Document ID: EPA-HQ-OPP-2005-0231-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2005-12-30T05:00Z

UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
WASHINGTON,
D.
C.
20460
OFFICE
OF
PREVENTION,
PESTICIDES
AND
TOXIC
SUBSTANCES
December
20,
2005
MEMORANDUM
SUBJECT:
Metaldehyde:
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED).
PC
Code:
053001;
DP
Barcode:
DP311884
FROM:
Matthew
Lloyd,
Risk
Assessor
Linda
Taylor
Ph.
D.
Felecia
Fort
Jeffrey
Dawson
Reregistration
Branch
1
Health
Effects
Division
(
7509C)

THROUGH:
Whang
Phang,
Ph.
D.
Branch
Senior
Scientist
Reregistration
Branch
1
Health
Effects
Division
(
7509C)

TO:
Jill
Bloom,
Chemical
Review
Manager
Special
Review
and
Reregistration
Division
(
7508C)

DP
Barcode:
DP311884
PC
Code:
053001
Attached
is
the
revised
Human
Health
Risk
Assessment
for
the
Metaldehyde
Reregistration
Eligibility
Decision
Document
(
RED).
Comments
from
the
registrant,
Lonza,
Inc.
have
been
reviewed
and
appropriately
been
incorporated
into
the
current
RED.
Information
was
drawn
from
Health
Effects
Division
(
HED)
team
members.
Additional
information
was
drawn
from
the
Environmental
Fate
and
Effects
Division
(
EFED)
Tier
1&
2
Drinking
Water
Assessment
and
the
review
of
Metaldehyde
Incident
Reports
from
HED,
Chemistry
and
Exposure
Branch.
A
complete
list
of
team
members
can
be
found
on
page
3.
Page
2
of
80
HUMAN
HEALTH
RISK
ASSESSMENT
Metaldehyde
U.
S.
Environmental
Protection
Agency
Office
of
Pesticide
Programs
Health
Effects
Division
(
7509C)
Matthew
Lloyd,
­
Risk
Assessor
Date:
December
20,
2005
Page
3
of
80
Risk
Assessment
Team:

Risk
Assessor:
Matthew
Lloyd
Residue
Chemistry:
Felecia
Fort
Occupational
and
Residential
Exposure:
Jeffrey
Dawson
Epidemiology:
Jerome
Blondell,
MPH,
Ph.
D.

Toxicology:
Linda
Taylor,
Ph.
D.

Drinking
Water
Estimates:
Lucy
Shanaman
HUMAN
HEALTH
RISK
ASSESSMENT
Metaldehyde
Page
4
of
80
Table
of
Contents
1.0
Executive
Summary.........................................................................................................
7
2.0
Ingredient
Profile.............................................................................................................
9
2.1.
Summary
of
Registered/
Proposed
Uses......................................................................
9
2.2.
Structure
and
Nomenclature
....................................................................................
12
2.3.
Physical
and
Chemical
Properties
............................................................................
12
3.0
Metabolism
Assessment.................................................................................................
13
3.1.
Comparative
Metabolic
Profile
................................................................................
13
3.2.
Nature
of
the
Residue
in
Foods.................................................................................
14
3.2.1.
Description
of
Primary
Crop
Metabolism...........................................................
14
3.2.2.
Description
of
Livestock
Metabolism
..................................................................
14
3.2.3.
Description
of
Rotational
Crop
Metabolism,
including
identification
of
major
metabolites
and
specific
routes
of
biotransformation
.......................................................
15
3.3.
Environmental
Degradation
.....................................................................................
15
3.4.
Tabular
Summary
of
Metabolites
and
Degradates..................................................
15
3.5.
Summary
of
Residues
for
Tolerance
Expression
and
Risk
Assessment..................
17
3.5.1.
Tabular
Summary
................................................................................................
17
3.5.2.
Rationale
for
Inclusion
of
Metabolites
and
Degradates......................................
17
4.0
Hazard
Characterization/
Assessment...........................................................................
17
4.1.
Hazard
Characterization
..........................................................................................
17
4.2
FQPA
Hazard
Considerations....................................................................................
22
4.1.1.
Adequacy
of
the
Toxicity
Database......................................................................
22
4.1.2.
Evidence
of
Neurotoxicity
....................................................................................
23
4.1.3.
Developmental
Toxicity
Studies...........................................................................
23
4.1.4.
Reproductive
Toxicity
Study................................................................................
23
4.1.5.
Additional
Information
from
Literature
Sources
...............................................
24
4.1.6.
Pre­
and/
or
Postnatal
Toxicity
.............................................................................
24
4.1.6.1.
Determination
of
Susceptibility........................................................................
24
4.1.6.2.
Degree
of
Concern
Analysis
and
Residual
Uncertainties
for
Pre­
and/
or
Postnatal
Susceptibility....................................................................................................
24
4.2.
Recommendation
for
a
Developmental
Neurotoxicity
Study
..................................
24
4.2.1.
Evidence
in
favor
of
retaining
the
10X/
requiring
further
evaluation
of
neurobehavioral
development............................................................................................
24
4.2.2.
Evidence
against
retaining
the
10X/
requiring
further
evaluation
of
neurobehavioral
development............................................................................................
25
4.2.2.1.
Rationale
for
the
UFDB
(
when
a
DNT
is
recommended)..................................
25
4.3.
Hazard
Identification
and
Toxicity
Endpoint
Selection
..........................................
25
4.3.1.
Margins
of
Exposure
............................................................................................
28
4.3.2.
Recommendation
for
Aggregate
Exposure
Risk
Assessments
............................
28
4.3.3.
Classification
of
Carcinogenic
Potential
..............................................................
28
4.4.
Endocrine
disruption
................................................................................................
29
5.0
Public
Health
Data.........................................................................................................
29
5.1.
Incident
Reports........................................................................................................
29
6.0
Exposure
Characterization/
Assessment........................................................................
31
6.1.
Dietary
Exposure/
Risk
Pathway...............................................................................
31
Page
5
of
80
6.1.1.
Residue
Profile......................................................................................................
31
6.1.2.
Acute
and
Chronic
Dietary
Exposure
and
Risk
..................................................
31
6.2.
Water
Exposure/
Risk
Pathway.................................................................................
33
6.3.
Residential
(
Non­
Occupational)
Exposure/
Risk
Pathway.......................................
33
6.3.1.
Home
Uses.............................................................................................................
33
6.3.1.1.
Residential
Handler
Risk
Assessment..............................................................
37
6.3.1.2.
Residential
Postapplication
Risk
Assessment
....................................................
43
6.3.2.
Recreational
Uses
.................................................................................................
48
6.3.3.
Other
(
Spray
Drift,
etc.).......................................................................................
48
7.0
Aggregate
Risk
Assessments
and
Risk
Characterization.............................................
48
7.1.
Acute
Aggregate
Risk................................................................................................
49
7.2.
Short­
Term
Aggregate
Risk
.....................................................................................
50
7.3.
Long­
Term
Aggregate
Risk
......................................................................................
52
8.0
Cumulative
Risk
Characterization/
Assessment............................................................
53
9.0
Occupational
Exposure/
Risk
Pathway..........................................................................
53
9.1.
Short/
Intermediate/
Long­
Term
Handler
Risk.........................................................
54
9.2.
Short/
Intermediate/
Long­
Term
Postapplication
Risk.............................................
65
10.0
Data
Needs
and
Label
Requirements............................................................................
65
10.1.
Toxicology
...............................................................................................................
65
10.2.
Residue
Chemistry..................................................................................................
65
10.3.
Occupational
and
Residential
Exposure
................................................................
66
References:
..............................................................................................................................
66
Appendices:
Appendix
A:
Relevant
Toxicology
Executive
Summaries
.....................................................
67
Appendix
B:
Tolerance
Reassessment
Summary
..................................................................
78
List
of
Tables
Table
1
­
Metaldehyde
End­
Use
Products
(
EPs)
with
Registered
Food/
Feed
Uses.
............
10
Table
2
­
Metaldehyde
Nomenclature
....................................................................................
12
Table
3
­
Physicochemical
Properties
of
Metaldehyde
..........................................................
12
Table
4
­
Tabular
Summary
of
Metabolites
and
Degradates
................................................
16
Table
5
­
Summary
of
Metabolites
and
Degradates
to
be
included
in
the
Risk
Assessment
and
Tolerance
Expression...............................................................................................
17
Table
6
­
Acute
Toxicity
Profile
­
Metaldehyde
.....................................................................
19
Table
7
­
Subchronic,
Chronic
and
Other
Toxicity
Profile
...................................................
20
Table
8
­
Summary
of
Toxicology
Endpoint
Selection
for
Metaldehyde
..............................
27
Table
9
­
Summary
of
Dietary
Exposure
and
Risk
for
Metaldehyde....................................
32
Table
10
­
Summary
of
Estimated
Surface
and
Ground
Water
Concentrations
for
Metaldehyde
....................................................................................................................
33
Table
11
­
Summary
of
Registered
Metaldehyde
Residential
Uses.......................................
34
Table
12
­
Metaldehyde
Residential
Non­
Cancer
Inhalation
Exposure
and
Risk................
40
Table
13
­
Summary
of
Non­
Cancer
Short­
term
Postapplication
MOEs
for
Toddlers
.......
47
Table
14
­
Aggregate
Risk
Assessment
for
Acute
Dietary
Exposure
to
Metaldehyde..........
50
Table
15
­
Short­
Term
Aggregate
Risk..................................................................................
51
Table
16
­
Aggregate
Risk
Assessment
for
Chronic
Dietary
Exposure
to
Metaldehyde
......
52
Page
6
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks.................................................................................................................................
58
Page
7
of
80
1.0
Executive
Summary
This
risk
assessment
was
performed
to
support
the
reregistration
eligibility
decision
for
metaldehyde
[
2,4,6,8­
tetramethyl­
1,3,5,7­
tetraoxyacyclooctane].
Metaldehyde
is
used
to
control
slugs
and
snails
on
a
wide
variety
of
tree,
fruit
and
vegetable
crops.
Metaldehyde
is
formulated
as
granules
(
G),
pelleted
(
P/
T)
baits,
emulsifiable
concentrate
(
EC),
flowable
concentrate
(
FlC),
and
ready­
to­
use
liquid
(
RTU/
L)
formulations.
Formulated
products
generally
contain
0.13­
25%
active
ingredient.

The
use
of
metaldehyde
is
being
supported
by
Lonza,
Inc.,
which
manufactures
the
only
technical
grade
product
registered
in
the
U.
S.
(
OPPIN
query
on
11/
15/
04).
There
are
a
total
of
68
end­
use
products
with
feed/
food
uses
that
are
registered
or
conditionally
registered
to
22
different
registrants.

In
the
past,
it
was
assumed
that
acetaldehyde,
which
can
be
formed
in
an
acidic
environment
like
the
stomach,
was
responsible
for
the
toxic
effects
observed
following
metaldehyde
exposure.
However,
this
seems
unlikely
since
acetaldehyde
was
not
found
in
the
plasma
or
urine
of
dogs
exposed
to
metaldehyde.
Metaldehyde
has
been
shown
to
cross
the
blood­
brain
barrier
and
has
been
detected
in
the
brain,
blood,
and
liver
of
rodents.
When
molluscs
and
slugs
are
exposed
to
metaldehyde,
the
chemical
causes
the
pests
to
be
torpid,
increasing
the
secretion
of
mucus
leading
to
dehydration
and
death.

Metaldehyde
has
low
acute
toxicity
via
the
dermal
and
inhalation
routes
of
exposure
[
Toxicity
Category
III]
and
via
the
oral
route
in
males
[
Toxicity
Category
III].
Moderate
acute
oral
toxicity
[
Toxicity
Category
II]
is
observed
in
females.
Metaldehyde
is
a
mild
eye
irritant
[
Toxicity
Category
III]
but
is
not
a
skin
irritant
[
Toxicity
Category
IV]
or
a
dermal
sensitizer.
No
dermal
or
systemic
toxicity
was
observed
at
the
limit
dose
[
1000
mg/
kg/
day]
in
the
21­
day
dermal
toxicity
study
in
the
rabbit.

The
liver
is
a
target
organ
following
subchronic
and
chronic
oral
exposure,
as
evidenced
by
increased
liver
weight,
increased
incidence
of
liver
lesions
[
hepatocellular
necrosis,
hepatocellular
hypertrophy,
inflammation],
and
an
increased
incidence
of
hepatocellular
adenomas/
carcinomas
in
female
rats
and
hepatocellular
adenomas
in
both
sexes
of
mice.
The
testes
and
prostate
are
also
target
organs,
as
evidenced
by
atrophy
of
both
organs
following
subchronic
and
chronic
exposure
in
dogs.

There
is
a
concern
for
neurotoxicity
following
oral
exposure
to
metaldehyde,
as
evidenced
by
hindlimb
paralysis,
along
with
mortality,
in
rats
following
both
acute
[
one
to
two
doses
in
pregnant
rats]
and
repeated
exposure
(
lactation
days
16­
18),
neurotoxic
signs
[
ataxia,
tremors,
twitching,
salivation,
and/
or
prostration]
in
female
rats
[
1­
2
doses]
and
dogs
of
both
sexes
[
within
first
week
of
exposure
and
persisting
through
week
19],
and
neuropathology
[
spinal
cord
necrosis
and
hemorrhage]
in
the
maternal
animal.

Developmental
toxicity
was
not
observed
in
either
the
rat
or
rabbit
study
at
adequate
dose
levels.
Reproductive
toxicity
was
not
observed.
Offspring
toxicity
[
decreased
pup
body
weight/
body­
weight
gain]
occurred
at
the
same
dose
level
producing
mortality,
clinical
signs
[
hindlimb
paralysis]
and
histopathology
[
spinal
cord
necrosis
and
hemorrhage]
in
the
maternal
animal.
Page
8
of
80
The
mutagenicity
database
is
not
complete,
and
a
complete
battery
of
studies
is
required.

The
weight
of
evidence
for
metaldehyde
is
"
Suggestive
Evidence
of
Carcinogenic
Potential",
based
on
the
presence
of
benign
liver
tumors
in
female
rats,
benign
liver
tumors
in
both
sexes
of
mice,
and
a
lack
of
adequate
mutagenicity
data.
No
quantification
of
cancer
risk
has
been
recommended.

The
available
toxicology
data
are
adequate
for
toxicity
endpoint
selection
for
risk
assessment
as
summarized
below:

Dose
Study
Type/
Endpoint
Acute
dietary:
NOAEL
75
mg/
kg
Developmental
toxicity
in
rats
Chronic
dietary:
NOAEL
10
mg/
kg
Chronic
oral
toxicity
study
in
dogs
Short
term
incidental
oral:
NOAEL
30
mg/
kg
Chronic
oral
toxicity
study
in
dogs
(
ataxia,
tremor,
twitching
from
week
1)
UF
=
1000
for
dietary
and
residential
assessment
There
was
no
evidence
of
increased
susceptibility
following
in
utero
exposure
in
rats
and
rabbits
and
pre­/
postnatal
exposure
in
the
2­
generation
reproduction
study
in
rats.
Since
there
are
no
residual
uncertainties
that
indicate
the
need
for
a
special
safety
factor,
the
FQPA
special
(
hazard)
factor
can
be
reduced
to
1X.
However,
a
developmental
neurotoxicity
study
is
recommended
due
to:
1)
the
neuropathology
observed
in
the
F0
dams
that
also
displayed
clinical
signs
of
neurotoxicity,
bilateral
hindlimb
paralysis,
and
death
in
the
2­
generation
reproduction
study;
2)
the
clinical
signs
of
neurotoxicity
and
death
in
dams
in
the
rat
developmental
toxicity
study;
and
3)
bilateral
hindlimb
paralysis
observed
in
one
high­
dose
female
sacrificed
[
day
22]
due
to
poor
condition
in
the
90­
day
subchronic
neurotoxicity
study
in
rats.
A
database
uncertainty
factor
of
10X
was
recommended
to
be
applied
to
all
exposure
durations.

Dietary
Exposure:
Acute
and
chronic
dietary
exposure
and
risk
assessments
were
conducted
applying
tolerance
level
residues.
Food
and
water
were
considered
in
these
assessments.
Risk
estimates
were
below
HED's
level
of
concern
for
both
the
acute
and
chronic
assessments
for
the
U.
S.
general
population
and
various
population
subgroups.
The
highest
exposed
population
subgroup
was
children
1­
2
years
old
(
25%
aPAD
and
49%
cPAD
for
acute
and
chronic
risks,
respectively.
The
dietary
risk
estimates
could
be
further
refined
with
the
incorporation
of
anticipated
residues,
cooking/
processing
factors
and
usage
information
(
percent
crop
treated).

Residential
Exposure:
Residential
handler
scenarios
and
some
residential
post­
application
scenarios
have
not
been
assessed
because
dermal
exposure
is
not
considered
a
hazard
for
metaldehyde
and
inhalation
exposures
are
not
anticipated.
All
of
the
residential
handler
scenarios
have
Margins
of
Exposure
(
MOEs)
that
were
not
of
concern
( 
5600).
The
post
application
residential
exposure
scenarios
include
hand­
to­
mouth,
object­
to­
mouth,
soil
ingestion
for
toddlers,
and
the
possible
ingestion
of
metaldehyde
granules.
The
combined
risk
estimate
represents
a
high
level
of
exposure
based
on
what
may
be
reasonably
expected
to
occur
in
the
metaldehyde
user
population.
Short­
term
risks
from
exposure
to
treated
turf
were
not
of
concern
(
combined
MOE=
1600).
.
A
rangefinder
intermediateterm
assessment
was
also
completed
resulting
in
risks
that
were
not
of
concern.
Page
9
of
80
Uncertainty
related
to
the
issue
of
a
lack
of
residue
dissipation
data
would
be
reduced
if
residue
dissipation
data
were
available.

Aggregate
Exposures:
HED
considered
and
aggregated
metaldehyde
pesticide
exposures
and
risks
from
several
major
sources:
food,
drinking
water,
residential,
and
other
nonoccupational
exposures.
Intermediate
term
exposures
were
expected
to
occur
infrequently,
if
at
all.
For
the
acute
aggregate
risk
assessment
with
dietary
and
ground
water,
the
highest
subgroup
was
children
(
1­
2
years
old)
with
29%
of
the
aPAD
at
the
95th
percentile.
The
short
term
aggregate
risk
was
aggregated
from
oral
and
inhalation
exposures,
and
was
based
on
the
same
endpoint.
None
of
the
scenarios
for
the
relevant
population
sub­
groups
demonstrated
risks
of
concern.
Long
term
aggregate
risk
included
only
food
and
drinking
water
as
there
were
no
long
term
residential
uses
for
metaldehyde.
The
most
highly
exposed
sub­
group
was
children
1­
2
years
old
where
69%
of
the
cPAD
was
occupied
in
the
chronic
aggregate
assessment.

Occupational
Exposures:
A
variety
of
handler
exposure
scenarios
were
assessed
including
chemigation,
groundboom
application,
airblast,
various
granular
application
scenarios,
and
various
handheld
sprayer
scenarios
(
e.
g.
handgun
and
hose­
end).
For
all
short­
and
intermediate­
term
occupational
handler
scenarios,
risks
were
not
of
concern.

Occupational
post­
application
exposures
were
not
assessed
for
metaldehyde
because
no
dermal
hazard
was
identified.
Inhalation
exposures
were
expected
to
be
negligible
in
outdoor
post­
application
scenarios
since
metaldehyde
has
low
vapor
pressure
and
the
dilution
factor
outdoors
is
considered
infinite.

2.0
Ingredient
Profile
Metaldehyde
[
2,4,6,8­
tetramethyl­
1,3,5,7­
tetraoxyacyclooctane]
is
used
to
control
slugs
and
snails
on
a
wide
variety
of
tree,
fruit
and
vegetable
crops.
Metaldehyde
is
formulated
as
granules
(
G),
pelleted
(
P/
T)
baits,
emulsifiable
concentrate
(
EC),
flowable
concentrate
(
FlC),
and
ready­
to­
use
liquid
(
RTU/
L)
formulations
at
concentrations
ranging
from
0.13­
25%
a.
i.
The
use
of
metaldehyde
is
being
supported
by
Lonza,
Inc.,
which
manufactures
the
only
technical
grade
product
registered
in
the
U.
S.

2.1.
Summary
of
Registered/
Proposed
Uses
A
summary
of
end­
use
products
is
presented
below
in
Table
1.
Page
10
of
80
Table
1
­
Metaldehyde
End­
Use
Products
(
EPs)
with
Registered
Food/
Feed
Uses.

EPA
Reg.
No.
Formulation
1
Label
Date
Registrant
Product
Name
11656­
20
2
2%
P/
T
6/
19/
74
Western
Farm
Service,
Inc
Coastox
Meta
Carbaryl
2­
4
Snail
Pellets
19713­
389
4%
4/
24/
96
Drexel
Chemical
Co
Drexel
Slug
and
Snail
Bait
239­
2373
3.25%
P/
T
6/
22/
71
Bug­
geta
Snail
&
Slug
Pellets
239­
2514
2
2%
1/
24/
85
Get­
a­
Bug
Snail,
Slug
&
Insect
Killer
239­
2651
2%
P/
T
10/
01/
96
The
ORTHO
Business
Goup
Bug­
Geta
Snail
&
Slug
Pellets
3
2935­
418
4%
10/
28/
82
Wilbur
Ellis
Co.
Metaldehyde
4
Bait
34911­
8
2
1%
9/
15/
76
Hi­
Yield
Chemical
Company
Hi­
Yield
Bug
Bait
4­
333
2
2%
8/
21/
86
Bonide
Slug,
Snail
&
Sowbug
Bait
4­
334
3.25%
8/
21/
86
Bonide
Slug
and
Snail
Beater
4­
351
4%
7/
31/
89
Last
Slime
Slug­
n­
Snail
Beater
RTU
4­
352
12.5%
12/
14/
89
Bonide
Last
Slime
Slug­
n­
Snail
Beater
4­
442
0.13%
8/
30/
00
N­
Slugs­
N­
Snails
4­
443
2
0.13%
2/
22/
96
Micro
Flow
Slug
N
Snail
Plus
4­
449
2
2%
11/
01/
02
Bonide
Snail,
Slug
&
Sowbug
Bait
4­
450
2
0.13%
10/
29/
02
Bonide
Snail
N
Slug
Plus
4­
451
3.25%
10/
29/
02
Bonide
Snail­
N­
Slug
Beater
4­
452
0.13%
3/
26/
03
N­
Snails­
N­
Slugs
4­
453
12.5%
10/
29/
02
Bonide
Products,
Inc.

Bonide
Snail­
n­
Slug
Beater
Concentrate
42057­
39
2
4%
3/
09/
79
MORGRO
Chemical
Co
MORGRO
Pest
Meal
49585­
27
2%
7/
02/
93
Alljack,
Division
of
United
Industries
Corp
K
Gro
Snail
&
Slug
Bait
5887­
170
2
2.5%
11/
16/
87
Black
Leaf
Snailicide
769­
643
3.25
P/
T
7/
29/
71
Value
Gardens
Supply,
LLC
Smcp
Slug
and
Snail
Bait
Pellets
59639­
53
4%
P/
T
11/
16/
89
Valent
U.
S.
A.
Corporation
Valent
Metaldehyde
4%
Bait
6973­
10
1%
P/
T
10/
09/
67
SOILSERV
Inc
SOILSERV
Sevin
Metaldehyde
Bait
61282­
10
2
3.5%
P/
T
6/
29/
92
Snail
and
Slug
Ag
Pelleted
Bait
61282­
11
3.5%
P/
T
6/
29/
92
Snail
and
Slug
Ag
Pelleted
Bait
61282­
34
2.75%
P/
T
1/
10/
67
HACCO,
Inc.

Hopkins
Snail
and
Slug
Pellets
5481­
100
2
2.5%
G
2/
26/
73
Durham
carbaryl
Metaldehyde
Granules
5­
2.5
5481­
103
7.5%
G
2/
26/
73
Durham
Metaldehyde
Granules
7.5
5481­
318
20%
G
7/
23/
86
Slugit
5481­
451
2
3%
3/
27/
95
Snail,
Slug
&
Sowbug
Killer
for
Lawn
&
Garden
5481­
507
4%
P/
T
9/
10/
86
Deadline
Bullets
5481­
511
4%
P/
T
2/
03/
98
Deadline
M­
PS
Mini­
Pellets!
5481­
91
3.5%
G
2/
26/
73
Durham
Metaldehyde
Granules
3.5
5481­
95
2
3%
G
2/
26/
73
Durham
End
of
Trail
Snail­
Slug
&
Insect
Granules
5481­
97
2
3%
2/
26/
73
AMVAC
Chemical
Corp
Alco
Snail,
Slug
and
Sowbug
Killer
71096­
10
1.5%
RTU
6/
26/
02
OR­
CAL
Inc
Slug­
Feast
All
Weather
Formula
RTU
Page
11
of
80
Table
1
­
Metaldehyde
End­
Use
Products
(
EPs)
with
Registered
Food/
Feed
Uses.

EPA
Reg.
No.
Formulation
1
Label
Date
Registrant
Product
Name
71096­
12
10.5%
4/
25/
73
Lilly/
Miller
Go
West
Slug
Killer
71096­
13
4%
P/
T
8/
16/
94
SOILSERV
Metaldehyde
Snail
Bait
71096­
4
2.1
lb/
gal
FlC
10/
10/
73
Slug­
Fest
Colloidal
25
71096­
7
3.25%
P/
T
10/
01/
80
OR­
CAL
Slug
&
Snail
Bait
71096­
8
2.75%
P/
T
10/
01/
80
(
OR­
CAL
cont'd)

Snail
&
Slug
Pellets
7401­
265
2
1%
P/
T
7/
14/
76
Ferti­
Lome
Home
Garden
Bug
Bait
7401­
450
2.75%
P/
T
9/
25/
00
Hi­
Yield
Snail
&
Slug
Killer
Pellets
7401­
72
2
1%
9/
10/
71
Voluntary
Purchasing
Group
Inc
Ferti­
Lome
Improved
Bug
Bait
74941­
1
2%
11/
21/
03
Metarex
2%
Snail
Slug
Bait
74941­
2
4%
5/
08/
03
De
Sangosse
UK
Metarex
4%
Snail
and
Slug
Bait
33116­
3
10.5%
11/
06/
02
Lilly
Miller
Slug
&
Snail
Spray
802­
351
2
2%
10/
24/
63
Miller's
Slug,
Snail
and
Insect
Killer
Bait
802­
549
2%
1/
03/
83
Lilly/
Miller
Slug,
and
Snail
'
Em
Bait
909­
83
2
3%
G
5/
31/
85
Central
Garden
&
Pet
D/
B/
A
Lilly
Miller
Brands/
Excel
Garden
Cooke
Slug­
N­
Snail
Granules
8119­
1
2%
9/
26/
63
Corry's
Slug
and
Snail
Death
8119­
11
3.25%
P/
T
12/
05/
02
Corry's
Slug
&
Snail
3.25
8119­
13
3.25%
P/
T
12/
05/
02
Corry's
Slug
&
Snail
Pellets
MP
8119­
2
4%
1/
16/
87
Corry's
Liquid
Slug
&
Snail
Control
8119­
5
2
2%
4/
11/
88
Corry's
Slug,
Snail
&
Insect
Killer
8119­
6
4%
1/
14/
75
Deadline­
40
8119­
9
4%
11/
13/
98
Matson,
LLC
Deadline
Rain
Trough
8278­
3
2
3.5%
8/
03/
90
Metro
Tested
All
Purpose
Bug
Bait
8278­
4
7.5%
4/
30/
93
Metro
Biological
Laboratory
Metro
That's
It
Dry
829­
182
2
3.25%
P/
T
11/
17/
67
Southern
Agricultural
Insecticides,
Inc.
SA­
50
Brand
Bait
Pellets
Kill
Land
Snails
&
Slugs
8660­
196
2.75%
3/
23/
71
Pursell
Snail
&
Slug
Killer
Meal
8660­
197
2.75%
P/
T
2/
19/
71
Snail
&
Slug
Killer
Pellets
8660­
250
2%
P/
T
2/
24/
99
Sta­
Gone
Snail
&
Slug
Killer
Pellets
8660­
251
2%
2/
24/
99
Sta­
Gone
Snail
&
Slug
Killer
Meal
8660­
73
3%
3/
12/
85
Vertagreen
Slug
&
Snail
Bait
8660­
73
3%
3/
12/
85
SYLORR
Plant
Corp.

