Document ID: EPA-HQ-OPP-2005-0507-0004
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-02-01T05:00Z

UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
WASHINGTON,
D.
C.
20460
OFFICE
OF
PREVENTION,
PESTICIDES
AND
TOXIC
SUBSTANCES
January
26,
2006
MEMORANDUM
SUBJECT:
Revised
Inorganic
Chlorates.
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED).
Case
#:
4049
DP
Barcode:
D303550
PC
Codes:
Sodium
chlorate:
073301
(
active)
and
873301
(
inert)
Calcium
chlorate:
073302
(
active)
and
875606
(
inert)
Potassium
chlorate:
073303
(
active)
and
900583
(
inert)
Magnesium
chlorate:
530200
(
active)
Regulatory
Action:
Phase
1
Reregistration
Action
Risk
Assessment
Type:
Multiple
Chemicals/
Aggregate
FROM:
Susan
V.
Hummel,
Branch
Senior
Scientist
Reregistration
Branch
4
Health
Effects
Division
(
7509C)

THROUGH:
Raymond
Kent,
Branch
Chief
Reregistration
Branch
4
Health
Effects
Division
(
7509C)

TO:
Jacqueline
Guerry,
Chemical
Review
Manager
Reregistration
Branch
3
Special
Review
and
Reregistration
Division
(
7508C)

This
document
provides
a
summary
of
the
findings
from
the
data
evaluation
and
the
subsequent
assessment
of
human
health
risk
resulting
from
the
uses
of
Inorganic
Chlorates.
The
hazard
characterization
was
completed
by
Abdallah
Khasawinah
(
HED/
RRB4);
the
occupational
and
residential
exposure
assessment
was
completed
by
Matthew
Crowley
(
HED/
RRB4);
the
residue
chemistry
data
evaluation
and
dietary
(
food)
exposure
estimates
for
the
dietary
risk
assessment
were
completed
by
Bonnie
Cropp­
Kohlligian
(
HED/
RRB4);
the
dietary
risk
assessment
analysis
was
completed
by
Thurston
Morton
(
HED/
RRB4);
the
incident
report
was
completed
by
Jerome
Blondell
(
HED/
CEB);
the
environmental
fate
characterization
for
chlorate
residues
resulting
from
terrestrial
food/
feed
uses
was
completed
by
Silvia
Termes
(
EFED);
the
risk
assessment
was
compiled
by
Susan
Hummel
(
HED/
RRB4).
The
drinking
water
exposure
characterization
and
exposure
estimate
calculations
for
chlorate
residues
as
a
byproduct
of
the
disinfection
of
drinking
water
for
the
dietary
(
water)
risk
assessment
analysis
were
provided
by
Patricia
Fair
of
the
Office
of
Ground
Water
and
Drinking
Water
Technical
Support
Center.
ii
Table
of
Contents
1.0
Executive
Summary
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1
2.0
Ingredient
Profile
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13
2.1
Summary
of
Registered/
Proposed
Uses
of
the
Active
Ingredient
Sodium
Chlorate
(
073301)
Under
Discussion
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13
2.2
Summary
of
Registered
Conventional
Uses
of
the
Inert
Ingredients
Sodium
Chlorate
(
873301)
and
Potassium
Chlorate
(
900583)
Under
Discussion
.
.
.
.
.
.
15
2.3
Summary
of
Uses
of
the
Inert
Ingredients
Sodium
Chlorate
(
873301)
and
Calcium
Chlorate
(
875606)
in
Antimicrobial
Agents
Under
Discussion
Due
to
Dietary
Concerns
Only
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15
2.4
Chemical
Formula
and
Nomenclature
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16
2.5
Physical
and
Chemical
Properties
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17
3.0
Metabolism
Assessment
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17
3.1
Comparative
Metabolic
Profile
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17
3.2
Nature
of
the
Residue
in
Foods
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17
3.2.1
Description
of
Primary
Crop
Metabolism
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17
3.2.2
Description
of
Livestock
Metabolism
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18
3.2.3
Description
of
Rotational
Crop
Metabolism
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18
3.3
Environmental
Degradation
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18
4.0
Hazard
Characterization/
Assessment
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19
4.1
Hazard
Characterization
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19
4.1.1
Database
Summary
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19
4.1.1.1
Studies
available
and
considered
(
animal,
human,
general
literature)
.
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19
4.1.1.2
Mode
of
action,
metabolism
and
toxicokinetic
data
.
.
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19
4.1.1.3
Sufficiency
of
studies/
data
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19
4.1.2
Toxicological
Effects
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19
4.1.3
Dose­
response
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21
4.2
FQPA
Hazard
Considerations
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30
4.2.1
Adequacy
of
the
Toxicity
Data
Base
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30
4.2.2
Evidence
of
Neurotoxicity
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30
4.2.3
Developmental
Toxicity
Studies
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30
4.2.4
Reproductive
Toxicity
Study
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31
4.2.5
Additional
Information
from
Literature
Sources
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34
4.2.6
Pre­
and/
or
Postnatal
Toxicity
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34
4.2.6.1
Determination
of
Susceptibility
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34
4.2.6.2
Degree
of
Concern
Analysis
and
Residual
Uncertainties
for
Pre
and/
or
Post­
natal
Susceptibility
.
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34
iii
4.3
Safety
Factor
for
Infants
and
Children
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34
4.4
Hazard
Identification
and
Toxicity
Endpoint
Selection
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35
4.4.1
Acute
Reference
Dose
(
aRfD)
­
Females
age
13­
49
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35
4.4.2
Acute
Reference
Dose
(
aRfD)
­
General
Population
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35
4.4.3
Chronic
Reference
Dose
(
cRfD)
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36
4.4.4
Incidental
Oral
Exposure
(
Short
and
Intermediate
Term)
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37
4.4.5
Dermal
Absorption
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38
4.4.6
Dermal
Exposure
(
Short,
Intermediate
and
Long
Term)
.
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38
4.4.7
Inhalation
Exposure
(
Short
and
Intermediate
Term)
.
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38
4.4.8
Margins
of
Exposure
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38
4.4.9
Recommendation
for
Aggregate
Exposure
Risk
Assessments
.
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38
4.4.10
Classification
of
Carcinogenic
Potential
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38
4.5
Endocrine
disruption
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41
5.0
Public
Health
Data
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42
5.1
Incident
Reports
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42
5.2
Other
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42
6.0
Exposure
Characterization/
Assessment
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44
6.1
Dietary
Exposure/
Risk
Pathway
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44
6.1.1
Residue
Profile
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44
6.1.2
Chronic
(
non­
cancer)
Dietary
(
food
only)
Exposure
and
Risk
.
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50
6.1.3
Cancer
Dietary
(
food
only)
Exposure
and
Risk
.
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50
6.2
Water
Exposure/
Risk
Pathway
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52
6.2.1
Environmental
Fate
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50
6.2.2
Drinking
Water
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50
6.2.2.1
Sources
and
Control
of
Chlorate
Ion
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50
6.2.2.2
Chlorate
Ion
Occurrence
Data
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.
.
.
.
.
.
.
.
.
.
.
50
6.2.2.3
Chronic
Exposure
to
Chlorate
Ion
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
50
6.2.2.4
Estimated
Concentrations
for
Chlorate
Ion
Deemed
Appropriate
for
Inclusion
in
the
Dietary
Risk
Assessment(
s)
50
6.3
Residential
(
Non­
Occupational)
Exposure/
Risk
Pathway
­
Conventional
Pesticides
57
6.3.1
Home
Uses
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
57
6.3.1.1
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
pesticide
products
­
Short­
Term
Residential
Handler
Exposure
via
Inhalation
Route
only
.
.
.
.
.
.
.
.
.
57
6.3.1.2
Sodium
Chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­
Term
Residential
Postapplication
Exposure
via
Incidental
Oral
Route
only
60
6.3.2
Recreational
Uses
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
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.
.
.
.
.
.
.
.
.
61
6.3.3
Other
(
Spray
Drift,
etc.)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
61
7.0
Aggregate
Risk
Assessments
and
Risk
Characterization
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
62
iv
7.1
Short­
Term
Aggregate
Risk
­
Residential
Handler
via
Inhalation
plus
background
(
chronic
dietary
(
food
+
water))
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
62
7.2
Chronic
(
non­
cancer)
Dietary
Risk
­
Food
+
Water
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
62
7.3
Cancer
Dietary
Risk
­
Food
+
Water
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
62
8.0
Cumulative
Risk
Characterization/
Assessment
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
63
9.0
Occupational
Exposure/
Risk
Pathway
­
Conventional
Pesticide
Products
Only
.
.
63
9.1
Short/
Intermediate/
Long­
Term
Handler
Risk
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
63
9.1.1
Sodium
chlorate
(
073301)
as
the
active
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
63
9.1.2
Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
69
9.1.3
Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
71
9.2
Short/
Intermediate/
Long­
Term
Postapplication
Risk
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
72
10.0
Data
Needs
and
Label
Requirements
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
72
10.1
Toxicology
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
.
.
.
.
.
.
72
10.2
Residue
Chemistry
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
72
10.3
Occupational
and
Residential
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
72
References:
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
72
Appendix
A
Toxicology
Data
Requirements
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
74
Appendix
B
Toxicology
Studies
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
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.
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.
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.
.
.
.
.
.
.
.
.
.
75
Appendix
C
Residue
Chemistry
Considerations
for
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
95
Appendix
D
Tolerance
Reassessment
Summary
For
Inorganic
Chlorates
as
active
or
inert
ingredients
in
conventional
(
agricultural)
pesticides
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
118
Appendix
E
Chlorate
(
ClO3
b
)
Dietary
Exposure
Estimates
in
Food
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
121
Page
1
of
141
1.0
Executive
Summary
A
Human
Health
Risk
Assessment
is
being
conducted
for
Inorganic
Chlorates
(
List
D
Reregistration
Case
#
4049).
Of
the
inorganic
chlorates
listed
as
active
ingredients
in
Office
of
Pesticide
Programs
Information
Network
(
i.
e.,
sodium
chlorate
(
073301),
calcium
chlorate
(
073302),
potassium
chlorate
(
073303),
and
magnesium
chlorate
(
530200)),
only
sodium
chlorate
(
073301)
is
present
as
an
active
ingredient
in
currently
registered
products.
Sodium
chlorate
(
873301),
calcium
chlorate
(
875606),
and
potassium
chlorate
(
900583)
are
present
as
inert
ingredients
in
currently
registered
products
and
will
also
be
addressed
in
this
risk
assessment.

Chlorates
are
strong
oxidizers
used
in
the
manufacture
of
dyes,
explosives,
matches,
printing
fabric,
paper
pulp
processing,
agricultural
desiccant/
defoliant,
weed
killers,
and
as
a
weak
antiseptic,
2­
3%
solutions
have
been
used
in
mouth
washes
(
OEHHA,
2002).
The
primary
pesticidal
use
for
sodium
chlorate
(
073301)
is
as
an
agricultural
defoliant/
desiccant,
primarily
on
cotton,
however
it
is
also
applied
to
a
wide
variety
of
other
agricultural
crops.
Sodium
chlorate
is
also
used
as
a
precursor
for
chlorine
dioxide
generation,
through
a
closed
system,
to
bleach
wood
pulp/
paper.
Only
a
small
percentage
(
less
than
2
percent)
is
used
in
water
systems
as
a
precursor
to
chlorine
dioxide
generation
or
as
a
defoliant/
desiccant
on
a
number
of
crops
to
aid
harvest.
As
inert
ingredients,
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
are
present
in
conventional
(
agricultural)
pesticides
used
on
food
crops
or
in
poultry
premises.
Also,
as
inert
ingredients,
sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
are
present
in
antimicrobial
agents
used:
(
1)
as
fruit,
vegetable,
and
egg
sanitizing
washes;
(
2)
to
control
bacterial
blotch
on
mushrooms;
(
3)
as
treatment
to
seed
used
for
sprouting;
(
4)
for
conditioning
live
oysters;
(
5)
in
poultry
drinking
water;
(
6)
in
fish
filleting;
(
7)
pecan
cracking/
dyeing.

Understanding
that
sodium
chlorate
and
sodium
chlorite
have
common
uses
such
as
use
in
water
systems
as
precursors
in
chlorine
dioxide
generation
and
the
potential
for
interconversion
of
chlorate
and
chlorite
anions
in
water,
the
environment
and
animals,
Chemical
Review
Managers
(
CRMs)
in
the
Special
Review
and
Reregistration
Division
(
SRRD)
responsible
for
completing
the
Inorganic
Chlorates
Reregistration
Eligibility
Decision
(
List
D
Reregistration
Case#
4049)
and
those
in
the
Antimicrobial
Division
(
AD)
responsible
for
completing
the
Chlorine
Dioxide
and
Sodium
Chlorite
Reregistration
Eligibility
Decision
(
List
D
Reregistration
Case#
4023)
developed
a
plan
to
coordinate
the
two
reregistration
cases.
Through
a
series
of
negotiations,
it
was
agreed
that
with
regards
to
the
Inorganic
Chlorates
Risk
Assessments
that:
(
1)
the
Inorganic
Chlorates
Risk
Assessments
will
consider
residues
of
chlorate
only;
(
2)
the
scope
of
the
Health
Effects
Division
(
HED)
Occupational
and
Residential
Risk
Assessments
will
be
limited
to
considerations
of
the
conventional
(
agricultural)
uses
of
inorganic
chlorates
only;
and
(
3)
AD
will
address
the
Occupational
and
Residential
Assessment
for
the
antimicrobial
uses
of
the
inorganic
chlorates
using
toxicological
endpoints
selected
by
HED.

We
note
that
AD
has
completed
an
Occupational
and
Residential
Risk
Assessment
for
the
antimicrobial
uses
of
the
inorganic
chlorates
under
separate
cover
(
D312200,
T.
Leighton,
01/
24/
2005)
using
the
appropriate
toxicological
endpoints
selected
by
HED.
There
are
no
Page
2
of
141
residential
exposures
associated
with
these
uses.
HED
will
not
discuss
this
topic
further
herein
except
to
note
that
no
risks
above
the
Agency's
level
of
concern
were
identified.

We
note
that
tolerances
and/
or
exemptions
from
the
requirement
of
a
tolerance
for
inorganic
chlorates
as
active
or
inert
ingredients
in
antimicrobial
agents
is
not
the
purview
of
HED
and
should
be
addressed
by
AD.
HED
will
not
discuss
this
topic
further.

We
note
that
since
Inorganic
Chlorates
is
a
List
D
reregistration
case,
the
Product
Chemistry
Chapter
for
the
Inorganic
Chlorates
Reregistration
Eligibility
Decision
(
RED)
is
the
responsibility
of
the
Antimicrobials
Division.
HED
will
not
discuss
this
topic
in
detail.

Hazard
Profile
The
database
for
the
inorganic
chlorates
is
substantially
complete
in
terms
of
endpoint
studies
and
dose
response
information
to
characterize
any
potential
for
prenatal
or
postnatal
risk
for
infants
and
children.
No
additional
FQPA
or
database
factor
is
required.
A
28­
Day
Inhalation
study
is
required
to
fulfill
Guideline
870.3465.

Sodium
chlorate
is
a
thyroid
toxicant
producing
thyroid
gland
follicular
cell
hypertrophy
in
rats
and
mice
following
chronic
exposures
and
some
evidence
of
follicular
cell
tumors
in
rats.
The
primary
target
of
chlorate
acute
toxicity
is
rupture
of
red
blood
cell
membranes
with
intravascular
hemolysis
and
the
irreversible
oxidation
of
hemoglobin
to
methemoglobin.
Potassium
chlorate
has
produced
renal
tubular
necrosis
in
animals.
Metabolism
studies
in
rats
and
dogs
have
shown
that
chlorates
are
readily
absorbed
by
the
gastrointestinal
tract
and
are
excreted
in
the
urine
primarily
as
chlorate
(
ClO
3
b
;
ca.
13%
of
the
administered
dose),
chlorite
(
ClO
2
b
;
ca.
4%
of
the
administered
dose),
and
chloride
(
Cl
b
;
ca.
20%
of
the
administered
dose).
Using
36Cl­
potassium
chlorate,
peak
blood
concentration
levels
were
reached
after
an
hour
of
ingestion
by
rats.
Elimination
of
the
labeled
chlorate
from
the
blood
was
biphasic
with
half­
lives
of
6
and
36.5
hours.

In
acute
toxicity
tests,
sodium
chlorate
is
slightly
toxic
by
the
oral
(
Toxicity
Category
IV),
dermal
(
Toxicity
Category
IV),
and
inhalation
routes
(
Toxicity
Category
IV
of
a
33%
aerosol).
Sodium
chlorate
crystals
were
mildly
irritating
to
the
rabbit
eye
(
Toxicity
Category
III
for
the
dry
crystals
or
moistened
crystals),
and
minimal
to
mild
dermal
irritant
(
Toxicity
Category
III
for
the
moistened
material
and
Toxicity
Category
IV
for
the
dry
crystal).
Ingestion
of
toxic
doses
of
sodium
chlorate
by
humans
produce
gastritis,
hemolysis,
methemoglobinemia,
hemoglobinurea,
late
toxic
nephritis,
and
acute
renal
failure.
Doses
in
excess
of
100
mg/
kg
are
generally
fatal
to
humans.

There
are
conflicting
findings
regarding
the
subchronic/
chronic
toxicity
of
sodium
chlorate.
In
one
series
of
studies,
rats
exposed
to
relatively
low
concentrations
of
sodium
chlorate
(
equivalent
to1.5
or
15
mg/
kg/
day)
for
up
to
11
months
exhibited
decreased
blood
glutathione,
increased
fragility
of
erythrocytes,
inhibition
of
incorporation
of
tritiated
thymidine
into
nuclei
in
rat
testes,
Page
3
of
141
decreased
RBC
count
and
hematocrit
and
decreased
body
weight.
In
another
study,
exposure
of
male
F344
rats
to
1%
sodium
or
potassium
chlorate
in
drinking
water
(
654­
686
mg/
kg/
day)
for
25
weeks,
the
only
effect
reported
was
significant
body
weight
reduction.
Relative
kidney
weights
were
significantly
increased
in
potassium
chlorate
treated
rats.
Rats
orally
administered
10­
1000
mg/
kg/
day
sodium
chlorate
for
90
days
did
not
exhibit
histological
or
clinical
chemistry
treatmentrelated
effects,
but
had
lower
red
blood
cell
counts,
hematocrit
and
hemoglobin
levels,
particularly
in
the
females.
The
adrenal
weight
was
also
depressed
in
males
and
females
at
the
1000
mg/
kg/
day
level.
In
another
published
study
in
which
rats
were
administered
sodium
chlorate
in
the
drinking
water
at
concentrations
equivalent
to
512
and
800
mg/
kg/
day
for
males
and
females,
respectively
for
90
days,
final
body
weights
were
significantly
lower
in
both
sexes
with
some
relative
organ
weight
changes
including
the
adrenal
glands
and
reduction
in
RBC
counts
and
percent
hemoglobin,
and
prominent
pituitary
gland
vacuolization
and
thyroid
gland
colloid
depletion
in
both
sexes.
The
thyroid
effects
were
confirmed
in
a
recent
study
in
rats
where
subchronic
treatment
for
21
or
90
days
with
sodium
chlorate
in
the
drinking
water
at
concentrations
up
to
2,000
mg/
L
(
225
mg/
kg/
day)
induced
a
concentration
dependent
increase
in
the
incidence
and
severity
of
thyroid
follicular
cellular
hyperplasia.
Colloid
depletion
and
hypertrophy
were
the
most
sensitive
histopathological
indicators
of
sodium
chlorate
exposure,
with
male
rats
more
susceptible
than
females
rats.
Decreases
in
serum
hormone
levels
triiodothyronine
(
T
3
)
and
thyroxine
(
T
4
)
were
also
reported
following
exposure
to
sodium
chlorate.
Mice
were
less
susceptible
to
the
adverse
effect
from
exposure
to
high
levels
of
sodium
chlorate.
In
a
subchronic
exposure
study
in
primates
where
sodium
chlorate
was
administered
in
drinking
water
for
8
weeks
at
400
mg/
L
(
58.4
±
27.6
mg/
kg/
day)
to
6
male
and
7
female
adult
African
Green
Monkeys
(
Cercopithecus
aethiops)
there
was
no
effect
on
the
thyroid
function
and
the
total
thyroxine
levels.
In
dogs,
the
only
reported
treatment
related
effect
following
subchronic
administration
of
sodium
chlorate
up
to
360
mg/
kg/
day
was
emesis.

A
2­
year
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
(
DRAFT
NTP
Report
2004).
In
these
tests,
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
the
imbalance
of
thyroid
hormones
(
reduced
T
3
and
T
4
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
sodium
chlorate.
Current
EPA
HED
policy
states
that
"
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
be
classified
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis"
(
Assessment
of
Thyroid
Follicular
Cell
Tumors;
USEPA
March
1998
EPA/
630/
R­
97/
002).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.

Sodium
chlorate
was
negative
in
most
bacterial
gene
mutation
assays.
In
one
assay,
it
showed
positive
effect
in
the
TA1535
strain
in
the
presence
of
metabolic
activation.
It
also
caused
DNA
damage
in
repair
deficient
E.
coli
strains
at
concentrations
above
1000
ug/
mL
in
the
presence
of
metabolic
activation
but
was
negative
in
the
unscheduled
DNA
synthesis
assay.
In
cytogenetics
tests,
sodium
chlorate
was
negative
in
the
in
vitro
cell
gene
mutation
assay,
mammalian
Page
4
of
141
erythrocyte
micronucleus
assay,
bone
marrow
cytogenetics
assay
and
sperm
head
abnormality
assay.

Sodium
chlorate
did
not
cause
developmental
effects
in
rats
tested
at
doses
up
to
1000
mg/
kg/
day
or
in
rabbits
tested
at
doses
up
to
500
mg/
kg/
day.
In
a
two
generation
reproductive
toxicity
study
in
the
rat,
postnatal
toxicity
did
not
exceed
parental
toxicity.
Sodium
chlorate
has
not
been
evaluated
for
neurotoxic
effects,
but
acute
and
subchronic
toxicity
studies
did
not
indicate
a
neurotoxic
potential.

There
are
no
repeated
dermal
toxicity
or
dermal
absorption
data
available
for
sodium
chlorate.
Based
on
its
high
water
solubility
and
ionic
nature,
potential
sodium
chlorate
(
or
any
other
inorganic
chlorate)
absorption
by
the
intact
skin
is
considered
negligible.

No
increase
in
prenatal
susceptibility
of
rats
or
rabbits
was
seen
in
developmental
studies
with
chlorate.
No
pre­
or
post­
natal
susceptibility
was
observed
in
a
reproduction
study
in
the
rat.

Note:
Lubbers
et
al
(
1984a,
1984b)
conducted
a
series
of
studies
with
human
volunteers
which
was
evaluated;
however,
due
to
the
limitations
of
these
studies,
the
data
were
not
deemed
useful
for
dose­
response
evaluation
and
were
not
relied
upon
in
the
risk
assessment.

Exposure
and
Aggregate
Risk
Assessment
Residue
Chemistry
The
residue
chemistry
database
is
not
complete.
New
ruminant
and
poultry
feeding
studies
are
required
to
fulfill
Guideline
860.1480.
These
data
are
considered
important
to
the
risk
assessment
and
are
needed
to
refine
the
meat/
milk/
poultry/
egg
exposure
estimates
in
the
dietary
risk
assessment.
Also
reference
standards
must
be
submitted
to
the
Pesticide
Repository
to
fulfill
Guideline
860.1650.

No
plant
metabolism
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
plant
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
available
published
information
(
Loomis
et
al.,
J.
Am.
Soc.
Agron.;
25,
724
(
1933)),
sodium
chlorate
is
highly
soluble
in
water
and
is
expected
to
readily
absorb
and
translocate
throughout
plants.
However,
given
the
proposed
use
conditions,
the
means
of
translocation
in
treated
plants
may
be
substantially
disrupted.
Translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses
may
occur.
Terminal
residues
are
expected
to
be
primarily
surface
residues.

Since
sodium
chlorate
is
a
strong
oxidizing
agent,
depending
on
environmental
factors,
it
is
expected
to
be
easily
reduced
to
chloride
and
possibly
chlorite
in
plants.
Total
redox
conversion
Page
5
of
141
to
these
reduced
species
is
not
expected;
hence,
the
terminal
residues
of
sodium
chlorate
in/
on
plants
are
likely
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
By
agreement
within
OPP,
the
residue
of
concern
is
the
chlorate
anion.

No
ruminant,
swine,
or
poultry
metabolism
or
feeding
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
animal
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
published
rat
metabolism
data
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985),
terminal
residues
of
sodium
chlorate
in
animal
tissues
are
expected
to
be
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
as
chlorate,
chlorite,
and
chloride
in
urine
primarily
and
feces.
Within
72
hours,
about
40%
of
the
administered
dose
was
excreted
in
the
urine
as
chlorate
(
ca.
13%),
chlorite
(
ca.
4%),
and
chloride
(
ca.
20%)
and
about
2­
4%
was
excreted
in
the
feces
in
the
same
time
period.
Less
than
1%
of
the
administered
dose
was
found
in
any
of
the
tissues
analyzed
including
kidney,
liver,
and
skin.
By
agreement
within
OPP,
the
residue
of
concern
is
the
chlorate
anion.

Although
some
previous
residue
chemistry
reviews
for
specific
exemptions
from
the
requirement
of
a
tolerance
have
concluded
that
there
is
no
reasonable
expectation
of
transfer
of
residues
to
meat,
milk,
poultry
or
eggs
in
specific
cases,
re­
evaluation
of
the
available
crop
field
trial
data
taken
as
a
whole,
indicate
that
there
is
the
possibility
of
detectable
residues
of
sodium
chlorate
on
animal
feedstuffs
at
harvest.
Hence,
secondary
residues
of
concern
in
meat,
milk,
poultry,
and
eggs
are
possible
and;
therefore,
new
ruminant
and
poultry
feeding
data
are
hereby
required
to
support
the
reregistration
of
sodium
chlorate.
These
data
are
considered
confirmatory.

The
analytical
method
used
to
support
the
established
exemptions
from
the
requirement
of
a
tolerance
is
a
non­
specific
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection.
The
method
was
originally
developed
to
estimate
residual
chlorate
concentrations
in
soil
and
as
a
rapid
diagnostic
test
for
chlorate
toxicity
in
plants.
Briefly,
the
method
involves
acid
extraction,
clean­
up
by
shaking
with
activated
charcoal,
and
filtration.
A
solution
of
ortho­
toluidine
in
HCl
is
then
added
to
the
concentrated
extract
and
the
resulting
color
is
measured
at
448
nm
for
low
concentrations
and
at
490
nm
for
higher
concentrations
of
dye.
The
method
is
not
specific
for
chlorate
since
it
measures
any
oxidizing
agent
capable
of
oxidizing
chloride
ion
to
free
chlorine.
A
standard
curve
is
prepared
with
sodium
chlorate
for
comparison.
The
lowest
limit
of
quantitation
of
the
method
is
estimated
at
1
ppm
based
on
available
fortification
data
from
field
trials.
Chloride
does
not
interfere
with
the
method
but
residues
of
chlorite,
which
might
be
present,
may
also
be
detected
with
this
method.
This
method
is
hereby
deemed
adequate
for
enforcement
of
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
A
more
selective
HPLC
method
("
Determination
of
Residues
of
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
is
available
for
the
detection
of
sodium
chlorate
residues
in
or
on
raw
agricultural
commodities
(
RACs).

Only
crop
field
trial
data
have
been
submitted
to
support
the
reregistration
of
sodium
chlorate.
No
storage
stability
or
processing
data
are
available.
The
available
crop
field
trial
data
have
been
Page
6
of
141
re­
evaluated
herein.
No
additional
plant
magnitude
of
the
residue
or
storage
stability
data
are
required
to
support
the
reregistration
of
sodium
chlorate.

Exemptions
from
the
requirement
of
tolerances
are
appropriate
for
sodium
chlorate
when
used
as
defoliant
or
desiccant
on
beans
(
dry),
corn,
cotton,
cowpeas,
flax,
guar,
peppers
(
non­
bell),
potatoes,
rice,
safflower,
sorghum
(
grain),
soybeans,
sunflower,
and
wheat
since
no
enforcement
action
can
be
anticipated
given
the
extremely
low
levels
of
chlorate
expected
in
food
commodities
(
most
of
the
residues
are
on
the
surface),
limitations
of
the
enforcement
method,
and
possible
interconversion
between
chlorate
and
chlorite
in
the
environment
making
misuse
determinations
difficult.

Sodium
chlorate
exemptions
under
40
CFR
180.1020(
a)
from
the
requirement
of
a
tolerance
should
be
amended
as
follows
to
(
1)
specify
defoliant
and
desiccant
use
only,
(
2)
specify
use
on
crops
rather
than
raw
agricultural
commodities,
(
3)
and
include
wheat:

40
CFR
180.1020(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
when
used
as
a
defoliant
or
desiccant
in
accordance
with
good
agricultural
practice
on
the
following
crops:
Bean
(
dry),
Corn,
Cotton,
Cowpea,
Flax,
Guar,
Pepper
(
non­
bell),
Potato,
Rice,
Safflower,
Sorghum
(
grain),
Soybean,
Sunflower,
and
Wheat.

Exemptions
from
the
requirement
of
a
tolerance
are
needed
for
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
pesticides
under
40
CFR
180.920
and
40
CFR
180.930,
respectively.

Environmental
Fate
Sodium
chlorate
is
used
as
a
desiccant/
defoliant
because
it
is
a
strong
oxidizer.
As
a
strong
oxidizing
agent,
chlorate
(
ClO
3
b
,
oxidation
state
V)
gets
reduced
to
chlorine
species
in
lower
oxidation
states,
such
as
the
oxyanions
chlorite
(
ClO
2
b
,
oxidation
state
III)
and
hypochlorite
(
ClO
b
,
oxidation
state
I),
chlorine
dioxide
(
oxidation
state
IV),
and
chloride
(
oxidation
state
­
I).
Thus,
at
least
some
and
possibly
substantial
reduction
of
the
applied
chlorate
is
likely
to
occur
in
the
field
prior
to
any
runoff
to
surface
water.
Under
environmental
(
terrestrial
field)
redox
conditions
and
based
on
chemical
equilibria
alone,
the
thermodynamically
favored,
end
reduction
product
of
chlorate
in
soil
and
in
water
is
the
chloride
anion.
Any
intermediate
chlorine
dioxide
that
may
form
under
environmental
conditions
will
undergo
photochemical
reactions
when
exposed
to
sunlight.
The
chlorine
oxyanions
chlorite
and
hypochlorite
(
other
possible
more
reduced
intermediates
in
the
ultimate
reduction
of
chlorate
to
chloride)
are
strong
oxidizers
in
themselves
and
thus,
they
are
also
reduced
and/
or
undergo
disproportionation
reactions.
Although
reduction
reactions
of
chlorate,
chlorite,
and
hypochlorite
are
said
to
occur
"
very
fast",
how
fast
they
occur
is
not
known
(
i.
e.,
the
actual
rate
constants
in
the
environment
are
not
known).
Therefore,
at
any
given
time
the
distribution
of
reduced
species
(
type
and
concentration)
cannot
be
estimated.
However,
it
is
unlikely
that
a
single
reduced
species
would
be
present.

Dietary
­
Food
Only
Page
7
of
141
Dietary
exposure
(
food
only)
to
inorganic
chlorates
as
the
chlorate
ion
(
ClO
3
b
)
may
be
expected
from
the
following
dietary
exposure
routes:
(
1)
from
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
used
on
food
crops;
(
2)
from
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
pesticides
used
on
food
crops
or
in
poultry
premises;
(
3)
from
secondary
residues
in
meat/
milk/
poultry/
eggs
due
to
residues
on
animal
feedstuffs;
(
4)
from
sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
as
inert
ingredients
in
antimicrobial
agents
used
as
fruit,
vegetable,
and
egg
sanitizing
washes,
on
mushrooms
to
control
bacterial
blotch,
as
treatments
to
seed
used
for
sprouting,
for
conditioning
live
oysters,
in
poultry
drinking
water,
in
fish
filleting,
and
in
pecan
cracking/
dyeing;
(
5)
as
a
potential
redox
of
chlorine
dioxide
and
sodium
chlorite
in
conventional
and
antimicrobial
pesticides;
(
6)
from
degradation
of
hypochlorites
in
antimicrobial
agents
used
as
fruit
and
vegetable
washes;
and,
(
7)
from
translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses.

A
chronic
Population
Adjusted
Dose
(
cPAD)
of
0.03
mg
chlorate/
kg/
day
was
used
in
the
chronic
(
non­
cancer
and
cancer)
dietary
risk
assessment
based
on
a
chronic
rat
study
(
DRAFT
NTP
Report
2004)
with
sodium
chlorate
which
found
increased
thyroid
gland
follicular
cell
hypertrophy
and
follicular
cell
mineralization.
A
NOAEL
was
not
identified
in
this
study.
Therefore,
a
bench
mark
dose
(
BMD)
analysis
was
performed.
Using
the
BMDL
as
an
approximation
of
the
NOAEL
(
0.9
mg
chlorate/
kg/
day)
and
an
uncertainty
factor
of
30x
(
3x
for
interspecies
extrapolation
and
10x
for
intraspecies
extrapolation),
the
cPAD
was
calculated
at
0.03
mg
chlorate/
kg/
day.

In
the
same
chronic
study
(
DRAFT
NTP
Report
2004)
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
changes
of
thyroid
hormones
(
reduced
T
3
and
T
4
and
elevated
TSH)
as
a
result
of
exposure
to
high
doses
of
sodium
chlorate.
Current
EPA
HED
policy
states
that
"
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
be
classified
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis"
(
Assessment
of
Thyroid
Follicular
Cell
Tumors;
USEPA
March
1998
EPA/
630/
R­
97/
002).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.
Therefore,
a
cancer
dietary
risk
assessment
was
conducted
using
an
MOE
approach
and
the
BMDL
as
an
approximation
of
the
NOAEL
(
0.9
mg
chlorate/
kg/
day).
The
level
of
concern
for
the
Margin
of
Exposure
was
30.
(
The
cancer
risk
assessment
is
the
same
as
the
chronic
(
non­
cancer)
risk
assessment
for
the
U.
S.
General
Population.)

A
chronic
(
non­
cancer
and
cancer)
dietary
risk
assessment
for
food
only
were
conducted
using
the
Dietary
Exposure
Evaluation
Model­
FCID
 
software
with
the
Food
Commodity
Intake
Database
(
DEEM­
FCID
 
Version
2.03)
and
food
and
water
consumption
data
from
the
United
States
Department
of
Agriculture's
(
USDA's)
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII)
from
1994­
1996
and
1998.
No
food
monitoring
data
are
available
for
this
risk
assessment;
only
limited,
chemical­
specific
field
trial
data
are
available.
Exposure
estimates
in
Page
8
of
141
food
were
based
on
field
trial
data
or,
in
the
case
of
fruit/
vegetable/
other
washes,
was
derived
from
a
film
thickness
model.
No
chemical­
specific
livestock
metabolism
or
feeding
data
are
available;
exposure
estimates
in
meat,
milk,
poultry,
and
eggs
were
derived
from
rat
metabolism
data,
field
trial
data,
and
livestock
reference
information
concerning
feed
consumption,
tissue
weights,
and
milk
production.
In
some
cases,
due
to
raw
data
limitations,
food
exposure
estimates
are
calculated
as
sodium
chlorate.
Default
concentration
factors
(
no
chemical­
specific
processing
data
are
available),
percent
crop
treated
data,
and
the
effects
of
washing
after
foliar
treatments
were
also
incorporated
into
the
risk
assessments.

The
chronic
(
non­
cancer
and
cancer)
dietary
risk
assessment
for
food
only
is
below
the
Agency's
level
of
concern
for
the
General
U.
S.
Population
and
all
subgroups.
The
highest
exposed
population
subgroup,
Children
1­
2
years
of
age,
was
28%
of
the
chronic
Population
Adjusted
Dose
(
cPAD).

Dietary
­
Drinking
Water
Only
Levels
of
chlorate
ion
(
ClO
3
b
)
found
in
finished
drinking
water
are
more
likely
a
consequence
of
drinking
water
treatment
with
chlorine
dioxide
or
hypochlorite
than
from
possible
source
water
contamination
due
to
inorganic
chlorate
pesticide
uses
and/
or
discharge
from
pulp
mills
which
use
inorganic
chlorates
in
their
bleaching
process.
Chlorate
ion
(
ClO
3
b
)
is
a
disinfection
by­
product
(
DBP)
of
water
treatment
which
can
be
formed
during
the
on­
site
generation
of
chlorine
dioxide
(
ClO
2
),
the
decomposition
of
chlorine
dioxide
in
the
water
treatment
system,
the
decomposition
of
hypochlorite
feedstock
during
storage,
and
the
interaction
of
chlorite
ion
and
free
chlorine.
Chlorate
ion
(
ClO
3
b
)
may
also
be
present
in
drinking
water
resulting
from
the
use
of
sodium
chlorate
(
073301)
in
water
systems
as
a
precursor
to
chlorine
dioxide
generation
due
to
incomplete
reaction
of
sodium
chlorate
in
the
formation
of
chlorine
dioxide
resulting
in
unreacted
chlorate
ion
in
the
chlorine
dioxide
feed
stream.

Data
are
available
concerning
the
levels
of
chlorate
ion
(
ClO
3
b
)
found
in
finished
drinking
water
collected
from
water
treatment
facilities
which
use
chlorine
dioxide
or
hypochlorite
to
treat
drinking
water.
No
data
are
available
concerning
the
levels
of
chlorate
ion
(
ClO
3
b
)
in
finished
drinking
water
collected
from
the
small
number
of
water
treatment
facilities
which
use
sodium
chlorate
as
a
precursor
for
chlorine
dioxide
generation,
through
a
closed
system,
to
treat
drinking
water.

While
EPA
Office
of
Ground
Water
and
Drinking
Water
(
OGWDW)
has
not
established
a
Maximum
Contamination
Level
(
MCL)
for
chlorate,
data
concerning
the
occurrence
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
have
been
collected
under
the
Information
Collection
Rule
(
ICR).
Under
the
ICR,
large
water
treatment
systems
(
those
serving
more
than
100,000
customers)
that
use
chlorine
dioxide
or
hypochlorite
for
disinfection
were
required
to
monitor
levels
of
chlorate
over
an
18­
month
period.
Data
were
collected
from
66
water
treatment
systems
(
90
water
treatment
plants)
which
use
chlorine
dioxide
or
hypochlorite
for
disinfection.
Data
from
these
systems
are
presented
separately
and
combined
in
Table
6.2.2.2.1.
Concentrations
of
chlorate
ion
(
ClO
3
b
)
in
finished
water
from
these
treatment
facilities
ranged
from
<
0.020
mg/
L
to
2.2
mg/
L.
Page
9
of
141
The
average
concentrations
of
chlorate
ion
(
ClO
3
b
)
in
the
distribution
systems
from
these
treatment
facilities
ranged
from
<
0.020
mg/
L
to
0.69
mg/
L;
the
90th
Percentile
was
0.24
mg/
L
and
the
median
was
0.11
mg/
L.

The
American
Water
Works
Association
Research
Foundation
(
AwwaRF
(
1995))
sponsored
a
project
to
study
how
water
systems
could
minimize
ClO
3
b
formation
in
the
hypochlorite
solutions
they
use
for
disinfection.
As
part
of
the
data
gathering
effort,
they
obtained
information
from
185
water
treatment
systems
concerning
their
use
of
hypochlorite
solutions.
Samples
of
source
water,
hypochlorite
solution,
and
finished
drinking
water
from
111
of
the
water
systems
were
analyzed
for
ClO
3
b
.
Only
one
set
of
samples
was
collected
for
each
system.
Concentrations
of
chlorate
ion
(
ClO
3
b
)
in
finished
water
from
these
treatment
facilities
ranged
from
<
0.010
mg/
L
to
9.2
mg/
L
(
ca.
9
mg/
L);
the
90th
Percentile
was
1.160
mg/
L
(
ca.
1.2
mg/
L)
and
the
median
was
0.161
mg/
L
(
ca.
0.2
mg/
L).

Based
on
the
available
occurrence
data
(
essentially
at
the
tap)
from
the
ICR
AUX1
Database
(
USEPA,
2000d)
and
the
AwwaRF
(
1995)
study,
the
following
estimated
concentrations
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
are
deemed
appropriate
for
inclusion
in
the
dietary
risk
assessments
for
inorganic
chlorates:

°
The
highest
annual
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
is
estimated
at
0.69
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).
°
The
90th
percentile
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
is
estimated
at
0.24
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).
°
The
treated
system
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
is
estimated
at
0.11
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).

Use
of
the
ICR
AUX1
database
could
underestimate
concentrations
in
drinking
water
since
higher
levels
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
were
found
at
the
small
water
treatment
utilities
sampled
in
the
AwwaRF
(
1995)
project
than
at
the
large
water
treatment
plants
included
in
the
ICR
AUX1
Database
(
USEPA,
2000d).
However,
the
AwwaRF
(
1995)
study
is
a
less
robust
data
set
consisting
of
only
one
sample
per
utility
and,
therefore,
the
ICR
AUX1
Database
(
USEPA,
2000d)
was
considered
the
more
appropriate
source
for
estimating
averages
from
individual
water
treatment
plants.

Chronic
(
non­
cancer
and
cancer)
dietary
(
water
only)
risk
assessments
were
conducted
using
the
Dietary
Exposure
Evaluation
Model­
FCID
 
software
with
the
Food
Commodity
Intake
Database
(
DEEM­
FCID
 
Version
2.03)
and
food
and
water
consumption
data
from
the
United
States
Department
of
Agriculture's
(
USDA's)
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII)
from
1994­
1996
and
1998.
Available
ICR
monitoring
data
essentially
at
the
tap
were
used
to
estimate
chlorate
concentrations
in
drinking
water.
Exposures
were
single
point
estimates.
Page
10
of
141
The
chronic
(
non­
cancer)
dietary
(
water
only)
risk
assessment
for
chlorate
in
drinking
water,
using
the
highest
annual
average
concentration
estimated
at
0.69
mg/
L,
is
below
the
Agency's
level
of
concern
for
the
General
U.
S.
Population
and
all
subgroups
except
all
infants
<
1
year
of
age.
The
highest
exposed
population
subgroup,
all
infants
<
1
year
of
age,
was
159%
of
the
chronic
Population
Adjusted
Dose
(
cPAD).
Using
the
90th
percentile
annual
average
concentration
estimated
at
0.24
mg/
L,
the
chronic
(
non­
cancer)
dietary
(
water
only)
risk
for
all
infants
<
1
year
of
age
was
55%
of
the
cPAD
and
25%
of
the
cPAD
using
the
median
annual
average
concentration
estimated
at
0.11
mg/
L.

No
separate
cancer
dietary
risk
assessment
for
chlorate
in
drinking
water
was
conducted.
The
estimated
cancer
dietary
risk
for
the
General
U.
S.
Population
is
based
on
the
chronic
(
non­
cancer)
dietary
risk,
and
is
below
the
Agency's
level
of
concern
(
i.
e.,
%
cPAD
is
less
than
the
level
of
concern
of
100%).

Residential
Exposure
All
residential
(
non­
occupational)
risk
estimates
for
inorganic
chlorates,
as
active
or
inert
ingredients
in
conventional
pesticide
products
used
in
residential
environments,
are
below
the
Agency's
level
of
concern
(
i.
e.,
Margin
of
Exposures
are
greater
than
the
Level
of
Concern
of
100).
These
uses
are
considered
to
be
short­
term
only
due
to
the
episodic
uses
associated
with
homeowner
products.
Since
the
episodic
nature
of
residential
exposure
is
inconsistent
with
the
mechanism
of
chlorate
carcinogenicity,
a
residential
cancer
risk
assessment
was
not
conducted.

There
is
the
potential
for
exposure
to
sodium
chlorate
by
residential
handlers
in
outdoor
residential
settings
during
application
of
conventional
pesticide
products
containing
sodium
chlorate
(
073301)
as
the
active
ingredient.
Sodium
chlorate
(
073301)
can
be
used
as
a
nonselective
herbicide
in
outdoor
residential
environments
as
a
spot
treatment/
edging
treatment
to
driveway
cracks
and
crevices,
around
foundations,
and
underneath
and
around
wood
decks
as
required.
Although
there
is
the
potential
for
dermal
exposure,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.

There
is
the
potential
for
postapplication
exposure
in
outdoor
residential
settings
from
entering
areas
previously
treated
by
professional
handlers
with
conventional
pesticide
products
containing
sodium
chlorate
(
873301)
as
an
inert
ingredient.
Although
there
is
the
potential
for
dermal
exposure,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.
Also,
postapplication
inhalation
exposure
for
sodium
chlorate
is
not
expected
due
to
negligible
vapor
pressure.

Aggregate
Risk
Evaluation
of
the
hazard
and
exposure
(
food,
water,
and
residential)
components
for
inorganic
chlorates
indicates
the
need
to
estimate
potential
risks
for
the
following
scenarios:
short­
term
inhalation,
chronic
(
non­
cancer)
dietary
(
food
+
water),
and
cancer
dietary
(
food
+
water).
Page
11
of
141
The
short­
term
aggregate
risks,
from
residential
(
non­
occupational)
exposures
(
including
background,
chronic
dietary
(
food
+
water))
are
below
the
Agency's
level
of
concern
for
the
Margins
of
Exposure
(
i.
e.,
Margin
of
Exposures
are
greater
that
the
Level
of
Concern
of
100).

The
chronic
(
non­
cancer)
dietary
(
food
+
water)
risk
assessment,
using
the
highest
annual
average
concentration
estimated
at
0.69
mg/
L
for
drinking
water,
is
below
the
Agency's
level
of
concern
for
the
General
U.
S.
Population
and
all
subgroups
except
all
infants
<
1
year
of
age
and
Children
1­
2
years.
The
highest
exposed
population
subgroup,
all
infants
<
1
year
of
age,
was
174%
of
the
chronic
Population
Adjusted
Dose
(
cPAD).
Using
the
90th
percentile
annual
average
concentration
estimated
at
0.24
mg/
L,
the
chronic
(
non­
cancer)
dietary
(
food
+
water)
risk
for
all
infants
<
1
year
of
age
was
70%
of
the
cPAD.
As
previously
indicated,
there
is
some
concern
that
the
exposure
estimates
for
water
may
be
underestimates.

The
cancer
dietary
(
food
+
water)
risk
assessment
is
below
the
Agency's
level
of
concern
and
is
based
on
the
chronic
(
non­
cancer)
dietary
(
food
+
water)
risk
assessment
for
the
general
population.

Occupational
Exposure
and
Risk
Assessment
for
Inorganic
Chlorates
in
Conventional
Pesticides
With
the
addition
of
PPE
(
dust/
mist
respirator)
or
engineering
controls
(
enclosed
cockpits
or
cabs),
all
occupational
handler
scenarios
for
the
use
of
inorganic
chlorates
as
an
active
or
inert
ingredient
in
conventional
pesticides
are
below
the
Agency's
level
of
concern
(
i.
e.,
Margin
of
Exposures
are
greater
than
the
Level
of
Concern
of
100).
Exposure
durations
are
short­
and
intermediate­
term
only.
Since
the
exposure
durations
for
occupational
handlers
are
inconsistent
with
the
mechanism
of
chlorate
carcinogenicity,
an
occupational
cancer
risk
assessment
was
not
conducted.

There
is
potential
for
occupational
handler
exposure
to
inorganic
chlorates
from:
(
1)
the
application
of
sodium
chlorate
(
073301)
as
the
active
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
non­
agricultural)
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators);
(
2)
the
application
of
sodium
chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
non­
agricultural)
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators);
and
(
3)
the
application
of
potassium
chlorate
(
900583)
as
an
inert
ingredient
in
conventional
pesticide
products
used
in
poultry
premises.
Only
the
inhalation
route
of
exposure
needs
to
be
included
in
the
occupational
handler
risk
assessment.

