NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

1
May
5,
2003
Public
Information
and
Records
Integrity
Branch
Information
Resources
and
Services
Division
(
7502C),
Office
of
Pesticide
Programs
Environmental
Protection
Agency,
1200
Pennsylvania
Avenue,
N.
W.
Washington,
DC
20460­
0001
Submitted
by
Email
to
opp­
docket@
epa.
gov
Attn:
Docket
#
OPP­
2003­
0072
Atrazine
IRED,
68
Fed.
Reg.
9652
(
Feb.
28,
2003)

On
behalf
of
the
Natural
Resources
Defense
Council
(
NRDC),
we
submit
these
comments
on
the
Environmental
Protection
Agency's
(
EPA)
Interim
Reregistration
Eligibility
Decision
(
IRED)
for
Atrazine
(
Jan.
31,
2003).
These
comments
supplement
our
prior
filings
regarding
this
chemical,
and
our
prior
comments
on
the
atrazine
human
health
and
ecological
risk
assessments.
NRDC
reiterates
its
previous
comments
urging
EPA
to
cancel
atrazine's
registration
and
revoke
all
atrazine
tolerances.

NRDC
uses
law,
science,
and
the
support
of
more
than
500,000
members
nationwide
to
protect
the
planet's
wildlife
and
wild
places
and
to
ensure
a
safe
and
healthy
environment
for
all
living
things.
NRDC
has
no
direct
or
indirect
financial
or
fiduciary
interest
in
the
manufacture
or
sale
of
atrazine
or
any
other
pesticide
or
chemical.

SUMMARY
The
following
concerns
are
discussed
in
detail
in
these
comments:

I.
The
atrazine
IRED
inappropriately
permits
excessively
high
drinking
water
contamination,
drinking
water
clean­
up
costs
are
passed
to
the
consumer,
and
wildlife
is
unprotected.

II.
EPA
has
violated
its
special
review
regulations,
FIFRA,
the
Federal
Advisory
Committee
Act,
the
Administrative
Procedure
Act,
and
the
Agency's
September
1984
settlement
with
NRDC,
by
meeting
repeatedly
and
privately
with
atrazine's
registrant
and
cutting
a
special
private
deal
with
the
registrant
that
is
contrary
to
the
public
interest.

III.
EPA's
atrazine
decision
allows
and
even
encourages
violations
of
the
safe
drinking
water
act
(
SDWA),
and
thus
contravenes
the
FFDCA
and
FIFRA
as
well.

IV.
EPA's
NOAEL
is
unjustified
because
it
is
a
level
at
which
adverse
effects
were
observed.
Moreover,
Congress
required
EPA
to
regulate
based
on
NOELs
not
NOAELs.

V.
Agriculture
and
lawn
care
risks
are
unacceptably
high,
and
EPA's
proposed
mitigation
is
insufficient.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