Vertagreen
Slug
&
Snail
Bait
869­
119
2
1%
11/
17/
72
Green
Light
Company
Green
Light
Bug
&
Snail
Bait
1
Information
on
the
formulation
type
for
numerous
EPs
was
not
available
to
the
reviewer.
2
These
are
MAI
formulations
also
containing
4­
5%
carbaryl.
Page
12
of
80
2.2.
Structure
and
Nomenclature
The
nomenclature
of
metaldehyde
are
presented
in
Table
2.

Table
2
­
Metaldehyde
Nomenclature
Chemical
structure
O
O
O
O
C
H
3
CH
3
CH
3
C
H
3
Common
name
Metaldehyde
(
PC
Code
 
053001)

Molecular
Formula
C8H16O4
Molecular
Weight
176.2
IUPAC
name
r­
2,
c­
4,
c­
6,
c­
8­
tetramethyl­
1,3,5,7­
tetroxocane
or
2,4,6,8­
tetramethyl­
1,3,5,7­
tetraoxacyclo­
octane
CAS
name
2,4,6,8­
tetramethyl­
1,3,5,7­
tetraoxacyclooctane
CAS
#
108­
62­
3
2.3.
Physical
and
Chemical
Properties
The
physicochemical
properties
of
metaldehyde
are
listed
below
in
Table
3.

Table
3
­
Physicochemical
Properties
of
Metaldehyde
Parameter
Value
Reference
Melting
point
246
EC
MRID
00131972;
Metaldehyde
Registration
Standard,
10/
7/
88,
Chuck
Trichilo.

pH
Not
applicable
due
to
the
low
solubility
of
metaldehyde
in
water.
N/
A
Density,
bulk
density,
or
specific
gravity
1.27
g/
cm3
Metaldehyde,
IPCS
Inchem,
WHO/
FAO
Data
Sheet
(
PDS
93).

Water
solubility
0.222
g/
L
at
20
EC
MRID
40733901;
RD
letter
dated
4/
5/
89
from
D.
Edwards
to
J.
Conti,
Lonza,
Inc.
Page
13
of
80
Table
3
­
Physicochemical
Properties
of
Metaldehyde
Parameter
Value
Reference
Solvent
solubility
At
20.3­
22.4
EC:
5.21
x
10­
2
g/
L
in
hexane
0.53
g/
L
in
toluene
1.56
g/
L
in
tetrahydrofuran
1.73
g/
L
in
methanol
MRID
00131972;
Metaldehyde
Registration
Standard,
10/
7/
88,
Chuck
Trichilo.

Vapor
pressure
6.6
±
0.3
Pa
at
25
EC
MRID
40733902;
Letter
dated
4/
5/
89
from
D.
Edwards
(
RD)
to
J.
Conti
(
Lonza,
Inc.)

Dissociation
constant,
pKa
3.5
Pa
(
m3/
mol)
(
Henry's
Law
Constant)
MRID
40733904;
Letter
dated
4/
5/
89
from
D.
Edwards
(
RD)
to
J.
Conti
(
Lonza,
Inc.)

Octanol/
water
partition
coefficient
1.33
(
log
POW
=
0.12)
at
20
EC
MRID
40733903;
Letter
dated
4/
5/
89
from
D.
Edwards
(
RD)
to
J.
Conti
(
Lonza,
Inc.)

UV/
visible
absorption
spectrum
N/
A
N/
A
3.0
Metabolism
Assessment
Previously,
the
toxicologically
active
substance
was
thought
to
be
the
degradation
product
acetaldehyde,
which
can
be
formed
at
a
low
pH
in
the
stomach.
However,
the
old
theory
that
acetaldehyde
is
responsible
for
the
toxic
effects
observed
following
metaldehyde
exposure
seems
unlikely
since
acetaldehyde
was
not
found
in
the
plasma
or
urine
of
dogs
exposed
orally
to
metaldehyde.
Metaldehyde
has
been
shown
to
cross
the
blood­
brain
barrier
and
has
been
detected
in
the
brain,
blood,
and
liver
of
rodents.

Metaldehyde
is
rapidly
absorbed,
distributed,
and
metabolized,
with
most
of
the
radiolabel
being
recovered
as
14CO2
in
expired
air
within
24
hours
for
male
rats
and
within
48
hours
in
female
rats
(
MRID
42300901).
Recovery
in
urine/
feces
is
low
[
2.5%­
5.1%],
and
the
sexes
differ
slightly.
In
plasma,
the
ratio
of
metaldehyde
to
acetaldehyde
was
found
to
be
4:
1
in
males
and
12:
1
in
females
at
peak
blood
level
(
1­
2
hrs
in
males
and
2­
4
hrs
in
female,
post
dosing).
In
addition,
the
half­
life
of
metaldehyde
was
longer
in
females
(
8.8
hrs)
than
in
males
(
3.4
hrs).

3.1.
Comparative
Metabolic
Profile
The
major
residue
found
in
plant
metabolism
studies
on
lettuce
and
sugar
beets
was
the
parent
compound,
metaldehyde.
There
were
considerable
non­
extractable
residues
in
sugar
beet
root
and
tops
that
were
not
further
characterized.
The
Confined
Rotational
Crop
study
was
waived
since
the
metabolism
in
secondary
crops
is
likely
to
be
similar
to
the
primary
crops.
Page
14
of
80
Livestock
metabolism
studies
have
been
waived
because
metaldehyde
is
expected
to
be
rapidly
metabolized
in
mammalian
systems
with
subsequent
incorporation
of
degradates
into
naturally
occurring
components.
This
conclusion
is
supported
by
the
extensive
metabolism
observed
in
rat
metabolism
studies.

Metaldehyde
is
rapidly
absorbed,
distributed,
and
metabolized
in
the
rat.
Between
78­
98%
of
the
administered
dose
was
recovered
as
expired
air
within
24
hours
as
14CO2
in
the
rat
metabolism
study
(
MRID
42300901).

There
was
extensive
metabolism
of
metaldehyde
in
both
plants
and
animals.

3.2.
Nature
of
the
Residue
in
Foods
3.2.1.
Description
of
Primary
Crop
Metabolism
The
qualitative
nature
of
metaldehyde
residues
in
plants
is
understood
based
on
the
adequate
lettuce
and
sugar
beet
metabolism
studies.
The
HED
Metabolism
Committee
(
7/
2/
96)
concluded
that
the
regulated
residue
of
concern
in
plants
is
parent
metaldehyde,
per
se.

In
the
lettuce
metabolism
study,
radioactive
residues
were
taken
up
and
translocated
to
leaves
following
a
single
directed
application
of
[
14C]
metaldehyde
to
the
soil
at
a
rate
equivalent
to
13.76
lb
ai/
A
(
10X).
The
maximum
total
radioactive
residues
(
TRR)
were
4.43
ppm
and
3.78
ppm
in
the
inner
and
outer
lettuce
leaves,
respectively,
with
a
PHI
of
28
days.
Up
to
95.3%
of
TRR
was
identified
as
the
parent
metaldehyde.

In
the
sugar
beet
metabolism
study,
a
single
directed
application
of
[
14C]
metaldehyde
was
made
to
the
soil
at
a
rate
equivalent
to
13.76
lb
ai/
A
(
10X).
The
TRR
were
1.65­
5.60
ppm
in/
on
sugar
beet
foliage
and
0.30­
1.13
ppm
in/
on
sugar
beet
root
(
PHI
=
48
days),
indicating
uptake
and
translocation
to
foliage.
Metaldehyde
was
the
only
radioactive
residue
identified
in
the
organic
fractions
of
foliage
(­
33%
TRR,
1.84
ppm)
and
root
(­
35%
TRR,
0.39
ppm).
Although
no
analytical
analyses
of
the
nonextractable
residues
of
foliage
(
43.2%
TRR,
2.42
ppm)
and
root
(
43.4%
TRR,
0.49
ppm)
were
conducted,
the
aggregate
of
plant
metabolism
data
for
this
chemical
support
the
HED
Metabolism
Committee's
decision
to
regulate
only
the
parent
in
the
tolerance
expression
for
plant
commodities.

3.2.2.
Description
of
Livestock
Metabolism
Requirements
for
livestock
metabolism
and
feeding
studies
have
been
waived.
The
Agency
concluded
that
residues
are
unlikely
to
occur
in
livestock
commodities
based
upon
the
rapid
degradation
of
metaldehyde
in
mammalian
systems
and
the
subsequent
incorporation
of
degradates
into
naturally
occurring
components.
(
HED;
3/
11/
97).
Page
15
of
80
3.2.3.
Description
of
Rotational
Crop
Metabolism,
including
identification
of
major
metabolites
and
specific
routes
of
biotransformation
A
request
for
a
data
waiver
of
the
confined
rotational
crop
study
for
metaldehyde
was
submitted.
The
registrant
is
proposing
to
conduct
a
field
accumulation
in
rotational
crops
study
rather
than
the
confined
accumulation
in
rotational
crop
study.

The
rationale
for
the
waiver
is
that
since
the
confined
rotational
crop
study
is
essentially
a
metabolism
study
and
metabolism
is
understood
for
metaldehyde,
the
confined
study
should
not
be
required.
The
Agency
made
the
determination
that
the
only
residue
of
interest
is
metaldehyde
per
se.
For
this
reason,
the
Agency
granted
Lonza
Inc.
waivers
for
nature
of
residue
studies
in
plants
and
livestock
and
required
quantification
of
metaldehyde
in
plant
translocation
studies
that
were
conducted
with
metaldehyde.
The
basis
for
this
decision
is
that
because
of
its
chemical
structure
(
a
tetramer
of
acetaldehyde),
the
primary
metabolite
would
be
acetaldehyde,
a
chemical
whose
metabolism
in
plants
and
animals
is
well
documented
in
basic
chemistry
texts.
The
second
reason
is
that
it
is
very
likely
that
total
radioactive
residues
(
TRR)
greater
than
0.01
ppm
would
be
found
in
the
one­
month
and
four­
month
rotational
crops
in
a
confined
rotational
crop
study.
This
in
turn
would
trigger
the
need
for
the
field
study
anyway.
Lonza,
Inc.
believes
that
the
TRR
would
be
greater
than
0.01
because
metaldehyde
is
a
soil
applied
slug
and
snail
bait
that
has
been
shown
to
translocate
through
the
soil
into
plant
matrices,
and
its
half
­
life
in
soil
under
aerobic
conditions
is
67.2
days.
The
third
reason
is
that
residues
ranging
between
0.168
and
0.298
ppm
have
been
found
in
several
crops
in
the
leafy
vegetable
crop
group
in
the
recent
crop
field
trial
program.

On
December
9,
2004,
the
Chemistry
Science
Advisory
Council
(
CHEMSAC)
granted
a
waiver
for
the
confined
accumulation
in
rotational
crop
study
for
the
chemical
metaldehyde.

3.3.
Environmental
Degradation
Metaldehyde
is
expected
to
be
mobile
and
moderately
persistent
in
the
environment.
Metaldehyde
degrades
aerobically
with
a
reported
half­
life
of
67
days,
anaerobically
with
a
reported
half­
life
of
222
days,
and
is
stable
to
abiotic
degradation
(
hydrolysis
and
photolysis).
There
were
no
toxic
residues
of
concern
identified
for
the
metaldehyde
transformation
products,
and
those
transformation
products
were
not
considered
in
the
EFED
drinking
water
assessment.
Acetaldehyde
is
an
environmental
degradate
resulting
from
metaldehyde,
although
because
acetaldehyde
undergoes
further
degradation,
it
is
not
included
in
the
tolerance
expression
or
this
risk
assessment.

3.4.
Tabular
Summary
of
Metabolites
and
Degradates
A
tabular
summary
of
metabolites
and
degradates
can
be
found
below
in
Table
4.
Page
16
of
80
Table
4
­
Tabular
Summary
of
Metabolites
and
Degradates
Percent
TRR
(
PPM)
1
Chemical
Name
Commodity
Matrices
­
Major
Residue2
(>
10%
TRR)
Matrices
­
Minor
Residue2
(<
10%
TRR)
Structure
Lettuce
95.3
Sugar
beet
­
root
35
Sugar
beet
­
top
33
Parent:
Metaldehyde
Rat
*
O
O
O
O
C
H
3
CH
3
CH
3
C
H
3
Lettuce
<
5
Sugar
beet
­
root
43.4
Sugar
beet
­
top
43.2
Degradate:
Non­
Extractable
Residues
Rat
ND
2.5­
5.1
CO2
Rat
78­
98
N/
A
Lettuce;
43923301;
13.8
lb
ai/
A;
10x;
single
directed
application;
28
days.

Sugar
beets;
43923302;
13.76
lb
ai/
A;
10x;
single
directed
application;
48
days.

Rat:
42300901;
single
gavage
dose
10
or
100
mg/
kg,
repeated
dose
10
mg/
kg/
day
for
14
days,
then
single
dose
14C
[
10
mg/
kg],
Sprague­
Dawley,
1
day
depuration
*
=
metaldehyde
and
acetaldehyde
detected
in
plasma;
no
quantification
available
at
this
time.
ND
=
not
detectable
Note
1:
Confined
Rotational
Crop
waiver
granted
by
CHEMSAC
on
12/
9/
04.
Note
2:
Livestock
metabolism
and
feeding
studies
(
ruminant
&
poultry)
waiver
granted
Metaldehyde:
3/
11/
97)
Page
17
of
80
3.5.
Summary
of
Residues
for
Tolerance
Expression
and
Risk
Assessment
3.5.1.
Tabular
Summary
Table
5
­
Summary
of
Metabolites
and
Degradates
to
be
included
in
the
Risk
Assessment
and
Tolerance
Expression
Matrix
Residues
included
in
Risk
Assessment
Residues
included
in
Tolerance
Expression
All
Primary
Crops
Parent
Parent
Plants
Rotational
Crop
Parent
Parent
Ruminant
Not
Applicable
Not
Applicable
Livestock
Poultry
Not
Applicable
Not
Applicable
Drinking
Water
Parent
Not
Applicable
3.5.2.
Rationale
for
Inclusion
of
Metabolites
and
Degradates
The
major
residue
found
in
plant
commodities
was
the
parent
compound,
metaldehyde.
Carbon
dioxide
and
acetaldehyde
are
expected
to
be
the
terminal
metabolites
and/
or
environmental
degradates.

As
mentioned
in
section
3.0,
acetaldehyde
previously
was
thought
to
be
a
major
metabolite
of
metaldehyde.
The
recent
data
indicated
that
metaldehyde
was
found
in
greater
concentrations
in
test
animals
than
acetaldehyde.
However,
acetaldehyde
occurs
naturally,
and
is
ubiquitous
in
the
body.
Acetaldehyde
is
used
as
a
flavorant/
adjuvant
and
background
levels
occur
in
foods
at
up
to
500
ppm.
It
is
also
listed
as
"
Generally
Recognized
As
Safe"
(
GRAS)
in
21
CFR
182.60.
Therefore,
acetaldehyde
is
not
a
residue
of
concern
for
either
risk
assessment
or
the
tolerance
expression.

4.0
Hazard
Characterization/
Assessment
4.1.
Hazard
Characterization
The
required
toxicological
database
on
metaldehyde
is
not
complete.
The
toxicological
data
gaps
for
metaldehyde
include
a
developmental
neurotoxicity
study
in
rats,
a
subchronic
inhalation
study,
and
a
mutagenicity
battery.
However,
adequate
information
was
available
for
establishing
toxicity
endpoints
and
doses
for
risk
assessment.

In
published
articles
on
metaldehyde,
signs
and
symptoms
of
toxicity
in
humans
may
be
delayed
several
hours
following
ingestion.
Depending
upon
the
dose,
initial
effects
may
Page
18
of
80
be
associated
with
gastrointestinal
irritation,
e.
g.
increased
salivation,
nausea,
abdominal
pain,
vomiting
and
diarrhea.
Other
signs
and
symptoms
may
include
elevated
body
temperature,
mental
confusion,
muscle
cramps
and
tremors,
loss
of
consciousness,
convulsions
and
coma.
In
case
of
severe
poisoning,
death
may
be
due
to
cyanosis
and
respiratory
failure.
There
may
also
be
some
liver
and
kidney
involvement
and
recovery
may
take
several
weeks.
It
should
be
noted
the
gastrointestinal
effect
of
metaldehyde
in
human
was
consistent
with
the
necropsy
found
in
the
developmental
rat
study.
In
that
study,
dams
dying
on
test
had
thinning
of
the
stomach
wall,
ulceration
of
the
glandular
and
nonglandular
portion
of
the
stomach.
These
results
were
seen
at
generally
high
dose
levels.

When
molluscs
and
slugs
are
exposed
to
metaldehyde,
the
chemical
causes
the
pests
to
be
torpid,
increasing
the
secretion
of
mucus
leading
to
dehydration
and
death.

Metaldehyde
has
low
acute
toxicity
via
dermal
[
Toxicity
Category
III]
and
inhalation
[
Toxicity
Category
IV]
routes
of
exposure.
The
acute
oral
toxicity
category
is
II.
Metaldehyde
is
a
mild
eye
irritant
[
Toxicity
Category
III],
but
is
not
a
skin
irritant
[
Toxicity
Category
IV]
or
a
dermal
sensitizer.
No
dermal
or
systemic
toxicity
was
observed
at
the
limit
dose
[
1000
mg/
kg/
day]
in
the
21­
day
dermal
toxicity
study
in
the
rabbit.

The
liver
is
a
target
organ
following
subchronic
and
chronic
oral
exposure,
as
evidenced
by
increased
liver
weight,
increased
incidence
of
liver
lesions
[
hepatocellular
necrosis,
hepatocellular
hypertrophy,
inflammation],
and
an
increased
incidence
of
hepatocellular
adenomas/
carcinomas
in
female
rats
and
hepatocellular
adenomas
in
both
sexes
of
mice.
In
dogs,
the
testes
and
prostate
are
target
organs,
as
evidenced
by
atrophy
of
both
organs
following
subchronic
and
chronic
exposure.
With
dermal
application
for
28­
days
in
rabbits,
no
systemic
effects
were
seen
at
doses
as
high
as
1000
mg/
kg.

Chronic
feeding
studies
in
rats
and
mice
indicated
that
metaldehyde
produced
liver
effects
characterized
by
liver
hypertrophy
and
liver
tumors.
The
carcinogenicity
of
metaldehyde
had
been
evaluated
by
the
Cancer
Assessment
Review
Committee
of
OPP,
and
it
classified
metaldehyde
as
"
suggestive
evidence
of
carcinogenicity".

The
developmental
toxicity
studies
in
rats
and
rabbits
did
not
find
any
developmental
effects
at
doses
as
high
as
150
mg/
kg;
however,
in
the
rat,
metaldehyde
produced
neurotoxic
signs
such
as
ataxia,
tremors,
and
twitching
in
dams
at
150
mg/
kg.
The
reproduction
study
in
rats
also
indicated
that
metaldehyde
did
not
affect
any
of
the
reproductive
parameters,
and
the
effects
on
the
offspring
consisted
of
decrease
pup
weight
and
body
weight
gains
only
at
133
mg/
kg
or
above.
However,
in
dams,
at
160
mg/
kg
or
above
metaldehyde
produced
mortality
and
clinical
signs
(
limb
paralysis,
spinal
cord
necrosis
and
hemorrhage)
similar
to
those
seen
in
the
rat
developmental
toxicity
study.

No
acute
neurotoxicity
study
on
metaldehyde
is
available.
The
90­
day
neurotoxicity
study
demonstrated
that
this
chemical
produced
increased
motor
activity
at
39
mg/
kg
or
Page
19
of
80
above.
At
185
mg/
kg,
it
produced
bilateral
hindlimb
paralysis
in
one
female
rat.
It
appeared
that
metaldehyde
at
dose
levels
greater
than
100
mg/
kg
could
produce
neurotoxicity
in
adult
rats
as
indicated
in
developmental
and
reproduction
studies
in
rats.

A
rat
metabolism
study
showed
that
metaldehyde
administered
by
gavage
was
rapidly
absorbed,
distributed,
and
metabolized.
78%­
98%
of
the
administered
dose
was
recovered
in
expired
air
within
24
hours
after
dosing.
More
14C
was
found
in
nervous
tissues,
fat,
liver,
and
reproductive
organs
than
other
tissue.

The
mutagenicity
battery
was
not
complete.
In
the
mutagenicity
studies
where
there
were
deficiencies
in
the
tests,
metaldehyde
was
suggested
to
be
negative
with
mouse
lymphoma
assay
and
chromosomal
aberrations
in
CHO
cell,
and
micronucleus
assay.

The
acute
toxicity
profile
for
metaldehyde
is
summarized
in
Table
6.
The
chronic,
subchronic
and
other
toxicity
profile
for
metaldehyde
is
summarized
in
Table
7.

Table
6
­
Acute
Toxicity
Profile
 
Metaldehyde
Guideline
No.
Study
Type
MRID(
s)
Results
Toxicity
Category
870.1100
Acute
oral
[
Sprague­
Dawley
rat]
LD50
=
283
mg/
kg
II
870.1200
Acute
dermal
[
CFY
rat]
00131434
LD50
=
>
5000
mg/
kg
III
870.1300
Acute
inhalation
[
Sprague­
Dawley
rat]
00131429
LC50
=
$
13.5
mg/
L/
4
hrs
IV
870.2400
Acute
eye
irritation
[
rabbit]
42068801
mild
irritant
III
870.2500
Acute
dermal
irritation
[
rabbit]
00131971
not
an
irritant
IV
870.2600
Skin
sensitization
[
guinea
pig]
N/
A
[
N/
A
]
[
N/
A
]
Page
20
of
80
Table
7
­
Subchronic,
Chronic
and
Other
Toxicity
Profile
Guideline
No./
Study
Type
MRID
No.
(
year)
Classification
/
Doses
Results
870.3100
90­
Day
oral
toxicity
[
rodents]
43297701
(
1990)
mouse
[
range­
finding
study]
0,
100,
300,
1000,
3000,
and
10000
ppm
[
19,
54,
178,
560,
and
1918
mg/
kg/
day
(
males);
24,
70,
235,
742,
and
2296
mg/
kg/
day
(
females)]
NOAEL
=
300
ppm
[
54/
70
mg/
kg/
day]
LOAEL
=
1000
ppm
[
178/
235
mg/
kg/
day],
based
on
increased
liver
weight
and
increased
incidence
of
liver
lesions
[
hepatocellular
necrosis,
hepatocellular
hypertrophy,
inflammation,
and
anisokaryosis
in
both
sexes.

Non­
guideline
28­
Day
oral
toxicity
[
rat]
44237704
(
1989)
acceptable/
non­
guideline
0,
2500,
5000,
10000,
20000
ppm
[
m/
f]­[
0,
197/
233,
382/
454,
761/
875
1545
(
males
only)
mg/
kg/
day]
Systemic
NOAEL
not
established
Systemic
LOAEL
=
2500
ppm
[
200
mg/
kg/
day],
based
on
increased
absolute
and
relative
liver
weights
at
all
dose
levels
in
both
sexes
Mortality,
hindlimb
paralysis
[
females
at
10000
ppm;
both
sexes
at
20000
ppm];
fracture/
luxation
of
vertebra,
hemorrhage
of
spinal
cord
870.3150
Subchronic
oral
toxicity
in
nonrodents
(
dog)
MRID
00131432
(
1980)
acceptable/
guideline
0,
20,
60,
90
mg/
kg/
day
[
26
weeks]
NOAEL
=
20
mg/
kg/
day
LOAEL
=
60
mg/
kg/
day
based
on
diffuse
or
focal
atrophy
of
the
testes
and
prostate;
at
HDT,
follicular
hyperplasia
of
mesenteric
lymph
node
in
both
sexes
870.3200
21/
28­
Day
dermal
toxicity
(
rabbit)
42063401
(
1991)
acceptable/
guideline
0,
100,
300,
1000
mg/
kg/
day
NOAEL
=
1000
mg/
kg/
day
[
highest
dose
tested]
LOAEL
=
no
effects
observed
870.3250
90­
Day
dermal
toxicity
no
study
located/
not
required
no
study
located/
not
required
870.3465
90­
Day
inhalation
toxicity
(
rat)
no
study
located
[
datagap]
[
datagap]

870.3700a
Prenatal
developmental
in
rodent
(
rat)
41656001
(
1990)
acceptable/
guideline
0,
25,
75,
150
mg/
kg/
day
gestation
days
6­
15
Maternal
NOAEL
=
75
mg/
kg/
day
]
LOAEL
=
150
mg/
kg/
day,
based
on
mortality,
clinical
signs
of
toxicity
[
ataxia,
tremors,
twitching,
rapid
respiration]
on
days
7
and
8,
and
decreased
body­
weight
gain
during
dosing,
and
decreased
food
consumption
during
dosing.
Developmental
NOAEL
=
150
mg/
kg/
day
[
HDT]
LOAEL
=
no
effects.

870.3700b
Prenatal
developmental
in
nonrodent
(
rabbit)
41590501
(
1990)
acceptable/
guideline
0,
10,
40,
80
mg/
kg/
day
gestation
days
6­
18
Maternal
toxicity
NOAEL
=
80
mg/
kg/
day
[
HDT]
Maternal
toxicity
LOAEL
=
no
effects
observed.
Developmental
toxicity
NOAEL
=
80
mg/
kg/
day
[
HDT]
Developmental
toxicity
LOAEL
=
no
effects.

870.3800
Reproduction
and
fertility
effects
(
rats)
MRID
42823101
(
1993)
acceptable/
guideline
0,
50,
1000,
2000
ppm
males:
F0
0,
3.4,
69.37,
138.36;
F1
0,
3.23,
64.93,
133.53
mg/
kg/
day
females:
F0
0,
4.16,
80.81,
160.42;
F1
0,
4.03,
80.51,
164.15
mg/
kg/
day
Parental
toxicity
NOAEL
=
1000
ppm
[
males
65
mg/
kg/
day;
females
81
mg/
kg/
day]
Parental
toxicity
LOAEL
=
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
based
on
mortality,
clinical
signs
(
hindlimb
paralysis
in
F0
females)
on
lactation
days
16­
18,
gross/
histopatholigical
lesions
in
females
(
spinal
cord
necrosis
and
hemorrhage,
vertebra
luxation
in
F0
females),
and
increased
liver
weight
in
both
sexes.

