Trial
1),
50­
1000

g/
mL
(
Trial
2),
both
w/
o
S9;
3.91­
62.5
(
Trial
1),
20­
100
(
Trial
2)
and
100­
200

g/
mL
(
Trial
3),
all
w/
S9.
Negative
in
L5178Y
TK+
mouse
lymphoma
cells
(
cytotoxicity
observed
at
1000

g/
mL
w/
o
S9
and

200

g/
mL
w/
S9).
Insoluble
at

62.5

g/
mL.

870.5300
Gene
Mutation
In
vitro
mammalian
cell
forward
gene
mutation
assay
00115729
(
1982)
Acceptable/
guideline
31.3­
1000

g/
mL
w/
o
S9
and
15.6­
250

g/
mL
w/
S9
Negative
in
L5178Y
TK+
mouse
lymphoma
cells
(
cytotoxicity
observed
at
1000

g/
mL
w/
o
S9
and
250

g/
mL
w/
S9).
Insoluble
at
250

g/
mL.

870.5375
Cytogenetics
In
vitro
mammalian
cell
chromosomal
aberration
assay
00115728
(
1982)
Acceptable/
guideline
2­
2000

g/
mL
w/
o
S9;
0.667­
2000

g/
mL
(
Trial
1)
and
200­
600

g/
mL
(
Trial
2),
both
w/
S9.
Negative
in
Chinese
hamster
ovary
(
CHO)
cells
(
cytotoxicity
observed
at
200

g/
mL
w/
o
S9
and
500

g/
mL
w/
S9).
Insoluble
at
667

g/
mL
w/
o
S9
and
200

g/
mL
w/
S9.
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
16
870.5375
Cytogenetics
In
vitro
mammalian
cell
chromosomal
aberration
assay
00115730
(
1982)
Acceptable/
guideline
0.416­
125

g/
mL
(
Trial
1)
and
12.5­
75

g/
mL
(
Trial
2),
both
w/
o
S9;
1.25­
125

g/
mL
w/
S9
(
trial
2).
Negative
in
Chinese
hamster
ovary
(
CHO)
cells
(
cytotoxicity
at
75

g/
mL
w/
o
S9
and
41.6

g/
mL
w/
S9).
Insoluble
at
416

g/
mL.

870.5395
Cytogenetics
Mammalian
erythrocyte
micronucleus
test
0073288
(
1980)
Unacceptable/
guideline
(
not
upgradable)
0,
500,
1000
or
2000
mg/
kg
100%
oxadiazon
Negative
up
to
limit
dose
of
2000
mg/
kg,
but
early
sampling
time
(
6
hr
post­
dosing)
may
have
missed
peak
time
of
mutagenic
effect.
No
signs
of
toxicity
were
observed.

870.5395
Cytogenetics
Mammalian
erythrocyte
micronucleus
test
0073289
(
1980)
Unacceptable/
guideline
(
not
upgradable)
0,
500,
1000
or
2000
mg/
kg
Negative
up
to
limit
dose
of
2000
mg/
kg
,
but
early
sampling
time
(
6
hr
post­
dosing)
may
have
missed
peak
time
of
mutagenic
effect.
No
signs
of
toxicity
were
observed.

870.5395
Cytogenetics
Mammalian
erythrocyte
micronucleus
test
00732890
(
1980)
Unacceptable/
guideline
(
not
upgradable)
0,
500,
1000
or
2000
mg/
kg
24865
RP
(
99%),
an
oxadiazon
impurity
Negative
up
to
limit
dose
of
2000
mg/
kg,
but
early
sampling
time
(
6
hr
post­
dosing)
may
have
missed
peak
time
of
mutagenic
effect.
Clinical
signs
of
toxicity
observed
at

1000
mg/
kg
including
2
deaths
at
2000
mg/
kg.

870.5550
Other
Effects
Unscheduled
DNA
synthesis
assay
00115723
(
1982)
Acceptable/
guideline
1.0
to
1000

g/
mL
Negative
in
primary
rat
hepatocytes
after
18
hrs
(
cytotoxicity
observed
at
100­
500

g/
mL).

870.5550
Other
Effects
Unscheduled
DNA
synthesis
assay
00115727
(
1982)
Acceptable/
guideline
0.5
to
50

g/
mL
Negative
in
primary
rat
hepatocytes
after
18
hrs
(
cytotoxicity
observed
at
50

g/
mL).
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
17
Nonguideline
Other
Effects
In
vitro
cell
transformation
00115703
(
1982)
Acceptable/
nonguideline
12.5­
200

g/
mL
w/
and
w/
o
S9
for
technical
oxadiazon;
25­
400

g/
mL
for
recrystallized
oxadiazon
(
100%)
w/
S9
or
w/
o
S9.
Positive,
dose­
related
induction
of
cell
transformation
above
background
levels
observed
w/
S9
and
w/
o
S9
activation
in
Syrian
hamster
kidney
cells
(
BHK21
C13/
HRC1
cells)
for
both
technical
and
recrystallized
oxadiazon.

METABOLISM,
DERMAL
PENETRATION
AND
SPECIAL
MECHANISTIC
STUDIES
870.7485
Metabolism
and
pharmacokinetics
(
Crl:
CD(
SD)
BR
rat)
42324701,
42663601
(
1992,
1993)
Acceptable/
guideline
5
mg/
kg
14C­
oxadiazon
(
single
dose),
5
mg/
kg
(
14­
day
dose
of
oxadiazon
+
1
dose
of
14C­
oxadiazon,
day
15)
or
500
mg/
kg
14Coxadiazon
(
gavage)
At
5
mg/
kg,
oxadiazon
is
completely
absorbed,
metabolized
and
excreted
in
urine
and
feces
(
no
parent
compound
in
urine;
<
5%
in
feces).
At
500
mg/
kg,
53%
of
administered
dose
was
excreted
in
feces
as
parent
compound.
For
both
groups,

83%
of
administered
dose
was
excreted
in
urine
and
feces
(
total
recovery

94%)
by
7
days'
post­
dosing.
Females
tended
to
excrete
more
radioactivity
in
urine
than
males.
Oxadiazon
was
metabolized
primarily
by
hydroxylation
and
glucuronide
conjugation,
but
benzene
and
pyrozolidine
rings
were
not
metabolized.
A
total
of
18
metabolites
were
identified
in
urine
and
feces
(
4
urinary,
5
fecal
metabolites
present
at
>
1%
of
administered
dose).

870.7600
Dermal
penetration
(
SD
rat)
44588101(
1996)
Acceptable/
guideline
5.45,
39.2
or
523

g/
cm2
(
exposure
times
of
0.5,
1,
2,
4,
10
or
24
hrs)
Total
absorption

9%
of
administered
dose
(
96%
a.
i.)
following
10
hr
exposure
(
2.65%
absorbed
and
6.05%
potentially
absorbed
by
skin).
Absorption
but
not
dermal
uptake
saturated
at
39.2
and
523

g/
cm2.

Special
studies
(
nonguideline)
­
Peroxisomal
proliferation
(
SD
rat)
42310001
(
1991)
Acceptable/
nonguideline
0,
20,
200
or
500
mg/
kg/
day
in
diet
for
14
days
NOAEL
<
20
mg/
kg/
day.

LOAEL
=
20
mg/
kg/
day,
based
on
increased
peroxisomal
enzyme
(
palmitoyl
CoA
and
acetylcarnitine
transferase)
activities.
At
200
mg/
kg/
day,
liver
enlargement
and
at
500
mg/
kg/
day,
ultrastructural
changes
(
peroxisomal
proliferation
and
microsomal
alterations)
were
also
observed.
However,
catalase
was
decreased
by
treatment.

NOAEL
No
Observable
Adverse
Effect
Level
LOAEL
Lowest
Observable
Adverse
Effect
Level
3.3
Dose
Response
Assessment
On
December
7,
2000,
the
Health
Effects
Division
(
HED)
Hazard
Identification
Assessment
Review
Committee
(
HIARC)
reviewed
the
recommendations
of
the
toxicology
reviewer
for
oxadiazon
with
regard
to
the
toxicological
endpoint
selection
for
use
as
appropriate
in
occupational/
residential
18
exposure
risk
assessments.
Based
on
these
deliberations,
the
HIARC
concluded
that
neither
an
acute
nor
a
chronic
reference
dose
was
required
because
there
are
no
food
or
feed
or
anticipated
food
or
feed
uses
for
oxadiazon.
The
HIARC
report,
nevertheless,
indicated
that
there
are
toxicological
endpoints
of
concern
for
oxadiazon.
A
short­
term
oral
endpoint
was
selected
for
incidental
oral
exposure
in
children,
using
a
No
Observed
Adverse
Effect
Level
(
NOAEL)
of
12
mg/
kg/
day
based
on
a
statistically
significant
decrease
in
maternal
body
weight
gains
at
40
mg/
kg/
day
(
LOAEL)
in
a
developmental
study
in
rats
(
McCarroll,
2001
b).

For
short­
term
and
intermediate
dermal
exposure,
an
oral
endpoint
was
selected
using
a
NOAEL
of
12
mg/
kg/
day
based
on
a
statistically
significant
decrease
in
maternal
body
weight
gains
at
40
mg/
kg/
day
(
LOAEL)
in
a
developmental
study
in
rats.
For
the
long­
term
dermal
exposure,
an
oral
endpoint
was
also
selected
using
a
NOAEL
of
0.36
mg/
kg/
day,
based
on
an
increased
incidence
of
hepatocellular
centrilobular
swelling
in
males
at
3.5
mg/
kg/
day
(
LOAEL)
in
a
combined
chronic/
oncogenicity
feeding
study
in
rats.
The
HIARC
recommended
that
a
dermal
absorption
factor
of
9%
(
rounded
up
from
8.7%)
be
used
in
the
calculations,
based
on
a
dermal
penetration
study.

Due
to
a
lack
of
inhalation
studies,
the
HIARC
selected
an
endpoint
from
oral
studies
for
inhalation
risk
assessments.
For
short
and
intermediate­
term
inhalation
exposure,
the
same
oral
study
was
chosen
as
for
dermal
exposure
of
this
duration,
with
a
NOAEL
of
12
mg/
kg/
day.
The
same
chronic/
oncogenicity
feeding
study
in
rats
chosen
for
dermal
exposure
of
this
duration
was
selected
for
the
long­
term
inhalation
exposure,
with
a
NOAEL
of
0.036
mg/
kg/
day.
An
absorption
factor
of
100%
was
applied
for
inhalation
exposures.
The
target
MOE
of
100
for
occupational
and
residential
exposure
scenarios
was
selected
based
upon
10x
for
intraspecies
variation
and
10x
for
interspecies
extrapolation.
Because
the
effects
from
dermal
and
inhalation
exposure
are
the
same,
the
doses
for
these
routes
and
duration
were
combined.
Dermal
and
incidental
oral
exposures
for
toddlers
were
also
combined
to
reflect
a
total
exposure
burden.

