Document ID: EPA-HQ-OW-2002-0021-0135
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-05-15T04:00Z

Health
Effects
Support
Document
for
Metribuzin
Printed
on
Recycled
Paper
Health
Effects
Support
Document
for
Metribuzin
U.
S.
Environmental
Protection
Agency
Office
of
Water
(
4304T)
Health
and
Ecological
Criteria
Division
Washington,
DC
20460
www.
epa.
gov/
safewater/
ccl/
pdf/
metribuzin.
pdf
EPA
822­
R­
03­
004
February
2003
iii
Metribuzin
 
February
2003
FOREWORD
The
Safe
Drinking
Water
Act
(
SDWA),
as
amended
in
1996,
requires
the
Administrator
of
the
Environmental
Protection
Agency
to
establish
a
list
of
contaminants
to
aid
the
agency
in
regulatory
priority
setting
for
the
drinking
water
program.
In
addition,
SDWA
requires
EPA
to
make
regulatory
determinations
for
no
fewer
than
five
contaminants
by
August
2001.
The
criteria
used
to
determine
whether
or
not
to
regulate
a
chemical
on
the
CCL
are
the
following:

The
contaminant
may
have
an
adverse
effect
on
the
health
of
persons.

The
contaminant
is
known
to
occur
or
there
is
a
substantial
likelihood
that
the
contaminant
will
occur
in
public
water
systems
with
a
frequency
and
at
levels
of
public
health
concern.

In
the
sole
judgment
of
the
administrator,
regulation
of
such
contaminant
presents
a
meaningful
opportunity
for
health
risk
reduction
for
persons
served
by
public
water
systems.

The
Agency's
finding
for
the
criteria
are
used
in
making
a
determination
to
regulate
a
contaminant.
The
Agency
may
determine
that
there
is
no
need
for
regulation
when
a
contaminant
fails
to
meet
one
of
the
criteria.
The
decision
not
to
regulate
is
considered
a
final
agency
action
and
is
subject
to
judicial
review.

This
document
provides
the
health
effects
basis
for
the
preliminary
regulatory
determination
for
metribuzin.
In
arriving
at
the
preliminary
regulatory
determination,
data
on
toxicokinetics,
human
exposure,
acute
and
chronic
toxicity
to
animals
and
humans,
epidemiology,
and
mechanisms
of
toxicity
were
evaluated.
In
order
to
avoid
wasteful
duplication
of
effort,
information
from
the
following
risk
assessments
by
the
EPA
and
other
government
agencies
were
used
in
development
of
this
document.

U.
S.
EPA.
1998a.
U.
S.
Environmental
Protection
Agency.
Registration
Eligibility
Decision
(
RED):
Metribuzin.
Office
of
Prevention,
Pesticides,
and
Toxic
Substances.
February
1998.

U.
S.
EPA.
1998b.
U.
S.
Environmental
Protection
Agency.
R.
E.
D.
Facts:
Metribuzin.
Office
of
Prevention,
Pesticides,
and
Toxic
Substances.
February
1998.

U.
S.
EPA.
1993.
U.
S.
Environmental
Protection
Agency.
Integrated
Risk
Information
System
(
IRIS):
Metribuzin.
Cincinnati,
OH.
December
1,
1993.

U.
S.
EPA.
1988.
U.
S.
Environmental
Protection
Agency.
Health
advisories
for
50
pesticides.
Office
of
Drinking
Water.
August
1988.
iv
Metribuzin
 
February
2003
Information
from
the
published
risk
assessments
was
supplemented
with
information
from
recent
studies
of
metribuzin
identified
by
literature
searches
conducted
in
1999
and
2000
and
the
primary
references
for
key
studies.

Generally
a
Reference
Dose
(
RfD)
is
provided
as
the
assessment
of
long­
term
toxic
effects
other
than
carcinogenicity.
RfD
determination
assumes
that
thresholds
exist
for
certain
toxic
effects
such
as
cellular
necrosis.
It
is
expressed
in
terms
of
milligrams
per
kilogram
per
day
(
mg/
kg­
day).
In
general,
the
RfD
is
an
estimate
(
with
uncertainty
spanning
perhaps
an
order
of
magnitude)
of
a
daily
exposure
to
the
human
population
(
including
sensitive
subgroups)
that
is
likely
to
be
without
an
appreciable
risk
of
deleterious
effects
during
a
lifetime.

The
carcinogenicity
assessment
for
metribuzin
includes
a
formal
hazard
identification.
Hazard
identification
is
a
weight­
of­
evidence
judgment
of
the
likelihood
that
the
agent
is
a
human
carcinogen
via
the
oral
route
and
the
conditions
under
which
the
carcinogenic
effects
may
be
expressed.

Guidelines
that
were
used
in
the
development
of
this
assessment
may
include
the
following:
the
Guidelines
for
Carcinogenic
Risk
Assessment
(
U.
S.
EPA,
1986a),
Guidelines
for
the
Health
Risk
Assessment
of
Chemical
Mixtures
(
U.
S.
EPA,
1986b),
Guidelines
for
Mutagenicity
Risk
Assessment
(
U.
S.
EPA,
1986c),
Guidelines
for
Developmental
Toxicity
Risk
Assessment
(
U.
S.
EPA,
1991),
Proposed
Guidelines
for
Carcinogen
Risk
Assessment
(
1996a),
Guidelines
for
Reproductive
Toxicity
Risk
Assessment
(
U.
S.
EPA,
1996b),
and
Guidelines
for
Neurotoxicity
Risk
Assessment
(
U.
S.
EPA,
1998c);
Recommendations
for
and
Documentation
of
Biological
Values
for
Use
in
Risk
Assessment
(
U.
S.
EPA,
1988);
and
Health
Effects
Testing
Guidelines
(
OPPTS
series
870,
1996
drafts;
U.
S.
EPA
40
CFR
Part
798,
1997);
Peer
Review
and
Peer
Involvement
at
the
U.
S.
Environmental
Protection
Agency
(
U.
S.
EPA,
1994a);
Use
of
the
Benchmark
Dose
Approach
in
Health
Risk
Assessment
(
U.
S.
EPA,
1995);
Science
Policy
Council
Handbook:
Peer
Review
(
U.
S.
EPA,
1998d,
2000f);
Memorandum
from
EPA
Administrator,
Carol
Browner,
dated
March
21,
1995,
Policy
for
Risk
Characterization;
Science
Policy
Council
Handbook:
Risk
Characterization
(
U.
S.
EPA,
2000g).

The
chapter
on
occurrence
and
exposure
to
metribuzin
through
potable
water
was
developed
by
the
Office
of
Ground
Water
and
Drinking
Water.
It
is
based
primarily
on
unregulated
contaminant
monitoring
(
UCM)
data
collected
under
SDWA.
The
UCM
data
are
supplemented
with
ambient
water
data
as
well
as
information
on
production,
use,
and
discharge.
v
Metribuzin
 
February
2003
ACKNOWLEDGMENTS
This
document
was
prepared
under
the
U.
S.
EPA
contract
No.
68­
C­
01­
002,
Work
Assignment
No.
B­
17
with
Sciences
International,
Inc.,
Alexandria,
Virginia.
The
Lead
U.
S.
EPA
Scientist
is
Octavia
Conerly,
Health
and
Ecological
Criteria
Division,
Office
of
Science
and
Technology,
Office
of
Water.
vi
Metribuzin
 
February
2003
Table
of
Contents
FOREWORD
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iii
ACKNOWLEDGMENTS
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v
LIST
OF
TABLES
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ix
LIST
OF
FIGURES
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x
1.0
EXECUTIVE
SUMMARY
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1­
1
2.0
IDENTITY:
PHYSICAL
AND
CHEMICAL
PROPERTIES
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2­
1
3.0
USES
AND
ENVIRONMENTAL
FATE
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3­
1
3.1
Production
and
Use
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3­
1
3.2
Environmental
Release
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3­
3
3.3
Environmental
Fate
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3­
4
4.0
EXPOSURE
FROM
DRINKING
WATER
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4­
1
4.1
Occurrence
and
Monitoring
Data
of
Ambient
Water
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4­
1
4.1.1
Data
Sources
and
Methods
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4­
1
4.1.2
Results
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4­
2
4.2
Occurrence
and
Monitoring
Data
in
Drinking
Water
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4­
5
4.2.1
Data
Sources,
Data
Quality,
and
Analytical
Methods
.
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4­
6
4.2.2
Data
Management
and
Analysis
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4­
10
4.2.3
Results
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4­
14
4.3
Conclusions
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4­
21
5.0
EXPOSURE
FROM
MEDIA
OTHER
THAN
WATER
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5­
1
5.1
Exposure
from
Food
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5­
1
5.1.1
Exposures
of
the
General
Population
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5­
1
5.1.2
Exposures
of
Subpopulations
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5­
3
5.2
Exposure
from
Air
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5­
3
5.2.1
Exposures
of
the
General
Population
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5­
3
5.2.2
Exposures
of
Subpopulations
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5­
3
5.3
Exposure
from
Soil
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5­
4
5.3.1
Exposures
of
the
General
Population
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5­
4
5.3.2
Exposures
of
Subpopulations
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5­
4
5.4
Other
Residential
Exposures
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5­
5
5.5
Summary
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5­
5
6.0
TOXICOKINETICS
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6­
1
6.1
Absorption
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6­
1
vii
Metribuzin
 
February
2003
6.2
Distribution
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6­
1
6.3
Metabolism
.
.
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.
6­
1
6.4
Excretion
.
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.
6­
1
7.0
HAZARD
IDENTIFICATION
.
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.
7­
1
7.1
Human
Effects
.
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.
7­
1
7.1.1
Short­
Term
Studies
.
.
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.
.
7­
1
7.1.2
Long­
Term
and
Epidemiological
Studies
.
.
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.
7­
1
7.2
Animal
Studies
.
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.
7­
1
7.2.1
Acute
Toxicity
.
.
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.
7­
1
7.2.2
Short­
Term
Studies
.
.
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.
7­
1
7.2.3
Subchronic
Studies
.
.
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.
.
7­
1
7.2.4
Neurotoxicity
.
.
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.
.
7­
3
7.2.5
Developmental/
Reproductive
Toxicity
.
.
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.
.
7­
3
7.2.6
Chronic
Toxicity
.
.
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.
7­
5
7.2.7
Carcinogenicity
.
.
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.
7­
6
7.3
Other
Key
Data
.
.
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.
.
7­
7
7.3.1
Mutagenicity/
Genotoxicity
.
.
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.
7­
7
7.3.2
Immunotoxicity
.
.
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.
.
7­
8
7.3.3
Hormonal
Disruption
.
.
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.
.
7­
8
7.3.4
Physiological
or
Mechanistic
Studies
.
.
.
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.
.
7­
8
7.3.5
Structure­
Activity
Relationship
.
.
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.
.
7­
9
7.4
Hazard
Characterization
.
.
.
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.
.
.
7­
9
7.4.1
Synthesis
and
Evaluation
of
Major
Non­
Cancer
Effects
.
.
.
.
.
.
.
.
.
.
.
.
7­
9
7.4.2
Synthesis
and
Evaluation
of
Carcinogenic
Effects
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
7­
10
7.4.3
Mode
of
Action
and
Implications
in
Cancer
Assessment
.
.
.
.
.
.
.
.
.
.
7­
10
7.4.4
Weight
of
Evidence
Evaluation
for
Carcinogenicity
.
.
.
.
.
.
.
.
.
.
.
.
.
.
7­
11
7.4.5
Sensitive
Populations
.
.
.
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.
7­
11
8.0
DOSE­
RESPONSE
ASSESSMENT
.
.
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.
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.
.
8­
1
8.1
Dose­
Response
for
Non­
Cancer
Effects
.
.
.
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.
.
8­
1
8.1.1
RfD
Determination
.
.
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.
.
8­
1
8.1.2
RfC
Determination
.
.
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.
.
8­
1
8.2
Dose­
Response
for
Cancer
Effects
.
.
.
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.
.
.
8­
2
9.0
REGULATORY
DETERMINATION
AND
CHARACTERIZATION
OF
RISK
FROM
DRINKING
WATER
.
.
.
.
.
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.
.
.
9­
1
9.1
Regulatory
Determination
for
Chemicals
on
the
CCL
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
9­
1
9.1.1
Criteria
for
Regulatory
Determination
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
9­
1
9.1.2
National
Drinking
Water
Advisory
Council
Recommendations
.
.
.
.
.
.
9­
2
9.2
Health
Effects
.
.
.
.
.
.
.
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.
.
9­
2
9.2.1
Health
Criterion
Conclusion
.
.
.
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.
.
.
.
.
.
9­
3
9.2.2
Hazard
Characterization
and
Mode
of
Action
Implications
.
.
.
.
.
.
.
.
.
9­
3
viii
Metribuzin
 
February
2003
9.2.3
Dose­
Response
Characterization
and
Implications
in
Risk
Assessment
.
.
.
.
.
.
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.
.
.
.
.
9­
4
9.3
Occurrence
in
Public
Water
Systems
.
.
.
.
.
.
.
.
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.
.
.
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.
.
.
.
.
9­
4
9.3.1
Occurrence
Criterion
Conclusion
.
.
.
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.
.
.
.
9­
5
9.3.2
Monitoring
Data
.
.
.
.
.
.
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.
.
.
9­
5
9.3.3
Use
and
Fate
Data
.
.
.
.
.
.
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.
.
9­
6
9.4
Risk
Reduction
.
.
.
.
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.
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.
.
9­
7
9.4.1
Risk
Criterion
Conclusion
.
.
.
.
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.
.
.
.
9­
7
9.4.2
Exposed
Population
Estimates
.
.
.
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.
.
9­
7
9.4.3
Relative
Source
Contribution
.
.
.
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.
.
.
.
.
.
9­
8
9.4.4
Sensitive
Populations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
9­
8
9.5
Regulatory
Determination
Summary
.
.
.
.
.
.
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.
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.
.
.
9­
9
10.0
REFERENCES
.
.
.
.
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.
.
10­
1
APPENDIX
A:
Abbreviations
and
Acronyms
.
.
.
.
.
.
.
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.
.
.
.
A­
1
APPENDIX
B:
Round
2
Metribuzin
Occurrence
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
B­
1
ix
Metribuzin
 
February
2003
LIST
OF
TABLES
Table
3­
1.
Metribuzin
Use,
1990­
1999.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
3­
3
Table
3­
2.
Environmental
Releases
(
in
pounds)
for
Metribuzin
in
the
United
States,

1995­
1998.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
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.
.
.
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.
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.
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.
.
.
.
.
.
.
.
.
.
.
.
3­
4
Table
4­
1.
Metribuzin
Detections
and
Concentrations
in
Streams
and
Ground
Water.
.
.
.
4­
3
Table
4­
2.
Metribuzin
Detections
in
Shallow
Ground
Water
from
Various
Land­
Use
Settings.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
4
Table
4­
3.
Metribuzin
Occurrence
in
Midwest
Surface
and
Ground
Water.
.
.
.
.
.
.
.
.
.
.
.
4­
5
Table
4­
4.
Summary
Occurrence
Statistics
for
Metribuzin.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
12
Table
4­
5.
SDWA
Compliance
Monitoring
Data
from
the
States
of
Illinois,
Indiana,

and
Ohio.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
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.
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.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
16
Table
4­
6.
Metribuzin
Occurrence
in
Midwest
Drinking
Water.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
18
Table
5­
1.
Exposures
of
the
General
Population
to
Metribuzin
in
Media
Other
Than
Water.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
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.
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.
.
.
.
5­
6
Table
5­
2.
Exposures
of
Subpopulations
to
Metribuzin
in
Media
Other
Than
Water.
.
.
.
.
5­
6
Table
7­
1.
Acute
Toxic
Effects
of
Metribuzin
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
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.
.
.
.
.
.
.
.
.
.
.
7­
2
x
Metribuzin
 
February
2003
LIST
OF
FIGURES
Figure
3­
1.
Estimated
Annual
Agricultural
Use
for
Metribuzin
(
1992).
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
3­
2
Figure
4­
1.
Geographic
Distribution
of
Cross­
Section
States
for
Round
2
(
SDWIS/
FED).
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
9
Figure
4­
2.
States
with
PWSs
with
Detections
of
Metribuzin
for
All
States
with
Data
in
SDWIS/
FED
(
Round
2).
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
4­
19
Figure
4­
3.
Round
2
cross­
section
states
with
PWSs
with
detections
of
metribuzin
(
any
PWSs
with
results
greater
than
the
Minimum
Reporting
Level
[
MRL];
above)
and
concentrations
greater
than
the
Health
Reference
Level
(
HRL;
below).
.
4­
20
1­
1
Metribuzin
 
February
2003
1.0
EXECUTIVE
SUMMARY
The
U.
S.
Environmental
Protection
Agency
(
EPA)
has
prepared
this
Health
Effects
Support
Document
for
Metribuzin
to
support
a
preliminary
determination
regarding
whether
to
regulate
metribuzin
with
a
National
Primary
Drinking
Water
Regulation
(
NPDWR).
The
available
data
on
occurrence,
exposure,
and
other
risk
considerations
suggest
that,
because
metribuzin
does
not
occur
in
public
water
systems
at
frequencies
and
levels
of
public
health
concern,
regulating
metribuzin
will
not
present
a
meaningful
opportunity
to
reduce
health
risk.
EPA
will
present
a
determination
and
further
analysis
in
the
Federal
Register
Notice
covering
the
CCL
proposals.

Metribuzin
(
Chemical
Abstracts
Services
Registry
Number
21087­
64­
9)
is
a
synthetic
organic
compound
used
as
a
selective
triazinone
herbicide.
It
is
a
white
crystalline
solid,
is
soluble
in
water
up
to
1,200
ppm
(
1.2
g/
L),
and
has
a
sulfurous
odor.
Metribuzin
is
released
into
the
environment
primarily
during
agricultural
spraying
operations
and
is
moderately
absorbed
on
soils
with
high
clay
or
organic
content.
It
may
be
released
into
surface
and
ground
waters
during
runoff
events
in
agricultural
regions.
Metribuzin
is
listed
as
a
Toxic
Release
Inventory
(
TRI)
chemical,
with
air
emissions
constituting
the
majority
of
on­
site
releases.

Human
exposure
to
metribuzin
occurs
through
inhalation
and
ingestion,
usually
in
agricultural
settings.
Although
it
is
applied
to
food
crops
to
discourage
the
growth
of
broadleaf
weeds
and
grasses,
metribuzin
has
not
been
detected
in
any
food
samples
tested.
Occupational
exposure
to
metribuzin
includes
agricultural
workers,
sprayers,
and
handlers.
General
population
exposures
are
thought
to
be
minimal.
There
are
no
reports
of
accidental
human
exposures
to
metribuzin.

There
is
little
information
on
the
adverse
health
effects
of
metribuzin
exposure
to
humans.
Hazard
characterization
has
therefore
been
accomplished
in
animal
toxicity
studies.
Acute
studies
in
animals
indicate
that
metribuzin
exhibits
a
low
order
of
toxicity,
as
indicated
by
high
LD
50
values.
Acute
exposure
studies
also
indicate
that
metribuzin
does
not
possess
ocular
or
dermal
irritation
properties.
Subchronic
studies
suggest
that
metribuzin
could
cause
adverse
effects
in
body
weight
gain,
organ
weight,
and
hematological
parameters.
Specifically,
studies
in
Wistar
rats
indicate
that
liver
and
thyroid
weights
were
increased
and
body
weight
gain
was
decreased.
In
rats,
chronic
effects
may
include
changes
in
body
weight
gain,
liver
enzyme
activities
and
histopathological
changes.
In
addition,
increases
in
corneal
neovascularization
and
discolored
zones
in
the
liver,
and
enlarged
adrenal
and
thyroid
glands,
have
been
observed
in
rats.
At
high
doses,
chronic
metribuzin
exposure
has
been
observed
to
cause
significant
increases
in
mortality,
liver
dysfunction,
and
thyroid
weight
in
Beagle
dogs.
Developmental
studies
in
rats
and
rabbits
indicate
that
effects
to
the
fetus
only
occur
subsequent
to
maternal
toxicity.
Similarly,
in
reproductive
studies,
both
parents
and
pups
experienced
decreased
body
weight
and
exaggerated
liver
cell
growth.

Drinking
water
monitoring
of
metribuzin
is
conducted
under
the
Unregulated
Contaminant
Monitoring
(
UCM)
program.
Metribuzin
was
not
among
the
contaminants
1­
2
Metribuzin
 
February
2003
monitored
in
Round
1
of
the
UCM
program;
metribuzin
monitoring
began
in
Round
2.
A
crosssection
analysis
of
20
states
participating
in
Round
2
of
the
UCM
program
indicate
that
the
frequency
of
detection
of
metribuzin
in
public
water
systems
(
PWSs)
is
low.
The
20­
state
crosssection
analysis
indicates
that
0.007%
of
PWSs
detected
metribuzin
at
levels
above
the
Minimum
Reporting
Level
(
MRL).
The
percentage
of
the
population
served
by
PWSs
reporting
metribuzin
detections
is
0.0003%.
National
extrapolation
of
this
data
indicates
that
5
PWSs
nationally
would
contain
detectable
levels
of
metribuzin,
and
that
1000
people
would
be
exposed.
However,
no
drinking
water
concentrations
of
metribuzin
in
the
cross­
section
analysis
were
greater
than
the
Health
Reference
Level
(
HRL)
or
half
the
HRL.
Using
more
conservative
estimates
of
occurrence
from
all
states
reporting
Round
2
monitoring
data,
including
states
with
biased
data,
0.28%
of
the
nation's
PWSs
(
approximately
182
systems
and
3.4
million
people
served)
are
affected
by
metribuzin
concentrations
>
MRL,
while
no
PWSs
are
affected
by
concentrations
>
½
HRL
or
>
HRL.

In
accordance
with
current
cancer
guidelines
(
U.
S.
EPA,
1986a),
metribuzin
is
classified
as
a
Class
D
carcinogen
due
to
inadequate
carcinogenicity
data
in
humans
and
animals.
Chronic
exposure
studies
in
rats
and
mice
were
negative
for
the
induction
of
tumors
by
metribuzin.
Based
on
a
2­
year
feeding
study
in
rats,
the
oral
Reference
Dose
(
RfD)
was
determined
to
be
0.013
mg/
kg­
day.
2­
1
Metribuzin
 
February
2003
H3C
CH
3
H3C
O
N
N
N
NH
2
S
CH
3
2.0
IDENTITY:
PHYSICAL
AND
CHEMICAL
PROPERTIES
Metribuzin
is
a
white
crystalline
solid
with
a
melting
point
of
126
°
C.
Pure
metribuzin
is
soluble
in
water
up
to
1,200
ppm
(
1.2
g/
L).
It
is
also
soluble
in
dimethylformamide
at
1,780,
cyclohexanone
at
1,000,
chloroform
at
850,
acetone
at
820,
ethylacetate
at
470,
methanol
at
450,
dichloromethane
at
333,
benzene
at
220,
n­
butanol
at
150,
ethanol
at
190,
toluene
at
120,
xylene
at
90
and
n­
hexane
at
2
g/
kg
at
20
°
C.
Metribuzin
has
a
slight
sulfurous
odor.
It
is
reported
to
have
a
vapor
pressure
of
between
5
and
10
mm
Hg
at
20
°
C
and
a
density
of
1.28
between
4
and
20
°
C
(
U.
S.
EPA,
1998a;
HSDB,
2000).

Common
Name:
Metribuzin
Chemical
Name:
4­
amino­
6­(
1,1­
dimethylethyl)­
3­(
methylthio)­
1,2,4­
triazin­
5(
4H)­
one
Chemical
Family:
Triazinone
CAS
Registry
Number:
21087!
64!
9
Molecular
Weight:
214.28
Empirical
Formula:
C
8
H
14
N
4
OS
Metribuzin
Structural
Formula:

Metribuzin
has
several
trade
names
and
synonyms.
These
names
and
synonyms
are
listed
below
in
alphabetical
order
(
RTECS,
2000;
HSDB,
2000;
U.
S.
EPA,
1998a).

4­
Amino­
6­
tert­
butyl­
4,5­
dihydro­
3­
methylthio­
1,2,4­
triazin­
5­
one
4­
Amino­
6­
tert­
butyl­
3­(
methylthio)­
as­
triazin­
S(
4H)­
one
4­
Amino­
6­
tert­
butyl­
3­(
methylthio)­
as­
triazin­
5(
4H)­
one
4­
Amino­
6­(
1,1­
dimethylethyl)­
3­(
methylthio)­
1,2,4­
triazin­
5(
4H)­
one
4­
Amino­
6­
tert­
butyl­
3­(
methylthio)­
1,2,4­
triazin­
5­
one
Bay
61597,
Bayer
94337,
Bay
DIC
1468,
Bayer
6159H,
Bayer
6443H
DIC
1468,
NTN
70
Lexone,
Lexone
DF,
Lexone
4L
Metribuzine,
Preview
Sencor,
Sencor
4,
Sencoral,
Sencor
DF,
Sencorer,
Sencorex
,
Sengoral
Zenkor
3­
1
Metribuzin
 
February
2003
3.0
USES
AND
ENVIRONMENTAL
FATE
3.1
Production
and
Use
Metribuzin
is
a
synthetic
organic
compound
(
SOC).
It
is
a
selective
triazinone
herbicide
used
primarily
to
discourage
growth
of
broadleaf
weeds
and
annual
grasses
among
vegetable
crops
and
turf
grass.
Metribuzin
accomplishes
this
by
inhibiting
electron
transport
in
photosynthesis
(
EXTOXNET,
1998;
U.
S.
EPA,
1998a).
Common
uses
include
application
to
soybeans,
potatoes,
alfalfa,
sugarcane,
barley,
and
tomatoes
(
Larson
et
al.,
1999;
U.
S.
EPA,
1998a).