Reproductive
NOAEL
=
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
the
highest
dose
tested.

Offspring
NOAEL
=
1000
ppm
[
males
65
mg/
kg/
day;
females
81
mg/
kg/
day];
Offspring
LOAEL
=
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
based
on
decreased
pup
body
weight
and
body­
weight
gain
in
both
sexes/
both
generations.
Page
21
of
80
Table
7
­
Subchronic,
Chronic
and
Other
Toxicity
Profile
Guideline
No./
Study
Type
MRID
No.
(
year)
Classification
/
Doses
Results
870.4100a
Chronic
toxicity
rodents
(
SD
rat)
MRID
42203601
(
1992)
acceptable/
guideline
0,
50,
1000,
5000
ppm
M
0,
2,
44,
244
mg/
kg/
day
F
0,
3,
60,
314
mg/
kg/
day
NOAEL
=
50
ppm
[
males
2
mg/
kg/
day;
females
3
mg/
kg/
day]
LOAEL
=
1000
ppm
[
males
44
mg/
kg/
day;
females
60
mg/
kg/
day],
based
on
increased
incidence
of
hepatocellular
hypertrophy
(
both
sexes)
and
increased
cholesterol
(
females),
and
decreased
bodyweight
gain
in
females.
[
see
under
870.4200
below]

870.4100b
Chronic
toxicity
nonrodent
(
dogs)
MRID
46378401
(
2003)
acceptable/
guideline
0,
10,
30,
90
mg/
kg/
day
NOAEL
=
10
mg/
kg/
day
LOAEL
=
30
mg/
kg/
day,
based
on
deaths
and
atrophy
of
testes/
prostate
870.4200
Carcinogenicity
rats
MRID
42203601
(
1992)
acceptable/
guideline
0,
50,
1000,
5000
ppm
M
0,
2,
44,
244
mg/
kg/
day
F
0,
3,
60,
314
mg/
kg/
day
NOAEL
=
50
ppm
[
2
mg/
kg/
day;
females
3
mg/
kg/
day]
LOAEL
=
1000
ppm
[
males
44
mg/
kg/
day;
females
60
mg/
kg/
day],
based
on
increased
incidence
of
hepatocellular
hypertrophy
(
both
sexes)
and
increased
cholesterol
(
females),
and
decreased
bodyweight
gain
in
females.
evidence
of
carcinogenicity:
females
displayed
a
treatmentrelated
increase
in
hepatocellular
adenomas
and
adenomas
and
carcinomas
combined
[
positive
trend
at
5000
ppm]
at
the
highdose
level
[
adenomas
6/
60,
10%]
compared
to
both
control
groups
[
0/
60
and
1/
60];
carcinomas
1/
60,
1.7%
compared
to
both
controls
[
0/
60
and
1/
60];
and
combined
7/
60,
11.7%
compared
to
both
controls
[
0/
60
and
2/
60];
the
incidence
was
within
the
historical
control
range
[
adenomas
0%­
10%;
carcinomas
0%;
combined
0%­
10%].

870.4300
Carcinogenicity
mice
42737201
(
1993)
acceptable/
guideline
2
control
groups
25,
100,
300
ppm
M
4.0,
15.9,
48.9
mg/
kg/
day
F
4.8,
19.7,
59.8
mg/
kg/
day
NOAEL
=
100
ppm
[
males
15.9/
females
19.7
mg/
kg/
day]
LOAEL
=
300
ppm
[
males
48.9/
females
59.8
mg/
kg/
day
based
on
increased
incidence
of
hepatocellular
hypertrophy
in
both
sexes.
Dose
levels
not
adequate
to
assess
carcinogenicity
potential;
slight
increase
in
hepatocellular
adenomas
in
both
sexes
compared
to
both
control
groups
870.4300
Carcinogenicity
mice
MRID
44625101
(
1998)

Acceptable/
guideline
2
control
groups,
1000
ppm
increased
liver
weight,
increase
in
incidence
of
hepatocellular
hypertrophy
(
both
sexes),
single
cell/
focal/
multifocal
necrosis
(
males),
and
an
increase
in
the
incidence
of
hepatocellular
adenomas
in
both
sexes
Gene
Mutation
­
Ames
assay
870.5265
MRID
41553205
(
1978)
unacceptable
0,
0.26,
1.28,
6.4,
32,
160
Fg/
plate
(+/­
S9;
initial);
4,
8,
16,
32
Fg/
plate
(+/­
S9;
repeat)

[
datagap]
does
not
provide
sufficient
evidence
of
a
negative
response
in
strains
TA98,
TA100,
TA1535,
TA1537,
TA1538
with
and
without
metabolic
activation;
no
MTD;
poor
performance
of
some
strains
Gene
Mutation
­
mouse
lymphoma
L5178Y
(
TK+/­)
cell
line
870.5300
MRID
41553206
(
1986)
unacceptable
20,
50,
100,
200
Fg/
mL
­
S9
20,
50,
100,
167
Fg/
mL
+
S9
[
datagap]
no
conclusions
can
be
drawn;
doses
evaluated
were
said
to
be
"
not
completely
dissolved
in
the
selected
solvent
(
culture
medium);
all
concentrations
precipitated.
Additionally,
the.
exposure
time
(
2
hours)
was
shorter
than
the
standard
exposure
time
for
this
test
system
(
4
hours).

Gene
Mutation
­
mouse
lymphoma
L5178Y
(
TK+/­)
cell
line
870.5300
MRID
42044007
(
1986;
revised
1991)
clarification
of
MRID
41553206
unacceptable
w/
S9
­
20,
50,
100,
167
Fg/
mL
w/
out
S9
­
20,
50,
100,
200
Fg/
mL
[
datagap]
negative
for
inducing
forward
gene
mutation
at
TK
locus
in
mouse
lymphoma
(
L5178Y)
cell
with/
without
S9
activation
up
to
precipitating
concentrations
(
100­
200
Fg/
mL
(­
S9);
100­
167
Fg/
mL
(+
S9),
but
the
exposure
time
(
2
hours)
was
shorter
than
the
standard
exposure
time
for
this
test
system
(
4
hours).

Chromosomal
aberrations
in
CHO
cells
870.5375
MRID
00163832
(
1986)
unacceptable
w/
S9
­
20,
50,
100,
167
Fg/
mL
w/
out
S9
­
20,
50,
100,
200
Fg/
mL
[
datagap]
Negative
for
inducing
chromosome
aberrations
in
CHO
cells
up
to
a
precipitating
concentration
(
200
Fg/
mL
­
S9).
With
S9,
negative
up
to
the
highest
dose
tested
(
167
Fg/
mL)
but
no
cytotoxicity
or
compound
precipitation
at
this
level.
Page
22
of
80
Table
7
­
Subchronic,
Chronic
and
Other
Toxicity
Profile
Guideline
No./
Study
Type
MRID
No.
(
year)
Classification
/
Doses
Results
Micronucleus
assay
870.5395
MRID
42044006
(
1990)
unacceptable
25,
50,
100
mg/
kg
Negative
up
to
HDT
(
100
mg/
kg)
but
MTD
not
reached
870.6200a
Acute
neurotoxicity
screening
battery
no
study
located
no
study
located
870.6200b
Subchronic
neurotoxicity
screening
battery
MRID
46223401
(
2003)
unacceptable/
guideline
0
[
basal
diet],
100,
500,
and
2500
ppm
(
equivalent
to
0,
8,
39,
185
mg/
kg
bw/
day)
NOAEL
=
100
ppm
[
8
mg/
kg/
day]
LOAEL
=
500
ppm
[
39
mg/
kg/
day],
based
on
increased
motor
activity
in
females.
At
the
HDT
[
185
mg/
kg],
bilateral
hindlimb
paralysis
[
one
female]
and
decreased
body­
weight
gains
in
females
during
the
first
week
of
the
study.

870.6300
Developmental
neurotoxicity
no
study
available
[
datagap]
[
datagap]

870.7485
Metabolism
and
pharmacokinetics
(
Sprague­
Dawley
rat)
MRID
42300901
(
1992)
single
gavage
dose
10
or
100
mg/
kg
repeated
dose
10
mg/
kg/
day
for
14
days,
then
single
dose
14C
[
10
mg/
kg]

Classification:
acceptable/
guideline
rapidly
absorbed,
distributed,
metabolized;
most
recovered
in
expired
air
[
78%­
98%
of
administered
dose]
within
24
hours
[
48
hr
high­
dose
females]
as
14CO2;
recovery
in
urine/
feces
low
[
2.5%­
5.1%]
;
sexes
differ
slightly;
peak
blood
levels
[
males
1­
2
hrs;
females
2­
4
hrs]
and
excretion
faster
in
males
[
T1/
2
males
3.4
hrs.;
females
8.8
hrs.];
recovery
greater
following
low­
dose
than
highdose
and
repeat
exposure;
concentration
of
total
14C
in
blood
at
peak
similar
for
sexes
but
concentration
of
intact
metaldehyde
was
>
50%
higher
in
females
than
in
males
at
peak,
first
and
second
blood
half­
lives;
14C
in
tissues/
carcass
after
7
days
similar
for
all
groups
[
7%­
11%
of
administered
dose];
high
concentrations
14C
recovered
in
nervous
tissue,
fat,
liver,
female
reproductive
organs;
2
major
peaks
[
plasma]
were
metaldehyde
and
acetaldehyde
870.7600
Dermal
penetration
no
study
available
no
study
available
Special
studies
(
CD­
1
mouse)
MRID
44810901
(
1999)
retrospective
analysis
of
cell
proliferation/
apoptosis
[
liver
tissue]
males
­
correlation
between
cell
proliferation,
liver
weight
increase,
and
an
increased
incidence
of
liver
necrosis
and/
or
hypertrophy
at
1000
ppm
and
3000
ppm];
clear
evidence
of
cell
proliferation
and
hepatotoxicity
not
evident
at
lower
doses;
females
­
suggestive
evidence
of
a
similar
correlation
at
1000
ppm
and
3000
ppm;
however,
lack
of
a
dose­
response
and
extreme
variability
of
data
renders
findings
equivocal
for
proposed
mode
of
carcinogenic
action
[
liver
tumors];
no
data
on
whether
proliferative
response
sustained.

4.2
FQPA
Hazard
Considerations
4.1.1.
Adequacy
of
the
Toxicity
Database
The
available
toxicology
database
is
adequate
for
toxicity
endpoint
selection.
A
developmental
neurotoxicity
study
in
rats
is
considered
a
datagap.
The
studies
available
for
FQPA
considerations
are:
Page
23
of
80
 
rat
developmental
toxicity
study
(
acceptable)
 
rabbit
developmental
toxicity
study
(
acceptable)
 
two­
generation
reproduction
study
in
rats
(
acceptable)
 
90­
neurotoxicity
study
in
rats
(
unacceptable)

4.1.2.
Evidence
of
Neurotoxicity
There
is
a
concern
for
neurotoxicity
resulting
from
exposure
to
metaldehyde,
based
on
(
1)
clinical
signs
[
ataxia,
twitching,
tremors,
prostration,
paresis
of
hind
legs]
in
female
rats
in
the
developmental
toxicity
study;
(
2)
hindlimb
paralysis,
necrosis
and
hemorrhage
in
the
spinal
cord
and
vertebra
luxation
in
F0
dams
during
lactation
period
in
the
twogeneration
reproduction
study;
(
3)
bilateral
hindlimb
paralysis
observed
initially
on
day
10
in
one
high­
dose
female
sacrificed
[
day
22]
due
to
poor
condition
in
the
90­
day
subchronic
neurotoxicity
study
in
rats;
(
4)
clinical
signs
[
ataxia,
tremors,
twitching,
salivation]
in
the
chronic
dog
study,
which
occurred
within
the
first
week
of
exposure
and
persisted
through
week
19;
other
signs
included
lateral
position,
reduced
mobility,
convulsions,
and
vocalization
in
one
female,
and
agitation
in
another.
It
should
be
noted
that
most
of
these
neurotoxic
signs
(
such
limb
paralysis,
ataxia,
and
tremors)
were
seen
in
rats
at
dose
levels
above
100
mg/
kg
except
the
increased
motor
activity
at
39
mg/
kg
in
the
90­
day
neurotoxicity
study.

4.1.3.
Developmental
Toxicity
Studies
In
a
developmental
toxicity
study
in
rats
metaldehyde
was
tested
up
to
150
mg/
kg;
no
developmental
effects
were
seen
at
any
dose.
However,
there
were
increased
mortality
and
clinical
signs
such
as
ataxia,
tremors,
twitching,
and
rapid
respiration
seen
in
150
mg/
kg
dams.
In
the
developmental
toxicity
study
in
rabbits,
metaldehyde
was
tested
up
to
only
80
mg/
kg,
no
developmental
and
maternal
toxicity
was
found.
The
developmental
toxicity
studies
in
rats
and
rabbits
did
not
demonstrate
an
increase
in
sensitivity
or
susceptibility
in
developing
fetuses
of
either
species.

The
executive
summaries
of
the
above
are
presented
in
Appendix
A.

It
should
be
noted
that
although
no
maternal
or
developmental
effects
were
observed
in
rabbit
developmental
toxicity
study,
the
dose
levels
are
considered
adequate
based
on
effects
observed
in
the
range­
finding
study.
All
does
[
5/
group]
in
the
200,
350
and
500
mg/
kg/
day
groups
died
[
following
1
or
2
doses]
or
were
sacrificed
moribund
[
gestation
days
8­
12],
and
one
doe
at
100
mg/
kg/
day
died.
A
repeat
study
at
higher
dose
levels
would
not
provide
useful
data.
This
was
also
supported
by
the
results
in
the
rat
developmental
toxicity
study
where
no
maternal
effect
was
seen
at
75
mg/
kg
and
no
developmental
effect
was
seen
at
150
mg/
kg.

4.1.4.
Reproductive
Toxicity
Study
In
a
2­
generation
reproduction
study
in
rats,
metaldehyde
was
administered
in
the
diet
at
concentrations
of
50,
1000,
and
2000
ppm
(
F1
males:
0,
3.23,
64.93,
and
133.53
Page
24
of
80
mg/
kg/
day;
F1
females:
0,
4.03,
80.51,
and
164.15
mg/
kg/
day).
Offspring
toxicity
was
seen
at
2000
ppm
(
133
mg/
kg)
consisting
of
decreased
pup
weight
and
body
weight
gain,
and
parental
toxicity
consisted
of
increased
mortality,
clinical
signs
such
as
hindlimb
paralysis,
spinal
cord
necrosis
and
hemorrhage,
and
increased
liver
weights.
As
demonstrated
in
the
developmental
toxicity
studies
in
rats
and
rabbits,
the
data
of
the
2­
generation
reproduction
study
also
showed
no
increase
in
sensitivity
or
susceptibility
in
pups
under
the
conditions
of
this
study.
The
executive
summary
is
presented
in
Appendix
A.

4.1.5.
Additional
Information
from
Literature
Sources
The
published
literature
noted
that
with
oral
exposure
metaldehyde
was
hydrolyzed
in
the
stomach
acid
to
acetaldehyde
polymers
that
readily
enter
the
brain.
Poisoning
might
result
from
reduced
levels
of
brain
serotonin,
norepinephrine,
and
the
inhibitory
neurotransmitter
(
­
aminobutyric
acid
[
GABA].
Clinical
signs
of
toxicosis
were
similar
in
all
mammals.
Neurotoxicity
signs
are
prominent
and
include
severe
muscle
tremors,
ataxia,
hyperesthesia,
nystagmus,
and
hyperpnea,
followed
by
opisthotonos
and
continuous
tonic
convulsions.

4.1.6.
Pre­
and/
or
Postnatal
Toxicity
There
is
low/
no
concern
for
pre­
and/
or
postnatal
toxicity
resulting
from
exposure
to
metaldehyde.
4.1.6.1.
Determination
of
Susceptibility
There
is
no
evidence
of
increased
susceptibility
[
qualitative
and
quantitative]
following
in
utero
exposure
to
metaldehyde
in
either
the
rat
or
rabbit
developmental
toxicity
study.
There
is
no
evidence
of
increased
susceptibility
[
qualitative
or
quantitative]
following
in
utero
and/
or
pre­/
postnatal
exposure
in
the
2­
generation
reproduction
study
in
rats.

4.1.6.2.
Degree
of
Concern
Analysis
and
Residual
Uncertainties
for
Pre­
and/
or
Postnatal
Susceptibility
There
are
no
residual
concerns
for
pre­
or
post
natal
toxicity
based
on
the
currently
available
data.

4.2.
Recommendation
for
a
Developmental
Neurotoxicity
Study
4.2.1.
Evidence
in
favor
of
retaining
the
10X/
requiring
further
evaluation
of
neurobehavioral
development
Neurotoxicity
was
observed
in
both
the
F0
and
F1
dams
during
the
gestation
and/
or
lactation
periods
in
the
reproduction
study
following
long­
term
exposure
and
in
the
dams
in
the
developmental
toxicity
study
in
rats
following
acute
(
1­
2
days)
exposure.
Additionally,
neuropathology
was
observed
in
those
dams
that
displayed
neurotoxicity
in
the
reproduction
study.
There
is
no
acute
neurotoxicity
study
on
metaldehyde,
but
there
is
Page
25
of
80
a
subchronic
neurotoxicity
study.
Although
no
neuropathological
lesions
were
observed
in
the
latter
study,
the
high­
dose
female
that
was
sacrificed
on
day
22
due
to
hindlimb
paralysis
and
poor
condition
was
not
subjected
to
a
histopathological
examination.
There
was
an
apparent
increase
in
motor
activity
in
females
in
the
subchronic
neurotoxicity
study,
although
the
adequacy
of
the
procedures
and
reporting
in
that
study
are
still
under
review.
Based
on
the
finding
of
neuropathy
in
the
reproduction
study
in
rats,
a
developmental
neurotoxicity
study
[
DNT]
in
rats
is
recommended.

4.2.2.
Evidence
against
retaining
the
10X/
requiring
further
evaluation
of
neurobehavioral
development
There
is
no
increased
susceptibility
and
no
developmental
toxicity
in
either
the
rat
or
rabbit,
and
the
apparent
neurotoxic
effects
in
adult
animals
occur
at
relatively
high
dose
levels
e.
g.,
at
160
mg/
kg
(
neuropathy
and
clinical
signs
observed
in
F0
dams
during
lactation
days
16­
18)
in
the
reproduction
study
and
150
mg/
kg
(
clinical
signs)
following
exposure
of
rats
during
gestation
days
7­
8
[
1­
2
doses].

4.2.2.1.
Rationale
for
the
UFDB
(
when
a
DNT
is
recommended)

Based
on
clinical
signs
indicating
neurotoxicity
seen
in
the
several
studies,
a
developmental
neurotoxicity
study
is
required
for
metaldehyde.
A
database
uncertainty
factor
of
10X
is
required
for
risk
assessment
under
the
current
policy
to
account
for
potential
increase
in
response
to
the
neurotoxic
effects
produced
by
metaldehyde
in
infants
and
children.

4.3.
Hazard
Identification
and
Toxicity
Endpoint
Selection
The
available
toxicology
data
are
adequate
for
toxicity
endpoint
selection
for
risk
assessment
as
summarized
below.
A
summary
of
selected
toxicity
endpoints
and
doses
are
presented
in
Table
8.
A
summary
of
each
study
used
in
selecting
appropriate
endpoints
and
doses
are
presented
in
Appendix
A.

Acute
dietary:
The
selected
endpoint
is
mortality
and
clinical
signs
[
ataxia,
tremors,
twitching,
rapid
respiration]
based
on
the
developmental
toxicity
study
in
rats.
The
effects
were
seen
at
150
mg/
kg
(
LOAEL)
or
above
after
a
single
or
more
doses.
The
NOAEL
was
75
mg/
kg.
The
route
and
duration
of
exposure
were
appropriate
for
acute
dietary
exposure
assessment
for
all
population.
No
developmental
toxicity
was
seen
in
this
study,
and
no
single­
dose
endpoint
specific
for
females
13­
49
years
old
could
be
identified.
The
selected
endpoint
applies
to
the
general
population
including
females
13+
subpopulation.

Chronic
dietary:
The
chronic
oral
toxicity
study
in
dogs
was
selected
as
the
basis
for
selecting
the
NOAEL
(
10
mg/
kg)
for
the
chronic
RfD.
The
LOAEL
was
30
mg/
kg
which
produced
death
and
atrophy
of
testes
and
prostate.
Also
considered
for
this
exposure
scenario
was
the
chronic
toxicity/
carcinogenicity
study
in
rats,
which
provided
a
lower
NOAEL
(
2
mg/
kg).
However,
the
endpoint
of
concern
[
liver
effects
(
hepatocellular
hypertrophy)]
was
seen
at
44
mg/
kg
(
LOAEL);
the
effects
were
considered
an
adaptive
Page
26
of
80
effect
and
not
appropriate
for
selection
of
the
chronic
dietary
endpoint.
In
addition
the
lower
NOAEL
seen
in
the
rat
study
might
be
influenced
by
dose
selection.
The
dog
study
was
selected
because
the
route
and
duration
of
exposure
are
appropriate
for
this
risk
assessment.

Incidental
oral
(
short­
term):
The
endpoint
[
clinical
signs
(
ataxia,
tremor,
twitching,
salivation,
emesis]
from
a
chronic
oral
toxicity
study
in
dogs
was
selected
for
the
shortterm
incidental
oral
exposure
scenario
because
the
toxicity
occurred
from
week
one
on
at
90
mg/
kg
and
no
effect
was
seen
at
30
mg/
kg.
It
is
appropriate
for
this
exposure
duration.

Incidental
oral
(
intermediate­
term):
The
endpoints
[
death
(
between
weeks
37
and
46)
and
atrophy
of
the
testes
and
prostate]
from
the
chronic
dog
study
was
selected
for
the
intermediate­
term
incidental
oral
exposure
scenario
because
the
toxicity
occurred
in
relatively
young
dogs
and
atrophy
of
the
testes
and
prostate
was
observed
at
study
termination
in
the
26­
week
dog
study
also.
The
NOAELs
are
20
mg/
kg/
day
[
subchronic]/
10
mg/
kg/
day
[
chronic],
and
the
LOAELs
are
60
[
subchronic]/
30
mg/
kg/
day
[
chronic].

Dermal
(
short­
intermediate­,
and
long­
term):
The
repeated
[
21­
day]
dermal
toxicity
study
was
considered
for
these
exposure
scenarios
because
the
route
of
exposure
is
appropriate.
Although
no
effects
were
observed,
the
limit
dose
was
tested,
no
clinical
signs
were
observed,
the
target
organs
[
liver
and
testes]
were
evaluated,
and
there
is
no
reproductive
toxicity
concern.
It
was
concluded
that
no
dermal
exposure
risk
assessment
is
required.

Inhalation
(
short
and
intermediate
term):
same
as
for
short­
and
intermediate­
term
incidental
oral.
The
inhalation
exposure
limits
for
all
durations
were
based
on
the
NOAELs
from
oral
studies
for
each
exposure
scenario
since
no
route­
specific
study
was
available.
Because
no
inhalation
absorption
data
are
available,
toxicity
by
the
inhalation
route
was
considered
to
be
equivalent
to
toxicity
by
the
oral
route
of
exposure.
A
subchronic
inhalation
toxicity
study
is
required.

Inhalation
(
long­
term):
see
chronic
RfD.
Page
27
of
80
Table
8
­
Summary
of
Toxicology
Endpoint
Selection
for
Metaldehyde
Exposure
Scenario
Dose
Used
in
Risk
Assessment,
UF
Special
FQPA
SF*
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Acute
Dietary
(
All
populations)
NOAEL
=
75
mg/
kg/
day
UF
=
1000
Acute
RfD
=
0.075
mg/
kg/
day
FQPA
SF
=
1X
aPAD
=
acute
RfD
(
0.075)
FQPA
SF
(
1)

=
0.075
mg/
kg/
day
developmental
toxicity
study
in
rats
LOAEL
=
150
mg/
kg/
day
based
on
mortality,
clinical
signs
[
ataxia,
tremors,
twitching,
rapid
respiration],
decreased
body­
weight
gain
during
dosing
in
females
Chronic
Dietary
(
All
populations)
NOAEL
=
10
mg/
kg/
day
UF
=
1000
Chronic
RfD
=
0.01
mg/
kg/
day
FQPA
SF
=
1X
cPAD
=
chronic
RfD
(
0.01)
FQPA
SF
(
1)

=
0.01
mg/
kg/
day
dog
chronic
oral
toxicity
study
LOAEL
30
mg/
kg/
day,
based
on
death
and
atrophy
of
the
testes
and
prostate
Short­
Term
Incidental
Oral
(
1­
30
days)
NOAEL
=
30
mg/
kg/
day
Residential
LOC
for
MOE
=
1000
Occupational
=
NA
dog
chronic
oral
toxicity
study
LOAEL
90
mg/
kg/
day
for
clinical
signs
seen
beginning
the
first
week
dosing.

Intermediate­
Term
Incidental
Oral
(
1­
6
months)
NOAEL
=
10
mg/
kg/
day
Residential
LOC
for
MOE
=
1000
Occupational
=
NA
chronic
oral
toxicity
study
­
dog
LOAEL
=
30
mg/
kg/
day
based
on
deaths
and
atrophy
of
testes
and
prostate
Short­
Term
Inhalation
(
1
to
30
days)
oral
NOAEL=
30
(
inhalation
absorption
rate
=
100%)
Residential
LOC
for
MOE
=
1000
Occupational
LOC
for
MOE
=
100
dog
chronic
oral
toxicity
study
LOAEL
=
90
mg/
kg/
day
for
clinical
signs
Intermediate­
Term
Inhalation
(
1
to
6
months)
oral
NOAEL
=
10
mg/
kg/
day
(
inhalation
absorption
rate
=
100%)
Residential
LOC
for
MOE
=
1000
Occupational
LOC
for
MOE
=
100
chronic
oral
toxicity
study
­
dog
LOAEL
=
30
mg/
kg/
day
based
on
deaths
and
testes/
prostate
atrophy
Long­
Term
Inhalation
(>
6
months)
oral
NOAEL=
10
mg/
kg/
day
(
inhalation
absorption
rate
=
100%)
Residential
LOC
for
MOE
=
1000
Occupational
LOC
for
MOE
=
100
chronic
oral
toxicity
study
­
dog
LOAEL
=
30
mg/
kg/
day,
based
on
deaths
and
atrophy
of
the
testes
and
prostate
Cancer
(
oral,
dermal,
inhalation)
Classification:
"
Suggestive
Evidence
of
Carcinogenic
Potential"

A
quantification
of
cancer
risk
for
metaldehyde
was
not
recommended.