2
VI.
Ecological
risks
are
unacceptably
high,
and
no
effective
mitigation
is
proposed.

VII.
The
ongoing
registration
of
atrazine
jeopardizes
endangered
species
and
their
critical
habitat.

VIII.
Atrazine
has
been
associated
with
an
increased
risk
of
cancer
in
several
studies.

IX.
Substantial
data
demonstrate
that
atrazine
is
an
endocrine
disruptor.

X.
Conclusion.

DETAILED
COMMENTS
I.
THE
ATRAZINE
IRED
INAPPROPRIATELY
PERMITS
EXCESSIVELY
HIGH
DRINKING
WATER
CONTAMINATION.
DRINKING
WATER
CLEAN­
UP
COSTS
ARE
PASSED
TO
THE
CONSUMER.
WILDLIFE
IS
UNPROTECTED
Most
dietary
atrazine
exposure
occurs
through
drinking
water,
with
almost
none
from
food.
Therefore,
the
drinking
water
level
of
comparison
(
DWLOC)
represents
essentially
the
amount
of
atrazine
that
EPA
believes
is
safe
to
consume.
When
model
or
monitoring
data
exceed
the
atrazine
DWLOC,
then
EPA
states
that
it
has
exceeded
the
Agency's
level
of
concern
(
LOC).
The
Agency
had
determined
that
the
DWLOC
for
infants,
the
most
vulnerable
population
subgroup,
was
12.5
ppb,
based
on
a
NOAEL
of
1.8
mg/
kg/
day
(
six­
month
LH
surge
in
a
rat)
and
a
1000X
UF
(
10X
inter,
10X
intra,
10X
FQPA
for
uncertainties
associated
with
atrazine's
toxic
effects
on
the
developing
child
and
the
extent
and
magnitude
of
exposure
to
atrazine
in
drinking
water).
EPA
suggests
that
the
increased
monitoring
program
could
allow
the
removal
of
that
portion
of
the
10X
FQPA
associated
with
exposure
uncertainties,
thereby
reducing
the
10X
to
3X
for
any
risk
assessments
conducted
in
monitored
areas.
Therefore,
in
the
IRED,
the
new
DWLOC
is
re­
calculated
to
be
37.5
ppb,
based
on
an
endpoint
of
1.8
with
a
300X
UF
(
10X
inter,
10X
intra,
3X
FQPA
for
uncertainty
associated
with
atrazine's
toxic
effects
on
the
developing
child)
(
IRED,
p.
84).

The
intermediate­
chronic
DWLOC
for
infants
is
12.5
ppb
(
seasonal
average)
for
unmonitored
areas,
and
37.5
ppb
for
monitored
areas.
There
are
37
community
water
systems
(
CWS)
that
exceed
12.5
ppb,
the
Agency's
level
of
concern
at
the
99.9th
exposure
percentile
for
infants,
children
1­
6
yrs,
and
adults,
according
to
the
manufacturer's
monitoring
data.
The
acute
dietary
drinking
water
risks,
and
chronic
food
risks
are
below
the
EPA's
LOC.

EPA
states
in
the
IRED
that
"
if
an
exceedence
of
37.5
is
detected
in
raw
drinking
water
(
pre­
treatment)
in
any
of
these
watersheds,
further
use
of
atrazine
will
be
prohibited
in
that
watershed"
(
IRED,
p.
84).
Unfortunately,
this
level
is
far
from
protective
for
two
reasons:
first,
adverse
effects
in
aquatic
plants
and
animals
have
been
reported
at
levels
of
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

3
10
ppb,
and
in
some
studies
at
levels
as
low
as
0.1
ppb;
second,
the
level
of
37.5
ppb
is
a
seasonal
average
that
would
allow
peak
levels
far
in
excess
of
this
level
during
the
spring
 
the
key
time
for
reproduction
of
aquatic
plants
and
animals.

Furthermore,
exposure
through
domestic
wells
exceeds
the
level
of
concern.
Eight
wells
out
of
1505
wells
monitored
in
high
atrazine
use
areas
had
residues
greater
than
12.5
ppb.
Approximately
ten
percent
of
the
US
population
gets
their
drinking
water
from
13
million
wells,
therefore
the
sample
taken
is
highly
inadequate.
Thus,
EPA
has
completely
ignored
the
known
aggregate
risks
of
atrazine
contamination
to
private
well
owners
(
and
users
of
springs
and
other
non­
regulated
water
systems),
in
direct
violation
of
the
aggregate
risk
requirements
of
FFDCA
§
408(
b).

II.
EPA
HAS
VIOLATED
ITS
SPECIAL
REVIEW
REGULATIONS,
FIFRA,
THE
FEDERAL
ADVISORY
COMMITTEE
ACT,
THE
ADMINISTRATIVE
PROCEDURE
ACT,
AND
THE
AGENCY'S
SEPTEMBER
1984
SETTLEMENT
WITH
NRDC,
BY
MEETING
REPEATEDLY
AND
PRIVATELY
WITH
ATRAZINE'S
REGISTRANT
AND
CUTTING
A
SPECIAL
PRIVATE
DEAL
WITH
THE
REGISTRANT
THAT
IS
CONTRARY
TO
THE
PUBLIC
INTEREST.