Recent
national
estimates
of
agricultural
use
for
metribuzin
are
available.
Using
its
own
proprietary
data,
data
from
the
United
States
Department
of
Agriculture
(
USDA)
and
the
National
Center
for
Food
and
Agricultural
Policy
(
NCFAP),
the
U.
S.
EPA
(
1998a)
estimated
U.
S.
average
annual
use
for
the
years
1990­
94
at
approximately
2.8
million
pounds
of
active
ingredient
(
a.
i.)
with
approximately
8.5
million
acres
treated.
The
United
States
Geological
Survey
(
USGS)
estimated
approximately
2.7
million
pounds
of
active
ingredient
used
for
the
year
1992,
with
roughly
8.4
million
acres
treated
(
USGS,
2000a).
These
estimates
were
derived
using
state­
level
data
sets
on
pesticide
use
rates
available
from
NCFAP
combined
with
county­
level
data
on
harvested
crop
acreage
from
the
Census
of
Agriculture
(
CA)
(
Thelin
and
Gianessi,
2000).

Figure
3­
1
shows
the
geographic
distribution
of
estimated
average
annual
metribuzin
use
in
the
United
States
for
1992.
A
breakdown
of
use
by
crop
is
also
included.
Non­
agricultural
uses
are
not
reflected
here
and
any
sharp
spatial
differences
in
use
within
a
county
are
not
well
represented
(
USGS,
1998a).
Existing
data
suggest
that
non­
agricultural
use
of
metribuzin
is
minimal
(
U.
S.
EPA,
1998a).

Metribuzin
use
patterns
have
been
documented
by
the
USDA
as
well.
USDA
Cropping
Practices
Surveys
(
CPS)
for
field
crops
(
1964­
1995)
merged
with
the
Farm
Costs
and
Returns
Survey
(
FCRS)
in
1996
to
form
the
Agricultural
Resources
Management
Study
(
ARMS).
As
was
the
case
with
the
CPSs,
the
ARMS
is
conducted
in
major
producing
states
and
provides
information
on
metribuzin
use
on
particular
field
crops
(
corn,
soybeans,
cotton,
winter
wheat,
spring
and
durum
wheat,
and
fall
potatoes).
Farm
operators
are
surveyed
for
crop
practice
information
on
a
field­
by­
field
basis
(
USDA,
1997;
USDA,
2000).
Table
3­
1
shows
the
amount
of
metribuzin
used
annually
and
the
number
of
acres
treated.
Metribuzin
use
appears
to
be
modestly
declining
over
the
ten­
year
period.
3­
2
Metribuzin
 
February
2003
Figure
3­
1.
Estimated
Annual
Agricultural
Use
for
Metribuzin
(
1992).

USGS,
1998b
3­
3
Metribuzin
 
February
2003
Table
3­
1.
Metribuzin
Use,
1990­
1999.

Year
Pounds
of
Active
Ingredient
(
x
1000)
Acres
Treated
(
x
1000)

1999
1,214
4,542*

1998
1,261
6,432
1997
2,207
8,646
1996
1,785
6,547
1995
1,498
5,892
1994
1,773
5,811
1993
2,003
6,437
1992
1,975
6,705
1991
2,537
7,706
1990
2,959
8,924
Data
for
the
years
1990­
1995,
USDA,
1997
Data
for
the
years
1996­
1999,
USDA,
2000
*
average
figure
based
on
available
data
3.2
Environmental
Release
Metribuzin
is
also
listed
as
a
toxic
release
inventory
(
TRI)
chemical.
In
1986,
the
Emergency
Planning
and
Community
Right­
to­
Know
Act
(
EPCRA)
established
the
Toxic
Release
Inventory
(
TRI)
of
hazardous
chemicals.
Created
under
the
Superfund
Amendments
and
Reauthorization
Act
(
SARA)
of
1986,
EPCRA
is
also
sometimes
known
as
SARA
Title
III.
The
EPCRA
mandates
that
larger
facilities
publicly
report
when
TRI
chemicals
are
released
into
the
environment.
This
public
reporting
is
required
for
facilities
with
more
than
10
full­
time
employees
that
annually
manufacture
or
produce
more
than
25,000
pounds,
or
use
more
than
10,000
pounds,
of
TRI
chemical
(
U.
S.
EPA,
1996;
U.
S.
EPA,
2000d).

Under
these
conditions,
facilities
are
required
to
report
the
pounds
per
year
of
metribuzin
released
into
the
environment
both
on­
and
off­
site.
The
on­
site
quantity
is
subdivided
into
air
emissions,
surface
water
discharges,
underground
injections,
and
releases
to
land
(
see
Table
3­
2).
For
metribuzin,
air
emissions
constitute
most
of
the
on­
site
releases;
these
emissions
decrease
throughout
the
period
of
record.
A
sharp
decrease
is
evident
between
the
1996
and
1997
reporting
years.
In
contrast,
over
the
period
for
which
data
are
available
(
1995­
1998),
surface
water
discharges
generally
increase.
Again,
the
trend
is
exaggerated
between
the
reporting
3­
4
Metribuzin
 
February
2003
Table
3­
2.
Environmental
Releases
(
in
pounds)
for
Metribuzin
in
the
United
States,
1995­
1998.

Year
On­
Site
Releases
Off­
Site
Releases
Total
On­
&
Off­
site
Releases
Air
Emissions
Surface
Water
Discharges
Underground
Injection
Releases
to
Land
1998
339
26
0
0
255
620
1997
359
24
0
0
0
383
1996
1,012
5
0
0
0
1,017
1995
1,936
9
0
0
0
1,945
U.
S.
EPA,
2000b
years
1996
and
1997.
Whether
these
abrupt
shifts
reflect
actual
increases
in
surface
water
discharges
and
decreases
in
air
emissions
is
unclear.
Interpretation
is
confounded
by
the
relatively
short
period
of
record.
These
TRI
data
for
metribuzin
were
reported
from
three
states
and
one
territory
(
IA,
MO,
NB,
Puerto
Rico;
U.
S.
EPA,
2000b).

Although
the
TRI
data
can
be
useful
in
giving
a
general
idea
of
release
trends,
it
is
far
from
exhaustive
and
has
significant
limitations.
For
example,
only
industries
that
meet
TRI
criteria
(
at
least
10
full­
time
employees,
and
manufacture
and
process
quantities
exceeding
25,000
lbs/
yr,
or
use
of
more
than
10,000
lbs/
yr)
are
required
to
report
releases.
These
reporting
criteria
do
not
account
for
releases
from
smaller
industries.
Threshold
manufacturing
and
processing
quantities
also
changed
from
1988­
1990
(
dropping
from
75,000
lbs/
yr
in
1988
to
50,000
lbs/
yr
in
1989
to
its
current
25,000
lbs/
yr
in
1990)
creating
possibly
misleading
data
trends.
Also,
the
TRI
data
is
meant
to
reflect
releases
and
should
not
be
used
to
estimate
general
exposure
to
a
chemical
(
U.
S.
EPA,
2000c;
U.
S.
EPA,
2000a).

In
summary,
metribuzin
is
used
as
an
herbicide
on
crops
and
has
limited
non­
agricultural
use.
Applications
are
primarily
targeted
to
soybeans,
potatoes,
alfalfa,
and
sugar
cane,
and
the
geographic
distribution
of
use
largely
reflects
the
distribution
of
these
crops
across
the
United
States
(
Figure
3­
1).
Estimated
annual
use
appears
to
be
modestly
declining
in
the
last
decade
(
Table
3­
1).
Metribuzin
is
also
a
TRI
chemical.
Industrial
releases
have
been
reported
since
1995
in
three
states
and
one
U.
S.
territory.

3.3
Environmental
Fate
Metribuzin
is
released
into
the
environment
primarily
during
agricultural
spraying
operations.
It
is
moderately
adsorbed
on
soils
with
high
clay
or
organic
content,
as
reflected
by
the
organic
carbon
partition
coefficient
(
K
oc
=
95)
(
HSDB,
2000).
Adsorption
decreases
with
increasing
soil
pH
since
metribuzin
is
adsorbed
via
a
hydrogen­
bonding
mechanism.
Although
little
leaching
occurs
in
soils
with
a
high
organic
content,
metribuzin
is
readily
leached
in
sandy
soils.
The
soil
half­
life
ranges
from
14­
60
days.
3­
5
Metribuzin
 
February
2003
Based
on
its
low
vapor
pressure,
metribuzin
should
exist
in
the
vapor
and
particulate
phases
at
ambient
temperature
(
HSDB,
2000).
In
the
vapor
phase,
metribuzin
is
degraded
by
reaction
with
photochemically
formed
hydroxyl
radicals
with
a
half­
life
of
approximately
11
hours
(
HSDB,
2000).
In
the
particulate
phase,
metribuzin
is
removed
from
the
atmosphere
by
dry
deposition.
In
addition,
metribuzin
has
been
detected
in
rainwater,
indicating
that
it
can
be
removed
from
air
by
wet
deposition
(
HSDB,
2000).

The
primary
fate
process
for
metribuzin
in
soil
is
microbial
degradation
(
HSDB,
2000).
The
rate
of
degradation
is
increased
by
the
activity
of
soil
microorganisms,
higher
temperatures,
and
aerobic
conditions.
Metribuzin
is
degraded
to
carbon
dioxide
in
soil.
Metabolites
observed
in
plants,
such
as
the
3,5­
diketo
and
deaminated
diketo
metribuzin,
have
been
found
in
soil
(
HSDB,
2000).
Loss
from
soil
surfaces
by
photodecomposition
and
volatilization
are
not
expected
(
HSDB,
2000).

In
the
aquatic
environment,
volatilization
from
water
and
bioconcentration
in
fish
are
not
anticipated
to
be
relevant
(
HSDB,
2000).
No
data
are
available
for
the
biodegradation
of
metribuzin
in
water.
4­
1
Metribuzin
 
February
2003
4.0
EXPOSURE
FROM
DRINKING
WATER
4.1
Occurrence
and
Monitoring
Data
of
Ambient
Water
To
understand
the
presence
of
a
chemical
in
the
environment,
an
examination
of
ambient
occurrence
is
useful.
In
a
drinking
water
context,
ambient
water
is
source
water
existing
in
surface
waters
and
aquifers
before
treatment.
The
most
comprehensive
and
nationally
consistent
data
describing
ambient
water
quality
in
the
United
States
are
being
produced
through
the
United
States
Geological
Survey's
(
USGS)
National
Ambient
Water
Quality
Assessment
(
NAWQA)
program.
NAWQA,
however,
is
a
relatively
young
program
and
complete
national
data
are
not
yet
available
from
their
entire
array
of
sites
across
the
nation.

4.1.1
Data
Sources
and
Methods
The
USGS
instituted
the
NAWQA
program
in
1991
to
examine
water
quality
status
and
trends
in
the
United
States.
NAWQA
is
designed
and
implemented
in
such
a
manner
to
allow
consistency
and
comparison
between
representative
study
basins
located
around
the
country,
facilitating
interpretation
of
natural
and
anthropogenic
factors
affecting
water
quality
(
Leahy
and
Thompson,
1994).

The
NAWQA
program
consists
of
59
significant
watersheds
and
aquifers
referred
to
as
"
study
units."
The
study
units
represent
approximately
two­
thirds
of
the
overall
water
usage
in
the
United
States
and
a
similar
proportion
of
the
population
served
by
public
water
systems.
Approximately
one
half
of
the
nation's
land
area
is
represented
(
Leahy
and
Thompson,
1994).

To
facilitate
management
and
make
the
program
cost­
effective,
approximately
one­
third
of
the
study
units
at
a
time
engage
in
intensive
assessment
for
a
period
of
3
to
5
years.
This
is
followed
by
a
period
of
less
intensive
research
and
monitoring
that
lasts
between
5
and
7
years.
This
way
all
59
study
units
rotate
through
intensive
assessment
over
a
ten­
year
period
(
Leahy
and
Thompson,
1994).
The
first
round
of
intensive
monitoring
(
1991­
96)
targeted
20
watersheds
which
were
slanted
toward
agricultural
basins.
A
national
synthesis
of
results
from
these
study
units
focusing
on
pesticides
and
nutrients
has
been
compiled
and
analyzed
(
Kolpin
et
al.,
1998;
Larson
et
al.,
1999;
USGS,
1999).

Metribuzin
is
an
analyte
for
both
surface
and
ground
water
NAWQA
studies.
Two
of
the
first
round
study
units,
the
Central
Nebraska
Basins
and
the
White
River
Basin
in
Indiana,
are
located
in
the
corn
belt
where
metribuzin
is
heavily
used
(
see
Figure
3­
1).
The
Method
Detection
Limit
(
MDL)
for
metribuzin
is
0.004
µ
g/
L
(
Kolpin
et
al.,
1998),
substantively
lower
than
most
drinking
water
monitoring
reporting
levels.
Additional
information
on
analytical
methods
used
in
the
NAWQA
study
units,
including
method
detection
limits,
are
described
by
Gilliom
and
others
(
in
press).

Data
are
also
available
for
metribuzin
occurrence
in
ground
water
and
surface
water
for
key
corn
belt
states.
The
majority
of
these
data
are
the
result
of
USGS
regional
water
quality
4­
2
Metribuzin
 
February
2003
investigations
with
a
focus
on
near­
surface
aquifers
and
surface
waters.
Additionally,
EPA's
Pesticides
in
Ground
Water
Database
(
PGWD)
provides
a
large
data
set
on
pesticide
occurrence
in
ground
water
that
spans
a
period
of
20
years
and
contains
data
from
68,824
sites.
It
is
a
compilation
of
numerous
national,
regional,
state,
and
local
studies
and
therefore
the
data
are
a
mix
of
the
results
of
a
variety
of
study
designs,
sampling
techniques,
and
reporting
limits.
However,
the
size
and
temporal
scope
of
the
data
set
make
it
a
valuable
resource.
Details
regarding
sampling
and
analytical
methods
for
the
USGS
studies
and
the
PGWD
report
are
described
in
the
respective
reports.

4.1.2
Results
NAWQA
National
Synthesis
Detection
frequencies
and
concentrations
of
metribuzin
in
ambient
surface
and
ground
water
are
low,
especially
in
ground
water
(
Table
4­
1).
Most
herbicides
monitored
in
the
first
round
of
the
NAWQA
program
were
detected
in
the
greatest
concentrations
and
frequencies
in
surface
water
compared
to
ground
water.
Surface
waters
show
the
highest
maximum
concentration
of
metribuzin
at
0.5
µ
g/
L,
well
below
the
Health
Reference
Level
(
HRL)
of
91
µ
g/
L.
The
Health
Reference
Level
is
a
preliminary
estimated
health
effect
level
used
for
the
present
analysis.

Frequencies
and
concentrations
of
metribuzin
in
streams
in
agricultural
settings
are
greater
than
those
in
urban
settings,
with
integrator
sites
(
a
combination
of
agricultural
and
urban)
having
the
highest
occurrence
(
Table
4­
1).
Larson
and
others
(
1999)
found
that
for
50
stream
sites
monitored
over
a
1­
year
period,
one
site
had
a
detection
frequency
of
>
50%
of
all
samples
(
detections
were
reported
for
metribuzin
concentrations
$
0.01
µ
g/
L).
Ninety
percent
of
sites,
however,
had
detection
frequencies
of
less
than
20%
of
all
samples.
The
annual
mean
frequency
of
metribuzin
detection
was
less
than
15%
in
all
land­
use
settings
at
all
concentrations
(
calculated
as
the
average
of
the
12
monthly
detection
frequencies
from
each
site;
Larson
et
al.,
1999).

While
occurrence
in
ground
water
is
considerably
lower
than
in
surface
water,
detection
in
>
1%
of
ground
water
samples
at
concentrations
$
0.05
µ
g/
L
makes
metribuzin
one
of
the
21
most
commonly
detected
pesticides
in
the
first
round
of
intensive
NAWQA
monitoring
(
the
21
are
detected
at
concentrations
$
0.05
µ
g/
L
in
more
than
10%
of
stream
samples
or
more
than
1%
of
ground
water
samples).
Metribuzin
exceeded
the
ground
water
criteria
partly
because
its
high
water
solubility
and
low
soil
adsorption
potential
allow
it
to
leach
into
ground
water
(
USGS,
2000b;
U.
S.
EPA,
1998b;
EXTOXNET,
1998).
Also,
the
herbicide
ranks
among
the
top
200
agricultural
pesticides
in
use
(
USGS,
1999).
4­
3
Metribuzin
 
February
2003
Table
4­
1.
Metribuzin
Detections
and
Concentrations
in
Streams
and
Ground
Water.

Detection
frequency
(%
samples
$
MDL*)
Concentration
percentiles
(
all
samples
µ
g/
L)

%
$
0.004
µ
g/
L
%
$
0.01
µ
g/
L
median
95th
maximum
streams
urban
6.73%
5.50%
nd**
0.011
0.100
integrator
14.29%
9.39%
nd
0.020
0.130
agricultural
13.70%
8.20%
nd
0.016
0.330
all
sites
13.82%
9.94%
nd
0.026
0.530
ground
water
shallow
urban
1.66%
0.33%
nd
nd
0.043
shallow
agricultural
3.46%
2.81%
nd
nd
0.300
major
aquifers
0.75%
0.32%
nd
nd
0.045
all
sites
1.95%
1.36%
nd
nd
0.300
USGS,
2000b
*
MDL
(
Method
Detection
Limit)
for
metribuzin
in
water
studies:
0.004
µ
g/
L
**
not
detected
in
concentration
greater
than
MDL
Herbicides
often
demonstrate
detection
frequencies
in
streams
that
correlate
with
patterns
of
use
(
USGS,
2000b).
Patterns
of
pesticide
use
often
do
not
correlate
with
detection
frequency
in
ground
water,
probably
because
of
the
variable
effect
of
local
hydrogeologic
conditions
(
depth
and
type
of
aquifer,
soil
conditions)
on
pesticides
in
ground
water
(
USGS,
2000b).
Metribuzin,
however,
is
one
of
six
pesticides
that,
for
shallow
ground
water,
demonstrate
a
statistically
significant
correlation
between
detection
frequency
and
intensity
of
use
(
Kolpin
et
al.,
1998).
Metribuzin
detection
frequencies
are
higher
in
shallow
ground
water
in
agricultural
areas
when
compared
with
shallow
ground
water
in
urban
areas
(
Table
4­
1).
This
is
most
likely
a
result
of
metribuzin's
primary
use
as
an
agricultural
pesticide
(
U.
S.
EPA,
1998a).
Metribuzin
is
detected
most
frequently
in
shallow
ground
water
from
land­
use
categories
containing
wheat,
wheat
and
alfalfa,
corn
and
soybeans,
and
corn
and
alfalfa
as
major
crops
or
crop­
groups
(
Table
4­
2).
4­
4
Metribuzin
 
February
2003
Table
4­
2.
Metribuzin
Detections
in
Shallow
Ground
Water
from
Various
Land­
Use
Settings.

Land­
use
settings*
Detection
frequency
$
0.004
µ
g/
L
Detection
frequency
$
0.010
µ
g/
L
All
3.1%
nr**

Corn
and
soybeans
>
20%
6.6%
#
10%

Corn
and
alfalfa
>
20%
2.1%
0
­
2%

Corn
>
50%
0.0%
0
­
2%

Peanuts
>
50%
1.6%
<
5%

Wheat
and
small
grains
>
50%
9.3%
<
10%

Wheat
and
small
grains
and
alfalfa
>
20%
6.2%
#
5%

Alfalfa
>
50%
0.0%
0
­
2%

Pasture
>
90%
0.0%
0
­
2%

Orchards
or
vineyards
>
50%
0.0%
0
­
2%

Urban
1.8%
0
­
2%

after
Kolpin
et
al.,
1998
*
evaluated
as
crop­
groups
occupying
a
percent
of
the
total
land
**
not
reported
Water
Quality
Investigations
from
the
Corn
Belt
USGS
regional
water
quality
investigations
and
other
state
and
national
studies
are
summarized
below
to
provide
ambient
data
in
states
where
metribuzin
use
is
high
(
see
Figure
3­
1).
Midwest
ground
water
concentrations
and
detection
frequencies
were
low
during
the
years
1991­
1994
(
Table
4­
3).
The
highest
detected
ground
water
concentration,
25.1
µ
g/
L,
is
found
in
the
national
Pesticides
in
Ground
Water
Database,
which
draws
only
a
portion
of
its
data
from
Midwestern
states.
This
concentration
is
still
well
below
the
Health
Reference
Level
(
HRL)
of
91
µ
g/
L.

Maximum
concentrations
of
metribuzin
in
surface
waters
of
the
Mississippi
River
and
major
tributaries
for
all
years,
peaking
at
<
0.1
µ
g/
L,
were
considerably
lower
than
the
HRL.
Although
all
9
sampling
sites
in
the
Mississippi
River
and
major
tributaries
had
a
least
one
detection
of
metribuzin
(
100%
of
sites)
from
April
1991
to
March
1992,
the
percentage
of
samples
with
detections
was
40%.
4­
5
Metribuzin
 
February
2003
Table
4­
3.
Metribuzin
Occurrence
in
Midwest
Surface
and
Ground
Water.

Ground
water
$
MRL
Surface
water
$
MRL
Max.
conc.
µ
g/
L
%
sites
%
samples
%
sites
%
samples
USGS
Midwest
Near­
Surface
Aquifers
(
1991)
1
1.3%
1.0%
0.57
Midwest
Near­
Surface
Aquifers
(
1992­
94)
2
nr
1.4%
0.22
Miss.
River
and
Major
Tributaries
(
1991)
3
54%
nr
0.08
Miss.
River
and
Major
Tributaries
(
1991­
92)
4
100%
40%
0.03
Midwest
Reservoirs
(
1992)
5
12%
6.5%
nr
Pesticides
in
Ground
Water
Database
(
1971­
91)
6
4.3%
nr
25.1
1
Kolpin
et
al.,
1994
2
Kolpin
et
al.,
1996
3
Periera
and
Hostettler,
1993
(
cited
in
Larson
et
al.,
1997)
4
Goolsby
and
Battaglin,
1993
(
cited
in
Larson
et
al.,
1997)
5
Goolsby
et
al.,
1993
(
cited
in
Larson
et
al.,
1997)
6
U.
S.
EPA,
1992
(
cited
in
Barbash
and
Resek,
1996);
data
are
national
results
including
some
Midwestern
states
­
The
Health
Reference
Level
(
HRL)
used
for
metribuzin
is
91
µ
g/
L.
This
is
a
draft
value
for
working
review
only.
­
Minimum
Reporting
Levels
(
MRL)
vary
by
study.
­
nd
=
results
below
the
respective
reporting
level
­
nr
="
not
reported"

4.2
Occurrence
and
Monitoring
Data
in
Drinking
Water
The
Safe
Drinking
Water
Act
(
SDWA),
as
amended
in
1986,
required
Public
Water
Systems
(
PWSs)
to
monitor
for
specified
"
unregulated"
contaminants
on
a
five­
year
cycle
and
to
report
the
monitoring
results
to
the
states.
Unregulated
contaminants
do
not
have
an
established
or
proposed
National
Primary
Drinking
Water
Regulation
(
NPDWR),
but
they
are
contaminants
that
were
formally
listed
and
were
required
for
monitoring
under
federal
regulations.
The
intent
was
to
gather
scientific
information
on
the
occurrence
of
these
contaminants
to
enable
a
decision
as
to
whether
or
not
regulations
were
needed.
All
non­
purchased
community
water
systems
(
CWSs)
and
non­
purchased
non­
transient
non­
community
water
systems
(
NTNCWSs),
with
greater
than
150
service
connections,
were
required
to
conduct
this
unregulated
contaminant
monitoring.
Smaller
systems
were
not
required
to
conduct
this
monitoring
under
federal
regulations,
but
were
required
to
be
available
for
monitoring
if
the
state
decided
such
monitoring
was
necessary.
Many
states
collected
data
from
smaller
systems.
Additional
contaminants
were
added
to
the
Unregulated
Contaminant
Monitoring
(
UCM)
program
in
1991
(
56
FR
3526)
for
required
monitoring
that
began
in
1993
(
57
FR
31776).
4­
6
Metribuzin
 
February
2003
Metribuzin
has
been
monitored
under
the
SDWA
Unregulated
Contaminant
Monitoring
(
UCM)
program
since
1993
(
57
FR
31776).
Monitoring
ceased
for
small
PWSs
under
a
direct
final
rule
published
January
8,
1999
(
64
FR
1494),
and
ended
for
large
PWSs
with
promulgation
of
the
new
Unregulated
Contaminant
Monitoring
Regulation
(
UCMR)
issued
September
17,
1999
(
64
FR
50556)
and
effective
January
1,
2001.
At
the
time
the
UCMR
lists
were
developed,
the
Agency
concluded
there
were
adequate
monitoring
data
for
a
regulatory
determination.
This
obviated
the
need
for
continued
monitoring
under
the
new
UCMR
list.