UF
=
uncertainty
factor,
FQPA
SF
=
Special
FQPA
safety
factor,
NOAEL
=
no
observed
adverse
effect
level,
LOAEL
=
lowest
observed
adverse
effect
level,
PAD
=
population
adjusted
dose
(
a
=
acute,
c
=
chronic)
RfD
=
reference
dose,
MOE
=
margin
of
exposure,
LOC
=
level
of
concern,
N/
A
=
Not
Applicable
Page
28
of
80
4.3.1.
Margins
of
Exposure
Margins
of
exposure
of
1000
(
10X
for
intraspecies
variability,
10X
for
interspecies
variability,
and
10X
for
a
database
uncertainty
factor)
should
be
applied
to
all
appropriate
exposure
scenarios
for
metaldehyde.

4.3.2.
Recommendation
for
Aggregate
Exposure
Risk
Assessments
As
per
FQPA
(
1996),
when
there
are
potential
residential
exposures
to
the
pesticide,
an
aggregate
risk
assessment
must
consider
exposures
from
three
major
sources:
oral,
dermal,
and
inhalation
exposures.
No
endpoint
was
identified
for
dermal
exposure,
so
dermal
exposures
need
not
be
considered
in
the
aggregate
assessment.
Inhalation
exposures
are
not
expected
because
of
the
use
pattern
(
typically
a
pellet
formulation).
Only
food
and
water
are
generally
aggregated
for
acute
(
one­
day)
exposures
to
metaldehyde.
For
short­
term
oral
exposure
to
metaldehyde,
food,
water,
and
residential
exposures
are
aggregated.

4.3.3.
Classification
of
Carcinogenic
Potential
In
a
chronic
toxicity/
carcinogenicity
study,
Sprague­
Dawley
CD
®
rats
were
administered
metaldehyde
in
the
diet
at
concentrations
of
0,
50,
1000,
and
5000
ppm
for
104
weeks.
An
increase
in
liver
tumors
was
seen
in
mid­
and
high­
dose
males
and
in
high
dose
female.
In
a
mouse
carcinogenicity
study,
CD­
1
mice
received
metaldehyde
in
the
diet
at
concentrations
of
0,
25,
100,
and
300
ppm
for
18
months.
There
was
no
statisticallysignificant
increase
in
the
incidence
of
liver
tumors
in
either
sex.
A
supplemental
mouse
carcinogenicity
study
using
the
same
strain
of
mice
and
a
single
dose
(
1000
ppm)
was
conducted.
Under
the
conditions
of
this
study,
increased
liver
weight
(
both
sexes),
hepatocellular
hypertrophy
(
both
sexes),
liver
single
cell/
focal/
multifocal
necrosis
(
males),
liver
pigment
accumulation
(
males),
sinusoidal
histiocytosis
(
males),
hepatocellular
eosinophilic
cell
foci
(
females),
and
hepatocellular
adenomas
(
both
sexes)
were
observed.
The
Cancer
Assessment
Review
Committee
evaluated
all
the
available
carcinogenicity
and
other
toxicology
data
and
classified
metaldehyde
in
accordance
with
the
EPA
Final
Guidelines
for
Carcinogen
Risk
Assessment
(
March
29,
2005),
as
"
Suggestive
Evidence
of
Carcinogenic
Potential"
based
on
the
presence
of
benign
liver
tumors
in
female
rats,
benign
liver
tumors
in
both
sexes
of
mice,
and
a
lack
of
adequate
mutagenicity
data.

A
summary
of
both
carcinogenicity
studies
is
presented
in
Appendix
A.

Special
FQPA
Safety
Factor
Based
on
the
hazard
data,
the
metaldehyde
risk
assessment
team
recommended
the
special
FQPA
SF
be
reduced
to
1X
because
there
are
no
residual
uncertainties
with
regard
to
pre­
and/
or
postnatal
toxicity.
A
clear
dose
response
relationship
was
observed
in
the
toxicity
studies
selected
for
risk
assessment
endpoints,
and
clear
NOAEL's
were
Page
29
of
80
established
which
were
used
as
risk
assessment
points
of
departure.
The
recommendation
is
also
based
on
the
following:

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

The
dietary
drinking
water
assessment
(
Tier
1
estimates)
utilizes
values
generated
by
model
and
associated
modeling
parameters
which
are
designed
to
provide
conservative,
health
protective,
high­
end
estimates
of
water
concentrations.

The
residential
exposure
assessment
relies
on
sufficiently
protective
default
assumptions
that
are
unlikely
to
underestimate
exposure/
risk.

4.4.
Endocrine
disruption
EPA
is
required
under
the
FFDCA,
as
amended
by
FQPA,
to
develop
a
screening
program
to
determine
whether
certain
substances
(
including
all
pesticide
active
and
other
ingredients)
"
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen,
or
other
such
endocrine
effects
as
the
Administrator
may
designate."
Following
recommendations
of
its
Endocrine
Disruptor
and
Testing
Advisory
Committee
(
EDSTAC),
EPA
determined
that
there
was
a
scientific
basis
for
including,
as
part
of
the
program,
the
androgen
and
thyroid
hormone
systems,
in
addition
to
the
estrogen
hormone
system.
EPA
also
adopted
EDSTAC's
recommendation
that
the
Program
include
evaluations
of
potential
effects
in
wildlife.
For
pesticide
chemicals,
EPA
will
use
FIFRA
and,
to
the
extent
that
effects
in
wildlife
may
help
determine
whether
a
substance
may
have
an
effect
in
humans,
FFDCA
authority
to
require
the
wildlife
evaluations.
As
the
science
develops
and
resources
allow,
screening
of
additional
hormone
systems
may
be
added
to
the
Endocrine
Disruptor
Screening
Program
(
EDSP).

In
the
available
toxicity
studies
on
metaldehyde,
there
was
no
apparent
estrogen,
androgen,
and/
or
thyroid
mediated
toxicity.
However,
atrophy
of
the
testes
and
prostate
occurred
in
both
the
subchronic
[
26­
week]
and
chronic
oral
toxicity
studies
in
the
dog.

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

5.0
Public
Health
Data
5.1.
Incident
Reports
The
following
databases
have
been
consulted
for
the
poisoning
incident
data
on
the
active
ingredient
metaldehyde:
OPP
Incident
Data
System
(
IDS),
Poison
Control
Centers,
California
Department
of
Pesticide
Regulation,
National
Pesticide
Information
Center
(
NPIC),
and
the
National
Institute
of
Occupational
Safety
and
Health's
Sentinel
Event
Notification
System
for
Occupational
Risks
(
NIOSH
SENSOR).
Page
30
of
80
There
are
35
cases
documented
from
IDS
between
1994
and
2004.
Another
8­
10
lawsuits
were
reported
but
excluded
from
tabulation
because
of
lack
of
medical
documentation.
Fifty­
one
percent
of
cases
reported
either
irritation
to
the
skin
or
allergic
type
reaction.
A
total
of
2268
cases
were
located
in
the
Poison
Control
Center
records
from
1993
through
2003.
Of
these
2268
cases,
9
were
of
moderately
or
life
threatening
concern,
and
those
cases
were
due
to
ingestion.
Children
under
age
six
were
involved
in
1648
cases,
594
were
adults
exposed
in
a
non­
occupational
setting
and
26
were
adults
in
an
occupational
setting.

Incident
data
on
domestic
animals
allegedly
exposed
to
metaldehyde
were
reviewed
from
two
sources,
the
National
Pesticide
Information
Center
(
NPIC)
and
EPA's
Incident
Data
System
for
6(
a)(
2)
reporting.
Data
for
the
period
January
1,
2000
to
December
31,
2004
were
reported
from
the
NPIC,
a
toll­
free
telephone
service
that
provides
pesticide
information
without
treatment
advice
to
the
general
public
and
medical
and
veterinary
professionals.
If
an
animal
is
in
need
of
immediate
veterinary
care,
the
caller
is
referred
to
the
ASPCA's
Animal
Poison
Control
Center
(
APCC).
The
APCC
is
a
24­
hour
emergency
hotline
for
animals
similar
to
human
poison
control
centers.
The
NPIC
determines
if
a
pesticide
product
is
responsible
for
clinical
signs
and
assigns
the
following
categories:
definite,
probable,
possible
or
unlikely.
Only
probable
and
possible
cases
were
included
with
the
metaldehyde
data.
A
probable
case
has
a
clearly
documented
and
highly
plausible
exposure
pathway
with
specific
health
effects
that
are
consistent
with
exposure
to
the
active
ingredient(
s).
With
possible
cases,
there
is
a
report
of
exposure
and
clinical
signs,
but
there
is
uncertainty
with
respect
to
the
likelihood
of
exposure,
the
circumstances
surrounding
the
exposure
or
the
consistency
of
the
reported
signs
based
upon
the
active
ingredient(
s).

The
metaldehyde
data
from
NPIC
were
analyzed
and
tabulated
to
determine
the
product
type
(
bait,
liquid,
etc.)
involved,
the
outcome
of
the
case
(
died,
referred
to
APCC,
unknown,
recovered)
and
species
affected
(
dog,
cat).
For
the
five­
year
period,
there
were
104
cases
in
the
probable
and
156
in
the
possible
categories
for
a
total
of
260
cases
involving
274
animals.
The
number
of
probable
cases
increased
yearly
from
8
in
2000
to
43
in
2004.
The
number
of
possible
cases
was
similar
from
2000­
2003
but
increased
in
2004.
Ingestion
was
the
most
common
route
of
exposure.
Most
animals
were
exposed
to
metaldehyde
products
applied
to
yards/
gardens;
however,
dogs
also
chewed
into
bags
or
boxes
in
storage
areas.
Granular
and
bait
formulations
were
the
most
common
form
ingested.
A
total
of
17
animals
in
the
probable
and
five
in
the
possible
categories
died
during
the
five­
year
period,
while
10
animals
in
the
probable
and
possible
categories
recovered.
A
total
of
35
animals
in
the
probable
and
46
in
the
possible
categories
were
referred
to
APCC.
The
outcome
was
unknown
in
54
animals
in
the
probable
and
108
in
the
possible
categories.
Most
of
the
outcomes
were
unknown
because
the
NPIC
advised
that
the
caller
consult
a
veterinarian
about
the
animal.
The
NPIC
has
no
follow­
up
capabilities
for
these
cases.
Animals
affected
include
both
dogs
(
252/
274)
and
cats
(
22/
274).
Data
reviewed
from
the
APCC
confirm
that
the
clinical
signs
in
the
cases
referred
by
the
NPIC
were
compatible
with
metaldehyde
exposure.
Page
31
of
80
6.0
Exposure
Characterization/
Assessment
6.1.
Dietary
Exposure/
Risk
Pathway
6.1.1.
Residue
Profile
The
qualitative
nature
of
metaldehyde
residues
in
plants
is
understood
based
on
the
adequate
lettuce
and
sugar
beet
metabolism
studies.
The
HED
Metabolism
Committee
(
7/
2/
96)
concluded
that
the
regulated
residue
of
concern
in
plants
is
parent
metaldehyde,
per
se.
Requirements
for
animal
metabolism
and
feeding
studies
have
been
waived.
The
Agency
concluded
that
residues
are
unlikely
to
occur
in
livestock
commodities
based
upon
the
rapid
degradation
of
metaldehyde
in
mammalian
systems
and
the
subsequent
incorporation
of
degradates
into
naturally
occurring
components.
The
tolerance
reassessment
summary
for
metaldehyde
is
presented
in
Appendix
B.

A
tolerance
of
"
zero"
has
been
established
for
residues
of
metaldehyde
on
strawberry
[
40
CFR
§
180.523(
a)(
2)].
There
are
currently
no
other
tolerances
on
other
primary
crops,
animal
commodities
or
rotational
crops.
No
analytical
methods
are
listed
in
the
Pesticide
Analytical
Manual
(
PAM
Vol.
II)
for
the
enforcement
of
the
established
tolerance.

An
adequate
GC/
MS
method
(
EN­
CAS
Method
No.
ENC­
3/
99,
Revision
1)
is
available
for
collecting
data
on
metaldehyde
residues
in/
on
plant
commodities.
This
method
has
been
validated
using
a
wide
variety
of
plant
matrices,
and
it
has
a
validated
method
LOQ
of
0.05
ppm.
The
method
has
also
undergone
a
successful
independent
laboratory
validation
trial
and
has
been
proposed
as
the
tolerance
enforcement
method.

Adequate
field
trial
data
are
available
to
support
the
use
of
metaldehyde
on
Brassica
leafy
vegetables
(
group
5),
citrus
fruits
(
group
10),
berries
(
group
13),
tomato,
artichoke,
lettuce,
strawberry,
prickly
pear
cactus
and
watercress.
An
adequate
number
of
tests
were
conducted
on
these
crops
in
the
appropriate
geographical
regions
using
representative
formulations
applied
at
the
maximum
supported
use
rates.
These
studies
are
also
supported
by
adequate
storage
stability
data.
The
residue
data
from
these
field
trials
will
support
permanent
tolerances
on
the
above
crops
or
crop
groups
The
available
residue
data
from
the
limited
field
trials
indicate
that
detectable
residues
($
0.05
ppm)
of
metaldehyde
are
likely
to
occur
on
a
wide
variety
of
plant
commodities
following
application(
s)
of
metaldehyde
formulations
at
the
maximum
supported
label
rates.
Therefore,
tolerances
for
metaldehyde
and
supporting
field
trial
data
are
required
on
all
crops
and/
or
crop
groups
with
registered
uses
of
metaldehyde.

The
available
processing
studies
on
tomatoes
and
oranges
are
adequate
and
indicate
that
metaldehyde
residues
do
not
concentrate
in
processed
commodities
derived
from
these
crops.

6.1.2.
Acute
and
Chronic
Dietary
Exposure
and
Risk
Page
32
of
80
An
unrefined
Tier
1
[
tolerance
level
and
100%
crop
treated
(%
CT)]
acute
dietary
risk
assessment
was
conducted
for
all
supported
metaldehyde
food
uses.
Dietary
risk
estimates
are
provided
for
the
general
U.
S.
population
and
various
population
subgroups.
This
assessment
showed
that
at
the
95th
percentile
of
exposure,
the
acute
risk
estimates
are
below
the
Agency's
level
of
concern
(<
100%
aPAD)
for
the
general
U.
S.
population
(
11%
of
the
aPAD)
and
all
population
subgroups
(<
25%
of
the
aPAD).
The
highest
exposed
population
subgroup
was
children
1­
2
years
old.

Tolerance
level
residues
and
100%
CT
were
also
used
to
determine
the
chronic
dietary
exposure
and
risk
estimates.
This
assessment
showed
that
for
all
included
commodities,
the
chronic
risk
estimates
were
below
the
Agency's
level
of
concern
(<
100%
cPAD)
for
the
general
U.
S.
population
(
22%
of
the
cPAD)
and
all
population
subgroups
(<
49%
cPAD).
The
highest
exposed
population
subgroup
was
children
1­
2
years
old.

Table
9
contains
a
summary
of
dietary
exposure
and
risks
for
metaldehyde
for
a
number
of
population
sub­
groups.

Table
9
­
Summary
of
Dietary
Exposure
and
Risk
for
Metaldehyde
Acute
Dietary
(
95th
Percentile)
Chronic
Dietary
DEEM­
FCID
DEEM­
FCID
Population
Subgroup*
Dietary
Exposure
(
mg/
kg/
day)
%
aPAD*
Dietary
Exposure
(
mg/
kg/
day)
%
cPAD
General
U.
S.
Population
0.008551
11
0.002215
22
All
Infants
(<
1
year
old)
0.003560
4.8
0.000674
6.7
Children
1­
2
years
old
0.018514
25
0.004890
49
Children
3­
5
years
old
0.016881
23
0.004442
44
Children
6­
12
years
old
0.011224
15
0.003002
30
Youth
13­
19
years
old
0.007551
10
0.001843
18
Adults
20­
49
years
old
0.007251
9.7
0.001830
18
Adults
50+
years
old
0.007776
10
0.002067
21
Females
13­
49
years
old
0.007320
9.8
0.001910
19
Page
33
of
80
6.2.
Water
Exposure/
Risk
Pathway
When
surface
water
modeling
residues
are
included
in
the
acute
and
chronic
assessments,
HED's
level
of
concern
is
not
exceeded
(<
100%
aPAD
and
cPAD).
The
most
highly
exposed
population
subgroup
was
children
1­
2
years
old
at
26%
aPAD
(
95th
percentile)
and
59%
cPAD,
respectively.
When
ground
water
modeling
residues
are
included
in
the
acute
and
chronic
assessments,
HED's
level
of
concern
is
not
exceeded
(<
100%
aPAD
and
cPAD).
For
ground
water,
children
1­
2
years
old
were
also
the
most
highly
exposed
population
subgroup.
For
children
1­
2
years
old,
29%
and
69%
of
the
aPAD
and
cPAD
were
occupied
in
the
acute
and
chronic
aggregate
assessment,
respectively.
For
groundwater,
EDWCs
were
generated
from
a
Tier
I
SCI­
GROW
analysis.
A
EDWC
of
62.5
ppb
from
a
scenario
based
on
use
of
metaldehyde
on
ornamental
plants
was
used
in
both
the
chronic
and
acute
aggregate
assessments.
The
EDWCs
are
considered
to
be
somewhat
conservative,
although
it
can
not
be
precluded
that
higher
concentrations
in
drinking
water
will
not
be
found
based
on
uncertainties
in
the
half­
life
determined
from
a
single
soil
aerobic
metabolism
study.
The
Commodity
Contribution
Analysis
shows
that
water
is
the
most
significant
contributor.

Table
10
­
Summary
of
Estimated
Surface
and
Ground
Water
Concentrations
for
Metaldehyde
Metaldehyde
Exposure
Duration
Surface
Water
Conc.,
ppb
a
Ground
Water
Conc.,
ppb
b
Acute
110
62.5
Chronic
(
non­
cancer)
55.8
62.5
Chronic
(
cancer)
31.9
62.5
a
From
the
Tier
II
PRZM­
EXAMS
­
Index
Reservoir
model.
Input
parameters
are
based
on
use
on
Brassica
and
leafy
vegetables
in
FL
&
CA.
b
From
the
SCI­
GROW
model
assuming
a
maximum
seasonal
use
rate
of
6.4
lb
ai/
A,
a
Koc
of
57
(
loam
soil),
and
a
half­
life
of
67
days.

6.3.
Residential
(
Non­
Occupational)
Exposure/
Risk
Pathway
The
residential
risk
assessment
addresses
exposures
that
individuals
receive
through
their
use
of
consumer
products
that
contain
metaldehyde
and
through
exposures
they
could
receive
from
frequenting
areas
that
have
been
previously
treated
with
metaldehyde,
such
as
a
home
lawn
or
a
park.

6.3.1.
Home
Uses
Page
34
of
80
Metaldehyde
is
available
as
a
consumer
product
for
snail
and
slug
control
on
lawns
and
around
fruit,
vegetable,
and
ornamental
gardens
in
the
following
formulations:
liquid
concentrate,
ready­
to­
use
liquid/
paste,
and
ready­
to­
use
granules/
pellets/
minipellets/
meal
baits.
The
methods
of
application
include
hose­
end
sprayers,
trigger­
pump
sprayers,
low
pressure
handwand
sprayers,
sprinkling
cans,
belly
grinders,
push­
type
spreaders,
and
applying
ready­
to­
use
products
by
hand.

A
Use
Closure
Memo
was
issued
for
metaldehyde
on
March
1,
2005.
Subsequently
on
March
21,
2005,
EPA's
metaldehyde
team
met
with
representatives
of
Lonza,
the
sole
technical
registrant
of
metaldehyde.
On
April
14,
2005,
an
addendum
(
addendum
1)
to
the
original
use
closure
memo
was
issued
that
contained
a
listing
of
the
agricultural
crop
uses
supported
by
Lonza
and
a
listing
of
the
formulations
supported
by
Lonza.
That
addendum
stated
Lonza's
decisions
regarding
the
maximum
application
rates,
the
maximum
seasonal
(
yearly)
application
rates,
minimum
retreatment
intervals,
and
the
pre­
harvest
intervals
for
each
supported
use
pattern.
The
addendum
stated
that
for
home
and
garden
products,
only
those
fruit
and
vegetable
crops
listed
for
agricultural
use
may
be
listed
on
product
labels.
[
Note:
All
assessments
contained
herein
are
based
on
the
aforementioned
use
closure
memo
and
associated
addenda
per
personal
communication
with
Chemical
Review
Manager,
Jill
Bloom.]
On
May
25,
2005,
a
second
addendum
(
addendum
2)
to
the
original
use
closure
memo
was
issued
that
contained
the
Lonza
proposed
maximum
application
rates,
the
maximum
seasonal
(
yearly)
application
rates,
minimum
retreatment
intervals,
and
the
maximum
applications
per
year
for
ornamentals
and
turf/
dichondra
use
patterns.

Table
11
provides
a
summary
of
residential
use
sites,
product
formulations,
maximum
application
rates,
frequency
of
application,
and
application
equipment.

Table
11
­
Summary
of
Registered
Metaldehyde
Residential
Uses
Crop
Target
Formulation
Maximum
Application
Ratea
and
Frequency
of
Applicationb
Application
Equipmentc
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
RTU
solution/
paste
squeeze
solution/
paste
from
bottle
or
tube
Ornamentals
Soluble
concentrate
3.5
lb
ai/
A
Maximum
number
of
applications/
yr:
12
Minimum
retreatment
interval:
21
days
hose­
end
sprayer,
low
pressure
handwand
sprayer,
trigger­
pump
sprayer,
and
sprinkler
can
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Lawns
and
Recreational
Turfgrass
Snails
and
slugs
Soluble
concentrate
1
lb
ai/
A
Maximum
number
of
applications/
yr:
12
Minimum
retreatment
interval:
21
days
hose­
end
sprayer,
low
pressure
handwand
sprayer,
trigger­
pump
sprayer,
and
sprinkler
can
Page
35
of
80
Table
11
­
Summary
of
Registered
Metaldehyde
Residential
Uses
Crop
Target
Formulation
Maximum
Application
Ratea
and
Frequency
of
Applicationb
Application
Equipmentc
Citrus
Granular
1
lb
ai/
A
Apply
when
needed
(
winter
through
spring)
up
to
day
of
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
6
lb
ai/
A
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Brassica
RTU
solution/
paste
1
lb
ai/
A
Apply
when
needed
up
to
72
hours
before
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
4
lb
ai/
A
squeeze
solution/
paste
from
bottle
or
tube
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Lettuce
RTU
solution/
paste
1
lb
ai/
A
Apply
when
needed
up
to
72
hours
before
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
4
lb
ai/
A
squeeze
solution
from
bottle
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Tomato
RTU
solution/
paste
1
lb
ai/
A
Apply
when
needed
up
to
72
hours
before
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
4
lb
ai/
A
squeeze
solution/
paste
from
bottle
or
tube
Strawberry
Granular
1
lb
ai/
A
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Page
36
of
80
Table
11
­
Summary
of
Registered
Metaldehyde
Residential
Uses
Crop
Target
Formulation
Maximum
Application
Ratea
and
Frequency
of
Applicationb
Application
Equipmentc
RTU
solution/
paste
Apply
when
needed
up
to
72
hours
before
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
5
lb
ai/
A
(
perennials)
and
3
lb
ai/
A
(
annuals)
squeeze
solution/
paste
from
bottle
or
tube
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Berries
RTU
solution/
paste
0.8
lb
ai/
A
Apply
up
to
day
before
harvest
Minimum
retreatment
interval:
2
weeks
Maximum
amount
applied
per
year:
4
lb
ai/
A
squeeze
solution/
paste
from
bottle
or
tube
Granular
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
Artichoke
RTU
solution/
paste
0.8
lb
ai/
A
Apply
up
to
day
before
harvest
Minimum
retreatment
interval:
18
days
Maximum
amount
applied
per
year:
5.6
lb
ai/
A
squeeze
solution/
paste
from
bottle
or
tube
Prickly
pear
cactus
Snails
and
slugs
Granular
0.8
lb
ai/
A
Apply
up
to
day
before
harvest
Minimum
retreatment
interval:
30
days
Maximum
amount
applied
per
year:
5.6
lb
ai/
A
push­
type
spreader,
belly
grinder,
by
hand,
shaker
can
a
Application
rates
are
the
maximum
application
rates
determined
from
EPA
registered
labels
for
metaldehyde
b
Amount
handled
per
day
values
are
HED
estimates
of
acres,
square
feet,
or
cubic
feet
treated
or
gallons
applied
based
on
Exposure
SAC
SOP
#
9
"
Standard
Values
for
Daily
Acres
Treated
in
Agriculture,"
industry
sources,
and
HED
estimates.
Page
37
of
80
6.3.1.1.
Residential
Handler
Risk
Assessment
The
anticipated
use
patterns
and
current
labeling
indicate
several
major
residential
exposure
scenarios,
based
on
the
types
of
equipment
and
techniques,
in
which
homeowners
can
be
exposed
to
metaldehyde
during
the
application
process.
The
quantitative
exposure/
risk
assessment
developed
for
residential
handlers
is
based
on
these
scenarios.
The
major
scenarios
include:

(
1)
Mixing/
loading/
applying
liquid
concentrates
with
low
pressure
handwand
sprayer
(
ORETF
data
for
ground­
directed
applications),
(
2)
Mixing/
loading/
applying
liquid
concentrates
with
hose­
end
sprayer
(
ORETF
data
for
hose­
end
sprayer
applications
to
turfgrass),
(
3)
Mixing/
loading/
applying
liquid
concentrates
with
sprinkling
can
(
using
ORETF
data
for
hose­
end
sprayer
applications
to
turfgrass
as
surrogate
data),
(
4)
Mixing/
loading/
applying
liquid
concentrates
with
pump­
trigger
sprayer
(
ORETF
pump­
trigger
data),
(
5)
Applying
granulars
by
hand
(
PHED
data),
(
6)
Loading/
applying
granulars
via
push
type
spreader
(
ORETF
data)
(
7)
Loading/
applying
granulars
via
belly
grinder
(
PHED
data),
and
(
8)
Applying
ready­
to­
use
liquid/
paste
formulations
via
squeeze
bottle
or
tube
(
using
ORETF
pump­
trigger
data
as
surrogate
data)

Data
and
Assumptions
A
series
of
assumptions
and
exposure
factors
served
as
the
basis
for
completing
the
residential
handler
risk
assessments,
as
described
below.

$
Label
maximum
use
rates
and
use
information
specific
to
residential
products
as
specified
in
the
use
closure
memo
(
Bloom,
2005)
served
as
the
basis
for
the
risk
calculations.

$
The
unit
exposure
values
used
in
this
assessment
were
based
on
the
Outdoor
Residential
Exposure
Task
Force
(
ORETF)
and
the
Pesticide
Handlers
Exposure
Database
(
Version
1.1
August
1998)
(
PHED)
1.
The
quality
of
the
data
in
PHED
varies
from
scenarios
that
meet
study
guideline
requirements
to
others
where
a
limited
number
of
poor
quality
data
points
are
available.
However,
in
all
cases,
the
data
used
represent
the
best
available
for
the
scenario.
The
PHED
unit
exposure
values
range
between
geometric
mean
and
median
of
available
exposure
data.
When
data
from
other
studies
were
used,
the
appropriate
statistical
measure
of
central
tendency
was
used.
Central
tendency
values,
coupled
with
other
inputs
used
by
HED,
are
thought
to
result
in
conservative,
deterministic
estimates
of
risk.
[
Note:
Lonza,
the
technical
registrant
is
not
a
member
of
the
ORETF
and
as
such,
the
use
of
ORETF
data
may
be
subject
to
data
compensation.]