Since
1987,
the
Agency's
decision
on
the
carcinogenic
potential
of
oxadiazon
has
been
in
concurrence
with
the
Scientific
Advisory
Panel's
(
SAP)
classification
of
oxadiazon
as
a
Group
C
carcinogen
and
the
Q1*
has
been
set
at
1.4
x
10­
1(
mg/
kg/
day)­
1
in
human
equivalents.
Since
that
time,
new
chronic/
carcinogenicity
data
have
been
submitted
and
reviewed
by
the
CARC.
Based
on
this
revisit,
CARC
has
reclassified
oxadiazon
as
a
"
Likely
To
Be
Carcinogenic
To
Humans"
(
Diwan,
2001).
For
the
purpose
of
the
lifetime
cancer
risk
assessment
by
the
Agency,
the
most
potent
unit
risk,
Q
1
*,
is
that
for
male
mouse
liver
adenoma
and/
or
carcinoma
combined
tumor
rates
at
7.11
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents.
All
unit
risks
have
been
converted
from
animals
to
humans
by
use
of
the
3/
4'
s
scaling
factor
(
Brunsman,
2001).
The
endpoints
that
were
selected
for
this
risk
assessment
are
summarized
in
Table
3.
19
Table
3:
Endpoints
Selected
by
HIARC
for
Assessing
Occupational
and
Residential
Risks
for
Oxadiazon
EXPOSURE
SCENARIO
DOSE
(
mg/
kg/
day)
ENDPOINT
STUDY
Incidental
Oral,
Short­
Term
NOAEL=
12
Maternal
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL).
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Incidental
Oral,
Intermediate­
Term
NOAEL=
12
Maternal
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL).
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Dermal,
Short­
Term
NOAEL=
12
Maternal
effects/
Developmental
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL)
/
Increased
fetal
resorptions/
postimplantation
loss,
increased
incidence
of
incomplete
ossification
at
40
mg/
kg/
day
(
LOAEL).
For
this
risk
assessment,
the
dermal
absorption
rate
of
9%
is
applied.
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Dermal,
Intermediate­
Term
NOAEL=
12
Maternal
effects/
Developmental
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL)
/
Increased
fetal
resorptions/
postimplantation
loss,
increased
incidence
of
incomplete
ossification
at
40
mg/
kg/
day
(
LOAEL).
For
this
risk
assessment,
the
dermal
absorption
rate
of
9%
is
applied.
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Dermal,
Long­
Term
NOAEL=
0.36
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL)
/
Increased
centrilobular
swelling
in
male
livers
at
3.5
mg/
kg/
day
(
LOAEL).
For
this
risk
assessment,
the
dermal
absorption
rate
of
9%
is
applied.
Combined
Chronic
Feeding/
Oncogenicity
­
Rat
MRID
Nos.
40993401,
00149003/
00157780
Inhalation,
Short­
Term
NOAEL=
12
Maternal
effects/
Developmental
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL)
/
Increased
fetal
resorptions/
postimplantation
loss,
increased
incidence
of
incomplete
ossification
at
40
mg/
kg/
day
(
LOAEL).
For
this
risk
assessment,
route­
to­
route
extrapolation
and
a
100%
absorption
rate
are
applied
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Inhalation,
Intermediate­
Term
NOAEL=
12
Maternal
effects/
Developmental
effects
Reduced
body
weight/
body
weight
gain
at
40
mg/
kg/
day
(
LOAEL)
/
Increased
fetal
resorptions/
postimplantation
loss,
increased
incidence
of
incomplete
ossification
at
40
mg/
kg/
day
(
LOAEL).
For
this
risk
assessment,
route­
to­
route
extrapolation
and
a
100%
absorption
rate
are
applied.
Developmental
Toxicity
­
Rat
MRID
No.
40470202
Inhalation,
Long­
Term
NOAEL=
0.36
Increased
centrilobular
swelling
in
male
livers
at
3.5
mg/
kg/
day
(
LOAEL).
Route­
to­
route
extrapolation
and
a
100%
absorption
rate
aplied.
Combined
Chronic
Feeding/
Oncogenicity
­
Rat
MRID
Nos.
40993401,
00149003/
00157780
Cancer
Q
1*
of
7.11
x
10­
2
(
mg/
kg/
day)­
1
Significant
increase
(
pair­
wise
and
trend,
p<
0.01)
in
liver
adenomas
and
adenomas
and/
or
carcinomas
combined
in
males
at

9.3
mg/
kg/
day).
Combined
Chronic
Feeding/
Carcinogenicity
­
Mouse
MRID
Nos.
40993301
20
4.0
EXPOSURE
ASSESSMENT
4.1
Summary
of
Registered
Uses
Oxadiazon
is
applied
as
a
pre­
plant
or
pre­
emergent
herbicide
on
non­
food/
outdoor
crops.
The
Registrant,
Bayer
Environmental
Science
is
supporting
use
of
oxadiazon
on
turf
(
e.
g.,
golf
courses,
apartment/
condo
lawns,
athletic
fields,
parks,
playgrounds
and
cemeteries)
and
ornamentals
(
Gorrell,
2001).
Bayer
is
not
supporting
any
tolerances
for
oxadiazon
in
the
United
States
(
Gorrell,
2001).
There
is
also
no
CODEX
(
Canadian
or
Mexican
tolerances)
for
oxadiazon
(
Piper,
2001a).
The
request
for
revocation
of
tolerances
for
residues
of
oxadiazon
on
food
and
feed
has
been
granted
and
tolerances
will
be
revoked
(
Piper,
2001b).
Occupational
applications
(
i.
e.,
to
turf
and
ornamentals)
are
made
to
established
areas
such
as
lawns
or
golf
course
greens
prior
to
the
emergence
of
the
target
plant
species.
The
oxadiazon
labels
indicate
that
use
of
this
pesticide
is
limited
to
licenced
operators
and
the
product
is
not
available
to
homeowners.
Residential/
non­
occupational
applications
by
commercial
operators
are
made
to
residential
lawns,
parks,
cemeteries,
schools,
athletic
fields
and
golf
courses.
The
frequency
of
application
ranges
from
1
to
3
applications
per
season.
Oxadiazon
can
be
applied
at
a
minimum
application
rate
of
2.0
pounds
of
active
ingredient
(
ai)
per
acre
up
to
a
maximum
application
rate
of
4.0
pounds
ai/
acre
to
turf
and
ornamentals.
Oxadiazon
use
sites
are
classified
as
nonfood
sites
(
i.
e.,
primarily
golf
course
greens),
residential
outdoor
use,
roadside
and
nurseries.
The
granular
formulations
account
for
the
majority
of
oxadiazon
that
is
used
on
turf.

Occupational­
use
sites
include:

Oxadiazon
is
registered
for
occupational­
use
only
on
conifer
nurseries,
landscape
­
industrial
sites,
ornamental,
roadside
landscape
planting,
woody
ornamental
shrubs,
vines
and
trees,
herbaceous
ornamental,
and
turf
grass
for
lawns,
fairways,
and
sod
production.

Residential/
Non­
occupational­
use
sites
include:

Oxadiazon
is
registered
for
commercial
use
on
lawns
and
turf
grown
in
parks,
playgrounds,
athletic
fields,
cemeteries,
schools
and
other
residential
(
i.
e.,
residential
buildings)
areas.
It
is
also
used
on
sod
farms
and
golf
courses.

Methods
and
types
of
equipment
used:

Chemigation,
groundboom,
rights­
of­
way
sprayer,
handgun
sprayer,
tractor
drawn
spreader,
backpack
sprayer,
low
pressure
handwand,
high
pressure
handwand,
lawn
handgun,
belly
grinder
and
push
type
spreader
are
examples
of
the
application
equipment
associated
with
the
use
patterns
for
oxadiazon.
(
Aerial
application
was
voluntarily
canceled
by
the
registrant).
26
Estimated
Environmental
Concentrations
21
4.2
Dietary
Exposure
4.2.1
Food
Exposure
There
are
no
food
or
feed
or
anticipated
food
or
feed
uses
for
oxadiazon.
The
Registrant
is
not
supporting
any
tolerances
for
oxadiazon
in
the
United
States
(
Gorrell,
2001).
There
is
also
no
CODEX
(
Canadian
or
Mexican
tolerances)
for
oxadiazon
(
Piper,
2001a).
The
request
for
revocation
of
tolerances
for
residues
of
oxadiazon
on
food
and
feed
has
been
granted
and
tolerances
will
be
revoked
(
Piper,
2001a).
Consequently,
dietary
exposure
is
not
a
concern
for
this
product.

4.2.2
Water
Exposure
The
Enviromental
Fate
and
Effects
Division
(
EFED)
has
provided
a
surface
and
groundwater
analysis
for
oxadiazon
(
Melendez,
2001).
The
MARC
concluded
that
the
only
residue
of
concern
is
the
parent
compound,
oxadiazon
because
major
degradates
would
only
be
minor
components
in
the
environment
and
are
not
likely
to
be
significantly
more
toxic
than
the
parent
(
Piper,
2001b).
Thus,
they
are
not
likely
to
be
a
concern
in
surface
or
ground
water.
Based
on
environmental
fate
characteristics,
potential
exposures
and
risks
from
oxadiazon
residues
in
unfinished
drinking
water
were
assessed
using
Tier
II
PRZM/
EXAM
(
surface
waters)
and
SCIGROW
(
ground
water)
modeling
estimates.
For
risk
assessment
purposes,
surface
water
EDWCs26
of
oxadiazon
were
an
acute
(
peak)
value
of
181
ppb
(

g/
L)
using
PRZM/
EXAMS
modeling
and
basing
the
EDWCs
for
Oxadiazon
on
the
proposed
maximum
application
rate
of
8.0
lbs
a.
i./
A
and
3
applications
to
a
golf
course
(
constituting
the
major
use
of
the
pesticide).
The
EDWCs
for
groundwater
was
an
average
annual
value
of
100
ppb
(

g/
L).
These
values
generally
depict
worse­
case
scenarios,
and
represent
the
upper­
bound
estimates
of
the
concentration
that
might
be
found
in
surface
and
ground
water
due
to
the
use
of
oxadiazon
on
turf.
In
the
absence
of
oxadiazon
monitoring
data,
unique
turf
characteristics
(
i.
e.,
turf
offers
a
vegetation
interception
layer
that
prevents
rapid
deposition
of
pesticides
onto
the
surface
of
soil
and
promotes
runoff)
have
been
considered
in
the
rationale
for
developing
EDWCs.

4.2.2.1
Surface
Water
For
drinking
water
originating
in
surface
water
bodies,
an
acute
concentration
of
181

g/
L
was
used
to
evaluate
the
risk
to
human
health.
This
amount
represents
the
high­
end
value
that
might
be
found
in
a
small
drinking
water
reservoir.
A
chronic
value
of
100.0

g/
L
was
used
to
evaluate
the
chronic
and
cancer
risk
to
human
health.

4.2.2.2
Ground
Water
For
drinking
water
originating
in
ground
water,
the
SCI­
GROW
model
provided
a
value
of
27
Outdoor
Residential
Exposure
Task
Force
28
Lawn
Care
Operator
22
0.59

g/
L
to
evaluate
the
risk
to
human
health.
This
value
represents
the
ground
water
concentration
of
oxadiazon
at
the
maximum
allowable
rate
(
2
applications/
year
of
4lb.
ai/
acre).
It
also
assumes
that
the
ground
water
is
exceptionally
vulnerable
to
contamination.
This
estimate
is
applied
to
all
exposure
scenarios
regardless
of
the
duration
of
exposure
since
SCI­
GROW
calculates
only
the
90­
day
average
value.

4.3
Occupational
Exposure
HED
has
determined
that
there
are
potential
exposures
to
mixers,
loaders,
applicators,
or
other
handlers
during
standard
use­
patterns
associated
with
oxadiazon.
Although
postapplication
contact
of
workers
with
oxadiazon
is
minimal,
the
Agency
has
ascertained
that
there
are
potential
postapplication
exposures
to
individuals
re­
entering
treated
areas
associated
with
mowing
and
harvesting.

4.3.1
Handler
The
Agency
has
found
that
occupational
exposure
to
oxadiazon
via
the
dermal
and
inhalation
routes
of
exposure
may
occur
during
mixing,
loading
and
applying
through
the
use
of
ground
spray,
granular
and
other
lawn
application
methods.
Based
on
the
use
patterns,
14
major
occupational
exposure
scenarios
were
identified
for
oxadiazon:
(
1a)
mixing/
loading
wettable
powders
for
chemigation
application;
(
1b)
mixing/
loading
wettable
powders
for
groundboom
application;
(
1c)
mixing/
loading
wettable
powders
for
rights­
of­
way
sprayer;
(
2)
loading
granular
formulations;
(
3)
applying
with
a
groundboom;
(
4)
applying
with
a
rights­
of­
way
sprayer;
(
5)
applying
wettable
powders
for
handgun
applicators
(
ORETF)
27;
(
6)
applying
granular
with
a
tractor
drawn
spreader;
(
7)
backpack
sprayer
(
LCO)
28;
(
8)
low
pressure
handwand­
wettable
powder
formulations
(
LCO);
(
9)
high
pressure­
handwandwettable
powder
formulations
(
LCO);
(
10)
lawn
handgun­
wettable
powder
formulations
(
ORETF);
(
11)
granulars
with
a
push
type
spreader
(
ORETF)
and
(
12)
granulars
with
a
bellygrinder
(
LCO).
Typical
application
rates
for
oxadiazon
range
from
3
to
4
lb.
ai/
acre,
with
the
higher
rate
being
applied
to
golf
courses,
roadside
turf,
lawns,
parks,
recreational
areas
and
woody
ornamentals.