4.2.1
Data
Sources,
Data
Quality,
and
Analytical
Methods
Currently,
there
is
no
complete
national
record
of
unregulated
or
regulated
contaminants
in
drinking
water
from
PWSs
collected
under
SDWA.
Many
states
have
submitted
unregulated
contaminant
PWS
monitoring
data
to
EPA
databases,
but
there
are
issues
of
data
quality,
completeness,
and
representativeness.
Nonetheless,
a
significant
amount
of
state
data
are
available
for
UCM
contaminants
that
can
provide
estimates
of
national
occurrence.

The
National
Contaminant
Occurrence
Database
(
NCOD)
is
an
interface
to
the
actual
occurrence
data
stored
in
the
Safe
Drinking
Water
Information
System/
Federal
version
(
SDWIS/
FED)
and
can
be
queried
to
provide
a
summary
of
the
data
in
SDWIS/
FED
for
a
particular
contaminant.
The
drinking
water
occurrence
data
for
metribuzin
presented
here
were
derived
from
monitoring
data
available
in
the
SDWIS/
FED
database.

The
data
in
this
report
have
been
reviewed,
edited,
and
filtered
to
meet
various
data
quality
objectives
for
the
purposes
of
this
analysis.
Hence,
not
all
data
from
a
particular
source
were
used,
only
data
meeting
the
quality
objectives
described
below
were
included.
The
sources
of
these
data,
their
quality
and
national
aggregation,
and
the
analytical
methods
used
to
estimate
a
given
contaminant's
national
occurrence
(
from
these
data)
are
discussed
in
this
section
(
for
further
details
see
U.
S.
EPA,
2001a,
b).

UCM
Rounds
1
and
2
The
1987
UCM
contaminants
include
34
volatile
organic
compounds
(
VOCs)
(
52
FR
25720).
Metribuzin,
a
synthetic
organic
compound
(
SOC),
was
not
among
these
contaminants.
The
UCM
(
1987)
contaminants
were
first
monitored
coincident
with
the
Phase
I
regulated
contaminants,
during
the
1988­
1992
period.
This
period
is
often
referred
to
as
"
Round
1"
monitoring.
The
monitoring
data
collected
by
the
PWSs
were
reported
to
the
states
(
as
primacy
agents),
but
there
was
no
protocol
in
place
to
report
these
data
to
U.
S
EPA.
These
data
from
Round
1
were
collected
by
U.
S
EPA
from
many
states
over
time
and
put
into
a
database
called
the
Unregulated
Contaminant
Information
System,
or
URCIS.

The
1993
UCM
contaminants
include
13
SOCs
and
1
inorganic
contaminant
(
IOC)
(
56
FR
3526).
Monitoring
for
the
UCM
(
1993)
contaminants
began
coincident
with
the
Phase
II/
V
regulated
contaminants
from
1993
through
1998.
This
is
often
referred
to
as
"
Round
2"
monitoring.
The
UCM
(
1987)
contaminants
were
also
included
in
the
Round
2
monitoring.
As
4­
7
Metribuzin
 
February
2003
with
other
monitoring
data,
PWSs
reported
these
results
to
the
states.
EPA,
during
the
past
several
years,
requested
that
the
states
submit
these
historic
data
which
is
now
stored
in
the
SDWIS/
FED
database.

Monitoring
and
data
collection
for
metribuzin,
a
UCM
(
1993)
contaminant,
began
in
Round
2.
Therefore,
the
following
discussion
regarding
data
quality
screening,
data
management,
and
analytical
methods
focuses
on
SDWIS/
FED.
Discussion
of
the
URCIS
database
is
included
where
relevant,
but
it
is
worth
noting
that
the
various
quality
screening,
data
management,
and
analytical
processes
were
nearly
identical
for
the
two
databases.
For
further
details
on
the
two
monitoring
periods
as
well
as
the
databases,
see
U.
S.
EPA
(
2001a
and
2001b).

Developing
a
Nationally
Representative
Perspective
The
Round
2
data
contain
contaminant
occurrence
data
from
a
total
of
35
primacy
entities
(
including
34
states
and
data
for
some
tribal
systems).
However,
data
from
some
states
are
incomplete
and
biased.
Furthermore,
the
national
representativeness
of
the
data
is
problematic
because
the
data
were
not
collected
in
a
systematic
or
random
statistical
framework.
These
state
data
could
be
heavily
skewed
to
low­
occurrence
or
high­
occurrence
settings.
Hence,
the
state
data
were
evaluated
based
on
pollution­
potential
indicators
and
the
spatial/
hydrologic
diversity
of
the
nation.
This
evaluation
enabled
the
construction
of
a
cross­
section
from
the
available
state
data
sets
that
provides
a
reasonable
representation
of
national
occurrence.

A
national
cross­
section
from
these
state
Round
2
contaminant
databases
was
established
using
the
approach
developed
for
the
EPA
report
A
Review
of
Contaminant
Occurrence
in
Public
Water
Systems
(
U.
S.
EPA,
1999).
This
approach
was
developed
to
support
occurrence
analyses
for
EPA's
Chemical
Monitoring
Reform
(
CMR)
evaluation.
It
was
supported
by
peer
reviewers
and
stakeholders.
The
approach
cannot
provide
a
"
statistically
representative"
sample
because
the
original
monitoring
data
were
not
collected
or
reported
in
an
appropriate
fashion.
However,
the
resultant
"
national
cross­
section"
of
states
should
provide
a
clear
indication
of
the
central
tendency
of
the
national
data.
The
remainder
of
this
section
provides
a
summary
description
of
how
the
national
cross­
section
for
the
SDWIS/
FED
(
Round
2)
database
was
developed.
The
details
of
the
approach
are
presented
in
other
documents
(
U.
S.
EPA,
2001a,
b);
readers
are
referred
to
these
for
more
specific
information.

Cross­
Section
Development
As
a
first
step
in
developing
the
cross­
section,
the
state
data
contained
in
the
SDWIS/
FED
database
(
containing
the
Round
2
monitoring
results)
were
evaluated
for
completeness
and
quality.
Some
state
data
in
SDWIS/
FED
were
unusable
for
a
variety
of
reasons.
Some
states
reported
only
detections,
or
their
data
had
incorrect
units.
Datasets
only
including
detections
are
obviously
biased.
Other
problems
included
substantially
incomplete
data
sets
without
all
PWSs
reporting
(
U.
S.
EPA,
2001a
Sections
II
and
III).
4­
8
Metribuzin
 
February
2003
The
balance
of
the
states
remaining
after
the
data
quality
screening
were
then
examined
to
establish
a
national
cross­
section.
This
step
was
based
on
evaluating
the
states'
pollution
potential
and
geographic
coverage
in
relation
to
all
states.
Pollution
potential
is
considered
to
ensure
a
selection
of
states
that
represent
the
range
of
likely
contaminant
occurrence,
and
a
balance
with
regard
to
likely
high
and
low
occurrence.
Geographic
consideration
is
included
so
that
the
wide
range
of
climatic
and
hydrogeologic
conditions
across
the
United
States
are
represented,
again
balancing
the
varied
conditions
that
affect
transport
and
fate
of
contaminants,
as
well
as
conditions
that
affect
naturally
occurring
contaminants
(
U.
S.
EPA,
2001b
Sections
III.
A.
and
III.
B.).

The
cross­
section
states
were
selected
to
represent
a
variety
of
pollution
potential
conditions.
Two
primary
pollution
potential
indicators
were
used.
The
first
factor
selected
indicates
pollution
potential
from
manufacturing/
population
density
and
serves
as
an
indicator
of
the
potential
for
VOC
contamination
within
a
state.
Agriculture
was
selected
as
the
second
pollution
potential
indicator
because
the
majority
of
SOCs
of
concern
are
pesticides
(
U.
S.
EPA,
2001b
Section
III.
A.).
The
50
individual
states
were
ranked
from
highest
to
lowest
based
on
the
pollution
potential
indicator
data.
For
example,
the
state
with
the
highest
ranking
for
pollution
potential
from
manufacturing
received
a
ranking
of
1
for
this
factor
and
the
state
with
the
lowest
value
was
ranked
as
number
50.
States
were
ranked
for
their
agricultural
chemical
use
status
in
a
similar
fashion.

The
states'
pollution
potential
rankings
for
each
factor
were
subdivided
into
four
quartiles
(
from
highest
to
lowest
pollution
potential).
The
cross­
section
states
were
chosen
from
all
quartiles
for
both
pollution
potential
factors
to
ensure
representation,
for
example,
from:
states
with
high
agrichemical
pollution
potential
rankings
and
high
manufacturing
pollution
potential
rankings;
states
with
high
agrichemical
pollution
potential
rankings
and
low
manufacturing
pollution
potential
rankings;
states
with
low
agrichemical
pollution
potential
rankings
and
high
manufacturing
pollution
potential
rankings;
and
states
with
low
agrichemical
pollution
potential
rankings
and
low
manufacturing
pollution
potential
rankings
(
U.
S.
EPA,
2001b
Section
III.
B.).
In
addition,
some
secondary
pollution
potential
indicators
were
considered
to
further
ensure
that
the
cross­
section
states
included
the
spectrum
of
pollution
potential
conditions
(
high
to
low).
The
cross­
section
was
then
reviewed
for
geographic
coverage
throughout
all
sectors
of
the
United
States.

The
data
quality
screening,
pollution
potential
rankings,
and
geographic
coverage
analysis
established
a
national
cross­
section
of
20
Round
2
(
SDWIS/
FED)
states.
The
cross­
section
states
provide
good
representation
of
the
nation's
varied
climatic
and
hydrogeologic
regimes
and
the
breadth
of
pollution
potential
for
the
contaminant
groups
(
Figure
4­
1).
4­
9
Metribuzin
 
February
2003
Figure
4­
1.
Geographic
Distribution
of
Cross­
Section
States
for
Round
2
(
SDWIS/
FED).

Round
2
(
SDWIS/
FED)

Alaska
Arkansas
Colorado
Kentucky
Maine
Maryland
Massachusetts
Michigan
Minnesota
Missouri
New
Hampshire
New
Mexico
North
Carolina
North
Dakota
Ohio
Oklahoma
Oregon
Rhode
Island
Texas
Washington
Cross­
Section
Evaluation
To
evaluate
and
validate
the
method
for
creating
the
national
cross­
sections,
the
method
was
used
to
create
smaller
state
subsets
from
the
24­
state,
Round
1
(
URCIS)
cross­
section
and
aggregations.
Again,
states
were
chosen
to
achieve
a
balance
from
the
quartiles
describing
pollution
potential
and
a
balanced
geographic
distribution,
to
incrementally
build
subset
crosssections
of
various
sizes.
For
example,
the
Round
1
cross­
section
was
tested
with
subsets
of
4,
8
(
the
first
4
state
subset
plus
4
more
states),
and
13
(
8
state
subset
plus
5)
states.
Two
additional
cross­
sections
were
included
in
the
analysis
for
comparison:
a
cross­
section
composed
of
16
biased
states
eliminated
from
the
24
state
cross­
section
for
data
quality
reasons
and
a
crosssection
composed
of
all
40
Round
1
states
(
U.
S.
EPA,
2001b
Section
III.
B.
1).

These
Round
1
incremental
cross­
sections
were
then
used
to
evaluate
occurrence
for
an
array
of
both
high­
and
low­
occurrence
contaminants.
The
comparative
results
illustrate
several
points.
The
results
are
quite
stable
and
consistent
for
the
8­,
13­,
and
24­
state
cross­
sections.
They
are
much
less
so
for
the
4­
state,
16­
state
(
biased),
and
40­
state
(
all
Round
1
states)
crosssections
The
4­
state
cross­
section
is
too
small
to
provide
balance
both
geographically
and
with
pollution
potential,
a
finding
that
concurs
with
past
work
(
U.
S.
EPA,
1999).
The
CMR
analysis
suggested
that
a
minimum
of
6­
7
states
was
needed
to
provide
balance
both
geographically
and
with
pollution
potential,
and
the
CMR
report
used
8
states
out
of
the
available
data
for
its
nationally
representative
cross­
section
(
U.
S.
EPA,
1999).
The
16­
state
and
40­
state
crosssections
both
including
biased
states,
provided
occurrence
results
that
were
unstable
and
inconsistent
for
a
variety
of
reasons
associated
with
their
data
quality
problems
(
U.
S.
EPA,
2001b
Section
III.
B.
1).

The
8­,
13­,
and
24­
state
cross­
sections
provide
very
comparable
results,
are
consistent,
and
are
usable
as
national
cross­
sections
to
provide
estimates
of
contaminant
occurrence.
4­
10
Metribuzin
 
February
2003
Including
greater
data
from
more
states
improves
the
national
representation
and
the
confidence
in
the
results,
as
long
as
the
states
are
balanced
in
terms
of
pollution
potential
and
spatial
coverage.
The
20­
state
cross­
section
provides
the
best,
nationally
representative
cross­
section
for
the
Round
2
data.

4.2.2
Data
Management
and
Analysis
The
cross­
section
analyses
focused
on
occurrence
at
the
water
system
level;
i.
e.,
the
summary
data
presented
discuss
the
percentage
of
public
water
systems
with
detections,
not
the
percentage
of
samples
with
detections.
By
normalizing
the
analytical
data
to
the
system
level,
skewness
inherent
in
the
sample
data
is
avoided.
System
level
analysis
was
used
since
a
PWS
with
a
known
contaminant
problem
usually
has
to
sample
more
frequently
than
a
PWS
that
has
never
detected
the
contaminant.
The
results
of
a
simple
computation
of
the
percentage
of
samples
with
detections
(
or
other
statistics)
can
be
skewed
by
the
more
frequent
sampling
results
reported
by
the
contaminated
site.
The
system
level
of
analysis
is
conservative.
For
example,
a
system
need
only
have
a
single
sample
with
an
analytical
result
greater
than
the
Minimum
Reporting
Limit
(
MRL),
i.
e.,
a
detection,
to
be
counted
as
a
system
with
a
result
"
greater
than
the
MRL."

Also,
the
data
used
in
the
analyses
were
limited
to
only
those
data
with
confirmed
water
source
and
sampling
type
information.
Only
standard
SDWA
compliance
samples
were
used;
"
special"
samples,
or
"
investigation"
samples
(
investigating
a
contaminant
problem
that
would
bias
results),
or
samples
of
unknown
type
were
not
used
in
the
analyses.
Various
quality
control
and
review
checks
were
performed,
including
follow­
up
questions
to
the
states
providing
the
data.
Many
of
the
most
intractable
data
quality
problems
encountered
occurred
with
older
data.
These
problematic
data
were,
in
some
cases,
simply
eliminated
from
the
analysis.
For
example,
when
the
number
of
data
with
problems
were
insignificant
relative
to
the
total
number
of
observations
they
were
dropped
from
the
analysis
(
For
further
details
see
Cadmus,
2000).

As
indicated
in
Figure
4­
1,
Massachusetts
is
included
in
the
20­
state,
Round
2
national
cross­
section.
Noteworthy
for
SOCs
like
metribuzin,
however,
Massachusetts'
SOC
data
were
problematic.
Massachusetts
reported
Round
2
sample
results
for
SOCs
from
only
56
PWSs,
while
reporting
VOC
results
from
over
400
different
PWSs.
Massachusetts
SOC
data
also
contained
an
atypically
high
percentage
of
systems
with
analytical
detections
when
compared
to
all
other
states.
Through
communications
with
Massachusetts
data
management
staff
it
was
learned
that
the
state's
SOC
data
were
incomplete
and
that
the
SDWIS/
FED
record
for
Massachusetts
SOC
data
was
also
incomplete.
For
instance,
the
SDWIS/
FED
Round
2
data
for
Massachusetts
indicates
14.3%
of
systems
reported
detections
of
metribuzin.
The
cross­
section
state
with
the
next
highest
detection
frequency
reported
only
0.2%
of
systems
with
detections.
In
contrast,
Massachusetts'
data
characteristics
and
quantities
for
IOCs
and
VOCs
were
reasonable
and
comparable
with
other
states'
results.
Therefore,
Massachusetts
was
included
in
the
group
of
20
SDWIS/
FED
Round
2
cross­
section
states
with
usable
data
for
IOCs
and
VOCs,
but
its
metribuzin
(
SOC)
data
were
omitted
from
Round
2
cross­
section
occurrence
analyses
and
summaries
presented
in
this
report.
4­
11
Metribuzin
 
February
2003
Occurrence
Analysis
To
evaluate
national
contaminant
occurrence,
a
two­
stage
analytical
approach
has
been
developed.
The
first
stage
of
analysis
provides
a
straightforward,
conservative,
broad
evaluation
of
occurrence
of
the
CCL
preliminary
regulatory
determination
priority
contaminants
as
described
above.
These
descriptive
statistics
are
summarized
here.
Based
on
the
findings
of
the
Stage
1
Analysis,
EPA
will
determine
whether
more
intensive
statistical
evaluations,
the
Stage
2
Analysis,
may
be
warranted
to
generate
national
probability
estimates
of
contaminant
occurrence
and
exposure
for
priority
contaminants.
(
For
details
on
this
two
stage
analytical
approach
see
Cadmus,
2000.)

The
summary
descriptive
statistics
presented
in
Table
4­
4
for
metribuzin
are
a
result
of
the
Stage
1
analysis
and
include
data
from
Round
2
(
SDWIS/
FED,
1993­
1997)
cross­
section
states
(
minus
Massachusetts).
Included
are
the
total
number
of
samples,
the
percent
of
samples
with
detections,
the
99th
percentile
concentration
of
all
samples,
the
99th
percentile
concentration
of
samples
with
detections,
and
the
median
concentration
of
samples
with
detections.
The
percentages
of
PWSs
and
population
served
indicate
the
proportion
of
PWSs
whose
analytical
results
showed
a
detection(
s)
of
the
contaminant
(
simple
detection,
>
MRL)
at
any
time
during
the
monitoring
period;
or
a
detection(
s)
greater
than
one­
half
the
Health
Reference
Level
(
HRL);
or
a
detection(
s)
greater
than
the
Health
Reference
Level.
The
Health
Reference
Level,
91
µ
g/
L,
is
a
preliminary
estimated
health
effect
level
used
for
this
analysis.

The
HRL
was
derived
from
the
RfD
(
developed
in
Chapter
8
of
this
document)
as
a
preliminary
estimated
health
effect
level
as
follows:

HRL
=
RfD
×
Body
Weight
×
Relative
Source
Contribution
Drinking
Water
Intake
HRL
=
0.013
mg/
kg
×
70
kg
×
20%
2L
HRL
=
0.091
mg/
L
or
91
:
g/
L
The
99th
percentile
concentration
is
used
here
as
a
summary
statistic
to
indicate
the
upper
bound
of
occurrence
values
because
maximum
values
can
be
extreme
values
(
outliers)
that
sometimes
result
from
sampling
or
reporting
error.
The
99th
percentile
concentration
is
presented
for
both
the
samples
with
only
detections
and
all
of
the
samples
because
the
value
for
the
99th
percentile
concentration
of
all
samples
is
below
the
Minimum
Reporting
Level
(
MRL)
(
denoted
by
"<"
in
Table
4­
4).
For
the
same
reason,
summary
statistics
such
as
the
95th
percentile
4­
12
Metribuzin
 
February
2003
Table
4­
4.
Summary
Occurrence
Statistics
for
Metribuzin.

Frequency
Factors
20
State
Cross­
Section1
(
Round
2)
All
Reporting
States2
(
Round
2)
National
System
and
Population
Numbers3
Total
Number
of
Samples
Percent
of
Samples
with
Detections
99th
Percentile
Concentration
(
all
samples)
Health
Reference
Level
Minimum
Reporting
Level
(
MRL)
99th
Percentile
Concentration
of
Detections
Median
Concentration
of
Detections
Total
Number
of
PWSs
Number
of
GW
PWSs
Number
of
SW
PWSs
Total
Population
Populations
of
GW
PWSs
Populations
of
SW
PWSs
34,507
0.003%
<
(
Non
­
detect)
91
:
g/
L
Variable4
0.10
:
g/
L
0.10
:
g/
L
13,512
11,833
1,679
50,633,068
14,886,153
35,746,915
42,856
0.23%
<
(
Non
­
detect)
91
:
g/
L
Variable4
3.0
:
g/
L
1.0
:
g/
L
15,333
13,311
2,022
62,397,416
16,255,818
46,141,598
 
 
 
 
 
 
 
65,030
59,440
5,590
213,008,182
85,681,696
127,326,486
Occurrence
by
System
National
Extrapolation5
PWSs
with
detections
(>
MRL)
Range
GW
PWSs
with
detections
SW
PWSs
with
detections
PWSs
>
½
Health
Reference
Level
(
HRL)
Range
GW
PWSs
>
½
Health
Reference
Level
SW
PWSs
>
½
Health
Reference
Level
PWSs
>
Health
Reference
Level
Range
GW
PWSs
>
Health
Reference
Level
SW
PWSs
>
Health
Reference
Level
0.007%
0­
0.17%
0.008%
0.00%

0.00%
0­
0.00%
0.00%
0.00%

0.00%
0­
0.00%
0.00%
0.00%
0.28%
0­
14.29%
0.14%
1.24%

0.00%
0­
0.00%
0.00%
0.00%

0.00%
0­
0.00%
0.00%
0.00%
5
N/
A
5
0
0
N/
A
0
0
0
N/
A
0
0
182
N/
A
83
69
0
N/
A
0
0
0
N/
A
0
0
Occurrence
by
Population
Served
PWS
Populations
Served
with
detections
Range
GW
PWS
Population
with
detections
SW
PWS
Populations
with
detections
PWS
Population
Served
>
½
Health
Reference
Level
Range
GW
PWS
Population
>
½
Health
Reference
Level
SW
PWS
Population
>
½
Health
Reference
Level
PWS
Population
Served
>
Health
Reference
Level
Range
GW
PWS
Population
>
Health
Reference
Level
SW
PWS
Population
>
Health
Reference
Level
0.0003%
0­
0.01%
0.00%
0.00%

0.00%
0­
0.00%
0.00%
0.00%

0.00%
0­
0.00%
0.00%
0.00%
1.61%
0­
14.92%
0.24%
2.09%

0.00%
0­
0.00%
0.00%
0.00%

0.00%
0­
0.00%
0.00%
0.00%
1,000
N/
A
1,000
0
0
N/
A
0
0
0
N/
A
0
0
3,429,000
N/
A
206,000
2,661,000
0
N/
A
0
0
0
N/
A
0
0
1
Summary
Results
based
on
data
from
20­
State
Cross­
Section
(
minus
Massachusetts),
from
SDWIS/
FED,
UCM
(
1993)
Round
2.
2
Summary
Results
based
on
data
from
all
reporting
states
from
SDWIS/
FED,
UCM
(
1993)
Round
2.
3
Total
PWS
and
population
numbers
are
from
EPA
March
2000
Water
Industry
Baseline
Handbook
(
U.
S.
EPA,
2000e).
4
See
text
for
discussion.
5
National
extrapolations
are
from
the
20­
State
cross­
section
data
(
left)
and
all
Round
2
states
reporting
data
(
right)
using
the
Baseline
Handbook
system
and
population
numbers.
­
PWS
=
Public
Water
Systems;
GW
=
Ground
Water;
SW
=
Surface
Water;
MRL
=
Minimum
Reporting
Level
(
for
laboratory
analyses);
HRL
=
Health
Reference
Level,
an
estimated
health
effect
level
used
for
preliminary
assessment
for
this
review;
N/
A
=
Not
Applicable.
­
The
Health
Reference
Level
(
HRL)
used
for
metribuzin
is
91
µ
g/
L.
This
is
a
draft
value
for
working
review
only.
­
Total
Number
of
Samples
=
the
total
number
of
analytical
records
for
metribuzin.
­
99th
Percentile
Concentration
=
the
concentration
value
of
the
99th
percentile
of
either
all
analytical
results
or
just
the
detections
(
in
µ
g/
L)­
Median
Concentration
of
Detections
=
the
median
analytical
value
of
all
the
detections
(
analytical
results
greater
than
the
MRL)
(
in
µ
g/
L)
­
Total
Number
of
PWSs
=
the
total
number
of
public
water
systems
with
records
for
metribuzin
­
Total
Population
Served
=
the
total
population
served
by
public
water
systems
with
records
for
metribuzin
­
%
PWS
with
detections,
%
PWS
>
½
Health
Reference
Level,
%
PWS
>
Health
Reference
Level
=
percent
of
the
total
number
of
public
water
systems
with
at
least
one
analytical
result
that
exceeded
the
MRL,
½
Health
Reference
Level,
Health
Reference
Level,
respectively
­
%
PWS
Population
Served
with
detections,
%
PWS
Population
Served
>
½
Health
Reference
Level,
%
PWS
Population
Served
>
Health
Reference
Level
=
percent
of
the
total
population
served
by
PWSs
with
at
least
one
analytical
result
exceeding
the
MRL,
½
Health
Reference
Level,
or
the
Health
Reference
Level,
respectively
4­
13
Metribuzin
 
February
2003
concentration
of
all
samples
or
the
median
(
or
mean)
concentration
of
all
samples
are
omitted
because
these
also
are
all
"<"
values.
This
is
the
case
because
only
0.003%
of
all
samples
recorded
detections
of
metribuzin
in
Round
2.