1
PHED
is
a
generic
database,
which
includes
the
results
of
over
100
exposure
studies,
developed
by
US
EPA,
Pest
Management
Regulatory
Agency/
Health
Canada
and
the
California
Department
of
Pesticide
Regulation,
in
cooperation
with
the
pesticide
industry.
Page
38
of
80
$
Average
body
weight
of
adult
handlers
is
assumed
to
be
70
kg
because
the
toxicological
endpoint
of
concern
used
for
the
risk
assessments
is
appropriate
for
average
adult
body
weight
representing
the
general
population.
No
specific
effects
were
observed
consistently
in
the
toxicology
studies
to
indicate
an
increased
sensitivity
of
one
gender
over
another.

$
Homeowner
handler
assessments
were
completed
based
on
individuals
wearing
shorts
and
short­
sleeved
shirts.

$
Homeowner
handlers
are
expected
to
complete
all
tasks
associated
with
the
use
of
a
pesticide
product
including
mixing/
loading,
if
needed,
as
well
as
the
application.

$
Calculations
were
based
on
scenarios
in
the
home
that
would
reasonably
be
treated
in
a
day
(
but
would
not
take
more
than
an
hour
or
two)
such
as
the
size
of
a
lawn,
the
size
of
a
garden,
or
the
amount
that
can
be
applied
with
a
piece
of
equipment
and
are
based
on
Agency
Exposure
SAC
Policy
12:
Recommended
Revisions
To
The
Standard
Operating
Procedures
For
Residential
Exposure
Assessment.

Residential
Handler
Non­
cancer
Risks
Non­
cancer
risks
are
calculated
using
the
Margin
of
Exposure
(
MOE)
approach,
which
is
a
ratio
of
the
body
burden
to
the
toxicological
endpoint
of
concern.
Since
no
toxicological
endpoint
of
concern
was
selected
to
assess
risk
from
short­
term
dermal
exposures,
no
short­
or
intermediate­
term
dermal
risks
are
calculated.
Short­
term
inhalation
risks
were
calculated
using
a
NOAEL
of
30
mg/
kg/
day
from
a
chronic
oral
toxicity
study
in
dogs.
The
level
of
concern
for
inhalation
risks
to
residential
handlers
is
1000,
based
on
a
10X
factor
to
account
for
interspecies
extrapolation
to
humans
from
the
animal
test
species,
a
10X
factor
to
account
for
intraspecies
sensitivity,
and
a
database
uncertainty
factor
(
10X).
Intermediate­
and
long­
term
exposures
are
not
expected
for
residential
handlers,
because
of
the
sporadic
nature
of
applications
by
homeowners.

Body
burden
values
were
determined
by
first
calculating
daily
exposures
using
application
parameters
(
i.
e.,
application
rate
and
area
treated)
along
with
unit
exposure
levels.
Exposures
were
then
normalized
by
body
weight
and
adjusted
for
absorption
factors
(
100
percent
for
inhalation)
as
appropriate
to
calculate
average
daily
dose
levels
(
i.
e.,
body
burdens)
as
illustrated
in
equation
below.

Daily
Exposure
(
mg
ai/
day)
=

Unit
Exposure
(
mg
ai/
lb
ai)
x
Application
Rate
(
lb
ai/
A
or
lb
ai/
gal))
x
Daily
Area
Treated
(
A
or
Gal/
day)

Where:

Daily
Exposure
=
Amount
that
is
inhaled,
also
referred
to
as
potential
dose
(
mg
ai/
day);
Unit
Exposure
=
Normalized
exposure
value
derived
from
August
1998
PHED
Surrogate
Page
39
of
80
Exposure
Table
and
ORETF
Surrogate
Exposure
Data
(
µ
g
ai/
lb
ai);
Application
Rate
=
Normalized
application
rate
based
on
a
logical
unit
treatment
such
as
acres
or
gallons,
maximum
values
are
generally
used
(
lb
ai/
A
or
lb
ai/
gal);
and
Daily
Area
Treated
=
Normalized
application
area
based
on
a
logical
unit
treatment
such
as
acres
(
A/
day)
or
gallons
per
day
(
gal/
day).

No
specific
inhalation
absorption
factor
is
available
for
metaldehyde.
Therefore,
a
factor
of
100
percent
was
used
for
route­
to­
route
calculations.
MOEs
were
calculated
using
the
following
formula.

MOE
=
NOAEL
(
mg
ai/
kg/
day)________
Average
Daily
Dose
(
mg
ai/
kg/
day)

Where:

MOE
=
Margin
of
exposure,
value
used
to
represent
risk
or
how
close
a
chemical
exposure
is
to
being
a
concern
(
unitless);
Average
Daily
Dose
=
The
amount
as
absorbed
dose
received
from
exposure
to
a
pesticide
in
a
given
scenario
(
mg
pesticide
active
ingredient/
kg
body
weight/
day);
and
NOAEL
=
No
observed
adverse
effect
level
or
dose
level
in
a
toxicity
study
where
no
observed
adverse
effects
occurred
in
the
study
(
mg
pesticide
active
ingredient/
kg
body
weight/
day).

Short­
term
risks
for
residential
handlers
are
presented
in
Table
12.
For
all
scenarios,
residential
handler
risks
are
not
of
concern,
because
MOEs
meet
or
exceed
HED's
uncertainty
factor
of
1000
(
i.
e.,
MOEs
range
from
56000
to
~
34
million).
Page
40
of
80
Table
12
­
Metaldehyde
Residential
handler
Non­
Cancer
Inhalation
Exposure
and
Risk
Baseline
Short­
term
Exposure
Scenario
Crop
or
Target
Application
Rate
(
lb
ai/
acre)
a
Area
Treated
Daily
(
acres)
b
Baseline
Inhalationc
Unit
Exposure
(
µ
g/
lb
ai)
Inhalation
Dose
(
mg/
kg/
day)
Inhalation
MOE
Mixer/
Loader/
Applicator
ornamentals
3.5
0.023
2.7
0.0000031
9700000
Mixing/
Loading/
Applying
Liquid
Concentrates
with
Low
Pressure
Handwand
(
ORETF­­
ground
directed)
(
1)
turf
­
spot
1
0.023
2.7
0.00000089
34000000
ornamentals
3.5
0.023
17
0.00002
1500000
turf
­
spot
1
0.023
17
0.0000056
5400000
Mixing/
Loading/
Applying
Liquid
Concentrates
with
Hose­
End
Sprayer
(
ORETF
data
­
turfgrass
application)
(
2)
turf
­
broadcast
1
1
17
0.000243
124000
ornamentals
3.5
0.023
17
0.00002
1500000
Mixing/
Loading/
Applying
Liquid
Concentrates
with
a
Watering
Can
(
using
ORETF
hose­
end
data
for
turfgrass
application)
(
3)
turf
1
0.023
17
0.0000056
5400000
Page
41
of
80
Table
12
­
Metaldehyde
Residential
handler
Non­
Cancer
Inhalation
Exposure
and
Risk
Baseline
Short­
term
Exposure
Scenario
Crop
or
Target
Application
Rate
(
lb
ai/
acre)
a
Area
Treated
Daily
(
acres)
b
Baseline
Inhalationc
Unit
Exposure
(
µ
g/
lb
ai)
Inhalation
Dose
(
mg/
kg/
day)
Inhalation
MOE
ornamentals
3.5
0.023
19
0.000022
1400000
Brassica,
lettuce,

tomato,
strawberry
1
0.023
19
0.0000062
4800000
Applying
Ready
to
Use
Formulations
via
Trigger­
Pump
Sprayer
(
ORETF)
(
4)
berries,
artichoke
0.8
0.023
19
0.000005
6000000
ornamentals
3.5
0.023
467
0.00054
56000
citrus,
Brassica,

lettuce,
tomato,

strawberry
1
0.023
467
0.00015
200000
Loading/
Applying
Granulars
via
Hand
(
PHED)
(
5)
berries,
artichoke,

prickly
pear
cactus
0.8
0.023
467
0.00012
240000
ornamentals
3.5
0.5
0.88
0.000022
1400000
Loading/
Applying
Granulars
via
Push
Type
Spreader
(
ORETF
data)
(
6)
turf,
citrus,
Brassica,

lettuce,
tomato,

strawberry
1
0.5
0.88
0.0000063
4800000
Page
42
of
80
Table
12
­
Metaldehyde
Residential
handler
Non­
Cancer
Inhalation
Exposure
and
Risk
Baseline
Short­
term
Exposure
Scenario
Crop
or
Target
Application
Rate
(
lb
ai/
acre)
a
Area
Treated
Daily
(
acres)
b
Baseline
Inhalationc
Unit
Exposure
(
µ
g/
lb
ai)
Inhalation
Dose
(
mg/
kg/
day)
Inhalation
MOE
berries,
artichoke,

prickly
pear
cactus
0.8
0.5
0.88
0.000005
6000000
ornamentals
3.5
0.023
62
0.000071
420000
citrus,
Brassica,

lettuce,
tomato,

strawberry
1
0.023
62
0.00002
1500000
Loading/
Applying
Granulars
via
Belly
Grinder
(
7)
berries,
artichoke,

prickly
pear
cactus
0.8
0.023
62
0.000016
1800000
ornamentals
3.5
0.023
19
0.000022
1400000
Brassica,
lettuce,

tomato,
strawberry
1
0.023
19
0.0000062
4800000
Applying
Ready
to
Use
Liquid/
Paste
Formulations
via
Squeeze
Bottle
or
Tube
(
using
ORETF
pump­
trigger
data
as
surrogate
data)
(
8)
berries,
artichoke
0.8
0.023
19
0.000005
6000000
a
Application
rates
are
the
maximum
application
rates
determined
from
EPA
registered
labels
for
metaldehyde
b
Amount
handled
per
day
values
are
HED
estimates
of
acres,
square
feet,
or
cubic
feet
treated
or
gallons
applied
based
on
Exposure
SAC
SOP
#
9
"
Standard
Values
for
Daily
Acres
Treated
in
Agriculture,"
industry
sources,
and
HED
estimates.

c
Baseline
Inhalation:
no
respirator.
Page
43
of
80
Residential
Handler
Cancer
Risks
Metaldehyde
is
classified
as
"
suggestive
evidence
of
carcinogenic
potential
@

however,
cancer
risks
were
not
calculated,
since
no
cancer
toxicological
endpoint
or
potency
factor
was
identified
for
metaldehyde.

6.3.1.2.
Residential
Postapplication
Risk
Assessment
Metaldehyde
uses
include
home
gardens,
ornamentals,
and
turf
(
lawns).
As
a
result,
a
wide
array
of
individuals
of
varying
ages
can
potentially
be
exposed
when
they
do
activities
in
areas
that
have
been
previously
treated.
However,
since
dermal
exposure
is
not
considered
a
hazard
for
metaldehyde
and
inhalation
exposures
are
not
anticipated
(
i.
e.,
due
to
low
volatility
and
dilution
outdoors),
the
only
risks
which
were
quantitatively
addressed
were
those
associated
with
the
oral
exposure
of
toddlers
who
played
on
treated
turf
(
i.
e.,
hand­
to­
mouth
activities,
object­
to­
mouth
activities,
and
ingestion
of
treated
soil
were
included)
and
those
associated
with
the
possible
ingestion
of
metaldehyde
granules.

The
exposures
from
treated
turf
were
assessed
using
the
short­
term
incidental
oral
endpoint
defined
in
a
chronic
dog
study
(
NOAEL
=
30
mg/
kg/
day).
Granular
ingestion
was
assessed
using
the
acute
dietary
endpoint
which
was
defined
in
a
developmental
toxicity
study
in
rats
(
NOAEL
=
75
mg/
kg/
day).
Short­
term
noncancer
risks
were
calculated
using
the
MOE
approach
as
described
under
Section
6.3.1.1
(
Residential
Handler
Risk
Assessment).
The
level
of
concern
is
established
by
the
total
uncertainty
factor
(
or
target
MOE)
of
1000.
This
factor
is
based
on
a
10X
factor
to
account
for
interspecies
extrapolation
to
humans
from
the
animal
test
species,
a
10X
factor
to
account
for
intraspecies
sensitivity,
and
an
additional
10X
database
uncertainty
factor.

Methodology
The
Agency
relied
on
a
standardized
approach
for
completing
residential
risk
assessments
that
is
based
on
current
metaldehyde
labels
and
guidance
contained
in
the
following
documents
[
Note:
No
exposure
data
were
available
for
metaldehyde.]:

 
Standard
Operating
Procedures
For
Residential
Exposure
Assessment
(
Dec.
1997)
This
document
provides
the
overarching
guidance
for
developing
residential
risk
assessments
including
scenario
development,
algorithms,
and
values
for
inputs.

 
Science
Advisory
Council
For
Exposure
Policy
12
(
Feb.
2001):
Recommended
Revisions
To
The
Standard
Operating
Procedures
(
SOPs)
For
Residential
Exposure
Assessment
This
document
provides
additional,
revised
guidance
for
completing
residential
exposure
assessments.

Several
different
types
of
calculations
were
used
in
this
assessment.
In
essence,
all
can
be
summarized
by
saying
that
a
source
of
some
sort
(
e.
g.,
residue
on
turf)
comes
in
contact
with
a
toddler
as
they
are
doing
an
activity
(
e.
g.,
playing
on
treated
lawns).
Exposures
were
then
calculated
by
multiplying
the
source
concentration
by
some
factor
(
e.
g.,
frequency
of
hand­
to­
mouth
events
and
saliva
extraction
Page
44
of
80
factors)
and
the
duration
of
exposure.
The
procedures
and
algorithms
incorporated
in
these
documents
used
to
address
the
specific
scenarios
are
presented
below:

 
Dose
from
ingestion
of
metaldehyde
granules
from
treated
turf
calculated
using
SOP
2.3.1:
Postapplication
dose
among
toddlers
from
episodic
nondietary
ingestion
of
residues
from
a
child
potentially
ingesting
solid
metaldehyde
formulations
(
e.
g.,
granulars
or
pellets)
after
they
have
been
applied
to
areas
such
as
lawns
or
gardens.

 
Dose
from
hand­
to­
mouth
activity
from
treated
turf
calculated
using
SOP
2.3.2:
Postapplication
dose
among
toddlers
from
incidental
nondietary
ingestion
of
pesticide
residues
on
treated
turf
from
hand­
to­
mouth
transfer
(
i.
e.,
those
residues
that
end
up
in
the
mouth
from
a
child
touching
turf
and
then
putting
their
hands
in
their
mouth);

 
Dose
from
object­
to­
mouth
activity
from
treated
turf
calculated
using
SOP
2.3.3:
Postapplication
dose
among
toddlers
from
incidental
nondietary
ingestion
of
pesticide
residues
on
treated
turf
from
object­
to­
mouth
transfer
(
i.
e.,
those
residues
that
end
up
in
the
mouth
from
a
child
mouthing
a
handful
of
treated
turf
or
object
that
has
been
in
contact
with
such
turf);
and
 
Dose
from
soil
ingestion
activity
from
treated
turf
calculated
using
SOP
2.3.4:
Postapplication
dose
among
toddlers
from
incidental
nondietary
ingestion
of
pesticide
residues
from
ingesting
soil
in
a
treated
turf
area
(
i.
e.,
those
soil
residues
that
end
up
in
the
mouth
from
a
child
touching
treated
soil
and
turf
then
putting
their
hands
in
their
mouth).

Dose
from
ingestion
of
metaldehyde
granules
from
treated
turf
calculated
using
SOP
2.3.1:
The
following
illustrates
the
approach
used
to
calculate
exposures
that
are
attributable
to
the
ingestion
of
metaldehyde
formulations
such
as
pellets
or
granules:

Where:

D
=
dose
from
ingesting
solid
formulation
(
mg/
kg/
day);
IgR
=
ingestion
rate
for
granule
ingestion
per
day
(
g/
day);
F
=
fraction
of
active
ingredient
in
granules
(
unitless);
and
BW
=
body
weight
(
kg).

Dose
from
hand­
to­
mouth
activity
from
treated
turf
calculated
using
SOP
2.3.2:
Nondietary
ingestion
from
hand­
to­
mouth
behaviors
considers
the
environmental
concentrations
and
the
mouthing
behaviors
of
children.
The
following
equation
describes
how
these
exposures
have
been
calculated.

D
=
{(
TR
*
(
SE/
100)
*
SA
*
Freq
*
Hr
*
(
1mg/
1000Fg))}/
BW
Where:

D
=
dose
from
hand­
to­
mouth
activity
(
mg/
kg/
day);
TR
=
transferable
residues,
TR
is
assumed
to
be
5%
of
the
application
rate
on
day
0
for
treatments
to
lawns
or
other
turf
(
Fg/
cm2);
D
={(
IgR
*
F
*
(
1000
mg/
1g))}/
BW
Page
45
of
80
SE
=
saliva
extraction
factor
(%);
SA
=
surface
area
of
the
hands
(
cm2);
Freq
=
frequency
of
hand­
to­
mouth
events
(
events/
hour);
Hr
=
exposure
duration
(
hours);
and
BW
=
body
weight
(
kg).

Dose
from
object­
to­
mouth
activity
from
treated
turf
calculated
using
SOP
2.3.3:
The
following
illustrates
the
approach
used
to
calculate
exposures
that
are
attributable
to
object­
to­
mouth
behavior
on
treated
turf:

Where:

D
=
dose
from
mouthing
activity
(
mg/
kg/
day);
TR
=
transferable
residues,
TR
is
assumed
to
be
20%
of
the
application
rate
on
day
0
for
treatments
to
lawns
or
other
turf
(
Fg/
cm2);
IgR
=
ingestion
rate
for
mouthing
per
day
(
cm2/
day);
and
BW
=
body
weight
(
kg).

Dose
from
soil
ingestion
activity
from
treated
turf
calculated
using
SOP
2.3.4:
The
following
illustrates
the
approach
used
to
calculate
exposures
that
are
attributable
to
the
ingestion
of
soil
on
treated
turf:

Where:

D
=
dose
from
mouthing
activity
(
mg/
kg/
day);
SR
=
soil
residues,
SR
is
based
on
soil
density
and
considering
100%
of
the
application
rate
in
top
1
cm
of
soil
on
day
0
for
treatments
to
turf
(
Fg/
g
or
ppm);
IgR
=
ingestion
rate
for
mouthing
per
day
(
g/
day);
and
BW
=
body
weight
(
kg).

Combining
Appropriate
Risk
Estimates:
HED
combines
risk
values
resulting
from
separate
postapplication
exposure
scenarios
when
it
is
toxicologically
appropriate
and
it
is
likely
they
can
occur
simultaneously
based
on
the
use­
pattern
and
the
behavior
associated
with
the
exposed
population.
The
risks
from
hand­
to­
mouth,
object­
to­
mouth,
and
soil
ingestion
scenarios
were
combined,
since
they
could
logically
co­
occur.
The
following
formula
is
used
to
calculate
total
MOE
values
by
combining
the
route­
specific
MOEs:
MOE
total
=
1/((
1/
MOE
a)
+
(
1/
MOE
b)
+
(
1/
MOE
c)).
Where:
MOE
a
represents
hand­
to­
mouth
risk,
MOE
b
represents
object­
to­
mouth
risks,
and
MOE
c
represents
soil
ingestion
risks.

Inputs
The
inputs
used
in
the
risk
calculations
are
consistent
with
current
Agency
policy
for
completing
residential
exposure
assessments
(
i.
e.,
SOPs
for
Residential
Exposure
Assessment
and
related
D
={(
TR
*
IgR
*(
1mg/
1000Fg))}/
BW
D
={(
SR
*
IgR
*(
1mg/
1000Fg))}/
BW
Page
46
of
80
documents).
A
series
of
standard
exposure
factors
served
as
the
basis
for
assessing
the
residential
post­
application
risks
from
children's.
These
included:

$
5
percent
of
the
application
rate
(
1
lb
ai/
acre)
has
been
used
to
calculate
the
0­
day
transferable
residue
levels
for
defining
risks
from
hand­
to­
mouth
behaviors
(
i.
e.,
5
percent
of
the
application
rate
lb
ai/
acre
after
it
has
been
converted
to
µ
g/
cm2
is
used);

$
hand­
to­
mouth
exposures
are
based
on
a
frequency
of
20
events/
hour
and
a
surface
area
per
event
of
20
cm2
representing
the
palmar
surfaces
of
three
fingers;

$
saliva
extraction
efficiency
is
50
percent
which
indicates
that
every
time
the
hand
goes
in
the
mouth
approximately
½
of
the
residues
on
the
hand
are
removed;

$
a
dissipation
rate
of
10
percent/
day
for
metaldehyde
residues
was
used
to
complete
a
rangefinder
intermediate­
term
assessment;

$
20
percent
of
the
application
rate
has
been
used
to
calculate
the
0­
day
transferable
residue
levels
for
defining
risks
from
object­
to­
mouth
behaviors
for
short­
term
exposures
(
i.
e.,
20
percent
of
the
application
rate
lb
ai/
acre
after
it
has
been
converted
to
µ
g/
cm2
is
used);

$
object­
to­
mouth
exposures
are
based
on
a
25
cm2
surface
area;

$
when
soil
ingestion
is
considered,
100
percent
of
the
application
rate
and
a
soil
density
of
0.67
cm3/
gram
have
been
used
to
calculate
day
0
concentrations
in
the
top
centimeter
of
soil
(
i.
e.,
the
application
rate
is
converted
to
µ
g/
cm2,
then
it
is
converted
to
a
density
µ
g/
cm3
based
on
the
premise
residues
are
found
in
the
top
1
cm
of
soil,
finally
w/
w
soil
concentrations
were
calculated
by
adjusting
for
soil
density);

$
various
formulations
were
considered
in
the
calculation
of
the
risks
associated
with
the
ingestion
of
metaldehyde
formulations,
a
concentration
range
for
all
homeowner
solid
formulations
of
2
to
7.5
percent
active
ingredient
was
considered
and
to
specifically
evaluate
the
amount
ingested
2
specific
formulations
were
considered
with
a
particle
size
of
35
to
50
mini­
pellets/
gram
(
EPA
Reg
8119­
9
which
contains
4%
ai)
and
450
particles/
gram
(
EPA
Reg
8278­
3
which
contains
3.5%
ai);

$
an
ingestion
rate
of
100
mg
per
day
was
used
for
defining
risks
from
soil
ingestion
behaviors
for
acute
oral
exposures;

$
an
ingestion
rate
of
0.3
grams
per
day
was
used
for
defining
risks
from
possible
ingestion
of
metaldehyde
granules;
and
$
the
average
weight
of
toddlers
is
15
kg.

Summary
of
Residential
Post­
application
Non­
Cancer
Risks
Table
13
summarizes
the
post­
application
non­
cancer
risks
to
toddlers
following
applications
of
metaldehyde
to
turf.
In
this
table,
risks
for
each
scenario
considered,
as
well
as
a
combined
risk
estimate
are
presented.
To
summarize,
short­
term
risks
from
mouthing
exposures
on
treated
turf
were
not
of
concern
(
i.
e.,
the
combined
MOE
on
the
day
of
application
=
1600
and
the
major
exposure
component
is
hand­
to­
mouth
activity
with
an
associated
MOE
=
2000).
It
should
be
noted
that
the
approaches
and
inputs
used
are
generally
thought
to
result
in
high
calculated
levels
of
exposure
(
and
hence
risk)
for
each
distinct
scenario.
As
a
result,
the
combined
risk
estimate
is
thought
to
represent
an
extremely
high
level
of
exposure
based
on
what
may
be
reasonably
expected
to
occur
in
the
metaldehyde
user
population.
A
rangefinder
intermediate­
term
assessment
was
also
completed
resulting
in
risks
that
were
not
of
concern
(
i.
e.,
MOE
=
2900).
However,
no
metaldehyde
residue
dissipation
data
were
available
so
the
dissipation
estimate
of
10
percent
per
day
has
uncertainty
Page
47
of
80
associated
with
it
especially
given
its
half­
life
of
67
days
and
the
intended
nature
of
the
formulations
to
provide
residual
pest
control
over
extended
periods.
Uncertainty
related
to
this
issue
would
be
reduced
if
residue
dissipation
data
were
available.

Table
13
­
Summary
of
Non­
Cancer
Short­
term
Postapplication
MOEs
for
Toddlers
Exposure
Scenario
Route
of
Exposure
Formulation
App.
Rate
(
lb
ai/
A)
MOE
on
Day
0
Combined
MOE
Granular
Hand
to
Mouth
Activity
on
Turf
Spray
2000
Granular
Object
to
Mouth
Activity
on
Turf
Spray
8000
Granular
Incidental
Soil
Ingestion
Oral
Spray
1.0
600000
1600
Note:
To
ensure
that
the
Agency
adequately
addressed
all
nature
of
exposures,
an
intermediate­
term
"
rangefinder"
assessment
was
also
completed
based
on
a
10%
residue
decline
per
day
over
a
month
(
no
residue
decline
data
were
available
for
metaldehyde).
The
resulting
combined
MOE
=
2900.

Ingestion
of
metaldehyde
formulations
such
as
mini­
pellets
or
granules
is
a
possible
source
of
exposure
because
children
could
potentially
ingest
them
if
they
were
found
in
treated
lawns
or
gardens.
This
scenario,
however,
is
considered
to
be
episodic
in
nature
and
is
also
further
thought
to
be
unlikely
because
of
the
use
of
a
bittering
agent
which
makes
ingestion
of
metaldehyde
formulations
generally
not
palatable
to
toddlers
(
i.
e.,
who
are
the
population
most
likely
to
ingest
such
materials).
However,
it
is
of
interest
to
examine
such
a
scenario
in
the
interest
of
public
health
in
order
to
characterize
the
potential
risks
if
such
ingestion
events
did
occur.
These
potential
risks
can
be
estimated
in
2
distinct
manners
including
(
1)
calculating
the
risks
based
on
the
SOP
2.3.1
described
above
and
(
2)
describing
how
much
formulation
one
would
be
required
to
ingest
at
the
level
of
concern
defined
by
the
hazard
endpoint
and
associated
uncertainty
factor.
Because
ingestion
of
formulated
material
is
considered
episodic,
risks
were
calculated
using
the
acute
dietary
endpoint
(
NOAEL
=
75
mg/
kg/
day
and
UF=
1000).
The
exposure
from
ingestion
of
metaldehyde
formulations
is
based
on
homeowner
solid
formulation
products
where,
as
indicated
above,
w/
w
concentration
ranges
from
2
to
7.5
percent
by
weight.
Additionally,
in
order
to
provide
an
illustration
of
how
much
one
may
be
required
to
ingest
to
achieve
a
level
of
concern,
2
specific
formulations
were
considered.