Since
the
use
patterns
for
oxadiazon
do
not
suggest
any
long
term
use,
exposure
scenarios
of
a
longer
duration
were
not
considered.
The
exposure
scenarios
are
of
short­
term
(
1­
7
days)
and
intermediate­
term
(
1
week
to
several
months).
The
estimated
exposures
considered
baseline
protection
(
long
pants,
long
shirts
and
no
gloves
­
dermal;
no
respirator
­
inhalation),
additional
PPE
(
long
pants,
long
shirts
and
chemical
resistant
gloves
and/
or
double
layer
of
clothing
­
dermal;
all
of
the
dermal
protection
plus
80%
protection
from
dust/
mist
respirator
­
inhalation),
and
engineering
controls
(
use
of
water
soluble
packages).
Handler
exposure
assessments
were
completed
by
EPA
using
baseline
exposure
scenarios
previously
noted
and,
if
required,
increasing
levels
of
risk
mitigation
(
PPE
and
29
Pesticide
Handlers
Exposure
Database
23
engineering
controls)
to
achieve
an
MOE
of
100
for
non­
cancer
risks.
For
cancer,
there
is
a
concern
for
risk
estimates
>
1.0x
10­
4.

Chemical­
specific
data
for
assessing
human
exposures
during
pesticide
handling
activities
were
not
submitted
to
the
Agency
in
support
of
the
reregistration
of
oxadiazon.
In
such
instances,
it
is
the
policy
of
the
HED
to
use
data
from
the
PHED29
Version
1.1
to
assess
handler
exposures
for
regulatory
actions
when
chemical­
specific
monitoring
data
are
not
available.
HED's
level
of
confidence
in
these
data
are
shown
in
the
occupational
and
residential
exposure
assessment
and
recommendations
for
oxadiazon
(
Tadayon,
2001).

4.3.1.1
Noncancer
Handler
Exposure/
Risks
The
short­
term
and
intermediate­
term
MOEs
for
dermal
and
inhalation
exposures
were
calculated
using
an
oral
NOAEL
of
12
mg/
kg/
day
for
both
exposure
durations
(
see
Section
3.3
Dose
Response
Assessment).
The
Agency
also
used
route­
to­
route
extrapolations
from
this
oral
study
for
both
exposure
assessments.
A
dermal
absorption
rate
of
9%
was
applied
to
the
dermal
exposure
assessments
and
an
inhalation
absorption
rate
of
100%
was
applied
to
the
inhalation
exposure
assessments.

The
results
of
the
short
and
intermediate­
term
handler
assessments
are
presented
in
Table
5
and
indicate
that
all
potential
non­
cancer
exposure
scenarios
provide
at
least
one
application
rate
with
a
total
MOE(
s)
greater
than
or
equal
to
100
at
either
the
baseline
(
i.
e.,
long
pants,
long
sleeved
shirts,
no
gloves)
using
open
systems,
PPE
(
i.
e.,
long
pants,
long
sleeved
shirts,
and
chemical
resistant
gloves
while
using
open
systems)
or
using
engineering
controls
(
i.
e.,
closed
systems).
The
only
exception,
with
the
feasible
level
of
mitigation,
is
scenario
8
(
low
pressure
handwand­
wettable
powder
formulations).
As
further
shown,
dermal
exposure
rather
than
inhalation
exposure
drives
the
total
MOE
for
scenario
8
as
well
as
the
majority
of
cases.
Total
MOEs
for
all
scenarios
range
from
2
to
3000
and
37
MOEs
were
calculated
for
the
various
application
rates.
The
data
show
that
baseline
or
mitigation
measures
raised
the
MOEs
to
values
greater
than
or
equal
to
100
for
all
scenarios
except
scenario
8.
24
Table
5:
Exposure
Variables
(
Noncancer),
MOEs
for
Uses
of
Oxadiazon
Exposure
Scenario
(
Scenario
#)
Crop
Type
App
Rates
(
lb
ai/
acre)
Daily
Acres
Treated
Dermal
MOEs
Inhalation
MOEs
Total
MOEs
Base
line
PPE
Eng.
Control
Base
line
PPE
Eng.
Control
Base
line
PPE
Eng.
Control
Mixer/
Loader
Mixing/
Loading
Wettable
Powders
for
Chemigation
Application
(
1a)
sod
farms
3
350
2
59
780
16
80
2900
2
35
610
Mixing/
Loading
Wettable
Powders
for
Groundboom
Application
(
1b)
conifer
nurseries,
woody
ornamentals
4
40
14
380
NA
100
520
NA
12
220
NA
herbaceous
ornamentals
3
40
18
510
NA
140
700
NA
16
300
NA
sod
farms
3
80
9
260
NA
70
350
NA
8
150
NA
golf
courses
4
40
14
380
NA
100
520
NA
12
220
NA
Mixing/
Loading
Wettable
Powders
for
Rights­
of­
Way
Sprayer
(
1c)
roadside
turf,
ornamentals
4
40
14
380
NA
100
520
NA
12
220
NA
Loading
Granular
formulations
(
2)
sod
farms,
conifers
forest
4
80
3000
NA
NA
1300
NA
NA
920
NA
NA
golf
course
turf,
parks,

recreational
areas
4
40
6000
NA
NA
2600
NA
NA
1800
NA
NA
woody
ornamentals
4
40
6000
NA
NA
2600
NA
NA
1800
NA
NA
Applicator
Applying
with
a
Groundboom
(
3)
sod
farms
3
80
2400
NA
NA
4100
NA
NA
1500
NA
NA
herbaceous
ornamentals
3
40
4800
NA
NA
8100
NA
NA
3000
NA
NA
golf
courses
40
3600
NA
NA
6100
NA
NA
2300
NA
NA
conifer
nurseries,
woody
ornamentals
4
40
3600
NA
NA
6100
NA
NA
2300
NA
NA
Applying
with
a
Rights­
of­
Way
Sprayer
(
4)
roadsides
4
40
38
130
NA
1200
1200
NA
37
120
NA
Table
5:
Exposure
Variables
(
Noncancer),
MOEs
for
Uses
of
Oxadiazon
Exposure
Scenario
(
Scenario
#)
Crop
Type
App
Rates
(
lb
ai/
acre)
Daily
Acres
Treated
Dermal
MOEs
Inhalation
MOEs
Total
MOEs
Base
line
PPE
Eng.
Control
Base
line
PPE
Eng.
Control
Base
line
PPE
Eng.
Control
25
Applying
Wettable­
Powders
for
Handgun
Applicators
(
ORETF)

(
5)
lawns,
parks,
recreational
areas
4
5
See
PPE
550
NA
36000
3600
0
NA
See
PPE
540
NA
Applying
Granular
with
a
Tractor
Drawn
Spreader
(
6)
sod
farms
4
80
2500
NA
NA
1900
NA
NA
1100
NA
NA
golf
courses
4
40
5100
NA
NA
3800
NA
NA
2200
NA
NA
Mixer/
Loader/
Applicator
Backpack
Sprayer
(
LCO)
(
7)
l
awn
s
,
gol
f
c
o
u
r
s
e
s
,

ornamentals
nurseries
4
5
See
PPE
160
NA
1200
1200
NA
See
PPE
140
NA
Low
Pressure
Handwand
­

Wettable
Powder
Formulations
(
LCO)
(
8)
lawns,
golf
courses,

nursery
stock
4
5
14
65
NF
33
160
NF
10
46
NF
High
Pressure
Handwand
­­

(
Wettable
Powder
Formulations)

(
9)
woody
ornamentals,

conifer
nurseries.
4
5
See
PPE
160
NA
300
300
NA
See
PPE
100
NA
Lawn
Handgun
(
Wettable
Powder
Formulations)
(
ORETF)

(
10)
ornamentals,
lawns,
parks
rec
areas
4
5
560
NA
NA
580
NA
NA
280
NA
NA
Granulars
with
a
Push
Type
Spreader
(
ORETF)
(
11)
lawns,
golf
courses,
parks,

rec
r
ea
t
iona
l
areas,

ornamentals
4
5
1100
NA
NA
4800000
NA
NA
1100
NA
NA
Granulars
with
a
Bellygrinder
(
LCO)
(
12)
golf
courses,
parks,
rec
areas.
4
1
200
NA
NA
2900
NA
NA
190
NA
NA
Baseline
dermal
unit
exposure
scenarios
includes
long
pants,
long
shirts
and
no
gloves.

Baseline
inhalation
unit
exposure
represents
no
respirator
PPE
dermal
unit
exposure
includes
long
pants,
long
shirts
and
gloves
for
scenarios
5,
7,
and
9.

PPE
dermal
unit
exposure
includes
long
pants,
long
shirts
gloves
and
double
layer
(
50%
protection)
for
scenarios
1a,
1b,
1c,
and
8.

PPE
inhalation
unit
exposure
represents
dust/
mist
respirator
(
80
%
protection)
for
scenarios
1a,
1b,
1c,
and
8.

Engineering
Control
dermal
unit
exposure
scenarios
includes
long
pants,
long
shirts,
gloves
and
water
soluble
packages
for
scenario
1a.

Engineering
inhalation
unit
exposure
represents
no
respirator.
NA
=
Not
applicable
NF
=
Not
Feasible
30
The
Agency
has
defined
a
range
of
acceptable
cancer
risks
based
on
a
policy
memorandum
dated
August
14,
1996,
by
then
Office
of
Pesticide
Programs
Director
Dan
Barolo.
This
memo
refers
to
a
predetermined
quantified
"
level
of
concern"
for
occupational
carcinogenic
risk.
Occupational
carcinogenic
risks
that
are
1
x
10­
6
or
lower
require
no
risk
management
action.
For
those
chemicals
subject
to
reregistration,
the
Agency
is
carefully
examining
uses
with
estimated
risks
in
the
10­
6
to
10­
4
range
to
seek
ways
of
cost­
effectively
reducing
risks.
If
carcinogenic
risks
are
in
this
range
for
occupational
handlers,
increased
levels
of
personal
protection
are
warranted
as
is
commonly
applied
with
noncancer
risk
estimates
(
e.
g.,
additional
PPE
or
engineering
controls).
Carcinogenic
risks
that
remain
above
1.0
x
10­
4
at
the
highest
level
of
mitigation
appropriate
for
that
scenario
remain
a
concern.

31
Lifetime
Average
Daily
Dose
26
4.3.1.2
Cancer
Handler
Exposure/
Risks
The
cancer
risk
assessments
for
handlers
used
baseline
exposure
scenarios
and,
as
needed,
increasing
levels
of
risk
mitigation
(
PPE
and
engineering)
to
achieve
cancer
risks
that
would
be
considered
of
no
concern.
According
to
Agency
policy30,
acceptable
cancer
risks
for
occupational
exposure
to
pesticides
varies
from
1
x
10­
4
to
1
x
10­
6,
depending
on
the
course
of
action
taken
by
the
Agency
as
outlined
in
the
policy
memo
on
this
subject.
The
Q
1*
used
in
this
risk
assessment
is
7.11
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents
(
see
Section
3.3
Dose
Response
Assessment).

Potential
cancer
risks
(
LADD31)
to
handlers
were
assessed
using
the
following
assumptions:

The
average
body
weight
of
70
kg
is
used,
representing
a
typical
adult.

Career
duration
is
assumed
to
be
35
years.
This
represents
a
typical
working
lifetime.

Lifetime
is
assumed
to
be
70
years.

Dermal
absorption
is
assumed
to
be
9%,
and
inhalation
absorption
is
assumed
to
be
100%
of
the
oral
dose.
The
dermal
and
inhalation
doses
were
added
together
to
represent
total
daily
dose.