As
a
simplifying
assumption,
a
value
of
one­
half
the
MRL
is
often
used
as
an
estimate
of
the
concentration
of
a
contaminant
in
samples/
systems
whose
results
are
less
than
the
MRL.
For
a
contaminant
with
relatively
low
occurrence,
such
as
metribuzin
in
drinking
water
occurrence
databases,
the
median
or
mean
value
of
occurrence
using
this
assumption
would
be
half
the
MRL
(
0.5
×
MRL).
However,
for
these
occurrence
data
this
is
not
straightforward.
For
Round
2,
states
have
reported
a
wide
range
of
values
for
the
MRLs.
This
is
in
part
related
to
state
data
management
differences
as
well
as
real
differences
in
analytical
methods,
laboratories,
and
other
factors.

The
situation
can
cause
confusion
when
examining
descriptive
statistics
for
occurrence.
For
example,
most
Round
2
states
reported
non­
detections
as
zeros
resulting
in
a
modal
MRL
value
of
zero.
By
definition
the
MRL
cannot
be
zero.
This
is
an
artifact
of
state
data
management
systems.
Because
a
simple
meaningful
summary
statistic
is
not
available
to
describe
the
various
reported
MRLs,
and
to
avoid
confusion,
MRLs
are
not
reported
in
the
summary
table
(
Table
4­
4).

In
Table
4­
4,
national
occurrence
is
estimated
by
extrapolating
the
summary
statistics
for
the
20­
state
cross­
section
(
minus
Massachusetts)
to
national
numbers
for
systems,
and
population
served
by
systems,
from
the
Water
Industry
Baseline
Handbook,
Second
Edition
(
U.
S.
EPA,
2000e).
From
the
handbook,
the
total
number
of
community
water
systems
(
CWSs)
plus
nontransient
non­
community
water
systems
(
NTNCWSs)
is
65,030,
and
the
total
population
served
by
CWSs
plus
NTNCWSs
is
213,008,182
persons
(
see
Table
4­
4).
To
arrive
at
the
national
occurrence
estimate
for
the
cross­
section,
the
national
estimate
for
PWSs
(
or
population
served
by
PWSs)
is
simply
multiplied
by
the
percentage
for
the
given
summary
statistic
[
i.
e.,
the
national
estimate
for
the
total
number
of
PWSs
with
detections
(
5)
is
the
product
of
the
percentage
of
PWSs
with
detections
(
0.007%)
and
the
national
estimate
for
the
total
number
of
PWSs
(
65,030)].

Included
in
Table
4­
4,
in
addition
to
the
results
from
the
cross­
section
data,
are
results
and
national
extrapolations
from
all
Round
2
reporting
states.
The
data
from
the
biased
states
are
included
because
of
metribuzin's
very
low
occurrence
in
drinking
water
samples
in
all
states.
For
contaminants
with
very
low
occurrence,
such
as
metribuzin
where
very
few
states
have
detections,
any
occurrence
becomes
more
important,
relatively.
For
such
contaminants,
the
cross­
section
process
can
easily
miss
a
state
with
occurrence
that
becomes
more
important.
This
is
the
case
with
metribuzin.

Extrapolating
only
from
the
cross­
section
states,
metribuzin's
very
low
occurrence
clearly
underestimates
national
occurrence.
For
example,
while
data
from
biased
states
like
Massachusetts
exaggerate
occurrence
because
of
incomplete
reporting,
the
detections
are
real
and
need
to
be
accounted
for
because
extrapolations
from
the
cross­
section
states
do
not
predict
enough
detections
in
the
biased
states.
Therefore,
results
from
all
reporting
Round
2
states,
including
the
biased
states,
are
also
used
here
to
extrapolate
a
national
estimate.
Using
the
biased
states'
data
should
provide
conservative
estimates
of
national
occurrence
for
metribuzin.
4­
14
Metribuzin
 
February
2003
As
exemplified
by
the
cross­
section
extrapolations
for
metribuzin,
national
extrapolations
of
these
Stage
1
analytical
results
can
be
problematic,
especially
for
contaminants
with
very
low
occurrence,
because
the
State
data
used
for
the
cross­
section
are
not
a
strict
statistical
sample.
For
this
reason,
the
nationally
extrapolated
estimates
of
occurrence
based
on
Stage
1
results
are
not
presented
in
the
CCL
Federal
Register
Notice.
The
presentation
in
the
Federal
Register
Notice
of
only
the
actual
results
of
the
cross­
section
analysis
maintains
a
straight­
forward
presentation,
and
the
integrity
of
the
data,
for
stakeholder
review.
The
nationally
extrapolated
Stage
1
occurrence
values
are
presented
here,
however,
to
provide
additional
perspective.
A
more
rigorous
statistical
modeling
effort,
the
Stage
2
analysis,
could
be
conducted
on
the
crosssection
data
(
Cadmus,
2001).
The
Stage
2
results
would
be
more
statistically
robust
and
more
suitable
to
national
extrapolation.
This
approach
would
provide
a
probability
estimate
and
would
also
allow
for
better
quantification
of
estimation
error.

Additional
Drinking
Water
Data
from
the
Corn
Belt
To
augment
the
SDWA
drinking
water
data
analysis
described
above,
and
to
provide
additional
coverage
of
the
corn
belt
states
where
metribuzin
use
is
highest
(
Figure
3­
1),
independent
analyses
of
finished
drinking
water
data
from
the
states
of
Iowa,
Illinois,
Indiana,
and
Ohio
are
reviewed
below.
The
Iowa
analysis
examined
SDWA
compliance
monitoring
data
from
surface
and
ground
water
PWSs
for
the
years
1988­
1995
(
Hallberg
et
al.,
1996).
Illinois
and
Indiana
compliance
monitoring
data
for
surface
and
ground
water
PWSs
were
evaluated.
The
data
were
mostly
for
the
years
from
1993
to
1997,
though
some
earlier
data
were
also
analyzed
(
after
U.
S.
EPA,
1999).
These
state
data
sets
were
available
from
an
independent
review
of
contaminant
monitoring
in
drinking
water
(
U.
S.
EPA,
1999).
Finally,
the
Ohio
Round
2
data
analyzed
with
the
20­
state
cross­
section
are
examined
independently
for
comparison
with
the
other
supplemental
data
sets
from
corn
belt
states.

Additional
reviews
of
national
and
state
drinking
water
monitoring
results
are
included
for
further
perspective
on
corn
belt
occurrence
of
metribuzin.
The
Iowa
State­
Wide
Rural
Well­
Water
Survey
was
conducted
in
1988­
1989
to
assess
pesticide
occurrence
in
rural
private
wells
(
Kross
et
al.,
1990).
The
National
Pesticide
Survey
(
NPS)
provides
extensive
national
monitoring
data
for
drinking
water,
including
data
from
Midwestern
states,
for
the
years
1988­
1990
(
U.
S.
EPA,
1990).
Hallberg
(
1989)
reviewed
special
contaminant
occurrence
studies
of
raw
surface
water
supplies
in
Illinois
(
1985­
1987),
and
both
raw
and
finished
drinking
water
from
surface
water
in
Iowa
(
1986).
Data
sources,
data
quality,
and
analytical
methods
for
these
analyses
are
described
in
the
respective
reports.

4.2.3
Results
Occurrence
Estimates
As
noted,
the
extrapolation
from
cross­
section
states
underestimates
national
metribuzin
occurrence,
and
the
resulting
percentages
of
PWSs
with
detections
are
very
low
(
Table
4­
4).
The
cross­
section
shows
approximately
0.007%
of
PWSs
(
about
5
PWSs
nationally)
experienced
detections
of
metribuzin
above
the
MRL,
affecting
less
than
0.0003%
of
the
population
served
(
approximately
1,000
people
nationally)
(
see
also
Figure
4­
3).
No
PWSs
reported
detections
at
levels
>
½
HRL
or
>
HRL.
Detection
frequencies
are
higher
for
ground
water
systems
when
4­
15
Metribuzin
 
February
2003
compared
to
surface
water
systems,
as
surface
water
systems
reported
zero
detections.
For
samples
with
detections,
the
median
and
99th
percentile
concentrations
are
0.10
µ
g/
L.
These
figures
are
identical
because
for
metribuzin,
Washington
was
the
only
state
that
reported
a
detection
(
0.10
µ
g/
L)
and
thus
this
statistic
is
both
the
median
and
99th
percentile
concentration.

Because
metribuzin's
low
occurrence
yields
an
underestimate
from
cross­
section
states,
all
data
are
used,
even
the
biased
data,
to
present
a
conservative
upper
bound
estimate.
Conservative
estimates
of
metribuzin
occurrence
using
all
of
the
Round
2
reporting
states
still
show
relatively
low
detection
frequencies
(
Table
4­
4).
Approximately
0.28%
of
PWSs
(
estimated
at
182
PWSs
nationally)
experienced
detections
>
MRL,
while
no
PWSs
experienced
detections
>
½
HRL,
and
>
HRL.
These
figures
indicate
that
about
1.61%
of
the
population
is
affected
by
concentrations
>
MRL
(
approximately
3.4
million
people
nationally),
and
0%
of
the
population
is
affected
by
concentrations
>
½
HRL
or
>
HRL.
The
proportion
of
surface
water
PWSs
with
detections
is
greater
than
ground
water
systems.
The
median
and
99th
percentile
concentrations
of
detections
are
1
µ
g/
L
and
3
µ
g/
L,
respectively.

The
Round
2
reporting
states
and
the
Round
2
national
cross­
section
show
a
proportionate
balance
in
PWS
source
waters
compared
to
the
national
inventory.
Nationally,
91%
of
PWSs
use
ground
water
(
and
9%
surface
waters);
Round
2
national
cross­
section
states
show
88%
use
ground
water
(
and
12%
surface
waters);
Round
2
reporting
states
show
87%
use
ground
water
(
and
13%
surface
waters).
The
relative
populations
served
are
not
as
comparable.
Nationally,
about
40%
of
the
population
is
served
by
PWSs
using
ground
water
(
and
60%
by
surface
water).
For
the
Round
2
cross­
section,
29%
of
the
cross­
section
population
is
served
by
ground
water
PWSs
(
and
71%
by
surface
water).
For
all
Round
2
reporting
states,
26%
of
the
population
is
served
by
ground
water
PWSs
(
and
74%
by
surface
water).
The
resultant
national
extrapolations
are
not
additive
as
a
consequence
of
these
disproportions
(
Table
4­
4).

Occurrence
in
the
Corn
Belt
SDWA
compliance
monitoring
data
from
the
corn
belt
states
of
Illinois,
Indiana,
and
Ohio
also
show
very
low
occurrence
of
metribuzin.
The
pesticide
was
not
detected
above
the
Health
Reference
Level
in
any
case,
and
the
highest
99th
percentile
concentration
of
detections
among
the
three
states
was
for
Illinois
at
0.7
µ
g/
L
(
Table
4­
5).
Illinois
also
had
the
highest
maximum
concentration
at
20
µ
g/
L,
still
well
below
the
HRL
(
after
U.
S.
EPA,
1999).
SDWA
compliance
monitoring
from
Iowa
for
the
years
1988­
1995
show
similar
results,
although
the
data
are
not
presented
in
Table
4­
5
because
they
were
not
compiled
at
the
system
level
in
the
same
manner.
Approximately
0.8%
of
samples
analyzed
for
metribuzin
in
Iowa
drinking
water
had
detections
of
the
compound
with
a
maximum
concentration
of
1.6
µ
g/
L.
The
99th
percentile
concentration
of
all
samples
was
a
non­
detect
(
Hallberg
et
al.,
1996).

Metribuzin
detection
frequencies
are
generally
much
greater
in
surface
water
when
compared
to
ground
water
(
Tables
4­
5
and
4­
6).
Two
exceptions
are
the
Iowa
SDWA
compliance
data,
in
which
surface
and
ground
water
detection
frequencies
are
essentially
the
same
(
0.77%
and
0.76%,
respectively),
and
the
Indiana
SDWA
compliance
data
which
had
no
metribuzin
detections
in
surface
water
(
Table
4­
5).
4­
16
Metribuzin
 
February
2003
Table
4­
5.
SDWA
Compliance
Monitoring
Data
from
the
States
of
Illinois,
Indiana,
and
Ohio.

Frequency
Factors
Illinois1
Indiana2
Ohio3
Total
Number
of
Samples
Percent
of
Samples
with
Detections
99th
Percentile
Concentration
(
all
samples)
Health
Reference
Level
Minimum
Reporting
Level
(
MRL)
99th
Percentile
Concentration
of
Detections
Median
Concentration
of
Detections
Minimum
Concentration
of
Detections
Total
Number
of
PWSs
Number
of
GW
PWSs
Number
of
SW
PWSs
14,818
0.2%
<
(
ND)
91
:
g/
L
Variable4
0.7
:
g/
L
0.2
:
g/
L
0.1
:
g/
L
1,139
1,030
109
1,033
0.1%
<
(
ND)
91
:
g/
L
Variable4
0.2
:
g/
L
0.2
:
g/
L
0.2
:
g/
L
392
345
47
4,039
0.0%
<
(
ND)
91
:
g/
L
Variable4
0
:
g/
L
0
:
g/
L
0
:
g/
L
2,178
2,017
161
Occurrence
by
System
%
PWSs
with
detections
(>
MRL)
GW
PWSs
with
detections
SW
PWSs
with
detections
0.97%
0.10%
9.17%
0.26%
0.29%
0.00%
0.00%
0.00%
0.00%

%
PWSs
>
½
Health
Reference
Level
GW
PWSs
>
½
Health
Reference
Level
SW
PWSs
>
½
Health
Reference
Level
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%

%
PWSs
>
Health
Reference
Level
GW
PWSs
>
Health
Reference
Level
SW
PWSs
>
Health
Reference
Level
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%

1
After
an
independent
analysis
of
Illinois
SDWA
compliance
monitoring
data
from
1993­
1997
(
U.
S.
EPA,
1999).
2
After
an
independent
analysis
of
Indiana
SDWA
compliance
monitoring
data
from
1993­
1997
(
U.
S.
EPA,
1999).
3
Summary
results
based
on
analysis
of
Ohio
data
from
the
SDWIS/
FED
UCM
(
1993),
Round
2.
4
See
text
for
discussion.
­
PWS
=
Public
Water
Systems;
GW
=
Ground
Water;
SW
=
Surface
Water;
MRL
=
Minimum
Reporting
Level
(
for
laboratory
analyses);
­
HRL
=
Health
Reference
Level,
an
estimated
health
effect
level
used
for
preliminary
assessment
for
this
review
­
The
Health
Reference
Level
(
HRL)
used
for
metribuzin
is
91
µ
g/
L.
This
is
a
draft
value
for
working
review
only.
­
Total
Number
of
Samples
=
the
total
number
of
analytical
records
for
metribuzin
­
99th
Percentile
Concentration
=
the
concentration
value
of
the
99th
percentile
of
either
all
analytical
results
or
just
the
detections
(
in
µ
g/
L)
­
Median
Concentration
of
Detections
=
the
median
analytical
value
of
all
the
detections
(
analytical
results
greater
than
the
MRL
)
(
in
µ
g/
L)
­
Total
Number
of
PWSs
=
the
total
number
of
public
water
systems
with
records
for
metribuzin
­
%
PWS
with
detections,
%
PWS
>
½
Health
Reference
Level,
%
PWS
>
Health
Reference
Level
=
percent
of
the
total
number
of
public
water
systems
with
at
least
one
analytical
result
that
exceeded
the
MRL,
½
Health
Reference
Level,
or
Health
Reference
Level,
respectively
4­
17
Metribuzin
 
February
2003
Table
4­
6
presents
data
from
a
number
of
national
and
state
drinking
water
monitoring
studies
with
results
in
corn
belt
states.
The
National
Pesticide
Survey
reports
no
detections
for
metribuzin.
Compliance
monitoring
from
Ohio
surface
water
PWSs
show
the
highest
detection
frequency
of
metribuzin
by
system
(
79.9%),
but
the
data
are
from
a
targeted
study
of
sensitive
surface
waters
so
results
may
not
be
representative.
The
highest
reported
concentration
of
the
studies
summarized
in
Table
4­
6,
3.7
µ
g/
L,
is
well
below
the
HRL.
Environmental
Working
Group
reports
were
reviewed;
however
only,
preliminary
results
were
available
from
a
special
study
of
finished
tap
water
in
29
cities.
Metribuzin
was
found
in
unspecified
concentrations
in
7%
(
2)
of
the
29
cities
(
Cohen
et
al.,
1995).

The
Iowa
State­
Wide
Rural
Well­
Water
Survey
established
a
statistically
significant
correlation
between
increasing
well
depth
and
decreasing
pesticide
contamination,
as
evidenced
by
the
lower
detection
frequency
of
metribuzin
in
drinking
water
wells
$
50
ft
deep
(
Table
4­
6).
Comparisons
between
raw
and
finished
water
in
Iowa
show
detection
frequencies
of
metribuzin
in
surface
water
increased
from
the
raw
to
finished
state
(
Table
4­
6;
Hallberg,
1989).
This
is
probably
a
result
of
either
analytical
variance,
imprecise
matching
between
raw
and
finished
water
samples,
or
pesticide
adsorption
to
and
subsequent
release
from,
filtration/
treatment
materials
(
Hallberg,
1989).

Regional
Patterns
Occurrence
results
are
displayed
graphically
by
state
in
Figures
4­
2
and
4­
3
to
assess
whether
any
distinct
regional
patterns
of
occurrence
are
present.
Thirty­
four
states
reported
Round
2
data
but
10
of
those
states
have
no
data
for
metribuzin
(
Figure
4­
2).
Another
21
states
did
not
detect
metribuzin.
The
remaining
3
states
detected
metribuzin
in
drinking
water
and
are
located
on
the
east
and
west
coasts
of
the
United
States
(
Figure
4­
2).
In
contrast
to
the
summary
statistical
data
presented
in
the
previous
section,
this
simple
spatial
analysis
includes
the
biased
Massachusetts
data.
4­
18
Metribuzin
 
February
2003
Table
4­
6.
Metribuzin
Occurrence
in
Midwest
Drinking
Water.

%
sites
$
MRL
%
samples
$
MRL
maximum
concentration
(
µ
g/
L)

Ground
Water
Surveys
National
Pesticide
Survey
(
1988­
90)
1
nd
nd
nd
Iowa
State­
Wide
Rural
Well­
Water
Survey
2
Wells
<
50
ft
deep
3.0%
nr
0.43
Wells
$
50
ft
deep
1.4%
nr
0.72
Special
Surface
Water
Studies
Raw
water
Iowa
(
1986)
3
nr
7.0%
0.89
Illinois
(
1985­
87)
3
nr
15.0%
3.70
Finished
water
Ohio
(
1993­
)
4
79.9%
22.3%
1.8
Iowa
(
1986)
3
nr
12.0%
0.45
1
U.
S.
EPA,
1990
;
data
are
national
results
including
some
Midwestern
states
2
Kross
et
al.,
1990
3
cited
in
Hallberg,
1989
4
U.
S.
EPA,
1999
­
HRL
=
91
µ
g/
L
­
MRLs
vary
by
study.
­
nd
=
results
below
the
respective
reporting
level
­
nr
="
not
reported"

The
simple
spatial
analysis
presented
in
Figures
4­
2
and
4­
3
does
not
suggest
any
special
regional
patterns.
Further,
use
and
environmental
release
information
(
Chapter
3)
and
ambient
water
quality
data
(
Section
4.1)
indicate
that
metribuzin
has
low
detection
even
in
non­
drinking
water
sources.
According
to
TRI
data,
industrial
releases
have
occurred
since
1995
in
only
three
states
and
one
U.
S.
territory
(
IA,
MO,
NB,
Puerto
Rico;
U.
S.
EPA,
2000b).
However,
the
use
patterns
for
metribuzin
(
Figure
3­
1)
do
show
that
use
is
concentrated
in
soybean
producing
regions
(
similar
to
the
corn
belt)
in
the
Midwest
states
and
along
the
Mississippi
River
Valley
production
region.
These
states
are
missing
from
the
Round
2
data,
hence,
a
special
review
was
conducted
to
evaluate
data
from
Iowa,
Illinois,
Indiana,
and
Ohio.
Occurrence
rates
in
these
states
are
much
greater
than
other
areas,
but
even
in
these
states
no
PWSs
had
results
>
HRL.
4­
19
Metribuzin
 
February
2003
Metribuzin
Detections
in
Round
2
States
not
in
Round
2
No
data
for
Metribuzin
States
with
No
Detections
(
No
PWSs
>
MRL)
States
with
Detections
(
Any
PWSs
>
MRL)
All
States
Figure
4­
2.
States
with
PWSs
with
Detections
of
Metribuzin
for
All
States
with
Data
in
SDWIS/
FED
(
Round
2).
4­
20
Metribuzin
 
February
2003
*
State
of
Massachusetts
is
an
outlier
with
14.29%
PWSs
>
MRL
Metribuzin
Occurrence
in
Round
2
States
not
in
Cross­
Section
No
data
for
Metribuzin
0.00%
PWSs
>
MRL
0.01
­
1.00%
PWSs
>
MRL
>
1.00%
PWSs
>
MRL
*

Metribuzin
Occurrence
in
Round
2
States
not
in
Cross­
Section
No
data
for
Metribuzin
0.00%
PWSs
>
HRL
0.01
­
1.00%
PWSs
>
HRL
>
1.00%
PWSs
>
HRL
Figure
4­
3.
Round
2
cross­
section
states
with
PWSs
with
detections
of
metribuzin
(
any
PWSs
with
results
greater
than
the
Minimum
Reporting
Level
[
MRL];
above)
and
concentrations
greater
than
the
Health
Reference
Level
(
HRL;
below).
4­
21
Metribuzin
 
February
2003
4.3
Conclusions
Detection
frequencies
and
concentrations
of
metribuzin
in
ambient
surface
and
ground
water
are
low,
especially
in
ground
water.
Even
so,
it
is
one
of
the
21
most
commonly
detected
pesticides
in
ground
water
from
the
first
round
of
NAWQA
intensive
data
collection.
The
annual
mean
frequency
of
metribuzin
detection
in
surface
water
was
less
than
15%
for
all
land­
use
settings
and
concentrations.
Midwestern
ambient
surface
and
ground
water
concentrations
and
detection
frequencies
are
also
low.
Releases
of
metribuzin
to
the
environment
were
reported
in
the
TRI
from
only
three
states
and
one
territory.

Metribuzin
has
been
detected
in
PWS
samples
collected
under
the
Safe
Drinking
Water
Act
(
SDWA).
Cross­
section
occurrence
estimates
are
very
low
with
only
0.003%
of
all
samples
showing
detections.
Significantly,
the
values
for
the
99th
percentile
and
median
concentrations
of
all
samples
are
less
than
the
Minimum
Reporting
Level
(
MRL).
For
the
Round
2
cross­
section
samples
with
detections,
both
the
median
and
the
99th
percentile
concentrations
are
0.10
µ
g/
L.
Systems
with
detections
constitute
approximately
0.007%
of
Round
2
cross­
section
systems.
National
estimates
for
the
population
served
by
PWSs
with
detections
using
the
cross­
section
data
are
also
low:
approximately
1,000
people
(
about
0.0003%
of
the
national
PWS
population
)
are
served
by
PWSs
with
metribuzin
detections
>
MRL,
and
no
PWSs
reported
detections
>
½
HRL
or
>
HRL.
Using
more
conservative
estimates
of
occurrence
from
all
states
reporting
SDWA
Round
2
monitoring
data,
including
states
with
biased
data,
0.28%
of
the
nation's
PWSs
(
approximately
182
systems
and
3.4
million
people
served)
are
affected
by
metribuzin
concentrations
>
MRL,
while
no
PWSs
are
affected
by
concentrations
>
½
HRL
or
>
HRL.

The
heaviest
use
of
metribuzin
is
across
the
nation's
corn­
soybean
production
area.
These
states
are
not
well
represented
in
the
Round
2
database.
Therefore,
additional
data
from
the
Midwest
corn
belt
were
also
evaluated.
Drinking
water
data
from
the
corn
belt
states
of
Iowa,
Indiana,
Illinois,
and
Ohio
also
show
very
low
occurrence
of
metribuzin.
Special
targeted
surface
water
studies
from
Ohio
have
the
highest
detection
frequency
of
metribuzin
(
79.9%
of
systems).
The
pesticide
was
not
detected
above
the
Health
Reference
Level
in
any
sample,
with
the
highest
concentration
at
20
µ
g/
L.
5­
1
Metribuzin
 
February
2003
5.0
EXPOSURE
FROM
MEDIA
OTHER
THAN
WATER
This
section
summarizes
human
population
exposures
to
metribuzin
from
food,
air,
and
soil.
The
primary
purpose
is
to
estimate
average
daily
intakes
of
metribuzin
by
members
of
the
general
public.
When
exposure
data
on
subpopulations
were
located,
such
as
occupationally
exposed
persons,
these
data
were
also
summarized
and
included
in
this
section.