The
first
formulation
is
a
mini­
pellet
type
with
a
particle
size
of
35
to
50
mini­
pellets/
gram
or
0.029
grams/
pellet
based
on
the
35
count
(
EPA
Reg
8119­
9
contains
4%
a.
i.
so
each
35
count
mini­
pellet
contains
1
mg
metaldehyde).
The
second
is
a
small
granular
formulation
with
a
particle
size
of
450
granules/
gram
or
0.0022
grams/
granule
(
EPA
Reg
8278­
3
contains
3.5%
ai
so
each
granule
contains
0.078
mg
metaldehyde).
Risks
(
i.
e.,
MOEs)
for
ingestion
of
the
2
and
7.5
percent
w/
w
formulations
based
on
SOP
2.3.1
are
188
and
50,
respectively.
These
values
represent
potential
risks
of
concern
since
the
total
uncertainty
factor
(
i.
e.,
target
MOE)
that
is
applicable
to
this
scenario
is
1000.
Page
48
of
80
However,
it
is
important
to
consider
these
results
in
the
context
described
above
(
i.
e.,
episodic
events
and
use
of
a
bittering
agent).
It
is
also
important
to
consider
these
results
in
the
context
of
how
much
formulation
would
be
required
to
be
ingested
at
the
Agency's
level
of
concern
(
i.
e.,
1.125
mg
metaldehyde
based
on
NOAEL
75
mg/
kg/
day/
UF
=
1000
and
the
15
kg
body
weight
of
a
toddler)
in
order
to
further
characterize
the
MOE
results
presented
above.
Ingestion
of
2
mini­
pellets
would
exceed
the
Agency's
level
of
concern
while
ingestion
of
15
small
granules
would
exceed
the
Agency's
level
of
concern
(
e.
g.,
1.125
mg
metaldehyde
at
level
of
concern/
1
mg
metaldehyde
in
each
minipellet

6.3.2.
Recreational
Uses
The
use
patterns
supported
by
the
technical
registrant,
Lonza,
include
uses
on
turf,
dichondra,
and
ornamentals
on
sites
such
as
parks,
recreation
areas,
golf
courses,
etc.
These
applications
would
be
applied
by
occupational
handlers;
therefore,
no
residential
handler
assessment
is
needed.
Postapplication
exposures
to
children
are
likely
to
occur.
However,
a
separate
risk
assessment
for
these
exposures
was
not
completed,
since
the
application
rates
and
other
application
parameters
are
identical
to
uses
on
home
lawns
and
home
ornamentals.
Therefore
the
exposure
and
risk
assessment
conducted
in
6.3.1.2
is
considered
representative
of
post­
application
exposures
to
toddler
from
uses
in
recreational
settings.

6.3.3.
Other
(
Spray
Drift,
etc.)

Spray
drift
is
always
a
potential
source
of
exposure
to
residents
nearby
to
spraying
operations.
This
is
particularly
the
case
with
aerial
application,
but,
to
a
lesser
extent,
could
also
be
a
potential
source
of
exposure
from
the
ground
application
method
employed
for
metaldehyde.
The
Agency
has
been
working
with
the
Spray
Drift
Task
Force,
EPA
Regional
Offices
and
State
Lead
Agencies
for
pesticide
regulation
and
other
parties
to
develop
the
best
spray
drift
management
practices.
On
a
chemical
by
chemical
basis,
the
Agency
is
now
requiring
interim
mitigation
measures
for
aerial
applications
that
must
be
placed
on
product
labels/
labeling.
The
Agency
has
completed
its
evaluation
of
the
new
data
base
submitted
by
the
Spray
Drift
Task
Force,
a
membership
of
U.
S.
pesticide
registrants,
and
is
developing
a
policy
on
how
to
appropriately
apply
the
data
and
the
AgDRIFT
computer
model
to
its
risk
assessments
for
pesticides
applied
by
air,
orchard
airblast
and
ground
hydraulic
methods.
After
the
policy
is
in
place,
the
Agency
may
impose
further
refinements
in
spray
drift
management
practices
to
reduce
off­
target
drift
with
specific
products
with
significant
risks
associated
with
drift.
However,
metaldehyde
is
primarily
applied
in
a
granular
form
and
spray
drift
is
unlikely.

7.0
Aggregate
Risk
Assessments
and
Risk
Characterization
In
accordance
with
the
FQPA,
HED
must
consider
and
aggregate
metaldehyde
pesticide
exposures
and
risks
from
several
major
sources:
food,
drinking
water,
residential,
and
other
non­
occupational
exposures.
In
an
aggregate
assessment,
exposures
from
relevant
sources
are
added
together
and
compared
to
quantitative
estimates
of
hazard
(
e.
g.,
a
NOAEL
or
PAD),
or
the
risks
themselves
can
be
aggregated.
When
aggregating
exposures
and
risks
from
various
sources,
HED
considers
both
the
route
and
duration
of
exposure.
Page
49
of
80
No
endpoint
was
identified
for
dermal
exposure
to
metaldehyde,
so
dermal
exposures
need
not
be
considered
in
the
aggregate
assessment.

For
metaldehyde,
a
screening
level
assessment
indicated
that
short­
term
risks
will
be
higher
than
intermediate
term
risks.
For
this
reason,
and
because
intermediate­
term
exposures
(
continuous
exposures
for
1­
6
month
in
duration)
are
likely
to
occur
only
infrequently,
if
at
all,
aggregate
assessment
was
completed
only
for
the
short­
term
duration.

No
quantification
of
cancer
risk
is
required,
based
on
the
"
Suggestive
Evidence
of
Carcinogenicity,
but
Not
Sufficient
to
Assess
Human
Carcinogenic
Potential"
classification.

7.1.
Acute
Aggregate
Risk
Only
food
and
water
are
generally
aggregated
for
acute
(
one­
day)
exposures
to
pesticides.
The
following
section
elaborates
on
the
probabilistic
dietary
assessment
that
includes
both
food
and
water
exposures.

When
surface
water
modeling
residues
are
included
in
the
acute
assessments,
HED's
level
of
concern
is
not
exceeded
(<
100%
aPAD).
The
most
highly
exposed
population
subgroup
was
children
1­
2
years
old
at
26%
aPAD
(
95th
percentile).
For
ground
water,
children
1­
2
years
old
were
also
the
most
highly
exposed
population
subgroup.
For
children
1­
2
years
old,
29%
of
the
aPAD
was
occupied
in
the
acute
aggregate
assessment.
HED
is
generally
not
concerned
unless
the
exposure
substantially
exceeds
100%
of
the
aPAD.

The
Commodity
Contribution
Analysis
shows
that
water
is
the
most
significant
contributor
to
the
risk.
SCI­
GROW
is
a
Tier
1
conservative
modeling
analysis;
therefore,
water
concentration
estimates
could
be
significantly
lower
with
additional
refinements.
Page
50
of
80
Table
14
­
Aggregate
Risk
Assessment
for
Acute
Dietary
Exposure
to
Metaldehyde
Acute
Scenario
(
95th
percentile)
Dietary
Only
Dietary
+
Surface
Water
Dietary
+
Ground
Water
Population
Subgroup1
aPAD
mg/
kg/
day
Food
Exp
mg/
kg/
day
%
aPAD
Agg.
Exp
mg/
kg/
day
%
aPAD
Agg.
Exp
mg/
kg/
day
%
aPAD
U.
S.
Population
0.075
0.008551
11
0.008809
12
0.010396
14
All
Infants
(<
1
year
old)
0.075
0.003560
4.8
0.005713
7.6
0.013840
18
Children
1­
2
years
old
0.075
0.018514
25
0.019321
26
0.021634
29
Children
3­
5
years
old
0.075
0.016881
23
0.017325
23
0.019125
26
Children
6­
12
years
old
0.075
0.011224
15
0.011484
15
0.013144
18
Youth
13­
19
years
old
0.075
0.007551
10
0.007750
10
0.009096
12
Adults
20­
49
years
old
0.075
0.007251
9.7
0.007549
10
0.008890
12
Adults
50+
years
old
0.075
0.007776
10
0.008007
11
0.009326
12
Females
13­
49
years
old
0.075
0.007320
9.8
0.007610
10
0.008932
12
1
­
This
footnote
should
indicate
the
selected
subgroups
and
provide
rationale
for
selection.
Indicate
body
weights
(
70
kg
adult
male;
60
kg
adult
female;
10
kg
child).
*
Dietary
Only
 
based
on
DEEM­
FCID
(
version
2.00)
*
Dietary
+
Surface/
Ground
Water
values
 
based
on
DEEM­
FCID
(
version
2.00)
and
PRZM­
EXAMS
analysis.
*
PRZM­
EXAMS
acute
assessment
(
n=
11000)
based
on
max.
application
of
Brassica
leafy
vegetables
in
California.
*
EDWC
of
295ppb
generated
from
a
Tier
I
SCI­
GROW
analysis
based
on
use
of
metaldehyde
on
ornamental
plants
(
chronic
and
acute
aggregate
assessments).

7.2.
Short­
Term
Aggregate
Risk
Incidental
oral
and
inhalation
exposures
may
be
expected
as
a
result
of
the
residential
use
of
metaldehyde.
The
same
study
was
selected
for
short
term
risk
assessment
for
both
the
oral
and
inhalation
routes,
so
the
risks
may
be
aggregated.
Since
the
same
study
was
used
and
an
inhalation
absorbtion
factor
of
100%
was
used,
the
exposures
were
added
and
divided
into
the
NOAEL
in
order
to
calculate
aggregate
MOEs.
Page
51
of
80
Exposures
via
the
oral
route
may
be
expected
from
food,
water,
and
incidental
oral
exposures
around
the
residence.
Inhalation
exposure
is
not
expected
because
of
the
use
patterns
(
pellet­
formulation).
Average
food
and
water
exposure
values
were
used
to
aggregate
the
MOEs.
Incidental
oral
exposures
may
result
from
children
playing
on
treated
turf
and
ingesting
soil
or
inserting
their
hands
in
their
mouths
during
or
after
playing
on
treated
turf.
Since
these
activities
are
likely
to
occur
simultaneously,
the
combined
MOE
was
used
in
the
aggregate
assessment.

The
short
term
aggregated
risks
can
be
found
below
in
Table
15
aggregated
from
oral
and
inhalation
exposures.
The
target
MOE
for
all
short
term
aggregated
risks
is
1000
for
all
scenarios;
none
exceed
the
Agency
target
MOE.

Table
15
­
Short­
Term
Aggregate
Risk
Exposure
(
mg/
kg/
day)
Aggregate
MOE
Population
Food
only
Residential
Food
&
water
food/
residential3
food/
drinking
water/
residential4
Aggregate
MOE
using
chronic
surface
water
EDWC
Children
playing
on
turf1
0.00489
0.019
0.0059
1300
1200
Residential
Handler
 
adults2
0.002215
0.00054
0.0029
11000
8700
Aggregate
MOE
using
chronic
ground
water
EDWC
Children
playing
on
turf1
0.00489
0.019
0.0069
1300
1200
Residential
Handler
 
adults2
0.002215
0.00054
0.003533
11000
7400
Target
MOE
for
all
short
term
aggregate
risks
=
1000
Note:
To
ensure
the
Agency
adequately
addressed
all
nature
of
exposures,
an
intermediate­
term
"
rangefinder"
assessment
was
also
completed
based
on
a
10%
residue
decline
per
day
over
a
month
(
MRID
4657801
shows
a
daily
dissipation
of
~
0.1%
per
day
although
it
has
not
been
completely
reviewed
by
HED.
Once
a
review
is
completed,
the
result
may
be
incorporated
in
to
the
RA.
However,
incorporating
any
lower
residue
decline
values
will
only
increase
resulting
MOEs).
The
resulting
combined
MOE
=
2900
1
`
Children
playing
on
turf'
dietary
exposures
(
food
&
food
and
drinking
water)
from
children
1­
2
years
old
2
Residential
Handler
adult
dietary
exposures
(
food
&
food
and
drinking
water)
from
General
U.
S.
population
Page
52
of
80
3
Food/
residential
Aggregate
MOEs
=
Short­
Term
Incidental
Oral
NOAEL
(
30
mg/
kg/
day)/[
dietary
exposure
+
residential
exposure
(
in
mg/
kg/
day)]
4
Food/
drinking
water/
residential
Aggregate
MOEs
=
Short­
Term
Incidental
Oral
NOAEL
(
30
mg/
kg/
day)/[
dietary
(
food
&
surface
water
drinking
water)
exposure
+
residential
exposure
(
in
mg/
kg/
day)]

7.3.
Long­
Term
Aggregate
Risk
There
are
no
long
term
residential
exposures
expected
for
metaldehyde,
therefore,
long
term
aggregate
risk
incorporates
only
food
and
drinking
water.

Tolerance
level
residues
and
100%
CT
were
used
to
determine
the
chronic
dietary
exposure
and
risk
estimates.
This
assessment
showed
that
for
food
only,
the
chronic
risk
estimates
were
below
the
Agency's
level
of
concern
(<
100%
cPAD)
for
the
general
U.
S.
population
(
22%
of
the
cPAD).
The
highest
exposed
population
subgroup
was
children
1­
2
years
old
(<
49%
cPAD).

When
surface
water
modeling
residues
are
included
in
the
chronic
assessment,
HED's
level
of
concern
is
not
exceeded
(<
100%
cPAD).
The
most
highly
exposed
population
subgroup
was
children
1­
2
years
old
at
59%
cPAD
(
95th
percentile).
For
ground
water,
children
1­
2
years
old
were
also
the
most
highly
exposed
population
subgroup.
For
infants,
69%
of
the
cPAD
was
occupied
in
the
chronic
aggregate
assessment.
The
Commodity
Contribution
Analysis
shows
that
water
is
the
most
significant
contributor.

Table
16
­
Aggregate
Risk
Assessment
for
Chronic
Dietary
Exposure
to
Metaldehyde
Chronic
Scenario
(
95th
percentile)
Food
Only
Food
+
Surface
Water
Food
+
Ground
Water
Population
Subgroup1
cPAD
mg/
kg/

day
Food
Exp
mg/
kg/
day
%
cPAD
Agg.
Exp
(
Food+
SW)
mg/
kg/
day
%
cPAD
Agg.
Exp
(
Food+
GW)

mg/
kg/
day
%
cPAD
U.
S.
Population
0.01
0.002215
22
0.002888
29
0.003533
35
All
Infants
(<
1
year
old)
0.01
0.000674
6.7
0.002878
29
0.004993
50
Children
1­
2
years
old
0.01
0.004890
49
0.005888
59
0.006846
69
Children
3­
5
years
old
0.01
0.004442
44
0.005377
54
0.006274
63
Page
53
of
80
Table
16
­
Aggregate
Risk
Assessment
for
Chronic
Dietary
Exposure
to
Metaldehyde
Chronic
Scenario
(
95th
percentile)
Food
Only
Food
+
Surface
Water
Food
+
Ground
Water
Population
Subgroup1
cPAD
mg/
kg/

day
Food
Exp
mg/
kg/
day
%
cPAD
Agg.
Exp
(
Food+
SW)
mg/
kg/
day
%
cPAD
Agg.
Exp
(
Food+
GW)
mg/
kg/
day
%
cPAD
Children
6­
12
years
old
0.01
0.003002
30
0.003646
37
0.004265
43
Youth
13­
19
years
old
0.01
0.001843
18
0.002329
23
0.002795
28
Adults
20­
49
years
old
0.01
0.001830
18
0.002458
25
0.003060
31
Adults
50+
years
old
0.01
0.002067
21
0.002728
27
0.003362
34
Females
13­
49
years
old
0.01
0.001910
19
0.002536
25
0.003135
31
1
­
This
footnote
should
indicate
the
selected
subgroups
and
provide
rationale
for
selection.
Indicate
body
weights
(
70
kg
adult
male;
60
kg
adult
female;
10
kg
child).
*
Dietary
Only
 
based
on
DEEM­
FCID
(
version
2.00)
*
Dietary
+
Surface/
Ground
Water
values
 
based
on
DEEM­
FCID
(
version
2.00)
and
PRZM­
EXAMS
analysis.
*
PRZM­
EXAMS
chronic
assessment
(
n=
11000)
based
on
average
residues
for
Brassica
leafy
vegetables
in
CA.
*
EDWC
of
295ppb
generated
from
a
Tier
I
SCI­
GROW
analysis
based
on
use
of
metaldehyde
on
ornamental
plants
(
chronic
and
acute
aggregate
assessments).

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

9.0
Occupational
Exposure/
Risk
Pathway
Page
54
of
80
This
section
of
the
risk
assessment
addresses
exposures
to
individuals
who
are
exposed
as
part
of
their
employment.
These
exposures
can
occur
because
people
have
contact
with
metaldehyde
residues
while
using
commercial
products
containing
metaldehyde
(
i.
e.,
handlers)
or
by
being
in
areas
that
have
been
previously
treated
(
post­
application
workers).
A
thorough
understanding
of
how
metaldehyde
is
used
is
critical
to
the
development
of
a
quality
risk
assessment.

Because
this
information
is
also
critical
to
the
dietary
and
residential
exposure
assessments
presented
above,
available
use
information
has
already
been
summarized.
Please
refer
to
Section
2.1:
Summary
of
Registered/
Proposed
Uses
for
further
information
on
this
topic.
All
calculations
for
occupationally
exposed
people
are
based
on
this
information.

9.1.
Short/
Intermediate/
Long­
Term
Handler
Risk
The
Agency
completes
occupational
handler
risk
assessments
using
scenarios
as
the
basis
for
the
calculations
as
described
in
the
U.
S.
EPA
Guidelines
for
Exposure
Assessment.
For
commercial
pesticide
products,
the
Agency
categorizes
handler
exposures
based
on
the
kinds
of
formulations
(
e.
g.,
liquids
or
various
solids),
the
kinds
of
equipment
used
to
make
applications
(
e.
g.,
airblast,
tractor­
drawn
spreader,
or
handheld
equipment),
the
nature
of
the
task
(
e.
g.,
mixing/
loading,
applying,
or
both
combined),
and
the
level
of
personal
protection
used.
Identifying
the
duration
of
exposure
is
also
a
critical
element
in
the
development
of
a
risk
assessment
to
ensure
that
the
proper
hazard
component
is
used.

For
metaldehyde
uses,
the
Agency
identified
several
major
occupational
exposure
scenarios
based
on
the
types
of
equipment
and
techniques
that
potentially
can
be
used
for
metaldehyde
applications.
The
scenarios
associated
with
metaldehyde
use
were
classified
as
having
short­
term
and
intermediate­
term
exposures
(
up
to
30
days
and
30
days
to
several
months,
respectively).
The
quantitative
exposure/
risk
assessment
developed
for
occupational
handlers
was
based
on
the
following
scenarios:

Mixing/
Loading
(
1a)
Mixing/
loading
liquid
concentrates
for
chemigation
applications
(
PHED
data);
(
1b)
Mixing/
loading
liquid
concentrates
for
groundboom
applications
(
PHED
data);
(
1c)
Mixing/
loading
liquid
concentrates
for
airblast
applications
(
PHED
data);
(
2)
Loading
granulars
for
tractor
drawn
spreader
applications
(
PHED
data);

Applicator
(
3)
Applying
sprays
via
groundboom
equipment
(
PHED
data);
(
4)
Applying
sprays
via
airblast
equipment
(
PHED
data);
(
5)
Applying
granulars
via
tractor
drawn
spreader
(
PHED
data);

Mixer/
Loader/
Applicator
Page
55
of
80
(
6)
Mixing/
loading/
applying
liquid
concentrates
with
low
pressure
handwand
(
ORETF
data
for
ground­
directed
applications*);
(
7)
Mixing/
loading/
applying
liquid
concentrates
with
a
handgun
sprayer
(
LCO
ORETF
data*);
(
8)
Mixing/
loading/
applying
liquid
concentrates
with
hose­
end
sprayer
(
ORETF
data
for
applications
to
turfgrass*);
(
9)
Mixing/
loading/
applying
liquid
concentrates
with
sprinkling
can
(
ORETF
data
for
hose­
end
applications
to
turfgrass
as
surrogate
data*);
(
10)
Mixing/
loading/
applying
liquid
concentrates
with
pump­
trigger
sprayer
(
ORETF
pump­
trigger
data*);
(
11)
Applying
granulars
by
hand
(
PHED
data);
(
12)
Loading/
applying
granulars
via
belly
grinder
(
PHED
data);
(
13)
Loading/
applying
granulars
via
push
type
spreader
(
ORETF
data*);
and
(
14)
Applying
ready­
to­
use
liquid/
paste
formulations
via
squeeze
bottle
or
tube
(
ORETF
pump­
trigger
data
as
surrogate
data*).

[*
Note:
Lonza,
the
technical
registrant
is
not
a
member
of
the
ORETF
and
as
such,
the
use
of
ORETF
data
may
be
subject
to
data
compensation.]

For
each
of
these
scenarios,
risk
calculations
were
completed
based
on
three
levels
of
personal
protection
that
were
defined
based
on
different
combinations
of
the
following:

$
Baseline:
no
respiratory
protection;

$
PF5
respirator:
quarter­
face
cup­
style
dust/
mist
filtering
respirator
which
is
presumed
to
reduce
respiratory
exposure
80%
from
baseline;

$
PF10
respirator:
a
half
or
full­
face
respirator
equipped
with
a
dust/
mist
filter,
which
is
presumed
to
reduce
respiratory
exposure
at
least
90%
from
baseline;

$
Engineering
Controls:
use
of
an
appropriate
engineering
control
such
as
a
closed
tractor
cab
or
closed
loading
system
for
granulars
or
liquids.

Data
and
Assumptions
A
series
of
assumptions
and
exposure
factors
served
as
the
basis
for
completing
the
occupational
handler
risk
assessments.
The
inputs
are
consistent
with
current
Agency
policy
for
completing
occupational
exposure
assessments
(
e.
g.,
PHED
Surrogate
Exposure
Guide
and
Exposac
Policy
9:
Standard
Values
for
Daily
Acres
Treated
in
Agriculture).
[
Note:
PHED
is
a
database
that
contains
monitored
field
data
used
for
assessments.
See
Section
6.3.1.1
Residential
Handler
Risk
Assessment
above
for
further
information.]

$
Average
body
weight
of
an
adult
handler
is
70
kg
as
described
in
the
residential
handler
assessments
(
see
Section
6.3.1.1).
Page
56
of
80
$
An
80
percent
protection
factor
(
i.
e.,
PF5)
was
used
to
represent
a
quarter­
face
cup
style
respirator.
Additionally,
a
90
percent
protection
factor
(
i.
e.,
PF10)
was
used
to
represent
a
typical
half/
full
face
cartridge
air
purifying
respirator.

$
Proposed
label
maximum
use
rates
and
use
information
specific
to
residential
products
as
specified
in
the
use
closure
memo
and
associated
attachments
(
Bloom,
2005).

$
The
average
occupational
workday
is
assumed
to
be
8
hours.

$
The
daily
areas
to
be
treated
were
defined
for
each
handler
scenario
(
in
appropriate
units)
by
determining
the
amount
that
can
be
reasonably
treated
in
a
single
day
(
e.
g.
acres).
The
factors
used
for
the
metaldehyde
assessment
are
the
same
as
those
detailed
in
the
HED
Science
Advisory
Committee
on
Exposure
Policy
9:
Standard
Values
for
Daily
Acres
Treated
in
Agriculture.

$
There
were
several
scenarios
which
were
identified
for
which
no
directly
applicable
exposure
data
are
known
to
exist.
These
include:
applying
ready­
touse
liquids/
pastes
with
a
squeeze
bottle
or
tube
and
liquid
concentrates
applied
with
a
sprinkling
can.
As
such,
exposure
data
which
closely
approximate
these
activities
were
used
to
estimate
risks
from
these
exposure
scenarios.
Consequently,
the
estimates
based
on
these
values
should
be
considered
to
have
a
higher
degree
of
uncertainty
associated
with
them.

Handler
Exposure
Assessment
As
no
chemical­
specific
handler
exposure
data
were
submitted
in
support
of
the
reregistration
of
metaldehyde,
an
exposure
assessment
for
each
use
scenario
was
developed
using
surrogate
values
calculated
using
the
Pesticide
Handlers
Exposure
Database
(
V
1.1)
or
data
from
Outdoor
Residential
Exposure
Task
Force
(
ORETF).

Occupational
handler
scenarios
were
assessed
using
the
short­
and
intermediate­
term
endpoints
for
inhalation
exposures.
Dermal
exposures
were
not
assessed
since
no
toxicological
endpoint
of
concern
was
identified
for
the
dermal
route
of
exposure.
The
short­
term
inhalation
endpoint
is
a
NOAEL
of
30
mg/
kg/
day,
based
on
a
chronic
oral
toxicity
study
in
dogs.
The
intermediate­
term
inhalation
endpoint
is
a
NOAEL
of
10
mg/
kg/
day,
also
based
on
a
chronic
oral
toxicity
study
in
dogs.
The
inhalation
absorption
rate
was
assumed
to
be
100
percent.
The
uncertainty
factor
(
UF)
for
both
the
inhalation
endpoints
is
100
(
10X
for
intraspecies
variability
and
10X
for
interspecies
extrapolation).

Daily
inhalation
dose
levels
(
mg/
kg/
day)
were
calculated
and
used
to
calculate
Margins
of
Exposure
(
MOEs)
for
baseline
attire,
personal
protective
equipment
(
respirators),
and
engineering
controls
using
the
short­
and
intermediate­
term
toxicological
endpoints
for
inhalation.
All
calculations
were
completed
based
on
current
EPA
policies
pertaining
to
the
completion
of
occupational
exposure/
risk
assessments
(
e.
g.,
rounding
and
acceptable
data
sources).

Calculating
Dose
from
Inhalation
Exposure
Page
57
of
80
Daily
inhalation
dose
is
calculated
using
the
following
formula
[
Note:
The
same
formula
is
applied
regardless
of
the
risk
mitigation
level.
Only
the
unit
exposure
levels
vary
with
different
levels
of
risk
mitigation.]:

DDaily
Inhalation
=
[
UE
x
(
1
mg/
1000
Fg)
x
AR
x
A
x
(
IA/
100)]
/
BW
Where:

DDaily
Inhalation
=
Daily
absorbed
dose
(
mg/
kg/
day)
resulting
from
inhalation
exposure;
UE
=
Unit
exposure
(
Fg/
lb
ai
handled)
excerpted
from
PHED
surrogate
exposure
table
or
ORETF
data,
AR
=
Application
rate
(
pounds
active
ingredient
per
acre;
A
=
Area
treated
(
acres
per
day)
based
on
the
application
equipment
type;
IA
=
Inhalation
absorption
factor
(%);
and
BW
=
Body
weight
(
kg)
based
on
the
body
weight
of
an
average
adult,
since
the
endpoint
is
non­
sex­
specific.

The
calculations
of
the
daily
inhalation
dose
of
metaldehyde
received
by
handlers
are
used
to
assess
the
inhalation
risks
to
those
handlers.
Short­
and
intermediate­
term
MOEs,
regardless
of
the
exposure
scenario,
were
calculated
using
the
following
formula:

MOE
=
NOAEL
(
mg/
kg/
day)
/
Dose
Inhalation
(
mg/
kg/
day)

Non­
cancer
Occupational
Handler
Risks
For
all
short­
and
intermediate­
term
occupational
handler
scenarios,
risks
were
not
of
concern
even
without
the
use
of
a
respirator
(
i.
e.,
MOEs
 
100).
In
fact,
for
all
scenarios,
MOEs
are
much
greater
than
1000
without
the
use
of
a
respirator
(
e.
g.
 