In
addition,
two
exposure
frequencies
were
used
in
the
calculations,
the
first
represented
the
maximum
number
of
applications
per
site
per
season
to
represent
private
use
(
3),
and
the
second
frequency
applied
a
factor
of
ten
to
the
first
frequency
to
represent
commercial
handlers
making
multiple
applications
per
site
per
season
(
30).

The
results
of
the
short
and
intermediate­
term
handler
cancer
assessments
presented
in
Table
6
indicate
that
values
range
from
1.65E­
2
to
4.66E­
7
at
the
baseline
(
long
pants,
long
shirts
and
no
gloves),
2.56E­
3
to
4.11E­
7
at
PPE1
(
long
pants,
long
shirts,
gloves
and
no
respirator),
2.40E­
3
to
3.51
27
E­
7
at
PPE2
(
long
pants,
long
shirts,
double
layer,
gloves
and
no
respirator),
1.05E­
3
to
1.98E­
7
at
PPE3
Table
6:
Exposure
Variables
for
Handlers
with
Baseline
Exposure
Scenarios
and
Increasing
Levels
of
Risk
Mitigation
(
Cancer)
for
Uses
of
Oxadiazon
Exposure
Scenario
(
Scenario
#)
Crop/
Target
Appl
Rates
(
lb
ai/
acre)
Daily
Acres
Treated
Cancer
Base
line
PPE
1
PPE
2
PPE
3
PPE
4
Eng.
Control
Mixer/
Loader
Mixing/
Loading
Wettable
Powders
for
Chemigation
Application
(
1a)
sod
farms
3
350
1.65e­
03/

1.65e­
02
2.56e­
04/

2.56e­
03
2.40e­
04/

2.40e­
03
1.05e­
04/

1.05e­
03
8.90e­
05/

8.90e­
04
4.92e­
06/

4.92e­
05
Mixing/
Loading
Wettable
Powders
for
Groundboom
Application
(
1b)
conifer
nurseries,
woody
ornamentals
4
40
2.51e­
04/

2.51e­
03
3.89e­
05/

3.89e­
04
3.65e­
05/

3.65e­
04
1.60e­
05/

1.60e­
04
1.36e­
05/

1.36e­
04
7.49e­
07/

7.49e­
06
herbaceous
ornamentals
3
40
1.88e­
04/

1.88e­
03
2.92e­
05/

2.92e­
04
2.74e­
05/

2.74e­
04
1.20e­
05/

1.20e­
04
1.02e­
05/

1.02e­
04
5.62e­
07/

5.62e­
06
sod
farms
3
80
3.77e­
04/

3.77e­
03
5.84e­
05/

5.84e­
04
5.48e­
05/

5.48e­
04
2.39e­
05/

2.39e­
04
2.03e­
05/

2.03e­
04
1.12e­
06/

1.12e­
05
golf
courses
4
40
2.51e­
04/

2.51e­
03
3.89e­
05/

3.89e­
04
3.65e­
05/

3.65e­
04
1.60e­
05/

1.60e­
04
1.36e­
05/

1.36e­
04
7.49e­
07/

7.49e­
06
Mixing/
Loading
Wettable
Powders
for
Rights­
of­
Way
Sprayer
(
1c)
roadside
turf,
ornamentals
4
40
2.51e­
04/

2.51e­
03
3.89e­
05/

3.89e­
04
3.65e­
05/

3.65e­
04
1.60e­
05/

1.60e­
04
1.36e­
05/

1.36e­
04
7.49e­
07/

7.49e­
06
Loading
Granular
formulations
(
2)
sod
farms,
conifers
forest
4
80
3.28e­
06/

3.28e­
05
3.10e­
06/

3.10e­
05
2.68e­
06/

2.68e­
05
1.28e­
06/

1.28e­
05
8.63e­
07/

8.63e­
06
2.20e­
08/

2.20e­
07
golf
course
turf,
parks,

recreational
areas
4
40
1.64e­
06/

1.64e­
05
1.55e­
06/

1.55e­
05
1.34e­
06/

1.34e­
05
6.42e­
07/

6.42e­
06
4.31e­
07/

4.31e­
06
1.10e­
08/

1.10e­
07
woody
ornamentals
4
40
1.64e­
06/

1.64e­
05
1.55e­
06/

1.55e­
05
1.34e­
06/

1.34e­
05
6.42e­
07/

6.42e­
06
4.31e­
07/

4.31e­
06
3.29e­
08/

3.29e­
07
Applicator
Applying
with
a
Groundboom
(
3)
sod
farms
3
80
2.00e­
06/

2.00e­
05
2.00e­
06/

2.00e­
05
1.73e­
06/

1.73e­
05
1.41e­
06/

1.41e­
05
1.14e­
06/

1.14e­
05
4.94e­
07/

4.94e­
06
Table
6:
Exposure
Variables
for
Handlers
with
Baseline
Exposure
Scenarios
and
Increasing
Levels
of
Risk
Mitigation
(
Cancer)
for
Uses
of
Oxadiazon
Exposure
Scenario
(
Scenario
#)
Crop/
Target
Appl
Rates
(
lb
ai/
acre)
Daily
Acres
Treated
Cancer
Base
line
PPE
1
PPE
2
PPE
3
PPE
4
Eng.
Control
28
herbaceous
ornamentals
3
40
1.00e­
06/

1.00e­
05
1.00e­
06/

1.00e­
05
8.67e­
07/

8.67e­
06
7.06e­
07/

7.06e­
06
5.71e­
07/

5.71e­
06
2.47e­
07/

2.47e­
06
golf
courses
40
1.34e­
06/

1.34e­
05
1.34e­
06/

1.34e­
05
1.16e­
06/

1.16e­
05
9.42e­
07/

9.42e­
06
7.61e­
07/

7.61e­
06
3.29e­
07/

3.29e­
06
conifer
nurseries,
woody
ornamentals
4
40
1.34e­
06/

1.34e­
05
1.34e­
06/

1.34e­
05
1.16e­
06/

1.16e­
05
9.42e­
07/

9.42e­
06
7.61e­
07/

7.61e­
06
3.29e­
07/

3.29e­
06
Applying
with
a
Rights­
of­
Way
Sprayer
(
4)
roadsides
4
40
8.07e­
05/

8.07e­
04
2.60e­
05/

2.60e­
04
2.00e­
05/

2.00e­
04
2.40e­
05/

2.40e­
04
1.80e­
05/

1.80e­
04
NA
Applying
Wettable­
Powders
for
Handgun
Applicators
(
ORETF)
(
5)
lawns,
parks,
recreational
areas
4
5
See
PPE
5.57e­
06/

5.57e­
05
2.94e­
06/

2.94e­
05
5.50e­
06/

5.50e­
05
2.87e­
06/

2.87e­
05
NA
Applying
Granular
with
a
Tractor
Drawn
Spreader
(
6)
sod
farms
4
80
9.31e­
07/

9.31e­
06
8.23e­
07/

8.23e­
05
7.03e­
07/

7.03e­
06
3.95e­
07/

3.95e­
06
2.75e­
07/

2.75e­
06
1.82e­
07/

1.82e­
06
golf
courses
4
40
4.66e­
07/

4.66e­
06
4.11e­
07/

4.11e­
06
3.51e­
07/

3.51e­
06
1.98e­
07/

1.98e­
06
1.38e­
07/

1.38e­
06
9.11e­
08/

9.11e­
07
Mixer/
Loader/
Applicator
Backpack
Sprayer
(
LCO)
(
7)
l
awn
s
,
g
o
l
f
c
o
u
r
s
e
s
,

ornamentals
nurseries
4
5
See
PPE
2.13e­
05/

2.13e­
04
1.45e­
05/

1.45e­
04
1.93e­
05/

1.93e­
04
1.25e­
05/

1.25e­
04
NA
Table
6:
Exposure
Variables
for
Handlers
with
Baseline
Exposure
Scenarios
and
Increasing
Levels
of
Risk
Mitigation
(
Cancer)
for
Uses
of
Oxadiazon
Exposure
Scenario
(
Scenario
#)
Crop/
Target
Appl
Rates
(
lb
ai/
acre)
Daily
Acres
Treated
Cancer
Base
line
PPE
1
PPE
2
PPE
3
PPE
4
Eng.
Control
29
Low
Pressure
Handwand
­
Wettable
Powder
Formulations
(
LCO)
(
8)
lawns,
golf
courses,
nursery
stock
4
5
3.10e­
04/

3.10e­
03
1.56e­
04/

1.56e­
03
1.38e­
04/

1.38e­
03
8.30e­
05/

8.30e­
04
6.50e­
05/

6.50e­
04
NA
High
Pressure
Handwand
­­
(
Wettable
Powder
Formulations)
(
9)
woody
ornamentals,
conifer
nurseries.
4
5
See
PPE
1.88e05/

1.88e­
04
1.20e­
05/

1.20e­
04
1.98e­
05/

1.98e­
04
1.31e­
05/

1.31e­
04
NA
Lawn
Handgun
(
Wettable
Powder
Formulations)
(
ORETF)
(
10)
ornamentals,
lawns,
parks
rec
areas
4
5
1.06e­
05/

1.06e­
04
1.06e­
05/

1.06e­
04
8.03e­
06/

8.03e­
05
6.44e­
06/

6.44e­
05
3.89e­
06/

3.89e­
05
NA
Granulars
with
a
Push
Type
Spreader
(
ORETF)
(
11)
lawns,
golf
courses,
parks,

r
ec
r
eat
iona
l
areas
,

ornamentals
4
5
2.33e­
06/

2.33e­
05
1.80e­
06/

1.80e­
05
No
data
1.80e­
06/

1.80e­
05
No
data
NA
Granulars
with
a
Bellygrinder
(
LCO)
(
12)
golf
courses,
parks,
rec
areas.
4
1
1.61e­
05/

1.61e­
04
1.50e­
05/

1.50e­
04
9.60e­
06/

9.60e­
05
1.42e­
05/

1.42e­
04
8.77e­
06/

8.77e­
05
NA
Baseline
dermal
unit
exposure
scenarios
includes
long
pants,
long
shirts
and
no
gloves.

PPE
1
cancer
risk
includes
long
pants,
long
shirts,
gloves
and
no
respirator.
30
PPE
2
cancer
risk
includes
long
pants,
long
shirts,
double
layer,
gloves
and
no
respirator.

PPE
3
cancer
risk
includes
long
pants,
long
shirts,
gloves
and
respirator.

PPE
4
cancer
risk
includes
long
pants,
long
shirts,
double
layer,
gloves
and
respirator.

Engineering
Control
dermal
unit
exposure
scenarios
includes
long
pants,
long
shirts,
gloves
and
water
soluble
packages.

Engineering
inhalation
unit
exposure
represents
no
respirator.
31
(
long
pants,
long
shirts,
gloves
and
respirator),
8.90E­
4
to
1.38E­
07
at
PPE4
(
long
pants,
long
shirts,
double
layer,
gloves
and
respirator)
and
4.92E­
5
to
1.10E­
8
at
engineering
control.
Overall,
these
data
show
that
none
of
the
evaluated
scenarios
have
cancer
risks
that
exceed
1.00E­
4
at
the
highest
feasible
level
of
mitigation.