There
are
no
dermal
toxicity
or
dermal
absorption
data
available
for
inorganic
chlorates.
Although
the
potential
for
dermal
exposures
exists
for
occupational
handler,
based
on
its
high
water
solubility
and
ionic
nature,
significant
absorption
of
inorganic
chlorates
through
intact
skin
is
not
expected.
Page
12
of
141
Postapplication
scenarios
do
not
need
to
be
included
in
the
occupational
risk
assessment
for
inorganic
chlorates.
Although
dermal
and
inhalation
exposures
are
possible,
these
exposures
are
expected
to
be
negligible
due
to
the
physical
and
chemical
characteristics
of
inorganic
chlorates.
Significant
absorption
of
inorganic
chlorates
through
intact
skin
is
not
expected.
Postapplication
inhalation
exposure
is
not
expected
based
on
the
negligible
vapor
pressure
of
sodium
chlorate.
Page
13
of
141
2.0
Ingredient
Profile
Sodium
chlorate
is
a
non­
selective
herbicide,
considered
phytotoxic
to
all
green
plant
parts.
Sodium
chlorate
is
absorbed
rapidly
by
the
plant
through
both
roots
and
leaves
causing
cell
death.
Its
oxidizing
action
may
disrupt
normal
respiratory
functioning
leading
to
a
buildup
to
toxic
peroxides
and
greater
production
of
ethylene
which
causes
leaf
abscission.
It
is
30­
50
times
more
toxic
to
plants
than
sodium
chloride.
It
has
a
soil­
sterilant
effect.

Sodium
chlorate
has
a
salty
taste
and
is
palatable
to
livestock.
Animals
may
feed
on
enough
freshly
treated
areas
to
become
poisoned.

With
respect
to
pesticidal
uses,
most
sodium
chlorate
is
used
as
an
on­
site
precursor
to
chlorine
dioxide
generation
for
wood
pulp
bleaching;
other
uses
include
herbicides
and
water
treatment.
It
is
used
as
a
defoliant
and
desiccant
on
a
number
of
crops
and
as
spot
treatments
on
non­
crop
areas
to
control
weeds.
Agricultural
products
are
all
formulated
as
soluble
concentrates/
liquids;
non­
crop
products
are
formulated
as
soluble
concentrates/
liquids
and
granules
or
pellets/
tablets.

2.1
Summary
of
Registered/
Proposed
Conventional
Uses
of
the
Active
Ingredient
Sodium
Chlorate
(
073301)
Under
Discussion
Table
2.1.1.
Summary
of
Food/
Feed
Agricultural
Uses
of
Sodium
Chlorate
as
a
Defoliant/
Desiccant
Applic.
Timing,
Type,
and
Equip.
Formulation
Applic.
Rate
(
lb
ai/
A)
Max.
No.
Applic.
per
Season
Max.
Seasonal
Applic.
Rate
(
lb
ai/
A)
PHI
(
days)
PGI
(
days)

Dry
Beans,
Corn,
Flax,
Guar,
Rice,
Safflower,
Sorghum,
Southern
Peas
(
i.
e.,
Cowpeas),
Soybeans,
Sunflower
Preharvest
Spray
Aircraft/
Ground
SC
7.5
1
7.5
14
(
Corn)
7
(
All
others)
14
Cotton
Preharvest
Spray
Aircraft/
Ground
SC
7.5
2
15
7
14
Wheat
(
Proposed
Use
Rate)

Preharvest
Spray
Aircraft/
Ground
SC
6
1
6
3
??

Chili
peppers,
Potatoes
Preharvest
Spray
Aircraft/
Ground
SC
12.5
1
12.5
10
(
Chili
peppers)
7
(
Potatoes)
14
Page
14
of
141
Table
2.1.2.
Summary
of
Non
Food/
Feed
Agricultural
Uses
of
Sodium
Chlorate
as
a
Defoliant/
Desiccant
Applic.
Timing,
Type,
and
Equip.
Formulation
Applic.
Rate
(
lb
ai/
A)
Max.
No.
Applic.
per
Season
Max.
Seasonal
Applic.
Rate
(
lb
ai/
A)
PHI
(
days)
PGI
(
days)

Ornamental
gourds,
Cucurbits
(
grown
for
seed),
Fallow
land
Preharvest
Spray
Aircraft/
Ground
SC
6
1
6
Table
2.1.3.
Summary
of
Industrial
and
Other
Non­
Crop
Uses
of
Sodium
Chlorate
as
non­
selective
Herbicide
Use
Site
Formulations
Application
Equipment
Application
Rates
1
(
lbs
ai/
A
2)

Industrial/
Non­
Crop
Sites:
rightsof
way
areas,
building
perimeters,
ditch
banks,
bleachers,
airport
runways,
vacant
lots,
fire
hydrants,
or
as
a
pre­
paving
treatment.
Soluble
concentrate/
liquid
rights­
of­
way
sprayer,
handgun
sprayer,
groundboom,
lowpressure
handwand
1032
523
132
Granular
or
pellet/
tablet
belly
grinder,
push­
type
spreader,
tractor­
drawn
spreaders
523
240
161
1
Application
rates
are
presented
as
ranges
to
reflect
different
product
labels.
2
Although
area
treated
on
most
product
labels
is
expressed
as
lbs
ai/
ft2,
application
rates
have
been
calculated
by
the
reviewer
(
M.
Crowley
HED/
RRB4)
as
lbs
ai/
A
consistent
with
the
standard
expression
for
application
rates
used
for
calculation
and
comparison
purposes.

Table
2.1.4.
Summary
of
Residential
Uses
of
Sodium
Chlorate
as
non­
selective
Herbicide
Use
Site
Formulations
Application
Equipment
Application
Rates
Spot
treatment/
edging
treatment:
driveway
cracks
and
crevices,
around
foundations,
and
underneath
and
around
wood
decks.

Not
labeled
for
broadcast
on
residential
lawns
or
ornamentals.
Liquid
RTU
sprinkler
can
0.27
lb
ai/
gallon
Liquid
low­
pressure
handwand,
sprinkler
can
23.7
lb
ai/
1000
ft2
Liquid
trigger­
pump
sprayer
0.196
lb
ai/
gallon
Granular
belly
grinder,
push­
type
spreader,
hand
12
lb
ai/
1000
ft2
Page
15
of
141
2.2
Summary
of
Registered
Conventional
Uses
of
the
Inert
Ingredients
Sodium
Chlorate
(
873301)
and
Potassium
Chlorate
(
900583)
Under
Discussion
Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
herbicide
formulation
products
can
be
applied
professionally
to
agricultural
(
corn,
guava,
macadamia
nuts,
sorghum
grain,
sugarcane,
wheat),
commercial
(
non­
agricultural),
and
residential
sites.
These
conventional
pesticide
products
contain
<
1
%
sodium
chlorate
and
can
be
applied
at
rates
no
greater
than
0.07
lb
(
as
sodium
chlorate)
per
acre.

Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
airborne
fungicide
products
can
be
applied
in
poultry
premises.
These
conventional
pesticide
products
contain
<
20%
potassium
chlorate
and
can
be
applied
at
rates
not
greater
than
0.01
lb
(
as
potassium
chlorate)
per
500
ft3.

2.3
Summary
of
Uses
of
the
Inert
Ingredients
Sodium
Chlorate
(
873301)
and
Calcium
Chlorate
(
875606)
in
Antimicrobial
Agents
Under
Discussion
Due
to
Dietary
Concerns
Only
Sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
as
inert
ingredients
in
antimicrobial
products
are
used:
(
1)
as
fruit,
vegetable,
and
egg
sanitizing
washes;
(
2)
to
control
bacterial
blotch
on
mushrooms;
(
3)
as
treatment
to
seed
used
for
sprouting;
(
4)
for
conditioning
live
oysters;
(
5)
in
poultry
drinking
water;
(
6)
in
fish
filleting;
(
7)
pecan
cracking/
dyeing.
These
products
contain
<
2%
sodium
chlorate
or
calcium
chlorate
and
the
maximum
use
rate
is
500
ppm
total
available
chlorine
in
the
sanitizing
wash
water;
exposure
time
is
1­
2
minutes.
Page
16
of
141
2.4
Chemical
Formula
and
Nomenclature
Table
2.4.
Chemical
Formula
and
Nomenclature
Sodium
Chlorate
­
NaClO3
Common
name
Sodium
Chlorate
IUPAC
name
Sodium
Chlorate
CAS
name
Sodium
Chlorate
CAS#
7775­
09­
9
Current
Food/
Feed
Site
Registration
dry
beans,
corn,
cotton,
flax,
guar,
peppers
(
chili
type),
rice,
safflower,
sorghum
(
grain),
southern
peas
(
i.
e.,
cowpeas),
soybeans,
sunflowers,
wheat
(
Section
18
Registration)

Proposed
Food/
Feed
Site
Registration
wheat
Calcium
Chlorate
­
CaCl2O6
Common
name
Calcium
Chlorate
IUPAC
name
Calcium
Chlorate
CAS
name
Calcium
Chlorate
CAS#
10137­
74­
3
Current
Food/
Feed
Site
Registration
None
Potassium
Chlorate
­
KClO3
Common
name
Potassium
Chlorate
IUPAC
name
Potassium
Chlorate
CAS
name
Potassium
Chlorate
CAS#
3811­
04­
9
Current
Food/
Feed
Site
Registration
None
Magnesium
Chlorate
­
MgCl2O6
Common
name
Magnesium
Chlorate
IUPAC
name
Magnesium
Chlorate
CAS
name
Magnesium
Chlorate
CAS#
10326­
21­
3
Current
Food/
Feed
Site
Registration
None
Page
17
of
141
2.5
Physical
and
Chemical
Properties
Sodium
chlorate
is
a
white,
odorless,
crystalline
solid
that
looks
like
common
table
salt
(
sodium
chloride)
and
is
highly
water
soluble.
It
is
a
strong
oxidant,
not
combustible
buts
reacts
violently
with
combustible
and
reducing
materials.
Vapor
pressure
is
low
(
EXTOXNET
lists
vapor
pressure
as
Zero).

HED
is
not
responsible
for
the
Product
Chemistry
Chapter
for
the
Inorganic
Chlorates
Reregistration
Eligibility
Decision
(
RED);
hence
detailed
physical
and
chemical
properties
of
sodium
chlorate,
calcium
chlorate,
potassium
chlorate,
and
magnesium
chlorate
are
not
provided
herein.

3.0
Metabolism
Assessment
By
agreement
within
OPP,
the
residue
of
concern
for
inorganic
chlorates
is
the
chlorate
anion.
Discussions
concerning
residues
to
be
included
in
the
tolerance
expression
are
not
relevant
here
since
residues
of
concern
are
not
and
will
not
be
specified
in
the
exemptions
from
the
requirement
of
a
tolerance
for
sodium
chlorate
used
on
crops.

3.1
Comparative
Metabolic
Profile
Since
there
are
no
livestock
metabolism
data,
no
comparison
can
be
made.
Based
on
published
rat
metabolism
data
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985),
terminal
residues
of
sodium
chlorate
in
animal
tissues
are
expected
to
be
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
as
chlorate,
chlorite,
and
chloride
in
urine
and
feces.
Within
72
hours,
about
40%
of
the
administered
dose
was
excreted
in
the
urine
as
chlorate
(
ca.
13%),
chlorite
(
ca.
4%),
and
chloride
(
ca.
20%)
and
about
2­
4%
was
excreted
in
the
feces
in
the
same
time
period.
Less
than
1%
of
the
administered
dose
was
found
in
any
of
the
tissues
analyzed
including
kidney,
liver,
and
skin.

3.2
Nature
of
the
Residue
in
Foods
3.2.1
Description
of
Primary
Crop
Metabolism
No
plant
metabolism
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
plant
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
available
published
information
(
Loomis
et
al.,
J.
Am.
Soc.
Agron.;
25,
724
(
1933)),
sodium
chlorate
is
highly
soluble
in
water
and
is
expected
to
readily
absorb
and
translocate
throughout
plants.
However,
given
the
proposed
use
conditions,
the
means
of
translocation
in
treated
plants
may
be
substantially
disrupted.
Translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
may
occur
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants).
Terminal
residues
are
expected
to
be
primarily
surface
residues.
Page
18
of
141
Since
sodium
chlorate
is
a
strong
oxidizing
agent,
depending
on
environmental
factors,
it
is
expected
to
be
easily
reduced
to
chloride
and
possibly
chlorite
in
plants.
Total
redox
conversion
to
these
reduced
species
is
not
expected;
hence,
the
terminal
residues
of
sodium
chlorate
in/
on
plants
are
likely
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).

3.2.2
Description
of
Livestock
Metabolism
No
ruminant,
swine,
or
poultry
metabolism
or
feeding
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
animal
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Although
some
previous
residue
chemistry
reviews
for
specific
exemptions
from
the
requirement
of
a
tolerance
have
concluded
that
there
is
no
reasonable
expectation
of
transfer
of
residues
to
meat,
milk,
poultry
or
eggs
in
specific
cases,
re­
evaluation
of
the
available
crop
field
trial
data
taken
as
a
whole,
indicate
that
there
is
the
possibility
of
detectable
residues
of
sodium
chlorate
on
animal
feedstuffs
at
harvest.
Hence,
secondary
residues
of
concern
in
meat,
milk,
poultry,
and
eggs
are
possible
and;
therefore,
new
ruminant
and
poultry
feeding
data
are
required
to
support
the
reregistration
of
sodium
chlorate.
These
data
are
considered
confirmatory.

3.2.3
Description
of
Rotational
Crop
Metabolism
Considering
the
phytotoxic
nature
of
sodium
chlorate,
planting
crops
soon
after
treatment
of
primary
crops
would
not
seem
likely.
Rotational
crop
tolerances
or
plant
back
restrictions
are
not
necessary.
Translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses
may
occur.

3.3
Environmental
Degradation
Sodium
chlorate
is
used
as
a
desiccant/
defoliant
because
it
is
a
strong
oxidizer.
As
a
strong
oxidizing
agent,
chlorate
(
ClO
3
b
,
oxidation
state
V)
gets
reduced
to
chlorine
species
in
lower
oxidation
states,
such
as
the
oxyanions
chlorite
(
ClO
2
b
,
oxidation
state
III)
and
hypochlorite
(
ClO
b
,
oxidation
state
I),
chlorine
dioxide
(
oxidation
state
IV),
and
chloride
(
oxidation
state
­
I).
Thus,
at
least
some
and
possibly
substantial
reduction
of
the
applied
chlorate
is
likely
to
occur
in
the
field
prior
to
any
runoff
to
surface
water.
Under
environmental
(
terrestrial
field)
redox
conditions
and
based
on
chemical
equilibria
alone,
the
thermodynamically
favored,
end
reduction
product
of
chlorate
in
soil
and
in
water
is
the
chloride
anion.
Any
intermediate
chlorine
dioxide
that
may
form
under
environmental
conditions
will
undergo
photochemical
reactions
when
exposed
to
sunlight.
The
chlorine
oxyanions
chlorite
and
hypochlorite
(
other
possible
more
reduced
intermediates
in
the
ultimate
reduction
of
chlorate
to
chloride)
are
strong
oxidizers
in
themselves
and
thus,
they
are
also
reduced
and/
or
undergo
disproportionation
reactions.
Although
reduction
reactions
of
chlorate,
chlorite,
and
hypochlorite
are
said
to
occur
"
very
fast",
how
fast
they
occur
is
not
known
(
i.
e.,
the
actual
rate
constants
in
the
environment
are
not
known).
Page
19
of
141
Therefore,
at
any
given
time
the
distribution
of
reduced
species
(
type
and
concentration)
cannot
be
estimated.
However,
it
is
unlikely
that
a
single
reduced
species
would
be
present.

4.0
Hazard
Characterization/
Assessment
4.1
Hazard
and
Dose­
Response
Characterization
4.1.1
Database
Summary
4.1.1.1
Studies
available
and
considered
(
animal,
human,
general
literature)
Subchronic
­
Oral
90­
day
rat,
90­
day
mouse
and
90­
day
dog
Repro/
developmental
­
rat
and
rabbit
developmental;
2­
generation
reproductive
rat
Chronic/
cancer
­
Two­
year
drinking
water
studies
in
rats
and
mice
Other
­
mutagenicity
screens;
metabolism
in
the
rat;
many
published
studies
included
in
this
hazard
and
dose
response
characterization.

4.1.1.2
Mode
of
action,
metabolism
and
toxicokinetic
data
Sodium
chlorate
is
a
thyroid
toxicant
producing
thyroid
gland
follicular
cell
hypertrophy
in
rats
and
mice
following
chronic
exposures
and
some
evidence
of
follicular
cell
tumors
in
rats.
The
primary
target
of
chlorate
acute
toxicity
is
rupture
of
red
blood
cell
membranes
with
intravascular
hemolysis
and
the
irreversible
oxidation
of
hemoglobin
to
methemoglobin.
Potassium
chlorate
has
produced
renal
tubular
necrosis
in
animals.

Metabolism
studies
in
rats
and
dogs
have
shown
that
chlorates
are
readily
absorbed
by
the
gastrointestinal
tract
and
in
rats
are
excreted
in
the
urine
as
chlorate
(
ca.
13%
of
the
administered
dose),
chlorite
(
ca.
4%
of
the
dose)
and
chloride
(
ca.
20%
of
the
dose).
Using
36Cl­
potassium
chlorate,
peak
blood
concentration
levels
were
reached
after
an
hour
of
ingestion
by
rats.
Elimination
of
the
labeled
chlorate
from
the
blood
was
biphasic
with
half­
lives
of
6
and
36.5
hours.

4.1.1.3
Sufficiency
of
studies/
data
Data
are
sufficient
for
each
exposure
scenario
and
for
FQPA
evaluation.
Data
are
sufficient
for
endpoint
selection.

4.1.2
Toxicological
Effects
The
toxicology
profile
for
sodium
chlorate
is
presented
in
tables
4.1a
and
4.1b.
In
acute
toxicity
tests,
sodium
chlorate
is
slightly
toxic
by
the
oral
(
Toxicity
Category
IV),
dermal
(
Toxicity
Category
IV),
and
inhalation
routes
(
Toxicity
Category
IV
of
a
33%
aerosol).
Sodium
chlorate
crystals
were
mildly
irritating
to
the
rabbit
eye
(
Toxicity
Category
III
for
the
dry
crystals
or
moistened
crystals),
and
minimal
to
mild
dermal
irritant
(
Toxicity
Category
III
for
the
moistened
material
and
Toxicity
Category
IV
for
the
dry
crystal).
Ingestion
of
toxic
doses
of
sodium
chlorate
by
humans
produce
gastritis,
hemolysis,
methemoglobinemia,
hemoglobinurea,
late
toxic
Page
20
of
141
nephritis,
and
acute
renal
failure.
An
acute
or
cumulative
dose
of
7.5­
35
grams
is
lethal
in
adults.
Ingestion
of
1
g
amounts
of
potassium
chlorate
was
reported
to
be
fatal
in
infants.

There
are
conflicting
findings
regarding
the
subchronic/
chronic
toxicity
of
sodium
chlorate.
In
one
series
of
studies,
rats
exposed
to
relatively
low
concentrations
of
sodium
chlorate
(
equivalent
to1.5
and
15
mg/
kg/
day)
for
up
to
11
months
exhibited
decreased
blood
glutathione,
increased
fragility
of
erythrocytes,
inhibition
of
incorporation
of
tritiated
thymidine
into
nuclei
in
rat
testes,
decreased
RBC
count
and
hematocrit
and
decreased
body
weight.
In
another
study,
male
F344
rats
were
exposed
to
1%
sodium
or
potassium
chlorate
in
drinking
water
(
654­
686
mg/
kg/
day)
for
25
weeks
and
the
only
effect
reported
was
significant
body
weight
reduction.
Relative
kidney
weights
were
significantly
increased
in
potassium
chlorate
treated
rats.
Rats
orally
administered
10­
1000
mg/
kg/
day
sodium
chlorate
for
90
days
did
not
exhibit
histological
or
clinical
chemistry
treatment­
related
effects,
but
had
decreased
red
blood
cell
counts,
hematocrit
and
hemoglobin
levels,
particularly
in
the
females.
Adrenal
weights
were
also
depressed
in
males
and
females
at
the
1000
mg/
kg/
day
level.
In
another
published
study
in
which
rats
were
administered
sodium
chlorate
in
the
drinking
water
at
concentrations
equivalent
to
512
and
800
mg/
kg/
day
for
males
and
females,
respectively
for
90
days,
final
body
weights
were
significantly
lower
in
both
sexes
with
some
relative
organ
weight
changes
including
the
adrenal
glands
and
reduction
in
RBC
counts
and
percent
hemoglobin,
and
prominent
pituitary
gland
vacuolization
and
thyroid
gland
colloid
depletion
in
both
sexes.
The
thyroid
effects
were
confirmed
in
a
recent
study
in
rats
where
subchronic
treatment
for
21
or
90
days
with
sodium
chlorate
in
the
drinking
water
at
concentrations
up
to
2,000
mg/
L
(
225
mg/
kg/
day)
induced
a
concentration
dependent
increase
in
the
incidence
and
severity
of
thyroid
follicular
cellular
hyperplasia.
Colloid
depletion
and
hypertrophy
were
the
most
sensitive
histopathological
indicators
of
sodium
chlorate
exposure,
with
male
rats
more
susceptible
than
females
rats.
Decreases
in
serum
hormone
levels
of
triiodothyronine
(
T
3
)
and
thyroxine
(
T
4
)
were
also
reported
following
exposure
to
sodium
chlorate.
Mice
were
less
susceptible
to
the
adverse
effect
from
exposure
to
high
levels
of
sodium
chlorate.
In
dogs,
the
only
reported
treatment
related
effect
following
subchronic
administration
of
sodium
chlorate
up
to
360
mg/
kg/
day
was
emesis.

A
2­
year
study
to
determine
the
potential
of
sodium
chlorate
to
cause
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
(
NTP
2004).
A
final
report
of
this
study
is
expected
during
2005.
In
these
tests,
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
the
imbalance
of
thyroid
hormones
(
reduced
T
3
and
T
4
levels
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
sodium
chlorate.
Current
EPA
HED
policy
states
that
"
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
be
classified
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis"
(
Assessment
of
Thyroid
Follicular
Cell
Tumors;
USEPA
March
1998
EPA/
630/
R­
97/
002).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.
Page
21
of
141
Sodium
chlorate
was
negative
in
most
bacterial
gene
mutation
assays.
In
one
assay
(
Ames
test),
it
showed
positive
effect
in
the
TA1535
strain
in
the
presence
of
metabolic
activation.
It
also
caused
DNA
damage
in
repair
deficient
E.
coli
strains
at
concentrations
above
1000
ug/
mL
in
the
presence
of
metabolic
activation
but
was
negative
in
the
unscheduled
DNA
synthesis
assay.
In
cytogenetics
tests,
sodium
chlorate
was
negative
in
the
in
vitro
cell
gene
mutation
assay,
mammalian
erythrocyte
micronucleus
assay,
bone
marrow
cytogenetics
assay
and
sperm
head
abnormality
assay.

Sodium
chlorate
did
not
cause
developmental
effects
in
rats
tested
at
doses
up
to
1000
mg/
kg/
day
or
in
rabbits
tested
at
doses
up
to
500
mg/
kg/
day.
In
a
two
generation
reproductive
toxicity
study
in
the
rat,
postnatal
toxicity
did
not
exceed
parental
toxicity.
Sodium
chlorate
has
not
been
evaluated
for
neurotoxic
effects,
but
acute
and
subchronic
toxicity
studies
did
not
indicate
a
neurotoxic
potential.

There
are
no
repeated
dermal
toxicity
or
dermal
absorption
data
available
for
sodium
chlorate.
Based
on
its
high
water
solubility
and
ionic
nature,
potential
sodium
chlorate
(
or
any
other
inorganic
chlorate)
absorption
by
the
intact
skin
is
considered
negligible.

4.1.3
Dose­
response
Subchronic,
developmental
and
reproductive
studies
were
considered.
An
endpoint
of
concern
attributable
to
a
single
dose
was
not
identified,
and
therefore
an
acute
RfD
is
not
established.
The
oral
endpoints
for
other
durations
were
based
on
subchronic
and
chronic
studies
in
rats.
The
toxic
effects
seen
in
the
subchronic
study
were
on
the
pituitary
(
vacuolization)
and
thyroid
gland
(
colloid
depletion),
body
weight
decrease
and
organ
weight
changes
and
reduction
in
erythrocyte
counts
and
hemoglobin
content.
In
the
chronic
drinking
water
study
in
rats,
an
endpoint
of
toxicity
was
derived
on
the
basis
of
thyroid
follicular
cell
hypertrophy.
There
were
no
dermal
toxicity
studies
available.
Sodium
chlorate
is
an
inorganic
salt
and
its
dermal
absorption
is
unlikely.
Therefore,
a
toxicity
endpoint
for
dermal
exposure
is
not
selected.
There
were
no
inhalation
studies
available
suitable
for
assessment
of
inhalation
risks.
For
the
risk
assessment
of
inhalation
exposure
from
sodium
chlorate,
the
endpoint
of
oral
toxicity
for
short
and
intermediate
exposures
is
used
with
a
100%
absorption
factor.
Page
22
of
141
Table
4.1a.
Acute
Toxicity
Profile
­
Sodium
Chlorate
Guideline
No./
Study
Type
Study
Type
MRID
No.
Results
Toxicity
Category
870.1100
Acute
oral
­
Rats
41819901
$
5000
mg/
kg
(
rat)
IV
870.1200
Acute
dermal
­
Rabbits
41819902
42497601
LD50
=
>
2000
mg/
kg
(
dry
crystal)
LD50
=
>
2000
mg/
kg
(
moistened)
IV
IV
870.1300
Acute
inhalation
­
Rats
41819903
LC50
=
5.59
mg/
L
IV
870.2400
Acute
eye
irritation
­
Rabbit
00085090
00102998
41819904
mildly
irritating
mildly
irritating
III
III
870.2500
Acute
dermal
irritation
­
Rabbit
41819905
42497602
non­
irritating
(
dry
crystal)
minimally
irritating
(
moistened)
IV
III
870.2600
Skin
sensitization
­
guinea
pigs
41819906
not
a
dermal
sensitizer
NA
Page
23
of
141
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
870.3100
90­
Day
oral
toxicity
(
Sprague­
Dawley
Rats)
40444801(
1987)
Acceptable/
guideline
0,
10,
40,
100
or
1000
mg/
kg/
day,
oral
gavage
NOAEL
=
100
mg/
kg/
day
LOAEL
=
1000
mg/
kg/
day
based
on
hematological
effects
(
hemoglobin
concentration,
hematocrit,
RBC
counts
were
statistically
significantly
decreased,
and
reticulocyte
count
was
statistically
significantly
increased
in
females.
In
males,
only
the
hematocrit
was
statistically
significantly
decreased.
The
adrenal
weight
was
depressed
in
both
males
and
females.

Non­
Guideline
25­
week
tumor
promotion
toxicity
study
(
Male
F344
Rats)
Kurokawa
et
al,
1985
1%
NaClO3
or
KClO3
in
drinking
water(
654­
686
mg/
kg/
day)
for
25
weeks
following
2­
week
initiation
with
0.05%
Nethyl
Nhydroxyethylnitrosamine
LOAEL
=
654­
686
mg/
kg/
day
(
only
dose
tested).
Significant
decrease
in
mean
body
weights
compared
to
the
controls.
This
dose
was
the
maximum
tolerated
dose
based
on
a
6­
week
screening
study
at
0.25,
0.5,
1
and
2%
doses
in
drinking
water.
Relative
kidney
weights
of
the
chlorate
treated
rats
were
significantly
increased
over
the
control
group.
NaClO3
or
KClO3
showed
no
promoting
effect
in
rat
renal
carcinogenesis
Non­
Guideline
90­
Day
oral
toxicity
(
Sprague­
Dawley
Rats)
McCauley
et
al,
1995
SD
rats
(
10/
sex/
group)
NaClO3
in
the
drinking
water
3.0,
12.0,
or
48
mM
for
90
days
M:
30,
100
and
512
mg/
kg/
day
(
chlorate)
F:
42,
158,
and
800
mg/
kg/
day
(
chlorate)
NOAEL
=
30
and
42
mg
chlorate/
kg/
day
in
males
and
females.
LOAEL
=
100
mg
chlorate/
kg/
day
in
males
and
150
mg/
kg/
day
in
females,
based
on
the
pituitary
effects
(
vacuolization)
and
thyroid
gland
effects
(
colloid
depletion),
the
body
weight
decrease
and
organ
weight
changes
and
reduction
in
erythrocyte
counts
and
hemoglobin
content.

Non­
Guideline
90­
Day
oral
toxicity
(
F344
rats
and
B6C3F1
mice)
Hooth
et
al,
2001
NaClO3
in
drinking
water
at
0,
0.125,
0.25,
0.5,
1.0
or
2
g/
L
for
21
days
or
90
days
in
rats
(
14,
28,
56,
112,
225
mg/
kg/
day
in
males;
20,
40,
80,
160
or
320
mg/
kg/
day
in
females).
Additional
groups
of
male
rats
at
0,
0.001,
0.01,
0.1,
1.0,
2.0
and
females
at
0,
0.5,
1.0,
2.0,
4.0,
6.0
g/
L
for
90­
105
days.
Groups
of
mice
were
also
treated.
NOAEL
=
0.25
g/
L
(
28
mg/
kg/
day
for
males)
LOAEL
=
1.0
g/
L
based
on
colloid
depletion
and
follicular
cell
hyperplasia,
(
112
mg/
kg/
day
for
males).
Females
were
less
susceptible
to
the
chlorate
toxicity.
Total
serum
triiodothyronine
(
T3)
and
thyroxine
(
T4)
concentrations
were
decreased
significantly
and
TSH
levels
increased
significantly
in
male
and
female
rats
after
4
days
of
treatment
with
1.0
or
2.0
g/
L
and
after
21
days
of
treatment
with
2.0
g/
L.
TSH
levels
also
increased
significantly
in
male
rats
after
21
days
of
treatment
with
1.0
g/
L.
Serum
T3
and
T4
levels
were
comparable
to
controls
in
male
and
female
rats
after
90
days
of
treatment,
but
TSH
levels
were
increased
in
both
sexes.
Follicular
cell
hyperplasia
was
not
present
in
male
or
female
mice.
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
24
of
141
Non­
Guideline
11­
month
oral
toxicity
­
Rats
Abdel­
Rahman
et
al.
1984
chlorine
dioxide
(
0,
1,
10,
100,
1000
mg/
L)
and
its
conversion
products
chlorite
and
chlorate
(
10,
100
mg/
L)
in
drinking
water
(
1.5,
15
mg/
kg/
day)
LOAEL
=
1.5
mg/
kg/
day
(
lowest
dose
tested).
At
9
months
the
osmotic
fragility
of
RBCs
was
decreased
in
all
treatment
groups,
while
a
decreased
blood
glutathione
was
only
observed
in
the
chlorite/
chlorate
groups.
At
2,
4
and
6
months,
no
significant
hematologic
changes
were
noted
in
treated
rats
compared
to
control.
After
9
month
RBC
counts,
hematocrit
and
Hb
were
decreased
in
all
treatment
groups.
The
incorporation
of
3H­
thymidine
into
nuclei
of
testes
was
inhibited
in
all
treated
groups,
also
in
the
liver
of
the
chlorite
groups
and
in
the
kidney
of
100
mg/
L
chlorine
dioxide
treatment.
The
incorporation
in
small
intestinal
nuclei
was
increased
in
10
and
100
mg/
L
chlorine
dioxide
and
in
10
mg/
L
chlorite
groups.
Rat
body
weight
was
decreased
in
all
groups
after
10
and
11
months
870.3150
90­
Day
oral
toxicity
(
Beagle
Dogs)
MRID
40460402
(
1987)
Acceptable/
Guideline
oral
gavage
0,
30,
60
or
360
mg/
kg/
day
for
90
d
NOAEL
=
360
mg/
kg/
day
(
HDT)
LOAEL
=
greater
than
360
mg/
kg/
day
based
on
lack
of
detectable
adverse
effects.
Higher
dose
levels
were
not
possible
due
to
occurrence
of
emesis
at
higher
doses.

Non­
Guideline
subacute
study
in
dogs
Heywood
et
al,
1972
doses
of
200
to
326
mg/
kg/
day
of
sodium
chlorate
administered
daily
by
intubation
as
50
ml
of
6%
solution
to
8
dogs
for
5
days
LOAEL
=
200
mg/
kg/
day
(
LDT).
Sodium
chlorate
caused
reduction
of
packed
cell
volume,
hemoglobin
and
red
blood
cells.
A
consistent
increase
in
plasma
urea
concentration
was
also
observed.
Two
animals
that
received
308
or
326
mg/
kg/
day
suffered
appetite
loss,
body
weight
decline
and
appearance
of
blood
in
their
urine
or
feces.
One
of
the
animals
died
after
4
days
of
exposure.
Postmortem
examination
of
both
animals
revealed
typical
signs
of
chlorate
poisoning,
including
cyanotic
kidney
surface
and
evidence
of
necrosis
and
hemolysis
in
the
kidney.
Five
of
the
8
animals
displayed
tissue
pathology
indicative
of
hemolysis
such
as
Kupffer
cells
containing
brown
pigment.

Non­
Guideline
21
day
oral
toxicity
study
(
B6C3F1
mice)
NTP
Study
(
2004)
10/
sex/
dose:
0,
125,
250,
500,
1000
or
2000
mg/
L
M:
20,
45,
90,
175
or
350
mg/
kg/
day
F:
0,
20,
45,
95,
190
or
365
mg/
kg/
day
NOAEL
=
350/
360
mg/
kg/
day
(
HDT).
Sodium
chlorate
had
no
effect
on
survival,
body
weights,
clinical
signs,
water
consumption,
hematology
parameters,
methemoglobin
concentration,
or
organ
weights
of
either
sex.
There
were
no
gross
or
microscopic
lesions
that
were
considered
to
be
due
to
sodium
chlorate
treatment.
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
25
of
141
Non­
Guideline
21
day
oral
toxicity
study
(
Fisher
344
rats)
NTP
Study
(
2004)
10/
sex/
dose:
0,
125,
250,
500,
1000
or
2000
mg/
L
M:
0,
20,
35,
75,
170,
300
mg/
kg/
day
F:
0,
20,
40,
75,
150
or
340
mg/
kg/
day
NOAEL/
LOAEL
unclear
from
study
summary.
Sodium
chlorate
had
no
effect
on
survival,
body
weights,
clinical
signs
or
water
consumption.
A
moderate
to
severe
neutropenia
was
observed
in
both
sexes
on
day
4
and
22.
Very
mild
decreases
in
erythrocyte
counts,
hemoglobin,
and
hematocrit
were
considered
not
to
be
biologically
significant.
The
only
gross
or
microscopic
lesion
that
was
considered
to
be
treatment
related
was
a
minimal
to
mild
follicular
cell
hyperplasia
of
the
thyroid
gland
seen
in
males
at
500
mg/
L
or
greater
and
in
females
at
250
mg/
L
or
greater.

870.3200
21/
28­
Day
dermal
toxicity
Not
required.
Sodium
chlorate
has
very
low
acute
dermal
toxicity.
Dermal
absorption
is
also
unlikely
due
to
its
ionic
nature
and
high
water
solubility.

870.3250
90­
Day
dermal
toxicity
Not
required.
Sodium
chlorate
has
very
low
acute
dermal
toxicity.
Dermal
absorption
is
also
unlikely
due
to
its
ionic
nature
and
high
water
solubility.

870.3465
90­
Day
inhalation
toxicity
NA
870.3700a
Prenatal
developmental
(
rats)
MRID
40460401(
1987)
Acceptable/
Guideline
oral
gavage
0,
10,
100
or
1000
mg/
kg/
d
on
GD
6­
15
Maternal
NOAEL
=
1000
mg/
kg/
day
(
HDT)
LOAEL
=
>
1000
mg/
kg/
day.
Developmental
NOAEL
=
1000
mg/
kg/
day
(
HDT)
LOAEL
=
>
1000
mg/
kg/
day
based
on
lack
of
effects
870.3700b
Prenatal
developmental
(
Rabbits)
NTP
(
2002)
Acceptable/
Guideline
0,
100,
250,
or
475
mg/
kg/
d
on
GD
6­
29.
Range
finding
study:
0,
100,
250,
500,
750
or
1000
mg/
kg/
d
Maternal
NOAEL
=
475
mg/
kg/
day
(
HDT)
LOAEL
=
500
mg/
kg/
day
based
on
mortality
in
range
finding
study.
Developmental
NOAEL
=
475
mg/
kg/
day
(
HDT)
LOAEL
=
>
475
mg/
kg/
day
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
26
of
141
870.3800
Reproduction
and
fertility
effects
(
Rats)
MRID
46524001(
2004)
Acceptable/
Guideline
0,
10,
70
or
500
mg/
kg/
day
(
gavage)
Parental/
Systemic
NOAEL
=
10/
70
(
M/
F)
mg/
kg/
day
LOAEL
=
70/
500
(
M/
F)
mg/
kg/
day
based
on
lower
BW
gain
and
food
consumption
(
F1
M),
decreased
RBC
counts
and
hemoglobin
(
P
males
and
females),
increased
absolute
and
relative
thyroid
weight
(
F1
males),
increased
incidence
of
slight
to
moderate
hyperactivity
of
the
thyroid
glands
(
P
and
F1
males
and
females)
(
only
in
P
and
F1
males
at
70
mg/
kg/
day).
Reproductive
NOAEL
=
500
mg/
kg/
day
(
HDT)
Offspring
NOAEL
=
70
mg/
kg/
day
LOAEL
=
500
mg/
kg/
day
based
on
increased
relative
thyroid
weight
(
F1
and
F2
males).

870.4100a
Chronic
toxicity
rodents
A
2­
year
NTP
bioassay
(
2004)
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
reported
in
a
draft
form.
F344
rats
(
50/
sex/
group)
were
exposed
to
drinking
water
at
0,
125,
1,000,
or
2,000
mg/
L
sodium
chlorate
for
2
years
(
5,
35,
and
75
mg/
kg
/
day
in
males
and
5,
45,
and
95
mg/
kg/
day
in
females).
T4
and
T3
were
significantly
reduced
in
1,000
and
2,000
mg/
L
on
day
4
and
in
2,000
mg/
L
males
and
females
at
week
3.
TSH
was
significantly
increased
in
1,000
and
2,000
mg/
L
males
on
day
4
and
at
week
3,
in
1,000
and
2,000
mg/
L
females
on
day
4,
in
2,000
mg/
L
females
at
week
3,
and
in
2,000
mg/
L
males
and
females
at
week
13.
There
were
positive
trends
in
the
incidences
of
thyroid
gland
follicular
cell
carcinoma
in
male
rats
(
0/
47,
0/
44,
0/
43,
4/
47)
and
of
thyroid
gland
follicular
cell
adenoma
or
carcinoma
(
combined)
in
males
(
1/
47,
0/
44,
0/
43,
6/
47)
and
females
(
1/
47,
0/
47,
1/
43,
4/
46).
The
incidences
of
thyroid
gland
follicular
cell
hypertrophy
were
significantly
increased
in
all
exposed
groups
of
males
(
4/
47,
13/
44,
33/
43,
40/
47)
and
in
1,000
and
2,000
mg/
L
females
(
3/
47,
7/
47,
27/
43,
42/
46).
Thyroid
gland
focal
follicle
mineralization
occurred
in
most
1,000
and
2,000
mg/
L
female
rats.
The
incidences
of
hematopoietic
cell
proliferation
in
the
spleen
of
2,000
mg/
L
males
(
2/
48,
6/
49,
4/
49,
11/
50)
and
bone
marrow
hyperplasia
in
1,000
and
2,000
mg/
L
males
(
28/
48,
35/
48,
41/
50,
40/
49)
were
significantly
greater
than
those
in
the
controls.
The
LOAEL
for
non
neoplastic
effects
derived
from
this
study
is
125
mg/
L
(
5
mg/
kg/
day)
based
on
increased
thyroid
gland
follicular
cell
hypertrophy
and
follicular
cell
mineralization.
The
NOAEL
is
less
than
5
mg/
kg/
day.

B6C3F1
mice
950/
sex/
group)
were
exposed
to
drinking
water
at
0,
500,
1,000,
or
2,000
mg/
L
sodium
chlorate
for
2
years
(
40,
80,
and
160
mg/
kg/
day
to
male
mice
and
30,
60,
and
120
mg/
kg/
day
to
female
mice).
There
was
a
positive
trend
in
the
incidences
of
pancreatic
islet
cell
adenoma
or
carcinoma
(
combined)
in
female
mice
(
0/
46,
2/
47,
2/
49,
4/
49).
Thyroid
gland
follicular
cell
hypertrophy
was
significantly
increased
in
2,000
mg/
L
females
(
3/
48,
2/
50,
5/
49,
14/
50).
The
incidences
of
bone
marrow
hyperplasia
were
significantly
increased
in
all
exposed
groups
of
females
(
14/
50,
28/
50,
29/
50,
31/
50).
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
27
of
141
870.4100b
Chronic
toxicity
dogs
Not
available
870.4200
Carcinogenicity
rats
A
2­
year
NTP
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
reported
in
a
draft
form
(
2004).
In
these
tests,
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
the
imbalance
of
thyroid
hormones
(
reduced
T3
and
T4
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
sodium
chlorate.
Current
EPA
HED
policy
considers
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis.

870.4300
Carcinogenicity
mice
NTP
2004
Study.
A
2­
year
NTP
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
reported
in
a
draft
form
(
2004).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.

Gene
Mutation
870.
5100
870.5500
Bacterial
DNA
damage/
Repair
MRID
41256201
(
1989)
Acceptable/
Guideline
Moriya
et
al,
1983
Eckhardt
et
al,
1982
Olivier
and
Marzin
1987
NTP,
2004
MRID
41256204
(
1989)
Acceptable/
Guideline
Sodium
chlorate
was
negative
for
inducing
reverse
gene
mutation
in
Ames
(
bacterial)
strains
of
Salmonella
typhimurium
exposed
with
or
without
activation
up
to
5000
ug/
plate
(
limit
dose).

Sodium
chlorate
was
negative
for
inducing
reverse
gene
mutation
in
Ames
(
bacterial)
strains
of
Salmonella
typhimurium
exposed
with
or
without
activation
up
to
5000
ug/
plate
(
limit
dose).

Sodium
chlorate
showed
mutagenic
activity
in
the
TA1535
strain
+
S9
Potassium
chlorate
was
not
mutagenic
in
the
SOS
chromotest
using
E.
coli
strain
PQ37
without
metabolic
activation
tested
at
1­
6000
nM/
ml.

Sodium
chlorate
tested
up
to
10,000
ug/
plate
was
negative
in
strains
TA97,
TA98,
TA100,
TA102,
TA1535
with
or
without
S9
Sodium
chlorate
caused
DNA
damage
in
repair
deficient
E.
coli
strains
at
concentrations
above
1000
ug/
mL
in
the
presence
or
absence
of
S9
fractions.
It
was
tested
up
to
10000
ug/
mL.
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
28
of
141
Cytogenetics
870.5300,
in
vitro
mammalian
cell
gene
mutation
assay
MRID
41256202
(
1989)
Acceptable/
Guideline
Sodium
chlorate
was
negative
for
inducing
forward
gene
mutation
at
the
hypoxanthine­
guanine
phosphoribosyl
transferase
(
HGPRT)
locus
in
the
Chinese
hamster
lung
(
V79)
cells
(
HGPRT
+,
­)
Exposed
in
activated
(+
s9)
or
non­
activated
(­
S9)
culture
tested
up
to
the
limit
dose
of
5000
ug/
mL.

870.5395
Mammalian
erythrocyte
micronucleus
test
MRID
41256203
(
1989)
Acceptable/
Guideline
Sodium
chlorate
was
negative
(
not
clastogenic)
for
inducing
micronuclei
in
polychromatic
erythrocytes
of
male
mice
with
single
oral
doses
of
200,
1000
or
5000
(
limit
dose)
mg/
kg.

870.5395
Mammalian
erythrocyte
micronucleus
test
NTP,
2004
Sodium
chlorate
did
not
increase
the
number
of
micronucleated
erythrocytes
in
B6C3F1
mice
treated
in
the
drinking
water
with
20,
45,
95,
190,
or
365
mg/
kg/
day
for
3
weeks.

micronucleus
test
Eckhardt
et
al,
1982
Sodium
chlorate
did
not
induce
chromosomal
damage.

micronucleus
test
Meier
et
al,
1985
Sodium
chlorate
did
not
increase
the
number
of
micronucleated
polychromatic
erythrocytes
in
CD­
1
mice
treated
by
gavage
with
8,
20
or
40
mg/
kg/
day
for
5
days.

870.5385
Bone
marrow
cytogenetics
assay
Meier
et
al,
1985
Sodium
chlorate
did
not
cause
structural
or
numerical
chromosomal
aberrations
in
mice
treated
by
gavage
with
8,
20
or
40
mg/
kg/
day
for
5
days.

Sperm
head
abnormality
assay
Meier
et
al,
1985
Sodium
chlorate
did
not
induce
sperm
head
abnormalities
in
B6C3FA
male
mice
treated
by
gavage
with
8,
20
or
40
mg/
kg/
day
for
5
days.

Other
Effects
870.5550,
Unscheduled
DNA
Synthesis
MRID412546205
Acceptable/
Guideline
Sodium
chlorate
was
negative
for
unscheduled
DNA
synthesis
(
UDS)
in
human
cells
(
HeLa­
S3)
exposed
up
to
10,000
ug/
mL,
with
or
without
metabolic
activation.
The
incorporation
of
thymidine
was
decreased
in
a
dosedependent
manner
between
doses
of
100
and
10,000
ug/
mL
indicating
cytotoxicity.

870.5275
recessive
lethal:
Drosophila
Eckhardt
et
al,
1982
Sodium
chlorate
was
mutagenic
in
this
system.

870.6200a
Acute
neurotoxicity
screening
battery
Not
required
for
this
chemical
Table
4.1b
Subchronic,
Chronic
and
Other
Toxicity
Profile:
Sodium
Chlorate
Guideline
No./
Study
Type
MRID
No.
(
year)/
Classification
/
Doses
Results
Page
29
of
141
870.6200b
Subchronic
neurotoxicity
screening
battery
Not
required
for
this
chemical
870.6300
Developmental
neurotoxicity
NA
870.7485
Metabolism
and
pharmacokinetics
Abdel­
Rahman
et
al,
1982,
984b,
1985­
rats
Non­
Guideline
National
Research
Council,
1980
­
dogs
(
OEHHA,
2002)
Non­
Guideline
There
are
no
guideline
studies
available.
However,
published
studies
provide
reasonable
information
on
the
pharmacokinetics
and
metabolism
of
the
chlorate
ion
in
the
rat
and
the
dog.
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
in
urine
mainly
and
feces.
In
dogs
the
excretion
is
entirely
as
chlorate
and
is
complete
after
72
hours.
In
rats,
about
40%
of
the
administered
dose
was
excreted
after
72
hours
and
it
is
excreted
as
chloride,
chlorite
and
chlorate.
In
Cl36
labeled
potassium­
chlorate
studies
in
rats,
Cl36
radioactivity
was
detected
at
the
end
or
72
hours
after
the
initial
oral
treatment
in
several
tissues.
Although
the
chlorites
and
the
chlorates
are
structurally
related,
their
pharmacokinetics
is
different.

870.7600
Dermal
penetration
Not
required
It
is
not
required
for
sodium
chlorate.
Acute
dermal
toxicity
is
low
and
sodium
chlorate
is
very
polar
being
an
inorganic
salt
would
not
be
readily
absorbed
through
the
skin.

Special
studies
Beinfeld
(
1994)
Mintz
et
al
(
1994)
Sodium
chlorate
is
in
vitro
inhibitor
of
ATP­
sulfurylase
and
protein
sulfation
Special
Studies
Roy
et
al
(
1988)
Sodium
chlorate
did
not
affect
bile
production
from
isolated
perfused
guinea
pig
livers
suggesting
that
it
is
not
a
general
liver
poison
4.2
FQPA
Hazard
Considerations
The
database
with
respect
to
the
standard
guideline
studies
is
adequate
to
characterize
potential
for
prenatal
or
postnatal
risk
for
infants
and
children.
No
increase
in
prenatal
susceptibility
of
rats
or
rabbits
was
seen
in
developmental
studies
with
chlorate,
and
no
increase
in
pre­
or
postnatal
susceptibility
was
evident
in
a
2­
generation
reproduction
study
in
rats.
Based
on
this,
there
are
no
residual
uncertainties
from
guideline
studies
and
the
special
FQPA
safety
factor
is
reduced
to
1X.
There
is,
however,
need
for
additional
data
on
potential
neuroendocrine
effects
on
the
developing
young
based
on
chlorate­
induced
thyroid
effects.