The
IRED
reflects
a
private
deal
between
atrazine's
registrant
Syngenta
and
the
agency.
The
agency
apparently
met
repeatedly
with
the
registrant
in
hammering
out
a
deal,
and
based
upon
our
review
of
the
docket
all
or
virtually
all
of
these
meetings
apparently
were
not
fully
and
timely
summarized
and
docketed
as
legally
required.
In
reaching
this
private
deal,
EPA
has
clearly
failed
to
follow
the
letter
and
spirit
of
its
Special
Review
regulations
governing
public
and
transparent
decision­
making
on
pesticides
such
as
atrazine
that
are
in
Special
Review.
See
40
C.
F.
R.
Part
154.
For
example,
EPA's
regulations
require
that
the
agency
fully
and
timely
docket
"
all
comments,
correspondence,
or
other
materials"
submitted
by
registrants
and
other
outside
parties
regarding
atrazine,
"
all
documents,
proposals,
or
other
materials
concerning"
atrazine
provided
by
EPA
to
outside
parties,
and
summaries
of
all
meetings
with
the
registrants
or
other
oputside
parties.
Id.
§
§
154.15(
b)(
7)­(
9);
154.27(
c).
The
memo
summarizing
the
meetings
with
registrants
and
outside
parties
"
shall
be
placed
in
the
docket
within
10
working
days
of
the
subject
meeting,"
and
the
materials
from
outside
parties
or
provided
by
EPA
to
outside
parties
must
be
docketed
within
15
working
days.
Id.
154.15(
d).
The
docket
index
must
reference
all
such
documents
and
be
publicly
disseminated.
Id.
154.15(
f).
In
addition,
the
rules
provide
that
while
meetings
with
private
parties
are
not
prohibited,
"
during
such
meetings,
the
Agency
will
not
commit
to
take
any
particular
action
concerning
a
pending
decision."
Id.
§
154.27(
b)(
emphasis
added).
Moreover,
the
final
decision
is
not
to
be
a
result
of
a
private
deal
cut
with
the
registrant;
the
rules
explicitly
mandate
that
"
the
Agency
will
make
the
final
administrative
decision
on
a
wholly
independent
basis
and
in
accordance
with
the
law."
Id.
§
154.27(
b)(
emphasis
added).

Contrary
to
EPA's
rules,
it
appears
that
the
agency
met
with
Syngenta
frequently
without
adequate
and
timely
docketing,
and
that
the
agency
reached
a
private
deal
with
Syngenta.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

4
Specifically,
the
agency
announced
in
its
January
31,
2003
Press
Release
that
"
The
provisions
of
this
action,
contained
in
the
IRED,
have
also
been
incorporated
into
an
agreement
with
the
principal
registrant
of
atrazine,
Syngenta."
Obviously,
as
is
evidenced
by
the
Press
Release
and
the
written
agreement
with
Syngenta,
EPA
did
"
commit
to
take
[
a]
particular
action
concerning
a
pending
decision"
in
consultation
only
with
Syngenta,
in
direct
violation
of
its
regulations.

Not
only
does
this
process
of
private
deal
making
violate
EPA's
Special
Review
rules
at
40
C.
F.
R.
Part
154,
it
also
violates
the
Federal
Insecticide,
Fungicide,
Rodenticide
and
Rodenticide
Act
(
FIFRA),
7
U.
S.
C.
§
136
et
seq.,
the
Federal
Advisory
Committee
Act
(
FACA),
5
U.
S.
C.
App.
II,
and
the
Administrative
Procedure
Act
(
APA),
5
U.
S.
C.
§
551
et
seq.
(
APA).
As
NRDC
alleged
in
detail
in
its
complaint
in
NRDC
et
al.
v.
EPA,
Civ.
Action
No.
83­
1509
(
D.
D.
C.,
filed
May
26,
1983),
EPA
simply
cannot
meet
repeatedly
with
registrants
(
in
this
case
Syngenta)
or
other
industry
representatives
to
reach
an
agreement
on
an
important
public
policy
and
public
health
issue
such
as
how
to
regulate
atrazine.

FIFRA
and
EPA
rules
require
that
EPA
act
independently
in
carrying
out
its
mandate
to
protect
public
health
and
the
environment.
Congress
expressed
its
intention
under
FIFRA
to
prohibit
such
private
or
closed
negotiations
or
protracted
and
secret
discussions
of
risks
and
benefits
between
the
industry
and
EPA.