4.3.2
Occupational
Postapplication
HED
uses
the
term
"
post­
application"
to
describe
those
individuals
who
can
be
exposed
to
pesticides
after
entering
areas
previously
treated
with
pesticides
and
performing
certain
jobs,
tasks
or
activities
(
also
often
referred
to
as
reentry
exposure).
Most
of
the
oxadiazon
used
in
agriculture
is
applied
either
pre­
plant
or
when
the
crops
are
quite
small
(
early
post­
emergence).
This
information
together
with
the
degree
of
mechanization
minimizes
the
postapplication
contact
of
workers
with
oxadiazon.
Nevertheless,
the
Agency
has
determined
that
there
are
potential
postapplication
exposures
to
individuals
re­
entering
oxadiazon
treated
areas
for
the
purpose
of:

c.
Roadsides:
mowing
d.
Bermuda
grass
rights­
of­
way:
mowing
e.
Sod
farms:
mowing
and
harvesting
f.
Golf­
course
turfgrass:
mowing
4.3.2.1
Data
Sources
and
Assumptions
for
Scenarios
Considered
Based
on
data
submitted
for
reregistration,
it
can
be
assumed
that
the
most
common
postapplication
exposures
will
occur
for
workers
on
turf.
Based
on
label
restrictions
and
patterns
of
use,
oxadiazon
is
applied
early
in
the
season,
either
pre­
plant
or
before
weeds
emerge
(
pre­
emergence).
Mowing
would
be
a
common
postapplication
activity
after
either
spraying
method.
Treated
turf
or
grasses
will
routinely
require
reentry
activities,
such
as
mowing
and
watering,
and
eventually
harvesting
in
the
case
of
sod
farms.
Although
two
transferable
turf
residue
(
TTR)
studies
and
one
Jazzercize
study
(
MRID
No.
43517801)
were
submitted
in
support
of
the
reregistration
of
oxadiazon,
only
the
Jazzercize
study
was
found
to
be
acceptable
for
this
assessment
because
the
TTR
values
obtained
from
the
two
TTR
studies
were
less
than
1%.
TTR
values
less
than
1%
are
not
considered
acceptable
by
HED
since
the
submitted
studies
were
performed
with
a
modified
California
Cloth
Roller
sampling
device,
which
has
been
replaced
with
new
equipment
accredited
by
ORETF.
TTR
values
derived
from
a
modified
California
Cloth
Roller
sampling
device
can
be
used
if
accompanied
by
concurrent
transfer
coefficient
measurements.
This
was
not
the
case
for
oxadiazon.

The
TTR
value
from
the
Jazzercise
study
utilized
a
wettable
powder
formulation
which
by
far
has
a
higher
potential
for
exposure
than
the
oxadiazon
granular
formulations.
Since
a
majority
of
the
total
use
involves
granular
formulations,
using
wettable
powder
TTR
values
is
a
conservative
approach
and
can
be
considered
the
upper
level
estimates
of
exposure.

A
linear
regression
to
calculate
a
dissipation
rate
(
T
½
)
for
oxadiazon
TTR
from
irrigated
and
nonirrigated
test
sites
was
performed,
using
all
non­
zero,
uncorrected,
averaged
data
point
from
DAT­
0
32
Agricultural
Reentry
Task
Force
32
through
DAT­
7.
Calculated
dissipation
half­
lives
for
the
irrigated
plot
was
1.7days
(
R2=
0.64)
and
for
the
non­
irrigated
plot
was
1.4
days
(
R2=
0.64)

Because
oxadiazon
has
a
low
vapor
pressure
(
1.0
x
10­
6mm
Hg)
and
is
only
used
outdoors,
the
inhalation
component
of
postapplication
exposure
is
anticipated
to
be
negligible.
Therefore,
all
calculations
of
postapplication
risk
estimates
have
been
done
for
dermal
exposure
only,
and
there
was
no
need
to
aggregate
postapplication
exposure
routes
for
workers.

4.3.2.2
Postapplication
Exposure
Risk
Estimates
For
turf
or
sod
mowing
and
harvesting,
transfer
coefficients
of
500
and
16,500
cm2/
hr
were
used,
based
on
the
ARTF
32
data.
The
TTR
values
are
assumed
to
be
5%
of
the
application
rate
on
Day
0
for
turfgrass
application
(
the
5%
rate
for
turfgrass
in
the
high
end
of
the
values
observed
in
the
studies
of
Hurto
and
Prinster,
1993;
Goh
et
al.,
1986
and
Cowell
et
al.,
1993).
As
shown
in
Table
7,
short
and
intermediate­
term
exposures
for
noncancer
risks
had
estimated
MOEs
of
300­
10,000,
which
exceed
the
target
value
of
100.
Similarly,
occupational
postapplication
cancer
risks
were
estimated
to
fall
within
the
acceptable
range
of
1
x
10­
4
to
1
x
10­
6.

4.3.3
Non­
Occupational
Postapplication
Exposures
and
Risk
The
Agency
has
determined
that
there
are
potential
postapplication
exposures
to
residents
entering
oxadiazon
treated
lawns,
either
as
a
result
of
commercial
or
private
application.
The
scenarios
likely
to
result
in
postapplication
exposures
are:

$
dermal
postapplication
risks
to
adults
and
toddlers
(
defined
as
5<
12
years
old
and
considered
by
HED
to
be
the
most
sensitive
subpopulation
of
children)
when
entering
oxadiazon­
treated
turf
and
lawns;

$
oral
postapplication
risks
to
toddlers
from
"
hand­
to­
mouth"
(
i.
e.,
ingestion
of
grass,
soil,
granular
pellets,
or
hand­
to­
mouth
contact)
exposure
when
reentering
lawns
treated
with
granular
and
wettable
powder
formulations.

Representative
turf
reentry
activities
include,
but
are
not
limited
to:

(
1)
Adults
involved
in
a
low
exposure
activity,
such
as
golfing
or
walking
on
treated
turf.
(
2)
Toddlers
involved
in
a
low
exposure
activity,
such
as
walking
on
treated
turf.
(
3)
Adults
mowing
or
other
moderate
contact
activity,
for
1­
2
hours.
(
4)
Adults
involved
in
a
high
exposure
activity,
such
as
heavy
yard
work
(
doses
similar
to
occupational
scenarios
for
cutting
and
harvesting
sod).
(
5)
Toddlers
involved
in
high
exposure
activities
on
turf.
33
34
Table
7:
Occupational
Short­
and
Intermediate­
Term
Postapplication
Risks
for
Oxadiazon
at
Day
0
Crop/
Use
Pattern
Application
Rate
(
lb
ai/
acre)
Postapplication
Activity
Transfer
Coefficienta
Short
Term
and
Intermediate
Term
Risks
Cancer
Risk
TTRb
(

g/
cm2)
MOEc
LADDd
mg/
kg/
day
Riske
Golf
Course
Turf
4
Mow,
seed,
scout,
mechanical
weed,
aerate,
fertilize,
prune
500
0.2
(
5%
of
application
rate)
10,000
4.23e­
6
3.01e­
7
Transplant,
hand
weed
16,500
300
1.39e­
4
9.92e­
6
Sod
Farms
4
Mow,
scout,
mechanical
weed,
irrigate
500
10,000
4.23e­
6
3.01e­
7
Transplant,
hand
weed,
harvest
(
hand
or
mechanical)
16,500
300
1.39e­
4
9.92e­
6
Bermuda
Grass
Rights
of
Way
4
Mow,
seed,
scout,
mechanical
weed,
aerate,
fertilize
500
10,000
4.23e­
6
3.01e­
7
a
Transfer
coefficient
from
Science
Advisory
Council
for
Exposure:
Policy
Memo
#
003
.1
"
Agricultural
Transfer
Coefficients,"
Revised
­
August
7,
2000.

b
TTR
source:
5%
of
application
rate,
"
Residential
SOP
Revised
February
2001
"
was
used
for
determination
of
MOE's.

c
MOE
=
Short­
term
NOAEL
(
12
mg/
kg/
day;
based
on
a
dermal
study)
/
dermal
dose
where
absorbed
dose
=
TTR
(

g/
cm2)
x
TC
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time(
8hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
60
kg;
adult).

d
Absorbed
dermal
dose
where
absorbed
dose
=
TTR
(

g/
cm2)
x
TC
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
8
hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
70
kg)
x
(
Number
of
days
(
3)
exposure
per
year
applicator)
/
365
days
per
year)
x
35
years
worked/
70
year
lifetime
e
Cancer
Risk
=
LADD
(
mg/
kg/
day)
x
(
Q
1*),
where
Q
1*
=
7.11e­
2
(
mg/
kg/
day)­
1.

Note:
TTR
­
Turf
Transferable
Residue
35
4.3.3.1
Non­
occupational
Postapplication
Dermal
Exposure
(
Adults
and
Toddlers)

4.3.3.1.1
Data
Sources
and
Assumptions
for
Scenarios
Considered
A
turf
re­
entry
exposure
study
(
Jazzercise
study),
using
a
spray
application,
was
mentioned
in
the
Occupational
Postapplication
section
(
see
Section
4.3.2,
Occupational
Postapplication).
As
the
study
was
found
to
be
acceptable
for
the
risk
assessment,
the
highest
mean
residues
were
also
used
to
estimate
short­
term
(
DAT
0­
1)
for
irrigated
and
non­
irrigated
plots
evaluated
for
these
scenarios.

The
duration
of
postapplication
dermal
exposure
is
expected
to
be
either
short­
term
or
intermediate­
term,
based
on
oxadiazon
turf
residue
dissipation
data.
The
short­
term
and
intermediate­
term
MOEs
for
dermal
exposures
were
calculated
using
an
oral
NOAEL
of
12
mg/
kg/
day
with
a
dermal
absorption
rate
of
9%;
this
value
was
derived
from
the
same
study
used
for
the
occupational
handler
noncancer
exposures
(
see
4.3.1.1,
Noncancer
Handler
Exposure/
Risks).
For
the
cancer
risk
estimates,
the
Q
1*
of
7.11
x
10­
2
(
mg/
kg/
day)­
1
in
human
equivalents
(
see
4.3.1.2,
Cancer
Handler
Exposure/
Risks)
was
used.

As
calculated
from
the
previously
discussed
Jazzercise
study,
oxadiazon
has
a
half­
life
on
turf
of
up
to
1.4
days
(
irrigated)
and
1.7
days
(
non­
irrigated)
after
spraying,
requiring
several
days
to
dissipate
to
non
detectable
levels
of
transferable
residues.
Because
the
label
prohibits
application
more
than
3
times
per
year,
and
even
with
the
slow
dissipation
rates,
it
is
not
expected
that
individual
residential
exposure
duration
would
exceed
30
days
in
duration.
Exposure
on
a
residential
lawn
would
diminish
continuously
with
time,
while
exposure
through
recreation
turf
contact
would
more
likely
be
random,
intermittent
events
of
varying
doses,
all
less
than
the
dose
predicted
in
this
assessment.
Residential
postapplication
exposure
assessments
assumed
residents
wear
the
following
attire:
short
sleeved
shirt,
short
pants,
shoes
and
socks,
and
no
gloves
or
respirator.
As
stated
earlier,
negligible
oxadiazon
inhalation
exposure
is
anticipated
for
non­
handlers,
due
to
the
low
chemical
vapor
pressure
and
the
dilution
of
the
vapor
outdoors.
Other
assumptions
and
all
equations
used
for
the
assessment
of
each
exposure
scenario
can
be
found
in
the
occupational
and
residential
exposure
assessment
and
recommendations
for
oxadiazon
document
(
Tadayon,
2001).

Dermal
postapplication
exposure
estimates
were
conducted
using
the
highest
mean
postapplication
residue
to
estimate
short­
term
DAT
0­
1
for
irrigated
and
non­
irrigated
plots
from
the
previously
discussed
Jazzercise
study
(
wettable
powder
formulations).
The
dermal
transfer
coefficients
from
the
Jazzercize
study
(
MRID
No.
43517801)
and
the
revised
residential
SOPs
were
also
used.
As
the
study
was
found
to
be
acceptable
for
the
risk
assessment.

4.3.3.1.2
Non­
occupational
Postapplication
Dermal
Exposure
Risk
Estimates
Utilizing
the
Jazzercize
wettable
powder
application
study
residue
data
and
revised
residential
SOPs,
all
of
the
non­
cancer
risks
scenario
developed
for
adults
and
toddlers
had
short­
term
and
intermediate­
term
dermal
MOEs
greater
than
100.
The
cancer
risks
for
all
adult
residential
36
\

dermal
postapplication
exposure
were
between
6.22x
10­
6
to
7.51
x
10­
8
.
The
resulting
risk
estimates
are
summarized
in
Tables
8
and
9.