4.2.1
Adequacy
of
the
Toxicity
Data
Base
The
toxicity
data
base
is
complete
with
respect
to
the
normal
complement
of
guideline
studies
except
for
a
21/
28
day
inhalation
study.
Because
the
inorganic
chlorates
affect
the
thyroid
gland
Page
30
of
141
in
rats
and
dogs,
there
is
concern
for
potential
neuroendocrine
pre­
and
postnatal
effects
to
developing
young
and
a
comparative
thyroid
study
in
which
T4,
T3
and
TSH
are
analyzed
in
adults
and
in
neonates
is
required
to
address
this
concern.

4.2.2
Evidence
of
Neurotoxicity
Sodium
chlorate
did
not
show
neurotoxic
effects
in
acute,
subchronic
testing.

4.2.3
Developmental
Toxicity
Studies
DEVELOPMENTAL
­
RAT
In
a
developmental
toxicity
study
(
MRID
40460401),
24
pregnant
Sprague­
Dawley
CD
rats
per
group
were
administered
technical
grade
sodium
chlorate
(
100%
a.
i.,
white
granular
solid)
by
oral
gavage
at
0
(
distilled
water)
10,
100,
or
1000
mg/
kg/
day
on
gestation
days
(
GD)
6­
15,
inclusive.
On
GD
20,
all
dams
were
sacrificed
and
all
fetuses
were
examined
for
external,
visceral,
and
skeletal
malformations/
variations.
All
animals
survived
until
scheduled
sacrifice
except
for
one
control
that
died
prior
to
terminal
sacrifice.
No
adverse
clinical
signs
were
reported.
There
were
no
dose
or
treatment
related
effects
detected
in
the
dams
or
embryos/
fetuses.
Maternal
body
weights,
food
consumption
were
comparable
to
controls.
Necropsy
of
treated
animals
did
not
reveal
any
treatment
related
effect.
There
was
no
treatment
related
effect
on
pregnancy
rate,
corpora
lutea,
implantation
sites,
viable
fetuses,
dead
fetuses,
resorptions
or
fetal
weights.
Fetal
examinations
did
not
reveal
any
anomalies
attributed
to
treatment.
The
LOAEL
derived
from
this
study
for
maternal
and
developmental
toxicity
in
the
rat
is
>
1000
mg/
kg/
day
and
the
NOAEL
is
at
least
1000
mg/
kg/
day.
This
study
is
considered
Acceptable/
guideline.

DEVELOPMENTAL
­
RABBIT
There
are
no
registrant
guideline
studies
available.
There
is
an
NTP
study
reported
in
2002,
where
24
timed
naturally
mated
female
New
Zealand
rabbits/
dose
were
dosed
by
gavage
with
sodium
chlorate
at
0
(
deionized
distilled
water),
100,
250,
or
475
mg/
kg/
day
on
gestation
days
6
through
29.
The
study
was
conducted
in
a
two
replicate
design
where
12
rabbits/
dose
were
dosed
in
each
replicate.
The
doses
were
selected
on
the
basis
of
a
range
finding
study
conducted
at
0,
100,
250,
500,
750,
or
1000
mg/
kg/
day.
In
this
range
finding
study,
excessive
maternal
toxicity
(
morbidity
and
mortality)
resulted
in
termination
of
the
groups
treated
with
750
and
1000
mg/
kg/
day
by
gestation
day
24.
One
maternal
death
occurred
in
the
500
mg/
kg/
day
group
and
one
doe
was
lethargic
with
respiratory
distress.
Clinical
signs
were
minimal
in
the
100
and
250
mg/
kg/
day
groups.
These
included
animals
with
discolored
urine
(
red,
orange,
orange/
white
or
brown).
Body
weights
were
decreased
during
treatment
only
at
doses
higher
than
500
mg/
kg/
day.
Developmental
toxicity
was
not
evident
at
doses
up
to
500
mg/
kg/
day.
In
the
final
study,
transient
changes
in
maternal
food
intake,
urinary
color
(
orange
or
brown)
and
/
or
urine
output
were
noted
at
100
mg/
kg/
day
and
greater,
but
clear
evidence
of
toxicity
occurred
only
at
doses
greater
than
475
mg/
kg/
day
as
observed
in
the
range
finding
study.
According
to
the
study
authors,
comparison
of
the
results
from
the
range
finding
study
and
the
developmental
toxicity
study
suggests
that
the
dose­
effect
curve
for
maternal
effects
is
very
steep
as
demonstrated
by
mortality
at
500
mg/
kg/
day
on
the
range
finding
study,
but
not
at
the
475
mg/
kg/
day
in
the
final
Page
31
of
141
study.
No
significant
treatment
related
developmental
toxicity
attributable
to
sodium
chlorate
occurred
under
the
conditions
of
this
study.
It
was
concluded
that
the
maternal
and
developmental
toxicity
NOAELs
were
equal
to
or
greater
than
475
mg/
kg/
day
(
the
HDT).
The
LOAEL
for
maternal
toxicity
is
500
mg/
kg/
day
based
on
mortality
observed
in
the
range
finding
study.
This
study
satisfies
guideline
requirements
and
is
acceptable/
guideline.

4.2.4
Reproductive
Toxicity
Study
In
an
Acceptable/
Guideline
2­
generation
reproduction
study
(
MRID
46524001),
sodium
chlorate
(
99.68%
a.
i.;
batch/
lot
1E012IUM)
was
administered
to
25
Sprague­
Dawley
rats
of
each
sex
per
dose
by
gavage
at
dose
levels
of
0,
10,
70,
or
500
mg/
kg/
day.
P
males
were
exposed
to
the
test
material
for
10
weeks
prior
to
mating
and
after
mating
until
the
pups
were
weaned;
P
females
were
exposed
for
10
weeks
prior
to
mating
and
then
throughout
gestation
and
lactation.
Selection
of
parents
(
4
males
and
4
females
per
litter)
for
the
F
1
generation
was
made
when
the
pups
were
4
days
of
age.
F
1
parents
were
exposed
in
the
same
manner
as
P
parents.

Oral
administration
of
sodium
chlorate
resulted
in
parental
toxicity
at
70
and
500
mg/
kg/
day.
Treatment­
related
effects
at
500
mg/
kg/
day
consisted
of
slightly
lower
body
weight
gain
and
food
consumption
(
F
1
males);
decreased
red
blood
cell
counts
(
P
males
and
females);
decreased
hemoglobin
concentration
(
P
males
and
females);
increased
absolute
and
relative
thyroid
weight
(
F
1
males);
increased
incidence
of
slight
to
moderate
follicular
hyperplasia
(
P
and
F
1
males
and
females);
and
increased
incidence
of
slight
to
moderate
hyperactivity
of
the
thyroid
glands
(
P
and
F
1
males
and
females).
The
thyroid
gland
appeared
to
be
the
target
organ.

At
70
mg/
kg/
day,
treatment­
related
effects
consisted
of
a
marginal
increased
incidence
of
hyperactivity
of
the
thyroid
glands
(
P
and
F
1
males).
Based
on
these
results,
a
NOAEL
of
10
mg/
kg/
day
for
males
(
LOAEL
70
mg/
kg/
day)
was
established.
In
females
a
NOAEL
of
70
mg/
kg/
day
and
a
LOAEL
of
500
mg/
kg/
day
was
established.

For
offspring,
exposure
to
sodium
chlorate
resulted
in
toxicity
at
500
mg/
kg/
day.
Treatmentrelated
effects
at
500
mg/
kg/
day
consisted
of
increased
relative
thyroid
weight
in
F
1
and
F
2
males.
The
offspring
LOAEL
is
500
mg/
kg/
day,
based
on
increased
relative
thyroid
weight.
The
offspring
NOAEL
is
70
mg/
kg/
day.

There
were
no
treatment­
related
reproductive
effects
observed
at
any
dose
level
for
either
generation.
Consequently,
the
reproductive
NOAEL
is
500
mg/
kg/
day.

4.2.5
Additional
Information
from
Literature
Sources
In
a
case
control
study
evaluating
chlorination
by­
products
in
drinking
water
and
adverse
pregnancy
outcomes
in
Italy
(
Aggazzotti
et
al,
2004),
no
association
was
found
between
preterm
births
and
exposure
to
chlorination
by
products
(
trihalomethanes,
chlorites
and
chlorates),
but
there
was
a
weak
association
between
small
weight
gestational
term
(
weighing
less
than
the
lowest
10th
percentile)
and
high
levels
of
trihalomethanes
($
30
ug/
L
drinking
water)
and
chlorites
and
chlorates
($
200
ug/
L
drinking
water).
Page
32
of
141
In
a
subchronic
exposure
study
in
primates
where
sodium
chlorate
was
administered
in
drinking
water
for
8
weeks
at
400
mg/
L
(
58.4
±
27.6
mg/
kg/
day)
to
6
male
and
7
female
adult
African
Green
Monkeys
(
Cercopithecus
aethiops)
there
was
no
effect
on
the
thyroid
function
and
the
total
thyroxine
levels
(
Bercz
et
al,
1982).
Based
on
this
study
the
NOAEL
for
sodium
chlorate
thyroid
effects
in
the
monkey
would
be
at
least
58
mg/
kg/
day.

4.2.6
Pre­
and/
or
Postnatal
Toxicity
Prenatal
toxicity
of
sodium
chlorate
has
been
evaluated
in
developmental
toxicity
studies
in
the
rat
and
the
rabbit.
In
both
species,
prenatal
toxicity
was
not
observed
at
the
highest
doses
tested
(
1000
mg/
kg/
day
in
the
rat,
and
475
mg/
kg/
day
in
the
rabbit).
In
a
2­
generation
reproduction
test
in
the
rat,
there
were
thyroid
effects
to
the
offspring
at
the
highest
dose
tested
­
500
mg/
kg.
No
other
offspring
effects
were
noted
in
the
study,

4.2.6.1
Determination
of
Susceptibility
Based
on
the
developmental
studies
in
rats
and
rabbits
and
the
reproductive
toxicity
study
in
rats,
fetal
or
neonatal
toxicity
from
administration
of
sodium
chlorate
did
not
occur
at
doses
lower
than
doses
causing
effects
in
parental
animals.

4.2.6.2
Degree
of
Concern
Analysis
and
Residual
Uncertainties
for
Pre
and/
or
Post­
natal
Susceptibility
No
increase
in
prenatal
susceptibility
of
rats
or
rabbits
was
seen
in
developmental
studies,
and
no
pre­
or
postnatal
susceptibility
was
observed
in
a
reproduction
study
in
the
rat.
Based
on
this,
there
are
no
residual
uncertainties
that
indicate
the
need
for
a
special
safety
factor.
The
hazard
factor
is
thus
1X.
Page
33
of
141
4.2.7
Recommendation
for
a
Developmental
Neurotoxicity
Study
4.2.7.1
Evidence
that
supports
requiring
a
Developmental
Neurotoxicity
study
There
is
no
evidence
for
requiring
such
a
study.
Sodium
chlorate
did
not
show
neurotoxic
effects
in
acute,
subchronic
testing.

4.2.7.2
Evidence
that
supports
not
requiring
for
a
Developmental
Neurotoxicity
study
No
neurotoxic
effects
were
seen
in
acute,
subchronic
studies
with
sodium
chlorate.

4.3
Safety
Factor
for
Infants
and
Children.
There
was
no
pre­
or
postnatal
sensitivity
or
susceptibility
observed
in
the
submitted
developmental
studies
in
rats
and
rabbits
and
the
2­
generation
reproduction
study
in
rats.
However,
there
is
a
concern
for
developing
offspring
because
of
the
effects
of
inorganic
chlorate
on
thyroid
function
in
rats
and
dogs.
The
thyroid
hormone
system
plays
a
critical
role
in
development,
and
it
is
therefore
important
to
understand
whether
the
thyroid
hormone
system
in
the
developing
young
differs
in
response
to
thyroid
toxicants
compared
to
adults.
There
exists
therefore
a
database
uncertainty
for
information
on
comparative
thyroid
response
in
young
vs
adult
rats;
however,
a
database
factor
reflecting
the
uncertainty
in
comparative
response
is
not
necessary
and
the
default
10X
FQPA
factor
can
be
removed.

The
rationale
for
removal
of
the
factor
lies
in
the
comparative
thyroid
physiology
of
rats
vs.
humans
(
see
further
discussion
of
the
differences
in
physiology
under
the
chronic
RfD).
As
a
consequence
of
these
dynamic
differences,
rats
are
much
more
sensitive
to
thyroid
toxicants
such
as
chlorate
than
humans
and
non­
human
primates.
As
discussed
in
section
4.4.3
below,
the
chronic
RfD
for
inorganic
chlorates
is
0.03
mg/
kg/
day
based
on
thyroid
hypertrophy
in
adult
rats.
There
is
a
study
of
the
effects
of
chlorate
on
adult
monkeys
(
Bercz
et
al,
1982),
in
which
the
NOAEL
for
effects
on
blood
thyroxine
levels
was
58
mg/
kg/
day.
If
the
NOAEL
from
the
monkey
study
were
used
to
derive
a
chronic
RfD
with
uncertainty
factors
of
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variability
and
an
FQPA
factor
of
10x
reflecting
uncertainties
in
effects
to
the
young,
the
chronic
RfD
would
be
0.06
mg/
kg/
day.
The
chronic
RfD
selected
by
the
risk
assessment
team
of
0.03
mg/
kg/
day
derived
from
the
chronic
rat
NTP
study
is
therefore
protective
of
thyroid
effects
in
primates
(
including
a
10X
factor
for
uncertainty
with
respect
to
developing
young)
without
the
necessity
of
an
additional
uncertainty
factor
applied
to
the
rat
data.

4.4
Hazard
Identification
and
Toxicity
Endpoint
Selection
4.4.1
Acute
Reference
Dose
(
aRfD)
­
Females
age
13­
49
An
acute
RfD
for
females
age
13­
49
was
not
identified
from
the
available
developmental
toxicity
studies
in
rats
and
rabbits.
Page
34
of
141
4.4.2
Acute
Reference
Dose
(
aRfD)
­
General
Population
An
endpoint
of
concern
attributable
to
a
single
dose
was
not
identified
although
several
studies
were
considered.
The
developmental
NTP
study
in
rabbits
discussed
above
provided
a
NOAEL
for
maternal
toxicity
of
475
mg/
kg/
day
based
on
maternal
morbidity
and
mortality
at
500
mg/
kg/
day
in
a
range
finding
study.
In
a
subacute
toxicity
study,
200
to
326
mg
of
sodium
chlorate/
kg
administered
daily
for
5
days
to
a
total
of
8
dogs,
all
dogs
experienced
toxicity
including
death
at
the
higher
dose.
However,
in
a
guideline
study
(
MRID
40460402)
sodium
chlorate
administered
to
dogs
by
oral
gavage
daily
for
90
days
did
not
exert
any
toxicity
at
the
highest
dose
tested
of
360
mg/
kg/
day.
None
of
these
studies
provided
an
endpoint
of
toxicity
attributable
to
a
single
exposure.
An
acute
RfD
for
the
general
population
is
not
established.

The
published
literature
provides
numerous
references
to
sodium
chlorate
poisoning
in
humans.
Doses
in
excess
of
100
mg/
kg
(
7
grams
for
a
70
kg
adult
and
0.5
grams
for
a
5
kg
child)
are
generally
fatal
(
Warrington
2002,
Cosmetic
Ingredient
Review
Panel
1995).
Pesticide
incident
data
are
not
used
for
establishing
dietary
endpoints,
but
the
chlorate
incident
data
indicate
that
there
is
a
concern
for
direct
ingestion
of
chlorate
formulations.

4.4.3
Chronic
Reference
Dose
(
cRfD)
A
chronic
study
with
sodium
chlorate
in
rats
has
been
completed
in
2004
and
reported
in
a
draft
form
(
NTP
2004).
In
this
NTP
study,
groups
of
50
male
and
50
female
F344
rats
were
exposed
to
drinking
water
containing
0,
125,
1,000,
or
2,000
mg/
L
sodium
chlorate
for
2
years
(
equivalent
to
average
daily
doses
of
approximately
5,
35,
and
75
mg/
kg
per
day
in
male
rats
and
5,
45,
and
95
mg/
kg
per
day
in
female
rats).
Survival
of
exposed
rats
was
similar
to
that
of
the
control
groups.
Mean
body
weights
of
all
exposed
groups
were
similar
to
those
of
the
control
groups
throughout
the
study.
Water
consumption
by
exposed
rats
was
generally
similar
to
that
by
controls
throughout
the
study
(
14­
17
g
of
water/
male
rat/
day
and
10.6­
13.2
g
of
water/
female
rat/
day).
Serum
concentrations
of
thyroxine
(
T
4
)
and
triiodothyronine
(
T
3
)
were
significantly
reduced
in
1,000
and
2,000
mg/
L
males
and
females
on
day
4
and
in
2,000
mg/
L
males
and
females
at
week
3.
Serum
concentrations
of
thyroid
stimulating
hormone
(
TSH)
were
significantly
increased
in
1,000
and
2,000
mg/
L
males
on
day
4
and
at
week
3,
in
1,000
and
2,000
mg/
L
females
on
day
4,
in
2,000
mg/
L
females
at
week
3,
and
in
2,000
mg/
L
males
and
females
at
week
13.
All
special
study
rats
in
the
1,000
and
2,000
mg/
L
groups
had
thyroid
gland
follicular
cell
hypertrophy
at
3
and
13
weeks.
There
were
positive
trends
in
the
incidences
of
thyroid
gland
follicular
cell
carcinoma
in
male
rats
(
0/
47,
0/
44,
0/
43,
4/
47)
and
of
thyroid
gland
follicular
cell
adenoma
or
carcinoma
(
combined)
in
males
(
1/
47,
0/
44,
0/
43,
6/
47)
and
females
(
1/
47,
0/
47,
1/
43,
4/
46).
The
incidences
of
thyroid
gland
follicular
cell
hypertrophy
were
significantly
increased
in
all
exposed
groups
of
males
(
4/
47,
13/
44,
33/
43,
40/
47)
and
in
1,000
and
2,000
mg/
L
females
(
3/
47,
7/
47,
27/
43,
42/
46).
Thyroid
gland
focal
follicle
mineralization
occurred
in
most
1,000
and
2,000
mg/
L
female
rats
(
25/
47,
26/
47,
40/
43,
44/
46).
The
incidences
of
hematopoietic
cell
proliferation
in
the
spleen
of
2,000
mg/
L
males
(
2/
48,
6/
49,
4/
49,
11/
50)
and
bone
marrow
hyperplasia
in
1,000
and
2,000
mg/
L
males
(
28/
48,
35/
48,
41/
50,
40/
49)
were
significantly
greater
than
those
in
the
controls.
The
LOAEL
for
non
neoplastic
effects
derived
from
this
study
is
125
mg/
L
(
5
mg/
kg/
day)
based
on
increased
thyroid
gland
follicular
cell
Page
35
of
141
hypertrophy
and
follicular
cell
mineralization.
A
NOAEL
for
non
neoplastic
effects
cannot
be
derived
from
this
study.
Therefore
a
bench
mark
dose
(
BMD)
analysis
was
performed
and
a
BMDL
of
28
mg/
L
as
sodium
chlorate
(
22
mg/
L
as
chlorate)
was
obtained
(
See
Memorandum
from
Becky
Daiss
to
Abdallah
Khasawinah,
Jan.
26,
2005).
This
corresponds
to
0.9
mg
chlorate/
kg/
day
oral
dose.
Using
the
BMDL
as
an
approximation
of
the
NOAEL,
the
oral
RfD
using
a
composite
30
X
uncertainty
factor
(
3X
for
interspecies
and
10X
for
intraspecies)
is:

The
usual
interspecies
uncertainty
factor
is
10X,
but
there
are
several
important
quantitative
dynamic
differences
between
rats
and
humans
with
respect
to
thyroid
function
that
permit
an
interspecies
factor
of
less
than
10X
for
a
thyroid
toxicant
like
chlorate.
The
half­
life
of
T4
in
rats
is
approximately
12
hours,
whereas
in
humans,
the
half­
life
is
5­
9
days
(
Dohler
et
al.,
1979).
The
shorter
half­
life
in
rats
is
likely
related
to
a
high­
affinity
binding
globulin
for
thyroxin
that
is
present
in
humans,
but
absent
in
rodents.
Specifically,
binding
of
the
hormone
to
thyroxin
binding
globulin
accounts
for
slower
metabolic
degradation
and
clearance
in
humans.
Increased
turnover
and
hepatic
clearance
of
T3
and
T4
renders
the
basal
activity
of
the
thyroid
gland
markedly
more
active
in
rats
compared
to
humans.
In
the
absence
of
a
functional
thyroid
gland,
a
rat
requires
approximately
10­
times
more
T4
than
an
adult
human
for
full
reconstitution
(
Dohler,
et
al.,
1979).
Constitutive
TSH
levels
are
nearly
25­
times
higher
in
rats
than
in
humans,
reflecting
the
increased
activity
of
the
thyroid­
pituitary
axis
in
rats
(
Dohler
et
al.,
1979;
McClain,
1992).
Therefore,
the
10X
interspecies
factor
(
which
is
subdivided
into
3X
for
differences
in
toxicokinetics
and
3X
for
differences
in
toxicodynamics)
can
be
reduced
to
3X
based
on
dynamic
considerations.

The
BMDL
of
0.9
mg/
kg/
day
for
chlorate
based
on
thyroid
effects
in
the
rat,
the
most
sensitive
species
for
such
an
effect,
will
be
protective
of
any
other
toxicity
produced
by
chlorate.

4.4.4
Incidental
Oral
Exposure
(
short
and
intermediate
durations:
1
day
­
6
months)
There
are
three
90­
day
toxicity
studies
in
rats
available
for
selecting
the
endpoint
to
assess
this
exposure.
In
MRID
40444801,
the
NOAEL
was
100
mg/
kg/
day
based
on
hematological
effects
(
hemoglobin
concentration,
hematocrit,
RBC
counts
were
statistically
significantly
decreased,
and
reticulocyte
count
was
statistically
significantly
increased
in
females
at
1000
mg/
kg/
day.
In
males,
only
the
hematocrit
was
statistically
significantly
decreased.
The
adrenal
weight
was
depressed
in
both
males
and
females.
In
the
McCauley
et
al,
1995
study,
the
NOAEL
was
30
and
42
mg/
kg/
day
(
as
chlorate)
for
males
and
females,
respectively,
based
on
the
pituitary
effects
(
vacuolization)
and
thyroid
gland
effects
(
colloid
depletion),
the
body
weight
decrease
and
organ
weight
changes
and
reduction
in
erythrocyte
counts
and
hemoglobin
content
at
the
LOAEL
of
100
and
150
mg/
kg/
day
in
males
and
females,
respectively.
In
the
third
study
(
Hooth
et
al,
2002),
the
NOAEL
was
28
and
40
mg/
kg/
day
in
males
and
females,
respectively,
based
on
thyroid
colloid
Chronic
RfD
=
0.9
mg/
kg/
day
(
BMDL)
=
0.03
mg/
kg/
day
30
(
UF)
Page
36
of
141
depletion
and
follicular
cell
hyperplasia,
at
112
&
160
mg/
kg/
day
for
males
and
females,
respectively.
Based
on
these
subchronic
studies
with
sodium
chlorate,
an
appropriate
endpoint
would
be
30
mg/
kg/
day
as
chlorate
(
McCauley
study).
For
the
incidental
oral
exposure,
the
30
mg/
kg/
day
dose
is
appropriate
for
this
risk
assessment
and
is
selected
for
the
toxic
endpoint
with
an
MOE
of
100.

4.4.5
Dermal
Absorption
There
are
no
dermal
absorption
studies
available
for
sodium
chlorate.
Based
on
its
high
water
solubility
and
ionic
nature,
sodium
chlorate
absorption
by
the
intact
skin
is
considered
negligible.

4.4.6
Dermal
Exposure
(
Short,
Intermediate
and
Long
Term)
There
are
no
subchronic
dermal
toxicity
studies
available.
Because
sodium
chlorate
is
unlikely
to
be
absorbed
by
the
skin,
a
risk
assessment
for
dermal
exposure
is
not
needed.

4.4.7
Inhalation
Exposure
(
Short
and
Intermediate
Term)
There
are
no
subacute
or
subchronic
inhalation
studies
available
for
sodium
chlorate.
The
toxic
endpoint
from
the
subchronic
oral
rat
study
discussed
above
with
a
NOAEL
of
30
mg/
kg/
day
is
used
for
assessing
the
risks
from
the
inhalation
exposure
to
sodium
chlorate
and
the
100%
default
absorption
factor
for
using
an
oral
dose
is
applied.

4.4.8
Margins
of
Exposure
The
Margin
of
Exposure
is
100
for
all
occupational
and
residential
exposure
scenarios.

4.4.9
Recommendation
for
Aggregate
Exposure
Risk
Assessments
As
per
FQPA
of
1996,
when
there
are
potential
residential
exposures
to
the
pesticide,
aggregate
risk
assessment
must
consider
exposures
from
residues
in
food
commodities
and
drinking
water,
as
well
as
exposures
arising
from
non­
dietary
sources
(
incidental
oral,
dermal
and
inhalation
exposures)
from
the
residential
scenarios.

4.4.10
Classification
of
Carcinogenic
Potential
A
2­
year
NTP
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
in
a
draft
form
(
NTP,
2004).
A
final
report
of
this
study
is
expected
during
2005.
In
these
tests,
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
changes
of
thyroid
hormones
(
reduced
T
3
and
T
4
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
high
doses
of
sodium
chlorate.
Current
EPA
HED
policy
states
that
"
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
be
classified
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis"
(
Assessment
of
Thyroid
Follicular
Cell
Tumors;
USEPA
March
1998
EPA/
630/
R­
97/
002).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.
Page
37
of
141
Table
4.4.
Summary
of
Toxicological
Doses
and
Endpoints
for
Chlorate
per
se
for
Use
in
Human
Risk
Assessments
for
Inorganic
Chlorates
Exposure
Scenario
Dose
(
as
chlorate)
per
se
Used
in
Risk
Assessment,
UF
Special
FQPA
SF*
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Chronic
Dietary
(
all
populations)
BMDL**
=
0.9
mg/
kg/
day
UF
=
30
1X
Chronic
Study
in
rats
(
NTP,
2004).
The
LOAEL=
5
mg/
kg/
day
based
on
increased
thyroid
gland
follicular
cell
hypertrophy
and
follicular
cell
mineralization.

Incidental
Oral
Short­
Term
(
1
­
30
days)
NOAEL
=
30
mg/
kg/
day
MOE
=
100
1X
Subchronic
study
in
rats
McCauley
et
al,
1995.
Pituitary
effects
(
vacuolization)
and
thyroid
gland
effects
(
colloid
depletion),
the
body
weight
decrease
and
organ
weight
changes
and
reduction
in
erythrocyte
counts
and
hemoglobin
content
at
the
LOAEL
of
100
and
150
mg/
kg/
day
in
males
and
females,
respectively
Incidental
Oral
Intermediate­
Term
(
1
­
6
months)
NOAEL
=
30
mg/
kg/
day
MOE
=
100
1X
McCauley
et
al,
1995
Dermal
all
durations
Not
required:
dermal
absorption
is
unlikely
due
to
the
ionic
nature
and
water
solubility
of
sodium
chlorate
Inhalation
Short­
Term
(
1
­
30
days)
NOAEL
=
30
mg/
kg/
day
UF
=
100
1X
McCauley
et
al,
1995
Inhalation
Intermediate­
Term
(
1
­
6
months)
NOAEL
=
30***
mg/
kg/
day
UF
=
100
1X
McCauley
et
al,
1995
Table
4.4.
Summary
of
Toxicological
Doses
and
Endpoints
for
Chlorate
per
se
for
Use
in
Human
Risk
Assessments
for
Inorganic
Chlorates
Exposure
Scenario
Dose
(
as
chlorate)
per
se
Used
in
Risk
Assessment,
UF
Special
FQPA
SF*
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Page
38
of
141
Cancer
(
oral,
dermal,
inhalation)
Classification:
A
2­
year
NTP
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
in
a
draft
form
(
NTP,
2004).
A
final
report
of
this
study
is
expected
during
2005.
There
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
the
imbalance
of
thyroid
hormones
(
reduced
T3
and
T4
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
high
doses
of
sodium
chlorate.
Current
EPA
HED
policy
states
that
"
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
should
be
classified
as
not
likely
to
be
carcinogenic
to
humans
at
doses
that
do
not
alter
thyroid
hormone
homeostasis"
(
Assessment
of
Thyroid
Follicular
Cell
Tumors;
USEPA
March
1998
EPA/
630/
R­
97/
002).
In
female
mice
there
was
equivocal
and
marginal
evidence
of
increased
pancreatic
islet
carcinoma.

UF
=
uncertainty
factor,
FQPA
SF
=
Special
FQPA
safety
factor,
NOAEL
=
no
observed
adverse
effect
level,
LOAEL
=
lowest
observed
adverse
effect
level,
PAD
=
population
adjusted
dose
(
a
=
acute,
c
=
chronic)
RfD
=
reference
dose,
MOE
=
Margin
of
Exposure,
LOC
=
level
of
concern,
NA
=
Not
Applicable
*
Refer
to
Section
4.5
**
A
NOAEL
was
not
identified
in
this
study.
Therefore
a
bench
mark
dose
(
BMD)
analysis
was
performed
and
a
BMDL
of
28
mg
sodium
chlorate/
L
(
22
mg
chlorate/
L)
was
calculated.
This
corresponds
to
0.9
mg
chlorate/
kg/
day
oral
dose.
***
A
100%
absorption
factor
is
used
for
using
an
oral
endpoint
of
toxicity.
Page
39
of
141
4.5
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).

The
available
toxicity
studies
on
sodium
chlorate,
demonstrate
the
thyroid
gland
to
be
its
target
of
toxicity.

When
additional
appropriate
screening
and/
or
testing
protocols
being
considered
under
the
Agency's
EDSP
have
been
developed,
sodium
chlorate
may
be
subjected
to
further
screening
and/
or
testing
to
better
characterize
effects
related
to
endocrine
disruption.
Page
40
of
141
5.0
Public
Health
Data
Sodium
chlorate
has
been
documented
to
cause
irritation
to
skin,
eyes,
and
mucous
membranes
of
the
upper
respiratory
tract.
Death
can
occur
from
ingestion
of
substantial
quantities,
almost
always
due
to
suicide.
Doses
in
excess
of
100
mg/
kg
are
generally
fatal
to
humans.

5.1
Incident
Reports
Available
sources
of
incident
data
in
humans
were
reviewed
for
the
active
ingredients
Sodium
Chlorate
(
073301)
and
Calcium
Chlorate
(
073302).
Data
were
available
from
the
following
sources:
OPP
Incident
Data
System
(
IDS)
consisting
of
reports
submitted
to
EPA
by
registrants,
other
federal
and
state
health
and
environmental
agencies
and
the
public
since
1992,
Poison
Control
Centers
(
1993­
2001),
California
Department
of
Pesticide
Regulation
for
pesticide
poisoning
since
1982,
National
Pesticide
Telecommunications
Network
(
NPTN)
for
ranking
of
the
top
200
active
ingredients
for
which
phone
calls
were
received
during
calender
years
1984­
1991,
and
National
Institute
of
Occupational
Safety
and
Health's
Sentinel
Event
Notification
System
for
Occupational
Risks
(
NIOSH
SENSOR)
from
1998­
2002.

A
total
of
21
cases
were
located
in
Poison
Control
Center
records
from
1993
through
2001.
Seven
reported
minor
symptoms
and
two
reported
moderate
medical
outcomes,
primarily
due
to
dermal
effects
such
as
swelling
and
rash.
It
is
difficult
to
draw
any
conclusions
on
such
a
small
number
of
cases.

Detailed
descriptions
of
36
cases
submitted
to
the
California
Pesticide
Illness
Surveillance
Program
(
1982­
2002)
were
reviewed.
However,
in
just
four
of
these
cases
was
sodium
chlorate
determined
to
be
the
primary
cause
of
illness
and
all
four
occurred
in
an
agricultural
setting
(
three
in
cotton
fields,
one
unknown).
Two
of
these
cases
were
classified
as
systemic
and
one
each
involved
skin
or
eye
effects.
The
two
systemic
cases
involved
applicators;
one
with
nausea
and
the
other
with
nausea,
headache,
and
itching
skin
after
spraying
for
one
week.
Both
of
these
cases
were
classified
as
possibly
due
to
sodium
chlorate.
The
skin
case
involved
a
worker
exposed
to
drift
from
an
adjacent
field
and
the
eye
case
occurred
when
a
worker
bumped
into
a
spray
nozzle
while
getting
off
the
tractor
and
was
splashed
in
the
face.
The
skin
case
was
classified
as
probably,
and
the
eye
case
as
definitely
due
to
sodium
chlorate.

5.2
Other
A
number
of
suicidal
ingestions
of
sodium
chlorate
have
been
reported
in
the
literature.
Many
of
these
have
led
to
death
and
were
summarized
by
Clarkson
(
2001).
The
following
is
taken
from
Clarkson's
review:

Accidental
and
Intentional
Poisoning
The
majority
of
deaths
caused
by
sodium
chlorate
have
been
the
result
of
suicide
(
Mengele
et
al.,
1969;
Motin
et
al.,
1970;
Oliver
et
al.,
1972;
Timperman
and
Maes,
1966).
The
chance
of
ingesting
a
fatal
dose
accidentally
is
small
unless
the
compound
is
mistaken
for
a
drug
and
taken
purposely,
as
Page
41
of
141
occurred
when
the
potassium
salt
mistakenly
was
substituted
for
potassium
chloride
(
Cochran
and
Smith,
1940).
However,
completely
typical,
near­
fatal
poisoning
occurred
when
a
13­
year­
old
boy
"
tasted"
crystals
of
this
weed
killer
which
he
found
in
his
father's
shed.
In
spite
of
intensive
treatment,
recovery
did
not
begin
until
about
the
15th
day
and
required
a
little
over
40
days
(
Starvou
et
al.,
1978).

Dermal
absorption
associated
with
agricultural
use
of
sodium
chlorate
is
not
sufficient
to
cause
systemic
poisoning.
Even
by
mouth,
a
large
dose
is
required
to
produce
illness.
A
6.35%
solution
of
potassium
chlorate
was
long
used
as
a
gargle,
or
a
300­
mg
tablet
was
allowed
to
dissolve
slowly
in
the
mouth
to
treat
pharyngitis
before
modern
antibiotics
became
available.
The
toxicities
of
the
sodium
and
potassium
salts
are
similar.
It
was
considered
that
a
dose
of
10,000
mg
was
fatal
(
Cochrane
ad
Smith,
1940;
Sollman,
1957).
The
smallest
recorded
fatal
dose
was
7500
mg
(
Bernstein,
1930).
However,
vigorous
treatment
saved
one
person
who
had
ingested
about
40,000
mg
(
Knight
et
al.,
1967).
Page
42
of
141
6.0
Exposure
Characterization/
Assessment
6.1
Dietary
Exposure/
Risk
Pathway
Dietary
exposure
(
food
only)
to
inorganic
chlorates
as
the
chlorate
ion
(
ClO
3
b
)
may
be
expected
from
the
following
dietary
exposure
routes:
(
1)
from
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
used
on
food
crops;
(
2)
from
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
pesticides
used
on
food
crops
or
in
poultry
premises;
(
3)
from
secondary
residues
in
meat/
milk/
poultry/
eggs
due
to
residues
in
animal
feedstuffs;
(
4)
from
sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
as
inert
ingredients
in
antimicrobial
agents
used
as
fruit,
vegetable,
and
egg
sanitizing
washes,
on
mushrooms
to
control
bacterial
blotch,
as
treatments
to
seed
used
for
sprouting,
for
conditioning
live
oysters,
in
poultry
drinking
water,
in
fish
filleting,
and
in
pecan
cracking/
dyeing;
(
5)
as
a
potential
redox
of
chlorine
dioxide
and
sodium
chlorite
in
conventional
and
antimicrobial
pesticides;
(
6)
from
degradation
of
hypochlorites
in
antimicrobial
agents
used
as
fruit
and
vegetable
washes;
and,
(
7)
from
translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses.

No
food
monitoring
data
are
available
for
this
risk
assessment;
only
limited,
chemical­
specific
field
trial
data
are
available.
Exposure
estimates
in
food
were
based
on
field
trial
data
or,
in
the
case
of
fruit/
vegetable/
other
washes,
was
derived
from
a
film
thickness
model.
No
chemical­
specific
livestock
metabolism
or
feeding
data
are
available;
exposure
estimates
in
meat,
milk,
poultry,
and
eggs
were
derived
from
rat
metabolism
data,
field
trial
data,
and
livestock
reference
information
concerning
feed
consumption,
tissue
weights,
and
milk
production.
In
some
cases,
due
to
raw
data
limitations,
food
exposure
estimates
are
calculated
as
sodium
chlorate.
Default
concentration
factors
(
no
chemical­
specific
processing
data
are
available),
percent
crop
treated
data
(
chronic
(
non­
cancer)
and
cancer
assessments
only),
and
the
effects
of
washing
after
foliar
treatments
were
also
incorporated
into
the
risk
assessments.

6.1.1
Residue
Profile
Sodium
chlorate
is
currently
registered
for
preharvest
and
foliar
applications
as
a
defoliant
or
desiccant
to
the
following
food/
feed
crops:
dry
beans,
corn,
cotton,
flax,
guar,
chili
peppers,
potatoes,
rice,
safflower,
sorghum
(
grain),
southern
peas
(
i.
e.,
cowpeas),
soybeans,
and
sunflowers.
For
food/
feed
uses,
sodium
chlorate
is
formulated
as
a
soluble
concentrate
(
SC)
with
the
active
ingredient
ranging
from
18%
to
47.2%.
Sodium
chlorate
may
be
applied
using
aircraft
or
ground
spray
equipment,
including
high
and
low
volume
equipment.

Uses
of
sodium
chlorate
as
a
defoliant
or
desiccant
on
cauliflower,
cucurbit
vegetables,
and
okra
grown
for
seed
only
are
considered
non­
food
uses.
Uses
of
sodium
chlorate
on
ornamental
gourds
and
fallow
lands
are
also
considered
non­
food
uses.
These
non­
food
uses
will
not
be
discussed
further
with
regards
to
residue
chemistry
or
dietary
exposure/
risk
considerations.
Page
43
of
141
Under
40
CFR
180.1020
(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
in
or
on
the
following
raw
agricultural
commodities
when
used
as
a
defoliant,
desiccant,
or
fungicide
in
accordance
with
good
agricultural
practice:
beans
(
dry,
edible),
corn
(
fodder),
corn
(
forage),
corn
(
grain),
cottonseed,
flaxseed,
flax
(
straw),
guar
beans,
peas
(
southern),
peppers
(
chili),
potatoes,
rice,
rice
(
straw),
safflower
(
grain),
sorghum
(
grain),
sorghum
(
fodder),
sorghum
(
forage),
soybeans
and
sunflower
seed.

Under
40
CFR
180.1020
(
b)
A
time­
limited
exemption
from
the
requirement
of
a
tolerance
is
established
for
residues
of
the
defoliant/
desiccant
in
connection
with
use
of
the
pesticide
under
section
18
emergency
exemptions
granted
by
EPA.
This
exemption
has
been
granted
for
wheat
and
will
expire
on
12/
31/
04.
As
requested
by
the
Registration
Division
(
Sodium
Chlorate
Use
Closure
Memo
Amendment;
J.
Guerry;
dated
11/
15/
2004)
the
use
of
sodium
chlorate
on
wheat
is
also
addressed
herein
with
the
intention
to
convert
the
time­
limited
exemption
status
to
a
permanent
exemption
from
the
requirement
of
a
tolerance
under
40
CFR.
1020
(
a).
The
proposed
use
rate
is
for
a
single
application
of
sodium
chlorate
to
wheat
at
6
lbs
ai/
A
with
a
3­
day
PHI.

No
plant
metabolism
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
plant
metabolism
data
are
required
to
support
the
established
sodium
chlorate
tolerance
exempts.
Based
on
available
published
information
(
Loomis
et
al.,
J.
Am.
Soc.
Agron.;
25,
724
(
1933)),
sodium
chlorate
is
highly
soluble
in
water
and
is
expected
to
readily
absorb
and
translocate
throughout
plants.
However,
given
the
proposed
use
conditions,
the
means
of
translocation
in
treated
plants
may
be
substantially
disrupted.
Translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses
may
occur.
Terminal
residues
are
expected
to
be
primarily
surface
residues.

Since
sodium
chlorate
is
a
strong
oxidizing
agent,
depending
on
environmental
factors,
it
is
expected
to
be
easily
reduced
to
chloride
and
possibly
chlorite
in
plants.
Total
redox
conversion
to
these
reduced
species
is
not
expected;
hence,
the
terminal
residues
of
sodium
chlorate
in/
on
plants
are
likely
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).

No
ruminant,
swine,
or
poultry
metabolism
or
feeding
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
animal
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
published
rat
metabolism
data
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985),
terminal
residues
of
sodium
chlorate
in
animal
tissues
are
expected
to
be
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
as
chlorate,
chlorite,
and
chloride
in
urine
primarily
and
feces.
Within
72
hours,
about
40%
of
the
administered
dose
was
excreted
in
the
urine
as
chlorate
(
ca.
13%),
chlorite
(
ca.
4%),
and
chloride
(
ca.
20%)
and
about
2­
4%
was
excreted
in
the
feces
in
the
same
time
period.
Less
than
1%
of
the
administered
dose
was
found
in
any
of
the
tissues
analyzed
including
kidney,
liver,
and
skin.
Page
44
of
141
Although
some
previous
residue
chemistry
reviews
for
specific
exemptions
from
the
requirement
of
a
tolerance
have
concluded
that
there
is
no
reasonable
expectation
of
transfer
of
residues
to
meat,
milk,
poultry
or
eggs
in
specific
cases,
re­
evaluation
of
the
available
crop
field
trial
data
taken
as
a
whole,
indicate
that
there
is
the
possibility
of
detectable
residues
of
sodium
chlorate
on
animal
feedstuffs
at
harvest.
Hence,
secondary
residues
of
concern
in
meat,
milk,
poultry,
and
eggs
are
possible
and;
therefore,
new
ruminant
and
poultry
feeding
data
are
hereby
required
to
support
the
reregistration
of
sodium
chlorate.
These
data
are
considered
confirmatory.

The
analytical
method
used
to
support
the
established
exemptions
from
the
requirement
of
a
tolerance
is
a
non­
specific
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection.
The
method
was
originally
developed
to
estimate
residual
chlorate
concentrations
in
soil
and
as
a
rapid
diagnostic
test
for
chlorate
toxicity
in
plants.
Briefly,
the
method
involves
acid
extraction,
clean­
up
by
shaking
with
activated
charcoal,
and
filtration.
A
solution
of
ortho­
toluidine
in
HCl
is
then
added
to
the
concentrated
extract
and
the
resulting
color
is
measured
at
448
nm
for
low
concentrations
and
at
490
nm
for
higher
concentrations
of
dye.
The
method
is
not
specific
for
chlorate
since
it
measures
any
oxidizing
agent
capable
of
oxidizing
chloride
ion
to
free
chlorine.
A
standard
curve
is
prepared
with
sodium
chlorate
for
comparison.
The
lowest
sensitivity
of
the
method
is
estimated
at
1
ppm
based
on
available
fortification
data
from
field
trials.
Chloride
does
not
interfere
with
the
method
but
residues
of
chlorite,
which
might
be
present,
may
also
be
detected
with
this
method.
This
method
is
hereby
deemed
adequate
for
enforcement
of
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
[
Note:
If
needed,
a
more
selective
HPLC
method
("
Determination
of
Residues
of
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
is
available
for
the
detection
of
sodium
chlorate
residues
in
or
on
raw
agricultural
commodities
(
RACs).]

New
reference
standards
must
be
supplied
to
the
EPA
National
Pesticide
Standards
Repository.

Only
crop
field
trial
data
have
been
submitted
to
support
the
reregistration
of
sodium
chlorate.
No
storage
stability
or
processing
data
are
available.
The
available
crop
field
trial
data
have
been
re­
evaluated
herein.
No
additional
plant
magnitude
of
the
residue
or
storage
stability
data
are
required
to
support
the
reregistration
of
sodium
chlorate.
Available
crop
field
trial
data
deemed
the
primary
sources
of
information
to
support
the
reregistration
of
sodium
chlorate
are
briefly
discussed
below
and
summarized
in
Table
C.
5.
All
other
available
crop
field
trial
data
are
considered
supplemental
and
will
not
be
discussed
further.

The
subject
data,
except
the
potato
tuber
data,
were
all
collected
using
the
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection
and
enforcement
of
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
The
potato
tuber
data
were
collected
with
a
more
selective
HPLC
method
("
Determination
of
Residues
of
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
deemed
adequate
for
data
collection.
The
lowest
limits
of
quantitation
(
LOQs)
of
these
methods
is
estimated
at
1
ppm.
Page
45
of
141
Based
on
the
available
flax,
guar,
southern
pea,
soybean,
and
sunflower
field
trial
data
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
dry
beans,
guar
beans,
southern
peas,
soybeans,
flaxseed,
safflower
seed,
and
sunflower
seed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
dry
beans,
guar,
southern
peas,
soybeans,
flax,
safflower,
and
sunflower
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI).
Furthermore,
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
cottonseed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
cotton
(
2
applications,
7.5
lbs
ai/
A/
application;
7­
day
PHI).
Any
residues
which
might
be
detected
at
the
point
of
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
prior
to
the
point
of
consumption.

Based
on
the
available
chili
pepper
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
13
ppm)
might
be
found
on
the
surface
of
unwashed
chili
peppers
treated
with
sodium
chlorate
at
the
maximum
use
rate
of
sodium
chlorate
on
chili
peppers
(
1
application;
12.5
lbs
ai/
A/
application;
10­
day
PHI).
However,
these
residues
are
primarily
surface
residues
present
at
the
point
of
harvest
which
would
be
substantially
removed
by
washing
(<
1
ppm)
prior
to
the
point
of
consumption.

Based
on
the
available
potato
field
trial
data,
no
detectable
residue
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
potato
tubers
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
potatoes
(
1
application;
12.5
lbs
ai/
A;
7­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
consumption.

Based
on
the
available
oat,
rice,
sorghum,
and
wheat
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
70
ppm
(
maximum)
as
demonstrated
by
sorghum
grain)
might
be
found
on
the
surface
of
cereal
grains
retaining
their
outer
hulls
at
harvest
(
such
as
oats
and
sorghum)
from
the
maximum
use
rate
of
sodium
chlorate
on
rice
and
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
and
wheat
(
1
application;
6
lbs
ai/
A;
3­
day
PHI).
However,
once
the
outer
hulls
are
removed
(
either
at
harvest
or
during
processing),
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
cereal
grains
such
as
rice
and
wheat
(
as
demonstrated
by
rice
w/
out
hulls
and
wheat
grain
data).

Based
on
the
available
sorghum
field
trial
data
alone,
maximum
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
for
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
70
ppm.
On
average,
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
on
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
40
ppm.

Translating
the
available
sorghum
field
trial
data
to
corn,
residues
of
sodium
chlorate
are
not
expected
to
exceed
20
ppm
(
ca.
10
ppm
on
average)
in/
on
corn
grain
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
corn
(
1
application,
7.5
lbs
ai/
A;
14­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
Page
46
of
141
consumption.
Hence,
residues
of
sodium
chlorate
in/
on
sweet
corn
after
washing
and
prior
to
consumption
would
not
be
expected
to
exceed
1
ppm.