5.1
Exposure
from
Food
5.1.1
Exposures
of
the
General
Population
Concentrations
of
Metribuzin
in
Food
Items
Metribuzin
is
a
triazine
herbicide
used
to
control
small
seeded
grasses
and
broadleaf
weeds
in
crops
such
as
soybeans,
potatoes
and
sugarcane
(
Bouchard,
1982).
Several
studies
have
evaluated
its
residues
in
food
(
as
mentioned
below).
However,
not
all
studies
may
be
representative
of
concentrations
that
the
general
population
would
typically
be
exposed
to
from
food
items.
In
the
animal
studies
summarized
below,
metribuzin
concentrations
administered
in
feed
were
greater
than
those
that
would
occur
under
typical
feeding
conditions.
In
the
plant
studies
summarized
below,
metribuzin
residues
in
plant
tissues
and
food
products
were
measured
at
the
point
of
application.
During
the
time
lapse
between
food
production
and
consumption
by
the
general
public,
metribuzin
may
further
be
metabolized
and
dissipated
in
the
food
product,
and
also
be
removed
through
washing
and
food
preparation.
Thus,
the
metribuzin
concentrations
reported
in
some
studies
are
most
likely
higher
than
those
that
the
general
population
would
encounter
in
their
diets.

In
1999,
approximately
9,438
domestically
produced
and
imported
food
samples
were
analyzed
for
366
different
pesticides
as
part
of
the
Food
and
Drug
Administration's
(
FDA)
Regulatory
Monitoring
Program.
Metribuzin
was
not
detected
(
detection
limit
not
reported)
in
any
samples
of
grains,
milk
products,
fruits
or
vegetables.
Metribuzin
was
also
not
detected
(
detection
limit
not
reported)
in
any
of
the
218
domestic
or
298
imported
fish
and
shellfish
samples
analyzed
(
US
FDA,
1999).

One
study
examined
the
uptake
and
metabolism
of
metribuzin
in
soybeans.
After
a
preemergence
soil
application
of
14C­
metribuzin
at
0.3
lb
ai/
A
(
active
ingredient/
acre),
soybean
plants
and
mature
soybean
seeds
contained
total
radioactive
residues
(
expressed
as
metribuzin
equivalents)
of
12.1
ppm
(
mg/
kg)
and
0.48
ppm
(
mg/
kg),
respectively.
The
major
metribuzin
metabolite
in
both
soybean
plants
and
mature
seeds
was
the
6­(
1,1­
dimethylethyl)­
3,5­(
diketo)­
1,2,4­
triazin­
5­(
2
H,
4H)­
dione
(
DADK)
(
U.
S.
EPA,
1998a).

Growth
chamber
experiments
measured
metribuzin
absorption
and
distribution
in
soybean
plants
during
a
6­
day
period
after
emergence.
Soybean
plants
grown
in
soils
treated
with
0.28
kg/
ha
(
kg/
hectare)
14C­
metribuzin
contained
metribuzin
concentrations
ranging
from
5­
2
Metribuzin
 
February
2003
8.86
to
9.99
:
g/
g
(
mg/
kg)
metribuzin.
Shoot
concentrations
were
not
as
high
as
those
in
roots,
and
little
radioactivity
was
found
in
leaves
of
plants
(
Hargroder
and
Rogers,
1974).

Post­
emergence
treatment
of
wheat
with
5­
14C­
metribuzin
at
0.15
lb
ai/
acre
resulted
in
0.2
ppm
(
ppm,
expressed
as
metribuzin
equivalents)
total
radioactive
residues
in
wheat
grains
after
33
days.
About
9.3%
of
these
residues
consisted
of
metribuzin
and
its
metabolites
(
U.
S.
EPA,
1998a).

Field
studies
conducted
in
California,
Delaware,
Illinois,
Michigan,
New
Jersey,
Texas
and
Washington
evaluated
metribuzin
residues
in
carrots
after
post­
emergence
herbicide
treatment.
Metribuzin
and
metribuzin
metabolite
residues
in
carrots
were
below
the
EPA
tolerance
level
of
0.3
ppm
after
multiple
applications
of
up
to
four
times
the
maximum
allowable
rate
(
U.
S.
EPA,
1998a).

Cessna
(
1998)
measured
metribuzin
residues
in
lentil
crops
in
Canada.
After
postemergence
application
of
0.28
kg/
ha,
lentils
contained
residues
of
1
mg/
kg
metribuzin.
Residues
in
lentils
decreased
five­
and
ten­
fold
after
one
and
two
weeks,
respectively,
and
were
not
detected
after
six
weeks.
At
lentil
maturity,
metribuzin
was
below
the
detection
limit
of
0.02
mg/
kg.

A
ruminant
(
goat)
metabolism
study
evaluated
the
distribution
of
metribuzin
and
its
metabolites
in
various
tissues
(
U.
S.
EPA,
1998a).
Goats
were
administered
410
ppm
5­
14Cmetribuzin
by
diet
for
three
consecutive
days.
This
corresponds
to
approximately
59
times
the
calculated
dietary
burden
of
metribuzin
for
ruminants.
Total
radioactive
residues
reported
in
various
tissues
were
2.66
mg/
kg
in
liver,
4.27
mg/
kg
in
kidney,
0.97
mg/
kg
in
fat,
0.44
mg/
kg
in
muscle,
and
0.25­
2.09
mg/
kg
in
milk
(
U.
S.
EPA,
1998a).
Because
animals
were
administered
metribuzin
in
their
diets
at
concentrations
of
up
to
59
times
their
dietary
burden,
the
resulting
tissue
residues
may
tend
to
be
up
to
59
times
higher
than
those
that
would
occur
under
typical
feeding
conditions.

In
a
poultry
metabolism
study,
hens
were
given
feed
at
a
concentration
of
400
ppm
5­
14Cmetribuzin
for
three
days.
This
corresponds
to
approximately
500
times
the
calculated
dietary
burden
of
metribuzin
for
poultry.
Radioactive
residues
of
33.6
mg/
kg
in
liver,
36.3
mg/
kg
in
kidney,
1.6
mg/
kg
in
muscle,
and
0.2­
1.0
mg/
kg
in
eggs
were
reported
(
U.
S.
EPA,
1998a).
Because
animals
in
this
study
were
administered
metribuzin
in
their
diets
at
concentrations
of
up
to
500
times
their
dietary
burden,
the
resulting
tissue
residues
may
tend
to
be
up
to
500
times
higher
than
those
that
would
occur
under
typical
feeding
conditions.

Intake
of
Metribuzin
from
Food
Items
From
the
studies
mentioned
above,
the
analysis
of
metribuzin
in
food
items
conducted
by
the
FDA
Regulatory
Monitoring
Program
appears
to
be
most
representative
of
general
population
exposures
to
metribuzin
in
food
items.
Although
additional
studies
reporting
metribuzin
residue
levels
in
food
items
were
identified,
these
studies
were
conducted
at
dietary
concentrations
that
5­
3
Metribuzin
 
February
2003
are
higher
than
anticipated
to
occur
under
typical
herbicide
use
conditions.
Metribuzin
was
not
detected
in
9,438
domestic
and
imported
food
items
analyzed
during
FDA
pesticide
regulatory
monitoring
(
US
FDA,
1999).
Based
on
this,
the
typical
average
daily
intake
of
metribuzin
from
food
for
the
general
population
is
anticipated
to
be
close
to
zero.

Both
imported
and
domestic
fish
and
shellfish
samples
analyzed
for
pesticides
during
FDA
regulatory
monitoring
did
not
contain
metribuzin
at
detectable
levels
(
US
FDA,
1999).
Based
on
this,
the
typical
average
daily
intake
of
metribuzin
from
fish
and
shellfish
for
the
general
population
is
anticipated
to
be
close
to
zero.

5.1.2
Exposures
of
Subpopulations
No
evidence
was
located
in
the
available
literature
indicating
the
existence
of
subpopulations
with
dietary
intakes
of
metribuzin
different
from
those
of
the
general
population.

5.2
Exposure
from
Air
5.2.1
Exposures
of
the
General
Population
Concentrations
of
Metribuzin
in
Air
Information
on
ambient
levels
of
metribuzin
measured
in
air
were
not
located
in
the
available
literature.

Intake
of
Metribuzin
from
Air
Concentration
data
on
ambient
levels
of
metribuzin
were
unavailable
to
estimate
average
intakes
by
the
general
population
from
air.
However,
based
upon
its
physical
properties,
metribuzin
is
not
expected
to
be
present
in
ambient
air.
Metribuzin
is
a
solid
at
ambient
temperatures,
and
has
a
low
vapor
pressure
(
4.4
×
10­
7
mm
Hg
at
20oC).
Therefore,
it
is
not
likely
to
readily
partition
into
ambient
air.
Additionally,
any
partitioning
of
metribuzin
into
air
would
most
likely
occur
in
areas
where
it
is
used.
These
areas
are
typically
agricultural
regions,
remote
from
the
general
population.
Based
upon
this,
ambient
air
concentrations
of
metribuzin
are
most
likely
close
to
zero.
Thus,
the
typical
average
daily
intake
for
the
general
population
is
anticipated
to
be
close
to
zero.

5.2.2
Exposures
of
Subpopulations
Concentrations
of
Metribuzin
in
Air
Occupational
exposures
to
metribuzin
may
occur
as
part
of
its
regular
use.
Persons
involved
in
mixing,
loading,
applying
or
handling
the
various
dry
and
liquid
formulations
of
metribuzin
during
its
ground
and
aerial
applications
have
the
potential
to
be
exposed.
Concentration
data
for
metribuzin
in
air
were
not
obtained
from
the
available
literature.
5­
4
Metribuzin
 
February
2003
However,
the
EPA
has
estimated
baseline
inhalation
exposures
for
workers
involved
in
the
regular
use
of
metribuzin
as
a
herbicide
ranging
from
0.006
to
91.14
mg/
day
(
U.
S.
EPA,
1998a).
The
greatest
inhalation
exposure
estimates
are
for
persons
involved
in
the
handling
of
powdered
and
dry
bulk
forms
of
metribuzin.
The
estimated
daily
inhalation
exposure
for
a
person
mixing
wettable
powder
for
application
to
sugarcane
crops
is
91.14
mg/
day,
and
31.3
mg/
day
for
a
worker
loading
or
mixing
dry
bulk
fertilizer.
The
lowest
daily
inhalation
exposures
(
0.006
mg/
day)
were
seen
in
workers
involved
in
the
liquid
applications
of
metribuzin
to
turf
grass
by
plane
(
U.
S.
EPA,
1998a).

Intake
of
Metribuzin
from
Air
The
EPA
estimated
inhalation
exposures
for
workers
involved
in
the
regular
use
of
metribuzin
to
range
from
0.006
to
91.14
mg/
day
(
U.
S.
EPA,
1998a).
Dividing
these
estimates
by
a
body
weight
of
70
kg
results
in
daily
metribuzin
intakes
for
adult
workers
ranging
from
8.6
×
10­
5
to
1.3
mg/
kg­
day.

5.3
Exposure
from
Soil
5.3.1
Exposures
of
the
General
Population
Concentrations
of
Metribuzin
in
Soil
Information
was
not
located
regarding
metribuzin
levels
in
residential
soils.
Metribuzin
is
not
labeled
for
residential
use
by
homeowners
or
certified
applicators.
Thus,
it
is
not
anticipated
to
be
found
in
residential
soils.

Intake
of
Metribuzin
from
Soil
Based
on
its
approved
uses,
exposure
to
metribuzin
in
soil
is
not
anticipated
to
be
a
typical
route
of
exposure
for
the
general
population.
Because
metribuzin
is
not
labeled
for
residential
use
by
homeowners
or
certified
applicators,
the
intake
of
metribuzin
through
soil
by
most
of
the
general
population
is
probably
close
to
zero.

5.3.2
Exposures
of
Subpopulations
Concentrations
of
Metribuzin
in
Soil
Several
studies
(
Burgard
et
al.,
1994;
Brown
et
al.,
1985;
Dao,
1995;
Gallaher
and
Meuller,
1996)
have
reported
metribuzin
levels
in
agricultural
soils,
which
may
be
a
source
of
occupational
exposure
for
those
involved
in
the
handling
or
application
of
this
chemical.
Soil
concentrations
were
dependant
upon
application
rate,
and
decreased
over
time
following
application.
At
application
rates
ranging
from
0.56
to
1.1
kg/
ha,
initial
metribuzin
concentrations
in
soil
ranged
from
0.09
to
0.78
mg/
kg.
After
86­
195
days,
concentrations
ranged
from
0.007
to
0.11
mg/
kg.
5­
5
Metribuzin
 
February
2003
Post­
application
exposures
to
metribuzin
in
soil
may
occur
for
persons
entering
areas
that
have
been
treated
with
metribuzin.
The
general
public
may
be
exposed
after
the
application
of
metribuzin
to
turfgrass
in
public
areas
(
e.
g.
parks,
athletic
fields,
or
golf
courses)
that
have
been
treated
with
metribuzin
(
U.
S.
EPA,
1998a).
Specific
information
on
post­
application
concentrations
in
recreational
areas
or
exposure
estimates
were
not
available
in
the
obtained
literature.

Intakes
of
Metribuzin
from
Soil
At
an
application
rate
of
0.56
kg/
ha,
metribuzin
concentrations
in
soil
may
be
as
high
as
0.78
mg/
kg
upon
first
application,
with
levels
decreasing
over
time
(
Gallaher
and
Mueller,
1996).
At
this
concentration,
and
a
daily
soil
intake
of
480
mg/
day
for
a
contact
intensive
worker
(
U.
S.
EPA,
1997),
the
maximum
total
daily
intake
of
metribuzin
for
a
70
kg
adult
worker
would
be
5.3
×
10­
3
mg/
kg­
day.

5.4
Other
Residential
Exposures
Metribuzin
may
be
transported
from
agricultural
fields
during
runoff
events.
Sediment
in
run­
off
water
from
winter
wheat
fields
in
eastern
Washington
contained
metribuzin
concentrations
ranging
from
below
detection
limits
(
200
:
g/
kg
sediment)
to
3440
:
g/
kg
wet
weight
(
Brown
et
al.,
1985).
These
samples
were
collected
from
three
major
runoff
events
during
1979­
1980
that
produced
more
than
7.5
grams
of
sediment.
Run­
off
samples
generating
less
than
7.5
grams
of
sediment
were
not
analyzed
for
metribuzin
in
this
study.
Metribuzin
concentrations
in
18
run­
off
water
samples
ranged
from
below
detection
limits
(
5
:
g/
L)
to
44
:
g/
L.

An
additional
study
evaluated
metribuzin
concentrations
in
surface
runoff
samples
collected
from
midwestern
streams
during
the
first
major
runoff
event
after
its
application.
The
90th
percentile
concentrations
of
metribuzin
collected
in
1989,
1994,
and
1995
were
1.4,
1.2,
and
0.5
ppb,
respectively
(
U.
S.
EPA,
1998a).

5.5
Summary
Concentration
and
intake
values
for
metribuzin
in
media
other
than
water
to
the
general
population
and
an
occupationally
exposed
adult
subpopulation
are
summarized
in
Tables
5­
1
and
5­
2.
Based
on
the
available
information,
the
general
population,
on
average,
is
not
typically
expected
to
be
exposed
to
metribuzin
from
food,
air
or
soil.
However,
for
persons
who
are
occupationally
exposed
to
metribuzin,
inhalation
appears
to
be
the
main
route
of
exposure
to
this
chemical.
5­
6
Metribuzin
 
February
2003
Table
5­
1.
Exposures
of
the
General
Population
to
Metribuzin
in
Media
Other
Than
Water.

Parameter
Medium
Food
Air
Soil
Adult
Child
Adult
Child
Adult
Child
Concentration
in
medium
not
detected
not
detected
NA
NA
Estimated
daily
intake
(
mg/
kg­
day)
0.0*
0.0*
0.0*
0.0*
0.0*
0.0*

NA=
Not
Available
in
literature
*
expected
to
be
close
to
zero
based
upon
physical
properties
and/
or
use
of
chemical
(
see
Sections
5.1.1,
5.2.1
and
5.3.1)

Table
5­
2.
Exposures
of
Subpopulations
to
Metribuzin
in
Media
Other
Than
Water.

Parameter
Medium
Food
Air
Soil
Adult
Worker
Adult
Worker
Adult
Worker*

Concentration
in
medium
NA
0.006
to
91.14
mg/
day
0.78
mg/
kg
Estimated
daily
intake
(
mg/
kg­
day)
­­
8.6
x
10­
5
to
1.3
**
mg/
kg­
day
5.3
x
10­
3***
mg/
kg­
day
NA=
Not
Available
in
literature.
­­
=
Unable
to
estimate
based
on
available
information
*
Estimates
are
for
a
contact
intensive
worker,
with
direct
soil
contact.
**
Based
on
U.
S.
EPA
(
1998a)
estimates
for
inhalation
exposures
of
workers
handling
or
applying
metribuzin
(
see
Section
5.2.2).
***
High­
end
estimate
based
upon
maximum
soil
concentration
after
application.
6­
1
Metribuzin
 
February
2003
6.0
TOXICOKINETICS
6.1
Absorption
Based
on
urinary
excretion
data,
36!
52%
of
orally
administered
metribuzin
was
absorbed
in
Sprague­
Dawley
rats
(
U.
S.
EPA,
1993).
In
dogs,
52!
60%
of
the
administered
oral
dose
was
absorbed
(
U.
S.
EPA,
1993).
However,
in
a
recent
study,
Mathew
et
al.
(
1998)
reported
poor
absorption
(<
15%)
of
metribuzin
in
Sprague­
Dawley
rats
fed
extracts
of
soybean
plants
containing
14C­
metribuzin
for
2
days
(
6,392!
156,000
disintegrations
per
minute/
g
body
weight).

6.2
Distribution
Mathew
et
al.
(
1998)
reported
on
the
distribution
of
14C­
metribuzin
in
Sprague­
Dawley
male
rats
(
n=
4)
after
a
2­
day
feeding
with
a
normal
rat
chow
containing
a
methanol
extract
of
beans
and
shoots
of
soybean
plants
radiolabeled
with
metribuzin
(
6,392!
156,000
dpm/
g
body
weight).
There
was
no
radioactivity
detected
in
tissues
such
as
heart,
kidney,
and
liver,
suggesting
that
the
metabolites
of
metribuzin,
or
the
parent
compound,
are
not
accumulated.

6.3
Metabolism
Animal
studies
suggest
that
metribuzin
undergoes
deamination
and
deketonization
during
its
metabolism.
The
presence
of
metribuzin
metabolites,
diketo
metribuzin
and
deaminateddiketo
metribuzin
in
urine
was
also
reported
(
U.
S.
EPA,
1993).
In
a
study
conducted
by
Cain
et
al.
(
1987),
the
authors
reported
the
metabolism
of
metribuzin
in
rats
to
involve
deamination,
dethioalkylation,
hydroxylation
of
the
t­
butyl
side
chain
and
conjugation
with
glutathione.

6.4
Excretion
Studies
in
Wistar
rats
performed
by
Cain
et
al.
(
1987)
used
either
a
single
low
dose
(
5
mg/
kg)
of
14C­
metribuzin
(
98.4!
99.4%
active
ingredient;
Specific
Activity
20.8
mCi/
nmol),
or
a
single
high
dose
(
500
mg/
kg).
No
significant
changes
were
observed
in
the
rates
or
the
routes
of
14C­
elimination
between
male
and
female
rats
in
either
the
low­
dose
or
high­
dose
administration
groups.
In
general,
27.3!
43.4%
of
the
radiolabel
was
excreted
in
the
urine
and
from
55.8
to
71.5%
of
the
radiolabel
was
excreted
in
feces
after
96
hours.

About
90%
of
administered
metribuzin
in
rats
was
excreted
within
16
days
in
one
study
or
within
5
days
by
another.
The
half­
life
for
elimination
of
radiolabeled
metribuzin
was
reported
as
19.1!
30.4
hours
for
male
rats
and
22.4!
33.6
hours
for
female
rats
(
U.
S.
EPA,
1993).
Moreover,
in
dogs,
over
90%
of
the
oral
dose
was
excreted
between
72
and
120
hours,
with
about
52!
60%
excreted
in
the
urine
as
metabolites
or
conjugates
and
about
30%
excreted
in
the
feces
predominantly
as
unchanged
metribuzin
(
U.
S.
EPA,
1993).
6­
2
Metribuzin
 
February
2003
Mathew
et
al.
(
1998)
reported
that
approximately
85%
of
the
radioactivity
was
eliminated
in
the
feces
of
rats
4
days
after
a
2­
day
feeding
with
extracts
of
soybean
plants
containing
radiolabeled
metribuzin.
About
1!
8%
of
the
radioactivity
was
eliminated
in
the
urine.
7­
1
Metribuzin
 
February
2003
7.0
HAZARD
IDENTIFICATION
7.1
Human
Effects
7.1.1
Short­
Term
Studies
There
are
no
short­
term
studies
available
which
report
the
effect
of
metribuzin
on
human
health.

7.1.2
Long­
Term
and
Epidemiological
Studies
There
are
no
long­
term
epidemiological
studies
available
which
have
examined
the
relationship
between
exposure
to
metribuzin
and
human
health
effects.

7.2
Animal
Studies
7.2.1
Acute
Toxicity
Animal
studies
have
demonstrated
that
metribuzin
exposure
induces
low
acute
toxicity.
The
doses
of
metribuzin
that
cause
acute
toxic
effects
are
summarized
in
Table
7­
1
(
U.
S.
EPA,
1998a).
Kimmerle
et
al.
(
1969)
found
that
metribuzin
was
not
an
eye
irritant
in
a
primary
eye
irritation
test
in
rabbits.
In
a
primary
dermal
irritation
study
also
conducted
by
Kimmerle
et
al.
(
1969),
metribuzin
exposure
produced
very
slight
irritation
of
rabbit
skin.
However,
metribuzin
exposure
has
not
been
shown
to
produce
sensitization
effects
in
guinea
pigs
(
ACGIH,
1986).

7.2.2
Short­
Term
Studies
There
are
no
short­
term
animal
studies
available
which
have
examined
the
relationship
between
metribuzin
exposure
and
adverse
health
effects.

7.2.3
Subchronic
Studies
Flucke
and
Hartmann
(
1989)
evaluated
systemic
and
dermal
toxicity
in
New
Zealand
rabbits
(
HC:
NZW
strain)
that
were
dermally
exposed
to
metribuzin
(
DIC
1468,
technical
94%)
at
0,
40,
200,
or
1,000
mg/
kg­
day
(
6
hours/
day;
5
days/
week)
for
3
weeks.
Neither
dermal
irritation
nor
mortality
were
observed
in
the
study.
However,
high­
dose
males
and
females
did
demonstrate
a
dose­
related
increase
in
cholesterol.
Triiodothyronine
(
T3)
was
decreased
in
all
males,
but
this
decrease
was
statistically
significant
only
at
the
high
dose.
The
authors
reported
statistically
significant
increases
in
liver
enzymes
such
as
N­
demethylase
and
cytochrome
P450
activities
in
high­
dose
males.

Chaisson
and
Cueto
(
1970)
studied
toxic
effects
in
Beagle
dogs
(
4
animals/
sex/
group)
orally
fed
metribuzin
in
the
diet
at
0,
50,
150
or
500
ppm
for
90
days.
No
differences
in
body
7­
2
Metribuzin
 
February
2003
Table
7­
1.
Acute
Toxic
Effects
of
Metribuzin
Species
Active
Ingredient
Route
of
Exposure
Results
Reference
Rats
Not
Specified
Oral
LD
50:
1,100
mg/
kg
Morgan,
1982
Rats
Technical
(%
not
specified)
Oral
LD
50:
Males
1,090
mg/
kg
Females
1,206
mg/
kg
Crawford
and
Anderson,
1974
Rat
Not
Specified
Oral
LD
50:
Males
2,379
mg/
kg
Females
2,794
mg/
kg
Mobay
Chemical,
1978a
Rat
Not
Specified
Oral
LD
50:
Males
2,300
mg/
kg
Females
2,200
mg/
kg
Kimmerle
et
al.,
1969
Mouse
Not
Specified
Oral
LD
50:
698!
711
mg/
kg
Hartley
and
Kidd,
1987
Cat
Not
Specified
Oral
LD
50:
>
500
mg/
kg
Hartley
and
Kidd,
1987
Guinea
Pig
Not
Specified
Oral
LD
50:
Males
245
mg/
kg
Females
274
mg/
kg
Crawford
and
Anderson,
1974
Guinea
Pig
Not
Specified
Oral
LD
50:
250
mg/
kg
Hartley
and
Kidd,
1987
Rat
and
Rabbit
Not
Specified
Dermal
LD
50:
>
2,000
mg/
kg
ACGIH,
1986
Rabbit
Technical
(%
not
specified)
Dermal
LD
50:
>
20,000
mg/
kg
Crawford
and
Anderson,
1972
Rat
Not
Specified
Percutaneous
LD
50:
>
20,000
mg/
kg
Hartley
and
Kidd,
1987
Rat
Not
Specified
Dermal
LD
50:
>
5,000
mg/
kg
Mobay
Chemical,
1978a
Mouse
Not
Specified
Inhalation
LC
50:
>
860
mg/
m3
ACGIH,
1986
Rat
Not
Specified
Inhalation
LC
50:
>
20,000
mg/
m3
Mobay
Chemical,
1978a
Rat
92.6%
Inhalation
LC
50:
>
648
mg/
m3
Shiotsuka,
1986
Mouse
Not
Specified
Intraperitoneal
LD
50:
210
mg/
kg
PCBPBS,
1984
7­
3
Metribuzin
 
February
2003
weight
gain
or
food
consumption
were
observed
at
any
of
the
doses
tested.
However,
in
both
male
and
female
animals,
dose­
related
increases
in
liver
weight,
and
liver:
body
weight
and
liver:
brain
weight
ratios,
were
reported.
Blood
chemistry
analysis
did
not
reveal
any
differences
between
the
control
and
treated
groups,
except
a
small
decrease
in
SGOT
(
serum
glutamateoxaloacetate
transaminase)
and
SGPT
(
serum
glutamate­
pyruvate
transaminase)
activities
in
the
high­
dose
male
group
at
the
end
of
the
study.
These
findings
implicate
the
liver
as
a
possible
target
organ.
However
the
dose
levels
were
not
verifiable.