4.3.3.2
Incidental
Oral
Exposure
for
Toddlers
Only
limited
information
was
received
regarding
the
size
and
distribution
of
granular
formulations.
This
information
would
help
to
refine
or
characterize
the
estimate
of
potential
risk
from
episodic
incidental
ingestion
of
granules
beyond
the
current
screening
level.
If
the
particles
are
very
fine,
individual
grains
would
be
difficult
to
pick
up,
or
even
to
see
when
applied
on
a
lawn.
If
used
according
to
label
directions,
it
is
unlikely
that
oxadiazon
granules
would
be
accessible
to
a
child.
However,
larger
granules
or
pellets
of
a
few
millimeters
diameter
might
be
attractive
and
easily
picked
up
by
a
toddler.

An
intermediate­
term
(
7­
30
days)
MOE
was
not
calculated
since
exposure
by
this
route
for
weeks
is
considered
less
likely
to
occur
than
short­
term
(
1­
7days)
exposure.
Similarly,
there
was
no
indication
from
the
studies
in
the
database
that
toxic
effects
observed
over
the
short­
term
would
be
any
different
over
a
longer
term
exposure.
Estimated
incidental
oral
short­
term
exposures
("
hand­
tomouth
for
toddlers
had
an
MOE
of
100
using
the
TTR
default
values
from
the
residential
SOP;
when
the
TTR
data
from
submitted
oxadiazon
study
were
used,
the
MOEs
were
90
and
240
(
Table
10).
The
former
MOE
of
90
does
not
exceed
the
target
value,
however,
the
submitted
study
TTR
data
were
from
the
wettable
powder
formulation
and
the
major
formulation
used
is
granular
oxadiazon.
It
is
probable,
therefore,
that
the
risk
indicated
for
irrigated
dormant
grass
is
an
overestimate
and
not
likely
to
be
a
cause
for
concern
(
also
see
Section
4.3.3.1,
Data
Sources
and
Assumptions
for
Scenarios
Considered).
MOEs
were
not
calculated
for
the
incidental
ingestion
of
oxadiazon
granules
because
an
acute
RfD
was
not
selected
for
this
non­
food
use
pesticide.
Additionally,
there
is
no
indication
from
the
studies
in
the
guideline
database
that
a
single
oral
administration
of
oxadiazon
presents
a
hazard.
This
statement
is
also
supported
by
the
high
rat
acute
LD
50
for
oxadiazon
(>
5000
mg/
kg).
It
is
thought,
therefore,
that
the
incidental
ingestion
of
granules
is
not
likely
to
be
a
cause
for
concern.

It
is
considered
reasonably
likely
that
dermal
and
oral
incidental
exposures
may
occur
in
the
same
day
for
children
playing
on
an
oxadiazon­
treated
lawn.
However,
these
exposures
were
not
aggregated
due
to
the
short­
term
hand­
to­
mouth
exposures
having
MOEs
less
than
or
equal
to
the
target
MOE
of
100.
Because
an
exposure
just
mets
or
exceeds
the
level
of
concern
by
a
single
route,
that
route
must
be
mitigated
prior
to
aggregating
exposures
by
other
routes
otherwise,
the
reported
risk
is
only
increased.
37
Table
8.
Residential
Dermal
Postapplication
Non­
Cancer
Risks
for
Oxadiazon
Dermal
Scenarios
Application
Rate
(
lb
ai/
acre)
Exposure
Time
(
hours/
day)
Short
Term
and
Intermediate
Term
Risks
Transfer
Coefficient
(
cm2/
hr)
a
Transfer
Coefficient
(
cm2/
hr)
Irrigatedb
Transfer
Coefficient
(
cm2/
hr)

Non­
Irrigatedc
TTRd
(
ug/
cm2)

DAT
0­
1
Dermal
Dose
(
mg/
kg/
day)
e
Dermal
Dose
(
mg/
kg/
day)

Irrigatedf
Dermal
Dose
(
mg/
kg/
day)

Non­
Irrigatedg
MOEsh
MOEs
i
Irrigated
MOEsj
Non­
Irrigated
Adult
dermal
turf
contact
4
2
14500
4300
7,400
1.53
NA
1.97e­
2
3.40e­
2
NA
610
350
2.0
8.70e­
2
NA
NA
140
NA
NA
Toddler
dermal
turf
contact
2
5200
1600
2,700
0.87
NA
1.67e­
2
2.82e­
2
NA
720
430
2.0
3.12e­
2
NA
NA
390
NA
NA
Adult
walking,
playing
golf
4
500
NA
NA
2.0
6.0e­
3
NA
NA
2000
NA
NA
Adult
push
mowing
lawn
2
500
NA
NA
2.0
3.0e­
3
NA
NA
4000
NA
NA
a
Transfer
coefficient
from
the
Residential
SOP's
(
2/
01)
used
for
fresh
grass
b
Transfer
coefficient
from
turf
study
MRID
#
435178­
01used
for
dormant
grass
c
Transfer
coefficient
from
turf
study
MRID
#
435178­
01used
for
dormant
grass
d
TTR
source:
wettable
powder
from
turf
studies
MRID
#
435178­
01,
DAT
0­
1
residue
or
residential
SOP
(
5%
application
rate)

e
Dermal
dose
(
mg/
kg/
day)
=
TTR
(
5%
application
rate)
(

g/
cm2)
x
TC
(
from
residential
SOP,
s)
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
or
4hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
60
kg
adult
or
15
kg
toddler).

f
Dermal
dose
(
mg/
kg/
day)
irrigated
=
TTR
(
from
MRID
#
435178­
01)
(

g/
cm2)
x
TC
(
MRID
#
435178­
01)
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
hrs/
day)
x
dermal
absorption
(
9
%)/
body
weight
(
60
kg
adult
or
15
kg
toddler).

g
Dermal
dose
(
mg/
kg/
day)
non­
irrigated
=
TTR
(
from
MRID
#
435178­
01)
(

g/
cm2)
x
TC
(
MRID
#
435178­
01)
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
60
kg
adult
or
15
kg
toddler).

h
MOE
=
Short­
term
NOAEL
(
12
mg/
kg/
day;
based
on
an
oral
study)
/
dermal
dose
(
mg/
kg/
day)

i
MOE
(
irrigated)
=
Short­
term
NOAEL
(
12
mg/
kg/
day;
based
on
an
oral
study)
/
dermal
dose
(
mg/
kg/
day)

j
MOE
(
non­
irrigated)
=
Short­
term
NOAEL
(
12
mg/
kg/
day;
based
on
an
oral
study)
/
dermal
dose
(
mg/
kg/
day)

Note:
TTR
­
Turf
Transferable
Residue
rounded
to
2.0
ug/
cm2
38
Table
9.
Residential
Dermal
Postapplication
Cancer
Risks
for
Oxadiazon
Dermal
Scenarios
Application
Rate
(
lb
ai/
acre)
Exposure
Time
(
hours/
day)
Transfer
Coefficient
(
cm2/
hr)
a
Transfer
Coefficient
(
cm2/
hr)
Irrigatedb
Transfer
Coefficient
(
cm2/
hr)

Non­
Irrigatedc
TTRd
(
ug/
cm2)

DAT
0­
1
LADDe
mg/
kg/
day
LADDf
mg/
kg/
day
irrigated
LADDg
mg/
kg/
dayf
Non­
Irrigated
Cancer
Riskh
Cancer
Risk
Irrigatedj
Cancer
Risk
Nonirrigatedj
Adult
dermal
turf
contact
4
2
14500
4300
7400
1.53
NA
6.95e­
5
1.2e­
4
NA
3.62e­
6
6.22e­
6
2.0
3.06e­
04
NA
NA
1.59e­
5
NA
NA
Toddler
dermal
turf
contact
2
5200
1600
2700
0.87
NF
NF
NF
NF
NF
NF
2.0
NF
NF
NF
NF
NF
NF
Adult
walking,
playing
golf
4
500
NA
NA
2.0
2.11e­
5
NA
NA
1.50e­
6
NA
NA
Adult
push
mowing
lawn
2
500
NA
NA
2.0
1.06e­
5
NA
NA
7.51e­
7
NA
NA
a
Transfer
coefficient
from
the
Residential
SOP's
(
2/
01)
used
for
fresh
grass
b
Transfer
coefficient
from
turf
study
MRID
#
435178­
01used
for
dormant
grass
c
Transfer
coefficient
from
turf
study
MRID
#
435178­
01used
for
dormant
grass
d
TTR
source:
wettable
powder
and
granular
turf
studies
MRID
#
435178­
01,
DAT
0­
1
residue
e
LADD
(
mg/
kg/
day)
=
TTR
(

g/
cm2)(
5%
of
application
rate)
x
TC(
residential
SOP)
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
or
4
hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
70
kg)
x
(
Number
of
days
(
3)
exposure
per
year
applicator)
/
365
days
per
year)
x
35
years
worked/
70
year
lifetime
f
LADD
(
mg/
kg/
day)(
irrigated)
=
TTR
(

g/
cm2)
(
from
MRID
#
435178­
01)
x
TC
(
cm2/
hr)(
from
MRID
#
435178­
01)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
70
kg)
x
(
Number
of
days
(
3)
exposure
per
year
applicator)
/
365
days
per
year)
x
35
years
worked/
70
year
lifetime
g
LADD
(
mg/
kg/
day)(
non­
irrigated)
=
TTR
(

g/
cm2)(
from
MRID
#
435178­
01)
x
TC(
from
MRID
#
435178­
01)
(
cm2/
hr)
x
conversion
factor
(
1
mg/
1,000

g)
x
exposure
time
(
2
hrs/
day)
x
dermal
absorption
(
9
%)
/
body
weight
(
70
kg)
x
(
Number
of
days
(
3)
exposure
per
year
applicator)
/
365
days
per
year)
x
35
years
worked/
70
year
lifetime
h
Cancer
Risk
=
LADD
(
mg/
kg/
day)
x
(
Q
1*),
where
Q
1*
=
7.11e­
2
(
mg/
kg/
day)­
1.

i
Cancer
Risk
(
irrigated)
=
LADD
(
mg/
kg/
day)
(
irrigated)
x
(
Q
1*),
where
Q
1*
=
7.11e­
2
(
mg/
kg/
day)­
1.

j
Cancer
Risk
(
non­
irrigated)
=
LADD
(
mg/
kg/
day)(
non­
irrigated)
x
(
Q
1*),
where
Q
1*
=
7.11e­
2
(
mg/
kg/
day)­
1.

NA=
Not
applicable
NF=
Not
Feasible
Note:
TTR
­
Turf
Transferable
Residue
rounded
to
2.0
ug/
cm2
39
Table
10
Residential
Oral
Nondietary
Postapplication
Risks
to
Toddlers
from
"
Hand­
to­
Mouth"
and
Ingestion
Exposure
When
Reentering
Lawns
Treated
with
Granular
or
wettable
powder
Oxadiazon
Formulations
Type
of
Exposure
Application
Ratea
(
lb
ai/
acre)
Ingestion
Rate
or
Other
Assumptionsb
Short­
Term
TTRc
(

g/
cm2)

DAT
0­
1
Oral
Dosed
(
mg/
kg/
day)
MOEe
Hand
to
Mouth
Activity
4
20
cm2/
event
surface
area
of
1­
3
fingers;
20
events/
hr;
fresh
grass
5%
of
ai
dislodgeable
with
potentially
wet
hands
2.0
1.19e­
01
100
20
cm2/
event
surface
area
of
1­
3
fingers;
20
events/
hr;

2.1%
of
ai
dislodgeable
with
potentially
wet
hands
(
dormant
grass,
irrigated)
1.0
5.02e­
02
240
20
cm2/
event
surface
area
of
1­
3
fingers;
20
events/
hr;

5.5%
of
ai
dislodgeable
with
potentially
wet
hands
(
dormant
grass,
non­
irrigated)
2.5
1.31e­
01
90
Incidental
Turfgrass
Ingestion
25
cm2/
day
of
turf
20%
application
rate
(
residential
SOP)
fresh
grass
9.0
1.49e­
02
805
25
cm2/
day
of
turf
Irrigated
(
MRID
#
435178­
01)
used
for
dormant
grass
0.87
2.60e­
03
4700
25
cm2/
day
of
turf
Non­
Irrigated(
MRID
#
435178­
01)
used
for
dormant
grass
1.53
1.45e­
03
8300
Incidental
Ingestion
of
Soil
100
mg/
day
ingestion;
0.67
cm3/
gm
soil
NA
2.12e­
04
57000
a
Application
rates
represent
maximum
label
rates
from
current
EPA
registered
labels.

b
Assumptions
from
Residential
SOP's
(
February,
2001).
fresh
grass
c
TTR
source:
wettable
powder
and
granular
oxadiazon
turf
studies
MRID
Nos.
43517801.
Short­
term
risks
assessed
using
DAT
0­
1
residue
values.

d
Oral
doses
calculated
using
formulas
presented
in
the
Residential
SOPs
(
February,
2001).
Short­
term
and
intermediate­
term
doses
were
calculated
using
the
following
formulas.
Intermediate
term
doses
were
each
multiplied
by
the
estimated
fraction
of
oxadiazon
residue
remaining
on
DAT
7
after
application.