10000).
[
Note:
Current
metaldehyde
labels
do
not
require
the
use
of
a
respirator.]
Table
17
summarizes
the
results
for
both
short­
term
and
intermediate­
term
occupational
handlers.
Page
58
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Mixer/
Loader
Mixing/
Loading
Liquid
Concentrates
for
Chemigation
Applications
(
1a)
watercress
2.1
350
2400
12000
24000
34000
790
4000
7900
11000
Mixing/
Loading
Liquids
Concentrates
for
Groundboom
Applications
(
1b)
Turf
(
golf
course
green
+
turf)
1
10
180000
880000
1800000
2500000
58000
290000
580000
840000
Mixing/
Loading
Liquids
Concentrates
for
Airblast
Applications
(
1c)
watercress
2.1
40
21000
100000
210000
300000
6900
35000
69000
100000
ornamentals
3.5
80
4400
22000
44000
220000
1500
7400
15000
74000
Loading
Granulars
for
Tractor
Drawn
Spreader
Applications
(
2)
grass
grown
for
seed
1.6
80
9700
48000
97000
480000
3200
16000
32000
160000
Page
59
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
turf,
citrus,

Brassica,

lettuce,
tomato,
strawberry
1
80
15000
77000
150000
770000
5100
26000
51000
260000
berries,
artichoke,

prickly
pear
cactus
0.8
80
19000
97000
190000
970000
6400
32000
64000
320000
Applicator
Applying
Sprays
via
Groundboom
Equipment
(
3)
turf
(
golf
course
green
+
turf)
1
10
280000
1400000
2800000
4900000
95000
470000
950000
1600000
Applying
Sprays
via
Airblast
Equipment
(
4)
watercress
2.1
40
5600
28000
56000
56000
1900
9300
19000
19000
ornamentals
3.5
80
6300
31000
63000
34000
2100
10000
21000
11000
Applying
Granulars
via
Tractor
Drawn
Spreader
(
5)
grass
grown
for
seed
1.6
80
14000
68000
140000
75000
4600
23000
46000
25000
Page
60
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
turf,
citrus,

Brassica,

lettuce,
tomato,
strawberry
1
80
22000
110000
220000
120000
7300
36000
73000
40000
berries,
artichoke,

prickly
pear
cactus
0.8
80
27000
140000
270000
150000
9100
46000
91000
50000
Mixer/
Loader/
Applicator
ornamentals
3.5
5
44000
220000
440000
NF
15000
74000
150000
NF
Mixing/
Loading
/
Applying
Liquid
Concentrates
with
Low
Pressure
Handwand
(
ORETF
data
for
ground
directed
application)
(
6)
turf
1
5
160000
780000
1600000
NF
52000
260000
520000
NF
Mixing/
Loading
/
Applying
Liquid
Concentrates
with
a
Handgun
Sprayer
(
LCO
ORETF
data)

(
7)
ornamentals
3.5
5
80000
330000
800000
NF
27000
110000
270000
NF
Page
61
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
turf
1
5
280000
1200000
2800000
NF
93000
390000
930000
NF
Ornamenttals
3.5
0.023
(
spot
trt.)
1500000
7700000
15000000
NF
510000
2600000
5100000
NF
Mixing/
Loading/
Applying
Liquids
with
a
Hose­
end
Sprayer
(
ORETF
data
for
turfgrass
applications)
(
8)
turf
1
0.023
(
spot
trt.)
5400000
27000000
54000000
NF
1800000
9000000
18000000
NF
ornamentals
3.5
0.023
(
spot
trt.)
1500000
7700000
15000000
NF
510000
2600000
5100000
NF
Mixing/
Loading
/
Applying
Liquids
with
a
Watering
Can
(
using
ORETF
hose­
end
data
for
turfgrass
applications)
(
9)
turf
1
0.023
(
spot
trt.)
5400000
27000000
54000000
NF
1800000
9000000
18000000
NF
Applying
Ready
to
Use
Formulations
via
Trigger­
Pump
Sprayer
ornamentals
3.5
0.023
(
spot
trt.)
1400000
6900000
14000000
NF
460000
2300000
4600000
NF
Page
62
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Brassica,

lettuce,
tomato,
strawberry
1
0.023
(
spot
trt.)
4800000
24000000
48000000
NF
1600000
8000000
16000000
NF
(
ORETF)
(
10)
berries,
artichoke
0.8
0.023
(
spot
trt.)
6000000
30000000
60000000
NF
2000000
10000000
20000000
NF
ornamentals
3.5
0.023
(
spot
trt.)
56500
280000
570000
NF
18000
93000
180000
NF
grass
grown
for
seed
1.6
0.023
(
spot
trt.)
120000
610000
1200000
NF
41000
200000
410000
NF
turf,
citrus,

Brassica,

lettuce,
tomato,
strawberry
1
0.023
(
spot
trt.)
190000
980000
1900000
NF
65000
330000
650000
NF
Applying
Ready
to
Use
Granular
by
Hand
(
11)
berries,
artichoke,

prickly
pear
cactus
0.8
0.023
(
spot
trt.)
240000
1200000
24000000
NF
80000
410000
800000
NF
Page
63
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
ornamentals
3.5
1
9700
48000
97000
NF
3200
16000
32000
NF
grass
grown
for
seed
1.6
1
21000
110000
210000
NF
7100
35000
71000
NF
turf,
citrus,

Brassica,

lettuce,
tomato,
strawberry
1
1
34000
170000
340000
NF
11000
56000
110000
NF
Loading/
Applying
Granulars
via
Belly
Grinder
(
12)
berries,
artichoke,

prickly
pear
cactus
0.8
1
42000
210000
420000
NF
14000
71000
140000
NF
ornamentals
3.5
5
16000
82000
160000
NF
5500
27000
55000
NF
grass
grown
for
seed
1.6
5
36000
180000
360000
NF
12000
60000
120000
NF
Loading/
Applying
Granulars
via
Push
Type
Spreader
(
ORETF)
(
13)
turf,
citrus,

Brassica,

lettuce,
tomato,
strawberry
1
5
58000
290000
580000
NF
19000
96000
190000
NF
Page
64
of
80
Table
17
­
Summary
of
Short­
and
Intermediate­
term
Occupational
Handler
Non­
cancer
Risks
Inhalation
Short­
term
MOEs
Inhalation
Intermediate­
term
MOEs
Exposure
Scenario
Crop
or
Target
ARa
(
lb
ai/
acre)
Area
Treated
Daily
(
acres)
b
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
Baselinec
PF
5
Respiratord
PF
10
Respiratore
Eng
Controlf
berries,
artichoke,

prickly
pear
cactus
0.8
5
72000
360000
720000
NF
24000
120000
240000
NF
ornamentals
3.5
0.023
(
spot
trt.)
1400000
6900000
14000000
NF
460000
2300000
4600000
NF
Brassica,

lettuce,
tomato,
strawberry
1
0.023
(
spot
trt.)
4800000
24000000
48000000
NF
1600000
8000000
16000000
NF
Applying
Ready­
to­
Use
Liquid/
Paste
Formulations
via
Squeeze
Bottle
or
Tube
(
ORETF
pumptrigger
data)

(
14)
berries,
artichoke
0.8
0.023
(
spot
trt.)
6000000
30000000
60000000
NF
2000000
10000000
20000000
NF
a
Application
rates
are
the
maximum
application
rates
determined
from
EPA
registered
labels
for
metaldehyde
b
Amount
handled
per
day
values
are
HED
estimates
of
acres
treated
or
amount
handled
per
day
based
on
Exposure
SAC
SOP
#
9
"
Standard
Values
for
Daily
Acres
Treated
in
Agriculture,"
industry
sources,
and
HED
estimates.

c
Baseline
inhalation
is
no
respirator.

d
80%
respirator
is
quarter­
face
dust/
mist
respirator
(
that
provides
an
80%
protection
factor).

e
90%
respirator
is
half­
face
or
full­
face
respirator
with
a
dust/
mist
filter
(
that
provides
a
90%
or
higher
protection
factor).

f
Engineering
controls
is
closed
mixing/
loading
system,
or
enclosed
cab,
or
enclosed
cockpit.
Page
65
of
80
Occupational
Handler
Cancer
Risks
Metaldehyde
is
classified
as
"
suggestive
evidence
of
carcinogenic
potential,@
however,
cancer
risks
were
not
calculated
for
metaldehyde,
since
no
cancer
endpoint
was
identified.

9.2.
Short/
Intermediate/
Long­
Term
Postapplication
Risk
The
exposures
typically
considered
for
occupational
post­
application
workers
result
from
dermal
contact
with
treated
plants
which
occurs
as
workers
engage
in
various
job
tasks
such
as
harvesting.
Occupational
post­
application
exposures
were
not
assessed
for
metaldehyde
because
no
dermal
hazard
was
identified.
Inhalation
exposures
are
thought
to
be
negligible
in
outdoor
post­
application
scenarios
since
metaldehyde
has
low
vapor
pressure
and
the
dilution
factor
outdoors
is
considered
infinite.
In
addition,
under
the
Worker
Protection
Standard
for
Agricultural
Pesticides
 
WPS
 
(
40
CFR
170)
greenhouses
must
be
appropriately
ventilated
(
ventilation
criteria
are
provided)
following
pesticide
applications
so
that
post­
application
inhalation
exposures
are
minimal.
[
Note:
The
current
restricted
entry
intervals
specified
on
various
metaldehyde
labels
range
from
12
to
24
hours.
The
results
of
this
assessment
do
not
impact
those
current
REIs.]

10.0
Data
Needs
and
Label
Requirements
10.1.
Toxicology

Developmental
neurotoxicity
study
(
rat)

90
day
inhalation
toxicity
study
(
rat)

Mutagenicity
battery
10.2.
Residue
Chemistry

All
end­
use
product
labels
must
be
amended
such
that
they
are
consistent
with
the
use
patterns
supported
by
the
available
field
trials.
Crop
uses
currently
not
being
supported
should
be
deleted
from
all
labels.

The
proposed
GC/
MS
tolerance
enforcement
method
will
be
forwarded
to
ACB
for
an
Agency
method
validation
trial.

Additional
field
trials
are
required
on
leafy
lettuce
(
2
tests),
spinach
(
6
tests),
celery
(
6
tests)
and
peppers
(
9
tests)
to
support
permanent
tolerances
on
the
leafy
and
fruiting
vegetable
crop
groups.
Page
66
of
80

Field
trial
data
are
required
on
the
following
crop
groups
and
individual
crops:
root
and
tuber
vegetables
(
group
1),
leaves
of
root
and
tuber
vegetables
(
group
2),
bulb
vegetables
(
group
3),
legume
vegetables
(
group
6),
foliage
of
legume
vegetables
(
group
7),
cucurbit
vegetables
(
group
9),
pome
fruits
(
group
11),
stone
fruits
(
group
12),
tree
nuts
(
group
14),
grass
forage,
fodder
and
hay
(
group
17),
nongrass
animal
feeds
(
group
18),
and
herbs
and
spices
(
group
19),
asparagus,
avocado,
banana,
coffee,
cotton,
cranberry,
kiwifruit,
grape,
mint,
okra,
and
papaya.

Processing
studies
are
required
on
apple,
sugar
beet,
cotton,
grape,
mint,
plum,
and
potato.

A
reference
standard
for
metaldehyde
must
be
submitted
to
the
National
Pesticide
Standards
Repository.

A
field
accumulation
in
rotational
crop
study
is
required.

10.3.
Occupational
and
Residential
Exposure

Turf
dissipation
study
(
TTR).
The
TTR
data
is
requested
to
ensure
that
intermediate­
term
exposure
estimates
are
commensurate
with
the
agreed
upon
use
interval.

References:

Bloom,
J.
2005.
Memorandum:
Use
Closure
Memorandum
for
Metaldehyde
PC#
053001.
Dated
March
1,
2005
Booze
TF,
Oehme
FW.
An
Investigation
of
Metaldehyde
and
Acetaldehyde
Toxicities
in
Dogs.
Fundamentals
of
Applied
Toxicology
1986
April
6(
3):
440­
446.

HED,
Metaldehyde;
DP
Barcode:
none.
Dated
March
11,
1997
Page
67
of
80
Appendix
A:
Relevant
Toxicology
Executive
Summaries
Page
68
of
80
Developmental
Toxicity
Studies
EXECUTIVE
SUMMARY:
In
a
developmental
toxicity
study
[
MRID
41656001],
female
Sprague­
Dawley
Crl:
CD(
SD)
BR
rats
[
25/
group]
were
administered
metaldehyde
[
99%]
via
gavage
at
dose
levels
of
0
[
Mazola
®
corn
oil],
25
mg/
kg/
day,
75
mg/
kg/
day,
and
150
mg/
kg/
day
from
gestation
day
6
through
gestation
day
15.

There
were
six
deaths
[
all
pregnant;
high­
dose
level
only],
which
occurred
between
gestation
days
7
and
8.
Clinical
signs
attributed
to
treatment
were
observed
at
the
highdose
level
in
those
dams
that
died
and
included
ataxia
[
all
six],
rapid
respiration
[
5
dams],
twitching
[
4
dams],
tremors
[
3
dams],
prostration
[
1
dam],
abdominal
breathing
[
1
dam],
hyperactivity
[
1
dam],
paresis
of
the
hind
legs
[
1
dam],
pallor
[
2
dams],
perioral
encrustation
[
3
dams],
and
perinasal
encrustation
[
2
dams].
Decreased
body
weight
[
96%
of
control]
was
observed
at
the
high­
dose
level
only
on
gestation
day
[
GD]
9.
Bodyweight
gain
was
significantly
decreased
[
74%
of
control]
initially
[
GD
6­
9]
and
throughout
the
dosing
period
at
the
high­
dose
level.
Although
dams
at
the
mid­
dose
level
displayed
only
a
slightly
lower
body­
weight
gain
during
the
dosing
period
[
91%
of
control]
compared
to
the
control,
based
on
their
pre­
dose
body­
weight
gain
[
115%
of
control],
the
decrease
is
considered
treatment­
related.
A
compensatory
weight
gain
was
noted
during
the
post­
dosing
period
at
the
high­
dose
level.
Corrected
body­
weight
gain
at
the
high­
dose
level
was
slightly
[
94%
of
control]
lower
than
the
control
value.
Food
consumption
was
decreased
at
the
high­
dose
level
during
the
dosing
period
and
increased
significantly
during
the
post­
dosing
period
at
the
mid­
and
high­
dose
levels.

Treatment­
related
necropsy
findings
in
the
dams
dying
on
test
included
thinning
of
the
stomach
wall
[
1
dam],
ulceration
of
the
glandular
[
2
dams]
and
nonglandular
[
2
dams]
portion
of
the
stomach,
red/
brown
lungs
[
6
dams],
dilated
renal
pelvis
[
2
dams],
and
hydronephrosis
[
1
dam].
Additionally,
perioral
encrustation
[
6
dams],
perinasal
encrustation
[
5
dams],
and
paravertebral
hemorrhage
[
1
dam]
were
observed
in
those
dying
on
test.
There
were
no
adverse
effects
observed
on
maternal
liver
weight
or
gravid
uterine
weight.

There
were
no
abortions,
and
the
pregnancy
rate
was
comparable
among
the
groups.
The
numbers
of
corpora
lutea,
implantation,
live
fetuses,
and
resorptions
[
both
total
and
per
dam],
as
well
as
pre­
and
post­
implantation
losses
were
comparable
among
the
groups.
There
was
one
dead
fetus
[
high
dose].
Fetal
body
weights
and
the
sex
ratio
were
comparable
among
the
groups.
There
were
no
statistically­
significant
or
dose­
related
differences
in
the
incidence
of
fetal
malformations
or
variations
[
external,
visceral,
and
skeletal].

The
maternal
toxicity
NOAEL
is
75
mg/
kg/
day,
and
the
maternal
toxicity
LOAEL
is
150
mg/
kg/
day,
based
on
mortality,
clinical
signs
of
toxicity
[
ataxia,
tremors,
twitching,
rapid
respiration],
decreased
body­
weight
gain
during
dosing,
and
decreased
food
consumption
during
dosing.
The
NOAEL
for
developmental
toxicity
is
150
mg/
kg/
day,
the
highest
dose
tested.
Page
69
of
80
This
guideline
developmental
toxicity
study
is
classified
Acceptable,
and
it
satisfies
the
guideline
[
OPPTS
870.3700;
§
83­
3(
a)]
for
a
developmental
toxicity
study
in
the
rodent.

EXECUTIVE
SUMMARY:
In
a
developmental
toxicity
study
[
MRID
41590501],
female
New
Zealand
white
rabbits
[
16/
group]
were
administered
metaldehyde
[
99%]
via
gavage
at
dose
levels
of
0
[
Mazola
®
corn
oil],
10
mg/
kg/
day,
40
mg/
kg/
day,
and
80
mg/
kg/
day
from
gestation
day
6
through
gestation
day
18.

There
were
no
treatment­
related
deaths
or
clinical
signs
of
toxicity.
Body­
weight
gains
were
extremely
variable,
and
there
was
no
dose­
response.
All
groups,
including
the
control,
displayed
negative
corrected
body­
weight
gains
but
there
was
no
dose­
response.
Food
consumption
was
decreased
at
all
dose
levels
during
the
dosing
period
compared
to
the
control,
but
there
was
no
dose­
response.

Necropsy
findings
were
comparable
among
the
groups.
There
were
no
adverse
effects
observed
on
maternal
liver
weight
or
gravid
uterine
weight.

There
were
no
abortions,
and
the
pregnancy
rate
was
not
adversely
affected
by
treatment.
The
numbers
of
corpora
lutea,
implantation,
live
fetuses,
resorptions
[
both
total
and
per
dam],
and
dead
fetuses,
as
well
as
pre­
and
post­
implantation
losses
were
comparable
among
the
groups.
Fetal
body
weights
and
the
sex
ratio
were
comparable
among
the
groups.
There
were
no
statistically­
significant
or
dose­
related
differences
in
the
incidence
of
external
or
visceral
malformations,
but
a
slightly
higher
incidence
of
skeletal
malformations
[
5
fetuses
in
3
litters]
was
observed
at
the
high­
dose
level
compared
to
the
control
and
lower
dose
groups
[
1
fetus/
group].
This
latter
finding
is
considered
attributable
to
the
greater
number
of
fetus
examined
at
the
high­
dose
level
[
140
fetuses
in
16
litters]
compared
to
the
other
groups
[
112
fetuses/
12
litters;
104
fetuses/
13
litters;
and
107
fetuses/
13
litters
in
the
control,
low­
and
mid­
dose
groups,
respectively].
External,
visceral,
and
skeletal
variations
were
comparable
among
the
groups.

The
maternal
toxicity
NOAEL
is
80
mg/
kg/
day,
the
highest
dose
tested.
The
NOAEL
for
developmental
toxicity
is
80
mg/
kg/
day,
the
highest
dose
tested.

This
guideline
developmental
toxicity
study
is
classified
Acceptable,
and
it
satisfies
the
guideline
[
OPPTS
870.3700;
§
83­
3(
b)]
for
a
developmental
toxicity
study
in
the
rodent.
NOTE:
Although
no
maternal
or
developmental
effects
were
observed,
the
dose
levels
are
considered
adequate
based
on
effects
observed
in
the
range­
finding
study.
All
does
[
5/
group]
in
the
200,
350
and
500
mg/
kg/
day
groups
died
[
following
1
or
2
doses]
or
were
sacrificed
moribund
[
gestation
days
8­
12],
and
one
doe
at
100
mg/
kg/
day
died.
A
repeat
study
at
higher
dose
levels
would
not
provide
useful
data.
This
is
supported
by
the
results
in
the
rat.
The
maternal
NOAEL
in
the
rat
developmental
toxicity
study
is
75
mg/
kg/
day,
based
on
mortality,
clinical
signs
of
toxicity
[
ataxia,
tremors,
twitching,
rapid
respiration],
decreased
body­
weight
gain
during
dosing,
and
decreased
food
consumption
during
dosing
at
the
LOAEL
of
150
mg/
kg/
day.
The
NOAEL
for
developmental
toxicity
is
150
mg/
kg/
day,
the
highest
dose
tested.
Page
70
of
80
Reproduction
Studies
EXECUTIVE
SUMMARY:
In
a
2­
generation
reproduction
study
[
MRID
42823101],
28
male/
28
female
F0
CD
®
rats/
sex/
group
were
administered
metaldehyde
[>
99%
a.
i.]
via
the
diet
for
10
weeks
prior
to
mating
and
through
gestation
and
lactation
of
one
litter
at
dose
levels
of
0
ppm,
50
ppm,
1000
ppm,
and
2000
ppm
[
F0
males:
0,
3.4,
69.37,
and
138.36mg/
kg/
day;
F0
females:
0,
4.16,
80.81,
and
160.42
mg/
kg/
day;
F1
males:
0,
3.23,
64.93,
and
133.53
mg/
kg/
day;
F1
females:
0,
4.03,
80.51,
and
164.15
mg/
kg/
day].
Rats
were
mated,
one
male
with
one
female.
The
resulting
F1
litters
were
weaned
at
day
28
post
partum.
The
F1
generation
[
28
rats/
sex/
group]
was
administered
the
test
material
at
the
same
dose
levels
as
F0
animals
and
mated
in
a
similar
manner,
avoiding
sibling
matings.
The
resulting
F2
litters
were
weaned
at
day
28
post
partum.

No
treatment­
related
clinical
signs
of
toxicity
or
mortality
were
observed
in
F0
males
at
any
time
point
or
in
F0
females
during
the
pre­
mating
and
mating
periods
or
during
gestation.
However,
at
2000
ppm,
three
F0
dams
were
sacrificed
moribund
during
the
lactation
period
[
lactation
days
16­
18;
days
110,
110,
113
on
test]
due
to
bilateral
hindlimb
paralysis.
No
treatment­
related
clinical
signs
of
toxicity
or
mortality
were
observed
in
F1
males
at
any
time
point
or
in
F1
females
during
the
pre­
mating
and
mating
periods.
However,
during
gestation/
lactation,
three
F1
dams
[
2000
ppm]
were
found
dead
[
days
95,
101,
and
125].
The
2000
ppm
F1
dam
that
was
found
dead
on
day
95
displayed
ataxia,
labored
breathing,
cold
extremities,
and
pallor
on
day
94.
An
additional
2000
ppm
F1
female
[
nongravid]
displayed
prostration,
tremors,
abdominal
breathing,
and
rapid
respiration
on
day
102
but
survived
until
terminal
sacrifice
[
day
134].
The
author
stated
that
the
relationship
of
these
latter
signs
to
treatment
was
unclear.
The
cause
of
death
of
two
of
the
F1
females
was
not
determined
[
third
female
due
to
septic
emboli
to
various
organs].
None
of
the
other
deaths
[
F0
male
and
2
F0
females
at
50
ppm,
2
F1
females
at
50
ppm,
and
one
F1
male
at
1000
ppm]
was
considered
treatment­
related.
No
additional
treatment­
related
clinical
signs
were
noted.

F0
parental
animals
Body
weights
for
the
treatment
groups
were
similar
to
control
throughout
the
study
for
both
sexes.
During
the
pre­
mating
dosing
period,
there
were
no
consistent
adverse
effects
on
body­
weight
gain
in
either
sex.
Body­
weight
gains
of
the
F0
high­
dose
males
were
decreased
initially
[
weeks
0­
1
(
91%
of
control)]
and
during
weeks
5­
6
(
89%
of
control)
and
weeks
8­
9
(
75%
of
control).
During
weeks
2­
3,
there
was
an
apparent
dose­
related
increase
in
body­
weight
gain
in
males
at
the
mid­
(
112%
of
control)
and
high­
dose
(
114%
of
control)
levels.
F0
females
displayed
a
decrease
in
body­
weight
gain
[
66%
of
control]
during
weeks
2­
3
at
the
high­
dose
level,
although
statistical
significance
was
not
attained,
and
the
standard
deviation
exceeded
the
group
mean.
Food
consumption
was
not
affected
in
either
sex.

There
were
no
consistent,
treatment­
related,
adverse
effects
on
body
weights
or
bodyweight
gains
of
the
F1
parental
animals
during
the
pre­
mating
dosing
period,
although
both
sexes
at
the
high
dose
displayed
a
smaller
body­
weight
gain
during
weeks
9­
10
Page
71
of
80
[
males
83%;
females
65%
of
control]
than
control.
Food
consumption
was
comparable
among
the
groups
[
both
sexes]
throughout
the
study.

At
sacrifice,
necrosis
and
hemorrhage
in
the
spinal
cord
and
vertebra
luxation
were
observed
in
the
three
high­
dose
F0
dams
that
displayed
hindlimb
paralysis.
An
additional
F0
dam
at
2000
ppm
displayed
spinal
cord
lesions
microscopically.

At
necropsy,
no
treatment­
related
adverse
effects
were
observed
in
F1
animals
at
any
dose
level.

At
2000
ppm,
F1
males
displayed
increased
relative
liver
weights
[
15%]
and
F1
females
displayed
increased
absolute
[
12%]
and
relative
[
11%]
liver
weights.
These
organ­
weight
changes
were
not
accompanied
by
histopathological
lesions
and
may
be
attributed
to
adaptation
to
the
test
material.
NOTE:
Liver
weights
were
not
determined
for
F0
animals.

F0
Generation.
No
apparent
adverse
effect
was
observed
on
fertility,
and
the
mating
and
gestation
indices
were
comparable
among
the
groups.
Pre­
coital
intervals
were
not
reported.
The
duration
of
gestation
was
comparable
among
the
groups.
The
number
of
live
pups
was
comparable
among
the
groups.
The
number
of
pups
born
dead/
dying
by
day
1
was
not
affected
by
treatment.
Litter
size
was
slightly
lower
at
the
high­
dose
level
[
Day
0
(
13.6),
Day
4
precull
(
13.3),
Day
21
(
7.5)]
compared
to
the
control
[
Day
0
(
13.7),
Day
4
precull
(
13.5),
Day
21
(
7.8)]
and
other
dose
groups
[
Day
0
(
14.0
and
13.8),
Day
4
precull
(
13.7
and
13.8),
Day
21
(
7.7
and
7.9)
for
low­
and
mid­
dose
groups,
respectively]
throughout
the
weaning
period.
The
live
birth
index
and
the
viability
index
were
comparable
among
the
groups,
but
the
lactation
index
was
slightly
lowered
[
89%]
at
the
high­
dose
level
compared
to
the
control
[
99%]
and
other
dose
groups
[
99%].
At
the
highdose
level,
a
slightly
lower
pup
body
weight
was
observed
on
lactation
days
7
[
males
96%/
females
95%
of
control]
and
21
[
95%
of
control],
although
statistical
significance
was
not
attained
for
either
timepoint.
Body­
weight
gains
were
slightly
lower
for
both
sexes
at
the
high­
dose
level
[
94%­
95%
of
control]
compared
to
the
control
throughout
lactation.
The
sex
ratio
was
comparable
among
the
groups.
F1
Generation.
No
apparent,
treatment­
related,
adverse
effect
was
observed
on
fertility,
and
the
mating
and
gestation
indices
were
comparable
among
the
groups.
Pre­
coital
intervals
were
not
reported.
The
duration
of
gestation
was
comparable
among
the
groups.
The
high­
dose
group
had
the
fewest
females
[
22]
with
live
born
pups
[
27
control
and
23
each
at
the
low­
and
mid­
dose
levels].
The
number
of
live
pups
was
comparable
among
the
groups.
The
number
of
pups
born
dead/
dying
by
day
1
was
not
affected
by
treatment.
Litter
size
was
comparable
among
the
groups,
and
the
live
birth
index,
viability
index,
and
the
lactation
index
were
comparable
among
the
groups.
At
the
high­
dose
level,
a
slightly
lower
pup
body
weight
was
observed
on
lactation
days
1
[
males
93%/
females
93%
of
control],
7
[
females
95%
of
control],
and
21
[
males
93%/
females
92%
of
control],
although
statistical
significance
was
attained
only
at
the
day
21
timepoint.
Body­
weight
gains
were
slightly
lower
for
both
sexes
at
the
high­
dose
level
[
91%­
93%
of
control]
compared
to
the
control
throughout
lactation.
The
sex
ratio
was
comparable
among
the
groups.
Page
72
of
80
The
NOAEL
for
parental
toxicity
is
1000
ppm
[
males
65
mg/
kg/
day;
females
81
mg/
kg/
day)
and
the
parental
LOAEL
is
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
based
on
mortality
(
F0
and
F1
females),
clinical
signs
(
hindlimb
paralysis
in
F0
females),
and
histopathology
(
spinal
cord
necrosis
and
hemorrhage,
and
vertebra
luxation
in
F0
females
and
increased
liver
weight
in
both
sexes
[
F1].