Loser
et
al.
(
1969)
reported
toxic
effects
in
Wistar
rats
(
5
animals/
sex/
group)
fed
metribuzin
at
0,
50,
150,
500
or
1,500
ppm
for
three
months.
The
authors
observed
no
statistically
significant
changes
in
food
consumption;
however,
there
was
a
significant
reduction
in
body
weight
gain
and
an
increase
in
liver
and
thyroid
weights
observed
in
the
high­
dose
(
1,500
ppm)
group.
Pathology
in
the
lung
and
liver
was
unremarkable
in
either
the
control
or
treatment
groups.

In
studies
conducted
by
Lindberg
and
Richter
(
1970),
Beagle
dogs
(
four/
sex/
dose)
which
were
administered
oral
doses
of
50,
150
or
500
ppm
(
about
1.25,
3.75
or
12.5
mg/
kg­
day,
based
on
dietary
assumptions
of
Lehman,
1959)
of
technical
metribuzin
for
90
days
showed
no
significant
differences
in
body
weights,
food
consumption,
behavior,
mortality,
hematological
findings,
urinalysis,
gross
pathology
or
histopathology.

In
a
study
reported
by
ACGIH
(
1986),
no
effects
were
observed
during
a
3­
week
period
of
daily
dermal
application
of
1,000
mg
metribuzin/
kg.
A
3­
week
inhalation
study
conducted
in
rats
(
ACGIH,
1986)
(
aerosol
exposure
six
hours
daily,
5x/
week)
at
an
air
concentration
of
31
mg/
m3
was
without
observable
effects.

In
a
21­
day
inhalation
toxicity
study,
Thyssen
(
1981)
administered
metribuzin
(
DIC
1468,
93.1!
98.2%
active
ingredient)
at
doses
ranging
from
0!
720
mg/
m3
daily
for
6
hours.
Increased
N­
demethylase,
O­
demethylase
and
cytochrome
P450
activities
along
with
increased
liver
and
thyroid
weights
were
noted
in
the
high
dose
(
720
mg/
m3)
group.

7.2.4
Neurotoxicity
There
are
no
studies
available
which
correlate
exposure
to
metribuzin
with
neurotoxic
effects.

7.2.5
Developmental/
Reproductive
Toxicity
In
a
developmental
toxicity
(
teratology)
study,
metribuzin
(
92.6%
active
ingredient)
was
administered
to
pregnant
Charles
River
rats
(
Crl:
CD
BR)
in
doses
of
0,
25,
70
or
200
mg/
kg­
day
by
gavage
on
gestation
days
6­
18.
Maternal
toxic
effects
such
as
a
reduction
in
body
weight
gain
during
the
entire
gestation
period,
and
a
decrease
in
food
consumption,
were
observed
at
all
doses.
The
high­
dose
(
200
mg/
kg­
day)
group
showed
a
statistically
significant
increase
in
thyroid
weight.
A
decrease
in
thyroxine
(
T4)
levels
was
reported
in
both
the
70
and
200
mg/
kg­
7­
4
Metribuzin
 
February
2003
day
dose
groups
(
Kowaski
et
al.,
1986).
In
another
developmental
toxicity
study,
Machemer
(
1972)
reported
a
reduction
in
maternal
weight
gain
only
in
the
high­
dose
rat
group
(
FB
30
Strain)
fed
metribuzin
at
0,
5,
15,
50
and
100
mg/
kg­
day
during
gestation
period
days
6!
15.
No
evidence
of
fetal
toxicity
was
reported
in
the
rats
administered
metribuzin
at
doses
of
100
mg/
kgday
or
below.

In
a
3­
generation
reproduction
study,
Loser
and
Siegmund
(
1974)
administered
technical
metribuzin
in
the
feed
at
dose
levels
of
0,
35,
100
or
300
ppm
(
about
0,
1.75,
5
or
15
mg/
kg­
day,
based
on
dietary
assumptions
of
Lehman,
1959)
to
FB30
(
Elberfeld
breed)
rats
during
mating,
gestation
and
lactation.
Following
treatment,
fertility,
lactation
performance,
and
pup
development
were
evaluated.
No
treatment­
related
effects
were
reported
at
any
dose
tested.

In
a
developmental
toxicity
(
teratology)
study
conducted
by
Clemens
and
Hartnagel
(
1989),
American
Dutch
rabbits
(
17
females/
dose
group)
were
dosed
with
0,10,
30
or
85
mg/
kgday
of
metribuzin
(
92.7%
active
ingredient)
by
gavage
on
gestation
days
6!
18.
Maternal
toxicity
was
noted
at
doses
of
30
mg/
kg­
day
and
above,
based
on
a
reduction
in
maternal
body
weight
gain
on
gestation
days
18!
28,
and
a
decrease
in
food
consumption
on
gestation
days
7!
19
at
the
high­
dose
level.
A
no­
observable­
adverse­
effects­
level
(
NOAEL)
for
maternal
toxicity
was
determined
to
be
10
mg/
kg­
day
and
a
maternal
lowest­
observable­
adverse­
effects­
limit
(
LOAEL)
of
30
mg/
kg­
day.

In
another
developmental
toxicity
(
teratology)
study,
New
Zealand
white
rabbits
were
administered
0,
15,
45,
or
135
mg/
kg­
day
of
metribuzin
by
gavage
on
gestation
days
6!
18.
Maternal
systemic
toxicity
was
noted
at
45
mg/
kg­
day
as
reduced
body
weight
gain,
and
reduced
food
and
water
intake.
Additionally,
at
135
mg/
kg­
day
there
was
an
increased
incidence
of
abortions
and
decreased
body
weights.
There
were
no
significant
differences
between
control
and
treatment
groups
reported
for
the
mean
number
of
corpus
lutea,
implantation
sites,
early
or
late
resorptions,
and
live
or
dead
fetuses
(
Unger
and
Shellenberger,
1981).

In
a
two­
generation
reproduction
study
conducted
by
Porter
et
al.
(
1988),
Cr:
CD
BR
rats
were
exposed
orally
via
diet,
with
0,
30,
150
or
750
ppm
of
metribuzin
(
Sencor
®
technical
92.6%
active
ingredient).
Compared
to
the
control
animals,
the
high­
dose
adult
males
and
females
of
both
the
F
0
and
F
1
generations
consumed
less
food
and
gained
less
body
weight.
Necropsy
findings
on
both
the
F
0
and
F
1
generations
were
not
affected
by
the
metribuzin
treatment.
There
were
no
treatment
related
effects
observed
in
the
pathology
of
the
reproductive
organs
or
the
pituitary
tissues.
However,
a
dose­
related
increase
in
the
hypertrophy
of
the
hepatocytes
of
the
centrilobular
and
mid
zonal
regions
was
noted
in
the
high­
dose
(
750
ppm)
males
and
mid­
and
high­
dose
(
150
and
750
ppm)
females.
No
other
biologically
relevant
observations
were
noted.
Therefore,
for
reproductive
toxicity
and
systemic
effects
a
NOAEL
of
30
ppm
and
LOAEL
of
150
ppm
were
established.
7­
5
Metribuzin
 
February
2003
7.2.6
Chronic
Toxicity
In
a
2­
year
feeding
study
conducted
by
Loser
and
Mohr
(
1974),
40
Wistar
rats/
sex/
group
received
25,
35,
100
and
300
ppm
of
metribuzin
(
99.5%
pure)
in
their
diets;
80
rats/
sex
served
as
controls.
These
doses
corresponded
to
0,
1.3,
1.9,
5.3
and
14.4
mg
metribuzin/
kg/
day,
respectively,
in
the
males
and
0,
1.7,
2.3,
6.5
and
20.4
mg
metribuzin/
kg/
day,
respectively,
in
females.
Metribuzin
exposure
resulted
in
no
significant
difference
in
either
food
consumption
or
mortality
rate
when
compared
to
the
control
groups.
The
body
weights
of
the
rats
in
the
25,
35
and
100
ppm
dose
groups
(
both
sexes)
at
the
end
of
2­
years
did
not
differ
significantly
from
their
respective
controls.
However,
body
weight
gains
in
the
male
high­
dose
groups
were
significantly
decreased
during
weeks
70!
80
and
90!
100;
high­
dose
female
body
weights
were
significantly
decreased
from
weeks
20!
100.

Hayes
(
1981)
investigated
the
systemic
effects
of
metribuzin
in
a
2­
year
feeding
study
in
outbred
CD­
1
mice.
In
this
study,
metribuzin
technical
(
92.9%
pure)
dissolved
in
corn
oil
and
added
to
a
commercial
diet
was
administered
to
the
mice
(
50/
sex/
group)
at
levels
of
0,
200,
800
or
3,200
ppm
(
about
30,
120
or
480
mg/
kg­
day,
based
on
the
dietary
assumptions
of
Lehman,
1959)
for
104
weeks.
The
body
weights
of
the
treated
males
(
all
dose
groups)
and
females
(
all
dose
groups
with
the
exception
of
800
ppm
group)
did
not
differ
significantly
from
those
of
the
control
group.
Metribuzin
treatment
induced
inconsistent
results
in
the
hematological
parameters.
Survival
rates
were
not
altered
by
metribuzin
exposure.

In
a
2­
year
feeding
study
conducted
by
Loser
and
Mirea
(
1974),
four
Beagle
dogs/
sex/
group
were
administered
0,
25,
100,
or
1,500
ppm
(
0,
0.8,
3.4
or
55.7
mg/
kg­
day
for
males;
0,
0.8,
3.6,
or
55.3
mg/
kg­
day
for
females)
of
metribuzin
(
Bay
94
337
technical
99.5%)
in
the
diet.
Mortality
rates
were
observed
in
the
high­
dose
(
1,500
ppm)
group
at
75%
in
both
males
and
females.
The
clinical
tests
performed
after
twelve
months
of
metribuzin
exposure
suggested
the
presence
of
liver
dysfunction
in
the
dogs.
Elevated
activities
of
liver
enzymes
such
as
SGOT,
SGPT,
OCT
(
ornithine­
carbamyl
transferase)
and
alkaline
phosphatase
along
with
an
increase
in
BSP
(
bromsulphthalein)
retention
were
reported
in
the
males.
Increased
SGPT,
OCT
and
serum
protein
levels
were
observed
in
high­
dose
females.
There
were
no
major
changes
in
kidney
function.
An
increase
in
thyroid
weight
was
observed
in
the
high­
dose
groups
of
both
sexes.

Christenson
and
Wahle
(
1993)
conducted
a
2­
year
feeding
study,
in
which
Fischer
344
rats
received
0,
30,
300
or
900
ppm
(
0,
1.3,
13.8,
42.2
mg/
kg­
day
in
males;
0,
1.6,
17.7,
53.6
mg/
kg­
day
females)
metribuzin
(
93.0%
active
ingredient)
for
104
weeks.
There
were
no
major
changes
in
the
food
consumption
or
the
mortality
rates
observed
subsequent
to
metribuzin
exposure.
A
decrease
in
body
weight
gain
was
noticed
in
high­
dose
males
(
900
ppm)
and
midand
high­
dose
females
(
300
and
900
ppm).
Increases
in
brain:
body
weight,
heart:
body
weight,
kidney:
body
weight,
and
liver:
body
weight
ratios
were
observed,
in
addition
to
increases
in
thyroid
weights
and
thyroid:
body
weight
ratios,
in
the
high­
dose
groups
for
both
sexes.
In
general,
thyroxine
(
T4)
levels
increased
in
all
dose
levels,
while
triiodothyronine
(
T3)
levels
decreased
at
all
dose
levels,
but
no
other
systemic
effects
were
observed.
A
significant
increase
in
corneal
neovascularization
was
observed
in
male
rats
receiving
300
and
900
ppm
metribuzin.
7­
6
Metribuzin
 
February
2003
An
incidence
of
macroscopic
changes
in
the
300
and
900
ppm
metribuzin
treated
male
rats
included
a
discolored
zone
in
the
liver,
an
enlarged
adrenal
and
thyroid
gland,
ocular
opacity,
an
enlarged
abdomen
and
epididymal
mass.
Ovarian
cysts
were
detected
in
the
300
and
900
ppm
metribuzin
treated
females.

7.2.7
Carcinogenicity
Hayes
(
1981)
conducted
studies
in
which
technical
metribuzin
was
administered
in
the
diet
to
albino
CD­
1
mice
(
50/
sex/
dose)
at
200,
800
or
3,200
ppm
(
approximately
30,
120
or
480
mg/
kg­
day)
for
24
months.
Although
some
increase
in
the
number
of
tumor­
bearing
animals
was
observed
in
low­
and
mid­
dose
animals,
significant
increases
in
the
incidence
of
specific
tumor
types
were
not
observed
at
any
dose
level.
The
authors
concluded
that,
under
the
conditions
of
the
test,
there
was
no
increase
in
the
incidence
of
tumors
in
mice.

Subsequently,
statistical
analysis
of
this
data
was
performed
by
the
EPA's
Office
of
Pesticide
Programs
using
the
Chi
square
test
(
U.
S.
EPA,
1993).
Reevaluations
resulted
in
a
statistically
significant
(
p=
0.037
and
p=
0.045,
respectively)
decrease
in
malignant
and
total
tumor­
bearing
male
mice
in
the
high­
dose
group.
The
number
of
tumor­
bearing
female
mice
appeared
to
increase
in
the
low­
dose
group
(
not
statistically
significant,
p=
0.071)
and
did
significantly
increase
in
the
middle­
dose
group
(
p=
0.45
for
malignant
tumors
and
p=
0.0499
for
benign
tumors).
The
tumor
incidence
in
high­
dose
females
was
comparable
to
that
of
the
female
control
group.
The
overall
conclusion
drawn
was
that,
under
the
test
conditions
in
the
Hayes
(
1981)
study,
metribuzin
exposure
did
result
in
an
increase
of
tumor
incidence
in
mice.

In
a
2­
year
feeding
study
by
Loser
and
Mohr
(
1974),
40
Wistar
rats/
sex/
group
received
25,
35,
100
and
300
ppm
metribuzin
(
99.5%
pure)
in
their
diets;
while
80
rats/
sex
served
as
a
control
group.
These
doses
corresponded
to
0,
1.3,
1.9,
5.3
and
14.4
mg
metribuzin/
kg/
day,
respectively,
in
the
males
and
0,
1.7,
2.3,
6.5
and
20.4
mg
metribuzin/
kg/
day,
respectively,
in
females.
Loser
and
Mohr
(
1974)
reported
through
initial
evaluation
that
there
were
statistically
significant
increases
in
the
incidence
of
liver
bile
duct
adenomas
and
pituitary
gland
adenomas
in
the
female
high­
dose
groups
by
pair­
wise
comparison.
The
incidence
of
bile
duct
adenoma
in
the
females
was
13/
71,
4/
10,
5/
10,
1/
10
and
19/
35
in
the
control,
25,
35,
100
and
300
ppm
groups,
respectively,
while,
the
incidence
in
males
was
19/
66,
10/
10,
8/
10,
5/
10
and
9/
29,
respectively.
The
incidence
of
pituitary
gland
adenomas
in
the
female
control
and
high­
dose
groups
was
27/
71
and
21/
35
respectively,
while
in
males
the
incidences
were
10/
62
and
6/
29,
respectively.
It
was
determined
that
the
incidence
of
tumors
in
male
rats
was
not
significantly
different
in
any
of
the
tissues
examined.

The
EPA's
Office
of
Pesticide
Programs
reevaluated
the
original
histopathological
findings
reported
by
Loser
and
Mohr
(
1974).
In
this
reevaluation,
all
of
the
female
liver
bile
duct
adenomas
were
reclassified
as
bile
duct
proliferation.
The
pituitary
glands
from
all
animals
were
also
histopathologically
reevaluated.
It
was
determined
that
the
incidences
of
pituitary
adenoma
in
the
female
groups
were
16/
71
(
23%),
6/
34
(
18%),
9/
31
(
29%),
11/
33
(
33%)
and
14/
35
(
40%)
in
the
control,
25­,
35­,
100­
and
300­
ppm
groups,
respectively
(
U.
S.
EPA,
1993).
7­
7
Metribuzin
 
February
2003
In
another
2­
year
feeding
cancer
study
conducted
by
Christenson
and
Wahle
(
1993),
Fischer
344
rats
received
0,
30,
300
or
900
ppm
(
0,
1.3,
13.8,
42.2
mg/
kg­
day
in
males
and
0,
1.6,
17.7,
53.6
mg/
kg­
day
females)
of
metribuzin
(
93.0%
active
ingredient)
for
104
weeks.
The
most
significant
change
observed
was
thyroid
follicular
hyperplasia
in
male
rats
at
the
highest
dose.
There
were
no
significant
changes
in
the
neoplastic
lesions
of
other
tissues
(
kidney,
pituitary)
observed
in
both
the
high­
dose
males
and
females.
Christenson
and
Wahle
(
1993)
concluded
that
there
was
no
evidence
of
carcinogenicity
in
any
of
the
tissues
examined.

7.3
Other
Key
Data
7.3.1
Mutagenicity/
Genotoxicity
Metribuzin
was
determined
to
be
nonmutagenic
when
tested
in
unspecified
strains
of
Salmonella
typhimurium
and
Escherichia
coli
(
Mobay
Chemical
Corp.,
1977,
1978b).
Metribuzin
exposure
did
not
induce
a
reverse
mutation
in
the
D7
strain
of
Saccharomyces
cerevisiae
either
in
the
presence
or
absence
of
metabolic
activation
(
Mobay
Chemical
Corp.,
1987).
Metribuzin
was
determined
to
be
negative
when
tested
for
dominant
lethal
effects
in
male
and
female
mice
(
unspecified
strain)
treated
with
doses
of
300
mg
metribuzin/
kg
(
Mobay
Chemical
Corp.,
1974a,
1975,
1976).
It
was
determined
that
doses
of
100
mg
metribuzin/
kg
did
not
induce
chromosomal
aberrations
in
Chinese
hamster
spermatogonia
(
Mobay
Chemical
Corp.,
1974b).
Metribuzin
exposure
did
not
cause
a
significant
increase
in
the
unscheduled
DNA
synthesis
when
added
to
test
cultures
of
rat
primary
hepatocytes
(
Mobay
Chemical
Corp.,
1986a)
and
was
determined
to
be
negative
in
the
CHO/
HGPRT
mutation
assay
(
Mobay
Chemical
Corp.,
1986b).
However,
S­
9
activated
(
but
not
nonactivated)
metribuzin
was
determined
to
be
clastogenic
in
CHO
cells
(
Mobay
Chemical
Corp.,
1990).

In
vitro
tests
suggest
that
metribuzin
(
Sencor)
exposure
can
result
in
adduct
formation.
Using
a
32P­
postlabeling
method,
Shah
et
al.
(
1997)
reported
that
adducts
were
formed
when
metribuzin
and
its
S9­
metabolites
(
1
mM)
were
reacted
with
calf
thymus
DNA
for
3.5
hours.
The
adducts
were
analyzed
using
either
nuclease
P1
or
butanol
enrichment
method.
Benzo(
a)
pyrene
was
used
as
the
positive
control.
Compared
to
the
adducts
formed
in
control
DNA
(
5.6
adducts
per
109
nucleotides),
metabolites
of
metribuzin
produced
48.0
total
adducts
per
109
nucleotides,
as
analyzed
by
nuclease
P1
enrichment
method.
Analysis
of
the
adducts
produced
by
metribuzin,
utilizing
the
butanol
enrichment
method,
yielded
three
unique
adducts.
The
major
adduct
was
produced
at
281.5
total
adducts
per
109
nucleotides.
Adduct
formation
by
metribuzin
is
less
than
the
adduct
formation
from
benzo(
a)
pyrene.
Benzo(
a)
pyrene
produced
1893
and
1707
adducts
per
109
nucleotides
as
analyzed
by
the
nuclease
P1
and
the
butanol
enrichment
methods,
respectively,
under
similar
conditions.
Utilizing
nuclease
P1
and
the
butanol
enrichment
methods,
Shah
et
al.
reported
that,
unlike
benzo(
a)
pyrene,
the
type
of
adducts
formed
by
metribuzin
metabolites
were
not
similar.
However,
metribuzin
(
Sencor)
did
test
positive
for
DNA
adduct
formation,
when
using
32P­
postlabeling
with
nuclease
P1
enrichment.

Metribuzin
exposure
produced
a
negative
response
in
the
SOS
Chromotest
(
DNA
damage)
conducted
in
Escherichia
coli
with
or
without
metabolic
activation
(
Xu
and
Schurr,
7­
8
Metribuzin
 
February
2003
1990).
In
a
recent
study,
Venkat
et
al.
(
1995)
reported
mild
genotoxic
effects
of
metribuzin
using
a
similar
SOS
chromotest.
The
test
compounds
were
tested
in
10%
dimethylsulfoxide
(
DMSO)
or
in
micellar
solution
in
sodium
taurocholate
in
order
to
simulate
conditions
that
are
present
in
the
gastrointestinal
tract.
The
activity
of
the
$­
galactosidase
was
199
and
636
per
:
mole
depending
on
whether
metribuzin
was
dissolved
in
DMSO
or
sodium
taurocholate
solution,
respectively.
The
genotoxic
activity
of
metribuzin
was
26!
43
times
less
than
that
of
the
positive
control,
4­
nitroquinoline
oxide
(
4­
NQO).
The
activity
of
the
$­
galactosidase
for
the
positive
control
(
4­
NQO)
was
8,557
and
16,734
per
:
mole
in
DMSO
and
sodium
taurocholate
solutions,
respectively.

7.3.2
Immunotoxicity
There
are
no
studies
available
which
examine
the
relationship
between
metribuzin
exposure
and
immunotoxic
effects.

7.3.3
Hormonal
Disruption
In
vivo
metribuzin
exposure
has
been
shown
to
affect
the
endocrine
system.
For
example,
Porter
et
al.
(
1993)
measured
thyroxine
and
somatotropin
levels
in
rats
after
exposure
to
metribuzin.
Metribuzin
was
administered
orally
in
drinking
water
to
Sprague­
Dawley
rats
(
n=
6;
125­
150g)
for
6
or
16
weeks.
It
was
observed
that
the
rats
treated
with
metribuzin
had
hyperthyroidism.
Metribuzin
exposure
(
0!
10,000
ppm)
caused
a
significant
(
p
<
0.0005)
increase
in
the
plasma
thyroxine
levels
after
7,
13
or
16
weeks
of
exposure
in
both
male
and
female
rats.
It
was
determined
that
somatotropin
levels
were
not
affected
by
metribuzin
exposure.

Christenson
and
Wahle,
(
1993)
reported
a
statistically
significant
increase
in
thyroxine
(
T4)
and
decrease
in
triiodothyronine
(
T3)
levels
at
all
dose
levels
in
Fischer
344
rats
receiving
0,
30,
300
or
900
ppm
metribuzin
(
93.0%
active
ingredient)
for
104
weeks.

Flucke
and
Hartmann
(
1989)
also
observed
a
decrease
in
triiodothyronine
(
T3)
in
male
New
Zealand
rabbits
exposed
dermally
to
metribuzin
(
DIC
1468,
technical
94%)
at
0,
40,
200,
or
1,000
mg/
kg­
day
(
6
hours/
day;
5
days/
week)
for
3
weeks.

Kowaski
et
al.
(
1986)
administered
metribuzin
(
92.6%
active
ingredient)
to
pregnant
Charles
River
rats
in
doses
of
0,
25,
70
or
200
mg/
kg­
day
by
gavage
on
gestation
days
6!
18.
The
high­
dose
(
200
mg/
kg­
day)
group
exhibited
a
statistically
significant
increase
in
thyroid
weight.
A
decrease
in
T4
levels
was
observed
in
both
the
70
and
200
mg/
kg­
day
dose
groups.

7.3.4
Physiological
or
Mechanistic
Studies
The
major
toxic
effects
that
result
from
metribuzin
exposure
are
changes
in
body
weight
gain,
survival
rate,
and
liver
and
thyroid
function.
These
effects
are
mainly
systemic
and
the
7­
9
Metribuzin
 
February
2003
mode
of
action
has
not
been
investigated.
In
addition,
metribuzin
exposure
has
also
been
shown
to
affect
hormonal
levels
such
as
triiodothyronine,
thyroxine,
and
somatotropin.

7.3.5
Structure­
Activity
Relationship
There
are
no
studies
available
which
examine
the
structure­
activity
relationship
of
metribuzin.