Hand­
to­
mouth
oral
dose
to
toddlers
on
the
day
of
treatment
(
mg/
kg/
day)
=
[
application
rate
(
lb
ai/
acre)
x
fraction
of
residue
dislodgeable
from
potentially
wet
hands
(
see
assumptions)
x
11.2
(
conversion
factor
to
convert
lb
ai/
acre
to

g/
cm2)]
x
median
surface
area
for
1­
3
fingers
(
20
cm2/
event)
x
hand­
to­
mouth
rate
(
ST:
20
events/
hour
)
x
exp.
time
(
2
hr/
day)
x
0.001
mg/
µ
g]
/
bw
(
15
kg
toddler).

Grass
ingestion
oral
dose
to
toddlers
on
the
day
of
treatment
(
mg/
kg/
day)
=
[
TTR
(

g/
cm2)
x
ingestion
rate
of
grass
(
25
cm2/
day)
x0.001
mg/
µ
g]
/
bw
(
15
kg
toddler).

Soil
ingestion
oral
dose
to
toddlers
on
the
day
of
treatment
(
mg/
kg/
day)
=
[(
application
rate
(
lb
ai/
acre)
x
fraction
of
residue
retained
on
uppermost
1
cm
of
soil
(
100%
or
1.0/
cm)
x
4.54E+
08

g/
lb
conversion
factor
x
2.47E­
08
acre/
cm2
conversion
factor
x
0.67
cm3/
g
soil
conversion
factor)
x
100
mg/
day
ingestion
rate
x
1.0E­
06
g/

g
conversion
factor]
/
bw
(
15
kg;
toddler).
Short
term
dose
based
residue
on
the
soil
on
day
of
application.

NA=
Not
applicable
Note:
TTR
­
Turf
Transferable
Residue
40
4.3.4
Incident
Data
Oxadiazon
has
not
been
reported
to
cause
life­
threatening
illness
or
death
in
humans.
Most
of
the
cases
appear
to
be
related
to
irritation
to
the
skin,
eyes
and
mucous
membranes.
Some
cases
may
be
related
to
an
allergic
reaction
On
the
list
of
the
top
200
chemicals
for
which
NPTN
received
calls
from
1984­
1991
inclusively,
oxadiazon
was
ranked
192nd
with
12
incidents
in
humans
reported
and
5
incidents
in
animals
(
mostly
pets).
33
Drinking
Water
Levels
of
Comparison
34
acute
Population
Adjusted
Dose
41
5.0
AGGREGATE
RISK
ASSESSMENTS
AND
RISK
CHARACTERIZATION
5.1
DWLOCs33
for
Acute
Exposure
An
aggregate
risk
assessment
is
defined
as
the
evaluation
of
the
likelihood
of
the
occurrence
of
an
adverse
health
effect
resulting
from
exposure
to
a
single
substance
via
all
relevant
routes.
As
part
of
the
aggregate
risk
assessment,
short­
and
intermediate­
term
risk
assessments
require
the
incorporation
of
drinking
water
exposure
and
the
calculation
of
DWLOC
values
to
estimate
the
total
exposure
from
all
sources.
DWLOCs
are
theoretical
upper
limits
on
a
pesticide's
concentration
in
drinking
water
that
are
used
to
determine
how
much
of
the
acceptable
exposure
is
available
for
exposure
through
drinking
water.
OPP
uses
DWLOCs
internally
in
the
risk
assessment
process
as
a
surrogate
measure
of
potential
exposure
associated
with
pesticide
exposure
through
drinking
water.
DWLOC
values
are
not
regulatory
standards
for
drinking
water;
however,
they
do
have
regulatory
impact
through
aggregate
exposure
and
risk
assessments.

DWLOCs
were
calculated
for
oxadiazon
based
on
an
oral
NOAEL
of
12
mg/
kg/
day
from
a
developmental
study,
which
was
selected
by
HIARC
for
the
short­
term
(
1­
7
day)
incidental
oral
exposure
(
McCarroll,
2001b).
An
acute
RfD
was
not
selected
for
oxadiazon
because
there
are
no
food
uses
(
McCarroll,
2001b).
However,
in
accordance
with
the
Updated
Interim
Guidance
for
Incorporating
Drinking
Water
Exposure
into
Aggregate
Risk
Assessments
(
Stasikowski,
1999),
this
NOAEL
was
used
to
calculate
the
acute
DWLOCs.
An
uncertainty
factor
of
100
was
applied
based
on
a
10x
for
intraspecies
variation
and
a
10x
for
interspecies
extrapolation.
Therefore,
the
theoretical
acute
RfD
or
the
theoretical
aPAD34
would
be
0.12
mg/
kg/
day.
The
default
body
weights
and
daily
water
consumption
values
were
applied
for
each
target
population
(
i.
e.,
U.
S.
population,
children
1­
6,
and
infants).
Default
body
weights
and
consumption
values
for
calculation
of
the
DWLOCs
were:
2L/
70
kg
(
adult
male),
2L/
60
kg
(
adult
female)
and
1L/
10
kg
(
children
and
infants),
respectively.
Based
on
a
comparison
of
DWLOCs
to
the
corresponding
PRZM/
EXAM
and
SCIGROW
values,
which
show
higher
values
for
the
DWLOCs,
acute
exposure
to
residues
of
oxadiazon
in
surface
and
ground
water
is
not
a
concern
(
Table
11a).

5.2
DWLOCs
for
Chronic
Exposure
A
chronic
RfD
was
also
not
selected
by
the
HIARC
because
of
the
lack
of
food
or
feed
uses
(
McCarroll,
2001b).
Using
the
line
of
reasoning
developed
for
the
acute
DWLOC
calculations
and
put
forth
in
the
interim
guidance
document,
a
combined
chronic/
oncogenicity
feeding
study
was
selected
by
HIARC
for
the
dermal
and
inhalation
risk
assessments
(
see
Section
3.3).
Accordingly,
this
35
chronic
Population
Adjusted
Dose
42
Table
11a.
Summary
of
Acute
DWLOC
Calculations
for
Oxadiazon
Population
Subgroup1
Acute
Scenario
Theoretical
aPAD
mg/
kg/
day
Acute
Food
Exp
mg/
kg/
day
Max
Acute
Water
Exp
mg/
kg/
day2
PRZM/
EXAM
Surface
Water
EDWC
(

g/
L)
SCIGROW
Ground
Water
EDWC
(

g/
L)
Acute
DWLOC
(

g/
L)
3
U.
S.
Population
0.12
0.00
0.12
181
0.59
4200
Females
13­
50
years
old
0.12
0.00
0.12
181
0.59
3600
Infants
<
1
year
old
0.12
0.00
0.12
181
0.59
1200
Children
1­
6
years
old
0.12
0.00
0.12
181
0.59
1200
1
Default
body
weights
and
consumption
values
for
calculation
of
the
DWLOCs
were:
2L/
70
kg
(
adult
male),
2L/
60
kg
(
adult
female)
and
1L/
10
kg
(
child),
respectively.
2
Maximum
acute
water
exposure
(
mg/
kg/
day)
=
[(
acute
PAD
(
mg/
kg/
day)
­
acute
food
exposure
(
mg/
kg/
day)]
3
Acute
DWLOC(

g/
L)
=
[
maximum
chronic
water
exposure
(
mg/
kg/
day)
x
body
weight
(
kg)]
[
water
consumption
(
L)
x
10­
3
mg/

g]

NOAEL
of
0.36
mg/
kg/
day,
based
on
adverse
liver
effects,
was
used
to
calculate
the
chronic
DWLOCs
(
DWLOC
chronic).
An
uncertainty
factor
of
100
was
applied
(
10x
for
intraspecies
and
a
10x
for
interspecies
variation).
Therefore,
the
theoretical
chronic
RfD
or
the
theoretical
cPAD35
would
be
0.0036
mg/
kg/
day.
Residential
exposures
were
not
factored
into
the
DWLOCchronic
since
no
long­
term
residential
exposures
(
handlers
or
postapplication)
are
expected.

As
shown
in
Table
11b,
only
the
adult
male
and
female
populations
as
a
whole
had
DWLOC
values
that
exceeded
the
surface
and
ground
water
targets;
consequently,
the
Agency
concludes
with
reasonable
certainty
that
there
is
no
drinking
water
risk
of
concern
for
these
populations
exposed
to
oxadiazon.
DWLOCs
values
derived
for
infants
and
children
also
exceeded
the
EDWCs
for
ground
water
and
are,
also
of
no
concern
to
the
Agency.
On
the
other
hand,
the
EDWCs
for
surface
water
(
65

g/
L)
based
on
the
Tier
II
modeling
from
PRZM/
EXAM,
were
higher
than
the
DWLOCs
calculated
for
infants
and
children.
Since
the
EDWCs
were
higher
than
the
chronic
values
derived
for
surface
and
ground
water
(
36

g/
L),
the
Agency
concludes
that
there
is
a
drinking
water
risk
of
concern
for
infants
and
children
chronically
exposed
to
oxadiazon
via
drinking
water.

5.3
DWLOCs
for
Cancer
For
the
cancer
(
Q
1*)
exposure
calculations,
the
Agency
used
multi­
year
mean
water
concentration
values.
The
DWLOC
cancer
is
the
concentration
in
drinking
water
as
a
part
of
the
aggregate
chronic
exposure
that
results
in
a
negligible
cancer
risk
(
10­
6).
43
No
residential
exposures
were
factored
into
the
equation
since
no
long­
term
residential
exposures
(
handlers
or
postapplication)
are
expected.
As
shown
in
Table
11c,
EFED's
EDWC
for
Table
11b.
Summary
of
Chronic
DWLOC
Calculations
for
Oxadiazon
Population
Subgroup1
Chronic
Scenario
Theoretical
cPAD
mg/
kg/
day
Chronic
Food
Exp
mg/
kg/
day
Max
Chronic
Water
Exp
mg/
kg/
day2
PRZM/
EXAMS
urface
Water
EDWC
(

g/
L)
SCIGROW
Ground
Water
EDWC
(

g/
L)
Chronic
DWLOC
(

g/
L)

U.
S.
Population
0.0036
0.00
0.0036
65
0.59
126
Females
13­
50
years
old
0.0036
0.00
0.0036
65
0.59
108
Infants
<
1year
old
0.0036
0.00
0.0036
65
0.59
36
Children
1­
6
years
old
0.0036
0.00
0.0036
65
0.59
36
1
Default
body
weights
and
consumption
values
for
calculation
of
the
DWLOCs
were:
2L/
70
kg
(
adult
male),
2L/
60
kg
(
adult
female)
and
1L/
10
kg
(
child),
respectively.
2
Maximum
Chronic
Water
Exposure
(
mg/
kg/
day)
=
[
Chronic
PAD
(
mg/
kg/
day)
­
Chronic
Dietary
Exposure
(
mg/
kg/
day)]
3
Chronic
DWLOC(

g/
L)
=
[
maximum
chronic
water
exposure
(
mg/
kg/
day)
x
body
weight
(
kg)]
[
water
consumption
(
L)
x
10­
3
mg/

g]