Based
on
the
available
straw
(
flax,
oat,
wheat,
rice)
and
forage
(
guar
plants,
sorghum
stalks,
soybean
forage)
data,
maximum
residues
of
sodium
chlorate
in/
on
straw
and
forage
livestock
feedstuffs
harvested
3­
7
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application)
are
not
expected
to
exceed
300
ppm
at
the
point
of
harvest.
On
average,
residues
in/
on
straw
and
forage
livestock
feedstuffs
should
not
exceed
100
ppm
when
harvested
7­
14
days
after
foliar
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application).

The
highest
average
residues
of
chlorate
(
excluding
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
expected
to
be
<
4
ppm
and
in
milk
are
expected
to
be
<
0.5
ppm
based
on
the
following
information
and
assumptions:

°
The
highest
average
theoretical
dietary
burden
for
livestock
is
175
ppm
for
cattle
feed
on
a
dry
wt.
basis
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
1600
mg
per
day
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
16
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Highest
Average
Theoretical
Dietary
Exposure
(
1600
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Highest
Average
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
4
ppm
Highest
Average
Residue
Estimate
in
Milk
=
<
0.5
ppm
The
maximum
residues
of
chlorate
(
excluding
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
expected
to
be
<
12
ppm
and
in
milk
are
expected
to
be
<
2
ppm
based
on
the
following
information
and
assumptions:
Page
47
of
141
°
The
maximum
theoretical
dietary
burden
for
livestock
is
500
ppm
for
cattle
feed
on
a
dry
wt.
basis
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
4600
mg
per
day
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
46
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Maximum
Theoretical
Dietary
Exposure
(
4600
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Maximum
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
12
ppm
Maximum
Residue
Estimate
in
Milk
=
<
2
ppm
Page
48
of
141
6.1.2
Chronic
(
non­
cancer)
Dietary
(
food
only)
Exposure
and
Risk
A
chronic
(
non­
cancer)
dietary
risk
assessment
was
conducted
for
all
potential
chlorate
dietary
exposure
routes,
using
the
Dietary
Exposure
Evaluation
Model­
FCID
 
software
with
the
Food
Commodity
Intake
Database
(
DEEM­
FCID
 
Version
2.03)
and
food
consumption
data
from
the
United
States
Department
of
Agriculture's
(
USDA's)
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII)
from
1994­
1996
and
1998.
In
this
analysis
the
chronic
dietary
exposure
and
risk
estimates
resulting
from
food
intake
were
determined
for
the
general
U.
S.
population
and
various
population
subgroups.

No
food
monitoring
data
are
available
for
this
risk
assessment;
only
limited,
chemical­
specific
field
trial
data
are
available.
Exposure
estimates
in
food
were
based
on
field
trial
data
or,
in
the
case
of
fruit/
vegetable/
other
washes,
was
derived
from
a
film
thickness
model.
No
chemical­
specific
livestock
metabolism
or
feeding
data
are
available;
exposure
estimates
in
meat,
milk,
poultry,
and
eggs
were
derived
from
rat
metabolism
data,
field
trial
data,
and
livestock
reference
information
concerning
feed
consumption,
tissue
weights,
and
milk
production.
In
some
cases,
due
to
raw
data
limitations,
food
exposure
estimates
are
calculated
as
sodium
chlorate.
Default
concentration
factors
(
no
chemical­
specific
processing
data
are
available)
and
the
effects
of
washing
after
foliar
treatments
were
also
incorporated
into
the
risk
assessment.
Percent
crop
treated
data
were
used
in
this
analysis.
Exposures
were
single
point
estimates.

The
chronic
(
non­
cancer)
dietary
(
food
only)
risk
assessment
is
below
the
Agency's
level
of
concern
for
the
General
U.
S.
Population
and
all
subgroups.
The
highest
exposed
population
subgroup,
Children
1­
2
years
of
age,
was
28%
of
the
chronic
Population
Adjusted
Dose
(
cPAD).
See
Table
6.1.2
below
for
details.

Table
6.1.2.
Summary
of
Chronic
(
non­
cancer)
Dietary
(
food
only)
Exposure
and
Risk
for
Inorganic
Chlorates
Population
Subgroup
cPAD
a
mg/
kg/
day
%
cPAD
General
U.
S.
Population
0.03
9
All
Infants
(<
1
yr)
15
Children
1­
2
yrs
28
Children
3­
5
yrs
23
Children
6­
12
yrs
14
Youth
13­
19
yrs
8
Adults
20­
49
yrs
7
Adults
50+
yrs
6
Females
13­
49
yrs
7
a
The
BMDL
is
0.9
mg
chlorate/
kg/
day.
The
level
of
concern
for
the
Margin
of
Exposure
(
MOE)
is
30.
Page
49
of
141
6.1.3
Cancer
Dietary
(
food
only)
Exposure
and
Risk
A
cancer
dietary
risk
assessment
was
conducted
for
all
potential
chlorate
dietary
exposure
routes,
using
the
same
dietary
(
food
only)
exposure
estimates
used
in
the
chronic
(
non­
cancer)
dietary
risk
assessment
for
the
U.
S.
Population,
with
a
9%
cPAD.

Note:
Sodium
chlorate
is
a
thyroid
toxicant
producing
thyroid
gland
follicular
cell
hypertrophy
in
rats
and
mice
following
chronic
exposures
and
some
evidence
of
follicular
cell
tumors
in
rats.
The
lack
of
mutagenicity
indicates
that
the
thyroid
tumors
are
induced
by
a
non­
mutagenic
mechanism.
Therefore,
for
the
purposes
of
this
risk
assessment,
the
Margin
of
Exposure
(
MOE)
approach
is
used
to
estimate
inorganic
chlorate
cancer
risk.
Children
are
not
expected
to
be
more
susceptible
to
chlorate­
induced
thyroid
effects
than
adults
and
the
endpoint
selected
for
the
thyroid
effects
is
protective
for
all
populations,
including
children.

6.2
Water
Exposure/
Risk
Pathway
6.2.1
Environmental
Fate
Sodium
chlorate
is
used
as
a
desiccant/
defoliant
because
it
is
a
strong
oxidizer.
As
a
strong
oxidizing
agent,
chlorate
(
ClO
3
b
,
oxidation
state
V)
gets
reduced
to
chlorine
species
in
lower
oxidation
states,
such
as
the
oxyanions
chlorite
(
ClO
2
b
,
oxidation
state
III)
and
hypochlorite
(
ClO
b
,
oxidation
state
I),
chlorine
dioxide
(
oxidation
state
IV),
and
chloride
(
oxidation
state
­
I).
Thus,
at
least
some
and
possibly
substantial
reduction
of
the
applied
chlorate
is
likely
to
occur
in
the
field
prior
to
any
runoff
to
surface
water.
Under
environmental
(
terrestrial
field)
redox
conditions
and
based
on
chemical
equilibria
alone,
the
thermodynamically
favored,
end
reduction
product
of
chlorate
in
soil
and
in
water
is
the
chloride
anion.
Any
intermediate
chlorine
dioxide
that
may
form
under
environmental
conditions
will
undergo
photochemical
reactions
when
exposed
to
sunlight.
The
chlorine
oxyanions
chlorite
and
hypochlorite
(
other
possible
more
reduced
intermediates
in
the
ultimate
reduction
of
chlorate
to
chloride)
are
strong
oxidizers
in
themselves
and
thus,
they
are
also
reduced
and/
or
undergo
disproportionation
reactions.
Although
reduction
reactions
of
chlorate,
chlorite,
and
hypochlorite
are
said
to
occur
"
very
fast",
how
fast
they
occur
is
not
known
(
i.
e.,
the
actual
rate
constants
in
the
environment
are
not
known).
Therefore,
at
any
given
time
the
distribution
of
reduced
species
(
type
and
concentration)
cannot
be
estimated.
However,
it
is
unlikely
that
a
single
reduced
species
would
be
present.

6.2.2
Drinking
Water
Page
50
of
141
6.2.2.1
Sources
and
Control
of
Chlorate
Ion
Chlorate
ion
(
ClO
3
b
)
is
primarily
present
in
drinking
water
as
a
result
of
the
use
of
chlorine
dioxide
or
hypochlorite
solutions
for
oxidation/
disinfection
in
the
treatment
process.
It
may
also
be
present
in
the
untreated
source
water,
but
the
ClO
3
b
concentrations
contributed
to
drinking
water
by
ambient
water
are
generally
much
lower
than
those
resulting
from
the
treatment
process.

The
American
Water
Works
Association
(
AWWA)
Disinfection
Systems
Committee
tracks
disinfection
practices
in
US
community
water
systems.
Their
most
recent
comprehensive
survey
(
completed
in
1998)
estimated
that
approximately
20%
of
the
systems
serving
populations
greater
than
10,000
use
sodium
hypochlorite
(
2%
generated
it
on­
site),
8%
use
chlorine
dioxide,
and
<
1%
use
calcium
hypochlorite.
(
AWWA,
2000a)
For
systems
serving
populations
less
than
10,000,
the
survey
estimated
that
approximately
34%
use
sodium
hypochlorite,
none
use
chlorine
dioxide,
and
at
least
4.5%
use
calcium
hypochlorite.
(
AWWA,
2000b)

Chlorine
Dioxide:
The
use
of
chlorine
dioxide
can
introduce
ClO
3
b
into
the
finished
water
by
several
routes.
Drinking
water
plants
generally
use
sodium
chlorite
as
a
starting
material
in
the
production
of
chlorine
dioxide.
Chlorate
ion
may
be
present
as
a
contaminant
in
the
feedstock
material
(
usually
less
than
four
percent
of
the
active
chlorite
is
chlorate).
A
typical
range
of
ClO
3
b
carryover
to
the
finished
water
from
chlorite
feedstock
contamination
is
about
50
µ
g/
L
for
a
1­
mg/
L
dose
of
chlorine
dioxide.
(
Gates,
1998)
Technology
to
generate
chlorine
dioxide
using
sodium
chlorate
is
now
available
to
the
drinking
water
industry,
which
introduces
the
possibility
of
ClO
3
b
carryover
to
the
finished
water
from
the
chlorate
feedstock.

Chlorate
ion
may
also
be
produced
due
to
inefficient
generation
of
chlorine
dioxide.
Excess
chlorine
will
favor
the
production
of
ClO
3
b
over
chlorine
dioxide,
as
will
keeping
the
generator
mixtures
at
highly
alkaline
(
pH
>
11)
or
acidic
(
pH
<
3)
conditions.
If
the
concentrations
of
feedstock
reactants
are
too
low
or
too
much
dilution
water
is
added
during
the
reaction,
ClO
3
b
formation
is
also
favored.

Chlorite
ion
(
ClO
2
b
)
is
a
major
degradation
product
resulting
from
the
reaction
of
chlorine
dioxide
with
inorganic
and
organic
constituents
in
the
water.
When
free
chlorine
is
used
after
the
application
of
chlorine
dioxide
in
the
treatment
process,
ClO
2
b
is
oxidized
to
ClO
3
b
.
This
conversion
will
continue
over
time
as
the
water
travels
through
the
distribution
system.
Chlorate
ion
is
also
formed
by
photodecomposition
of
chlorine
dioxide
when
treated
water
is
exposed
to
bright
sunlight
in
open
basins.

The
primary
ways
in
which
water
systems
can
control
the
levels
of
ClO
3
b
in
the
finished
water
is
through
high
efficiency
operation
of
their
chlorine
dioxide
generators
and
by
reducing
ClO
2
b
concentrations
prior
to
the
addition
of
free
chlorine.
Careful
control
of
the
generation
process
minimizes
ClO
3
­
formation.
Ferrous
ion,
which
is
a
coagulant
aid,
can
be
used
to
convert
ClO
2
b
to
chloride
ion
and
thus
prevent
it
from
reacting
with
free
chlorine
to
form
ClO
3
b
.
Page
51
of
141
Hypochlorite:
Some
water
systems
use
sodium
hypochlorite
or
calcium
hypochlorite
as
their
source
of
free
chlorine.
Chlorate
ion
can
be
formed
in
these
products
during
the
manufacturing
process,
but
the
decomposition
of
hypochlorite
solutions
during
storage
is
the
more
significant
source
of
ClO
3
b
in
systems
using
hypochlorite.
Sodium
hypochlorite
is
usually
purchased
as
a
solution,
and
ClO
3
b
concentrations
increase
between
the
time
of
manufacture
and
delivery
to
the
water
plant.
Calcium
hypochlorite
is
a
solid,
and
thus
ClO
3
b
concentrations
don't
increase
until
calcium
hypochlorite
solutions
are
prepared
for
use
at
the
water
treatment
plant.

The
rate
at
which
hypochlorite
ion
(
OCl
b
)
disproportionates
to
ClO
3
b
is
influenced
by
concentration
of
OCl
b
,
pH,
and
temperature.
The
rate
of
decomposition
increases
as
the
concentration
of
OCl
b
increases,
so
water
systems
can
use
dilution
as
one
control
strategy.
The
pH
should
be
in
the
12
to
13
range
to
minimize
decomposition;
a
pH
below
11
greatly
increases
the
rate
of
decomposition.
Hypochlorite
solutions
should
be
protected
from
high
temperatures
and
sunlight.
Storage
time
should
be
minimized;
both
from
the
time
of
manufacture
to
delivery
and
from
the
time
of
delivery
to
use.

6.2.2.2
Chlorate
Ion
Occurrence
Data
Data
on
the
occurrence
of
ClO
3
b
in
drinking
water
are
available
from
two
primary
sources:
the
Information
Collection
Rule
(
ICR)
Auxiliary
1
Database,
Version
5.0
(
USEPA,
2000)
and
the
AwwaRF
research
study
on
the
control
of
ClO
3
b
in
hypochlorite
solutions
(
Gordon
et
al,
1995).

Information
Collection
Rule:
The
most
extensive
data
on
the
occurrence
of
ClO
3
b
in
drinking
water
is
from
the
ICR
(
USEPA,
1996).
Source
water
and
drinking
water
were
monitored
for
ClO
3
b
between
July
1997
and
December
1998.
Water
systems
serving
a
population
of
at
least
100,000
were
required
to
monitor
for
ClO
3
b
at
treatment
plants
using
chlorine
dioxide
or
hypochlorite
solutions
in
the
treatment
process.
Plants
using
chlorine
dioxide
collected
monthly
samples
of
the
source
water
entering
the
plant,
the
finished
water
leaving
the
plant,
and
at
three
sample
points
in
the
distribution
system
(
near
the
first
customer,
an
average
residence
time
and
a
maximum
residence
time).
Plants
using
hypochlorite
solutions
were
only
required
to
collect
quarterly
samples
of
the
water
entering
and
leaving
the
plant.
If
chlorine
dioxide
or
hypochlorite
solutions
were
used
intermittently
at
a
plant,
ClO
3
b
samples
were
only
required
in
sample
periods
in
which
they
were
in
use.

Chlorine
dioxide
was
used
by
22
water
systems
(
29
treatment
plants)
during
at
least
one
of
the
18
monthly
ICR
sampling
periods.
Data
from
413
samples
collected
at
the
entry
point
to
the
distribution
system
showed
ClO
3
b
concentrations
ranging
from
<
20
µ
g/
L
to
1,600
µ
g/
L.
The
ClO
3
b
concentrations
ranged
from
<
20
µ
g/
L
to
2,200
µ
g/
L
in
the
1084
samples
collected
in
the
distribution
system.
The
distribution
of
average
ClO
3
b
concentrations
calculated
for
each
treatment
plant
and
sample
point
are
summarized
in
Table
6.2.2.2.1.
The
distribution
system
average
concentrations
determined
for
each
water
plant
by
averaging
the
data
from
the
three
distribution
system
sample
points
are
summarized
in
the
last
column
of
Table
6.2.2.2.1.
The
median
distribution
system
average
concentration
is
129
µ
g/
L
with
a
range
from
<
20
µ
g/
L
to
691
µ
g/
L.
Page
52
of
141
Sodium
hypochlorite
solutions
were
in
use
in
44
water
systems
(
61
treatment
plants)
during
the
six
quarterly
ICR
sampling
periods.
(
None
of
the
systems
reported
using
calcium
hypochlorite
as
the
source
of
their
chlorine
solutions.)
Data
from
312
samples
were
reported
with
concentrations
ranging
from
<
20
µ
g/
L
to
a
maximum
of
1,400
µ
g/
L.
The
average
ClO
3
b
concentration
in
the
finished
drinking
water
for
each
treatment
plant
ranged
from
<
20
µ
g/
L
to
502
µ
g/
L
with
a
median
concentration
of
99
µ
g/
L.
The
table
below
summarizes
the
distribution
of
average
ClO
3
b
concentrations
calculated
for
each
plant.

Table
6.2.2.2.1.
Chlorate
Concentrations1
(
µ
g/
L)
­
ICR
Data
Hypochlorite
Plants
Chlorine
Dioxide
Plants
Combined
Hypochlorite
and
Chlorine
Dioxide
Plants
10th
Percentile
23
56
24
20th
Percentile
37
77
53
50th
Percentile
99
119
108
80th
Percentile
155
195
179
90th
Percentile
239
226
242
Maximum
502
687
691
#
WTPs
61
29
90
#
PWSs
44
22
66
1The
average
chlorate
concentration
was
calculated
for
each
sample
point
at
each
water
treatment
plant
(
WTP)
over
the
entire
ICR
monitoring
program.
The
distribution
of
these
averages
is
presented
in
this
table.
2The
distribution
system
average
chlorate
concentration
was
calculated
for
each
WTP
using
the
three
distribution
system
sample
points.
The
distribution
of
these
averages
is
presented
in
this
column.

AwwaRF
Hypochlorite
Project:
The
American
Water
Works
Association
Research
Foundation
sponsored
a
project
to
study
how
water
systems
could
minimize
ClO
3
b
formation
in
the
hypochlorite
solutions
they
use
for
disinfection.
As
part
of
the
data
gathering
effort,
they
obtained
information
from
185
water
systems
concerning
their
use
of
hypochlorite
solutions.
Samples
of
source
water,
hypochlorite
solution,
and
finished
drinking
water
from
111
of
the
water
systems
were
analyzed
for
ClO
3
b
.
Only
one
set
of
samples
was
collected
for
each
system.

Background
information
on
the
subset
of
111
water
systems
that
provided
samples
was
not
reported
separately
from
the
185
systems
who
answered
the
questionnaire.
Therefore,
the
ClO
3
b
Page
53
of
141
concentrations
cannot
be
directly
related
to
the
size
of
the
water
system
or
type
of
hypochlorite
solution
in
use.
However,
73.5
%
of
the
systems
who
responded
to
the
questionnaire
served
populations
less
than
100,000
with
a
subset
of
66%
serving
populations
less
than
10,000.
There
is
a
possibility
that
a
few
systems
using
calcium
hypochlorite
were
sampled
in
the
AwwaRF
project,
since
13%
of
the
185
systems
reported
using
calcium
hypochlorite
and
85%
reported
using
sodium
hypochlorite.

The
ClO
3
b
concentrations
reported
in
the
finished
water
are
summarized
in
Table
2.
The
median
concentration
in
the
finished
water
is
161
µ
g/
L.
The
distribution
of
ClO
3
b
is
shown
below
in
Table
6.2.2.2.2.
The
ClO
3
b
concentrations
in
the
hypochlorite
solutions
used
to
treat
the
water
ranged
from
0.03
to
113
g/
L.

Table
6.2.2.2.2.
Chlorate
Concentrations
­
AwwaRF
Project
(
PWSs
using
Hypochlorite
Solutions)
1
Finished
Water
Chlorate
Concentration
(
µ
g/
L)

Minimum
<
10
10th
Percentile
15
20th
Percentile
41
50th
Percentile
161
80th
Percentile
611
90th
Percentile
1,160
Max
9,180
#
PWSs
111
#
States
13
1
A
single
sample
was
collected
from
each
of
the
public
water
systems
(
PWSs)
in
the
survey.

6.2.2.3
Chronic
Exposure
to
Chlorate
Ion
The
ICR
data
were
collected
from
systems
suspected
of
having
ClO
3
b
contamination
due
to
the
treatment
process
in
use.
It
is
reasonable
to
assume
that
there
were
not
significant
ClO
3
b
levels
in
the
systems
in
the
same
size
category
that
were
not
sampled.
This
is
based
on
earlier
drinking
water
studies
that
found
ClO
3
b
concentrations
in
source
water
were
too
low
to
impact
the
levels
in
drinking
water
on
the
same
scale
as
treating
the
water
with
either
chlorine
dioxide
or
hypochlorite
(
Bolyard
et
al,
1993).
Page
54
of
141
The
ICR
data
confirm
the
presence
of
ClO
3
b
in
source
water
(
75
of
744
samples
of
water
entering
the
treatment
plants
contained
measurable
ClO
3
b
),
but
also
demonstrate
that
the
concentrations
are
generally
very
low,
can
vary
considerably
over
time
at
the
same
sample
site,
and
are
minor
compared
to
those
observed
from
chlorine
dioxide
or
hypochlorite
use.
Data
were
reported
from
105
treatment
plant
influent
sample
points
in
the
ICR
and
samples
from
33
of
those
sites
contained
ClO
3
b
concentrations
of
20
µ
g/
L
or
greater.
Chlorate
concentrations
were
reported
in
influent
samples
from
both
surface
and
ground
water
sources.
Samples
from
fifteen
of
the
33
sites
contained
measurable
ClO
3
b
in
more
than
one
sampling
period,
but
with
one
exception,
the
concentrations
were
all
#
120
µ
g/
L;
70%
were
between
20
and
50
µ
g/
L.
One
influent
water
had
a
ClO
3
b
concentration
of
944
µ
g/
L
in
one
sample
period,
but
the
concentrations
were
#
100
µ
g/
L
in
the
other
sample
periods.
Three
influent
waters
contained
a
high
ClO
3
b
concentration
(
1,300
to
1,600
µ
g/
L)
in
one
sample
period
and
none
in
the
other
sample
periods.
The
ICR
data
indicate
that
the
influence
of
source
water
ClO
3
b
(
as
reflected
by
the
influent
samples)
on
the
concentrations
in
finished
drinking
water
is
minimal
compared
to
the
contribution
from
using
chlorine
dioxide
or
hypochlorite
solutions
in
the
treatment
process.

The
ICR
data
set
provides
the
best
available
estimate
of
long
term
exposure
to
ClO
3
b
from
drinking
water,
because
multiple
samples
were
collected
over
an
18
month
period.
Only
systems
serving
populations
of
at
least
100,000
were
sampled
during
the
ICR.
Even
though
this
size
category
includes
roughly
one
percent
of
the
total
number
of
drinking
water
systems
in
the
United
States,
it
serves
almost
60
percent
of
the
population.
During
the
ICR,
there
were
296
water
systems
in
this
size
category;
7%
used
chlorine
dioxide
and
15%
used
hypochlorite
solutions.

When
chlorine
dioxide
is
the
source
of
ClO
3
b
in
drinking
water,
it
is
appropriate
to
use
the
average
concentration
in
the
distribution
system
to
estimate
exposure.
This
is
because
the
concentration
is
expected
to
change
within
the
system
due
to
the
conversion
of
ClO
2
b
to
ClO
3
b
in
the
presence
of
chlorine.
Fifty
percent
of
the
chlorine
dioxide
plants
had
average
distribution
system
ClO
3
b
concentrations
of
#
129
µ
g/
L.
Ninety
percent
had
concentrations
#
264
µ
g/
L.

The
average
ClO
3
b
concentration
at
the
entry
point
to
the
distribution
system
can
be
used
to
estimate
exposure
when
hypochlorite
solutions
are
the
source
of
the
ClO
3
b
contamination.
No
additional
ClO
3
b
is
expected
to
be
formed
in
the
distribution
system.
Fifty
percent
of
the
plants
using
hypochlorite
solutions
had
finished
water
ClO
3
b
concentrations
of
#
99
µ
g/
L.
Ninety
percent
had
concentrations
#
239
µ
g/
L.

The
AwwaRF
data
set
is
much
smaller
than
the
ICR
data
set,
because
the
111
systems
from
13
states
were
only
sampled
once.
Low
levels
of
ClO
3
b
were
measured
in
almost
20%
of
the
source
waters
with
90
percent
of
the
samples
having
concentrations
less
than
35
µ
g/
L.
(
Over
30%
of
the
source
waters
sampled
during
the
ICR
contained
measurable
concentrations
of
ClO
3
b
with
90
percent
having
concentrations
less
than
23
µ
g/
L.)
The
finished
water
ClO
3
b
concentrations
measured
in
the
AwwaRF
study
are
generally
higher
than
those
observed
in
the
ICR.
This
difference
could
be
the
result
of
a
number
of
factors
such
as:
1)
The
AwwaRF
data
represents
a
single
point
in
time
while
the
ICR
data
reflects
an
average
over
18
months;
2)
Most
of
the
Page
55
of
141
AwwaRF
samples
were
collected
from
utilities
that
served
population
of
less
than
100,000,
while
all
of
the
ICR
samples
were
from
utilities
serving
at
least
100,000;
and
3)
Hypochlorite
treatment
practices
may
have
changed
between
when
the
AwwaRF
samples
were
collected
(
1993)
and
the
ICR
samples
were
collected
(
1997­
98).

Section
6.2.2.1
explains
the
mode
of
conversion
of
hypochlorite
ion
(
OCl­)
to
ClO
3
­
for
systems
using
hypochlorite
as
their
source
of
free
chlorine.
The
conversion
is
influenced
by
the
solution
concentration,
pH,
and
ambient
temperature.
For
systems
using
chlorine
dioxide,
ClO
3
­
level
in
the
finished
water
depends
on
concentration
of
chlorate
ion
in
the
feedstock,
the
efficiency
of
chlorine
dioxide
generation,
and
subsequent
disinfection
techniques.
Awareness
of
these
factors
is
critical
in
controlling
chlorate
concentrations
in
finished
water.
Smaller
systems
using
chlorine
dioxide
or
hypochlorite,
those
serving
fewer
than
100,000,
may
be
more
likely
to
have
finished
water
with
higher
levels
of
chlorate
due
to
smaller
budgets
and,
consequently,
fewer
resources
to
devote
to
running
their
systems
or
training
their
staff.
An
untrained
staff
may
not
know,
for
example,
that
when
free
chlorine
is
used
after
the
application
of
chlorine
dioxide,
that
ClO
2
­
is
oxidized
to
ClO
3
­.

Both
the
AwwaRF
study
and
the
ICR
data
reveal
high
concentrations
of
chlorate
ion
to
be
a
local
problem
affecting
a
relatively
small
number
of
systems.
Section
6.2.2.1
outlines
simple
measures
that
systems
of
any
size
can
use
to
maintain
low
levels
of
chlorate
ion
in
finished
drinking
water.

6.2.2.4.
Estimated
Concentrations
of
Chlorate
Ion
Deemed
Appropriate
for
Inclusion
in
the
Dietary
Risk
Assessment(
s)

Based
on
the
available
occurrence
data
(
essentially
at
the
tap)
from
the
ICR
AUX1
Database
(
USEPA,
2000d)
and
the
AwwaRF
(
1995)
survey
study,
which
are
discussed
above,
the
following
estimated
concentrations
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
are
deemed
appropriate
for
inclusion
in
the
dietary
risk
assessment
for
inorganic
chlorates:

°
The
highest
annual
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
is
estimated
at
0.69
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).
°
The
90th
percentile
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
is
estimated
at
0.24
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).
°
The
treatment
system
median
average
concentration
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
in
tested
large
treatment
systems
is
estimated
at
0.11
mg/
L
and
is
based
on
the
ICR
AUX1
Database
(
USEPA,
2000d).

Use
of
the
ICR
AUX1
database
could
underestimate
concentrations
in
drinking
water
since
higher
levels
of
chlorate
ion
(
ClO
3
b
)
in
drinking
water
were
found
at
the
small
water
treatment
utilities
sampled
in
the
AwwaRF
(
1995)
project
than
at
the
large
water
treatment
plants
included
in
the
ICR
AUX1
Database
(
USEPA,
2000d).
However,
the
AwwaRF
(
1995)
survey
study
is
a
less
robust
data
set
consisting
of
only
one
sample
per
utility
and,
therefore,
the
ICR
AUX1
Database
Page
56
of
141
(
USEPA,
2000d)
was
considered
the
more
appropriate
source
for
estimating
averages
from
individual
water
treatment
plants.

Chronic
(
non­
cancer)
dietary
and
cancer
dietary
risk
assessments
for
water
only
were
conducted
using
the
Dietary
Exposure
Evaluation
Model­
FCID
 
software
with
the
Food
Commodity
Intake
Database
(
DEEM­
FCID
 
Version
2.03)
and
food
and
water
consumption
data
from
the
United
States
Department
of
Agriculture's
(
USDA's)
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII)
from
1994­
1996
and
1998.
Available
ICR
and
AwwaRF
monitoring
data
were
used
to
estimate
chlorate
concentrations
in
drinking
water.
Exposures
were
single
point
estimates.

The
chronic
(
non­
cancer)
dietary
risk
assessment
for
chlorate
in
drinking
water
(
highest
annual
average
concentration
estimated
at
0.69
mg/
L)
is
below
the
Agency's
level
of
concern
for
the
General
U.
S.
Population
and
all
subgroups,
except
all
infants
(<
1
year
of
age).
The
highest
exposed
population
subgroup,
all
infants
<
1
year
of
age,
was
159%
of
the
chronic
Population
Adjusted
Dose
(
cPAD).
See
Table
6.2.2.4
below
for
details.

Table
6.2.2.4.
Summary
of
Estimated
Chronic
(
non­
cancer
and
cancer)
Dietary
(
water
only)
Exposure
and
Risk
for
Inorganic
Chlorates
by
Average
Annual
Concentration
in
Large
Drinking
Water
Systemsa
Population
Subgroup
b
cPAD
mg/
kg/
dayc
%
cPAD
Water
Estimated
at
the
Highest
Annual
Average
(
0.69
mg/
L)
Water
Estimated
at
the
90th
Percentile
Annual
Average
(
0.24
mg/
L)
Water
Estimated
at
the
Median
Annual
Average
(
0.11
mg/
L)

General
U.
S.
Population
0.03
49
17
8
All
Infants
(<
1
yr)
159
55
25
Children
1­
2
yrs
72
25
12
Children
3­
5
yrs
67
23
11
Children
6­
12
yrs
47
16
7
Youth
13­
19
yrs
35
12
6
Adults
20­
49
yrs
45
16
7
Adults
50+
yrs
48
17
8
Females
13­
49
yrs
45
16
7
a
The
estimated
exposures
and
risks
are
based
on
the
ICR
data
(
multiple
data
points
per
water
system).
Higher
concentrations
of
chlorate
ion
(
ClO3
­)
in
drinking
water
were
reported
in
the
AwwaRF
data
set
(
only
a
single
data
point
per
water
system),
which
sampled
smaller
water
systems.
b
The
values
for
the
population
with
the
highest
risk
for
each
type
of
risk
assessment
are
bolded.
C
The
BMDL
is
0.9
mg
chlorate/
kg/
day.
The
level
of
concern
for
the
Margin
of
Exposure
(
MOE)
is
30.

The
Office
of
Water
characterizes
the
population
included
in
the
ICR
data
as
follows:
Page
57
of
141
o
"
EPA
collected
data
required
by
the
Information
Collection
Rule
(
ICR)
to
support
future
regulation
of
microbial
contaminants,
disinfectants,
and
disinfection
byproducts.
The
systems
represented
in
the
ICR
database
serve
60%
of
the
US
population.
o
"
Included
in
the
ICR
are
levels
of
chlorate
ion
concentrations
in
the
finished
water
of
these
systems.
The
agency's
level
of
concern
for
chlorate
ion
is
370
ppb.
During
the
ICR,
four
water
treatment
plants
had
average
chlorate
ion
levels
above
the
agency's
level
of
concern
and
represented
0.5%
of
the
ICR
population
(
621,000
persons).
o
"
One
treatment
plant
serving
218,000
persons
had
average
chlorate
ion
concentrations
of
0.69
mg/
L.
This
corresponds
to
0.17%
of
the
ICR
population;
98
percent
of
this
ICR
population
received
finished
water
with
average
chlorate
ion
concentrations
at
or
below
0.2
mg/
L;
93
percent
received
finished
water
with
average
chlorate
ion
concentration
at
or
below
0.1
mg/
L;
and
over
99
percent
receives
finished
water
below
the
Agency's
level
of
concern
of
0.37
mg/
L.
o
"
1
percent
of
the
ICR
population
(
1,260,000
persons)
is
exposed
to
chlorate
concentrations
at
or
greater
than
the
90th
percentile
concentration
of
0.24
mg/
L,
while,
6.5
percent
(
8,490,000
persons)
is
exposed
to
chlorate
concentrations
at
or
greater
than
the
median
concentration
of
0.11
mg/
L.
o
"
The
best
way
for
these
systems
to
lower
the
level
of
chlorate
ion
in
their
finished
water
is
to
implement
the
simple
measures
explained
above."

No
separate
cancer
dietary
risk
assessment
for
chlorate
in
drinking
water
(
lifetime
average
concentration
estimated
at
0.1
mg/
L)
was
conducted.
The
cancer
dietary
risk
assessment
is
based
on
the
chronic
(
non­
cancer)
dietary
risk
assessment
for
the
General
U.
S.
Population
The
cancer
dietary
risk
assessment
for
chlorate
in
drinking
water
is
below
the
Agency's
level
of
concern
(
i.
e.,
%
cPAD
less
than
100).
Page
58
of
141
6.3
Residential
(
Non­
Occupational)
Exposure/
Risk
Pathway
­
Conventional
Pesticides
All
residential
(
non­
occupational)
risk
estimates
for
inorganic
chlorates,
as
active
or
inert
ingredients
in
conventional
pesticide
products
used
in
residential
environments,
are
below
the
Agency's
level
of
concern
(
i.
e.,
Margin
of
Exposures
(
MOEs)
are
greater
than
the
Level
of
Concern
(
LOC)
of
100).
These
uses
are
considered
to
be
short­
term
only
due
to
the
episodic
uses
associated
with
homeowner
products.
Since
the
episodic
nature
of
residential
exposure
is
inconsistent
with
the
mechanism
of
chlorate
carcinogenicity,
a
residential
cancer
risk
assessment
was
not
conducted.

6.3.1
Home
Uses
6.3.1.1
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
pesticide
products
­
Short­
Term
Residential
Handler
Exposure
via
Inhalation
Route
only
There
is
the
potential
for
exposure
to
sodium
chlorate
by
residential
handlers
in
outdoor
residential
settings
during
the
application
of
conventional
pesticide
products
containing
sodium
chlorate
(
073301)
as
the
active
ingredient.
Sodium
chlorate
(
073301)
can
be
used
as
a
non­
selective
herbicide
in
outdoor
residential
environments
as
a
spot
treatment
or
edging
treatment
around
patios,
along
fence
lines,
lawn
edges,
around
foundations,
underneath
or
around
wood
decks,
and
in
cracks
and
crevices
of
driveways.
Residential
handler
exposure
scenarios
are
considered
to
be
short­
term
only
due
to
the
episodic
uses
associated
with
homeowner
products.
Although
there
is
the
potential
for
dermal
exposure
by
residential
handlers,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.
Hence,
a
short­
term
risk
assessment
for
residential
handlers
via
the
inhalation
exposure
route
was
conducted
for
sodium
chlorate
as
the
active
ingredient
in
conventional
pesticide
products.

Although
there
is
the
potential
for
exposure
to
sodium
chlorate
in
outdoor
residential
settings
from
entering
areas
previously
treated
with
sodium
chlorate
(
073301),
as
the
active
ingredient
in
conventional
pesticide
products,
a
residential
postapplication
exposure
risk
assessment
for
sodium
chlorate
was
not
conducted
because:

°
Although
there
is
the
potential
for
postapplication
dermal
exposure
in
residential
settings,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
dermal
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.
°
Postapplication
inhalation
exposure
for
sodium
chlorate
is
not
expected
due
to
negligible
vapor
pressure.
°
Postapplication
exposure
assessments
for
residential
settings
are
not
typically
performed
for
spot
treatments.

A
series
of
assumptions
and
exposure
factors
served
as
the
basis
for
completing
the
residential
handler
risk
assessment.
Each
assumption
and
factor
is
detailed
below.
In
addition
to
these
factors,
Page
59
of
141
unit
exposures
were
used
to
calculate
risk
estimates.
Unit
exposures
were
taken
from
PHED,
ORETF
studies,
and
one
proprietary
study.
[
Note:
Several
of
the
assumptions
and
factors
used
for
the
assessment
are
similar
to
those
used
in
the
occupational
assessment
presented
under
Section
9.1.
As
such,
only
factors
that
are
unique
to
the
residential
scenarios
are
presented
here.]
The
assumptions
and
factors
used
in
the
risk
calculations
include:

C
Due
to
the
lack
of
chemical
specific
data,
exposures
from
a
scenario
deemed
similar
might
be
used.
As
an
example,
mixer/
loader/
applicator
data
for
hose­
end
sprayers
were
used
to
assess
sprinkler
can
applications.
These
application
methods
are
believed
to
be
similar
enough
to
bridge
the
data.

C
HED
always
considers
the
maximum
application
rates
allowed
by
labels
in
its
risk
assessments.
If
additional
information
such
as
average
or
typical
rates
are
available,
these
values
also
may
be
used
to
allow
risk
managers
to
make
a
more
informed
risk
management
decision.

C
Residential
risk
assessments
are
based
on
estimates
of
what
homeowners
would
typically
treat,
such
as
the
size
of
a
lawn,
or
the
size
of
a
garden.
The
factors
used
for
the
sodium
chlorate
assessment
were
from
the
Health
Effects
Division
Science
Advisory
Council
for
Exposure
Policy
12:
Recommended
Revisions
To
The
Standard
Operating
Procedures
For
Residential
Exposure
Assessment
which
was
completed
on
February
22,
2001
and
on
professional
judgement.
The
daily
volumes
handled
and
area
treated,
used
in
each
residential
scenario,
include:

°
1000
square
feet
when
mixing/
loading/
applying
liquids
as
a
spot
treatment
with
a
lowpressure
handwand
and
sprinkler
cans;
°
1
gallon
when
applying
with
a
RTU
sprinkler
can
and
trigger
pump
sprayer;
and,
°
1000
square
feet
for
granular
formulation
spot
treatments.

Short­
term
risks
for
residential
handlers
via
the
inhalation
exposure
route
are
presented
below
in
Table
6.3.1.1.
All
risks
are
below
the
Agency's
level
of
concern
(
i.
e,
Margin
of
Exposures
(
MOEs)
are
greater
than
the
Level
of
Concern
(
LOC)
of
100).
The
scenarios
assessed
represent
worse­
case
exposures
and
risks.
It
should
also
be
noted
that
there
were
many
other
scenarios
where
medium
to
low
PHED
quality
data
were
used
to
complete
the
assessment.
Data
quality
should
be
considered
in
the
interpretation
of
the
uncertainties
associated
with
each
risk
value
presented.
Page
60
of
141
Table
6.3.1.1.
Sodium
Chlorate
(
073301)
­
Short
Term
Residential
Inhalation
Exposure1
Exposure
Scenario
(
Scenario
#)
Daily
Area
Treated2
Crop/
Target3
Application
Rate4
Inhalation
MOE5
Mixer/
Loader/
Applicators,
Loader/
Applicators,
&
Applicators
M/
L/
A
liquids
with
a
Low
Pressure
Handwand
Sprayer
(
1)
1000
Spot/
edging
treatment
23.7
3000
L/
A
RTU
liquid
with
a
Trigger
Pump
Sprayer
(
2)
1
Spot/
edging
treatment
0.196
87000
M/
L/
A
liquids
with
a
Sprinkler
Can
(
3)
1000
Spot/
edging
treatment
23.7
5200
Applying
liquid
with
a
RTU
Sprinkler
Can
(
4)
1
Spot/
edging
treatment
0.27
710000
Applying
granules
by
Hand
(
5)
1000
Spot/
edging
treatment
12
370
L/
A
granules
with
a
Belly
Grinder
(
6)
1000
Spot/
edging
treatment
12
2800
L/
A
granules
with
a
Push­
type
Spreader
(
7)
1000
Spot/
edging
treatment
12
200000
1
Residential
exposures
assessments
do
not
include
PPE.

2
Amount
treated
is
presented
in
ft2/
day,
except
for
Scenario
#
s
2
and
4
which
are
presented
in
gallons/
day.
(
Standard
EPA/
OPP/
HED
values).

3
Crops
and
use
patterns
are
from
label
extractions
(
Appendix
1),
BEAD's
LUIS
reports,
and
the
Sodium
Chlorate
Use
Closure
Memo
(
J.
Guerry,
8/
5/
04;
10/
13/
04;
11/
15/
04).

4
Ranges
of
application
rates
are
based
on
values
from
label
extractions
(
Appendix
1),
BEAD's
LUIS
reports,
and
the
Sodium
Chlorate
Use
Closure
Memo
(
J.
Guerry,
8/
5/
04;

10/
13/
04;
11/
15/
04).
Application
rates
upon
which
the
analysis
is
based
are
presented
as
lb
ai/
1000
ft2,
except
for
Scenario
#
s
2
and
4
which
are
presented
in
lb
ai/
gallon.

5
Inhalation
MOE
=
Oral
NOAEL
(
30
mg/
kg/
day)
/
Daily
Inhalation
Dose.
HED
LOC
for
MOE
is
100.
Page
61
of
141
6.3.1.2
Sodium
Chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­
Term
Residential
Postapplication
Exposure
via
Incidental
Oral
Route
only
There
is
the
potential
for
postapplication
exposure
in
outdoor
residential
settings
from
entering
areas
previously
treated
with
conventional
pesticide
products
containing
sodium
chlorate
(
873301)
as
an
inert
ingredient.
Hence,
a
residential
postapplication
risk
assessment
was
conducted.
However,
since
these
products
are
professionally
applied,
residential
handler
exposure
is
not
of
concern.

Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
herbicide
formulation
products
can
be
applied
professionally
to
residential
sites.
These
conventional
pesticide
products
contain
<
1
%
sodium
chlorate
and
can
be
applied
at
rates
no
greater
than
0.07
lb
(
as
sodium
chlorate)
per
acre.

As
an
inert
ingredient
in
herbicide
formulations
broadcast
on
residential
sites,
there
is
potential
for
children
to
have
incidental
oral
exposures
(
hand­
to­
mouth
(
HTM),
object­
to­
mouth(
OTM),
and
soil
ingestion
(
SI));
however,
residential
postapplication
exposures
via
dermal
and
inhalation
routes
are
not
of
concern
because:

°
Although
there
is
the
potential
for
postapplication
dermal
exposure
in
residential
settings,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
dermal
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.

°
Postapplication
inhalation
exposure
for
sodium
chlorate
is
not
expected
due
to
negligible
vapor
pressure.

A
series
of
assumptions
and
exposure
factors
served
as
the
basis
for
completing
the
residential
postapplication
risk
assessments.
Each
assumption
and
factor
is
detailed
below.

°
Residential
exposure
and
risk
estimates
are
conducted
assuming
no
personal
protective
equipment
(
i.
e.,
short­
sleeved
shirt,
shorts,
shoes/
socks,
and
no
respirator).
°
Residential
postapplication
exposures
are
assessed
on
the
day
of
pesticide
application.
°
15
kg
represents
the
body
weight
of
a
toddler
(
3
year
old).
°
5%
of
the
application
rate
has
been
used
to
calculate
the
day­
zero
residue
levels
used
for
assessing
risks
from
HTM
behaviors.
°
20%
of
the
application
rate
has
been
used
to
calculate
the
day­
zero
residue
levels
used
for
assessing
risks
from
OTM
behaviors.
°
100%
of
the
application
rate
has
been
used
to
calculate
the
day­
zero
soil
residue
levels
used
for
assessing
risks
from
SI.
°
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;
°
50%
saliva
extraction
factor
for
HTM
exposures.
°
OTM
exposures
are
based
on
a
25
cm2
surface
area.
°
Exposure
durations
are
expected
to
be
2
hours.
Page
62
of
141
°
Soil
residues
are
contained
in
the
top
1
centimeter
and
soil
density
is
0.67
cm3/
gram.

Table
6.3.1.2
below
shows
the
risk
estimates
for
incidental
oral
exposures
to
sodium
chlorate
(
877301)
for
children
playing
in
treated
areas
following
its
application.

Table
6.3.1.2.
Short­
term
Residential
Postapplication
Risk
Estimates
for
Sodium
Chlorate
(
873301)

Population
Subgroup
Scenario
Route
MOE
Combined
MOE
Child
Hand­
to­
Mouth
Oral
29000
23000
Object­
to­
Mouth
Oral
110000
Soil
Ingestion
Oral
8600000
6.3.2
Recreational
Uses
Recreational
exposures
are
expected
to
be
similar
to,
or
in
many
cases,
less
than,
those
evaluated
in
Section
6.3.1
Home
Uses;
therefore,
a
separate
recreational
exposure
assessment
was
not
conducted.

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
sodium
chlorate.
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.
Page
63
of
141
7.0
Aggregate
Risk
Assessments
and
Risk
Characterization
Evaluation
of
the
hazard
and
exposure
(
food,
water,
and
residential)
components
for
inorganic
chlorates
indicates
the
need
to
estimate
potential
risks
for
the
following
scenarios:
Short­
term
inhalation,
screening
level
acute
dietary
(
food
+
water),
chronic
(
non­
cancer)
dietary
(
food
+
water),
and
cancer
dietary
(
food
+
water).

7.1
Short­
Term
Aggregate
Risk
­
Residential
Handler
Inhalation
plus
background
(
chronic
dietary
(
food
+
water))

Table
7.1.
Short­
Term
Aggregate
Risk
Calculations
Population
Target
Aggregate
MOE
1
MOE
food+
water
2
MOE
inhalation
3
Aggregate
MOE
(
food+
water
and
residential)
4
Adult
100
1715
400
324
1
Inhalation
MOE
=
Oral
NOAEL
(
30
mg/
kg/
day)
/
Daily
Inhalation
Dose.
HED
LOC
for
MOE
is
100.
2
MOE
food+
water
=
[(
Short­
Term
oral
NOAEL
=
30
mg/
kg/
day)/(
chronic
dietary
exposure
food
+
water)
Chronic
dietary
exposure
food
+
water
=
0.002730mg/
kg/
day(
food)
+
0.01476mg/
kg/
day(
water)
=
0.01749mg/
kg/
day
3
MOE
inhalation
=
[(
Short­
Term
inhalation
NOAEL
=
30
mg/
kg/
day)/(
high­
end
inhalation
residential
exposure)]
4
Aggregate
MOE
(
food+
water
and
residential)
=
1
÷
[
[(
1
÷
MOE
food+
water)
+
(
1
÷
MOE
inhalation)]]

7.2
Chronic
(
non­
cancer)
Dietary
Risk
­
Food
+
Water
Table
7.2.
Summary
of
Chronic
(
non­
cancer)
Dietary
(
food
+
water)
Exposure
and
Risk
for
Inorganic
Chlorates
Population
Subgroup
a
cPAD
mg/
kg/
day
%
cPAD
Food
+
Water
Estimated
at
the
Highest
Annual
Average
(
0.69
mg/
L)
Food
+
Water
Estimated
at
the
90th
Percentile
Annual
Average
(
0.24
mg/
L)
Food+
Water
Estimated
at
the
Median
Annual
Average
(
0.11
mg/
L)

General
U.
S.
Population
0.03
58
26
17
All
Infants
(<
1
yr)
174
70
40
Children
1­
2
yrs
100
53
39
Children
3­
5
yrs
90
47
34
Children
6­
12
yrs
60
30
21
Youth
13­
19
yrs
43
20
14
Adults
20­
49
yrs
52
23
14
Adults
50+
yrs
54
23
14
Females
13­
49
yrs
52
23
14
a
The
values
for
the
population
with
the
highest
risk
for
each
type
of
risk
assessment
are
bolded.
Page
64
of
141
b
The
BMDL
is
0.9
mg
chlorate/
kg/
day.
The
level
of
concern
for
the
Margin
of
Exposure
(
MOE)
is
30.

7.3
Cancer
Dietary
Risk
­
Food
+
Water
No
separate
cancer
dietary
(
food
+
water)
risk
assessment
was
conducted.
The
chronic
(
food
+
water)
dietary
risk
assessment
is
protective
for
cancer
for
the
General
U.
S.
Population.
(
See
Table
7.2.)
The
estimated
risk
does
not
exceed
our
level
of
concern
(
less
than
100%
cPAD).