7.4
Hazard
Characterization
7.4.1
Synthesis
and
Evaluation
of
Major
Non­
Cancer
Effects
While
the
studies
relating
to
the
metribuzin
exposure
on
human
health
effects
are
lacking,
the
hazard
characterization
is
performed
from
the
available
animal
studies.
Studies
conducted
in
animals
suggest
that
metribuzin
exposure
causes
low
acute
toxicity
as
evidenced
by
the
reported
high
LD
50
values
(
Kimmerle
et
al.,
1969;
Morgan,
1982;
Hartley
and
Kidd,
1987).
Also,
acute
exposure
studies
suggest
that
metribuzin,
at
the
doses
tested,
does
not
result
in
eye
or
dermal
irritations
(
Kimmerle
et
al.,
1969).
Subchronic
studies
suggest
that
metribuzin
could
cause
adverse
effects
in
body
weight
gain,
organ
weight,
and
hematological
parameters.
For
example,
a
significant
reduction
in
body
weight
gain
and
an
increase
in
liver
and
thyroid
weights
were
reported
in
Wistar
rats
exposed
to
metribuzin
at
1,500
ppm
(
Loser
et
al.,
1969).
Three
weeks
of
dermal
exposure
to
metribuzin
(
1,000
mg/
kg)
in
rabbits
also
resulted
in
an
increase
in
liver
enzymes
such
as
N­
demethylase
and
cytochrome
P450
(
Flucke
and
Hartmann,
1989).
These
effects
are
not
pronounced
when
the
studies
were
conducted
at
lower
doses
in
dogs.
Threemonth
metribuzin
exposure
to
Beagle
dogs
did
not
affect
body
weight
gain
or
food
consumption,
but
altered
the
clinical
parameters
such
as
SGOT
and
SGPT
levels
(
Chaisson
and
Cueto,
1970).

Chronic
effects
of
metribuzin
exposure
may
include
changes
in
body
weight
gain,
mortality,
liver
enzyme
activities
and
histopathological
changes.
Two­
year
feeding
studies
were
performed
on
rats
(
Loser
and
Mohr,
1974;
Christenson
and
Wahle,
1993),
mice
(
Hayes,
1981)
and
Beagle
dogs
(
Loser
and
Mirea,
1974).
In
general,
there
were
no
significant
differences
in
body
weight
gain,
food
consumption
or
mortality
after
two
years
of
exposure
to
metribuzin
to
rats
(
Loser
and
Mohr,
1974)
and
mice
(
Hayes,
1981).
However,
Christenson
and
Wahle
(
1993)
observed
a
decrease
in
body
weight
gain
in
rats
after
metribuzin
treatment.
The
differences
in
body
weight
gain
observed
in
rats
could
possibly
be
attributed
to
the
higher
dose
(
900
ppm)
administered
by
Christenson
and
Wahle
(
1993)
as
compared
to
a
maximum
dose
of
100
ppm
given
by
Loser
and
Mohr
(
1974).

Major
histopathological
changes
reported
by
one
study
after
chronic
feeding
of
metribuzin
include
a
significant
increase
in
corneal
neovascularization,
the
incidence
of
a
discolored
zone
in
the
liver,
an
enlarged
abdomen,
enlarged
adrenal
and
thyroid
glands,
ocular
opacity,
and
enlarged
epididymal
mass
in
male
rats
and
the
presence
of
ovarian
cysts
in
female
rats
(
Christenson
and
Wahle
1993).
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February
2003
Chronic
exposure
to
metribuzin
(
1,500
ppm)
could
cause
a
significant
increase
in
the
mortality
rate
in
Beagle
dogs.
Liver
dysfunction
was
also
observed
as
evidenced
by
elevation
in
the
activities
of
liver
enzymes
such
as
SGOT,
SGPT
and
OCT.
In
addition,
an
increase
in
thyroid
weight
was
observed
in
the
high
dose
group
of
both
males
and
females
(
Loser
and
Mirea,
1974).
However,
inconsistent
hematological
results
were
observed
in
mice
following
chronic
exposure
to
metribuzin
(
Hayes,
1981).

There
are
a
few
studies
available
on
metribuzin
treatment
and
developmental
and
reproductive
effects.
These
studies
were
performed
using
rats
(
Kowaski
et
al.,
1986;
Machemer,
1972)
and
rabbits
(
Unger
and
Shellenberger,
1981;
Clemens
and
Hartnagel,
1989).
In
general,
the
maternal
toxic
effects
are
accompanied
by
little
toxic
effect
to
the
fetus.
These
maternal
toxic
effects
are
characterized
by
a
reduction
in
body
weight
gain
and
food
consumption.
In
a
twogeneration
reproduction
study,
Porter
et
al.
(
1988)
reported
that
F
0
and
F
1
generations
consumed
less
food
and
gained
less
body
weight.
Necropsy
findings
in
both
the
F
0
and
F
1
generations
were
not
affected
by
metribuzin
exposure.
Also,
no
treatment­
related
effects
were
reported
in
a
3­
generation
reproduction
study
in
rats
(
Loser
and
Siegmund,
1974).

There
are
no
animal
studies
available
which
have
examined
neurotoxic
or
immunotoxic
effects
of
metribuzin.
However,
metribuzin
exposure
could
produce
some
endocrine
effects
in
vivo.
For
example,
evidence
suggests
that
metribuzin
could
elevate
plasma
thyroxine
(
T4)
levels
in
rats
(
Porter
et
al.,
1993;
Christenson
and
Wahle,
1993)
and
decrease
triiodothyronine
(
T3)
levels
in
rats
(
Christenson
and
Wahle,
1993)
and
rabbits
(
Flucke
and
Hartmann,
1989).

A
few
inhalation
studies
are
available
on
metribuzin
exposure
and
the
effects
are
comparable
to
the
existing
oral
exposure
studies.
An
increase
in
thyroid
and
liver
weights
as
well
as
liver
enzyme
activities
such
as
N­
demethylase,
O­
demethylase
and
cytochrome
P450
was
reported
in
Wistar
rats
exposed
to
metribuzin
at
720
mg/
m3
(
Thyssen,
1981).

7.4.2
Synthesis
and
Evaluation
of
Carcinogenic
Effects
There
are
no
human
studies
available
which
have
examined
the
relationship
between
exposure
to
metribuzin
and
cancer.
Metribuzin
exposure
did
not
increase
the
incidence
of
tumors
in
a
lifetime
dietary
study
using
CD­
1
mice
when
compared
to
both
concurrent
and
historic
controls
(
Hayes,
1981).
In
a
2­
year
feeding
study
utilizing
Wistar
rats,
there
were
no
significant
differences
in
neoplastic
findings
between
the
test
and
control
groups
(
Loser
and
Mohr,
1974;
Christenson
and
Wahle,
1993).
Short­
term
studies
in
bacteria
and
mammalian
systems
suggest
that
metribuzin
is
not
mutagenic.
Recent
in
vitro
studies
suggest,
however,
that
metribuzin
can
induce
adduct
formation
(
Shah
et
al.,
1997).

7.4.3
Mode
of
Action
and
Implications
in
Cancer
Assessment
The
available
evidence
from
animal
studies
suggest
that
there
is
little
data
to
support
metribuzin­
induced
carcinogenicity
and
therefore
no
studies
are
reported
which
examine
the
mode
of
action
of
metribuzin
for
cancer
effects.
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2003
7.4.4
Weight
of
Evidence
Evaluation
for
Carcinogenicity
There
are
no
studies
identified
that
examine
the
carcinogenic
effects
of
metribuzin
on
humans.
There
are
three
lifetime
studies
which
have
been
reported,
one
in
mice
and
two
in
rats,
that
examine
the
relationship
between
metribuzin
exposure
and
tumor
incidence.
Evidence
from
these
animal
studies
is
inadequate
and
therefore,
metribuzin
is
classified
as
a
class
D
carcinogen,
applying
the
criteria
described
in
the
EPA's
guidelines
for
the
assessment
of
carcinogenic
risk
(
U.
S.
EPA,
1986).

7.4.5
Sensitive
Populations
There
are
no
human
studies
available
which
examine
the
toxic
effects
of
metribuzin
and
its
effect
on
sensitive
populations.
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February
2003
8.0
DOSE­
RESPONSE
ASSESSMENT
8.1
Dose­
Response
for
Non­
Cancer
Effects
8.1.1
RfD
Determination
Choice
of
Principal
Study
The
oral
Reference
Dose
(
RfD)
is
based
on
the
assumption
that
thresholds
exist
for
certain
toxic
effects.
The
RfD
is
expressed
in
units
of
mg/
kg­
day.
In
general,
the
RfD
is
an
estimate
(
with
uncertainty
spanning
perhaps
an
order
of
magnitude)
of
a
daily
exposure
to
the
human
population
(
including
sensitive
subgroups)
that
is
likely
to
be
without
an
appreciable
risk
of
deleterious
effects
during
a
lifetime.

The
principal
study
utilized
for
RfD
derivation,
as
recommended
by
the
OPP/
HED
RfD
Committee,
was
the
chronic
study
in
rats
conducted
by
Christenson
and
Wahle
(
1993)
in
rats
described
in
section
7.2.6.
A
2­
year
feeding
study
was
conducted
in
which
Fischer
344
rats
received
0,
30,
300
or
900
ppm
(
0,
1.3,
13.8,
42.2
mg/
kg­
day
in
males;
0,
1.6,
17.7,
53.6
mg/
kgday
females)
metribuzin
(
93.0%
active
ingredient)
for
104
weeks.
At
30
ppm
(
1.3
mg/
kg­
day
for
males
and
1.6
mg/
kg­
day
for
females),
both
sexes
exhibited
increased
absolute
and
relative
thyroid
weights,
statistically
significant
increases
in
blood
levels
of
thyroxine
(
T4),
and
statistically
significant
decreases
in
blood
levels
of
triiodothyronine
(
T3).
Females
also
exhibited
decreased
lung
weight.
However,
these
effects
were
considered
to
be
of
marginal
biological
significance.
Therefore,
the
RfD
Committee
determined
that
the
30
ppm
dose
(
1.3
mg/
kg­
day
in
males)
should
be
considered
the
NOAEL.

RfD
Derivation
RfD
=
1.3
mg/
kg­
day
=
0.013
mg/
kg­
day
100
Based
on
a
chronic
exposure
study,
an
uncertainty
factor
of
100
was
used
to
account
for
inter­
species
extrapolation
(
10)
and
intra­
species
variability
(
10).

8.1.2
RfC
Determination
There
is
insufficient
data
available
from
which
to
derive
the
RfC
at
this
time.
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February
2003
8.2
Dose­
Response
for
Cancer
Effects
In
a
study
by
Hayes
(
1981),
metribuzin
was
orally
administered
via
the
diet
to
mice
(
50/
sex/
dose)
at
dose
levels
of
200,
800
or
3,200
ppm
(
30,
120
or
480
mg/
kg­
day)
for
24
months.
Following
treatment,
the
incidence
of
tumor
formation
was
analyzed
in
a
variety
of
tissues.
Neoplasms
of
various
tissues
and
organs
were
similar
in
type,
location,
time
of
occurrence,
and
incidence
in
control
and
treated
animals.
The
mice
study
is
supported
by
the
tumor
incidence
data
observed
in
2­
year
feeding
cancer
studies
in
rats
(
Loser
and
Mohr,
1974;
Christenson
and
Wahle,
1993).

Applying
the
criteria
described
in
EPA's
guidelines
for
assessment
of
carcinogenic
risk
(
U.
S.
EPA,
1986),
metribuzin
should
be
classified
in
Group
D:
not
classifiable
as
to
human
carcinogenicity.
This
category
is
used
for
substances
with
inadequate
animal
evidence
of
carcinogenicity.
9­
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February
2003
9.0
REGULATORY
DETERMINATION
AND
CHARACTERIZATION
OF
RISK
FROM
DRINKING
WATER
9.1
Regulatory
Determination
for
Chemicals
on
the
CCL
The
Safe
Drinking
Water
Act
(
SDWA),
as
amended
in
1996,
required
the
U.
S.
Environmental
Protection
Agency
(
EPA)
to
establish
a
list
of
contaminants
to
aid
the
agency
in
regulatory
priority
setting
for
the
drinking
water
program.
EPA
published
a
draft
of
the
first
Contaminant
Candidate
List
(
CCL)
on
October
6,
1997
(
62
FR
52193,
U.
S.
EPA,
1997a).
After
review
of
and
response
to
comments,
the
final
CCL
was
published
on
March
2,
1998
(
63FR
10273,
U.
S.
EPA,
1998).
The
CCL
grouped
contaminants
into
three
major
categories
as
follows:

Regulatory
Determination
Priorities
­
Chemicals
or
microbes
with
adequate
data
to
support
a
regulatory
determination.

Research
Priorities
­
Chemicals
or
microbes
requiring
research
for
health
effects,
analytical
methods,
and/
or
treatment
technologies.

Occurrence
Priorities
­
Chemicals
or
microbes
requiring
additional
data
on
occurrence
in
drinking
water.

The
March
2,
1998
CCL
included
one
microbe
and
19
chemicals
in
the
regulatory
determination
priority
category.
More
detailed
assessments
of
the
completeness
of
the
health,
treatment,
occurrence
and
analytical
method
data
led
to
a
subsequent
reduction
of
the
regulatory
determination
priority
chemicals
to
a
list
of
12
(
one
microbe
and
11
chemicals)
which
was
distributed
to
stakeholders
in
November
1999.

SDWA
requires
EPA
to
make
regulatory
determinations
for
no
fewer
than
five
contaminants
in
the
regulatory
determination
priority
category
by
August,
2001.
In
cases
where
the
Agency
determines
that
a
regulation
is
necessary,
the
Agency
has
two
years
to
propose
an
NPDWR
and
one
and
a
half
years
to
finalize
the
rule.
The
Agency
is
given
the
freedom
to
also
determine
that
there
is
no
need
for
a
regulation
if
a
chemical
on
the
CCL
fails
to
meet
the
statutory
criteria
established
by
SDWA
and
described
in
section
9.1.1.

9.1.1
Criteria
for
Regulatory
Determination
These
are
the
three
criteria
used
to
determine
whether
or
not
to
regulate
a
chemical
on
the
CCL:

The
contaminant
may
have
an
adverse
effect
on
the
health
of
persons
The
contaminant
is
known
to
occur
or
there
is
a
substantial
likelihood
that
the
contaminant
will
occur
in
public
water
systems
with
a
frequency
and
at
levels
of
public
health
concern
9­
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Metribuzin
 
February
2003
In
the
sole
judgment
of
the
administrator,
regulation
of
such
contaminant
presents
a
meaningful
opportunity
for
health
risk
reduction
for
persons
served
by
public
water
systems.

The
findings
for
all
three
criteria
are
used
in
making
a
determination
to
regulate
a
contaminant.
As
required
by
SDWA,
a
decision
to
regulate
commits
the
EPA
to
publication
of
a
Maximum
Contaminant
Level
Goal
(
MCLG)
and
promulgation
of
a
National
Primary
Drinking
Water
Regulation
(
NPDWR)
for
that
contaminant.
The
Agency
may
determine
that
there
is
no
need
for
a
regulation
when
a
contaminant
fails
to
meet
one
of
the
criteria.
A
decision
not
to
regulate
is
considered
a
final
Agency
action
and
is
subject
to
judicial
review.
The
Agency
can
choose
to
publish
a
Health
Advisory
(
a
nonregulatory
action)
or
other
guidance
for
any
contaminant
on
the
CCL,
independent
of
the
regulatory
determination.

9.1.2
National
Drinking
Water
Advisory
Council
Recommendations
In
March
2000,
the
U.
S
EPA
convened
a
Working
Group
under
the
National
Drinking
Water
Advisory
Council
(
NDWAC)
to
help
develop
an
approach
for
making
regulatory
determinations.
The
Working
Group
developed
a
protocol
for
analyzing
and
presenting
the
available
scientific
data
and
recommended
methods
to
identify
and
document
the
rationale
supporting
a
regulatory
determination
decision.
The
NDWAC
Working
Group
report
was
presented
to
and
accepted
by
the
entire
NDWAC
in
July
2000.

Because
of
the
intrinsic
difference
between
microbial
and
chemical
contaminants,
the
Working
Group
developed
separate
but
similar
protocols
for
microorganisms
and
chemicals.
The
approach
for
chemicals
was
based
on
an
assessment
of
the
impact
of
acute,
chronic,
and
lifetime
exposures,
as
well
as
a
risk
assessment
that
includes
evaluation
of
occurrence,
fate,
and
dose­
response.
The
NDWAC
Protocol
for
chemicals
is
a
semi­
quantitative
tool
for
addressing
each
of
the
three
CCL
criteria.
The
NDWAC
requested
that
the
Agency
use
good
judgement
in
balancing
the
many
factors
that
need
to
be
considered
in
making
a
regulatory
determination.
The
U.
S.
EPA
modified
the
semi­
quantitative
NDWAC
suggestions
for
evaluating
chemicals
against
the
regulatory
determination
criteria
and
applied
them
in
decision
making.
The
quantitative
and
qualitative
factors
for
metribuzin
that
were
considered
for
each
of
the
three
criteria
are
presented
in
the
sections
that
follow.

9.2
Health
Effects
The
first
criterion
asks
if
the
contaminant
may
have
an
adverse
effect
on
the
health
of
persons.
Because
all
chemicals
have
adverse
effects
at
some
level
of
exposure,
the
challenge
is
to
define
the
dose
at
which
adverse
health
effects
are
likely
to
occur,
and
to
estimate
a
dose
at
which
adverse
health
effects
are
either
not
likely
to
occur
(
threshold
toxicant),
or
have
a
low
probability
for
occurrence
(
non­
threshold
toxicant).
The
key
elements
that
must
be
considered
in
evaluating
the
first
criterion
are
the
mode
of
action,
the
critical
effect(
s),
the
dose­
response
for
critical
effect(
s),
the
RfD
for
threshold
effects,
and
the
slope
factor
for
non­
threshold
effects.
9­
3
Metribuzin
 
February
2003
A
full
description
of
the
health
effects
associated
with
exposure
to
metribuzin
is
presented
in
Chapter
7
of
this
document
and
summarized
below
in
Section
9.2.2.
Chapter
8
and
Section
9.2.3
present
dose­
response
information.

9.2.1
Health
Criterion
Conclusion
Although
there
are
no
studies
reporting
the
adverse
effects
of
metribuzin
on
human
health,
animal
studies
indicate
that
metribuzin
has
the
potential
to
cause
adverse
health
effects
at
high
doses.
Exposure
to
metribuzin
may
occur
primarily
in
an
occupational
setting,
particularly
in
the
agriculture
industry
where
it
is
used
as
an
herbicide.
The
RfD
of
0.013
mg/
kg­
day
was
derived
from
a
study
reporting
the
adverse
health
effects
of
metribuzin
in
rats.

9.2.2
Hazard
Characterization
and
Mode
of
Action
Implications
There
are
no
epidemiology
studies
that
have
assessed
adverse
human
health
effects
caused
by
exposure
to
metribuzin.
Acute
toxicity
animal
studies
indicate
that
metribuzin
induces
low
toxicity
as
evidenced
by
the
relatively
high
LD
50
values
(
Kimmerle
et
al.,
1969;
Morgan,
1982;
Hartley
and
Kidd,
1987).
In
addition,
metribuzin
has
not
been
found
to
cause
eye
irritation
in
rabbits,
and
causes
only
slight
dermal
irritation
in
rabbits
(
Kimmerle
et
al.,
1969).

Subchronic
studies
in
animals
suggest
that
metribuzin
may
cause
adverse
effects
on
body
weight
gain,
organ
weight
and
hematological
parameters.
Wistar
rats
exposed
to
metribuzin
in
the
diet
at
1500
ppm
for
three
months
exhibited
a
significant
reduction
in
body
weight
gain,
and
increased
liver
and
thyroid
weights
(
Loser
et
al.,
1969).
However
a
3­
month
dietary
exposure
in
Beagle
dogs
did
not
affect
body
weight
gain
or
food
consumption,
and
only
altered
clinical
parameters
such
as
SGOT
and
SGPT
levels
(
Chaisson
and
Cueto,
1970).

Chronic
studies
of
metribuzin
report
effects
on
body
weight
gain,
mortality,
liver
enzyme
activities
and
histopathological
changes.
Two­
year
feeding
studies
conducted
in
rats
(
0,
25,
35,
100
or
300
ppm)
and
mice
(
0,
200,
800
or
3200
ppm)
indicated
no
significant
differences
in
body
weight
gain,
food
consumption,
or
mortality
(
Loser
and
Mohr,
1974;
Hayes,
1981).
Another
two­
year
feeding
study
in
rats
using
a
higher
dose
(
900
ppm)
of
metribuzin
did
report
a
decrease
in
body
weight
gain
(
Christenson
and
Wahle,
1993).
This
study
also
reported
histopathological
changes
such
as
significant
increases
in
corneal
neovascularization,
discolored
zones
in
the
liver,
an
enlarged
abdomen,
enlarged
adrenal
and
thyroid
glands,
ocular
opacity,
an
enlarged
epididymal
mass
in
males,
and
the
presence
of
ovarian
cysts
in
female
rats
(
Christenson
and
Wahle,
1993).
In
Beagle
dogs,
chronic
exposure
to
the
highest
dose
of
1,500
ppm
caused
a
significant
increase
in
the
mortality
rate
and
liver
dysfunction
as
evidenced
by
increases
in
the
activity
of
liver
enzymes
such
as
SGOT,
SGPT
and
OCT
(
Loser
and
Mirea,
1974).
Thyroid
weight
was
also
increased
in
the
highest
dose
group.
Histopathologic
findings
included
liver
and
kidney
damage
at
the
highest
dose.
The
liver
and
kidney
effects,
decreased
body
weight
gain,
and
mortality
at
the
highest
dose
are
considered
the
critical
effects
of
metribuzin
exposure.
9­
4
Metribuzin
 
February
2003
There
are
few
studies
that
have
assessed
the
developmental
and
reproductive
effects
of
metribuzin
exposure.
In
general,
maternal
toxicity
effects
observed
in
rats
and
rabbits
include
reduced
body
weight
gain
and
food
consumption,
and
are
accompanied
by
slight
toxicity
to
the
fetus
(
Kowaski
et
al.,
1986;
Machemer,
1972;
Unger
and
Shellenberger,
1981;
Clemens
and
Hartnagel,
1989).
A
two­
generation
study
in
rats
reported
that
both
F
0
and
F
1
generations
consumed
less
food
and
gained
less
body
weight
(
Porter
et
al.,
1988).
Necropsy
findings
in
both
generations
were
not
affected
by
exposure
to
metribuzin.
Another
3­
generation
reproduction
study
in
rats
found
no
treatment­
related
effects
(
Loser
and
Siegmund,
1974).

No
animal
studies
have
addressed
the
neurologic
or
immunotoxic
effects
of
metribuzin.
There
is
evidence
of
endocrine
effects
induced
by
metribuzin,
including
elevated
plasma
thyroxine
levels
in
rats
and
decreased
triiodothyronine
levels
in
rats
and
rabbits
(
Porter
et
al.
1993;
Christenson
and
Wahle,
1993;
Flucke
and
Hartmann,
1989).

The
EPA
has
classified
metribuzin
as
a
class
D
carcinogen
due
to
inadequate
carcinogenicity
data
in
humans
and
animals.
A
lifetime
dietary
study
in
CD­
1
mice
and
2­
year
feeding
studies
in
Wistar
rats
were
negative
for
the
induction
of
tumors
compared
to
control
incidences
(
Hayes,
1981;
Loser
and
Mohr,
1974;
Christenson
and
Wahle,
1993).

9.2.3
Dose­
Response
Characterization
and
Implications
in
Risk
Assessment
The
principal
study
utilized
for
RfD
derivation,
as
recommended
by
the
OPP/
HED
RfD
Committee,
was
the
chronic
study
in
rats
conducted
by
Christenson
and
Wahle
(
1993)
in
rats
described
in
section
7.2.6.
A
2­
year
feeding
study
was
conducted
in
which
Fischer
344
rats
received
0,
30,
300
or
900
ppm
(
0,
1.3,
13.8,
42.2
mg/
kg­
day
in
males;
0,
1.6,
17.7,
53.6
mg/
kgday
females)
metribuzin
(
93.0%
active
ingredient)
for
104
weeks.
At
30
ppm
(
1.3
mg/
kg­
day
for
males
and
1.6
mg/
kg­
day
for
females),
both
sexes
exhibited
increased
absolute
and
relative
thyroid
weights,
statistically
significant
increases
in
blood
levels
of
thyroxine
(
T4),
and
statistically
significant
decreases
in
blood
levels
of
triiodothyronine
(
T3).
Females
also
exhibited
decreased
lung
weight.
However,
these
effects
were
considered
to
be
of
marginal
biological
significance.
Therefore,
the
RfD
Committee
determined
that
the
30
ppm
dose
(
1.3
mg/
kg­
day
in
males)
should
be
considered
the
NOAEL.
The
RfD
of
0.013
mg/
kg­
day
was
derived
by
dividing
the
NOAEL
by
an
uncertainty
factor
of
100,
which
was
used
to
account
for
inter­
and
intraspecies
variability.