Table
11c.
Summary
of
Cancer
DWLOC
Calculations
for
Oxadiazon
Population
Q*
Negligible
Risk
Level1
Target
Max
Exposure2
mg/
kg/
day
Chronic
Food
Exposure
mg/
kg/
day
Max
Water
Exposure3
mg/
kg/
day
PRZM/
EXAM
SurfaceWater
EDWC
(

g/
L)
SCIGROW
Ground
Water
EDWC
(

g/
L)
Cancer
DWLOC4
(

g/
L)

U.
S.
Pop
7.11e­
02
0.000001
0.000014
0.000000
0.00001400
56
0.59
0.490000
1
DWLOC
CANCER
was
calculated
for
U.
S.
population
only.
Default
body
weights
and
consumption
values
for
calculation
of
the
DWLOCs
were:
2L/
70
kg
2
Target
Maximum
Exposure
(
mg/
kg/
day)
=
[
negligible
risk/
Q*]
3
Maximum
Water
Exposure
(
mg/
kg/
day)
=
[
Target
Maximum
Exposure
­
(
Chronic
Food
Exposure
+
Residential
Exposure
(
Lifetime
Average
Daily
Dose))]
4
Cancer
DWLOC(

g/
L)
=
[
maximum
water
exposure
(
mg/
kg/
day)
x
body
weight
(
kg)]
[
water
consumption
(
L)
x
10­
3
mg/

g]
2
oxadiazon
residues
in
surface
and
ground
water
are
higher
than
the
Agency's
calculated
DWLOCs
for
the
adult
U.
S.
population.
Therefore,
the
cancer
risk
exceeds
HED's
level
of
concern
for
lifetime
exposure
to
oxadiazon
in
drinking
water
derived
from
surface
and
ground
water.
It
should
be
noted,
however,
that
EDWC
values
derived
from
the
SCI­
GROW
model
for
the
ground
water
analysis,
are
based
on
high
concentrations
observed
in
shallow
ground
water
after
agricultural
treatment
of
permeable
soils.
Since
this
combination
of
conditions
is
encountered
in
only
1%
of
the
agricultural
use
area
in
the
U.
S.,
it
is
not
likely
that
oxadiazon
would
pose
a
potential
cancer
concern
for
exposure
to
oxadiazon
in
ground
water
(
Barrett,
1998).
44
5.4
Aggregrate
Risk
Assessments
HED
did
not
perform
an
aggregate
risk
assessment
as
part
of
this
reregistration
review
for
oxadiazon
because
the
calculated
DWLOC
values
are
based
on
conservative
default
values
since
no
monitoring
data
were
available
on
oxadiazon
and
the
refined
model
for
turf
analysis
is
not
completed
at
this
time.
In
addition,
data
used
to
develop
residential
exposure
estimates
(
dermal
exposure
values)
were
also
conservative
because
the
highest
mean
postapplication
TTR
residue
value
from
the
Jazzercize
study
(
MRID
No.
43517801)
along
with
the
data
from
the
wettable
powder
formulation
instead
of
the
the
major
formulation
(
granular)
were
used.
Thus,
any
aggregation
of
a
conservative
water
number
with
a
conservative
residential
exposure
estimate
would
result
in
an
even
more
conservative
expression
of
aggregate
risk.
The
RARC
also
noted
that
guidance
from
management
on
this
issue
is
forthcoming.

6.0
CUMULATIVE
RISK
FQPA
of
1996
stipulates
that
when
determining
the
safety
of
a
pesticide
chemical,
EPA
shall
base
its
assessment
of
the
risk
posed
by
the
chemical
on,
among
other
things,
available
information
concerning
the
cumulative
effects
to
human
health
that
may
result
from
dietary,
residential,
or
other
non­
occupational
exposure
to
other
substances
that
have
a
common
mechanism
of
toxicity.
The
reason
for
consideration
of
other
substances
is
due
to
the
possibility
that
low­
level
exposures
to
multiple
chemical
substances
that
cause
a
common
toxic
effect
by
a
common
mechanism
could
lead
to
the
same
adverse
health
effect
as
would
a
higher
level
of
exposure
to
any
of
the
other
substances
individually.
A
person
exposed
to
a
pesticide
at
a
level
that
is
considered
safe
may
in
fact
experience
harm
if
that
person
is
also
exposed
to
other
substances
that
cause
a
common
toxic
effect
by
a
mechanism
common
with
that
of
the
subject
pesticide,
even
if
the
individual
exposure
levels
to
the
other
substances
are
also
considered
safe.

HED
did
not
perform
a
cumulative
risk
assessment
as
part
of
this
reregistration
review
for
oxadiazon
because
HED
has
not
yet
initiated
a
comprehensive
review
to
determine
if
there
are
any
other
chemical
substances
that
have
a
mechanism
of
toxicity
common
with
that
of
oxadiazon.
For
purposes
of
this
reregistration
decision,
EPA
has
assumed
that
oxadiazon
does
not
have
a
common
mechanism
of
toxicity
with
other
substances.

On
this
basis,
the
Registrant,
Bayer
Environmental
Science,
must
submit,
upon
EPA's
request
and
according
to
a
schedule
determined
by
the
Agency,
such
information
as
the
Agency
directs
to
be
submitted
in
order
to
evaluate
issues
related
to
whether
oxadiazon
shares
a
common
mechanism
of
toxicity
with
any
other
substance
and,
if
so,
whether
any
tolerances
for
oxadiazon
need
to
be
modified
or
revoked.
If
HED
identifies
other
substances
that
share
a
common
mechanism
of
toxicity
with
oxadiazon,
HED
will
perform
aggregate
exposure
assessments
on
each
chemical,
and
will
begin
to
conduct
a
cumulative
risk
assessment
once
the
final
guidance
HED
will
use
for
conducting
cumulative
risk
assessments
is
available.

HED
has
recently
developed
a
framework
that
it
proposes
to
use
for
conducting
cumulative
risk
assessments
on
substances
that
have
a
common
mechanism
of
toxicity.
This
guidance
was
issued
for
45
public
comment
on
June
30,
2000
(
65
FR
40644­
40650)
and
is
available
from
the
OPP
Website
at:
http://
www.
epa.
gov/
fedrgstr/
EPA­
PEST/
2000/
June/
Day­
30/
6049.
pdf
.
In
the
draft
guidance,
it
is
stated
that
a
cumulative
risk
assessment
of
substances
that
cause
a
common
toxic
effect
by
a
common
mechanism
will
not
be
conducted
until
an
aggregate
exposure
assessment
of
each
substance
has
been
completed.
The
proposed
guidance
on
cumulative
risk
assessment
of
pesticide
chemicals
that
have
a
common
mechanism
of
toxicity
is
expected
to
be
finalized
by
the
summer
of
2001.

Before
undertaking
a
cumulative
risk
assessment,
HED
will
follow
procedures
for
identifying
chemicals
that
have
a
common
mechanism
of
toxicity
as
set
forth
in
the
"
Guidance
for
Identifying
Pesticide
Chemicals
and
Other
Substances
that
Have
a
Common
Mechanism
of
Toxicity"
(
64
FR
5795­
5796,
February
5,
1999).

7.0
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,
oxadiazon
may
be
subjected
to
additional
screening
and/
or
testing
to
better
characterize
effects
related
to
endocrine
disruption.

8.0
DATA
NEEDS/
LABEL
REQUIREMENTS
8.1
Toxicology
28­
day
Inhalation
Study
(
870.3465)
46
8.2
Product
and
Residue
Chemistry
Current
Confidential
Statement
of
Formula
containing
nominal
concentration,
upper
limits
for
all
components
and
lower
limits
for
the
a.
i.

8.3
Occupational
and
Residential
Exposure
Concurrent
Transfer
Coefficient
measurements
along
with
TTR
studies.

9.0
BIBILOGRAPHY
Litt,
B.
D.
(
1984).
Carcinogenicity
Risk
Assessment
for
Oxadiazon,
dated
November
21,
1984
(
HED
Document
No.
004097).

Farber,
T
(
1987).
Classification
of
Oncogenic
Potential
of
Oxadiazon,
dated
August
27,
1987
(
HED
Document
No.
007798).

Quest,
J.
(
1987).
Second
Peer
Review
of
Oxadiazon,
dated
August
14,
1987
(
HED
Document
No.
007798).

Barrett,
M.
(
1998).
Updated
Documentation
on
the
SCI­
GROW
Method
to
Determine
Screening
Concentration
Estimates
for
Drinking
Water
Derived
from
Ground
Water
Sources,
dated
May
29,
1998.

Brunsman,
L.
(
2001).
REVISED
Oxadiazon
Qualitative
Risk
Assessment
(
Q
1
*)
Based
on
SPF
Wistar
Rat
and
ICR_
JCL
Mouse
Dietary
Studies
with
3/
4'
s
interspecies
Scaling
Factor,
dated
February
1,
2001
(
HED
Document
No.
014465).

Diwan,
S.
(
2001).
Cancer
Assessment
Document
Evaluation
of
the
Carcinogenic
Potential
of
Oxadiazon
(
Third
Review),
dated
May
1,
2001
(
HED
Document
No.
014555).

Hansen,
L
and
McCarroll,
N.
(
2001).
Oxadiazon:
Toxicology
Disciplinary
Chapter
for
the
Reregistration
Eligibility
Decision
Document,
dated
July
7,
2001
(
HED
Document
No.
014614).

Dockter,
K.
(
2001).
Oxadiazon.
List
B
Registration
Case
2485.
PC
Code
109001.
Product
Chemistry
Chapter
for
the
Reregistration
Eligibility
Decision
[
RED]
Document,
dated
March
2,
2001.
D273104.

Gorrell.
M.
(
2001).
Revocation
Letter
for
Oxadiazon
Tolerances
March
12,
1991.
Letter
from
Mike
Gorrell,
Manager,
Registrations,
Aventis
Environmental
Science
USA
to
Veronique
La
Capra,
SRRD,
USEPA,
dated
January
24,
2001.

Kahn,
F.
A.
(
200@
0.
Tier
II
Estimated
Drinking
Water
Concentrations
(
EDWCs)
for
Human
Health
Risk
for
oxadiazon
on
Florida
Golf
Course,
dated
April
15,
2002
(
DP
Code
D281176).
47
McCarroll,
N.
(
2001a).
Oxadiazon:
Assessment
of
Mode
of
Action
on
Liver
Carcinogenicity,
dated
February
28,
2001.
D266361(
TXR#
0050506).

McCarroll,
N.
(
2001b).
Oxadiazon:
Report
of
the
Hazard
Identification
Assessment
Review
Committee
(
HIARC),
dated
February
8,
2001
(
HED
Document
No.
014469)
D266361.

Melendez,
J.
L.
(
2001).
Tier
I
Estimated
Environmental
Concentrations
of
Oxadiazon,
dated
May
8,
2001.

Piper,
S.
(
2001a).
Oxadiazon:
List
B
Registration
Case
2485.
PC
Code
109001.
Product
Chemistry
and
Residue
Chemistry
Chapter
for
the
Registration
Eligibility
Decision
[
RED]
Document,
dated
March
27,
2001.
DP
Barcode
D273740.

Piper,
S.
(
2001b).
Oxadiazon:
(
List
B,
Case
No.
2485)
The
Outcome
of
the
HED
Metabolism
Assessment
Review
Committee
Meeting
Held
on
01/
31/
01,
dated
February
13,
2001.
D272425.

Piper,
S.
and
McCarroll,
N.
(
2001).
Oxadiazon:
(
List
B,
Case
No.
2485)
Issues
to
be
Presented
to
the
HED
Metabolism
Assessment
Review
Committee
(
MARC),
dated
January
10,
2001.
D271728.

Stasikowski,
M.
(
1999).
Updated
"
Interim
Guidance
for
Incorporating
Drinking
Water
Exposure
into
Aggregate
Risk
Assessments",
dated
August
1,
1999.

Tadayon,
S.
(
2001).
Occupational
and
Residential
Exposure
Assessment
and
Recommendationsfor
the
Reregistration
Eligibility
Decision
Document
for
Oxadiazon,
dated
May
7,
2001.
DP
Barcode
D273742.
48
SignOff
Date:
XXXXXXX
DP
Barcode:
D290005
HED
DOC
Number:
XXXXXX
Toxicology
Branch:
TOX1