FACA
requires
that
if
EPA
establishes
a
group
of
outside
advisors
on
an
issue,
or
utilizes
advice
from
outside
parties,
it
may
do
so
only
in
compliance
with
FACA.
To
establish
or
utilize
such
advice,
EPA
must
establish
a
balanced
advisory
committee
that
meets
in
the
open
and
in
accordance
with
all
FACA
procedural
requirements,
is
"
fairly
balanced,"
and
is
not
"
inappropriately
influenced 
by
any
special
interest."
5
U.
S.
C.
App.
II.
EPA
obviously
solicited
and
in
an
ongoing
fashion
utilized
the
advice
of
Syngenta
on
what
regulatory
actions
would
be
appropriate
to
deal
with
atrazine,
yet
the
agency
failed
to
comply
with
any
of
FACA's
procedural
and
substantive
requirements,
in
direct
violation
of
the
Act.

Moreover,
the
APA
requires
that
in
making
regulatory
decisions,
EPA
may
not
give
preferential
access
to
any
one
side
of
the
debate,
and
may
not
cut
private
deals
with
a
regulated
industry.
The
agency
may
not
issue
a
rule
that
has
been
negotiated
with
only
one
party,
and
then
provide
what
amounts
to
an
empty
opportunity
for
public
comment.

Finally,
EPA
entered
into
a
consent
agreement
with
NRDC
on
September
20,
1984
in
which
the
agency
agreed
to
open
up
its
pesticide
review
process.
EPA
agreed
to,
inter
alia:
use
a
comprehensive
public
docketing
system;
docket
minutes
of
all
meetings
with
persons
outside
of
the
government;
prohibitions
against
providing
draft
decisions
or
other
documents
solely
to
industry
representatives;
procedures
to
assure
that
EPA
independently
makes
all
decisions
with
docket
summaries
of
meetings;
and
to
refuse
to
make
private
deals
with
registrants.
See
NRDC
Motion
to
Dismiss
NRDC
v.
EPA,
Civ.
Action
No.
83­
1509
(
D.
D.
C.,
Motion
filed
January
24,
1986),
(
attached).
Many
of
these
requirements
were
embodied
in
EPA
regulations
noted
above.
It
is
profoundly
troubling
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

5
that
history
seems
to
be
repeating
itself,
and
that
EPA
appears
to
be
reverting
to
cutting
private
deals
after
private
negotiations
with
registrants.
We
note
that
EPA
agreed
that
if
the
agreed
procedures
were
not
followed
for
a
chemical,
that
NRDC
has
a
right
to
move
the
Court
to
enforce
the
agreement
with
respect
to
such
pesticides.

The
clear
evidence
that
EPA
has
shunted
aside
legal
restrictions
on
its
decision­
making
procedures
would
be
somewhat
less
troubling
if
the
Agency
had
reached
a
decision
that
fully
protected
public
health
and
the
environment.
However,
by
mandating
nothing
more
than
additional
monitoring
and
setting
a
"
trigger
level"
at
37.5
ppb,
which
is
over
12
times
the
3
ppb
MCL
for
atrazine,
EPA
has
effectively
punted
the
cost
of
clean­
up
to
the
water
utilities,
and
eventually
to
the
consumer.
We
believe
that
this
is
a
bad
policy
and
is
unfair.
The
EPA
decision
also
leaves
essentially
helpless
hundreds
of
thousands
or
millions
of
people
who
use
groundwater­
supplied
systems
that
will
not
be
required
to
have
their
source
water
monitored,
who
use
private
wells,
or
who
use
smaller
public
or
private
water
systems
in
areas
with
high
atrazine
use
that
are
unaware
of
atrazine
problems
and
have
not
installed
treatment.
Moreover,
it
leaves
environmental
harms
unaddressed.
Aquatic
wildlife
remains
unprotected.