9.3
Occurrence
in
Public
Water
Systems
The
second
criterion
asks
if
the
contaminant
is
known
to
occur
or
if
there
is
a
substantial
likelihood
that
the
contaminant
will
occur
in
public
water
systems
with
a
frequency
and
at
levels
of
public
health
concern.
In
order
to
address
this
question,
the
following
information
was
considered:
9­
5
Metribuzin
 
February
2003
°
Monitoring
data
from
public
water
systems
°
Ambient
water
concentrations
and
releases
to
the
environment
°
Environmental
Fate
Data
on
the
occurrence
of
metribuzin
in
public
drinking
water
systems
were
the
most
important
determinants
in
evaluating
the
second
criterion.
EPA
looked
at
the
total
number
of
systems
that
reported
detections
of
metribuzin,
as
well
as
those
that
reported
concentrations
of
metribuzin
above
an
estimated
drinking
water
health
reference
level
(
HRL).
For
noncarcinogens
the
estimated
HRL
risk
level
was
calculated
from
the
RfD
assuming
that
20%
of
the
total
exposure
would
come
from
drinking
water.
For
carcinogens,
the
HRL
was
the
10­
6
risk
level.
The
HRLs
are
benchmark
values
that
were
used
in
evaluating
the
occurrence
data
while
the
risk
assessments
for
the
contaminants
were
being
developed.

The
available
monitoring
data,
including
indications
of
whether
or
not
the
contamination
is
a
national
or
a
regional
problem,
are
included
in
Chapter
4
of
this
document
and
are
summarized
below.
Additional
information
on
production,
use,
and
environmental
fate
are
found
in
Chapters
2
and
3.

9.3.1
Occurrence
Criterion
Conclusion
The
available
data
on
metribuzin
production
and
use
indicate
a
modestly
declining
trend.
Although
detection
of
metribuzin
is
found
in
both
surface
and
ground
waters
of
urban
and
agricultural
regions,
concentrations
are
extremely
low
and
well
below
the
HRL
or
half
the
HRL.
In
regards
to
drinking
water,
metribuzin
detection
frequencies
and
concentrations
are
extremely
low
to
undetectable,
with
the
exception
of
detections
in
Pennsylvania,
Indiana,
Illinois
and
Washington.
These
data
indicate
that
although
metribuzin
is
found
in
ambient
waters,
little
to
no
metribuzin
is
detected
in
drinking
water
systems.

9.3.2
Monitoring
Data
Drinking
Water
A
national
cross­
section
of
20
states
reported
metribuzin
detection
data
in
the
SDWIS/
FED
database.
This
cross­
section
provides
a
good
representation
of
the
nation's
varied
climatic
and
hydrogeologic
regions,
and
the
breadth
of
pollution
potential.
In
addition,
occurrence
data
is
presented
from
all
the
states
participating
under
the
Unregulated
Contaminant
Monitoring
(
UCM)
program
begun
in
1991.
Metribuzin
was
not
included
in
this
program
until
Round
2,
which
began
in
1993.

In
the
cross­
section
of
20
states,
approximately
0.007%
of
Public
Water
Systems
(
PWS)
reported
detections
of
metribuzin
above
the
minimum
reporting
level
(
MRL),
affecting
about
0.0003%
of
the
population.
Only
the
state
of
Washington
reported
a
metribuzin
detection
above
the
MRL,
at
a
level
of
0.10
:
g/
L,
which
is
far
below
the
Health
Reference
Level
(
HRL)
of
91
9­
6
Metribuzin
 
February
2003
:
g/
L.
A
national
extrapolation
of
this
data
indicates
that
approximately
5
PWSs
would
experience
detections
of
metribuzin
above
the
MRL,
and
that
approximately
1,000
people
would
be
affected.
When
all
the
states
participating
in
Round
2
of
the
UCM
program
were
considered,
0.28%
of
PWSs
experienced
detections
above
the
MRL.
This
indicates
that
approximately
1.61%
of
the
population,
or
3.4
million
people
nationally,
is
affected
by
concentrations
of
metribuzin
above
the
MRL.
No
PWSs
experienced
detections
>
½
HRL
or
>
HRL.
Therefore,
0%
of
the
population
is
affected
by
metribuzin
concentrations
>
½
HRL
or
>
HRL.
The
median
and
99th
percentile
concentrations
of
detections
are
1.0
µ
g/
L
and
3
µ
g/
L,
respectively.

Ambient
Water
The
USGS
began
the
National
Ambient
Water
Quality
Assessment
(
NAWQA)
program
in
1991
to
monitor
water
quality
status
and
trends
in
the
U.
S.
This
program
consists
of
59
watersheds
and
aquifers
referred
to
as
"
study
units"
and
represents
approximately
two­
thirds
of
the
overall
water
usage
and
a
similar
proportion
of
the
population
served
by
public
water
systems.
The
Method
Detection
Limit
(
MDL)
for
metribuzin
is
0.004
:
g/
L.

Detection
frequencies
and
concentrations
of
metribuzin
in
ambient
surface
and
ground
waters
are
low.
Surface
waters
exhibited
the
highest
maximum
concentration
of
metribuzin
at
0.530
:
g/
L,
with
a
reported
frequency
of
13.82%
of
samples
with
concentrations
greater
than
the
MDL.
Although
the
occurrence
in
ground
water
is
lower
than
in
surface
water,
detection
in
1.95%
of
ground
water
samples
at
a
maximum
concentration
of
0.300
:
g/
L
make
metribuzin
one
of
the
21
most
commonly
detected
pesticides
in
intensive
NAWQA
monitoring.
In
both
surface
and
ground
waters,
metribuzin
was
more
frequently
detected
in
agricultural
regions
as
compared
to
urban
areas.

9.3.3
Use
and
Fate
Data
Metribuzin,
a
synthetic
organic
compound,
is
a
selective
triazinone
herbicide
used
to
discourage
growth
of
broadleaf
weeds
and
annual
grasses
among
vegetable
crops
and
turf
grass.
Using
data
from
the
USDA
and
NCFAP,
the
EPA
estimates
that
the
average
annual
use
for
the
years
1990­
94
at
2.8
million
pounds
of
active
ingredient
with
8.5
million
acres
treated.
The
USGS
estimates
that
2.7
million
pounds
of
metribuzin
treating
8.4
million
acres
were
used
in
1992.
The
non­
agricultural
use
of
metribuzin
is
minimal.
Table
3­
1
of
Chapter
3
indicates
a
modest
decline
of
metribuzin
use
from
1990­
1999.

Data
from
the
Toxic
Release
Inventory
(
TRI)
indicate
a
general
decline
in
environmental
releases
of
metribuzin
between
1995
and
1998
(
Table
3­
2).
Air
emissions
are
reported
to
have
declined
although
surface
water
discharges
have
increased.

Metribuzin
is
a
solid
at
ambient
temperatures
and
has
a
low
vapor
pressure.
Therefore,
it
is
unlikely
to
readily
partition
to
air.
Since
metribuzin
is
not
labeled
for
residential
use,
it
is
not
anticipated
to
be
found
in
residential
soils.
The
Organic
Carbon
Partition
Coefficient
(
K
oc)
is
95,
9­
7
Metribuzin
 
February
2003
and
indicates
that
metribuzin
is
highly
mobile
in
soil.
It
is
also
moderately
adsorbed
on
soils
with
high
clay
or
organic
content
and
leaches
more
readily
from
sandy
soils.
In
soil,
biodegradation
is
the
primary
fate
process
(
HSDB,
2000).
In
the
aquatic
environment,
volatilization
from
water
and
bioconcentration
in
fish
are
not
anticipated
to
be
relevant
(
HSDB,
2000).
No
data
are
available
for
the
biodegradation
of
metribuzin
in
water.

9.4
Risk
Reduction
The
third
criterion
asks
if,
in
the
sole
judgement
of
the
Administrator,
regulation
presents
a
meaningful
opportunity
for
health
risk
reduction
for
persons
served
by
public
water
systems.
In
evaluating
this
criterion,
EPA
looked
at
the
total
exposed
population,
as
well
as
the
population
exposed
above
the
estimated
HRL.
Estimates
of
the
populations
exposed
and
the
levels
to
which
they
were
exposed
were
derived
from
the
monitoring
results.
These
estimates
are
included
in
Chapter
4
of
this
document
and
summarized
in
Section
9.4.2
below.

In
order
to
evaluate
risk
from
exposure
through
drinking
water,
EPA
considered
the
net
environmental
exposure
in
comparison
to
the
exposure
through
drinking
water.
For
example,
if
exposure
to
a
contaminant
occurs
primarily
through
ambient
air,
regulation
of
emissions
to
air
provides
a
more
meaningful
opportunity
for
EPA
to
reduce
risk
than
regulation
of
the
contaminant
in
drinking
water.
In
making
the
regulatory
determination,
the
available
information
on
exposure
through
drinking
water
(
Chapter
4)
and
information
on
exposure
through
other
media
(
Chapter
5)
were
used
to
estimate
the
fraction
that
drinking
water
contributes
to
the
total
exposure.
The
EPA
also
evaluated
effects
on
potentially
sensitive
populations,
including
fetuses,
infants
and
children.
The
sensitive
population
considerations
are
included
in
Section
9.4.4.

9.4.1
Risk
Criterion
Conclusion
Based
on
the
data
from
the
cross­
section
analysis
of
20
states,
metribuzin
exposure
from
drinking
water
would
be
very
low
with
only
1,000
people
exposed
nationally.
When
all
the
Round
2
data
are
considered,
including
data
from
the
state
of
Pennsylvania,
approximately
3.4
million
people
nationally
are
exposed
to
any
concentration
of
metribuzin.
Aside
from
the
potential
of
occupational
exposure,
no
other
source
of
exposure
would
lead
to
significant
doses
of
metribuzin.
These
observations
indicate
that
regulation
of
metribuzin
in
drinking
water
would
have
little
impact
on
human
risk
reduction.

9.4.2
Exposed
Population
Estimates
As
described
in
9.3.1,
a
cross­
section
survey
of
20
states
reported
that
0.007%
of
Public
Water
Systems
had
detections
of
metribuzin
above
the
minimum
reporting
level
(
MRL),
affecting
less
than
0.0003%
of
the
population.
A
national
extrapolation
of
this
data
indicates
that
approximately
1,000
people
would
be
exposed
to
metribuzin
through
the
drinking
water.
Of
the
20
states
in
this
cross­
section
survey,
only
the
state
of
Washington
reported
a
detection
of
metribuzin.
Since
Washington
is
the
only
state
to
report
a
metribuzin
detection
at
0.10
:
g/
L,
this
value
is
both
the
median
and
99th
percentile
concentrations.
9­
8
Metribuzin
 
February
2003
However,
when
all
of
the
participating
states
in
Round
2
of
the
UCM
program
were
considered,
0.28%
of
PWSs
reported
detections
above
the
MRL.
National
extrapolation
of
this
data
indicates
that
approximately
1.6%
of
the
population,
or
3.4
million
people,
are
exposed
to
concentrations
above
the
MRL.

9.4.3
Relative
Source
Contribution
Relative
source
contribution
analysis
compared
the
magnitude
of
exposure
to
metribuzin
expected
via
drinking
water
and
the
magnitude
of
exposure
from
other
media,
such
as
food,
air
and
soil.
The
intake
of
metribuzin
from
drinking
water
can
be
calculated
from
the
median
concentrations
described
above
for
both
the
cross­
section
study
and
the
study
of
all
the
Round
2
states.
Using
the
median
metribuzin
level
from
the
20
state
cross­
section
study
of
0.10
:
g/
L,
an
average
daily
intake
of
2
L/
day
for
an
adult,
and
an
average
weight
of
70
kg
for
an
adult,
the
corresponding
dose
would
be
2.8
×
10­
3
mg/
kg­
day
for
adults.
For
children,
assuming
an
intake
of
1
L/
day
and
an
average
weight
of
10
kg,
the
dose
would
be
1.0
×
10­
2
mg/
kg­
day.

As
part
of
the
FDA's
Regulatory
Monitoring
Program,
9,438
domestic
and
imported
food
samples
were
analyzed
for
pesticides,
including
metribuzin.
Metribuzin
was
not
detected
in
any
samples
of
grains,
milk
products,
fruits
or
vegetables.
In
addition,
no
detections
were
found
in
218
domestic
and
298
imported
fish
and
shellfish
samples.
The
daily
intake
of
metribuzin
from
food
is
anticipated
to
be
close
to
zero.

No
data
are
available
for
the
ambient
levels
of
metribuzin
in
air.
However,
metribuzin
is
a
solid
at
ambient
temperatures
and
has
a
low
vapor
pressure;
partitioning
of
metribuzin
into
air
is
highly
unlikely.
Therefore,
the
average
daily
intake
for
the
general
population
is
anticipated
to
be
close
to
zero.
However,
inhalation
of
metribuzin
may
be
potentially
significant
for
occupational
exposure.
The
occupational
subgroup
may
include
workers
involved
in
the
mixing,
loading,
handling
and
application
of
metribuzin.
The
EPA
has
estimated
that
inhalation
exposures
of
this
subgroup
range
from
0.006
to
91.14
mg/
day.
Calculations
of
doses
based
on
this
range
of
exposure
and
70
kg
body
weight
are
8.6
×
10­
5
to
1.3
mg/
kg­
day.

Metribuzin
is
not
labeled
for
residential
use
and
so
it
is
not
anticipated
to
be
found
in
residential
soils.
General
population
exposures
are
anticipated
to
be
close
to
zero.
In
agricultural
regions
where
metribuzin
is
applied,
metribuzin
may
be
found
in
soils
in
concentrations
as
high
as
0.78
mg/
kg.
Based
on
an
average
body
weight
of
70
kg
and
a
daily
soil
intake
of
480
mg/
day,
the
maximum
daily
intake
for
a
contact
intensive
worker
would
be
5.3
×
10­
3
mg/
kg­
day,
which
is
below
the
RfD.

For
estimating
the
HRL
from
the
RfD,
the
default
value
of
20%
was
used
for
the
relative
source
contribution
assuming
that
the
total
exposure
to
metribuzin
is
not
from
drinking
water.

9.4.4
Sensitive
Populations
No
sensitive
populations
to
metribuzin
have
been
identified.
9­
9
Metribuzin
 
February
2003
9.5
Regulatory
Determination
Summary
Although
there
is
evidence
from
animal
studies
that
metribuzin
may
cause
adverse
health
effects
at
high
doses,
its
occurrence
in
public
water
systems
and
the
numbers
of
people
potentially
exposed
through
drinking
water
are
low.
In
addition,
there
are
no
available
studies,
either
epidemiological
or
case­
studies
of
accidentally
exposed
agricultural
workers,
assessing
adverse
health
effects
in
humans
due
to
metribuzin.
Overall,
metribuzin
is
not
anticipated
to
cause
adverse
health
effects
in
humans
at
the
concentrations
detected
in
public
water
systems
and
is
unlikely
to
expose
a
large
number
of
people
outside
of
an
occupational
setting.
For
these
reasons,
EPA
may
not
propose
to
regulate
metribuzin
with
NPDWR.
All
final
determinations
and
future
analysis
will
be
presented
in
the
Federal
Register
Notice
covering
CCL
proposals.
10­
1
Metribuzin
 
February
2003
10.0
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February
2003
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*
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A­
1
Metribuzin
 
February
2003
APPENDIX
A:
Abbreviations
and
Acronyms
AA
­
Atomic
Absorption
ACGIH
­
American
Conference
of
Governmental
Industrial
Hygienists
a.
i.
­
active
ingredient
ANPRM
­
Advanced
Notice
of
Proposed
Rule­
Making
APHA
­
American
Public
Health
Association
ARMS
­
Agricultural
Resources
Management
Study
ATSDR
­
Agency
for
Toxic
Substances
and
Disease
Registry
CA
­
Census
of
Agriculture
CAS
­
Chemical
Abstract
Service
CASRN
­
Chemical
Abstract
Service
Registry
Number
CCL
­
Contaminant
Candidate
List
CEC
­
cation
exchange
capacity
CERCLA
­
Comprehensive
Environmental
Response,
Compensation
&
Liability
Act
CMR
­
Chemical
Monitoring
Reform
CPS
­
Cropping
Practices
Survey
CWS
­
Community
Water
System
DBCP
­
dibromochloropropane
DCIs
­
Data
Call­
Ins
DEA
­
deethyl­
atrazine
DWEL
­
Drinking
Water
Equivalent
Level
ECD
­
Electron
Capture
Detectors
EDB
­
ethylene
dibromide
EDL
­
Estimated
Detection
Limit
Eh
­
oxidation­
reduction
potential
EHS
­
Extremely
Hazardous
Substance
EPA
­
Environmental
Protection
Agency
EPCRA
­
Emergency
Planning
and
Community
Right­
to­
Know
Act
ESA
­
ethanesulfonic
acid
FCRS
­
Farm
Costs
and
Returns
Survey
FDA
­
Food
and
Drug
Administration
FIFRA
­
Federal
Insecticide,
Fungicide,
and
Rodenticide
Act
FQPA
­
Food
Quality
Protection
Act
GAC
­
granular
activated
carbon
(
treatment
technology
for
organic
compounds)
GC
­
gas
chromatography
(
a
laboratory
method)
GW
­
ground
water
A­
2
Metribuzin
 
February
2003
GWP
­
ground
water
­
purchased
GUDI
­
Ground
Water
Under
the
Direct
Influence
(
of
surface
water)
GUP
­
Ground
Water
Under
Direct
Influence
­
Purchased
HA
­
Health
Advisory
HAL
­
Health
Advisory
Level
HRL
­
Health
Reference
Level
IDL
­
Instrument
Detection
Level
IGWM
­
Iowa
Ground
Water
Monitoring
Program
IOC
­
inorganic
compound
IRIS
­
Integrated
Risk
Information
System
MCL
­
Maximum
Contaminant
Level
MDL
­
Method
Detection
Limit
MMT
­
methylcyclopentadienyl
manganese
tricarbonyl
MRL
­
Minimum
Reporting
Level
MS
­
mass
spectrometry
(
a
laboratory
method)

NAWQA
­
National
Water
Quality
Assessment
Program
NCFAP
­
National
Center
for
Food
and
Agricultural
Policy
NCOD
­
National
Drinking
Water
Contaminant
Occurrence
Database
NDWAC
­
National
Drinking
Water
Advisory
Council
NERL
­
National
Environmental
Research
Laboratory
NIOSH
­
National
Institute
for
Occupational
Safety
and
Health
NPD
­
nitrogen/
phosphorus
detector
NPDES
­
National
Pollution
Discharge
Elimination
System
NPDWR
­
National
Primary
Drinking
Water
Regulation
NPS
­
National
Pesticide
Survey
NRMRL
­
National
Risk
Management
Research
Laboratory
NTIS
­
National
Technical
Information
Service
NTNCWS
­
Non­
Transient
Non­
Community
Water
System
NTTAA
­
National
Technology
Transfer
and
Advancement
Act
OA
­
oxanilic
acid
OCT
­
ornithine­
carbamyl
transferase
OGWDW
­
Office
of
Ground
Water
and
Drinking
Water
OMB
­
Office
of
Management
and
Budget
ORD
­
Office
of
Research
and
Development
OSHA
­
Occupational
Safety
and
Health
Administration
PAH
­
polycyclic
aromatic
hydrocarbon
PB
­
particle
beam
PBMS
­
performance­
based
measurement
system
A­
3
Metribuzin
 
February
2003
PCE
­
tetrachloroethylene
PEL
­
permissible
exposure
limit
PGWD
­
Pesticides
in
Ground
Water
Database
ppm
­
part
per
million
PWS
­
Public
Water
System
PWSF
­
Public
Water
System
Facility
PWSID
­
Public
Water
System
Identifier
QA
­
quality
assurance
QC
­
quality
control
RCRA
­
Resource
Conservation
and
Recovery
Act
RFA
­
Regulatory
Flexibility
Act
RFF
­
Resources
for
the
Future
RO
­
reverse
osmosis
RPD
­
relative
percent
difference
RSD
­
relative
standard
deviation
SARA
Title
III
­
Superfund
Amendments
and
Reauthorization
Act
SBREFA
­
Small
Business
Regulatory
Enforcement
Fairness
Act
SD
­
standard
deviation
SDWA
­
Safe
Drinking
Water
Act
SDWIS
­
Safe
Drinking
Water
Information
System
SDWIS
FED
­
the
Federal
Safe
Drinking
Water
Information
System
SGOT
­
serum
glutamate­
oxaloacetate
transaminase
SGPT
­
serum
glutamate­
pyruvate
transaminase
SM
­
standard
methods
SMCL
­
Secondary
Maximum
Contaminant
Level
SMF
­
Standard
Compliance
Monitoring
Framework
SOC
­
synthetic
organic
compound
SPE
­
solid
phase
extraction
(
a
laboratory
method)
SRF
­
State
Revolving
Fund
STORET
­
Storage
and
Retrieval
System
SW
­
surface
water
SWP
­
surface
water
­
purchased
TBD
­
to
be
determined
TCE
­
trichloroethylene
TDS
­
total
dissolved
solids
THM
­
trihalomethane
TNCWS
­
Transient
Non­
Community
Water
System
TPQ
­
Threshold
Planning
Quantity
TRI
­
Toxic
Release
Inventory
A­
4
Metribuzin
 
February
2003
UCM
­
Unregulated
Contaminant
Monitoring
UCMR
­
Unregulated
Contaminant
Monitoring
Regulation/
Rule
UMRA
­
Unfunded
Mandates
Reform
Act
of
1995
URCIS
­
Unregulated
Contaminant
Monitoring
Information
System
USDA
­
United
States
Department
of
Agriculture
U.
S.
EPA
­
United
States
Environmental
Protection
Agency
USGS
­
United
States
Geological
Survey
VOC
­
volatile
organic
compound
µ
g/
L
­
micrograms
per
liter
mg/
L
­
milligrams
per
liter
>
MCL
­
percentage
of
systems
with
exceedances
>
MRL
­
percentage
of
systems
with
detections
B­
1
Metribuzin
 
February
2003
APPENDIX
B:
Round
2
Metribuzin
Occurrence
Metribuzin
Occurrence
in
Public
Water
Systems
in
Round
2,
UCM
(
1993)
results
State
Total
Unique
PWS
#
GW
PWS
#
SW
PWS
%
PWS
>
MRL
%
GW
PWS
>
MRL
%
SW
PWS
>
MRL
%
PWS
>
HRL
%
GW
PWS
>
HRL
%
SW
PWS
>
HRL
99%
Value
(:
g/
L)

Tribes
(
06)
1
1
0
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
AK
20
17
3
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
AL
AR
536
431
105
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
AZ
CA
CO
750
538
212
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
CT
69
35
34
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
IN
KY
418
204
214
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
10.00
LA
MA
56
29
27
14.29%
13.79%
14.81%
0.00%
0.00%
0.00%
2.00
MD
684
627
57
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.30
ME
M
I
2,650
2,570
80
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
M
N
1,264
1,234
30
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
M
O
638
437
101
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.60
MS
NC
623
567
56
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
ND
296
258
38
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.02
NH
557
524
33
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
NJ
NM
715
686
29
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.60
OH
2,178
2,017
161
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
2.00
OK
107
82
25
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
OR
1,135
984
151
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
PA
358
231
127
9.50%
5.63%
16.54%
0.00%
0.00%
0.00%
3.00
RI
15
6
9
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.53
Appendix
B
(
continued)

State
Total
Unique
PWS
#
GW
PWS
#
SW
PWS
%
PWS
>
MRL
%
GW
PWS
>
MRL
%
SW
PWS
>
MRL
%
PWS
>
HRL
%
GW
PWS
>
HRL
%
SW
PWS
>
HRL
99%
Value
(:
g/
L)

B­
2
Metribuzin
 
February
2003
SC
940
842
98
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
SD
TN
7
2
5
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
TX
426
121
305
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.20
VT
390
338
52
0.00%
0.00%
0.00%
0.00%
0.00%
0.00%
<
0.00
WA
600
530
70
0.17%
0.19%
0.00%
0.00%
0.00%
0.00%
<
0.00
WI
Total
15,333
13,311
2,022
0.28%
0.14%
1.24%
0.00%
0.00%
0.00%
<
2.00
20
States
13,568
11,862
1,706
0.07%
0.04%
0.23%
0.00%
0.00%
0.00%
<
2.00
19
States
13,512
11,833
1,697
0.01%
0.01%
0.00%
0.00%
0.00%
0.00%
<
2.00
1.
Massachusetts
data
not
included
in
"
19
States"
summary
for
metribuzin.
PWS
=
Public
Water
System;
GW
=
Ground
Water
(
PWS
Source
Water
Type);
SW
=
Surface
Water
(
PWS
Source
Water
Type);
MRL
=
Minimum
Reporting
Limit
(
for
laboratory
analyses)
The
Health
Reference
Level
(
HRL)
is
the
estimated
health
effect
level
as
provided
by
EPA
for
preliminary
assessment
for
this
work
assignment.
"%
>
HRL"
indicates
the
proportion
of
systems
with
any
analytical
results
exceeding
the
concentration
value
of
the
HRL.
The
Health
Reference
Level
(
HRL)
used
for
Metribuzin
is
91
:
g/
L.
This
is
a
draft
value
for
working
review
only.
The
highlighted
States
are
part
of
the
SDWI/
FED
20
State
Cross­
Section.