Note:
Sodium
chlorate
is
a
thyroid
toxicant
producing
thyroid
gland
follicular
cell
hypertrophy
in
rats
and
mice
following
chronic
exposures
and
some
evidence
of
follicular
cell
tumors
in
rats.
The
lack
of
mutagenicity
indicates
that
the
thyroid
tumors
are
induced
by
a
non­
mutagenic
mechanism.
Therefore,
for
the
purposes
of
this
risk
assessment,
the
Margin
of
Exposure
(
MOE)
approach
is
used
to
estimate
inorganic
chlorate
cancer
risk.
Children
are
not
expected
to
be
more
susceptible
to
chlorate­
induced
thyroid
effects
than
adults
and
the
endpoint
selected
for
the
thyroid
effects
is
protective
for
all
populations,
including
children.
Page
65
of
141
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
inorganic
chlorates
and
any
other
substances.
However,
available
data
indicate
that
there
may
be
some
interconversion
between
chlorate
and
chlorite
in
water,
in
the
environment,
and
in
the
gut.

For
the
purposes
of
this
tolerance
action,
EPA
has
not
assumed
that
inorganic
chlorates
have
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/.
Page
66
of
141
9.0
Occupational
Exposure/
Risk
Pathway
­
Conventional
Pesticide
Products
Only
9.1
Short/
Intermediate/
Long­
Term
Handler
Risk
There
is
potential
for
occupational
handler
exposure
to
inorganic
chlorates
from:
(
1)
the
application
of
sodium
chlorate
(
073301)
as
the
active
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
non­
agricultural)
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators);
(
2)
the
application
of
sodium
chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
nonagricultural
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators);
and
(
3)
the
application
of
potassium
chlorate
(
900583)
as
an
inert
ingredient
in
conventional
pesticide
products
used
in
poultry
premises.

With
the
addition
of
PPE
(
dust/
mist
respirator)
or
engineering
controls
(
enclosed
cockpits
or
cabs),
all
occupational
handler
scenarios
for
the
use
of
inorganic
chlorates
as
an
active
or
inert
ingredient
in
conventional
pesticides
are
below
the
Agency's
level
of
concern
(
i.
e.,
Margin
of
Exposures
(
MOEs)
are
greater
than
the
Level
of
Concern
(
LOC)
of
100).
Exposure
durations
are
short­
and
intermediate­
term
only.
Since
the
exposure
durations
for
occupational
handlers
are
inconsistent
with
the
mechanism
of
chlorate
carcinogenicity,
an
occupational
cancer
risk
assessment
was
not
conducted.

9.1.1
Sodium
chlorate
(
073301)
as
the
active
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
There
is
potential
for
occupational
handler
exposure
to
sodium
chlorate
from
the
application
of
sodium
chlorate
(
073301)
as
the
active
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
non­
agricultural)
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators).
Occupational
handler
scenarios
were
identified
for
which
exposure
to
sodium
chlorate
is
expected
(
see
Table
9.1.1).

Sodium
chlorate
is
an
agricultural
defoliant/
desiccant
and
a
commercial
herbicide.
Use
patterns
vary
from
short­
to
intermediate­
term
exposure
durations.
Occupational
handlers
may
be
exposed
dermal
and
inhalation
routes;
however,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.
Hence,
only
short­
and
intermediate­
term
sodium
chlorate
risk
assessment
for
occupational
handlers
via
the
inhalation
exposure
route
was
conducted.

Risk
for
most
occupational
handler
baseline
(
without
a
respirator)
inhalation
exposure
scenarios
do
not
exceed
the
Agency's
level
of
concern
(
i.
e.,
Margin
of
Exposures
(
MOEs)
are
greater
than
the
Level
of
Concern
(
LOC)
of
100).
However,
occupational
handler
risks
for
some
of
the
high
end
application
rates
(
1032
and
523
lb
ai/
A)
did
exceed
the
Agency's
level
of
concern
at
baseline.
Risk
mitigation
for
these
scenarios
was
accomplished
with
the
addition
of
a
dust/
mist
respirator
(
with
an
Page
67
of
141
80%
reduction
factor),
or,
for
certain
scenarios,
with
engineering
controls
(
enclosed
cabs
or
cockpits).

No
chemical­
specific
handler
exposure
data
are
available
and,
therefore,
the
following
data
and
assumptions
were
used
to
assess
the
subject
handler
exposures
and
risks:

C
Occupational
handler
exposure
estimates
were
based
on
surrogate
data
from:
(
1)
the
Pesticide
Handlers
Exposure
Database
(
PHED),
and
(
2)
Outdoor
Residential
Exposure
Task
Force
(
ORETF).

C
Average
body
weight
of
an
adult
handler
is
70
kg
because
the
toxicity
endpoint
values
used
for
the
assessments
are
appropriate
for
average
adult
body
weight
representing
the
general
population.
This
is
the
case
because
none
of
the
effects
identified
in
the
selected
toxicity
studies
were
sex
specific.

C
Exposure
factors
used
to
calculate
daily
exposures
to
handlers
are
based
on
applicable
data
if
available.
For
lack
of
appropriate
data,
values
from
a
scenario
deemed
similar
enough
by
the
assessor
might
be
used.
As
an
example,
for
sodium
chlorate
handler
exposures,
ORETF
data
for
hose­
end
sprayer
equipment
were
used
to
assess
sprinkling
can
applications.
The
nature
of
these
application
methods
are
believed
to
be
similar
enough
to
bridge
the
data.

C
HED
always
considers
the
maximum
application
rates
allowed
by
labels
in
its
risk
assessments.
If
additional
information
such
as
a
different
range
of
rates
are
available,
these
values
also
may
be
used
to
allow
risk
managers
to
make
a
more
informed
risk
management
decision.

C
The
typical
occupational
workday
is
assumed
to
be
8
hours.

C
The
daily
area
treated
was
defined
for
each
handler
scenario
(
in
appropriate
units)
by
determining
the
amount
that
can
be
reasonably
treated
in
a
single
day
(
e.
g.
acres,
square
feet,
or
gallons
per
day).
When
possible,
the
assumptions
for
daily
areas
treated
is
taken
from
ExpoSAC
SOP
#
9:
Standard
Values
for
Daily
Acres
Treated
in
Agriculture
which
was
completed
on
July
5,
2000.
Assumptions
for
these
scenarios,
including
further
refinements
based
on
HED
estimates,
are
listed
below.

Agricultural
Scenarios
S
Aerial
applications:
350
acres
(
typical
field
crop
assumption)
for
guar
beans,
southern
peas,
chili
peppers
(
for
processing
only),
potatoes,
ornamental
gourds,
and
cucurbits
(
grown
for
seed);
1200
acres
(
high
acreage
crop
assumption)
for
cotton,
corn,
rice,
dry
beans,
sorghum,
flax,
safflower,
sunflower,
soybeans,
wheat,
and
fallow
land.

S
Groundboom:
80
acres
(
typical
field
crop
assumption)
for
guar
beans,
southern
peas,
chili
peppers
(
for
processing
only),
potatoes,
ornamental
gourds,
and
cucurbits
(
grown
for
seeds);
200
acres
(
high
acreage
crop
assumption)
for
cotton,
corn,
rice,
dry
beans,
sorghum,
flax,
safflower,
sunflower,
soybeans,
wheat
and
fallow
land.
Page
68
of
141
S
Flaggers:
350
acres.

Refinements
into
"
typical
field"
and
"
high
acreage"
crops
was
performed
with
help
from
HED
crop
expert
Bernard
Schneider
(
email
from
B.
Schneider,
5/
24/
04).

Industrial/
Non­
Crop
Sites
S
Rights­
of­
Way
Sprayer
and
Handgun
Sprayer:
5
acres
per
day;

S
Low
Pressure
Handwand
Sprayer:
2
acres
per
day;

Note:
Although
assessments
for
applications
involving
rights­
of­
way
sprayers
and
low
pressure
handwands
typically
use
a
volume­
based
approach
for
amount
handled/
treated
per
day
(
1000
gallons
and
40
gallons,
respectively,
from
ExpoSAC
Policy
#
9),
label­
specific
application
rates
and
their
respective
dilution
factors
for
larger
application
settings
are
better
represented
by
a
daily
unit
area
treated
than
a
volume
based
approach.
For
example,
the
label­
specific
application
of
8
pints
per
100
square
feet
[
EPA
Reg.
No.
7701­
34]
yields
the
application
rate
of
1032
lb
ai
in
2196
gallons
of
solution
per
acre.
At
this
rate,
the
volumebased
approach
of
1000
gallons
per
day
would
have
a
worker
treating
approximately
½
acres
per
day.
Because
a
rights­
of­
way
sprayer
would
likely
treat
more
than
½
acre
per
day,
a
daily
unit
area
of
5
acres
was
used
as
more
appropriate
estimate.

S
Belly
grinder:
1
acre
per
day.

S
Push­
type
spreader:
5
acres
per
day
S
Groundboom
and
Tractor­
drawn
Spreader:
40
acres
per
day.
Page
69
of
141
Table
9.1.1.
Sodium
Chlorate
(
073301):
Short­
and
Intermediate­
Term
Occupational
Inhalation
Exposure
Exposure
Scenario
(
Scenario
#)
Daily
Area
Treated1
Crop/
Target2
Application
Rate3
Inhalation
MOE4
Mitigation
Level5
Mixer/
Loader
Mixing/
Loading
liquids
for
Aerial
application
(
1a)
1200
Cotton,
Corn,
Rice,
Dry
Beans,
Grain
Sorghum,
Flax,

Safflower,
Sunflower,
Soybeans
7.5
190
Baseline
Fallow
Land,
Wheat
6
240
Baseline
350
Chili
Peppers
(
for
processing
only),
Potatoes
12.5
400
Baseline
Ornamental
Gourds,
Cucurbits
(
grown
for
seed)
6
830
Baseline
Guar
Beans,
Southern
Peas
7.5
670
Baseline
Mixing/
Loading
liquids
for
Groundboom
application
(
1b)
200
Cotton,
Corn,
Rice,
Dry
Beans,
Grain
Sorghum,
Flax,

Safflower,
Sunflower,
Soybeans
7.5
1200
Baseline
Fallow
Land,
Wheat
6
1500
Baseline
80
Chili
Peppers
(
for
processing
only),
Potatoes
12.5
1800
Baseline
Ornamental
Gourds,
Cucurbits
(
grown
for
seed)
6
3600
Baseline
Guar
Beans,
Southern
Peas
7.5
2900
Baseline
40
Industrial/
Non­
Crop
Sites
1032
210
PPE
­
80%
R
523
420
PPE
­
80%
R
132
330
Baseline
Mixing/
Loading
liquids
for
Rights­
of­

Way
Sprayer
application
(
1c)
5
Rights­
of­
Way
&
Industrial/
Non­
Crop
Sites
1032
340
Baseline
523
670
Baseline
132
2700
Baseline
Loading
granules
for
Tractor­
drawn
Spreader
application
(
2)
40
Industrial/
Non­
Crop
Sites
523
300
PPE
­
80%
R
240
130
Baseline
161
190
Baseline
Applicator
Table
9.1.1.
Sodium
Chlorate
(
073301):
Short­
and
Intermediate­
Term
Occupational
Inhalation
Exposure
Exposure
Scenario
(
Scenario
#)
Daily
Area
Treated1
Crop/
Target2
Application
Rate3
Inhalation
MOE4
Mitigation
Level5
Page
70
of
141
Aerial
spray
applications
(
3a)
1200
Cotton,
Corn,
Rice,
Dry
Beans,
Grain
Sorghum,
Flax,

Safflower,
Sunflower,
Soybeans
7.50
3400
Engineering
Control
Fallow
Land,
Wheat
6
4300
Engineering
Control
350
Guar
Beans,
Southern
Peas
7.5
12000
Engineering
Control
Chili
Peppers
(
for
processing
only),
Potatoes
12.5
7100
Engineering
Control
Ornamental
Gourds,
Cucurbits
(
grown
for
seed)
6
15000
Engineering
Control
Groundboom
spray
applications
(
3b)
1200
Cotton,
Corn,
Rice,
Dry
Beans,
Grain
Sorghum,
Flax,

Safflower,
Sunflower,
Soybeans
7.5
1900
Baseline
Fallow
Land,
Wheat
6
2400
Baseline
350
Guar
Beans,
Southern
Peas
7.5
4700
Baseline
Chili
Peppers
(
for
processing
only),
Potatoes
12.5
2800
Baseline
Ornamental
Gourds,
Cucurbits
(
grown
for
seed)
6
5900
Baseline
40
Industrial/
Non­
Crop
Sites
1032
350
PPE
­
80%
R
1200
Engineering
Control
523
140
Baseline
2300
Engineering
Control
132
540
Baseline
9200
Engineering
Control
Rights­
of­
Way
Sprayer
Applications
(
3c)
5
Rights­
of­
Way
&
Industrial/
Non­
Crop
Sites
1032
110
Baseline
523
210
Baseline
132
820
Baseline
Tractor­
drawn
Spreader
Applications
(
4)
40
Industrial/
Non­
Crop
Sites
523
420
PPE
­
80%
R
460
Engineering
Control
240
180
Baseline
Table
9.1.1.
Sodium
Chlorate
(
073301):
Short­
and
Intermediate­
Term
Occupational
Inhalation
Exposure
Exposure
Scenario
(
Scenario
#)
Daily
Area
Treated1
Crop/
Target2
Application
Rate3
Inhalation
MOE4
Mitigation
Level5
Page
71
of
141
990
Engineering
Control
161
270
Baseline
1500
Engineering
Control
Table
9.1.1.
Sodium
Chlorate
(
073301):
Short­
and
Intermediate­
Term
Occupational
Inhalation
Exposure
Exposure
Scenario
(
Scenario
#)
Daily
Area
Treated1
Crop/
Target2
Application
Rate3
Inhalation
MOE4
Mitigation
Level5
Page
72
of
141
Flagger
Flagging
for
Aerial
Spray
applications
(
5)
350
Various
Agricultural
Crops
12.5
1400
Baseline
Mixer/
Loader/
Applicators
&
Loader/
Applicators
M/
L/
A
liquids
with
a
Low
Pressure
Handwand
Sprayer
(
6)
2
Industrial/
Non­
Crop
Sites
1032
170
PPE
­
80%
R
523
330
PPE
­
80%
R
132
270
Baseline
M/
L/
A
liquids
with
a
Handgun
Sprayer
(
7)
5
Industrial/
Non­
Crop
Sites
1032
230
Baseline
523
450
Baseline
132
1800
Baseline
L/
A
granules
with
a
Belly
Grinder
(
8)
1
Industrial/
Non­
Crop
Sites
523
320
PPE
­
80%
R
240
140
Baseline
161
210
Baseline
L/
A
granules
with
a
Push­
type
Spreader
(
9)
5
Industrial/
Non­
Crop
Sites
523
110
Baseline
240
240
Baseline
161
360
Baseline
1
Amount
treated
is
presented
in
acres/
day.
(
Standard
EPA/
OPP/
HED
values).

2
Crops
and
use
patterns
are
from
label
extractions
(
Appendix
1),
BEAD's
LUIS
reports,
and
the
Sodium
Chlorate
Use
Closure
Memo
(
J.
Guerry,
8/
5/
04;
10/
13/
04;
11/
15/
04).

3
Ranges
of
application
rates
are
based
on
values
from
label
extractions
(
Appendix
1),
BEAD's
LUIS
reports,
and
the
Sodium
Chlorate
Use
Closure
Memo
(
J.
Guerry,
8/
5/
04;
10/
13/
04;

11/
15/
04).
Application
rates
upon
which
the
analysis
is
based
are
presented
as
lb
ai/
acre.

4
Inhalation
MOE
=
Oral
NOAEL
(
30
mg/
kg/
day)
/
Daily
Inhalation
Dose.
HED
LOC
for
MOE
is
100.

5
Mitigation
Levels
Baseline:
No
respirator
PPE
­
80%
R:
Dust/
mist
respirator
with
an
80%
reduction
factor
Engineering
Control:
Closed
cockpit
or
cab
Page
73
of
141
9.1.2
Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
There
is
potential
for
occupational
handler
exposure
to
chlorate
from
the
application
of
sodium
chlorate
(
873301)
as
an
inert
ingredient
in
conventional
pesticide
products
used
on
both
agricultural
and
commercial
(
non­
agricultural)
sites
(
i.
e.,
mixer/
loaders,
applicators,
flaggers,
and
mixer/
loader/
applicators).
Occupational
handler
scenarios
were
identified
for
which
exposure
to
sodium
chlorate
is
expected
(
see
Table
9.1.2).

Herbicide
formulations
containing
<
1%
sodium
chlorate
(
873301)
as
an
inert
ingredient
may
be
professionally
applied
to
agricultural
and
commercial
(
non­
agricultural)
sites
at
the
maximum
use
rate
of
0.07
lb
(
as
sodium
chlorate)
per
acre.
Use
patterns
vary
from
short­
to
intermediate­
term
exposure
durations.
Occupational
handlers
may
be
exposed
dermal
and
inhalation
routes;
however,
sodium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
sodium
chlorate
through
intact
skin
is
not
expected.
Hence,
only
short­
and
intermediate­
term
sodium
chlorate
risk
assessment
for
occupational
handlers
via
the
inhalation
exposure
route
was
conducted.

No
chemical­
specific
handler
exposure
data
are
available
and,
therefore,
the
following
data
and
assumptions
were
used
to
assess
the
subject
handler
exposures
and
risks:

C
Assumptions
for
daily
area
treated
are
taken
from
ExpoSAC
SOP
#
9:
Standard
Values
for
Daily
Acres
Treated
in
Agriculture
(
July
5,
2000)
or
from
professional
judgement.

C
Unit
exposures
are
from
the
PHED
Surrogate
Exposure
Guide
(
August,
1998)
or
data
from
the
Outdoor
Residential
Exposure
Task
Force
(
ORETF).

C
Baseline
personal
protective
equipment
(
PPE)
represents
(
in
terms
of
inhalation
exposure
and
risk)
a
worker
without
a
respirator.

C
Average
body
weight
of
an
adult
handler
is
70
kg
because
the
toxicity
endpoint
values
used
for
the
assessments
are
appropriate
for
average
adult
body
weight
representing
the
general
population.
This
is
the
case
because
none
of
the
effects
identified
in
the
selected
toxicity
studies
were
sex
specific.
Page
74
of
141
Table
9.1.2.
Short­/
Intermediate­
Term
Occupational
Inhalation
Exposure
Risk
Estimates
for
Sodium
Chlorate
(
873301)
as
an
Inert
Ingredient
in
Herbicide
Formulations
Exposure
Scenario
Unit
Exposure
Daily
Area
Treated
Crop/
Target
Application
Rate
Non­
Cancer
MOE
Mitigation
Level
Mixer/
Loader
Mixing/
Loading
liquids
for
Aerial
application
0.0012
1200
Agricultural
crops
0.07
21000
Baseline
Mixing/
Loading
liquids
for
Groundboom
application
0.0012
350
Agricultural
crops
0.07
71000
Baseline
Mixing/
Loading
liquids
for
Rights­
of­
Way
Sprayer
application
0.0012
5
Non­
agricultural
sites
0.07
5000000
Baseline
Mixing/
Loading
liquids
for
Handgun
Sprayer
application
0.0012
100
Residential
sites
0.07
250000
Baseline
Applicator
Aerial
spray
applications
0.000068
1200
Agricultural
crops
0.07
370000
Engineering
Control
Groundboom
spray
applications
(
open
cab)
0.00074
350
Agricultural
crops
0.07
120000
Baseline
Rights­
of­
Way
Sprayer
Applications
0.0039
5
Non­
agricultural
sites
0.07
1500000
Baseline
Flagger
Flagging
for
Aerial
Spray
applications
0.00035
350
Agricultural
Crops
0.07
240000
Baseline
Mixer/
Loader/
Applicators
M/
L/
A
liquids
with
a
Low
Pressure
Handwand
Sprayer
0.03
1
Residential
sites
0.07
1000000
Baseline
M/
L/
A
liquids
with
a
Handgun
Sprayer
0.0018
5
Residential
sites
0.07
3300000
Baseline
M/
L/
A
liquids
with
a
Backpack
Sprayer
0.03
1
Residential
sites
0.07
1000000
Baseline
Page
75
of
141
9.1.3
Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
conventional
pesticide
products
­
Short­/
Intermediate­
Term
Occupational
Handler
Exposure
via
Inhalation
Route
only
There
is
potential
for
occupational
handler
exposure
to
potassium
chlorate
from
the
application
of
potassium
chlorate
(
900583)
as
an
inert
ingredient
in
conventional
pesticide
products
used
in
poultry
premises.
Occupational
handler
scenarios
were
identified
for
which
exposure
to
potassium
chlorate
is
expected
(
see
Table
9.1.3).

Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
airborne
fungicide
products
can
be
applied
in
poultry
premises.
These
conventional
pesticide
products
contain
<
20%
potassium
chlorate
and
can
be
applied
at
rates
not
greater
than
0.01
lb
(
as
potassium
chlorate)
per
500
ft3.

Use
patterns
vary
from
short­
to
intermediate­
term
exposure
durations.
Occupational
handlers
may
be
exposed
dermal
and
inhalation
routes;
however,
potassium
chlorate
is
an
inorganic
salt,
therefore,
significant
absorption
of
potassium
chlorate
through
intact
skin
is
not
expected.
Hence,
only
short­
and
intermediate­
term
potassium
chlorate
risk
assessment
for
occupational
handlers
via
the
inhalation
exposure
route
was
conducted.

No
chemical­
specific
handler
exposure
data
are
available
and,
therefore,
the
following
data
and
assumptions
were
used
to
assess
the
subject
handler
exposures
and
risks:

C
This
risk
calculation
is
assumed
to
be
a
very
conservative
estimate.
It
assumes
that
all
the
potassium
chlorate
(
no
greater
than
0.01
lb)
is
present
in
the
air,
and
available
for
inhalation,
following
application
of
the
airborne
fungicide.

C
Baseline
PPE
represents
(
in
terms
of
inhalation
exposure
and
risk)
a
worker
without
a
respirator.

C
Exposure
duration
is
estimated
to
be
1
minute
per
day.

C
Adult
inhalation
rate
for
light
activity
is
16.6
l/
min.

C
Average
body
weight
of
an
adult
handler
is
70
kg
because
the
toxicity
endpoint
values
used
for
the
assessments
are
appropriate
for
average
adult
body
weight
representing
the
general
population.
This
is
the
case
because
none
of
the
effects
identified
in
the
selected
toxicity
studies
were
sex
specific.

Table
9.1.3.
Short­/
Intermediate­
Term
Occupational
Inhalation
Exposure
Risk
Estimates
for
Potassium
Chlorate
(
900583)
as
an
Inert
Ingredient
Used
in
Airbourne
Fungicides
Exposure
Scenario
Application
Rate
Maximum
Potential
Airborne
Concentration
(
mg
KClO3/
l)
Non­
Cancer
MOE
Mitigation
Level
Airborne
Application
of
Fungicide
0.01
lb/
500
ft3
0.32
400
Baseline
Page
76
of
141
9.2
Short/
Intermediate/
Long­
Term
Postapplication
Risk
Postapplication
exposures
do
not
need
to
be
included
in
the
occupational
risk
assessment
for
inorganic
chlorates.
Although
dermal
and
inhalation
exposures
are
possible,
these
exposures
are
expected
to
be
negligible
due
to
the
physical
and
chemical
characteristics
of
inorganic
chlorates.

10.0
Data
Needs
and
Label
Requirements
10.1
Toxicology
870.3465
28­
Day
Inhalation
Study
These
data
are
needed
to
refine
the
need
for
additional
PPE
(
dust/
mist
respirator)
or
engineering
controls
(
enclosed
cockpit
or
cabs)
to
protect
occupational
handlers
from
potential
inhalation
exposure
resulting
from
conventional
agricultural
use
of
sodium
chlorate.

10.2
Residue
Chemistry
860.1480
Magnitude
of
the
Residue
­
Meat,
Milk,
Poultry,
Eggs
New
ruminant
and
poultry
feeding
studies
are
required.
860.1650
Submittal
of
Analytical
Reference
Standards
Submission
of
a
reasonable
amount
of
the
analytical
reference
standards
for
sodium
chlorate
to
the
Pesticide
Repository
is
required
and
replenishment
of
standards
as
requested
by
the
repository.

10.3
Occupational
and
Residential
Exposure
Sodium
chlorate
(
073301)
end­
use
product
labels
should
be
amended,
as
necessary,
to
include
application
rates
in
terms
of
lbs/
acre
treated
for
clarification.

Unpublished
References:

Benchmark
Dose
Analysis
of
Sodium
Chlorate
FCH
Response
in
Rats:
No
DP
Barcode,
B.
Daiss,
01/
26/
2005.

Chlorate
Ion
in
Drinking
Water,
memo
from
Patricia
Fair
(
Office
of
Ground
Water
and
Drinking
Water
Technical
Support
Center)
to
Jacqueline
Guerry
(
OPPTS/
OPP/
SRRD/
RB3),
dated
08/
10/
2005.

Drinking
Water
Assessment
of
Sodium
Chlorate
as
a
Desiccant/
Defoliant
on
Food/
Feed
Terrestrial
Uses:
D303556,
S.
Termes,
01/
05/
2005.
Page
77
of
141
Incident
Report:
D310573,
J.
Blondell,
03/
31/
2005.

Inorganic
Chlorates
Dietary
Exposure
Assessment
for
the
Reregistration
Eligibility
Decision:
D303555.
T.
Morton,
01/
26/
2006.

Occupational
and
Residential
Exposure
Assessment
for
Sodium
Chlorate
(
073301)
as
an
Active
Ingredient
in
Conventional
Pesticides:
D307365,
M.
Crowley,
06/
13/
2005.

Occupational
and
Residential
Exposure
Assessment
for
Inorganic
Chlorates
in
Antimicrobial
Pesticides:
D312200,
T.
Leighton,
01/
24/
2005.

Occupational
and
Residential
Exposure
Assessment
for
Inorganic
Chlorates
as
Inert
Ingredients
in
Conventional
Pesticides:
D318045,
M.
Crowley,
06/
13/
2005.

Response
to
Sodium
Chlorate
Preliminary
Risk
Assessment,
memo
of
OW
to
Jacqueline
Guerry,
SRRD,
10/
20/
2005.

Note:
Residue
Chemistry
Considerations
are
addressed
under
Appendix
C.

Published
References:

AWWA
Water
Quality
Division
Disinfection
Systems
Committee,
Committee
Report:
Disinfection
at
Large
and
Medium­
Size
Systems,
May
2000a,
p
32­
43.

AWWA
Water
Quality
Division
Disinfection
Systems
Committee,
Committee
Report:
Disinfection
at
Small
Systems,
May
2000b,
p
24­
31.

Bolyard,
M.,
Fair,
P.
S.,
and
Hautman,
D.
P.
"
Sources
of
Chlorate
Ion
in
US
Drinking
Water,"
Journal
AWWA
Vol
85(
9)
81­
88,
1993.

Dohler,
K.
D.,
Wong,
C.
C.,
Von
Zur
Muhlen,
A.
(
1979)
The
rat
as
a
model
for
the
study
of
drug
effects
on
thyroid
function:
Consideration
of
methodological
problems.
Pharmacol.
Ther.
5,
305­
318
Gates,
D.
J.
The
Chlorine
Dioxide
Handbook.
American
Water
Works
Association,
Denver,
CO,
1998.

Gordon,
G.
G.,
Adam,
L.,
and
Bubnis,
B.
Minimizing
Chlorate
Ion
Formation
in
Drinking
Water
When
Hypochlorite
Ion
is
the
Chlorinating
Agent.
American
Water
Works
Association
Research
Foundation,
Denver,
CO,
1995.
Page
78
of
141
McClain,
R.
M.
(
1992).
Thyroid
gland
neoplasia:
non­
genotoxic
mechanisms.
Toxicol.
Lett.
64/
65,
397­
408.

USEPA,
1996.
National
Primary
Drinking
Water
Regulation:
Monitoring
Requirements
for
Public
Drinking
Water
Supplies:
Cryptosporidium,
Giardia,
Viruses,
Disinfection
Byproducts,
Water
Treatment
Plant
Data
and
Other
Information
Requirements.
Final
Rule.
FR
61:
94:
24354­
24388
(
May
14,
1996).

USEPA,
2000.
ICR
Auxiliary
1
Database.
EPA
815­
C­
00­
002.
Office
of
Water,
Cincinnati,
OH,
April
2000.
Page
79
of
141
APPENDIX
A
TOXICOLOGY
DATA
REQUIREMENTS
Test
Technical
Required
Satisfied
870.1100
Acute
Oral
Toxicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.1200
Acute
Dermal
Toxicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.1300
Acute
Inhalation
Toxicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.2400
Primary
Eye
Irritation
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.2500
Primary
Dermal
Irritation
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.2600
Dermal
Sensitization
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
870.3100
Oral
Subchronic
(
Rodent)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.3150
Oral
Subchronic
(
Non­
Rodent)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.3200
21­
Day
Dermal
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.3250
90­
Day
Dermal
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.3465
28­
Day
Inhalation
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
yes
yes
no
no
yes
yes
yes
­­

no
870.3700a
Developmental
Toxicity
(
Rodent)
.
.
.
.
.
.
.
.
.
.
.
.
.
870.3700b
Developmental
Toxicity(
Non­
rodent)
.
.
.
.
.
.
.
.
.
.
.
870.3800
Reproduction
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
yes
yes
yes
yes
yes*
yes**

870.4100a
Chronic
Toxicity
(
Rodent)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.4100b
Chronic
Toxicity
(
Non­
rodent)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.4200a
Oncogenicity
(
Rat)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.4200b
Oncogenicity
(
Mouse)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.4300
Chronic/
Oncogenicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
yes
yes
yes
yes
yes
yes*
yes***
yes*
yes*
yes*

870.5100
Mutagenicity 
Gene
Mutation
­
bacterial
.
.
.
.
.
.
.
.
870.5300
Mutagenicity 
Gene
Mutation
­
mammalian
.
.
.
.
.
870.5395
Mutagenicity 
Erythrocyte
Micronucleus
.
.
.
.
.
.
.
870.5385
Mutagenicity 
Bone
Marrow
Cytogenetics
.
.
.
.
.
.
870.5550
Mutagenicity 
Unscheduled
DNA
Synthesis
.
.
.
.
.
870.5275
Mutagenicity 
Recessive
lethal
in
Drosophila
.
.
.
.
yes
yes
yes
yes
yes
yes
yes
yes
yes*
yes*
yes
yes*

870.6100a
Acute
Delayed
Neurotox.
(
Hen)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.6100b
90­
Day
Neurotoxicity
Hen)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.6200a
Acute
Neurotoxicity.
Screening
Battery
(
Rat)
.
.
.
.
.
870.6200b
90
Day
Neurotoxicity
Screening
Battery
(
Rat)
.
.
.
.
.
870.6300
Develop.
Neurotoxicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
no
no
no
no
no
­­­­­

870.7485
General
Metabolism
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
870.7600
Dermal
Penetration
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
yes
no
yes*
­

Special
Studies
for
Ocular
Effects
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
Acute
Oral
(
Rat)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
Subchronic
Oral
(
Rat)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
Six­
month
Oral
(
Dog)
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
no
no
no
­­­

­
Not
Applicable
*
Chlorate
published
study
**
Chlorite
published
study
***
The
2­
year
NTP
(
DRAFT
NTP
Report
2004)
study
in
the
rat
satisfies
this
requirement.
No
toxicity
was
seen
in
the
subchronic
study
in
dogs
administered
sodium
chlorate
by
oral
gavage
except
for
emesis
at
the
highest
dose
of
360
mg/
kg/
day.

APPENDIX
B
TOXICOLOGY
STUDIES
The
executive
summaries
of
tox
studies
presented
in
the
sodium
chlorate
toxicology
profile
are
provided
below.
Page
80
of
141
Acute
Toxicity
The
acute
oral
LD50
of
potassium
chlorate
has
been
reported
to
be
1870
mg/
kg
in
rats
and
the
lowest
oral
lethal
dose
in
rats
was
7000
mg/
kg,
in
rabbits
2000
mg/
kg
and
in
dogs
1200
mg/
kg
(
Cosmetic
Ingredient
Review
Panel,
1995)

The
published
literature
provides
numerous
references
to
sodium
chlorate
poisoning.
In
one
report
(
Helliwell
&
Nunn,
1979),
14
cases
of
deliberate
and
accidental
sodium
chlorate
poisonings
in
individuals
(
males
and
females)
ranging
in
age
from
3­
55
years
old
are
described.
In
one
case
a
48
year
old
female
died
after
20
hours
of
accidentally
ingesting
15
g
of
sodium
chlorate.
Death
is
described
occurring
from
massive
intra
vascular
hemolysis
and
acute
renal
failure.
Recovery
from
sodium
chlorate
poisoning
was
low
even
with
medical
intervention.
The
clinical
features
of
sodium
chlorate
poisonings
in
these
cases
were
nausea
and
vomiting,
cyanosis,
abdominal
pain,
diarrhea,
dyspnea.
In
the
patients
who
died,
a
"
constant
necropsy
finding
was
a
chocolate
discoloration
of
the
blood
and
viscera
due
to
staining
by
bilirubin
and
methemoglobin".

The
acute
toxic
effects
of
potassium
chlorate
are
summarized
in
the
1995
Cosmetic
Ingredient
Review
Panel,
1995.
The
toxic
dose
of
potassium
chlorate
is
often
reported
to
be
5
g
with
the
lethal
adult
dose
being
15­
35
g.
Mortality
of
a
child
has
been
reported
after
ingestion
of
1
g
of
potassium
chlorate.
Human
chlorate
ingestion
can
produce
gastritis,
a
late
toxic
nephritis,
hemolysis,
methemoglobinemia,
hemoglobinuria
and
acute
renal
failure.
The
toxic
effects
of
potassium
chlorate
appear
cumulative
because
of
the
slow
excretion
of
the
chlorate
ion;
repeated
1
g
ingestions
have
been
fatal.
Dermal
irritation
and
burns
have
been
reported
in
industrial
uses.
Use
of
potassium
chlorate
in
toothpastes
may
have
caused
inflammation
and
bleeding
of
the
gums.

In
a
case
of
severe
chlorate
poisoning
of
a
26
year
old
female
who
ingested
150­
200
grams
of
sodium
chlorate,
methemoglobinaemia
was
described
as
the
early
symptom
of
intoxication
(
Steffen
and
Seitz,
1981).
Methemoglobin
was
converted
to
hematin.
The
patient
was
deeply
cyanotic
when
admitted
to
hospital
approximately
5
hours
after
ingesting
the
material.
After
extensive
gastric
lavage
and
administration
of
methylene
blue
and
ascorbic
acid
intravenously,
7.4
grams
of
sodium
chlorate
were
excreted
in
the
urine.
The
patient
voided
clear
urine
initially,
turning
dark
brown
becoming
muddy
before
it
completely
subsided,
the
result
of
renal
failure.
After
the
renal
failure,
the
patient
required
several
weeks
of
hemodialysis.
Renal
function
was
absent
for
10
days
and
recovered
slowly
and
the
patient
was
discharged
after
3
months.
Liver
function
was
only
moderately
disturbed.
Serum
tranasaminases
were
elevated
during
the
first
10
days.
Bilirubin
was
only
slightly
elevated
for
3
weeks.

Subchronic
Toxicity
870.3100
90­
Day
Oral
Toxicity
­
Rat
In
a
subchronic
oral
toxicity
study
(
MRID
40444801),
Sprague­
Dawley
CD
rats
(
15/
sex/
group)
were
dosed
with
technical
grade
sodium
chlorate
(
100%
a.
i.,
white
granular
solid)
gavage
at
0
Page
81
of
141
(
distilled
water),
10,
40,
100,
or
1000
mg/
kg/
day
for
90
consecutive
days.
Body
weight
gain
was
lower
in
females
of
all
dosed
groups
compared
to
controls
which
had
abnormal
body
weight
gain.
The
body
weights
of
males
were
minimally
lower
(
not
statistically
significant)
in
the
two
highest
dose
groups.
The
most
notable
effects
of
sodium
chlorate
dosing
were
on
the
hematological
parameters.
At
the
1000
mg/
kg/
dose,
hemoglobin
concentration,
hematocrit,
red
blood
cell
counts
were
statistically
significantly
decreased,
and
reticulocyte
count
was
statistically
significantly
increased
in
females.
In
males,
only
the
hematocrit
was
statistically
significantly
decreased
at
the
highest
dose
tested
(
HDT).
The
adrenal
weight
was
depressed
in
both
males
and
females
at
the
HDT.
Histological
lesions
were
detected
in
all
groups
but
with
no
apparent
dose
relationship.
The
LOAEL
derived
from
this
study
was
1000
mg/
kg/
day
based
on
the
hematological
effects
and
the
NOAEL
was
100
mg/
kg/
day.
This
study
is
considered
Acceptable/
guideline.

In
a
published
study
(
Kurokawa
et
al,
1985)
it
was
reported
that
administration
of
1%
sodium
or
potassium
chlorate
in
the
drinking
water
(
654­
686
mg/
kg/
day)
to
male
F344
rats
for
25
weeks
produced
significant
decrease
in
mean
body
weights
compared
to
the
controls.
This
dose
was
the
maximum
tolerated
dose
based
on
a
6­
week
screening
study
at
0.25,
0.5,
1
and
2%
doses
in
drinking
water.
Relative
kidney
weights
of
the
potassium
chlorate
treated
rats
were
significantly
increased
over
the
control
group,
suggesting
renal
toxicity.

Studies
were
conducted
to
determine
the
toxicity
of
chlorine
dioxide
(
0,
1,
10,
100,
1000
mg/
L)
and
its
conversion
products
chlorite
and
chlorate
(
10,
100
mg/
L)
in
drinking
water
in
rats.
After
9
month
treatment
the
osmotic
fragility
of
the
red
blood
cells
(
RBC)
was
decreased
in
all
treatment
groups,
while
a
decreased
blood
glutathione
was
only
observed
in
the
chlorite/
chlorate
groups.
At
2,
4
and
6
months,
no
significant
hematologic
changes
were
noted
in
treated
rats
compared
to
control.
After
9
month
RBC
counts,
hematocrit
and
Hb
were
decreased
in
all
treatment
groups.
Chlorine
dioxide,
chlorite
and
chlorate
administered
chronically
in
drinking
water
for
3
months
inhibited
the
incorporation
of
3H­
thymidine
into
nuclei
of
rat
testes.
This
inhibition
was
observed
in
the
liver
of
the
chlorite
groups
and
in
the
kidney
of
100
mg/
L
chlorine
dioxide
treatment.
The
incorporation
in
small
intestinal
nuclei
was
increased
in
10
and
100
mg/
L
chlorine
dioxide
and
in
10
mg/
L
chlorite
groups.
Rat
body
weight
was
decreased
in
all
groups
after
10
and
11
months
(
Abdel­
Rahman
et
al.
1984)
Page
82
of
141
EPA/
PATHOLOGY
ASSOCIATES
Study
In
a
published
study
conducted
by
USEPA
Risk
Reduction
Engineering
Laboratory/
Environmental
Monitoring
Systems
Laboratory
in
Cincinnati,
Ohio
and
by
Pathology
Associates
in
Ohio
(
McCauley
et
al,
1995),
Sprague
Dawley
rats
(
10/
sex/
group)
were
exposed
to
sodium
chlorate
in
the
drinking
water
at
concentrations
of
0
(
distilled
water
control),
48
mM
saline
(
sodium
chloride)
control,
3.0
mM
sodium
chlorate,
12
mM
sodium
chlorate
or
48
mM
sodium
chlorate
for
90
days.
The
final
sodium
concentration
was
48.0
mM
for
each
group
except
for
the
distilled
water
control.
At
the
end
of
90
day
exposure
animals
were
sacrificed
and
organs
were
collected
for
gross
pathological
and
histopathological
examination.
Blood
was
collected
for
clinical
and
hematological
evaluation.

During
the
course
of
chlorate
exposure,
no
behavioral
or
clinical
abnormalities
were
noted
and
there
were
no
compound
related
deaths.
The
water
consumption
was
100
g/
kg/
day
for
the
distilled
water
control
group
males
and
the
mid­
dose
group
males.
The
other
male
groups
consumed
20
to
30%
more.
The
water
consumption
for
the
females
was
133,
167,
172,
163,
and
200
g/
kg/
day
for
the
distilled
water
control,
saline
control,
low­,
mid­
and
high­
dose
groups,
respectively.
Based
on
the
water
consumption,
the
mean
delivered
doses
were
calculated
to
be
0.36
mM
(
30
mg),
1.2
mM
(
100
mg),
and
6.14
mM
(
510
mg)
chlorate/
kg/
day
for
the
low­,
midand
high­
dose
males
and
0.5
(
42
mg),
1.9
(
158
mg),
and
9.6
mM
(
797
mg)
chlorate/
kg/
day
for
the
low­,
mid­
and
high­
dose
females,
respectively.
Treatment­
related
effects
were
conspicuous
in
the
high
dose
group.
These
included
significant
body
weight
reduction
throughout
the
exposure
group
in
both
sexes,
significant
decreases
in
male
relative
organ
weights
of
the
heart,
kidneys
and
liver
with
relative
brain
and
testes
weights
increased,
significant
declines
in
female
relative
weights
of
adrenals,
thymus
and
spleen
with
significant
brain
weight
increased,
significant
decreases
in
clinical
chemistry
parameters:
ALT,
AST,
calcium,
creatine,
and
phosphorus
and
an
increase
in
the
serum
cholesterol.
Calcium
and
creatinine
also
declined
in
the
mid­
dose
group,
serum
BUN
levels
were
decreased
in
the
low
dose
females.
The
biological
relevance
of
the
clinical
chemistry
changes
in
all
chlorate
groups
was
considered
doubtful,
since
most
of
the
values
were
within
the
normal
reference
ranges.
There
was
a
significant
decrease
in
hematocrit
concentration
and
red
and
white
blood
cell
counts
in
the
high
dose
animals
while
females
of
this
group
exhibited
a
trend
towards
decreased
erythrocyte
and
hematocrit
values.
Histopathologically,
thyroid
colloid
depletion
was
noted
in
both
control
and
treated
animals
in
a
dose
related
manner
and
was
characterized
by
an
increased
number
of
smaller
follicles
which
were
lined
by
a
prominent
cuboidal
epithelium
but
devoid
of
colloid.
The
control
group
had
an
incidence
of
30%
with
a
minimal
to
mild
severity
while
those
in
the
mid
and
high
dose
groups
exhibited
a
100%
incidence
level
with
a
moderate
to
marked
severity.
The
authors
cite
a
published
study
(
Harrington
and
Shertzer,
1985)
which
demonstrates
the
effects
of
chlorine
dioxide
on
the
bioavailability
of
iodide
in
drinking
water
and
diet.
In
that
paper,
it
was
concluded
that
chlorine
dioxide
in
drinking
water
oxidizes
iodide
to
a
reactive
form
which
binds
to
tissues
of
the
digestive
tract
while
with
dietary
chow
it
converts
iodide
to
a
less
easily
absorbed
by
organification
to
dietary
constituents.
According
to
current
study
authors
"
these
findings
suggest
a
possible
mechanism
by
which
chlorate,
a
by­
product
of
chloride
dioxide
degradation,
may
Page
83
of
141
accentuate
colloid
depletion
due
to
this
anti­
thyroid
effect
of
reducing
iodide
availability".
The
study
authors
concluded
that
based
on
the
biologically
significant
changes
noted
in
the
mid
and
high
dose
groups
of
both
sexes
(
thyroid
colloid
depletion)
and
hematological
effects
at
the
high
dose,
the
LOAEL
is
1.20
mM
(
100
mg
chlorate)/
kg
bw/
day
in
males
and
1.9
mM
(
158
mg
chlorate)/
kg
bw/
day
for
females
and
the
NOAEL
is
0.36
mM
(
30
mg
chlorate/
kg
bw/
day
in
males)
and
0.50
mM
(
42
mg
chlorate/
kg
bw/
day
for
females).

EPA/
NTP
Studies
In
a
21
day
oral
toxicity
study
(
NTP
1999a
and
1999b),
B6C3F1
mice
and
Fisher
344
rats
(
10/
sex/
dose)
were
exposed
to
sodium
chlorate
in
the
drinking
water
at
0,
125,
500,
1000
or
2000
mg/
L
.
Measured
consumption
was
0,
22,
43,
173
or
348
mg/
kg/
day
for
male
mice,
0,
20,
44,
94,
192
or
363
mg/
kg/
day
for
female
mice;
0,
20,
36,
77
or
170
mg/
kg/
day
for
male
rats
and
0,
21,
38,
73,
152
or
338
mg/
kg/
day
for
female
rats.
In
mice,
sodium
chlorate
had
no
effect
on
survival,
body
weights,
clinical
signs,
water
consumption,
hematology
parameters,
methemoglobin
concentration,
or
organ
weights
of
either
sex.
There
were
no
gross
or
microscopic
lesions
that
were
considered
to
be
due
to
sodium
chlorate
treatment.
In
rats,
sodium
chlorate
had
no
effect
on
survival,
body
weights,
clinical
signs
or
water
consumption.
A
moderate
to
severe
neutropenia
was
observed
in
both
sexes
on
day
4
and
22.
Very
mild
decreases
in
erythrocyte
counts,
hemoglobin,
and
hematocrit
were
considered
not
to
be
biologically
significant.
The
only
gross
or
microscopic
lesion
that
was
considered
to
be
treatment
related
was
a
minimal
to
mild
follicular
cell
hyperplasia
of
the
thyroid
gland
seen
in
males
at
500
mg/
L
or
greater
and
in
females
at
250
mg/
L
or
greater.
The
thyroid
gland
was
considered
to
be
a
target
organ
for
sodium
chlorate
toxicity
in
the
rat.

In
a
published
study
conducted
by
USEPA
National
Health
and
Environmental
Effects
Research
Laboratory
and
the
NTP
National
Institute
of
Environmental
Health
Sciences
in
North
Carolina
(
Hooth
et
al,
2001),
to
evaluate
development
of
thyroid
lesions
in
rodents
exposed
to
sodium
chlorate
in
the
drinking
water,
male
and
female
F344
rats
and
B6C3F
1
mice
(
10/
group)
were
exposed
to
sodium
chlorate
in
drinking
water
at
0,
0.125,
0.25,
1
or
2
g/
L
for
21
days
(
NTP
study)
.
In
another
test,
male
and
female
rats
(
10/
group)
were
exposed
at
0,
0.125,
1
or
2
g/
L
for
4,
21
or
90
days
(
NTP
study).
Additional
male
rats
(
10/
group)
were
exposed
to
0,
0.001,
0.01,
0.1,
1
or
2
g/
L
for
90
days
(
EPA
study).
Mean
compound
consumption
at
these
water
concentrations
was
estimated
by
the
reviewer
to
be
0.112,
1.12,
11.2,
112,
and
225
mg/
kg/
day
for
the
males
and
0.16,
1.6,
16.0,
160,
320
mg/
kg/
day
for
the
females
based
on
water
consumption
values
reported
in
the
McCauley
et
al,
1995
article.
Additional
female
rats
and
female
mice
(
6/
group)
were
exposed
to
0,
0.500,
1,
2,
4,
or
6
g/
L
for
105
days
(
EPA
study)
(
82,
165,
330,
660,
990
estimated
mg/
kg/
day).
Animals
were
observed
daily
and
moribund
animals
were
necropsied.
Prior
to
necropsy,
a
blood
sample
was
collected
from
animals
treated
for
4,
21
or
90
days
and
the
serum
was
separated
and
frozen
(
NTP
study).
Complete
necropsies
were
performed
on
all
animals
and
tissues
of
interest
were
removed,
examined
macroscopically,
and
fixed
in
10%
neutral
buffered
formalin.
Fixed
thyroid
tissues
were
processed
by
routine
methods
to
5
um
paraffin
sections
and
stained
with
hematoxylin
and
eosin
for
histological
examination
by
light
Page
84
of
141
microscopy.
The
thyroids
were
examined
for
the
presence
of
colloid
depletion,
follicular
cell
hypertrophy,
and
follicular
cell
hyperplasia.