III.
EPA'S
ATRAZINE
DECISION
ALLOWS
AND
EVEN
ENCOURAGES
VIOLATIONS
OF
THE
SAFE
DRINKING
WATER
ACT
(
SDWA),
AND
THUS
THE
FFDCA
AND
FIFRA
AS
WELL.

The
current
EPA
drinking
water
standard
(
Maximum
Contaminant
Level,
or
MCL)
for
atrazine,
codified
in
the
C.
F.
R.,
is
3
ppb
(
annual
average
of
4
quarterly
samples).
See
40
C.
F.
R.
§
141.62(
c).
Moreover,
EPA
has
determined,
through
notice
and
comment
rulemaking,
that
the
MCL
Goal
(
MCLG)
 
the
"
level
at
which
no
known
or
anticipated
adverse
effects
on
the
health
of
persons
occur,
and
which
allows
an
adequate
margin
of
safety"
 
for
atrazine
is
3
ppb,
a
level
also
codified
in
the
C.
F.
R.
See
40
C.
F.
R.
§
141.50(
b).

Yet
EPA's
private
deal
with
Syngenta
states
that
no
action
will
be
required
unless
water
used
by
a
public
water
system
exceeds
37.5
ppb,
a
concentration
over
12
times
higher
than
EPA's
duly­
promulgated
tap
water
standard.
It
is
impossible,
if
any
tap
water
sample
exceeds
even
12
ppb,
for
a
public
water
system
to
be
in
compliance
with
the
MCL.
Thus,
EPA's
private
deal
effectively
allows
or
even
encourages
widespread,
unabated
contamination
of
the
source
waters
used
by
potentially
millions
of
Americans
for
drinking
water
with
atrazine
at
levels
that
violate
the
agency's
own
tap
water
standard.
This
is
despite
the
Agency's
formal
determination,
through
a
notice
and
comment
rulemaking
that
has
not
been
repealed,
that
the
promulgated
MCL
is
the
highest
level
at
which
there
will
be
no
known
or
anticipated
adverse
effects
on
the
health
of
persons.
EPA
is
not
free
to
ignore
the
agency's
own
duly­
promulgated
drinking
water
safety
standard
and
MCLG
for
atrazine,
and
therefore
cannot
lawfully
find
under
the
FFDCA
that
it
is
"
safe"
for
drinking
water
to
contain
atrazine
at
a
level
in
excess
of
3
ppb.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

6
In
a
strange
twist,
under
EPA's
currently
enforceable
rules,
any
public
water
system
with
over
3
ppb
atrazine
in
its
water
must
issue
to
all
of
its
customers
the
following
notice:

The
United
States
Environmental
Protection
Agency
(
EPA)
sets
drinking
water
standards
and
has
determined
that
atrazine
is
a
health
concern
at
certain
levels
of
exposure.
This
organic
chemical
is
a
herbicide.
When
soil
and
climatic
conditions
are
favorable,
atrazine
may
get
into
drinking
water
by
runoff
into
surface
water
or
by
leaching
into
ground
water.
This
chemical
has
been
shown
to
affect
offspring
of
rats
and
the
heart
of
dogs.
EPA
has
set
the
drinking
water
standard
for
atrazine
at
0.003
parts
per
million
(
ppm)
to
protect
against
the
risk
of
these
adverse
health
effects.
Drinking
water
that
meets
the
[
3
ppb]
EPA
standard
is
associated
with
little
to
none
of
this
risk
and
is
considered
safe
with
respect
to
atrazine.

40
C.
F.
R.
§
141.32(
28)(
emphasis
added).
It
is
unfathomable
how
EPA
can
take
directly
conflicting
positions
under
the
SDWA
and
the
FFDCA/
FIFRA.
Under
the
SDWA,
EPA
has
promulgated
rules
setting
an
enforceable
MCL
of
3
ppb,
providing
that
the
3
ppb
MCLG
is
the
highest
safe
level
in
drinking
water,
and
explicitly
ordering
any
water
utility
serving
drinking
water
at
over
3
ppb
to
warn
their
customers
that
they
are
getting
drinking
water
containing
more
than
the
"
safe"
level
of
3
ppb.
Yet
on
the
other
hand
the
agency's
pesticide
program
now
says
that
it
is
perfectly
"
safe"
under
the
FFDCA
and
FIFRA
for
Syngenta
to
continue
to
sell
atrazine
and
for
it
to
contaminate
drinking
water
at
up
to
37.5
ppb.
This
is
arbitrary
and
capricious
decision­
making
at
its
most
clear.