The
NOAEL
for
reproductive
toxicity
is
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
the
highest
dose
tested.

The
NOAEL
for
offspring
toxicity
is
1000
ppm
[
males
65
mg/
kg/
day;
females
81
mg/
kg/
day)
and
the
LOAEL
for
offspring
toxicity
is
2000
ppm
[
males
133
mg/
kg/
day;
females
160
mg/
kg/
day],
based
on
decreased
pup
body
weight/
bodyweight
gain
[
F1
and
F2
pups].

This
2­
generation
reproduction
study
is
classified
Acceptable/
Guideline.
This
study
satisfies
the
guideline
requirement
(
OPPTS
870.3800;
§
83­
4)
for
a
2­
generation
reproduction
study.
The
original
DER
set
the
reproductive
toxicity
LOEL
at
2000
ppm,
based
on
decreased
pup
body
weight
and
weight
gain
in
both
sexes,
which
is
not
a
reproductive
toxicity
endpoint
but
an
offspring
endpoint.
Reproductive
toxicity
was
not
observed
in
this
study,
based
on
the
parameters
examined.
It
is
to
be
noted
that
several
parameters
in
the
current
protocol
that
measure
reproductive
effects,
such
as
age
of
vaginal
opening
and
preputial
separation;
anogenital
distance
for
F2
pups;
implantations
sites;
estrous
cycle
length
and
periodicity
(
F1
weanlings);
and
sperm
measures,
were
not
evaluated.
These
are
included
in
the
new
protocol,
which
was
not
in
effect
at
the
time
of
the
study.

Carcinogenicity
Study
­
rat
EXECUTIVE
SUMMARY:
In
a
chronic
toxicity/
carcinogenicity
study
[
MRIDs
42203601],
60
Sprague­
Dawley
CD
®
rats/
sex/
dose
were
administered
metaldehyde
[
99
%]
via
the
diet
at
concentrations
of
0
ppm
and
0
ppm
(
there
were
2
control
groups),
50
ppm
[
males
2
mg/
kg/
day;
females
3
mg/
kg/
day],
1000
ppm
[
males
44
mg/
kg/
day;
females
60
mg/
kg/
day],
5000
ppm
[
males
224
mg/
kg/
day;
females
314
mg/
kg/
day]
for
104
weeks.

There
was
no
adverse
effect
of
treatment
on
survival
of
either
sex,
although
females
at
the
mid­
[
60%]
and
high­
[
58%]
levels
displayed
a
slightly
greater
mortality
than
the
control
groups
[
50%
and
48%].
There
were
no
apparent
treatment­
related
clinical
signs
of
toxicity.
There
was
a
slight
reduction
in
body
weight
[.
95%
of
control]
throughout
most
of
the
study
in
both
sexes
at
the
high­
dose
level
compared
to
the
control
groups.
During
the
first
week,
females
in
all
treated
groups
displayed
a
dose­
related
[
statisticallysignificant
at
all
dose
levels]
decrease
in
body­
weight
gain
compared
to
the
2
control
groups
[
86%/
94%,
69%/
75%,
and
60%/
66%
of
control
with
increasing
dose].
During
the
same
time­
frame,
males
displayed
a
similar
dose­
related
decrease
in
body­
weight
gain,
which
was
statistically
significant
at
the
mid­
[
87%
of
control]
and
high­
[
78%
of
control]
dose
level
compared
to
one
of
the
control
groups.
Food
consumption
was
decreased
at
the
Page
73
of
80
high­
dose
level
in
both
sexes
during
the
first
few
weeks
of
the
study,
which
suggests
a
palatability
problem.

There
were
no
apparent,
treatment­
related,
effects
on
the
ophthalmological
or
hematological
parameters
monitored
in
either
sex.
Mid­
and
high­
dose
females
displayed
a
statistically­
significant,
dose­
related,
increase
in
cholesterol
levels
throughout
most
of
the
study.
Globulin
values
were
elevated
in
the
high­
dose
females
throughout
most
of
the
study
[
weeks
26,
52,
and
78]
and
in
mid­
dose
females
only
at
week
78.
There
were
no
treatment­
related
alterations
in
the
liver
enzymes
monitored.
There
was
a
dose­
related
increase
in
urine
volume
in
females
[
37%,
40%,
and
54%
with
increasing
dose]
at
week
77
only.

Increased
liver
weight
[
males
111%­
118%
of
control;
females
121%­
132%
of
control]
was
observed
in
both
sexes
at
the
high­
dose
level,
although
the
values
in
males
did
not
attain
statistical
significance.
Females
at
all
dose
levels
displayed
an
increase
in
ovarian
weight,
but
there
was
no
dose­
response,
and
the
standard
deviation
of
the
low­
and
highdose
female
groups
exceeded
the
means.

In
the
liver,
there
was
a
dose­
related
increase
in
hepatocellular
hypertrophy
in
both
sexes,
which
was
statistically­
significant
at
the
mid­
dose
level
in
males
and
at
the
high­
dose
level
in
both
sexes.
There
was
a
statistically­
significant
increase
in
hepatocellular
adenomas
in
high­
dose
females
[
10%]
compared
to
the
control
and
other
dose
groups.
The
majority
of
the
liver
adenomas
were
observed
at
the
terminal
sacrifice,
and
the
incidence
is
within
the
historical
control
incidence
of
the
testing
facility
[
0%­
10%].
One
hepatocellular
carcinoma
was
observed
in
one
of
the
control
groups
and
in
one
high­
dose
female.
The
combined
incidence
[
adenomas
and
carcinomas]
of
liver
tumors
in
the
highdose
females
[
11.7%]
is
slightly
outside
the
historical
control
incidence
of
the
testing
facility
[
0%­
10%].
Males
did
not
display
an
increase
in
liver
tumors.

The
systemic
toxicity
NOAEL
is
50
ppm
[
males
2
mg/
kg/
day;
females
3
mg/
kg/
day],
based
on
hepatocellular
hypertrophy
and
increased
cholesterol
in
both
sexes
and
decreased
body­
weight
gain
in
females
at
the
systemic
LOAEL
of
1000
ppm
[
males
44
mg/
kg/
day;
females
60
mg/
kg/
day].

This
guideline
chronic
toxicity/
carcinogenicity
study
is
classified
ACCEPTABLE,
and
it
satisfies
the
guideline
[
OPPTS
870.4300;
§
83­
5]
for
a
chronic
toxicity/
carcinogenicity
study
in
the
rat.

Carcinogenicity
Study
 
mouse
EXECUTIVE
SUMMARY:
In
a
carcinogenicity
study
[
MRID
42737201],
60
CD­
1
mice/
sex/
dose
were
administered
metaldehyde
[>
99%;
Lot
#
5448]
via
the
diet
at
concentrations
of
0
ppm
[
2
control
groups],
25
ppm
[
males
4.0
mg/
kg/
day;
females
4.8
mg/
kg/
day],
100
ppm
[
males
15.9
mg/
kg/
day;
females
19.7
mg/
kg/
day],
and
300
ppm
[
males
48.9
mg/
kg/
day;
females
59.8
mg/
kg/
day]
for
18
months.
Page
74
of
80
There
were
no
treatment­
related
effects
on
survival
or
clinical
signs
in
either
sex,
and
body
weights,
body­
weight
gains,
and
food
consumption
were
comparable
among
the
groups
for
both
sexes.

The
hematologic
parameters
monitored
were
comparable
among
the
groups
[
both
sexes].
Clinical
chemistry
and
urinalysis
parameters
were
not
monitored.

At
necropsy,
there
were
no
gross
lesions
attributed
to
treatment
in
either
sex.
With
the
exception
of
liver
weights
in
males,
which
displayed
a
dose­
related
increase
(
although
statistical
significance
was
not
attained),
organ
weights
were
comparable
among
the
groups
[
both
sexes].

Non­
neoplastic
lesions:
The
incidence
[
overall:
high­
dose
males
62%
vs
30%­
33%
control;
high­
dose
females:
30%
vs
7%­
15%
control]
and
severity
of
hepatocellular
hypertrophy
were
increased
in
both
sexes
at
the
high­
dose
level
compared
to
the
control
groups.
The
majority
of
the
mice
with
hepatocellular
hypertrophy
were
diagnosed
at
terminal
sacrifice.

Neoplastic
lesions:
There
was
no
statistically­
significant
increase
in
the
incidence
of
liver
tumors
in
either
sex,
although
the
high­
dose
males
displayed
a
slight
increase
[
15
adenomas
and
3
carcinomas]
compared
to
both
control
groups
[
8
adenomas/
1
carcinoma
and
8
adenomas/
3carcinomas].

The
systemic
toxicity
NOAEL
is
100
ppm
[
15.9
mg/
kg/
day
(
males);
19.7
mg/
kg/
day
(
females)],
based
on
a
significantly
increased
incidence
of
hepatocellular
hypertrophy
in
both
sexes
at
the
LOAEL
of
300
ppm
[
48.9
mg/
kg/
day
(
males);
59.8
mg/
kg/
day
(
females)].
No
other
toxicological
effects
were
observed
in
either
sex.
The
incidence
of
tumors
was
comparable
among
the
groups
[
both
sexes].

This
guideline
carcinogenicity
study
is
classified
ACCEPTABLE/
Guideline.
However,
the
dose
levels
were
not
considered
adequate
for
assessing
the
carcinogenic
potential
of
metaldehyde,
and
a
supplementary
study
was
performed
[
MRID
44625101;
separate
DER].
In
the
90­
day
mouse
study
[
not
submitted
to
the
Agency]
performed
to
determine
dose
levels
to
be
used
in
the
current
study,
mortality
was
said
to
have
been
observed
at
3000
ppm
and
10000
ppm
and
dose­
related
increases
in
liver
weight
and
hepatic
lesions
were
reported
in
both
sexes
at
$
300
ppm.
The
supplemental
carcinogenicity
study
[
MRID
44625101]
was
performed
using
one
dose
level
of
metaldehyde
[
1000
ppm].
At
1000
ppm,
there
was
a
treatment­
related
increase
in
the
incidence
of
hepatocellular
adenomas
in
both
sexes
when
compared
to
controls.
Dosing
was
considered
adequate
based
on
the
increased
incidence
of
liver
lesions
[
liver
single
cell/
focal/
multifocal
necrosis
(
males)
and
hepatocellular
eosinophilic
cell
foci
(
females)]
in
both
sexes,
in
addition
to
hepatocellular
hypertrophy
(
both
sexes),
which
was
the
only
treatmentrelated
finding
in
the
current
study
at
300
ppm.
When
all
the
information,
including
the
90­
day
study
(
MRID
43297701),
are
considered
together,
MRID
42737201
and
MRID
44625101
satisfy
the
guideline
requirement
[
OPPTS
870.4200;
§
83­
2]
for
a
carcinogenicity
study
in
the
mouse.
Page
75
of
80
In
a
carcinogenicity
study
[
MRID
44625101],
metaldehyde
(%
a.
i.,
batch/
lot
#)]
was
administered
to
60
Crl:
CD­
1
®
­
(
ICR)
BR
mice/
sex/
dose
via
the
diet
at
dose
levels
of
0,
0,
and
1000
ppm
[
equivalent
to
0,
0,
135
mg/
kg
bw/
day
(
males)/
163
mg/
kg
bw/
day
(
females)]
for
at
least
78
weeks.

There
were
no
compound­
related
effects
on
mortality,
clinical
signs,
body
weight,
food
consumption,
or
hematology
in
either
sex.
With
the
exception
of
the
liver,
organ
weights
were
comparable
to
those
of
the
control
groups
for
both
sexes.
Liver
weights
were
increased
significantly
in
both
sexes
at
1000
ppm
compared
to
both
of
their
respective
control
groups.
Gross
and
histologic
pathology
findings
were
comparable
among
the
groups
for
both
sexes,
with
the
exception
of
the
liver.
Hepatocellular
hypertrophy
was
observed
in
both
sexes
at
1000
ppm.
Males
at
1000
ppm
displayed
single
cell
necrosis,
focal
or
multifocal
necrosis,
pigment
accumulation,
and
sinusoidal.
Females
at
1000
ppm
displayed
a
small
increase
in
the
incidence
of
hepatocellular
eosinophilic
cell
foci.
There
was
a
significant
increase
in
the
incidence
of
hepatocellular
adenomas
in
both
sexes
[
males:
4
and
5
vs
14;
females:
1
and
0
vs
5],
with
the
males
displaying
the
greater
effect.
Males
also
displayed
a
slight
increase
in
hepatocellular
carcinomas
[
2
and
2
vs
4]
compared
to
both
control
groups.

Under
the
conditions
of
this
study,
at
the
only
dose
of
metaldehyde
tested
[
1000
ppm;
135
(
males)/
163
(
females)
mg/
kg/
day)],
increased
liver
weight
(
both
sexes),
hepatocellular
hypertrophy
(
both
sexes),
liver
single
cell/
focal/
multifocal
necrosis
(
males),
liver
pigment
accumulation
(
males),
sinusoidal
histiocytosis
(
males),
hepatocellular
eosinophilic
cell
foci
(
females),
and
hepatocellular
adenomas
(
both
sexes)
were
observed.
The
NOAEL
is
not
established
in
the
current
study.
However,
based
on
a
previous
mouse
carcinogenicity
study
in
the
same
strain
of
mouse
[
MRID
42737201],
in
which
an
increased
incidence
of
hepatocellular
hypertrophy
was
observed
in
both
sexes
at
the
highest
dose
tested
[
300
ppm;
48.9
(
males)/
59.8
(
females)
mg/
kg/
day],
the
NOAEL
is
100
ppm
[
15.9
(
males)/
19.7
(
females)
mg/
kg/
day],
with
the
LOAEL
based
on
an
increased
incidence
of
hepatocellular
hypertrophy
in
both
sexes.

At
the
dose
tested
in
the
current
study,
there
was
a
treatment
related
increase
in
the
incidence
of
hepatocellular
adenomas
in
both
sexes
when
compared
to
the
controls.
Dosing
was
considered
adequate
based
on
the
increased
incidence
of
liver
lesions
[
liver
single
cell/
focal/
multifocal
necrosis
(
males)
and
hepatocellular
eosinophilic
cell
foci
(
females)]
in
both
sexes,
in
addition
to
the
hepatocellular
hypertrophy
observed
in
the
previous
study
at
300
ppm.

This
carcinogenicity
study
in
the
mouse
is
Acceptable/
non­
guideline.
It
is
non­
guideline
since
only
one
dose
level
was
tested.
The
study
was
performed
as
a
supplement
to
a
previous
18­
month
mouse
carcinogenicity
study
[
MRID
42737201]
and
should
be
considered
along
with
the
previous
study.
Together,
the
two
studies
satisfy
the
guideline
requirement
for
a
carcinogenicity
study
[
OPPTS
870.4200;
OECD
451]
in
mice.
Page
76
of
80
STUDIES
FOR
ENDPOINT
SELECTION:

Chronic
Oral
Toxicity
Study
­
dog
EXECUTIVE
SUMMARY
In
a
chronic
oral
toxicity
study
(
MRID
46378401),
metaldehyde
(
98.3%
a.
i.;
batch
#
30202)
was
administered
once
daily
for
52
consecutive
weeks
to
groups
of
4
male
and
4
female
Beagle
dogs
at
dose
levels
of
10,
30,
and
90
mg/
kg/
day.
The
amount
of
test
material
given
was
adjusted
to
each
dog's
actual
body
weight
weekly.

There
were
three
deaths
[
one
each
sex
at
30
mg/
kg/
day
and
one
female
at
90
mg/
kg/
day],
which
occurred
between
weeks
37
and
46.
Treatment­
related
clinical
signs
were
observed
from
week
one
on
at
the
high
dose
and
included
ataxia,
emesis,
tremor,
twitching,
and
salivation.
The
incidence
and
severity
of
these
clinical
signs
lessened
with
time
from
week
19,
although
1
or
2
animals
continued
to
display
salivation
throughout
the
study.
One
high­
dose
female
displayed
lateral
position
early
in
the
study,
reduced
motility
during
most
of
the
study,
and
convulsion
and
vocalization
during
week
46.
Agitation
was
displayed
by
one
high­
dose
female
during
weeks
6­
9
and
24­
52.
Body
weight
was
slightly
lower
in
the
treated
dogs
[
males
83%­
93%;
females
81%­
94%]
throughout
most
of
the
study,
although
a
dose­
response
was
not
always
evident.
At
study
termination,
male
body
weights
were
84%,
88%,
and
83%
and
female
body
weights
were
96%,
90%,
and
81%
of
control
with
increasing
dose.
During
the
first
week
on
test,
males
displayed
decreased
body­
weight
gains
at
all
dose
levels,
although
the
decrease
was
inversely
related
to
dose
[
47%,
66%,
and
74%
of
control
with
increasing
dose].
Only
the
mid­
dose
females
displayed
a
decrease
in
body­
weight
gain
initially
[
36%
of
control].
During
the
0­
13
week
interval,
males
at
all
dose
levels
[
75%,
83%,
and
57%
with
increasing
dose]
and
females
at
the
mid­
[
63%]
and
high­
[
79%]
dose
levels
displayed
decreased
bodyweight
gains
compared
to
the
controls.
Food
consumption
was
not
adversely
affected.
Food
efficiency
values
were
not
provided.

No
lesions
of
the
eyes
or
optic
region
were
found,
and
there
were
no
differences
in
the
urinalysis
parameters
monitored
in
either
sex.
During
the
13­
week
assessment,
one
highdose
dog
of
each
sex
did
not
react
to
the
noise
test,
but
no
effects
were
noted
in
either
sex
at
the
26­
and
52­
week
assessments.
Increases
in
hemoglobin,
RBC,
and
hematocrit
were
observed
in
both
sexes
at
the
high­
dose
level
at
week
13,
but
only
in
females
at
week
26.
Alkaline
phosphatase
was
increased
throughout
the
study
in
both
sexes
at
the
high­
dose
level,
with
the
magnitude
of
the
response
from
control
increasing
with
time
[
both
sexes].
High­
dose
females
displayed
an
increase
in
gamma­
GT
throughout
the
study,
but
other
liver
enzyme
activities
[
AST,
ALT]
were
not
affected
by
treatment.
Triglycerides
were
increased
in
the
high­
dose
females
throughout
the
study
compared
to
the
control
values.

At
the
high­
dose
level
in
both
sexes,
liver
weight
was
increased
significantly
compared
to
the
control
values.
There
was
a
dose­
related
decrease
in
absolute
prostate
weight
[
82%,
71%,
and
68%
of
control
with
increasing
dose],
a
decrease
in
testes
weight
at
the
lowand
high­
dose
level,
and
an
increase
in
absolute
and
relative
lung
weight
in
high­
dose
Page
77
of
80
males.
Increased
brain
weight
was
observed
in
females
at
the
high­
dose
level
compared
to
the
control.
There
were
no
apparent
microscopic
lesions
in
the
liver,
but
atrophy
and/
or
degeneration
was
observed
in
the
testes
and
prostate.

The
lowest­
observed­
adverse­
effect
level
(
LOAEL)
for
metaldehyde
in
the
dog
is
30
mg/
kg/
day,
based
on
death
and
atrophy
of
the
testes
and
prostate.
The
NOAEL
is
10
mg/
kg/
day.

This
chronic
oral
toxicity
study
in
the
dog
is
Acceptable/
Guideline,
and
it
satisfies
the
guideline
requirement
for
a
chronic
oral
toxicity
study
[
OPPTS
870.4100);
OECD
452]
in
the
dog.

21
 
Day
Dermal
Toxicity
Study
EXECUTIVE
SUMMARY:
In
a
21­
day
dermal
toxicity
study
[
MRID
42063401],
5
New
Zealand
White
rabbits/
sex/
group
were
administered
metaldehyde
[
99.0%]
via
dermal
application
[
dry
powder
covered
with
a
gauze
patch
moistened
with
Milli­
Q
®
filtered
water;
once
a
day
for
6
hours,
5
days/
week]
for
22
days
at
concentrations
of
0,
100,
300,
and
1000
mg/
kg/
day.

Treatment
had
no
adverse
effect
on
survival,
clinical
signs,
mean
body
weight,
bodyweight
gain,
food
consumption,
hematology,
clinical
chemistry,
organ
weights,
or
gross
and
microscopic
pathology.
There
was
no
dose­
related
increase
in
the
incidence
or
severity
of
signs
of
dermal
toxicity.

The
NOAEL
for
systemic
and
dermal
toxicity
is
1000
mg/
kg/
day,
the
highest
dose
tested
This
guideline
21­
day
dermal
toxicity
study
is
classified
ACCEPTABLE,
and
it
satisfies
the
guideline
requirement
[
§
82­
2;
870.3200]
for
a
21­
day
dermal
toxicity
study.
Although
fewer
rabbits/
sex/
group
were
utilized
than
specified
in
the
Guideline,
this
does
not
by
itself
diminish
the
finding
of
no
effect
at
the
limit
dose.
Page
78
of
80
Appendix
B:
Tolerance
Reassessment
Summary
Page
79
of
80
TOLERANCE
REASSESSMENT
SUMMARY
Tolerance
Reassessments
for
Metaldehyde
The
current
tolerance
expression
for
metaldehyde
residues
is
adequate.
The
HED
Metabolism
Committee
has
determined
that
the
tolerance
expression
for
residues
in/
on
crop
commodities
should
include
only
metaldehyde
per
se.
A
summary
of
metaldehyde
tolerance
reassessments
is
presented
in
Table
5.

Tolerances
Listed
Under
40
CFR
§
180.523:

A
tolerance
of
"
zero"
has
been
established
for
residues
of
metaldehyde
on
strawberries
[
40
CFR
§
180.523(
a)].
No
other
tolerances
are
established.

The
residue
data
submitted
to
reassess
the
established
tolerance
for
strawberries
is
adequate
to
support
the
use
of
P/
T
and
G
formulations
of
metaldehyde
on
strawberry.
These
data
will
support
a
tolerance
of
0.10
ppm
for
residues
in/
on
strawberry.
The
RTU/
L
formulation
of
metaldehyde
is
not
currently
registered
for
use
on
strawberry.
However,
if
the
registrant
intends
to
support
the
use
of
RTU/
L
formulations
on
strawberry,
then
additional
field
trials
will
be
required
as
residues
resulting
from
use
the
RTU/
L
were
substantially
higher
than
from
either
the
P/
T
or
G
formulations.

Tolerances
Needed
Under
40
CFR
§
180.523(
a):

As
detectable
residues
($
0.05
ppm)
of
metaldehyde
were
found
in/
on
a
wide
variety
of
crops
in
the
limited
field
trials
conducted
at
the
reported
1x
rates,
tolerances
for
metaldehyde
will
be
required
on
all
crops
and/
or
crop
groups
with
registered
uses
of
metaldehyde.
The
available
field
trial
data
on
broccoli,
cabbage,
mustard
greens,
lemon,
orange,
grapefruit,
blueberry,
raspberry,
artichoke,
prickly
pear
cactus,
and
watercress
are
adequate.
These
data
will
support
permanent
tolerances
on
Brassica
leafy
vegetables
(
group
5)
at
2.5
ppm,
citrus
fruits
(
group
10)
at
0.26
ppm,
berries
(
group
13)
at
0.15
ppm,
globe
artichoke
at
0.06
ppm,
and
watercress
at
3.2
ppm.

The
adequate
residue
data
on
tomatoes
will
support
either
a
separate
permanent
tolerance
on
tomatoes
at
0.24
ppm
or
a
temporary
tolerance
on
the
crop
group.
If
at
a
later
date,
the
registant
wants
to
support
a
permanent
tolerance
on
fruiting
vegetables
(
group
8),
additional
field
trials
will
be
required
on
bell
and
non­
bell
peppers.

The
available
residue
data
on
lettuce
supports
a
permanent
tolerance
of
1.73
ppm
on
lettuce.
If
the
registrant
wants
to
support
a
crop
group
tolerance
on
leafy
vegetable,
except
Brassica
group
4,
then
additional
field
trials
will
be
required
on
leafy
lettuce,
spinach,
and
celery.
Page
80
of
80
Table
B1.
Tolerance
Reassessment
Summary
for
Metaldehyde.

Commodity
Current
Tolerance
(
ppm)
Range
of
Residues
(
ppm)
1
Tolerance
Reassessment
(
ppm)
Comment/[
Correct
Commodity
Definition]

Tolerances
Listed
Under
40
CFR
§
180.523(
a):

Strawberry
0
<
0.05­
2.42
6.25
The
available
residue
data
for
the
G
and
P/
T
formulations
are
adequate.

Tolerances
Needed
under
40
CFR
180.523(
a):

Artichoke,
globe
None
<
0.05
0.0625
The
available
residue
data
are
adequate.

Berry,
group
13
None
<
0.05­
0.06
0.15
The
available
residue
data
on
blueberry
and
raspberry
are
adequate.

Fruit,
citrus,
group
10
None
<
0.05­
0.103
0.26
The
available
residue
data
are
adequate.

Prickly
pear
cactus
None
<
0.05
0.0625
The
available
residue
data
are
adequate.

Vegetable,
brassica,
leafy,
group
5
None
<
0.05­
1.00
2.5
The
available
residue
data
on
broccoli,
cabbage
and
mustard
greens
are
adequate.

Lettuce
None
<
0.05­
0.691
1.73
The
available
residue
data
on
leafy
and
head
lettuce
are
adequate.

Vegetable,
fruiting,
group
8
Tomato
None
<
0.05­
0.096
0.24
The
available
residue
data
are
adequate.

Watercress
None
0.215­
1.28
3.2
The
available
residue
data
are
adequate.