Total
serum
triiodothyronine
(
T
3
)
and
thyroxine
(
T
4
)
concentrations
were
determined
as
well
as
the
thyroid
stimulating
hormone
(
TSH)
concentrations.
Serum
T
3
and
T
4
levels
were
decreased
significantly
and
TSH
levels
increased
significantly
in
male
and
female
rats
after
4
days
of
treatment
with
1.0
or
2.0
g/
L
sodium
chlorate
and
after
21
days
of
treatment
with
2.0
g/
L.
TSH
levels
also
increased
significantly
in
male
rats
after
21
days
of
treatment
with
1.0
g/
L.
Serum
T
3
and
T
4
levels
were
comparable
to
controls
in
male
and
female
rats
after
90
days
of
treatment,
but
TSH
levels
were
increased
in
both
sexes.

Thyroid
alterations
were
initially
diagnosed
using
standard
published
methods.
According
to
this
method,
follicular
cell
hyperplasia
and
severe
colloid
depletion
were
present
in
all
male
and
female
F344
rats
following
21
days
of
treatment
with
1.0
g/
L
treatment
of
sodium
chlorate
or
greater.
The
severity
of
the
lesions
was
the
same
in
all
animals.
The
present
study
utilized
a
"
novel"
method
of
diagnosis
detailed
in
the
article.
According
to
this
diagnosis
colloid
depletion
and
hypertrophy
were
present
in
male
and
female
rats
treated
with
0.125
g/
L
or
greater,
but
were
statistically
significant
(
p<
0.05)
at
0.5
g/
L
treatments.
In
males,
the
incidence
and
severity
of
thyroid
alterations
was
greater
at
1.0
g/
L
Sodium
chlorate
than
2.0
g/
L,
but
in
females,
it
was
the
opposite.
After
90
days
of
treatment,
significant
colloid
depletion
was
diagnosed
in
most
treated
male
F344
rats
but
the
incidences
were
similar
in
all
groups.
Colloid
depletion
was
more
significant
in
female
rats
treated
with
1.0
or
2.0
g/
L
sodium
chlorate
for
21
days
than
for
105
days.
Significant
colloid
depletion
was
diagnosed
in
female
F344
rats
treated
for
105
days
at
sodium
chlorate
concentrations
of
2.0
g/
L
or
greater.

Follicular
cell
hypertrophy
was
present
in
most
male
and
female
rats
after
21
or
90
days
of
sodium
chlorate
treatment,
but
the
incidence
did
not
increase
in
a
concentration
dependent
manner.
The
incidence
of
follicular
cell
hypertrophy
was
higher
in
female
rats
treated
with
1.0
or
2.0
g/
L
sodium
chlorate
for
21
days
than
for
105
days.
At
105
days,
6.0
g/
L
of
sodium
chlorate
caused
a
significant
increase
in
the
incidence
of
follicular
cell
hypertrophy.
Complex
papillary
infolding
or
branching
was
more
frequent
in
thyroid
tissue
from
male
rats
at
the
1.0
and
2.0
g/
L
concentrations.
The
area
of
the
thyroid
tissue
affected
in
male
rats
increased
in
a
concentration
dependent
manner
following
90
days
of
treatment.
Thyroid
alterations
were
not
present
in
male
or
female
mice.

It
was
concluded
by
the
study
authors
that
sodium
chlorate
treatment
induced
a
concentration
dependent
increase
in
the
incidence
and
severity
of
thyroid
follicular
cell
hyperplasia.
Colloid
depletion
and
hypertrophy
were
the
most
sensitive
histopathological
indicators
of
sodium
chlorate
exposure
in
male
F344
rats
at
21
and
90
days,
although
the
hypertrophy
response
was
variable
when
concentration
dependency
was
evaluated.
Male
rats
were
more
sensitive
to
the
effects
of
sodium
chlorate
treatment
than
female
rats.
Decreases
in
serum
hormone
levels
observed
in
the
present
study
may
suggest
that
sodium
chlorate
has
the
potential
to
induce
acute
detrimental
neurodevelopmental
effects.
Hormone
and
histological
alterations
may
reflect
a
transient
Page
85
of
141
physiologic
response
of
the
thyroid
to
sodium
chlorate
exposure.
It
is
not
known
whether
the
histological
effects
of
sodium
chlorate
are
reversible
following
cessation
of
chemical
exposure.
Alternatively,
the
concentration
dependent
increase
in
incidence
and
severity
of
thyroid
follicular
cell
hyperplasia
may
indicate
an
increased
likelihood
of
the
lesions
progressing
to
cancer.
The
study
authors
did
not
provide
a
NOAEL
for
the
effects
of
sodium
chlorate
treatment
in
rats,
but
based
on
the
article,
a
NOAEL
may
be
derived
at
0.5
g/
L
(
28
mg/
kg/
day
in
males
and
40
mg/
kg/
day
in
females)
based
on
colloid
depletion
and
follicular
cell
hyperplasia
at
a
LOAEL
of
1.0
g/
L
(
112
mg/
kg
day
for
males
and
160
mg/
kg/
day
for
females)
sodium
chlorate
after
90
days
of
exposure.
Chlorate
is
related
in
structure
to
bromate
and
perchlorate,
both
are
thyroid
toxicants
and
chemical
oxidants.

870.3150
90­
Day
Oral
Toxicity
­
Dog
In
a
subchronic
oral
toxicity
study
(
MRID
40460402),
beagle
dogs
(
4/
sex/
group)
were
dosed
with
technical
grade
sodium
chlorate
(
100%
a.
i.,
white
granular
solid)
by
oral
gavage
at
dose
levels
of
0
(
distilled
water),
30,
60,
or
360
mg/
kg/
day
for
90
consecutive
days.
All
dogs
survived
the
treatment.
Clinical
signs
were
sporadic,
one
female
in
the
high
dose
group
exhibited
emesis
during
the
first
three
weeks
of
dosing
and
two
other
females
developed
yellow/
brown
watery
stool.
There
were
no
effects
on
hematological
parameters,
clinical
chemistry
(
including
methemoglobin),
opthalmology
or
histopathology.
Urinalysis
was
not
conducted.
The
adrenal,
and
spleen
weights,
and
organ/
body
weight
ratios
in
males
were
increased
at
the
HDT.
Only
the
spleen
weights
in
females
were
increased
at
the
HDT.
Hypercellularality
of
the
bone
marrow
of
males
appeared
to
increase
in
severity
and
number
of
animals
responding
as
the
dose
was
increased.
The
effect
was
less
pronounced
in
females.
None
of
these
effects
are
sufficiently
adverse
to
establish
an
effect
level.
The
dose
levels
used
in
this
study
were
too
low
to
detect
unequivocal
toxicity.
At
higher
dose
levels
in
a
range­
finding
study,
emesis
occurred,
and
it
was
stated
that
emesis
would
have
precluded
a
study
at
higher
dose
levels.
The
LOAEL
derived
from
this
study
is
>
360
mg/
kg/
day
and
the
NOAEL
is
360
mg/
kg/
day
(
the
HDT).
This
study
is
considered
Acceptable/
guideline
(
The
study
was
originally
classified
supplementary
because
of
missing
data
regarding
incomplete
histopathological
examination
of
mammary
tissues,
and
number
of
animals
examined
opthalmologicaly
was
not
stated.
These
do
not
impact
the
acceptability
of
the
study).

In
a
sub­
acute
exposure
study
in
dogs,
doses
of
200
to
326
mg/
kg/
day
of
sodium
chlorate
administered
daily
by
intubation
as
50
ml
of
6%
solution
to
8
dogs
for
5
days
caused
reduction
of
packed
cell
volume,
hemoglobin
and
red
blood
cells
(
Heywood
et
al,
1972
cited
in
the
Final
Draft
Drinking
Water
Criteria,
Clement
International
Corp.,
1994).
A
consistent
increase
in
plasma
urea
concentration
was
also
observed,
suggesting
some
compromise
of
renal
function.
Two
animals
that
received
308
or
326
mg/
kg/
day
suffered
appetite
loss,
body
weight
decline
and
appearance
of
blood
in
their
urine
or
feces.
One
of
the
animals
(
not
specified)
died
after
4
days
of
exposure.
Postmortem
examination
of
both
animals
revealed
typical
signs
of
chlorate
poisoning,
including
cyanotic
kidney
surface
and
evidence
of
necrosis
and
hemolysis
in
the
kidney.
Five
of
the
8
animals
displayed
tissue
pathology
indicative
of
hemolysis
such
as
Kupffer
cells
containing
Page
86
of
141
brown
pigment.
Hematological
values
of
red
blood
cells
were
reduced
in
all
animals.
The
highest
methemoglobin
concentrations
was
seen
in
the
animal
that
died.
Methemoglobinemia
was
not
correlated
with
changes
in
the
other
hematological
parameters.

870.4100a
Chronic
Toxicity
­
Mouse
In
the
NTP
(
DRAFT
NTP
Report
2004)
study
presented
in
a
draft
form,
Groups
of
50
male
and
50
female
B6C3F
1
mice
were
exposed
to
drinking
water
containing
0,
500,
1,000,
or
2,000
mg/
L
sodium
chlorate
for
2
years
(
equivalent
to
average
daily
doses
of
approximately
40,
80,
and
160
mg/
kg
per
day
to
male
mice
and
30,
60,
and
120
mg/
kg
per
day
to
female
mice).
Survival
of
exposed
mice
was
similar
to
that
of
the
control
groups.
Mean
body
weights
of
exposed
females
were
generally
less
(
88­
90%
of
controls
in
all
treated
females
at
week
104)
than
those
of
the
control
groups
after
week
84
of
the
study.
Water
consumption
by
exposed
mice
was
generally
similar
to
that
by
controls
throughout
the
study
(
3.4­
4.2
g/
male/
day;
2.5­
3.6
g/
female/
day).
There
was
a
positive
trend
in
the
incidences
of
pancreatic
islet
cell
adenoma
or
carcinoma
(
combined)
in
female
mice
(
0/
46,
2/
47,
2/
49,
4/
49).
Thyroid
gland
follicular
cell
hypertrophy
was
significantly
increased
in
2,000
mg/
L
females
(
3/
48,
2/
50,
5/
49,
14/
50).
The
incidences
of
bone
marrow
hyperplasia
were
significantly
increased
in
all
exposed
groups
of
females
(
14/
50,
28/
50,
29/
50,
31/
50).

Carcinogenicity
870.4200a
Carcinogenicity
Study
­
rat
A
2­
year
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
in
a
draft
form.
A
final
report
of
this
study
is
expected
during
2005.
In
the
NTP
(
2004)
study
summarized
in
Section
4.4.3
of
the
main
body
of
this
memo,
there
was
some
evidence
of
thyroid
gland
follicular
cell
carcinogenicity
in
male
rats
which
may
be
attributed
to
the
imbalance
of
thyroid
hormones
(
reduced
T
3
and
T
4
and
elevated
TSH)
seen
in
these
studies
as
a
result
of
exposure
to
high
doses
of
sodium
chlorate.
Current
EPA
HED
policy
considers
nonmutagenic
pesticides
that
induce
elevated
levels
of
TSH
and
thyroid
follicular
cell
tumors
in
the
rat
as
not
likely
to
be
cargencogenic
to
humans
at
doses
that
do
not
alter
rat
thyroid
hormone
homeostasis.

In
a
published
study,
sodium
chlorate
and
potassium
chlorate
were
tested
for
potential
promoting
effect
in
a
two
stage
rat
renal
carcinogenesis
assay
(
Kurokawa
et
al,
1985).
In
this
assay
three
groups
of
15
male
F344
rats
were
given
N­
ethyl­
N­
hydroxyethylnitrosamine
(
EHEN)
at
0.05%
concentration
in
the
drinking
water
for
the
first
2
weeks
during
the
initiation
phase.
Subsequently,
one
group
of
the
initiated
rats
was
treated
with
1%
sodium
chlorate,
second
group
with
1%
potassium
chlorate
and
the
third
group
with
distilled
water
for
25
weeks.
Three
other
groups
(
controls)
were
treated
similarly,
except
that
distilled
water
was
given
in
the
initiation
phase.
Page
87
of
141
These
doses
were
selected
on
the
basis
of
6
week
study
where
male
F344
rats
were
administered
the
test
compounds
in
the
drinking
water
at
0,
0.25%,
1%
or
2%
concentrations
and
found
that
1%
concentration
was
the
maximum
tolerated
concentration
for
both
test
compounds.
All
animals
survived
the
treatment
in
the
main
study.
The
mean
final
body
weight
in
the
sodium
chlorate
and
potassium
chlorate
groups
with
or
without
initiation
were
significantly
lower
(
p
<
0.05­
0.01)
than
the
controls.
The
mean
intake
of
drinking
water
(
water
consumption)
in
rats
treated
with
sodium
chlorate
or
potassium
chlorate
was
slightly
lower
than
the
controls
and
it
ranged
from
19.2
­
22.1
ml/
day/
rat.
The
mean
consumption
of
sodium
chlorate
was
654­
686
mg/
kg/
day
for
sodium
chlorate
and
667
to
675
mg/
kg/
day
for
the
potassium
chlorate.
At
the
end
of
promotion
phase,
rats
were
sacrificed
and
kidneys
examined
histopathologically
for
renal
neoplastic
lesions
which
were
classified
as
dysplastic
foci
and
renal
cell
tumors.
The
mean
absolute
kidney
weights
were
comparable
in
all
groups,
but
the
mean
relative
kidney
weights
given
the
sodium
chlorate
or
potassium
chlorate
with
or
without
initiation
were
significantly
(
p<
0.01­
0.05)
lower
than
the
control
group.
There
were
no
statistically
significant
differences
in
the
incidences
in
the
mean
number
of
the
types
of
the
kidney
lesions
between
the
test
compounds
and
the
distilled
water
treated
rats
initiated
with
EHEN,
it
was
concluded
that
sodium
chlorate
and
potassium
chlorate
did
not
have
a
promoting
effect
in
rat
renal
carcinogenesis
assay
(
Kurokawa
et
al,
1985).

870.4200b
Carcinogenicity
(
feeding)
­
Mouse
A
2­
year
bioassay
to
determine
the
potential
of
sodium
chlorate
to
induce
thyroid
tumors
in
laboratory
animals
(
rats
and
mice)
has
been
recently
reported
in
a
draft
form
(
DRAFT
NTP
Report
2004).
A
final
report
of
this
study
is
expected
during
2005.
As
summarized
above,
there
was
a
positive
trend
in
the
incidences
of
pancreatic
islet
cell
adenoma
or
carcinoma
(
combined)
in
female
mice
(
0/
46,
2/
47,
2/
49,
4/
49).
This
finding
was
considered
to
be
equivocal
evidence.

870.7485
Metabolism
­
Rat
The
pharmacokinetics
of
chlorite
ion
and
chlorate
ion
was
studied
in
rats
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985).
Two
groups
of
male
Sprague­
Dawley
rats
(
4/
group)
were
administered
orally
36Cl­
labeled
potassium
chlorate
or
potassium
chlorite
at
concentrations
of
10
mg/
L.
In
one
group,
blood
samples
were
collected
at
selected
times
between
5
minutes
and
48
hours
after
dosing
and
assayed
for
36Cl­
activity
and
at
72
hours,
the
rats
were
killed
and
the
tissue
distribution
of
36Cl­
activity
was
determined.
In
the
other
group,
expired
air,
urine,
and
fecal
samples
were
obtained
for
up
to
72
hours
and
assayed
for
36Cl­
activity.
Maximum
blood
36Clconcentrations
occurred
2
hours
after
dosing
with
potassium
chlorite
and
1
hour
after
treatment
with
potassium
chlorate.
Potassium
chlorate
elimination
from
the
blood
was
biphasic,
with
half
lives
of
6
hours
for
the
first
phase
and
36.7
hours
for
the
second
phase.
Potassium
chlorite
elimination
was
monophasic
with
a
half
life
of
35
hours.
After
72
hours,
36Cl­
activity
was
highest
in
whole
blood
following
potassium
chlorite
administration
and
highest
in
plasma
following
potassium
chlorate
administration.
The
highest
measured
radioactivity
after
the
plasma
in
the
chlorate
treated
rats
was
in
the
whole
blood
followed
by
stomach,
testes,
lungs,
kidneys,
Page
88
of
141
skin,
duodenum,
spleen,
brain,
packed
cells,
ileum,
carcass,
liver,
and
bone
marrow.
36Clconcentration
in
the
plasma
was
2
ng/
g,
and
in
bone
marrow
was
less
than
0.5
ng/
g.
Significantly
high
levels
of
36Cl­
activity
after
dosing
with
both
compounds
were
found
in
the
testes.
Seventy
two
hours
after
dosing
with
potassium
chlorite,
35
percent
of
the
dose
was
eliminated
in
the
urine
and
5%
in
the
feces.
Approximately
43%
of
the
potassium
chlorate
dose
was
eliminated
by
the
urinary
and
feces
routes.
36Cl­
was
not
detected
in
exhaled
air
after
dosing
with
either
compound.
The
administered
chlorate
was
eliminated
as
chlorate
(
ca.
13%
of
the
administered
dose),
chlorite
(
ca.
4%
of
the
administered
dose)
and
chloride
(
ca.
20%
of
the
administered
dose).
The
authors
suggest
that
the
high
levels
of
36Cl­
activity
in
the
testes
after
72
hours
suggest
possible
pharmacological
action
at
this
site.

870.7485
Metabolism
­
Dog
A
metabolism
study
in
dogs
is
reported
in
the
National
Research
Council
1980
report
on
Drinking
Water
and
Health
and
is
summarized
in
California
EPA/
OEHHA
2002
Report
(
OEHHA,
2002).
In
this
study,
when
seven
female
dogs
were
given
500
mg/
kg
doses
of
chlorate
in
500
mL
water,
55­
70
%
of
the
dose
was
excreted
in
the
urine
in
the
first
6
hours.
By
24
to
48
hours,
76­
99%
of
the
dose
had
been
excreted
unchanged
in
urine.
The
chlorate
concentration
in
the
blood
peaked
at
2
hours
and
decreased
to
little
or
none
by
24
hours.
Page
89
of
141
Special/
Other
Studies
Sodium
Chlorate
as
an
Inhibitor
of
Protein
Sulfation
Sodium
chlorate
has
been
described
as
a
non­
toxic
inhibitor
of
tyrosine
sulfation
(
Beinfeld,
1994).
This
property
is
utilized
by
biochemists
to
study
peptide
and
protein
synthesis,
regulation
of
protein
secretion
and
function
(
Beinfeld,
1994;
Mintz
et
al,
1994).
Sodium
chlorate
is
an
in
vitro
inhibitor
of
ATP­
sulfurylase,
the
first
enzyme
in
the
biosynthesis
of
3'­
phosphoadenosine
5'­
phosphosulfate
which
is
the
ubiquitous
co­
substrate
for
sulfation
(
Baeuerle
and
Huttner,
1986).
Treatment
of
hybridoma
derived
cells
and
rat
pheochromocytoma
cell
cultures
with
1
mM
sodium
chlorate
in
a
medium
low
in
sulfate
and
sulfur­
containing
amino
acids
resulted
in
more
than
95%
inhibition
of
protein
sulfation
as
well
as
tyrosine
and
carbohydrate
sulfation,
but
did
not
inhibit
protein
synthesis
even
after
prolonged
incubation.
The
authors
concluded
from
this
study
that
sodium
chlorate
"
provides
powerful
tool
for
studying
the
biological
significance
of
protein
sulfation"
(
Baeuerle
and
Huttner,
1986).
The
sulfation
of
polyethylene
glycol
200
by
the
isolated
perfused
guinea
pig
liver
was
inhibited
to
about
60%
by
10
mM
of
sodium
chlorate
in
the
plasma
of
the
perfusate
when
the
concentration
of
the
sulfate
ion
was
1.18
mM,
but
in
a
low
sulfate
medium
(
0.1mM),
the
inhibition
was
almost
complete
(
94%)
(
Roy
et
al,
1988).
Bile
production
from
isolated
perfused
livers
was
not
affected
by
the
presence
of
sodium
chlorate
in
this
test,
suggesting
that
chlorate
is
not
a
general
liver
poison
according
to
the
authors
of
this
article
(
Roy
et
al,
1988).
When
bovine
aorta
endothelial
cells
were
cultured
in
a
medium
containing
3Hglucosamine
35S­
sulfate
and
various
concentrations
of
sodium
chlorate,
cell
growth
and
viability
was
not
affected
by
10mM
chlorate
and
slight
inhibition
at
30
mM
(
Humphries
and
Silbert,
1988).
Chlorate
concentrations
of
10
mM
and
greater
resulted
in
significant
inhibition
of
sulfation
of
chondroitin.
With
30
mM
chlorate
the
inhibition
was
90%
for
chondroitin
and
65%
for
heparin,
but
3H­
glucosamine
incorporation
was
not
inhibited.
Removal
of
chlorate
from
the
cell
culture
medium
restored
the
rapid
resumption
of
sulfation.

Chlorate
Toxicity
in
Humans
In
a
series
of
studies
by
Lubbers
et
al
(
1984a,
1984b),
investigating
the
physiological
impact
of
human
ingestion
of
chlorine
dioxide
and
its
water
breakdown
byproducts
(
chlorite
and
chlorate),
reported
no
effects
attributable
to
the
daily
consumption
of
water
treated
with
these
products
for
periods
extending
to
12
weeks.
In
these
studies
normal
healthy
adult
male
volunteers
(
21­
35
years
of
age)
divided
into
groups
(
10/
group)
drank
daily
500
mL
of
water
containing
5
ppm
of
chlorite,
or
chlorate
or
distilled
water
(
control)
for
12
weeks.
Subjects
were
monitored
weekly
during
the
12
week
treatment
and
for
8
additional
weeks
by
conducting
physical
medical
examination,
checking
vital
signs.
Special
chemical
tests
for
thyroid
function,
antibody
formation,
hepatoglobin
and
methemoglobin
concentrations,
and
blood
morphology
were
repeated
regularly
to
assess
physiological
functions
in
areas
"
suspected
to
be
most
sensitive
to
oxidative
challenge".
Subjective
evaluations
of
the
palatability
of
the
water
disinfectant
solutions
were
recorded
at
regular
intervals.
A
total
of
47
quantitative
chemical
parameters
derived
from
an
extensive
battery
of
blood
and
urine
testing
were
recorded
regularly.
Abnormalities
in
the
qualitative
blood
and
urine
analysis
were
few
and
appeared
to
be
randomly
distributed.
In
several
cases,
Page
90
of
141
statistically
significant
trends
(
mean
corpuscular
hemoglobin
levels)
were
associated
with
treatment,
but
"
none
of
these
were
judged
to
have
physiological
consequence".
The
authors
concluded
that
the
possibility
that
these
trends
might
achieve
proportions
of
clinical
importance
cannot
be
ruled
out,
but
"
within
the
limits
of
the
study,
the
relative
safety
of
oral
ingestion
of
chlorine
dioxide,
and
its
metabolites,
chlorite
and
chlorate,
was
demonstrated".
In
their
second
study
(
Lubbers
et
al,
1984b),
3
male
healthy
adult
volunteers
deficient
in
glucos­
6­
phosphate
dehydrogenase
and
receiving
500
mL
of
water
containing
500
ppm
of
sodium
chlorite
did
not
experience
any
adverse
effects
demonstrating
the
safety
of
this
chemical
to
a
susceptible
group
of
the
human
population.

These
data
were
not
deemed
useful
for
dose­
response
evaluation
and
were
not
relied
upon
in
the
risk
assessment.

Chlorates
Mechanism
of
Toxicity
The
mode
of
action
in
sodium
chlorate
poisoning
in
humans
is
summarized
by
Smith
and
Oehme
(
1991)
in
their
review
article.
The
chlorate
ion
initially
reacts
with
thiol
groups
on
the
red
blood
cells
and
may
cause
it
to
lyse,
similar
to
nitrite
ions,
converting
the
hemoglobin
to
methemoglobin.
The
chlorate
ion
is
a
strong
oxidizer,
and
it
oxidizes
the
ferrous
ion
of
the
hemoglobin
molecule
to
ferric
ion
to
result
in
methemoglobin
formation.
With
chlorate,
in
contrast
to
nitrite,
a
concentration
dependent
lag
phase
was
seen
before
methemoglobin
was
formed
(
Singelmann
et
al,
1984).
Sodium
chlorate
ranked
the
least
potent
among
six
direct­
acting
methemoglobin
agents
(
French
et
al,
1995).
These
were
(
most
to
least)
p­
dinitrobenzene
>
o­
dinitrobenzene
>
copper
=
nitrite
>
chlorite
>
chlorate.
The
ranking
was
based
on
linear
regression
analysis
of
dose­
response
data,
the
calculated
dose
expected
to
induce
a
given
amount
of
methemoglobin
formation
and
the
calculated
percentage
methemoglobin
response
induced
by
mmole/
L
of
the
agent
in
Dorset
sheep
erythrocytes.
Calbarese
et
al,
1995
also
investigated
the
potency
of
sodium
chlorate
to
produce
methemoglobin
in
mink
erythrocytes
and
it
was
the
least
potent
among
six
other
chemicals
(
anaphthol
nitrite>
copper>
p­
dinitrobenzene>
chlorite>
o­
dinitrobenzene>
chlorate).

Potassium
chlorate
incubated
with
washed
erythrocytes
from
human
venous
blood
(
0.1
to
6.0
mmol/
L)
caused
a
dose­
related
increase
in
glutathione
activity
and
mechanical
fragility
with
a
parallel
increase
in
Heinz
body
formation
(
Hopkins
and
Tudhope,
1974).
There
was
also
a
close
relationship
between
increased
mechanical
fragility
and
increased
inhibition
of
glutathione
peroxidase.
Spontaneous
hemolysis
in
this
test
was
less
than
10%.

The
mechanism
of
chlorate
poisoning
was
explored
in
a
set
of
in
vitro
and
in
vivo
experiments
by
Steffen
and
Wetzel
(
1993).
They
found
that
incubation
of
human
erythrocytes
with
5
mM
sodium
chlorate
oxidized
hemoglobin
to
methemoglobin
after
a
lag
period
of
approximately
60
minutes.
When
after
different
periods
of
contact
with
the
30
mM
chlorate,
samples
of
erythrocytes
were
washed
free
of
the
chlorate
and
incubated
with
methylene
blue,
reduction
of
methemoglobin
was
only
partial
during
the
first
hour
of
incubation
(
8%)
but
became
nil
after
2
hours
of
incubation.
Page
91
of
141
The
catalytic
reduction
of
methemoglobin
by
methylene
blue
was
found
to
be
dependent
on
the
availability
of
NADPH
formed
in
the
pentose
phosphate
cycle.
Therefore,
an
intact
enzyme
system
in
erythrocytes
is
required.
Incubation
of
homeliest
erythrocytes
with
5
mM
sodium
chlorate
showed
that
glucose­
6­
phosphate
dehydrogenase
and
glyceraldehyde
­
3­
phosphate
dehydrogenase
were
most
sensitive,
whereas
glutathione
reductase
was
very
stable.
When
human
erythrocyte
membranes
(
devoid
of
hemoglobin)
were
incubated
with
5
mM
sodium
chlorate,
there
was
a
rapid
inactivation
of
glyceraldehyde
­
3­
phosphate
dehydrogenase
when
hemoglobin
was
added,
but
not
in
its
absence.
This
suggests
that
sodium
chlorate
does
not
inactivate
the
membane­
bound
glyceraldehyde
­
3­
phosphate
dehydrogenase,
the
key
enzyme
in
the
NADPHdependent
methemoglobin
reduction.
Nearly
all
membrane
proteins
were
affected
by
the
hemoglobin
catalyzed
oxidation.
Earlier
work
by
Heubner
and
Jung,
1941
(
cited
by
Steffen
and
Wetzel,
1993)
demonstrated
that
methemoglobin
formation
by
chlorate
was
an
autocatalytic
reaction.
Both
the
lag
period
and
the
rate
were
dependent
on
the
actual
methemoglobin
concentration.

Steffen
and
Wetzel
(
1993)
also
explored
the
in
vitro
effects
of
chlorate
on
rabbit
erythrocytes
and
compared
them
to
the
in
vivo
effects
on
methemoglobin
formation
in
rabbits.
It
was
discovered
in
1888
by
Cahn
(
cited
by
Steffen
and
Wetzel,
1993)
that
rabbits
do
not
develop
methemoglobine
anemia
after
chlorate
administration.
When
rabbit
erythrocytes
were
incubated
with
sodium
chlorate
at
concentrations
ranging
from
7.5
to
75
mM,
methemoglobin
was
formed
in
a
dose
dependent
manner.
Higher
concentrations
of
the
chlorate
were
needed
for
rabbit
erythrocytes
than
for
the
human
erythrocytes.
No
methemoglobin
was
formed
after
the
oral
administration
of
sodium
chlorate
(
1000
mg/
kg
body
weight)
in
50
mL
water.
The
serum
concentration
of
the
chlorate
was
10
­
20
mM
for
at
least
12
hours.
The
highest
concentration
of
the
chlorate
in
the
serum
was
reached
after
90
minutes
(
16
±
4.3
mM)
and
in
the
urine
after
6
hours
(
246
±
99
mM).
The
elimination
half­
life
was
20
hours.
During
7
days
of
observation
period
there
were
no
changes
in
serum
values
of
urea,
creatinine,
aspartate
and
alanine
aminotransferases.
When
the
animals
were
killed
at
the
end
of
the
7
day
observation
period
and
kidneys
examined
histologically,
there
were
no
pathologic
findings
detected,
indicating
lack
of
nephrotoxicity
in
the
treated
rabbits.
Page
92
of
141
TOXICOLOGY
REFERENCES
UNPUBLISHED
MRID:
40444801
Barrett,
D.
(
1987)
A
Subchronic
(
3
Month)
Oral
Toxicity
Study
of
Sodium
Chlorate
in
the
Rat
Gavage:
Final
Report:
Project
No.
86­
3112.
Unpublished
study
prepared
by
Bio/
dynamics,
Inc.
464
p.

MRID:
40460401
Schroeder,
R.
(
1987)
A
Teratogenicity
Study
in
Rats
with
Sodium
Chlorate:
Project
No.
86­
3117.
Unpublished
study
prepared
by
Bio/
dynamics,
Inc.
372
p.

MRID:
40460402
Barrett,
D.
(
1987)
A
Subchronic
(
3
Month)
Oral
Toxicity
Study
in
the
Dog
Gavage
Administration
with
Sodium
Chlorate:
Project
No.
86­
3114.
Unpublished
study
prepared
by
Bio/
dynamics,
Inc.
323
p.

MRID:
41256201
May,
K.
(
1989)
Sodium
Chlorate:
Assessment
of
Mutagenic
Potential
in
Histidine
Auxotrophs
of
Salmonella
Typhimurium
(
Ames
Test):
Rept.
No.
89/
0285.
Unpublished
study
prepared
by
Life
Science
Research
Limited.
39
p.

MRID:
41256204
May,
K.
(
1989)
Sodium
Chlorate:
Assessment
of
Its
Ability
to
Cause
Lethal
DNA
Damage
in
Strains
of
Escherichia
Coli:
LSR
Report
No.
89/
SKR004/
0341.
Unpublished
study
prepared
by
Life
Science
Re­
search
Ltd.
34
p.

MRID:
41256202
Hudson­
Walker,
G.
(
1989)
Sodium
Chlorate:
Investigation
of
Mutage­
nic
Activity
at
the
HGPRT
Locus
in
a
Chinese
Hamster
V79
Cell
Mutation
System:
Report
No.
89/
0631.
Unpublished
study
prepared
by
Life
Science
Research.
42
p.

MRID:
41256203
Mackay,
J.
(
1989)
Sodium
Chlorate:
Assessment
of
Clastogenic
Action
on
Bone
Marrow
Erythrocytes
in
the
Micronucleus
Test:
LSR
Report
No.
89/
SKR003/
0253.
Unpublished
study
prepared
by
Life
Science
Research
Ltd.
34
p.

MRID:
41256204
May,
K.
(
1989)
Sodium
Chlorate:
Assessment
of
Its
Ability
to
Cause
Lethal
DNA
Damage
in
Strains
of
Escherichia
Coli:
LSR
Report
No.
89/
SKR004/
0341.
Unpublished
study
prepared
by
Life
Science
Re­
search
Ltd.
34
p.
Page
93
of
141
MRID:
41256205
Seeburg,
A.
(
1989)
Unscheduled
DNA
Synthesis
(
UDS)
in
Hela
S3
Cells
In
Vitro:
Sodium
Chlorate:
LSR­
RTC
Report
No.
102002­
M­
02289.
Unpublished
study
prepared
by
Life
Science
Research
Roma
Toxicology
Centre.
50
p.

PUBLISHED
Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1982.
Metabolism
and
pharmacokinetics
of
alternate
drinking
water
disinfectants.
Environ
Health
Perspect.
46:
19­
23.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1984a.
Toxicity
of
chlorine
dioxide
in
drinking
water.
J
AM
COLL
TOXICOL;
3
(
4)
277­
284.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1984b.
The
Kinetics
of
Chlorite
and
Chlorate
in
the
Rat.
Journal
of
the
American
College
of
Toxicology,
3(
4):
261­
267.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1985.
The
kinetics
of
chlorite
and
chlorate
in
rats.
J
Environ
Pathol
Toxicol
Oncol.
6(
1):
97­
103.

Aggazzotti
G,
Righi
E,
Fantuzzi
G,
Biasotti
B,
Ravera
G,
Kanitz
S,
Barbone
F,
Sansebastiano
G,
Battaglia
MA,
Leoni
V,
Fabiani
L,
Triassi
M,
Sciacca
S.
2004.
Chlorination
by­
products
(
CBPs)
in
drinking
water
and
adverse
pregnancy
outcomes
in
Italy.
J
Water
Health.
2(
4):
233­
47.

Baeuerle
PA,
Huttner
WB.
1986.
Chlorate
a
potent
inhibitor
of
protein
sulfation
in
intact
cells.
Biochem
biophys
res
commun;
141
(
2).
870­
877.

Beinfeld,
MC.
1994.
Inhibition
of
Cholecystokinin
(
CCK)
sulfation
by
treatment
with
Sodium
Chlorate
alters
its
processing
and
decreases
cellular
content
and
secretion
of
CCK
8.
Neuropeptides
26:
195­
200.

Bercz,
JP,
Jones
L,
Garner
L,
Murray
D,
Ludwig
DA,
Boston
J.
1982.
Subchronic
Toxicity
of
Chlorine
Dioxide
and
Related
Compounds
in
Drinking
Water
in
Nonhuman
Primate.
Env.
Hlth
Perspectives,
46:
47­
55.

Chang,
S.,
Crothers,
C.,
Lai,
S.,
Lamm,
S.
(
2003)
Pediatric
Neurobehavioral
Diseases
in
Nevada
Counties
with
respect
to
Perchlorate
in
Drinking
Water
­
An
Ecological
Inquiry.
Birth
Defects
Res
A
Clin
Mol
Teratol.
67(
10):
886­
92.

Cosmetic
Ingredient
Review
Panel.
1995.
Final
report
on
the
safety­
assessment
of
Potassium
Chlorate
J
Am
Coll
Toxicol.
14:
221­
30
Couri
D,
Abdel­
Rahman
MS,
Bull
RJ.
1982.
Toxicological
effects
of
chlorine
dioxide,
chlorite
and
chlorate.
Environ
Health
Perspect.
46:
13­
7.
Page
94
of
141
Dohler,
K.
D.,
Wong,
C.
C.,
Von
Zur
Muhlen,
A.
(
1979)
The
rat
as
a
model
for
the
study
of
drug
effects
on
thyroid
function:
Consideration
of
methodological
problems.
Pharmacol.
Ther.
5,
305­
318.

Eckhardt
K,
Gocke
E,
King
MT,
Wild
D.
1982.
Mutagenic
activity
of
chlorate,
bromate,
and
iodate
MUTAT
RES
97:
185.

French
CL,
Yaun
S­
S,
Baldwin
LA,
Leonard
DA,
Zhao
XQ,
Calabrese
EJ.
1995.
Potency
Ranking
of
Methemoglobin­
Forming
Agents.
J.
of
Appld.
Tox.,
15(
3):
167­
174.

Gill,
MW,
Swanson,
MS,
Murphy
SR,
Bailey
GP
.
2000.
Two­
Generation
Reproduction
and
Developmental
Neurotoxicity
Study
with
Sodium
Chlorite
in
the
Rat.
J.
Applied
Toxicology.
20(
4):
291­
203.

Helliwell,
M;
Nunn
J.
1979.
Mortality
in
Sodium
Chlorate
Poisoning.
British
Med.
J.
1:
1119
Heywood,
R,
Sortwell,
RJ,
Kelly,
PJ,
Street,
AE.
1972.
Toxicity
of
sodium
chlorate
to
the
dog.
Vet.
Rec.
90:
416­
418.

Hooth,
MJ,
DeAngelo
AB,
George
MH,
Gailard
ET,
Travlos
GS,
Boorman
GA,
Wolf
DC.
2001.
Subchronic
Sodium
Chlorate
Exposure
in
Drinking
Water
Results
in
a
Concentration­
Depndent
Increase
in
Rat
Thyroid
Follicular
Cell
Hyperplasia.
Toxicologic
Pathology.
29(
2):
250­
259.

Hopkins
J
and
Tudhope
GR,
1974.
The
effects
of
drugs
on
erythrocytes
in
vitro:
Heinz
body
formation,
glutahione
proxidase
inhibition,
and
changes
in
mechanical
fragility.
Br.
J.
Clin
Pharmacolo
1:
191­
195.

Kurokawa
Y,
Imazawa
T,
Matsushima
M,
Takamura
N,
Hayashi
Y.
1985.
Lack
of
promoting
effect
of
sodium
chlorate
and
potassium
chlorate
in
two­
stage
rat
renal
carcinogenesis.
J
Am
Coll
Toxicol
4:
331­
337.

Li,
F.
X.,
Byrd,
D.
M.,
Deyille,
G.
M.,
Sesser,
D.
E.,
Skeels,
M.
R.,
Katkowsky,
S.
R.,
Lamm,
S.
H.
(
2000)
Neonatal
Thyroid­
Stimulating
Hormone
Level
and
Perchlorate
in
Drinking
Water.
Teratology
62:
429­
431.

Li,
Z.,
Li,
X.
I.,
Byrd,
D.,
Deyhle,
G.
M.,
Sesser,
D.
E.,
Skeels,
M.
R.,
Lamm,
S.
H.
(
2000)
Natal
Thyroxine
Level
and
Perchlorate
in
Drinking
Water.
42:
200­
205.

Lubbers
JR,
Chauhan
S,
Miller
JK,
Bianchine
JR.
1984a.
The
effects
of
chronic
administration
of
chlorine
dioxide,
chlorite
and
chlorate
to
normal
healthy
adult
male
volunteers.
J
Environ
Pathol
Toxicol
Oncol
5(
4­
5):
229­
238.
Page
95
of
141
Lubbers
JR,
Chauhan
S,
Miller
JK,
Bianchine
JR.
1984b.
The
effects
of
chronic
administration
of
chlorite
to
glucose­
6­
phosphate
dehydrogenase
deficient
healthy
adult
male
volunteers.
J
Environ
Pathol
Toxicol
Oncol
5(
4­
5):
239­
242.

McCain,
R.
M.
(
1992)
Thyroid
gland
neoplasia:
non­
genotoxic
mechanisms.
Toxicol.
Lett.
64/
65,
397­
408.

McCauley
PT,
Robinson
M,
Daniel
FB,
Olson
GR.
1995.
The
effects
of
subchronic
chlorate
exposure
in
Sprague­
Dawley
rats.
Drug
and
Chemical
Toxicology
18(
2,3):
185­
199.

Meier
JR,
Bull
RJ,
Stober
JA,
Cimino
MC.
1985.
Evaluation
of
chemicals
used
for
drinking
water
disinfection
for
production
of
chromosomal
damage
and
sperm­
head
abnormalities
in
mice.
Environ
Mutagen
7
(
2):
201­
212.

Mintz
KP,
Fisher
LW,
Grzesik
WJ,
Hascall
VC,
Midura
RJ.
1994.
Chlorate­
induced
inhibition
of
tyrosine
sulfation
on
bone
sialoprotein
synthesis
by
a
rat
osteoblast
like
cell
line
(
UMR
106­
01
BSP).
JBiol.
Chem.
269(
7):
4845­
4852.

Moriya
M,
Ohta
T,
Watanabe
K,
Miyazawa
T,
Kato
K,
Shirasu
Y.
1983.
Further
mutagenicity
studies
on
pesticides
in
bacterial
reversion
assay
Systems.
MUTAT
RES
116:
185­
216.

NTP
(
1999a).
National
Toxicology
Program.
21­
day
toxicity
study
of
sodium
chlorate
administered
in
dosed
water
to
B6C3F1
mice.
NIEHS/
NTP
Contract
No.
N01­
ES­
85420.
Southern
Research
Institute,
February
11,
1999.

NTP
(
1999b).
National
Toxicology
Program.
21­
day
toxicity
study
of
sodium
chlorate
administered
in
dosed
water
to
Fisher­
344
rats.
NIEHS/
NTP
Contract
No.
N01­
ES­
85420.
Southern
Research
Institute,
February
11,
1999.

NTP
(
2002).
National
Toxicology
Program.
Final
Study
Report
on
the
Developmental
Toxicity
Evaluation
for
Sodium
Chlorate
(
CAS
No.
7775­
09­
9)
Administered
by
Gavage
to
New
Zealand
White
Rabbits
on
Gestational
Days
6
through
29.
Prepared
by
Julia
D.
George
and
Catherine
J
Price.
NIEHS/
NTP
Contract
No.
N01­
ES­
65405.
Govt
Reports
Announcements
&
Index
(
GRA&
I),
Issue
04,
2003
Research
Triangle
Inst.,
Research
Triangle
Park,
NC.
Center
for
Life
Sciences
and
Toxicology.

NTP
(
2004).
NTP
Technical
Report
on
the
Toxicology
and
Carcinogenesis
Studies
of
Sodium
Chlorate
(
CAS
No.
7775­
09­
9)
in
F344
rats
and
B6C3F1
Mice
(
Drinking
Water
Studies).
Scheduled
peer
review
date:
December
9­
10,
2004.
Draft
Report.

OEHHA.
2002.
Proposed
Action
Level
for
Chlorate.
Office
of
Environmental
Health
Hazard
Assessment,
California
EPA.
Memorandum
from
Robert
A.
Howd
to
David
P.
Spath.
January
7,
2002.
http://
www.
oehha.
ca.
gov/
water/
pals/
chlorate.
html
Page
96
of
141
Olivier
P,
Marzin
D.
1987.
Study
of
genotoxic
potential
of
48
inorganic
derivatives
with
the
SOS
chromotest.
Mutation
Research
189:
263­
270.

Roy
AB,
Curtis
CG,
Powell
GM.
1988..
The
inhibition
by
chlorate
of
the
sulfation
of
polyethyleneglycol
in
the
isolated
perfused
guinea
pig
liver.
Xenobiotica.
18(
9):
1049­
1055.

Singelmann
E,
Wetzel
E,
Adler
G,
Steffen
C.
1984.
Erythrocyte
membrane
alterations
as
the
basis
of
chlorate
toxicity.
Toxicology
30(
2):
135­
147.

Smith
EA;
Oehme
FW.
1991.
A
review
of
Selected
Herbicides
and
Their
Toxicities.
Vet.
Hum
Toxicol.
33:
596­
608
Steffen
C;
Seitz
R.
1981.
Severe
Chlorate
Poisoning.
Arch.
Toxicol.
48:
281­
288.

Steffen
C,
Wetzel
E.
1993.
Chlorate
Poisoning:
Mechanism
of
Toxicity.
Toxicology
84:
217­
231.

Suh
DH,
Abdel­
Rahman
MS,
Bull
RJ.
1983.
Effect
of
chlorine
dioxide
and
its
metabolites
in
drinking
water
on
fetal
development
in
rats.
J
Appl
Toxicol
3(
2):
75­
79.

Suh
DH
Abdel­
Rahman
MS
Bull
RJ.
1984.
Biochemical
Interactions
Of
Chlorine
Dioxide
And
Its
Metabolites
In
Rats.
Archives
of
Environmental
Contamination
and
Toxicology,
13(
2):
163­
169.

Tellez,
R.,
Chacon,
P.
M.,
Abarca,
R.
C.,
Blount,
B.
C.,
Van
Landingham,
C.
B.,
Crump,
K.
S.,
Lobo,
Gibbs,
J.
P.
(
2005)
Thyroid:
15:(
in
publication)

Tuthill
RW,
Giusti
RA,
Moore
GS,
Calabrese
EJ.
1982.
Health
Effects
Among
Newborns
after
Prenatal
Exposure
to
ClO2­
Disinfected
Drinking
Water.
Environmental
Health
Perspectives,
46:
39­
45.

USEPA.
1994.
Final
Draft
for
the
Drinking
Water
Criteria
Document
on
Chlorine
Dioxide,
Chlorite
and
Chlorate.
Prepared
for
the
Health
Effects
Division/
Office
of
Science
and
Technology/
Office
of
Water,
March
31,
1994,
under
contract
by
Clement
International
Corp.

USEPA
2000.
Toxicological
Review
of
Chlorine
Dioxide
and
Chlorite,
EPA/
635/
R­
00/
007.
http://
www.
epa.
gov/
IRIS/
toxreviews/
0496­
tr.
pdf
Warrington.
P.
2002.
Ambient
Water
Quality
Guidelines
for
Chlorate
­
technical
background
report.
Government
of
British
Columbia,
Ministry
of
Water,
Land
and
Air
Protection.
ISBN
0­
7726­
4734­
8.
http://
wlapwww.
gov.
bc.
ca/
wat/
wq/
BCguidelines/
chlorate.
html
Page
97
of
141
WHO.
2004.
Chlorite
and
chlorate
in
Drinking
Water.
Background
document
for
developing
WHO
Guidelines
for
Drinking­
water
Quality,
20
pages.
WHO/
SDE/
WSH/
03.04/
86
http://
www.
who.
int/
water_
sanitation_
health/
dwq/
chemicals/
en/
chloratechlorite.
pdf
Page
98
of
141
APPENDIX
C
RESIDUE
CHEMISTRY
CONSIDERATIONS
for
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
Preface:
Through
a
series
of
negotiations
between
members
of
SRRD
and
AD
to
coordinate
Inorganic
Chlorates
and
Chlorine
Dioxide
and
Sodium
Chlorite,
with
regards
to
the
risk
assessment
for
Inorganic
Chlorates,
the
residue
of
concern
from
sodium
chlorate
exposures
is
chlorate
by
agreement.
See
Section
1.0
Executive
Summary
above.

Sodium
chlorate
is
currently
registered
for
preharvest
and
foliar
applications
as
a
defoliant
or
desiccant
to
the
following
food/
feed
crops:
dry
beans,
corn,
cotton,
flax,
guar,
chili
peppers,
potatoes,
rice,
safflower,
sorghum
(
grain),
southern
peas
(
i.
e.,
cowpeas),
soybeans,
and
sunflowers.
For
food/
feed
uses,
sodium
chlorate
is
formulated
as
a
soluble
concentrate
(
SC)
with
the
active
ingredient
ranging
from
18%
to
47.2%.
Sodium
chlorate
may
be
applied
using
aircraft
or
ground
spray
equipment,
including
high
and
low
volume
equipment.

Uses
of
sodium
chlorate
as
a
defoliant
or
desiccant
on
cauliflower,
cucurbit
vegetables,
and
okra
grown
for
seed
only
are
considered
non­
food
uses.
Uses
of
sodium
chlorate
on
ornamental
gourds
and
fallow
lands
are
also
considered
non­
food
uses.
These
non­
food
uses
will
not
be
discussed
further
with
regards
to
residue
chemistry
or
dietary
exposure/
risk
considerations.

Under
40
CFR
180.1020
(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
in
or
on
the
following
raw
agricultural
commodities
when
used
as
a
defoliant,
desiccant,
or
fungicide
in
accordance
with
good
agricultural
practice:
beans
(
dry,
edible),
corn
(
fodder),
corn
(
forage),
corn
(
grain),
cottonseed,
flaxseed,
flax
(
straw),
guar
beans,
peas
(
southern),
peppers
(
chili),
potatoes,
rice,
rice
(
straw),
safflower
(
grain),
sorghum
(
grain),
sorghum
(
fodder),
sorghum
(
forage),
soybeans
and
sunflower
seed.