While
the
SDWA
MCL
applies
to
public
water
systems,
not
to
Syngenta
qua
registrant
of
atrazine,
the
agency's
private
deal
with
Syngenta
not
only
encourages
violations
of
the
EPA
atrazine
MCL
in
a
manner
contrary
to
public
policy
and
Congressional
intent,
it
directly
violates
the
SDWA,
FIFRA,
and
the
FFDCA.
Under
the
latter
two
statutes,
the
agency
may
not
authorize
contamination
of
water
used
for
drinking
in
excess
of
its
drinking
water
standard.
FIFRA
provides
that
EPA
may
not
register
a
pesticide
unless,
"
when
used
in
accordance
with
widespread
and
commonly
recognized
practice,
it
will
not
generally
cause
unreasonable
adverse
effects
on
the
environment."
FIFRA
§
3(
c)(
5)(
D).
Moreover,
FIFRA
§
2(
bb),
7
U.
S.
C.
§
136(
bb),
provides
in
defining
"
unreasonable
adverse
effects
on
the
environment"
that
there
shall
be
no
"
human
dietary
risk
from
residues
that
result
from
a
use
of
a
pesticide
in
or
on
any
food
inconsistent
with
the
standard
under"
FFDCA
§
408,
21
U.
S.
C.
§
346a.
The
term
"
food"
includes
drinking
water.
21
U.
S.
C.
§
321(
f).
Under
the
FFDCA,
EPA
must
determine
that
all
aggregate
exposure
to
atrazine,
including
all
exposure
to
atrazine
in
drinking
water,
is
"
safe,"
meaning
that
there
is
a
"
reasonable
certainty
of
no
harm"
to
any
person,
including
infants,
children,
and
other
vulnerable
populations.
EPA
simply
cannot
determine
that
exposure
to
atrazine
at
a
level
of
over
12
times
its
duly­
promulgated
drinking
water
standard
is
"
safe"
and
that
there
is
a
"
reasonable
certainty
of
no
harm"
from
that
exposure.

EPA's
decision
also
contravenes
the
Safe
Drinking
Water
Act,
because
the
agency
is
authorizing
and
indeed
encouraging
drinking
water
contamination
up
to
12
times
the
atrazine
MCL,
effectively
a
back­
door
relaxation
of
the
SDWA
health
standard
in
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

7
violation
of
the
SDWA.
EPA
is
prohibited
from
adopting
a
weaker
atrazine
MCL
under
the
anti­
backsliding
provision
of
the
SDWA
§
1412(
b)(
9),
42
U.
S.
C.
§
300g­
1(
b)(
9).
As
was
recently
reiterated
by
the
U.
S.
Court
of
Appeals
for
the
D.
C.
Circuit
in
a
decision
involving
the
radionuclides
MCLs,
City
of
Waukesha
v.
EPA,
No.
01­
1028,
slip
op.
at
21,
47
(
Feb.
25,
2003),
and
as
EPA
acknowledged
in
briefing
that
case,
the
agency
is
prohibited
from
weakening
MCLs
for
contaminants
under
the
anti­
backsliding
provision.
Even
if
EPA
were
not
prohibited
by
the
SDWA
anti­
backsliding
provision
from
weakening
the
atrazine
MCL,
the
agency
clearly
could
not
effectively
weaken
that
standard
without
going
through
the
full
SDWA
§
1412,
42
U.
S.
C.
§
300g­
1
process,
including
notice
and
comment
rulemaking
and
a
full
scientific
and
other
analysis
as
mandated
by
that
Act.
EPA
has
done
none
of
this
analysis.
Therefore,
EPA's
private
deal
also
contravenes
the
SDWA.