Under
40
CFR
180.1020
(
b)
A
time­
limited
exemption
from
the
requirement
of
a
tolerance
is
established
for
residues
of
the
defoliant/
desiccant
in
connection
with
use
of
the
pesticide
under
section
18
emergency
exemptions
granted
by
EPA.
This
exemption
has
been
granted
for
wheat
and
will
expire
on
12/
31/
04.
As
requested
by
the
Registration
Division
(
Sodium
Chlorate
Use
Closure
Memo
Amendment;
J.
Guerry;
dated
11/
15/
2004)
the
use
of
sodium
chlorate
on
wheat
is
also
addressed
herein
with
the
intention
to
convert
the
time­
limited
exemption
status
to
a
permanent
exemption
from
the
requirement
of
a
tolerance
under
40
CFR.
1020
(
a).
The
proposed
use
rate
is
for
a
single
application
of
sodium
chlorate
to
wheat
at
6
lbs
ai/
A
with
a
3­
day
PHI.

No
plant
metabolism
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
plant
metabolism
data
are
required
to
support
the
established
sodium
chlorate
tolerance
exempts.
Based
on
available
published
information
(
Loomis
et
al.,
J.
Am.
Soc.
Agron.;
25,
724
(
1933)),
sodium
chlorate
is
highly
soluble
in
water
and
is
expected
to
readily
absorb
and
translocate
throughout
plants.
However,
given
the
proposed
use
conditions,
the
means
of
translocation
in
treated
plants
may
be
substantially
disrupted.
Translocation
of
very
small
Page
99
of
141
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses
may
occur.
Terminal
residues
are
expected
to
be
primarily
surface
residues.

Since
sodium
chlorate
is
a
strong
oxidizing
agent,
depending
on
environmental
factors,
it
is
expected
to
be
easily
reduced
to
chloride
and
possibly
chlorite
in
plants.
Total
redox
conversion
to
these
reduced
species
is
not
expected;
hence,
the
terminal
residues
of
sodium
chlorate
in/
on
plants
are
likely
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).

No
ruminant,
swine,
or
poultry
metabolism
or
feeding
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
animal
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
published
rat
metabolism
data
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985),
terminal
residues
of
sodium
chlorate
in
animal
tissues
are
expected
to
be
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
as
chlorate,
chlorite,
and
chloride
in
urine
primarily
and
feces.
Within
72
hours,
about
40%
of
the
administered
dose
was
excreted
in
the
urine
as
chlorate
(
ca.
13%),
chlorite
(
ca.
4%),
and
chloride
(
ca.
20%)
and
about
2­
4%
was
excreted
in
the
feces
in
the
same
time
period.
Less
than
1%
of
the
administered
dose
was
found
in
any
of
the
tissues
analyzed
including
kidney,
liver,
and
skin.

Although
some
previous
residue
chemistry
reviews
for
specific
exemptions
from
the
requirement
of
a
tolerance
have
concluded
that
there
is
no
reasonable
expectation
of
transfer
of
residues
to
meat,
milk,
poultry
or
eggs
in
specific
cases,
re­
evaluation
of
the
available
crop
field
trial
data
taken
as
a
whole,
indicate
that
there
is
the
possibility
of
detectable
residues
of
sodium
chlorate
on
animal
feedstuffs
at
harvest.
Hence,
secondary
residues
of
concern
in
meat,
milk,
poultry,
and
eggs
are
possible
and;
therefore,
new
ruminant
and
poultry
feeding
data
are
hereby
required
to
support
the
reregistration
of
sodium
chlorate.
These
data
are
considered
confirmatory.

The
analytical
method
used
to
support
the
established
exemptions
from
the
requirement
of
a
tolerance
is
a
non­
specific
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection.
The
method
was
originally
developed
to
estimate
residual
chlorate
concentrations
in
soil
and
as
a
rapid
diagnostic
test
for
chlorate
toxicity
in
plants.
Briefly,
the
method
involves
acid
extraction,
clean­
up
by
shaking
with
activated
charcoal,
and
filtration.
A
solution
of
ortho­
toluidine
in
HCl
is
then
added
to
the
concentrated
extract
and
the
resulting
color
is
measured
at
448
nm
for
low
concentrations
and
at
490
nm
for
higher
concentrations
of
dye.
The
method
is
not
specific
for
chlorate
since
it
measures
any
oxidizing
agent
capable
of
oxidizing
chloride
ion
to
free
chlorine.
A
standard
curve
is
prepared
with
sodium
chlorate
for
comparison.
The
lowest
sensitivity
of
the
method
is
estimated
at
1
ppm
based
on
available
fortification
data
from
field
trials.
Chloride
does
not
interfere
with
the
method
but
residues
of
chlorite,
which
might
be
present,
may
also
be
detected
with
this
method.
This
method
is
hereby
deemed
adequate
for
enforcement
of
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
[
Note:
If
needed,
a
more
selective
HPLC
method
("
Determination
of
Residues
of
Page
100
of
141
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
is
available
for
the
detection
of
sodium
chlorate
residues
in
or
on
raw
agricultural
commodities
(
RACs).]

New
reference
standards
must
be
supplied
to
the
EPA
National
Pesticide
Standards
Repository.

Only
crop
field
trial
data
have
been
submitted
to
support
the
reregistration
of
sodium
chlorate.
No
storage
stability
or
processing
data
are
available.
The
available
crop
field
trial
data
have
been
re­
evaluated
herein.
No
additional
plant
magnitude
of
the
residue
or
storage
stability
data
are
required
to
support
the
reregistration
of
sodium
chlorate.
Page
101
of
141
Table
C.
1.
Residue
Chemistry
Science
Assessment
for
Reregistration
of
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
GLN
Data
Requirements
Current
Tolerances
(
ppm)
[
§
180.1020]
Additional
Data
Needed?
Citations
1
860.1200:
Directions
for
Use
NA
No
860.1300:
Nature
of
the
Residue
­
Plants
NA
No
00062497,
00066805
860.1300:
Nature
of
the
Residue
­
Animals
NA
No
None
860.1340:
Residue
Analytical
Method
NA
No
00049610,
00066802,
00066804,
00066808,
00066809,
00066810,
00123747,
00124680,
00135224
860.1360:
Multiresidue
Method
NA
No
None
860.1380:
Storage
Stability
Data
NA
No
None
860.1400:
Magnitude
of
the
Residue
­
Water,
Fish
and
Irrigated
Crops
None
No
None
860.1460:
Magnitude
of
the
Residue
­
Food
Handling
None
No
None
860.1480:
Magnitude
of
the
Residue
­
Meat,
Milk,
Poultry,
Eggs
­
Cattle
fat,
meat,
and
meat
byproducts
None
Yes
2
None
­
Goat
fat,
mean
and
meat
byproducts
­
Horse
fat,
meat
and
meat
byproducts
­
Sheep
fat,
meat
and
meat
byproducts
­
Milk
­
Eggs
and
the
Fat,
Meat
and
Meat
Byproducts
of
Poultry
860.1500:
Crop
Field
Trials
3
­
Beans
(
dried,
edible)
Exempt
No
­
Corn
(
fodder,
forage,
grain)
Exempt
No
­
Cottonseed
Exempt
No
­
Flaxseed
and
Flax
(
straw)
Exempt
No
00136326
­
Guar
beans
Exempt
No
00136388
Table
C.
1.
Residue
Chemistry
Science
Assessment
for
Reregistration
of
Sodium
Chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
GLN
Data
Requirements
Current
Tolerances
(
ppm)
[
§
180.1020]
Additional
Data
Needed?
Citations
1
Page
102
of
141
­
Peas
(
southern)
Exempt
No
00128727
­
Peppers
(
chili)
Exempt
No
00116554
­
Potatoes
Exempt
No
42464201,
42930601
­
Rice
and
Rice
straw
Exempt
No
00159210
­
Safflower
(
grain)
Exempt
No
None
­
Sorghum
(
grain,
fodder,
forage)
Exempt
No
00123727
­
Soybeans
Exempt
No
00128727
­
Sunflower
seed
Exempt
No
00135224
­
Wheat
Exempt
No
00136326
860.1520:
Processed
Food/
Feed
NA
No
None
860.1850:
Confined
Accumulation
in
Rotational
Crops
NA
No
None
860.1650:
Submittal
of
Analytical
Reference
Standards
NA
Yes
4
None
860.1900:
Field
Accumulation
in
Rotational
Crops
NA
No
None
1
Only
data
considered
primary
sources
of
information
to
support
the
reregistration
of
sodium
chlorate
are
included
here.
All
other
available
data
are
considered
supplemental.
2
New
ruminant
and
poultry
feeding
studies
are
required.
3
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
in
or
on
the
listed
raw
agricultural
commodities
when
used
as
a
defoliant,
desiccant,
or
fungicide
in
accordance
with
good
agricultural
practice
[
40
CFR
180.1020]
4
Replenish
standards
as
requested
by
the
repository.

860.1300
Nature
of
the
Residue
­
Plants
No
plant
metabolism
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
plant
metabolism
data
are
required
to
support
the
established
sodium
chlorate
tolerance
exempts.
Based
on
available
published
information
(
Loomis
et
al.,
J.
Am.
Soc.
Agron.;
25,
724
(
1933)),
sodium
chlorate
is
highly
soluble
in
water
and
is
expected
to
readily
absorb
and
translocate
throughout
plants.
However,
given
the
proposed
use
conditions,
the
means
of
Page
103
of
141
translocation
in
treated
plants
may
be
substantially
disrupted.
Translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses
may
occur.
Terminal
residues
are
expected
to
be
primarily
surface
residues.

Since
sodium
chlorate
is
a
strong
oxidizing
agent,
depending
on
environmental
factors,
it
is
expected
to
be
easily
reduced
to
chloride
and
possibly
chlorite
in
plants.
Total
redox
conversion
to
these
reduced
species
is
not
expected;
hence,
the
terminal
residues
of
sodium
chlorate
in/
on
plants
are
likely
chlorate,
chlorite,
and
chloride.

860.1300
Nature
of
the
Residue
­
Livestock
No
ruminant,
swine,
or
poultry
metabolism
or
feeding
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate;
however,
no
new
animal
metabolism
data
are
required
to
support
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
Based
on
published
rat
metabolism
data
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985),
terminal
residues
of
sodium
chlorate
in
animal
tissues
are
expected
to
be
chlorate
(
ClO
3
b
),
chlorite
(
ClO
2
b
),
and
chloride
(
Cl
b
).
Chlorate
is
readily
absorbed
from
the
digestive
tract
and
is
excreted
as
chlorate,
chlorite,
and
chloride
in
urine
primarily
and
feces.
Within
72
hours,
about
40%
of
the
administered
dose
was
excreted
in
the
urine
as
chlorate
(
ca.
13%),
chlorite
(
ca.
4%),
and
chloride
(
ca.
20%)
and
about
2­
4%
was
excreted
in
the
feces
in
the
same
time
period.
Less
than
1%
of
the
administered
dose
was
found
in
any
of
the
tissues
analyzed
including
kidney,
liver,
and
skin.

Metabolism
­
Rat
The
metabolism
and
distribution
of
chlorine
dioxide
(
ClO
2
),
chlorite
ion
(
ClO
2
b
),
and
chlorate
ion
(
ClO
3
b
)
were
studied
in
rats
(
Abdel­
Rahman
et
al,
1982,
1984b,
1985).
Three
groups
of
male
Sprague­
Dawley
rats
(
4/
group)
were
administered
a
single
oral
(
gavage)
dose
of
one
of
the
compounds
which
were
36Cl­
radiolabeled.
Expired
air,
fecal
and
urine
samples
were
collected
over
72
hours.
The
36Cl­
activity
in
these
samples
was
measured
and
the
radioactivity
in
the
urine
was
identified
as
chlorate
(
ca.
13%
of
the
administered
dose),
chlorite
(
ca.
4%
of
the
administered
dose)
and
chloride
(
ca.
20%
of
the
administered
dose).
At
72
hours,
the
rats
were
killed
and
the
distribution
of
36Cl­
activity
in
tissues
was
determined
(
see
Table
C.
2).
Total
radioactivity
in
each
of
the
tissues
examined
was
<
1%
of
the
initial
dose.
Page
104
of
141
Table
C.
2.
Distribution
of
radioactivity
in
rat
tissues
after
dosing
with
36Cl­
labeled
chlorine
dioxide,
potassium
chlorite,
or
potassium
chlorate.

Tissue
Percentage
of
initial
dose
1
Chlorine
dioxide
(
36ClO2)
Chlorite
(
36ClO2
b
)
Chlorate
(
36ClO3
b
)

Plasma
0.72
±
0.02
0.55
±
0.038
0.68
±
0.09
Packed
cells
­­
2
0.63
±
0.11
0.23
±
0.02
Whole
blood
­­
0.64
±
0.01
0.57
±
0.05
Kidney
0.81
±
0.15
0.30
±
0.06
0.42
±
0.07
Lung
0.74
±
0.15
0.37
±
0.04
0.45
±
0.07
Stomach
0.70
±
0.15
0.43
±
0.07
0.46
±
0.05
Duodenum
0.29
±
0.07
0.31
±
0.01
0.34
±
0.04
Ileum
0.48
±
0.09
0.17
±
0.03
0.21
±
0.02
Liver
0.38
±
0.09
0.06
±
0.03
0.20
±
0.03
Spleen
0.25
±
0.04
0.22
±
0.02
0.29
±
0.04
Bone
marrow
0.16
±
0.03
0.09
±
0.03
0.15
±
0.03
Testes
­­
0.39
±
0.04
0.45
±
0.07
Skin
­­
0.38
±
0.06
0.42
±
0.10
Carcass
­­
0.25
±
0.04
0.21
±
0.02
1
Value
represents
the
mean
±
SE
as
percentage
of
the
initial
dose
from
four
rats
per
treatment
after
72
hr.
2
Not
Determined
860.1340
Residue
Analytical
Methods
The
analytical
method
used
to
support
the
established
exemptions
from
the
requirement
of
a
tolerance
is
a
non­
specific
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection.
The
method
was
originally
developed
to
estimate
residual
chlorate
concentrations
in
soil
and
as
a
rapid
diagnostic
test
for
chlorate
toxicity
in
plants.
Briefly,
the
method
involves
acid
extraction,
clean­
up
by
shaking
with
activated
charcoal,
and
filtration.
A
solution
of
ortho­
toluidine
in
HCl
is
then
added
to
the
concentrated
extract
and
the
resulting
color
is
measured
at
448
nm
for
low
concentrations
and
at
490
nm
for
higher
concentrations
of
dye.
The
method
is
not
specific
for
chlorate
since
it
measures
any
oxidizing
agent
capable
of
oxidizing
chloride
ion
to
free
chlorine.
A
standard
curve
is
prepared
with
sodium
chlorate
for
comparison.
The
sensitivity
of
the
method
is
estimated
at
1
ppm
based
on
available
fortification
data
from
field
trials.
Chloride
does
not
interfere
but
residues
of
chlorite,
which
might
be
present,
may
also
be
detected
with
this
method.
This
method
is
hereby
deemed
adequate
Page
105
of
141
for
enforcement
of
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
A
more
selective
HPLC
method
("
Determination
of
Residues
of
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
is
available
for
the
detection
of
sodium
chlorate
residues
in
or
on
raw
agricultural
commodities
(
RACs).

860.1360
Multiresidue
Methods
It
does
not
appear
that
the
registrant
has
submitted
multiresidue
method
studies.
Sodium
chlorate
is
not
listed
in
the
FDA
PESTDATA
database
dated
11/
01
(
PAM
Volume
I,
Appendix
I).
However,
sodium
chlorate
would
not
be
expected
to
be
recovered
by
the
PAM
I
multiresidue
methods.
No
additional
multiresidue
methods
data
are
required
to
support
the
reregistration
of
sodium
chlorate.

860.1380
Storage
Stability
No
storage
stability
data
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate.
However,
the
available
data
continue
to
uphold
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance,
and
therefore,
no
new
storage
stability
data
are
required
to
support
the
reregistration
of
sodium
chlorate.

860.1400
Water,
Fish,
and
Irrigated
Crops
Sodium
chlorate
is
not
presently
registered
for
direct
use
on
water
and
aquatic
food
and
feed
crops
other
than
as
a
desiccant
on
rice.
Since
sodium
chlorate
is
used
to
desiccate
green
foliage
and
weeds
present
in
rice
fields
to
increase
harvest
efficiency,
residues
of
concern
are
not
expected
to
be
occurred
in
water,
fish,
and
irrigated
crops
from
the
use
of
sodium
chlorate
as
a
desiccant
on
rice.
Therefore,
no
residue
chemistry
data
are
required
under
these
guideline
topics.

860.1460
Food
Handling
Sodium
chlorate
is
not
presently
registered
for
use
in
food­
handling
establishments;
therefore,
no
residue
chemistry
data
are
required
under
these
guideline
topics.

860.1480
Meat,
Milk,
Poultry,
and
Eggs
No
ruminant,
swine
or
poultry
feeding
studies
have
been
submitted
in
support
of
the
reregistration
of
sodium
chlorate.
Although
some
previous
residue
chemistry
reviews
for
exemptions
from
the
requirement
of
a
tolerance
have
concluded
that
there
is
no
reasonable
expectation
of
transfer
of
residues
to
meat,
milk,
poultry
or
eggs
in
specific
cases,
re­
evaluation
of
the
available
crop
field
trial
data
taken
as
a
whole,
indicate
that
there
is
the
possibility
of
detectable
residues
of
sodium
chlorate
on
animal
feedstuffs
at
harvest.
Hence,
secondary
residues
of
sodium
chlorate
in
meat,
milk,
poultry,
and
eggs
are
possible
and;
therefore,
new
ruminant
and
poultry
feeding
data
are
hereby
required
to
support
the
reregistration
of
sodium
chlorate.
Page
106
of
141
Table
C.
3.
Calculation
of
the
highest
average
and
maximum
theoretical
dietary
burden
for
beef/
dairy
cattle
and
poultry
from
the
maximum
registered
use
rates
of
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides.

Feed
Commodity
%
Dry
Matter
%
Diet
Residue
Estimate
(
ppm)
Dietary
Contribution
1
(
ppm)
Max.
Feed
Per
Day
on
a
Dry
Wt.
Basis
(
Kg)
Dietary
Exposure
Estimate
(
mg)

Highest
Ave
Max
Highest
Ave
Max
Highest
Ave
Max
Beef
and
Dairy
Cattle
Cowpea
forage
30
40
100
2
300
2
133
400
Cowpea
hay
86
20
100
2
300
2
23
70
Sorghum
grain
86
40
40
3
70
3
19
33
Total
Burden
175
500
9.1
5
1600
4600
Poultry
Sorghum
grain
Not
Used
1
80
40
3
70
3
32
56
Rice
bran
20
40
4
70
4
8
14
Total
Burden
40
70
1
Dietary
Contribution
for
Cattle
=
(
Residue
Estimate
in
ppm
÷
%
DM)
x
%
Diet
Dietary
Contribution
for
Poultry
=
Residue
Estimate
in
ppm
x
%
Diet
2
Based
on
the
available
straw
(
flax,
oat,
wheat,
rice)
and
forage
(
guar
plants,
sorghum
stalks,
soybean
forage)
data,
maximum
residues
of
sodium
chlorate
in/
on
straw
and
forage
livestock
feedstuffs
harvested
3­
7
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application)
are
not
expected
to
exceed
300
ppm
at
the
point
of
harvest.
On
average,
residues
in/
on
straw
and
forage
livestock
feedstuffs
should
not
exceed
100
ppm
when
harvested
7­
14
days
after
foliar
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application).
3
Based
on
the
available
sorghum
field
trial
data
alone,
maximum
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
for
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
70
ppm.
On
average,
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
on
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
40
ppm.
4
Translated
from
sorghum
grain
estimate.
5
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993)
Page
107
of
141
The
highest
average
residues
of
chlorate
(
excluding
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
expected
to
be
<
4
ppm
and
in
milk
are
expected
to
be
<
0.5
ppm
based
on
the
following
information
and
assumptions:

°
The
highest
average
theoretical
dietary
burden
for
livestock
is
175
ppm
for
cattle
feed
on
a
dry
wt.
basis
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
1600
mg
per
day
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
16
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Highest
Average
Theoretical
Dietary
Exposure
(
1600
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Highest
Average
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
4
ppm
Highest
Average
Residue
Estimate
in
Milk
=
<
0.5
ppm
Page
108
of
141
The
maximum
residues
of
chlorate
(
excluding
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
expected
to
be
<
12
ppm
and
in
milk
are
expected
to
be
<
2
ppm
based
on
the
following
information
and
assumptions:

°
The
maximum
theoretical
dietary
burden
for
livestock
is
500
ppm
for
cattle
feed
on
a
dry
wt.
basis
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
4600
mg
per
day
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
46
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Maximum
Theoretical
Dietary
Exposure
(
4600
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Maximum
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
12
ppm
Maximum
Residue
Estimate
in
Milk
=
<
2
ppm
Page
109
of
141
860.1500
Crop
Field
Trials
Available
crop
field
trial
data
deemed
the
primary
sources
of
information
to
support
the
reregistration
of
sodium
chlorate
are
briefly
discussed
below
and
summarized
in
Table
C.
5.
All
other
available
crop
field
trial
data
are
considered
supplemental
and
will
not
be
discussed
further.
No
additional
crop
field
trial
data
are
required
to
support
the
reregistration
of
sodium
chlorate.

The
subject
data,
except
the
potato
tuber
data,
were
all
collected
using
the
colorimetric
method
(
Branderis,
J.
Sci.
Food
Agric.,
16,
558
(
1965)),
deemed
acceptable
for
data
collection
and
enforcement
of
the
established
sodium
chlorate
exemptions
from
the
requirement
of
a
tolerance.
The
potato
tuber
data
were
collected
with
a
more
selective
HPLC
method
("
Determination
of
Residues
of
Sodium
Chlorate
in
Potatoes",
Method
#
S57023,
4/
2/
91)
deemed
adequate
for
data
collection.
The
lowest
limits
of
quantitation
(
LOQs)
of
these
methods
is
estimated
at
1
ppm.

Based
on
the
available
flax,
guar,
southern
pea,
soybean,
and
sunflower
field
trial
data
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
dry
beans,
guar
beans,
southern
peas,
soybeans,
flaxseed,
safflower
seed,
and
sunflower
seed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
dry
beans,
guar,
southern
peas,
soybeans,
flax,
safflower,
and
sunflower
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI).
Furthermore,
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
cottonseed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
cotton
(
2
applications,
7.5
lbs
ai/
A/
application;
7­
day
PHI).
Any
residues
which
might
be
detected
at
the
point
of
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
prior
to
the
point
of
consumption.

Based
on
the
available
chili
pepper
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
13
ppm)
might
be
found
on
the
surface
of
unwashed
chili
peppers
treated
with
sodium
chlorate
at
the
maximum
use
rate
of
sodium
chlorate
on
chili
peppers
(
1
application;
12.5
lbs
ai/
A/
application;
10­
day
PHI).
However,
these
residues
are
primarily
surface
residues
present
at
the
point
of
harvest
which
would
be
substantially
removed
by
washing
(<
1
ppm)
prior
to
the
point
of
consumption.

Based
on
the
available
potato
field
trial
data,
no
detectable
residue
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
potato
tubers
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
potatoes
(
1
application;
12.5
lbs
ai/
A;
7­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
consumption.

Based
on
the
available
oat,
rice,
sorghum,
and
wheat
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
70
ppm
(
maximum)
as
demonstrated
by
sorghum
grain)
might
be
found
on
the
surface
of
cereal
grains
retaining
their
outer
hulls
at
harvest
(
such
as
oats
and
sorghum)
from
the
maximum
use
rate
of
sodium
chlorate
on
rice
and
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
and
wheat
(
1
application;
6
lbs
ai/
A;
3­
day
PHI).
However,
once
the
outer
hulls
are
removed
(
either
at
harvest
or
during
processing),
no
detectable
residues
of
sodium
chlorate
Page
110
of
141
(<
1
ppm)
are
expected
in/
on
cereal
grains
such
as
rice
and
wheat
(
as
demonstrated
by
rice
w/
out
hulls
and
wheat
grain
data).

Based
on
the
available
sorghum
field
trial
data
alone,
maximum
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
for
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
70
ppm.
On
average,
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
on
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
40
ppm.

Translating
the
available
sorghum
field
trial
data
to
corn,
residues
of
sodium
chlorate
are
not
expected
to
exceed
20
ppm
(
ca.
10
ppm
on
average)
in/
on
corn
grain
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
corn
(
1
application,
7.5
lbs
ai/
A;
14­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
consumption.
Hence,
residues
of
sodium
chlorate
in/
on
sweet
corn
after
washing
and
prior
to
consumption
would
not
be
expected
to
exceed
1
ppm.

Based
on
the
available
straw
(
flax,
oat,
wheat,
rice)
and
forage
(
guar
plants,
sorghum
stalks,
soybean
forage)
data,
maximum
residues
of
sodium
chlorate
in/
on
straw
and
forage
livestock
feedstuffs
harvested
3­
7
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application)
are
not
expected
to
exceed
300
ppm
at
the
point
of
harvest.
On
average,
residues
in/
on
straw
and
forage
livestock
feedstuffs
should
not
exceed
100
ppm
when
harvested
7­
14
days
after
foliar
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application).

Chili
peppers:
MRID
00116554
Chili
pepper
plants
were
treated
with
a
single
application
of
sodium
chlorate
at
8
or
16
lb
ai/
A.
Chili
pepper
samples
were
collected
7­
21
days
after
treatment.
Residues
of
chlorate
in/
on
chili
pepper
samples
were
<
0.1
to
13
ppm.
After
washing
the
treated
chili
peppers
with
water,
residues
of
chlorate
were
all
<
0.1
ppm.

Flax,
Oats,
Wheat:
MRID
00136326
Flax,
oats,
and
wheat
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
6
or
12
lbs
ai/
A.
Grain
and
straw
samples
were
collected
3­
10
days
after
treatment.
Residues
of
chlorate
in/
on
flax
grain/
straw,
wheat
grain/
straw
and
oat
straw
samples
were
<
2
ppm.
Residues
of
chlorate
in/
on
oat
grain
samples
treated
at
6
and
12
lbs
ai/
A
were
10­
36
ppm
(
20
ppm
average)
and
<
2­
125
ppm
(
80
ppm
average),
respectively.

Guar:
MRID
00136388
Guar
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
6
or
12
lbs
ai/
A.
Seed
and
plant
samples
were
collected
2­
14
days
after
treatment.
Residues
of
chlorate
in/
on
seed
samples
<
10
ppm.
Residues
of
chlorate
in/
on
plant
samples
were
18­
266
ppm.
Page
111
of
141
Potatoes:
MRID
42464201
(
Chromatograms
­
MRID
42930601)
Potato
plants
were
treated
with
a
single
application
of
sodium
chlorate
at
9
lbs
ai/
A.
Potato
tubers
were
collected
7­
10
days
after
treatment.
Residues
of
chlorate
in/
on
potato
tubers
were
<
1.0
ppm.

Rice:
MRID
00159210
Rice
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
6
or
12
lbs
ai/
A.
Grain
w/
out
hulls,
grain
with
hulls,
and
straw
samples
were
collected
2­
9
days
after
treatment.

While
residues
of
chlorate
in/
on
grain
with
hulls
collected
8
days
after
treatment
were
7­
160
ppm,
residues
in/
on
grain
w/
out
hulls
collected
7
days
after
treatment
were
essentially
nil
(
reported
as
0.0
ppm).
Detectable
residues
(
0.0­
30
ppm)
were
reported
in/
on
grain
w/
out
hulls
collected
2
days
after
treatment
at
12
lbs
ai/
A.

Residues
of
chlorate
in/
on
straw
samples
ranged
from
<
1
ppm
to
44
ppm
from
treatment
at
6
lbs
ai/
A
and
from
<
1
ppm
to
438
ppm
from
treatment
at
12
lbs
ai/
A.

Sorghum:
MRID
00123727
Sorghum
plots
were
treated
with
a
single
application
fo
sodium
chlorate
at
3,
6,
and
12
lbs
ai/
A.
Grain
and
stalk
samples
were
collected
2­
14
days
after
application.

Residues
of
chlorate
in/
on
grain
samples
collected
7
and
14
days
after
treatment
at
6
lbs
ai/
A
were
44­
69
ppm
(
59
ppm
average)
and
8­
21
ppm
(
13
ppm
average),
respectively.
Residues
of
chlorate
in/
on
grain
samples
collected
7
and
14
days
after
treatment
at
12
lbs
ai/
A
were
83­
132
ppm
(
106
ppm
average)
and
13­
40
ppm
(
30
ppm
average),
respectively.

Residues
of
chlorate
in/
on
stalk
samples
collected
7­
14
days
after
treatment
at
6
lbs
ai/
A
were
essentially
nil
(
0.0
ppm)
to
51
ppm
(
21
ppm
average).
Residues
of
chlorate
in/
on
stalk
samples
collected
7­
14
days
after
treatment
at
12
lbs
ai/
A
were
essentially
nil
(
0.0
ppm)
to
352
ppm
(
117
ppm
average).

Southern
Peas
(
cowpeas):
MRID
00128727
Southern
pea
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
6
lbs
ai/
A.
Shelled
pea
samples
were
collected
4
or
5
days
after
treatment.
Some
of
the
raw
shelled
peas
were
processed
into
frozen
peas.
Residues
of
sodium
chlorate
were
<
0.3
ppm
in/
on
all
samples.

Soybeans:
MRID
00128727
Soybean
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
6
or
12
lbs
ai/
A.
Soybean
and
foliage
samples
were
collected
2­
14
days
after
treatment.
Residues
of
chlorate
in/
on
soybeans
collected
7­
14
days
after
treatment
were
<
5.0
ppm.
Residues
of
chlorate
in/
on
soybean
foliage
collected
7
days
after
treatment
at
6
or
12
lbs
ai/
A
were
as
high
as
153
ppm
and
526
ppm,
respectively.
Residues
of
chlorate
in/
on
soybean
forage
collected
14
days
after
treatment
at
6
or
12
lbs
ai/
A
were
as
high
as
100
ppm
and
318
ppm,
respectively.
Page
112
of
141
Sunflower
Seeds:
MRID
00135224
Sunflower
plots
were
treated
with
a
single
application
of
sodium
chlorate
at
3,
6,
or
12
lbs
ai/
A.
Seed
samples
were
collected
2­
14
days
after
treatment.
Residues
of
sodium
chlorate
in/
on
all
samples
were
essentially
nil
(
reported
as
0
ppm)
except
1
seed
sample
collected
4
days
after
treatment
at
12
lbs
ai/
A
which
showed
residues
of
10
ppm
(
average
of
3
replicates;
one
replicate
showed
residues
of
30
ppm).
Page
113
of
141
Table
C.
4.
Summary
of
available
crop
field
trial
data.
Note:
Guar,
rice,
sorghum,
soybean,
and
sunflower
data
are
truncated
in
this
table.
Data,
except
wheat
grain
data,
collected
less
than
7
days
after
treatment
have
been
intentionally
excluded
in
this
table
but
may
be
included
in
the
brief
discussions
above.

Matrix
Crop
Application
Rate
(
lbs
ai/
A)
PHI
(
days)
Residues
(
ppm)

Maximum
1
Estimated
Average
2
Vegetable
Chili
pepper
(
raw)
8
or
16
7­
21
13
Not
Calculated
Chili
pepper
(
washed)
<
0.1
<
0.1
Potato
tuber
9
7­
10
<
1
<
1
Seed/
Bean
Flax
6
10
<
2
<
2
Guar
7
<
10
<
10
Southern
pea
4­
5
<
0.3
<
0.3
Soybean
7­
14
<
5
<
5
Sunflower
7­
14
essentially
nil
(
zero)
essentially
nil
(
zero)

Flax
12
10
<
2
<
2
Guar
7­
14
<
10
<
10
Soybean
7­
14
<
5
<
5
Sunflower
7­
14
essentially
nil
(
zero)
essentially
nil
(
zero)

Cereal
Grain
Oat
6
8
36
20
Rice
w/
out
hulls
7­
9
essentially
nil
(
zero)
essentially
nil
(
zero)

Rice
with
hulls
8
13
9.7
Sorghum
7
69
59
14
21
13
Wheat
3­
9
<
2
<
2
Oat
12
8
125
80
Rice
w/
out
hulls
7­
9
essentially
nil
(
zero)
essentially
nil
(
zero)

Rice
with
hulls
8
160
93
Page
114
of
141
Sorghum
7
132
106
14
40
30
Wheat
3­
9
<
2
<
2
Straw
Flax,
Oat,
Wheat
6
or
12
3­
10
<
2
<
2
Rice
6
7­
9
44
11
12
7­
9
438
75
Forage
Guar
plants
6
7
58
40
12
7­
14
106
70
Sorghum
stalk
6
7­
14
51
21
12
7­
14
352
117
Soybean
forage
6
7
153
Reviewer
Cannot
Determine
14
100
12
7
526
14
318
1
Maximum
residue
as
reported
in
the
data
submission.
2
Estimated
Average
calculated
by
the
reviewer.

860.1520
Processed
Food
and
Feed
No
processing
data
have
been
submitted
regarding
residues
of
sodium
chlorate
in/
on
processed
food/
feed
commodities
(
corn,
cotton,
flaxseed,
potato,
rice,
safflower,
sorghum,
and
wheat).
However,
since
no
significant
residues
were
found
in
the
raw
agricultural
commodities
subject
to
processing,
it
is
unlikely
that
significant
residues
will
occur
in
the
processed
fractions.

860.1650
Submittal
of
Analytical
Reference
Standards
As
of
8/
11/
04,
an
analytical
reference
standard
for
sodium
chlorate
is
not
available
at
the
EPA
National
Pesticide
Standards
Repository.

860.1850
Confined
Accumulation
in
Rotational
Crops
No
data
have
been
submitted
regarding
residues
of
sodium
chlorate
in/
on
confined
accumulation
in
rotational
crops.
Page
115
of
141
860.1900
Field
Accumulation
in
Rotational
Crops
No
data
have
been
submitted
regarding
residues
of
sodium
chlorate
in/
on
field
accumulation
in
rotational
crops.
Page
116
of
141
RESIDUE
CHEMISTRY
REFERENCES
Studies
Considered
Primary
Sources
of
Information
and
Used
in
the
Assessment
PUBLISHED
Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1982.
Metabolism
and
pharmacokinetics
of
alternate
drinking
water
disinfectants.
Environ
Health
Perspect.
46:
19­
23.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1984b.
The
Kinetics
of
Chlorite
and
Chlorate
in
the
Rat.
Journal
of
the
American
College
of
Toxicology,
3(
4):
261­
267.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1985.
The
kinetics
of
chlorite
and
chlorate
in
rats.
J
Environ
Pathol
Toxicol
Oncol.
6(
1):
97­
103.

Frank,
G.
2002.
Cost
of
Milk
Production
per
Hundredweight
Equivalent
in
Milk
Sold
per
Cow
Ranges.
Wisconsin
Dairy
Data.
Fact
Sheet
2002­
01.
Center
for
Dairy
Profitability.
Univ.
Wisconsin
Extension
Service.
Oct.
2002.

UNPUBLISHED
49610
Rhone­
Poulenc
Chemical
Company
(
1959)
Method
of
Analysis
for
Chlorates.
(
Unpublished
study
received
Jan
4,
1962
under
359­
400;
CDL:
119511­
B)

62497
Pernert,
J.
C.
(
1960)
On
the
Possibility
of
Toxic
Residues
following
Cotton
Defoliation
by
Chlorate.
(
Unpublished
study
received
Dec
18,
1969
under
0F0926;
prepared
by
Hooker
Chemical
Corp.,
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
093232­
G)

66802
Fenrich­
Vincent
Associates
(
1969)
Analytical
Methods
and
Results
of
Tests
on
the
Amount
of
Residue
Remaining
in
or
on
Raw
Cottonseed
When
an
(
Inert
Ingredient)
has
Been
Used
on
the
Cotton
Plant.
Unpublished
study;
14
p.

66804
Gauditz,
I.
(
1959)
The
Results
of
Tests
on
the
Amount
of
Residue
Remaining,
Including
a
Description
of
the
Analytical
Methods
Used:
(
Penco
De­
fol­
ate).
(
Unpublished
study
received
May
30,
1970
under
0F0926;
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
091580­
O)

66805
Banderis,
A.
(
1965)
Colorimetric
Determination
of
chlorate
in
soil
and
plant
extracts.
Journal
of
the
Science
of
Food
and
Agriculture
16(
Sep):
558­
564.
(
Also
In
unpublished
submission
received
May
30,
1970
under
0F0926;
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
091580­
P)
Page
117
of
141
66808
Peniston,
Q.
P.
(
1968)
Letter
sent
to
E.
H.
Karr
dated
Jan
3,
1968:
Determination
of
sodium
chlorate
residues
on
cottonseed:
Report
#
3.
(
Unpublished
study
received
May
30,
1970
under
0F0926;
prepared
by
Food,
Chemical
&
Research
Laboratories,
Inc.,
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
091580­
T)

66809
Peniston,
Q.
P.
(
1968)
Letter
sent
to
E.
H.
Karr
dated
Jul
30,
1968:
Determination
of
sodium
chlorate
residues
in
ground
cottonseed­­
report
#
4:
Lab.
No.
5639.
(
Unpublished
study
received
May
30,
1970
under
0F0926;
prepared
by
Food,
Chemical
&
Re­
search
Laboratories,
Inc.,
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
091580­
U)

66810
Peniston,
Q.
P.
(
1969)
Letter
sent
to
E.
H.
Karr
dated
Feb
18,
1969:
Further
studies
on
determination
of
sodium
chlorate
residues
in
ground
cottonseed­­
report
#
5:
Lab.
No.
5879;
prepared
by
Food,
Chemical
&
Research
Laboratories,
Inc.
Unpublished
study;
2
p.

116554
California,
Dept.
of
Agriculture
(
1971)
Application
of
Shed­
A­
Leaf
on
Chili
Peppers:
Results.
(
Compilation;
unpublished
study
received
Oct
13,
1972
under
2E1286;
CDL:
091822­
A)

123747
Banderis,
A.
(
1965)
Colorimetric
determination
of
chlorate
in
soil
and
plant
extracts.
J.
Sci.
Ef.
Agric.
16(
Sep):
558.
(
Also
In
unpublished
submission
received
1965
under
3E1386;
submitted
by
Interregional
Research
Project
No.
4,
New
Brunswick,
NJ;
CDL:
093699­
B)

124680
Roth,
F.
(
1967)
A
test
for
chlorate
residues.
Bulletin
of
Environmental
Contamination
&
Toxicology
2(
4):
251­
254.
(
Also
In
unpublished
submission
received
Jun
23,
1972
under
2E1286;
submitted
by
California,
Dept.
of
Agriculture,
Sacramento,
CA;
CDL:
094665­
A)

128727
Interregional
Research
Project
No.
4
(
1983)
The
Results
of
Tests
on
the
Amount
of
Residues
Remaining
in
or
on
Southern
Peas,
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Jun
10,
1983
under
3E2910;
CDL:
071699­
A)

135224
Interregional
Research
Project
No.
4
(
1975)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
in
or
on
Sunflower
Seeds,
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Jul
1,
1976
under
6E1825;
CDL:
097356­
A)

136326
Interregional
Research
Project
No.
4
(
1978)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
in
or
on
Flax,
Oats,
and
Wheat
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Oct
20,
1978
under
9E2142;
CDL:
097460­
A)

136388
Interregional
Research
Project
No.
4
(
1979)
Results
of
Tests
Concerning
the
Amount
of
Sodium
Chlorate
Residue
Remaining
in
or
on
Guar
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Jun
15,
1979
under
9E2220;
CDL:
098331­
A)
Page
118
of
141
159210
Kerr­
McGee
Chemical
Corp.
(
1975)
Sodium
Chlorate
on
Rice:
Summary
of
Experimental
Conditions
and
Data
from
Texas
and
Louisiana
in
1975.
Unpublished
study.
12
p.

42464201
McGaughey,
R.
(
1992)
Determination
of
the
Magnitude
of
Residues
of
Sodium
Chlorate
in
Potatoes
Treated
with
DEFOL6:
Final
Report:
Lab
Project
Number:
DREX­
9002:
9006­
010X:
04­
9012.
Unpublished
study
prepared
by
Compliance
Services
Intl.
112
p.

42930601
McGaughey,
R.
(
1993)
Determination
of
the
Magnitude
of
Residues
of
Sodium
Chlorate
in
Potatoes
Treated
with
DEFOL
6:
Lab
Project
Number:
DREX­
9002.
Unpublished
study
prepared
by
Minnesota
Valley
Testing
Labs.
22
p.

Study
Citations
Considered
Supplemental
Sources
of
Information
5620
United
States
Borax
&
Chemical
Corporation
(
1967)
Residue
Data.
(
Unpublished
study
received
Apr
1,
1969
under
9F0783;
CDL:
091347­
A)

48007
Abernathy,
J.;
Miller,
C.
S.;
Richard,
J.
(
1975)
Sodium
chlorate
on
Sunflowers.
Prepared
in
cooperation
with
Texas
A
&
M
Univ.,
Agricultural
Experiment
Station
and
Iowa
State
Univ.,
Ames
Laboratory.
Unpublished
study;
17
p.

48009
Smith,
D.
T.;
Eastin,
E.
F.;
Wiese,
A.
F.;
et
al.
(
1976)
Summary
of
Experimental
Conditions
and
Data
from
Texas
and
Oklahoma
in
1975.
(
Unpublished
study
received
Aug
12,
1980
under
2342­
964;
prepared
in
cooperation
with
Texas
A
&
M
Univ.,
Agricultural
Experiment
Station
and
others,
submitted
by
Kerr­
McGee
Chemical
Corp.,
Oklahoma
City,
Okla.;
CDL:
243078­
I)

48064
Abernathy,
J.;
Scrib,
J.;
Miller,
C.
S.;
et
al.
(
1975)
Sodium
chlorate
on
Sunflowers:
Summary
of
Experimental
Conditions
and
Data
from
Texas
in
1975;
prepared
in
cooperation
with
Texas
A
&
M
Univ.
Agricultural
Experiment
Station
and
Iowa
State
Univ.,
Ames
Laboratory
E.
R.
D.
A.
Unpublished
study;
17
p.

48065
Smith,
D.
T.;
Eastin,
E.
F.;
Wiese,
A.
F.;
et
al.
(
1975)
Summary
of
Experimental
Conditions
and
Data
from
Texas
and
Oklahoma
in
1975.
(
Unpublished
study
received
Aug
12,
1980
under
2342­
964;
prepared
in
cooperation
with
Texas
A
&
M
Univ.,
Agricultural
Ex­
periment
Station
and
others,
submitted
by
Kerr­
McGee
Chemical
Corp.,
Oklahoma
City,
Okla.;
CDL:
243079­
E)

49609
Chipman
Chemical
Company,
Incorporated
(
1962)
Progress
Report:
Residue
Data
following
the
Field
Use
of
Shed­
a­
Leaf
on
Tomatoes
as
a
Defoliant/
Desiccant
in
California
and
New
York
State
from
Applications
Made
Fall
of
1961.
(
Unpublished
study
received
Jan
4,
1962
under
359­
400;
submitted
by
Rhone­
Poulenc
Chemical
Co.,
Monmouth
Junction,
N.
J.;
CDL:
119511­
A)
Page
119
of
141
53626
Chipman
Chemical
Company,
Incorporated
(
1961)
Residue
Data
Sheet.
(
Unpublished
study
received
Jan
4,
1962
under
359­
400;
submitted
by
Rhone­
Poulenc
Chemical
Co.,
Monmouth
Junction,
N.
J.;
CDL:
119510­
A)

58490
Pennwalt
Corporation
(
1975)
Efficacy
of
Sodium
chlorate­­
Rice.
(
Reports
by
various
sources;
unpublished
study,
including
published
data,
received
Oct
14,
1976
under
4581­
328;
CDL:
232133­
T)

66803
Walaski,
L.
J.
(
1960)
Residue
Analysis
and
Reports.
(
Unpublished
study
received
May
30,
1970
under
0F0926;
prepared
by
Chipman
Chemical
Co.,
Inc.,
submitted
by
Fenrich­
Vincent
Associates,
Manhasset,
N.
Y.;
CDL:
091580­
N)

74958
Rhone­
Poulenc
Chemical
Company
(
1964)
Tests
with
Shed­
a­
leaf
L.
(
Compilation;
unpublished
study
received
Apr
16,
1964
under
359­
399;
CDL:
023331­
A)

74967
Walaski,
L.
J.
(
1962)
Analyses
of
Dry
Edible
Beans,
Stalks,
and
Pods
for
Possible
Residues
of
Borate
and
Chlorate:
BB/
9/
62.
(
Unpublished
study
received
Dec
3,
1962
under
359­
399;
prepared
by
Chipman
Chemical
Co.,
Inc.,
submitted
by
Rhone­
Poulenc
Chemical
Co.,
Monmouth
Junction,
N.
J.;
CDL:
101365­
B)

75021
Chipman
Chemical
Company,
Incorporated
(
1960)
Results
of
Analyses
for
Chlorate
and
Borate
Residues
on
Cottonseed
from
1959
&
1960
California
Cotton
Samples.
(
Unpublished
study
received
Jan
19,
1961
under
359­
399;
submitted
by
Rhone­
Poulenc
Chemical
Co.,
Monmouth
Junction,
N.
J.;
CDL:
119545­
A)

75023
Rhone­
Poulenc
Chemical
Company
(
1963)
Residues
in
Sorghum
and
Rice.
(
Compilation;
unpublished
study,
including
letter
dated
Jul
1,
1963
from
L.
R.
Reed
to
Commissioner
of
Food
&
Drugs,
Food
&
Drug
Administration,
Department
of
Health,
Education,
&
Wel­
fare,
received
Jul
2,
1963
under
unknown
admin.
no.;
CDL:
119636­
A)

75025
Walaski,
L.
J.
(
1963)
Analysis
of
Potatoes
for
Possible
Residues
of
Borate
following
Applications
of
Chlorate/
Sodium
Metaborate
Combinations
for
Vinekilling:
BB/
1/
63.
(
Unpublished
study
received
May
21,
1963
under
359­
399;
prepared
by
Chipman
Chemical
Co.,
Inc.,
submitted
by
Chipman
Chemical
Co.,
Bound
Brook,
NJ;
CDL:
119640­
A)

123745
Interregional
Research
Project
No.
4
(
1973)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
on
or
in
Grain
Sorghum,
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Apr
13,
1973
under
3E1386;
CDL:
093698­
C)
Page
120
of
141
140109
Interregional
Research
Project
No.
4
(
1975)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
in
or
on
Sunflower
Seeds,
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Jul
1,
1976
under
6E1825;
CDL:
095932­
A)

140483
Interregional
Research
Project
No.
4
(
1977)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
in
or
on
Corn
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Jun
24,
1977
under
7E1972;
CDL:
097261­
A)

140486
Interregional
Research
Project
No.
4
(
1976)
The
Results
of
Tests
on
the
Amount
of
Sodium
Chlorate
Residue
Remaining
on
or
in
Rice
and
Rice
Straw
Including
a
Description
of
the
Analytical
Method
Used.
(
Compilation;
unpublished
study
received
Apr
6,
1976
under
6E1996;
CDL:
097358­
A)

159211
Ladd,
R.
(
1976)
Meat
and
Milk
Residue
Study
with
Antor
Herbicide
in
a
Dairy
Cow
[
Dosing
Information
Only]:
Project
No.
76­
12:
IBT
No.
8580­
09096.
Unpublished
study
prepared
by
Industrial
Bio­
Test
Laboratories,
Inc.
21
p.
Page
121
of
141
APPENDIX
D
TOLERANCE
REASSESSMENT
SUMMARY
For
Inorganic
Chlorates
as
active
or
inert
ingredients
in
conventional
(
agricultural)
pesticides
NOTE:
Tolerances
and/
or
exemptions
from
the
requirement
of
a
tolerance
for
inorganic
chlorates
as
active
or
inert
ingredients
in
antimicrobial
agents
is
not
the
purview
of
HED
and
should
be
addressed
by
AD.

Existing
exemptions
from
the
requirement
of
a
tolerance
for
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
listed
under
40
CFR
180.1020
Sodium
chlorate
is
currently
registered
for
preharvest
and
foliar
applications
as
a
defoliant
or
desiccant
to
the
following
food/
feed
crops:
dry
beans,
corn,
cotton,
flax,
guar,
chili
peppers,
potatoes,
rice,
safflower,
sorghum
(
grain),
southern
peas
(
i.
e.,
cowpeas),
soybeans,
and
sunflowers.

Under
40
CFR
180.1020
(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
in
or
on
the
following
raw
agricultural
commodities
when
used
as
a
defoliant,
desiccant,
or
fungicide
in
accordance
with
good
agricultural
practice:
beans
(
dry,
edible),
corn
(
fodder),
corn
(
forage),
corn
(
grain),
cottonseed,
flaxseed,
flax
(
straw),
guar
beans,
peas
(
southern),
peppers
(
chili),
potatoes,
rice,
rice
(
straw),
safflower
(
grain),
sorghum
(
grain),
sorghum
(
fodder),
sorghum
(
forage),
soybeans
and
sunflower
seed.

Under
40
CFR
180.1020
(
b)
A
time­
limited
exemption
from
the
requirement
of
a
tolerance
is
established
for
residues
of
the
defoliant/
desiccant
in
connection
with
use
of
the
pesticide
under
section
18
emergency
exemptions
granted
by
EPA.
This
exemption
has
been
granted
for
wheat
and
will
expire
on
12/
31/
04.
As
requested
by
the
Registration
Division
(
Sodium
Chlorate
Use
Closure
Memo
Amendment;
J.
Guerry;
dated
11/
15/
2004)
the
use
of
sodium
chlorate
on
wheat
is
also
addressed
herein
with
the
intention
to
convert
the
time­
limited
exemption
status
to
a
permanent
exemption
from
the
requirement
of
a
tolerance
under
40
CFR.
1020
(
a).
The
proposed
use
rate
is
for
a
single
application
of
sodium
chlorate
to
wheat
at
6
lbs
ai/
A
with
a
3­
day
PHI.

Sodium
chlorate
exemptions
under
40
CFR
180.1020
(
a)
from
the
requirement
of
a
tolerance
should
be
amended
as
follows
to:
(
1)
specify
defoliant
and
desiccant
use
only,
(
2)
specify
use
on
crops
rather
than
raw
agricultural
commodities,
(
3)
include
wheat
concomitant
with
the
revocation
of
wheat
under
40
CFR
180.1020
(
b).

40
CFR
180.1020
(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
when
used
as
a
defoliant
or
desiccant
in
accordance
with
good
agricultural
practice
on
the
following
crops:
Bean
(
dry),
Corn,
Cotton,
Cowpeas,
Flax,
Guar,
Pepper
(
non­
bell),
Potato,
Rice,
Safflower,
Sorghum
(
grain),
Soybeans,
Sunflower,
and
Wheat.
Page
122
of
141
Table
D.
1.
Tolerance
Reassessment
Summary
for
Sodium
Chlorate
Listed
under
40
CFR
180.1020(
a)

Commodity
Current
Tolerance
(
ppm)
Tolerance
Reassessment
(
ppm)
[
Correct
Definition]
Comments
beans,
dry,
edible
Exempt
Exempt
[
Bean
(
dry)]

corn,
fodder
Exempt
Exempt
[
Corn]

corn,
forage
Exempt
corn,
grain
Exempt
cottonseed
Exempt
Exempt
[
Cotton]

flaxseed
Exempt
Exempt
[
Flax]

flax,
straw
Exempt
Revoke
Flax
straw
is
not
listed
in
Table
1
of
OPPTS
860.1000
guar
beans
Exempt
Exempt
[
Guar]

peas,
southern
Exempt
Exempt
[
Cowpea]

potatoes
Exempt
Exempt
[
Potato]

peppers,
chili
Exempt
Exempt
[
Pepper
(
nonbell)]

rice
Exempt
Exempt
[
Rice]

rice,
straw
Exempt
Exempt
safflower,
grain
Exempt
Exempt
[
Safflower]

sorghum,
grain
Exempt
Exempt
[
Sorghum
(
grain)]

sorghum,
fodder
Exempt
sorghum,
forage
Exempt
soybeans
Exempt
Exempt
[
Soybeans]

sunflower
seed
Exempt
Exempt
[
Sunflower]

Wheat
None
Exempt
[
Wheat]
Concomitant
with
the
revocation
of
wheat
under
40
CFR
180.1020
(
b)
Page
123
of
141
Needed
exemptions
from
the
requirement
of
a
tolerance
for
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
pesticides
Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
herbicide
formulation
products
can
be
applied
professionally
to
agricultural
(
corn,
guava,
macadamia
nuts,
sorghum
grain,
sugarcane,
wheat),
commercial
(
non­
agricultural),
and
residential
sites.
These
conventional
pesticide
products
contain
<
1
%
sodium
chlorate
and
can
be
applied
at
rates
no
greater
than
0.07
lb
(
as
sodium
chlorate)
per
acre.

Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
airborne
fungicide
products
can
be
applied
in
poultry
premises.
These
conventional
pesticide
products
contain
<
20%
potassium
chlorate
and
can
be
applied
at
rates
not
greater
than
0.01
lb
(
as
potassium
chlorate)
per
500
ft3.

Table
D.
2.
Tolerance
Exemption
Needed
Tolerance
Exemption
Expression
PC
Code
CAS
Reg
No.
40
CFR
§
Use
(
Pesticidal)
List
Classification
Sodium
chlorate
873301
7775­
09­
9
180.920
1
Stabilizer
3
Potassium
chlorate
900583
3811­
04­
9
180.930
2
Oxidizer
3
1
Residues
listed
in
40
CFR
§
180.920
[
formerly
40
CFR
§
180.100(
d)]
are
exempted
from
the
requirement
of
a
tolerance
when
used
in
accordance
with
good
agricultural
practice
as
inert
(
or
occasionally
active)
ingredients
in
pesticide
formulations
applied
to
growing
crops
only.
2
Residues
listed
in
40
CFR
§
180.930
[
formerly
40
CFR
§
180.100(
e)]
are
exempted
from
the
requirement
of
a
tolerance
when
used
in
accordance
with
good
agricultural
practice
as
inert
(
or
occasionally
active)
ingredients
in
pesticide
formulations
applied
to
animals.

Codex/
International
Harmonization
There
are
no
Codex
maximum
residue
limits
(
MRLs)
for
sodium
chlorate;
therefore,
no
questions
of
compatibility
with
U.
S.
tolerances
exist.
Page
124
of
141
APPENDIX
E
CHLORATE
(
ClO3
b
)
DIETARY
EXPOSURE
ESTIMATES
in
FOOD
Exposure
estimates
for
chlorate
residues
in
food
are
considered
conservative
and
the
dietary
(
food
only)
risk
assessments
are
deemed
upper
bound
estimates.

Dietary
exposure
(
food
only)
to
inorganic
chlorates
as
the
chlorate
ion
(
ClO
3
b
)
may
be
expected
from
the
following
dietary
exposure
routes:
(
1)
from
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
used
on
food
crops;
(
2)
from
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
pesticides
used
on
food
crops
or
in
poultry
premises;
(
3)
from
secondary
residues
in
meat/
milk/
poultry/
eggs
due
to
residues
in
animal
feedstuffs;
(
4)
from
sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
as
inert
ingredients
in
antimicrobial
agents
used
as
fruit,
vegetable,
and
egg
sanitizing
washes,
on
mushrooms
to
control
bacterial
blotch,
as
treatments
to
seed
used
for
sprouting,
for
conditioning
live
oysters,
in
poultry
drinking
water,
in
fish
filleting,
and
in
pecan
cracking/
dyeing;
(
5)
as
a
potential
redox
of
chlorine
dioxide
and
sodium
chlorite
in
conventional
and
antimicrobial
pesticides;
(
6)
from
degradation
of
hypochlorites
in
antimicrobial
agents
used
as
fruit
and
vegetable
washes;
and,
(
7)
from
translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
as
a
result
of
inorganic
chlorate
pesticide
uses.
These
dietary
(
food)
routes
of
exposure
are
discussed
below.
Dietary
exposure
estimates
for
food
only
to
be
incorporated
into
the
dietary
risk
assessments
for
inorganic
chlorate
are
summarized
in
Table
E.
1
below.

No
food
monitoring
data
are
available
for
this
risk
assessment;
only
limited,
chemical­
specific
field
trial
data
are
available.
Exposure
estimates
in
food
were
based
on
field
trial
data
or,
in
the
case
of
fruit/
vegetable/
other
washes,
was
derived
from
a
film
thickness
model.
No
Chemical­
specific
livestock
metabolism
or
feeding
data
are
available;
exposure
estimates
in
meat,
milk,
poultry,
and
eggs
were
derived
from
rat
metabolism
data,
field
trial
data,
and
livestock
reference
information
concerning
feed
consumption,
tissue
weights,
and
milk
production.
In
some
cases,
due
to
raw
data
limitations,
food
exposure
estimates
are
calculated
as
sodium
chlorate.
The
effects
of
washing
after
foliar
treatments
and,
in
some
cases
such
as
meat,
milk,
poultry
and
eggs
estimates,
percent
crop
treated
data
were
also
incorporated
into
these
exposure
estimates.
Page
125
of
141
Table
E.
1.
Summary
of
Chlorate
Dietary
(
Food)
Exposure
Estimates
for
the
Dietary
Risk
Assessments
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Vegetables
chili
peppers
0.5
0.5
/
0.2
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
chili
pepper,
potato,
and
cereal
grain
field
trial
data
and
considering
the
effects
of
washing
field
treated
RACs
as
demonstrated
by
the
chili
pepper
washing
data,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Note:

Incorporating
available
sodium
chlorate
percent
crop
treated
data
would
result
in
an
estimated
residue
level
below
that
from
sanitizing
fruit
and
vegetable
wash.

Maximum/
Average
Exposure
Estimate
from
sanitizing
fruit
and
vegetable
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

potatoes
0.5
0.5
/
0.2
sweet
corn
0.5
0.5
/
0.2
dry
beans,

guar
beans,

southern
peas,

soybeans
0.5
0.5
/
0.2
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
seed/
bean
field
trial
data
taken
as
a
whole,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Note:
Incorporating
available
sodium
chlorate
percent
crop
treated
data
would
result
in
an
estimated
residue
level
below
that
from
sanitizing
fruit
and
vegetable
wash.

Maximum/
Average
Exposure
Estimate
from
sanitizing
fruit
and
vegetable
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

all
others
0.2
N/
A
N/
A
0.2
Maximum/
Average
Exposure
Estimate
from
sanitizing
fruit
and
vegetable
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Page
126
of
141
Fruits
guava
0.5
0.5
0.5
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
the
exposure
estimates
for
sodium
chlorate,
as
an
active
ingredient,
in
conventional
(
agricultural)
pesticides
used
on
food
crops
and
considering
the
effects
of
washing
field
treated
RACs
as
demonstrated
by
the
chili
pepper
washing
data,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Note:
No
percent
crop
treated
data
are
currently
available.

Maximum/
Average
Exposure
Estimate
from
sanitizing
fruit
and
vegetable
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

citrus
fruits
(
except
peels),

bananas,
plantains,
and
coconuts
zero
N/
A
N/
A
zero
Maximum/
Average
Exposure
Estimate
from
sanitizing
fruit
and
vegetable
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.
For
citrus
fruits,
bananas/
plantains,
and
coconuts
which
have
substantial
outer
peels/
husks
which
are
removed
prior
to
consumption
and
processing,

residues
are
expected
to
be
essentially
nil;
the
exposure
estimate
is
zero.
Residues
in
citrus
fruit
peels
are
estimated
at
0.2
ppm.

citrus
fruit
peel
0.2
0.2
all
others
0.2
0.2
Seeds
cottonseed,

flaxseed,
safflower
seed,
sunflower
seed
0.5
0.5
/
0.5
/
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
seed/
bean
field
trial
data
taken
as
a
whole,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Page
127
of
141
Cereal
grains
rice
0.5
0.5
/
0.5
/
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
rice
field
trial
demonstrating
residues
in/
on
rice
w/
out
outer
hulls,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.

wheat
0.5
0.5
/
0.5
/
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
wheat
and
other
cereal
grain
field
trial
data,
residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.

corn
(
except
sweet)
20
10
/
10
/
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Translated
from
sorghum
field
trial
data,

maximum
and
average
residues
in/
on
corn
grain
are
not
expected
to
exceed
20
ppm
and
10
ppm,

respectively,
at
the
point
of
harvest
(
14­
day
PHI).

sorghum
70
40
/
40
/
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
sorghum
field
trial
data,

maximum
and
average
residues
in/
on
sorghum
grain
are
not
expected
to
exceed
70
ppm
and
40
ppm,

respectively,
at
the
point
of
harvest
(
7­
day
PHI).

Nuts
Macadamia
Nuts
0.5
0.5
0.5
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
the
exposure
estimates
for
sodium
chlorate,
as
an
active
ingredient,
in
conventional
(
agricultural)
pesticides
used
on
food
crops,

residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Note:
No
percent
crop
treated
data
are
currently
available.

Pecans
0.2
N/
A
N/
A
0.2
Maximum/
Average
Exposure
Estimate
from
pecan
cracking
and
dyeing:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Page
128
of
141
Animal
Tissues
Meat,
Poultry,

and
Eggs
10
0.1
0.1
Maximum/
Average
Exposure
Estimates
from
Agricultural
uses:
Conservative
estimates
based
on
the
rat
metabolism
data
that
demonstrated
that
<
1%
of
a
single
initial
dose
of
chlorate
is
expected
to
be
incurred
in
any
animal
tissue
72
hours
after
oral
exposure.

Maximum
residues
are
expected
to
be
<
12
ppm;
the
maximum
exposure
estimate
is
10
ppm
and
is
based
on:

°
Maximum
theoretical
dietary
burden
for
livestock
(
500
ppm)

°
Maximum
feed
rate
for
livestock
(
9.1
kg/
day)

°
Average
weight
(
4
kg)
of
the
smallest
(
by
weight)
organ
of
interest
(
kidney)

°
Percent
crop
treated
data
is
not
incorporated
into
the
estimate
Average
residues
are
expected
to
be
<
0.2
ppm;
the
average
exposure
estimate
is
0.1
ppm
and
is
based
on:

°
Highest
average
theoretical
dietary
burden
for
livestock
(
175
ppm)

°
Maximum
feed
rate
for
livestock
(
9.1
kg/
day)

°
Average
weight
(
4
kg)
of
the
smallest
(
by
weight)
organ
of
interest
(
kidney)

°
Incorporates
highest
percent
crop
treated
data
(
cotton
5%)
into
the
estimate
Maximum/
Average
Exposure
Estimates
from
sanitizing
washes:
Covered
by
estimates
from
agricultural
uses.
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Page
129
of
141
Milk
1
0.01
0.01
Maximum/
Average
Exposure
Estimates
from
Agricultural
uses:
Conservative
estimates
based
on
the
rat
metabolism
data
that
demonstrated
that
<
1%
of
a
single
initial
dose
of
chlorate
is
expected
to
be
incurred
in
any
animal
tissue
72
hours
after
oral
exposure.

Maximum
residues
are
expected
to
be
<
2
ppm;
the
maximum
exposure
estimate
is
1
ppm
and
is
based
on:

°
Maximum
theoretical
dietary
burden
for
cattle(
500
ppm)

°
Maximum
feed
rate
for
cattle
(
9.1
kg/
day)

°
Average
milk
production
per
day
(
ca.
30
kg)

°
Percent
crop
treated
data
are
not
incorporated
into
the
estimate
Average
residues
are
expected
to
be
<
0.03
ppm;
the
average
exposure
estimate
is
0.01
ppm
and
is
based
on:

°
Highest
average
theoretical
dietary
burden
for
cattle
(
175
ppm)

°
Maximum
feed
rate
for
(
9.1
kg/
day)

°
Average
milk
production
per
day
(
ca.
30
kg)

°
Incorporates
highest
percent
crop
treated
data
(
cotton
5%)
into
the
estimate
Food
Group
Food
Crop
Acute
Dietary
Screen
­
Do
Not
Use
%
Crop
Treated
Data
in
DEEM
Chronic
Dietary
Comments
From
Agricultural
Uses
Only
From
All
Uses
Exposure
Estimate
(
ppm)
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Exposure
Estimate
(
ppm)
/
=
Use
%
Crop
Treated
Data
in
DEEM
Page
130
of
141
Misc.
Fish
fillets
0.2
N/
A
N/
A
0.2
Maximum/
Average
Exposure
Estimate
from
sanitizing
fish
fillet
wash:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

Oysters
0.2
N/
A
N/
A
0.2
Maximum/
Average
Exposure
Estimate
from
conditioning
live
oysters:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

Mushrooms
0.2
N/
A
N/
A
0.2
Maximum/
Average
Exposure
Estimate
from
use
to
control
bacterial
blotch
on
mushrooms:
Estimate
derived
from
film
thickness
model
developed
by
FDA
for
sanitizing
non­
porous
surfaces.
Residues
are
expected
to
be
<
0.3
ppm;
the
exposure
estimate
is
0.2
ppm.

Sugarcane
0.5
0.5
0.5
Maximum/
Average
Exposure
Estimate
from
agricultural
use:
Based
on
exposure
estimates
from
sodium
chlorate,
as
an
active
ingredient,
in
conventional
(
agricultural)
pesticides
used
on
food
crops.

Residues
are
expected
to
be
<
1
ppm;
the
exposure
estimate
is
0.5
ppm.
Note:
No
percent
crop
treated
data
are
currently
available.

Note:
According
to
the
Usage
Report
in
Support
of
Reregistration
for
Sodium
Chlorate
(
Chemical
Code
073301/
Case
No.
4049)
dated
10/
27/
2004,
the
highest
average
Percent
Crop
Treated
(
PCT)
for
any
crop
reported
is
5%
PCT
for
cotton;
all
others
are
reported
as
<
1%
PCT
except
processed
lima
beans
and
safflower
which
are
reported
as
2%
PCT.
Page
131
of
141
Dietary
Exposure
Route
1.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
sodium
chlorate
(
073301)
as
an
active
ingredient
in
conventional
(
agricultural)
pesticides
used
on
food
crops
Sodium
chlorate
is
currently
registered
for
preharvest
and
foliar
applications
as
a
defoliant
or
desiccant
to
the
following
food/
feed
crops:
dry
beans,
corn,
cotton,
flax,
guar,
chili
peppers,
potatoes,
rice,
safflower,
sorghum
(
grain),
southern
peas
(
i.
e.,
cowpeas),
soybeans,
and
sunflowers.
For
food/
feed
uses,
sodium
chlorate
is
formulated
as
a
soluble
concentrate
(
SC)
with
the
active
ingredient
ranging
from
18%
to
47.2%.
Sodium
chlorate
may
be
applied
using
aircraft
or
ground
spray
equipment,
including
high
and
low
volume
equipment.

Uses
of
sodium
chlorate
as
a
defoliant
or
desiccant
on
cauliflower,
cucurbit
vegetables,
and
okra
grown
for
seed
only
are
considered
non­
food
uses.
Uses
of
sodium
chlorate
on
ornamental
gourds
and
fallow
lands
are
also
considered
non­
food
uses.
These
non­
food
uses
will
not
be
discussed
further
with
regards
to
dietary
exposure/
risk
considerations.

Under
40
CFR
180.1020
(
a)
Sodium
chlorate
is
exempt
from
the
requirement
of
a
tolerance
for
residues
in
or
on
the
following
raw
agricultural
commodities
when
used
as
a
defoliant,
desiccant,
or
fungicide
in
accordance
with
good
agricultural
practice:
beans
(
dry,
edible),
corn
(
fodder),
corn
(
forage),
corn
(
grain),
cottonseed,
flaxseed,
flax
(
straw),
guar
beans,
peas
(
southern),
peppers
(
chili),
potatoes,
rice,
rice
(
straw),
safflower
(
grain),
sorghum
(
grain),
sorghum
(
fodder),
sorghum
(
forage),
soybeans
and
sunflower
seed.

Under
40
CFR
180.1020
(
b)
A
time­
limited
exemption
from
the
requirement
of
a
tolerance
is
established
for
residues
of
the
defoliant/
desiccant
in
connection
with
use
of
the
pesticide
under
section
18
emergency
exemptions
granted
by
EPA.
This
exemption
has
been
granted
for
wheat
and
will
expire
on
12/
31/
04.
As
requested
by
the
Registration
Division
(
Sodium
Chlorate
Use
Closure
Memo
Amendment;
J.
Guerry;
dated
11/
15/
2004)
the
use
of
sodium
chlorate
on
wheat
is
also
addressed
herein
with
the
intention
to
convert
the
time­
limited
exemption
status
to
a
permanent
exemption
from
the
requirement
of
a
tolerance
under
40
CFR.
1020
(
a).
The
proposed
use
rate
is
for
a
single
application
of
sodium
chlorate
to
wheat
at
6
lbs
ai/
A
with
a
3­
day
PHI.

Based
on
the
available
flax,
guar,
southern
pea,
soybean,
and
sunflower
field
trial
data
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
dry
beans,
guar
beans,
southern
peas,
soybeans,
flaxseed,
safflower
seed,
and
sunflower
seed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
dry
beans,
guar,
southern
peas,
soybeans,
flax,
safflower,
and
sunflower
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI).
Furthermore,
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
cottonseed
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
cotton
(
2
applications,
7.5
lbs
ai/
A/
application;
7­
day
PHI).
Any
residues
which
might
be
detected
at
the
point
of
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
prior
to
the
point
of
consumption.

Based
on
the
available
chili
pepper
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
13
ppm)
might
be
found
on
the
surface
of
unwashed
chili
peppers
treated
with
Page
132
of
141
sodium
chlorate
at
the
maximum
use
rate
of
sodium
chlorate
on
chili
peppers
(
1
application;
12.5
lbs
ai/
A/
application;
10­
day
PHI).
However,
these
residues
are
primarily
surface
residues
present
at
the
point
of
harvest
which
would
be
substantially
removed
by
washing
(<
1
ppm)
prior
to
the
point
of
consumption.

Based
on
the
available
potato
field
trial
data,
no
detectable
residue
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
potato
tubers
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
potatoes
(
1
application;
12.5
lbs
ai/
A;
7­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
consumption.

Based
on
the
available
oat,
rice,
sorghum,
and
wheat
field
trial
data,
it
is
possible
that
detectable
residues
of
sodium
chlorate
(
ca.
70
ppm
as
demonstrated
by
sorghum
grain)
might
be
found
on
the
surface
of
cereal
grains
retaining
their
outer
hulls
at
harvest
(
such
as
oats
and
sorghum)
from
the
maximum
use
rate
of
sodium
chlorate
on
rice
and
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
and
wheat
(
1
application;
6
lbs
ai/
A;
3­
day
PHI).
However,
once
the
outer
hulls
are
removed
(
either
at
harvest
or
during
processing),
no
detectable
residues
of
sodium
chlorate
(<
1
ppm)
are
expected
in/
on
cereal
grains
such
as
rice
and
wheat
(
as
demonstrated
by
rice
w/
out
hulls
and
wheat
grain
data).

Based
on
the
available
sorghum
field
trial
data
alone,
maximum
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
for
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
70
ppm.
On
average,
residues
in/
on
sorghum
grain
harvested
7­
14
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
on
sorghum
(
1
application;
7.5
lbs
ai/
A;
7­
day
PHI)
are
not
expected
to
exceed
40
ppm.

Translating
the
available
sorghum
field
trial
data
to
corn,
residues
of
sodium
chlorate
are
not
expected
to
exceed
20
ppm
(
ca.
10
ppm
on
average)
in/
on
corn
grain
at
the
point
of
harvest
from
the
maximum
use
rate
of
sodium
chlorate
on
corn
(
1
application,
7.5
lbs
ai/
A;
14­
day
PHI).
As
demonstrated
by
the
chili
pepper
field
trial
data,
any
residues
present
at
harvest
are
expected
to
be
primarily
surface
residues
which
would
be
substantially
removed
by
washing
prior
to
the
point
of
consumption.
Hence,
residues
of
sodium
chlorate
in/
on
sweet
corn
after
washing
and
prior
to
consumption
would
not
be
expected
to
exceed
1
ppm.

Based
on
the
available
straw
(
flax,
oat,
wheat,
rice)
and
forage
(
guar
plants,
sorghum
stalks,
soybean
forage)
data,
maximum
residues
of
sodium
chlorate
in/
on
straw
and
forage
livestock
feedstuffs
harvested
3­
7
days
after
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application)
are
not
expected
to
exceed
300
ppm
at
the
point
of
harvest.
On
average,
residues
in/
on
straw
and
forage
livestock
feedstuffs
should
not
exceed
100
ppm
when
harvested
7­
14
days
after
foliar
treatment
with
sodium
chlorate
at
the
maximum
use
rate
permitted
on
forage
crops
(
1
or
2
applications;
7.5
lbs
ai/
A/
application).
Page
133
of
141
Dietary
Exposure
Route
2.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
sodium
chlorate
(
873301)
and
potassium
chlorate
(
900583)
as
inert
ingredients
in
conventional
(
agricultural)
pesticides
used
on
food
crops
or
in
poultry
premises
Sodium
chlorate
(
873301)
as
an
inert
ingredient
in
herbicide
formulation
products
can
be
applied
professionally
to
agricultural
(
corn,
guava,
macadamia
nuts,
sorghum
grain,
sugarcane,
wheat),
commercial
(
non­
agricultural),
and
residential
sites.
These
conventional
pesticide
products
contain
<
1
%
sodium
chlorate
and
can
be
applied
at
rates
no
greater
than
0.07
lb
(
as
sodium
chlorate)
per
acre.

Taking
into
account
the
small
percentage
of
sodium
chlorate
(
873301)
in
the
product(
s)
and
the
application
rate(
s)
of
the
product(
s)
at
issue,
chlorate
dietary
exposure
estimates
in/
on
corn,
guava,
macadamia
nuts,
sorghum
grain,
sugarcane,
and
wheat
are
expected
to
be
<
1
ppm
based
on
the
exposure
estimates
for
sodium
chlorate
(
073301)
as
an
active
ingredient
used
in
conventional
(
agricultural)
pesticides
which
are
used
at
higher
rates
(
6­
12.5
lb
ai/
A).

Specifically,
based
on
the
available
chili
pepper
and
potato
data,
residues
of
chlorate
in/
on
guava,
macadamia
nuts,
and
sugarcane
are
expected
to
be
primarily
surface
residues
leaving
<
1
ppm
in/
on
these
commodities
after
washing
and/
or
removal
of
outer
surfaces
prior
to
consumption,
as
demonstrated
by
the
available
chili
pepper
washing
data
and
the
rice
with
and
w/
out
hulls
field
trial
data.

Potassium
chlorate
(
900583)
as
an
inert
ingredient
in
airborne
fungicide
products
can
be
applied
in
poultry
premises.
These
conventional
pesticide
products
contain
<
20%
potassium
chlorate
and
can
be
applied
at
rates
not
greater
than
0.01
lb
(
as
potassium
chlorate)
per
500
ft3.

No
chlorate
residues
are
expected
in
egg
commodities
from
the
use
of
potassium
chlorate
(
900583)
as
an
inert
ingredient
in
poultry
premises.
Page
134
of
141
Dietary
Exposure
Route
3.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
secondary
residues
incurred
in
meat,
milk,
poultry
and
eggs
from
consumption
of
feedstuffs
treated
with
sodium
chlorate
(
073301
or
873301)
as
an
active
or
inert
ingredient
in
conventional
(
agricultural)
pesticides
The
maximum
residues
(
excluding
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
estimated
at
10
ppm
and
in
milk
is
estimated
at
1
ppm
based
on
the
following
information
and
assumptions:

°
The
maximum
theoretical
dietary
burden
for
livestock
is
500
ppm
for
cattle
feed
on
a
dry
wt.
basis
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
4600
mg
per
day
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
46
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Maximum
Theoretical
Dietary
Exposure
(
4600
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Maximum
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
12
ppm;
estimated
at
10
ppm
Maximum
Residue
Estimate
in
Milk
=
<
2
ppm;
estimated
at
1
ppm
The
highest
average
residues
(
including
percent
crop
treated
data)
in
meat,
poultry,
and
eggs
are
estimated
at
0.1
ppm
and
in
milk
is
estimated
at
0.01
ppm
based
on
the
following
information
and
assumptions:

°
The
highest
average
theoretical
dietary
burden
for
livestock
is
175
ppm
for
cattle
feed
on
a
dry
wt.
basis
(
excluding
percent
crop
treated
data)
°
Cattle
eat
a
maximum
of
9.1
kg
of
feed
per
day
on
a
dry
wt.
basis
(
Update
of
Livestock
Feed
Consumption,
1993);
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
1600
mg
per
day
(
excluding
percent
crop
treated
data)
°
The
maximum
percent
crop
treated
is
5%
on
cotton
all
other
feed
crops
are
<
1%
(
Usage
Report
from
A.
Halvorson
to
B.
Cropp­
Kohlligian
and
J.
Guerry
dated
10/
27/
2004)
Page
135
of
141
hence,
the
highest
average
theoretical
dietary
exposure
for
sodium
chlorate
to
livestock
is
80
mg
per
day
(
including
percent
crop
treated
data
at
5%).
°
Based
on
the
available
rat
metabolism
data,
<
1%
of
the
initial
dose
of
chlorate
is
expected
to
be
incurred
in
animal
tissues
72
hours
after
exposure
(
Abdel­
Rahman
et
al,
1982,
1984b
and
1985);
hence
<
0.8
mg
is
expected
to
be
incurred
in
any
livestock
tissue
of
interest
°
Assuming
that
kidneys
have
the
lowest
weight
of
the
organs/
tissues
of
interest
(
other
than
milk)
in
livestock
(
i.
e.,
compared
to
meat,
liver,
fat,
and
eggs)
°
Assuming
that
the
average
weight
of
cattle
kidneys
is
about
4
kg
(
Update
of
Livestock
Feed
Consumption,
1993;
cattle
kidneys
weigh
3.6­
4.5
kg)
°
Assuming
that
the
average
milk
production
per
day
is
about
30
kg
(
Frank,
2002;
milk
production
is
50­
90
lb
milk/
cow/
day)

Calculations:

(
Highest
Average
Theoretical
Dietary
Exposure
(
80
mg)
x
Percent
of
Dietary
Exposure
Expected
in
Organs
(<
1%)
Average
Weight
of
the
Organ/
Tissue
of
Interest
(
Kidney
at
4
Kg
or
Milk
at
30
Kg)

Highest
Average
Residue
Estimate
in
Meat,
Poultry,
and
Eggs
=
<
0.2
ppm;
estimated
at
0.1
ppm
Highest
Average
Residue
Estimate
in
Milk
=
<
0.03
ppm;
estimated
at
0.01
ppm
Page
136
of
141
Dietary
Exposure
Route
4.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
sodium
chlorate
(
873301)
and
calcium
chlorate
(
875606)
as
inert
ingredients
in
antimicrobial
agents
used:
(
1)
as
fruit,
vegetable,
and
egg
sanitizing
washes;
(
2)
to
control
bacterial
blotch
on
mushrooms;
(
3)
as
treatment
to
seed
used
for
sprouting;
(
4)
for
conditioning
live
oysters;
(
5)
in
poultry
drinking
water;
(
6)
in
fish
filleting;
and
(
7)
pecan
cracking/
dyeing
Fruit
and
vegetable
sanitizing
washes:
Using
a
film
thickness
model,
residues
of
chlorate
in/
on
fruits
and
vegetables
treated
at
the
maximum
use
rate
are
expected
to
be
<
0.3
ppm;
estimated
at
0.2
ppm.

This
estimate
will
also
be
used
for
seed
sprouting,
mushrooms,
oysters,
fish
fillets,
and
pecans.

This
estimate
will
also
cover
estimates
on
fruits
and
vegetables
from
Dietary
Exposure
Routes
5,
6,
7,
and
8
identified
below.

Since
these
residues
are
expected
to
be
primarily
surface
residues
in
fruits
which
have
substantial
outer
peels
which
are
removed
prior
to
consumption,
residues
of
chlorate
in
citrus
fruits,
bananas
and
plantains
are
expected
to
be
essentially
nil
(
zero)
once
the
peels
are
removed.

No
chlorate
residues
are
expected
in
egg
commodities
from
surface
sanitizing
washes.
Chlorate
residue
estimates
in
poultry
commodities
from
chlorate
in
antimicrobial
agents
use
in
poultry
drinking
water
are
covered
by
the
secondary
residue
estimates
for
meat/
milk/
poultry/
egg
addressed
above
under
Dietary
Exposure
Route
3.

Calculation
for
percent
chlorate
in
the
sanitizing
washes:

For
the
active
ingredient(
s)
the
maximum
use
rate
is
500
ppm
as
total
chlorine
in
the
sanitizing
wash
water.
Exposure
time
is
1­
2
minutes.

Percent
of
chlorate
as
an
inert
in
the
product
is
at
most
2%.
This
is
equivalent
to
ca.
<
15
ppm
or
<
0.0015%
chlorate
in
the
sanitizing
wash
water.

Note:
The
maximum
or
peak
concentration
of
chlorate
ion
(
ClO3
b
)
in
drinking
water
is
estimated
at
9
mg/
L
and
is
based
on
the
available
AwwaRF
(
1995)
survey
study
report
data.

Calculation
of
the
surface
and
weight
of
treated
fruits
and
vegetables:

As
a
model
a
small
fruit
with
high
surface
to
volume
ratio
such
as
a
blueberry
was
selected
to
represent
all
fruits
and
vegetables.

Information
Provided
by
Cassi
Walls
of
AD:
Diameter
of
one
blueberry
=
20
mm
Page
137
of
141
Source:
Blueberry
Research
at
the
University
of
Georgia
http://
www.
ces.
uga.
edu/
ES­
pubs/
RR662.
htm#
CPPU%
20Enhances%
20Fruit%
20Set
Surface
area
of
one
blueberry
=
12.56
cm2
Based
on
surface
area
of
a
sphere
where
A
=
4Br2
(
where
r
=
10mm
=
1cm)
A
=
4(
3.14)(
1
cm2)
=
12.56
cm2
Information
Provided
by
Cassi
Walls
of
AD:
Mass
of
one
blueberry
=
0.00136
kg
(
where
50
berries
=
68
g
or
0.068
kg)
Source:
USDA's
nutrient
database
http://
www.
nal.
usda.
gov/
fnic/
foodcomp/
search/

Calculation
of
chlorate
residues
on
blueberries
Information
Provided
by
Cassi
Walls
of
AD:
Assumes
the
film
thickness
of
the
sanitizing
solution
on
the
surface
of
the
berry
is
0.0023
g
(
2.3
mg)
sanitizing
solution/
cm2
Source:
Proctor
and
Gamble
exposure
assessment
for
ingestion
of
dishwashing
product
residues
­
based
on
the
amount
of
rinse
water
in
contact
with
dishware
surfaces
http://
www.
scienceinthebox.
com/
en_
UK/
safety/
ingestionfromsurface_
en.
html
2.3
mg/
cm2
(
film
thickness)
x
12.56
cm2
(
surface
area)
x
<
0.0015%
chlorate
in
solution
0.00136
kg
blueberry
Chlorate
residues
on
blueberry
=
<
0.3
ppm;
estimated
at
0.2
ppm
Page
138
of
141
Dietary
Exposure
Route
5.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
potential
redox
of
chlorine
dioxide
as
the
antimicrobial
agent
in
fruit
and
vegetable
washes
and
water
used
in
poultry
processing
These
dietary
exposure
concerns
are
covered
by
the
estimates
from
Dietary
Exposure
Routes
3
and
4
discussed
above.

Under
173.300
concerning
secondary
direct
food
additives
permitted
in
food
for
human
consumption
chlorine
dioxide
(
CAS
Reg.
No.
10049­
04­
4)
may
be
safely
used
in
food
in
accordance
with
the
following
prescribed
conditions:
(
a)
The
additive
is
generated
by
one
of
the
following
methods:
Treating
an
aqueous
solution
of
sodium
chlorite
with
either
chlorine
gas
or
a
mixture
of
sodium
hypochlorite
and
hydrochloric
acid,
or
treating
an
aqueous
solution
of
sodium
chlorate
with
hydrogen
peroxide
in
the
presence
of
sulfuric
acid.
In
either
case,
the
generator
effluent
contains
at
least
90
percent
(
by
weight)
of
chlorine
dioxide
with
respect
to
all
chlorine
species
as
determined
by
Method
4500­
ClO2
E
in
the
  
Standard
Methods
for
the
Examination
of
Water
and
Wastewater,''
18th
ed.,
1992,
or
an
equivalent
method.
Method
4500­
ClO2
E
is
incorporated
by
reference
in
accordance
with
5
U.
S.
C.
552(
a)
and
1
CFR
part
51.
The
additive
may
be
used
as
an
antimicrobial
agent
in
water
used
in
poultry
processing
in
an
amount
not
to
exceed
3
parts
per
million
(
ppm)
residual
chlorine
dioxide
as
determined
by
Method
4500­
ClO2
E,
referenced
in
paragraph
(
a)
of
this
section,
or
an
equivalent
method.
(
2)
The
additive
may
be
used
as
an
antimicrobial
agent
in
water
used
to
wash
fruits
and
vegetables
that
are
not
raw
agricultural
commodities
in
an
amount
not
to
exceed
3
ppm
residual
chlorine
dioxide
as
determined
by
Method
4500­
ClO2
E,
referenced
in
paragraph
(
a)
of
this
section,
or
an
equivalent
method.
Treatment
of
the
fruits
and
vegetables
with
chlorine
dioxide
shall
be
followed
by
a
potable
water
rinse
or
by
blanching,
cooking,
or
canning.

Dietary
Exposure
Route
6.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
degradation
of
sodium
hypochlorite
or
calcium
hypochlorite
as
antimicrobial
agents
in
fruit
and
vegetable
washes
These
dietary
exposure
concerns
are
covered
by
the
estimates
from
Dietary
Exposure
Route
4
discussed
above.

Under
40
CFR
180.2
sodium
hypochlorite
is
generally
regarded
as
safe
Under
40
CFR
180.1054
(
a)
Calcium
hypochlorite
is
exempted
from
the
requirement
of
a
tolerance
when
used
preharvest
or
postharvest
in
solution
on
all
raw
agricultural
commodities.
(
b)
Calcium
hypochlorite
is
exempted
from
the
requirement
of
a
tolerance
in
or
on
grapes
when
used
as
a
fumigant
postharvest
by
means
of
a
chlorine
generator
pad.

Under
21
CFR
173.315
concerning
secondary
direct
food
additives
permitted
in
food
for
human
consumption,
chemicals
used
in
washing
or
to
assist
in
the
lye
peeling
of
fruits
and
vegetables
...
sodium
hypochlorite
...
The
use
of
the
chemicals
is
followed
by
rinsing
with
potable
water
to
remove,
to
the
extent
possible,
residues
of
the
chemical.
Page
139
of
141
Dietary
Exposure
Route
7.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
potential
redox
of
acidified
sodium
chlorite
as
an
antimicrobial
agent
used
in
fruit
and
vegetable
washes
and
poultry
carcass
and
red
meat
processing
water
These
dietary
exposure
concerns
are
covered
by
the
estimates
from
Dietary
Exposure
Routes
3
and
4
discussed
above.

Under
21
CFR
173.325
concerning
secondary
direct
food
additives
permitted
in
food
for
human
consumption,
acidified
sodium
chlorite
solutions
may
be
safely
used
in
accordance
with
the
following
prescribed
conditions:
(
a)
The
additive
is
produced
by
mixing
an
aqueous
solution
of
sodium
chlorite
(
CAS
Reg.
No.
7758­
19­
2)
with
any
generally
recognized
as
safe
(
GRAS)
acid.
(
b)(
1)
The
additive
is
used
as
an
antimicrobial
agent
in
poultry
processing
water
in
accordance
with
current
industry
practice
under
the
following
conditions:
(
i)
As
a
component
of
a
carcass
spray
or
dip
solution
prior
to
immersion
of
the
intact
carcass
in
a
prechiller
or
chiller
tank;
(
ii)
In
a
prechiller
or
chiller
solution
for
application
to
the
intact
carcass;
(
iii)
As
a
component
of
a
spray
or
dip
solution
for
application
to
poultry
carcass
parts;
(
iv)
In
a
prechiller
or
chiller
solution
for
application
to
poultry
carcass
parts;
or
(
v)
As
a
component
of
a
post­
chill
carcass
spray
or
dip
solution
when
applied
to
poultry
meat,
organs,
or
related
parts
or
trim.
(
2)
When
used
in
a
spray
or
dip
solution,
the
additive
is
used
at
levels
that
result
in
sodium
chlorite
concentrations
between
500
and
1,200
parts
per
million
(
ppm),
in
combination
with
any
GRAS
acid
at
a
level
sufficient
to
achieve
a
solution
pH
of
2.3
to
2.9.
(
3)
When
used
in
a
prechiller
or
chiller
solution,
the
additive
is
used
at
levels
that
result
in
sodium
chlorite
concentrations
between
50
and
150
ppm,
in
combination
with
any
GRAS
acid
at
levels
sufficient
to
achieve
a
solution
pH
of
2.8
to
3.2.
(
c)
The
additive
is
used
as
an
antimicrobial
agent
in
accordance
with
current
industry
practice
in
the
processing
of
red
meat,
red
meat
parts,
and
organs
as
a
component
of
a
spray
or
in
the
processing
of
red
meat
parts
and
organs
as
a
component
of
a
dip.
Applied
as
a
dip
or
spray,
the
additive
is
used
at
levels
that
result
in
sodium
chlorite
concentrations
between
500
and
1,200
ppm
in
combination
with
any
GRAS
acid
at
levels
sufficient
to
achieve
a
solution
pH
of
2.5
to
2.9.
(
d)
The
additive
is
used
as
an
antimicrobial
agent
in
water
and
ice
that
are
used
to
rinse,
wash,
thaw,
transport,
or
store
seafood
in
accordance
with
current
industry
standards
of
good
manufacturing
practice.
The
additive
is
produced
by
mixing
an
aqueous
solution
of
sodium
chlorite
with
any
GRAS
acid
to
achieve
a
pH
in
the
range
of
2.5
to
2.9
and
diluting
this
solution
with
water
to
achieve
an
actual
use
concentration
of
40
to
50
parts
per
million
(
ppm)
sodium
chlorite.
Any
seafood
that
is
intended
to
be
consumed
raw
shall
be
subjected
to
a
potable
water
rinse
prior
to
consumption.
(
e)
The
additive
is
used
as
an
antimicrobial
agent
on
raw
agricultural
commodities
in
the
preparing,
packing,
or
holding
of
the
food
for
commercial
purposes,
consistent
with
section
201(
q)(
1)(
B)(
i)
of
the
act,
and
not
applied
for
use
under
section
201(
q)(
1)(
B)(
i)(
I),
(
q)(
1)(
B)(
i)(
II),
or
(
q)(
1)(
B)(
i)(
III)
of
the
act,
in
accordance
with
current
industry
standards
of
good
manufacturing
practice.
Applied
as
a
dip
or
a
spray,
the
additive
is
used
at
levels
that
result
in
chlorite
concentrations
of
500
to
1200
parts
per
million
(
ppm),
in
combination
with
any
GRAS
acid
at
levels
sufficient
to
achieve
a
pH
of
2.3
to
2.9.
Treatment
of
the
raw
agricultural
commodities
with
acidified
sodium
chlorite
solutions
shall
be
followed
by
a
potable
water
rinse,
or
Page
140
of
141
by
blanching,
cooking,
or
canning.
(
f)
The
additive
is
used
as
an
antimicrobial
agent
on
processed,
comminuted
or
formed
meat
food
products
(
unless
precluded
by
standards
of
identity
in
9
CFR
part
319)
prior
to
packaging
of
the
food
for
commercial
purposes,
in
accordance
with
current
industry
standards
of
good
manufacturing
practice.
Applied
as
a
dip
or
spray,
the
additive
is
used
at
levels
that
result
in
sodium
chlorite
concentrations
of
500
to
1200
ppm,
in
combination
with
any
GRAS
acid
at
levels
sufficient
to
achieve
a
pH
of
2.5
to
2.9.
(
g)
The
additive
is
used
as
an
antimicrobial
agent
in
the
water
applied
to
processed
fruits
and
processed
root,
tuber,
bulb,
legume,
fruiting
(
i.
e.,
eggplant,
groundcherry,
pepino,
pepper,
tomatillo,
and
tomato),
and
cucurbit
vegetables
in
accordance
with
current
industry
standards
of
good
manufacturing
practices,
as
a
component
of
a
spray
or
dip
solution,
provided
that
such
application
be
followed
by
a
potable
water
rinse
and
a
24­
hour
holding
period
prior
to
consumption.
However,
for
processed
leafy
vegetables
(
i.
e.,
vegetables
other
than
root,
tuber,
bulb,
legume,
fruiting,
and
cucurbit
vegetables)
and
vegetables
in
the
Brassica
[
Cole]
family,
application
must
be
by
dip
treatment
only,
and
must
be
preceded
by
a
potable
water
rinse
and
followed
by
a
potable
water
rinse
and
a
24­
hour
holding
period
prior
to
consumption.
When
used
in
a
spray
or
dip
solution,
the
additive
is
used
at
levels
that
result
in
sodium
chlorite
concentrations
between
500
and
1,200
ppm,
in
combination
with
any
GRAS
acid
at
a
level
sufficient
to
achieve
a
solution
pH
of
2.3
to
2.9.
(
h)
The
concentration
of
sodium
chlorite
is
determined
by
a
method
entitled
  
Determination
of
Sodium
Chlorite:
50
ppm
to
1500
ppm
Concentration,''
September
13,
1995,
developed
by
Alcide
Corp.,
Redmond,
WA,
which
is
incorporated
by
reference
in
accordance
with
5
U.
S.
C.
552(
a)
and
1
CFR
part
51.

Dietary
Exposure
Route
8.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
potential
redox
of
sodium
chlorite
as
the
active
ingredient
in
conventional
(
agricultural)
pesticides
used
in
seed­
soak
treatments
These
dietary
exposure
concerns
are
covered
by
the
estimates
from
Dietary
Exposure
Route
4
discussed
above.

Under
40
CFR
180.1070,
sodium
chlorite
is
exempted
from
the
requirement
of
a
tolerance
for
residues
when
used
in
accordance
with
good
agricultural
practice
as
a
seed­
soak
treatment
in
the
growing
of
the
raw
agricultural
commodities
crop
group
Brassica
(
cole)
leafy
vegetables
and
radishes.
Page
141
of
141
Dietary
Exposure
Route
9.
Chlorate
(
ClO
3
b
)
dietary
exposure
estimates
from
translocation
of
very
small
amounts
of
chlorate
ion
(
ClO
3
b
)
by
plants
(
translocation
of
significant
amounts
would
be
phytotoxic
to
plants)
from
the
environment
which
may
be
present
due
to
inorganic
chlorate
pesticide
uses
These
dietary
exposure
concerns
are
covered
by
the
estimates
from
Dietary
Exposure
Routes
1,
2,
and
4
discussed
above.

REFERENCES
Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1982.
Metabolism
and
pharmacokinetics
of
alternate
drinking
water
disinfectants.
Environ
Health
Perspect.
46:
19­
23.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1984b.
The
Kinetics
of
Chlorite
and
Chlorate
in
the
Rat.
Journal
of
the
American
College
of
Toxicology,
3(
4):
261­
267.

Abdel­
Rahman
MS,
Couri
D,
Bull
RJ.
1985.
The
kinetics
of
chlorite
and
chlorate
in
rats.
J
Environ
Pathol
Toxicol
Oncol.
6(
1):
97­
103.

Frank,
G.
2002.
Cost
of
Milk
Production
per
Hundredweight
Equivalent
in
Milk
Sold
per
Cow
Ranges.
Wisconsin
Dairy
Data.
Fact
Sheet
2002­
01.
Center
for
Dairy
Profitability.
Univ.
Wisconsin
Extension
Service.
Oct.
2002.