IV.
EPA'S
NOAEL
IS
UNJUSTIFIED
BECAUSE
IT
IS
A
LEVEL
AT
WHICH
ADVERSE
EFFECTS
WERE
OBSERVED.
MOREOVER,
CONGRESS
MANDATED
THAT
EPA
MUST
USE
THE
NOEL,
NOT
A
NOAEL.

EPA
has
used
a
six
month
study
in
Sprague­
Dawley
(
SD)
rats
to
determine
a
No
Observable
Adverse
Effect
Level
(
NOAEL),
based
on
leutinizing
hormone
(
LH)
surge
attenuation
(
MRID44152102).
In
this
study,
EPA
determined
that
atrazine
had
adverse
effects
at
3.65
mg/
kg/
day
(
based
on
estrous
cycle
alterations
and
LH
surge
attenuation),
and
treated
this
dose
as
its
lowest
observed
adverse
effect
level
(
LOAEL).
Accordingly,
the
Agency
chose
the
next
lowest
dose
tested,
1.8
mg/
kg/
day,
as
its
NOAEL.

There
are
numerous
legal
and
scientific
problems
with
EPA's
approach.
First,
Congress
ordered
the
agency
to
set
tolerances
at
a
"
safe"
level
at
which
there
is
a
"
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
the
pesticide
chemical
residue
.
.
."
FFDCA
§
408(
c)(
2).
Congress
made
it
clear
in
the
Legislative
History
that
it
expected
the
tolerance
to
be
based
not
upon
a
LOAEL
or
even
a
NOAEL,
but
based
upon
a
No
Observable
Effect
Level
(
NOEL).
As
the
House
Report
states:

In
the
case
of
a
threshold
effect
for
a
pesticide
chemical
residue,
the
Committee
expects
that
a
tolerance
will
provide
a
"
reasonably
certainty
of
no
harm"
if
the
Administrator
determines
that
the
aggregate
exposure
to
the
pesticide
chemical
residue
will
be
lower
by
an
ample
margin
of
safety
than
the
level
at
which
the
pesticide
chemical
residue
will
not
cause
or
contribute
to
any
known
or
anticipated
harm
to
human
health.
The
Committee
further
expects,
based
on
discussions
with
the
Environmental
Protection
Agency,
that
the
Administrator
will
interpret
an
ample
margin
of
safety
to
be
a
100­
fold
safety
factor
applied
to
the
scientifically
determined
``
no
observable
effect''
level
when
data
are
extrapolated
from
animal
studies.

H.
R.
Rep.
No.
104­
669
part
2
at
41
(
July
23,
1996)
(
emphasis
added).
Thus,
EPA
must
use
the
NOEL,
not
a
LOAEL
or
NOAEL
as
it
has
here
for
atrazine.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

8
Moreover,
even
assuming
that
it
were
lawful
to
use
a
NOAEL
instead
of
a
NOEL,
EPA's
NOAEL
determination
is
seriously
flawed
on
scientific
grounds.
The
agency
relies
on
what
it
says
is
a
NOAEL
as
the
most
sensitive
toxicity
endpoint
for
its
chronic
and
intermediate­
term
health
assessment.
NRDC
raised
concerns
that
there
were
treatment
related
effects
at
the
lowest
dose
tested
(
NRDC
comments
July,
2002).
EPA
summarized
NRDC's
comments
and
presented
the
Agency's
response
as
follows:

Comment:
NRDC
believes
that
1.8
mg/
kg
bw
per
day
is
the
lowest
observed
adverse
effect
level
(
LOAEL)
rather
than
the
no
observed
adverse
effect
level
(
NOAEL)
for
suppression
of
the
LH
surge
in
the
6
month
LH
study
and
its
NOAEL.
HED
Response:
EPA's
position
is
that
1.8
mg/
kg
bw
per
day
is
a
NOAEL
in
the
6
month
LH
surge
study
by
Syngenta.
EPA
believes
it
is
justified
in
using
3.6
mg/
kg
bw
per
day
as
a
LOAEL
for
this
endpoint.
The
rationale
for
the
selection
of
3.6
mg/
kg
bw
per
day
as
a
LOAEL
and
1.8
mg/
kg
bw
per
day
as
a
NOAEL
for
suppression
of
the
LH
surge
is
based
on
a
weight
of
evidence
argument.
There
is
a
dose
response
trend
for
suppression
of
the
LH
surge.
While
the
3.6
mg/
kg
bw
per
day
dose
does
not
represent
a
statistically
significant
decrease
in
the
amount
of
LH,
the
dose
response
trend
is
supported
by
the
statistically
significant
difference
in
vaginal
cycling
at
3.6
mg/
kg
bw
per
day.
Vaginal
cycling
data
tends
to
be
less
variable
than
LH
data.
Thus,
EPA
acknowledges
that
selection
of
1.8
mg/
kg
bw
per
day
as
a
NOAEL
for
LH
suppression
is
conservative,
but
errs
on
the
side
of
health
protection.
Although
there
is
one
statistically
significant
response
for
suppression
of
the
LH
surge
in
the
1.8
mg/
kg
bw
per
day
dose
group
for
one
time
point,
this
is
not
sufficient
evidence
to
designate
1.8
mg/
kg
bw
per
day
as
a
LOAEL,
particularly
in
light
of
the
fact
there
were
no
statistically
significant
differences
found
for
vaginal
cycling
at
this
dose.
i
Although
EPA
acknowledges
that
the
lowest
dose
tested,
1.8,
did
have
one
statistically
significant
response
for
suppression
of
the
LH
surge,
the
endpoint
of
interest,
it
maintains
that
vaginal
cycling
(
number
of
days
in
estrus)
was
not
significantly
affected
at
this
dose.
However,
while
the
study
design
was
flawed
and
underpowered,
so
that
even
large
treatment
effects
are
not
statistically
significant,
a
dose­
dependent
trend
is
evident
from
the
data,
presented
in
the
Table
below.

TABLE
1:
Six
month
study
of
atrazine:
LH
surge
in
SD
rats
(
MRID
44152102).
Summary
data
for
each
relevant
toxicity
endpoint,
at
each
dose
of
atrazine
is
shown.
All
data
is
exactly
as
presented
in
the
EPA
data
evaluation
report.
An
asterisk
represents
EPA
determination
of
statistical
significance.
ii
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

9
Effect
Control
Low
dose
1.8
mg/
kg/
day
Med
dose
3.65
mg/
kg/
day
High
dose
29.44
mg/
kg/
day
Increase
in
mean
%
days
in
estrus
at
week
21­
22
Avg=
32%
SD=
25%
Avg=
41%
SD=
32%
Avg=
45%
*
SD=
32%
Avg=
51%
*
SD=
35%

Number
of
animals
with
estrus
blocks,
at
week
21­
22
21
31
38
50
Group
mean
LH
values
in
repeat
bleed
animals
At
1800
At
2000
+
267%
+
273%
+
237%
+
133%
+
157%
+
148%
­
15%*
+
4%*

It
is
clear
from
EPA
data
presented
in
the
Table
that
atrazine
adversely
affects
the
LH
surge,
with
expected
effects
on
the
estrus
cycle,
at
all
doses
tested.
The
LH
surge,
even
at
the
lowest
dose
of
atrazine
tested,
is
below
the
threshold
critical
for
ovulation,
as
evidenced
by
concomitant
increases
in
percent
days
in
estrus
and
increases
in
the
number
of
atrazine­
treated
animals
with
estrus
blocks.

While
the
EPA
dismisses
the
low­
dose
effects
as
not
statistically
significant,
it
is
evident
that
the
study
design
was
underpowered,
and
unable
to
detect
even
large
treatment
effects.
For
example,
none
of
the
increases
in
the
number
of
animals
with
estrus
blocks
are
significant,
at
any
dose,
despite
the
evident
dose­
dependent
increasing
trend
(
21
v.
31,
38,
50).
Further,
the
obvious
dose­
dependent
increase
in
mean
%
days
in
estrus
does
not
gain
statistical
significance
primarily
due
to
the
large
standard
deviations,
almost
as
large
as
the
mean
values
themselves,
even
in
the
control
group
(
mean=
32%,
SD=
25%).
This
large
variability
in
data
is
evidence
of
an
underpowered
study,
with
too
few
samples
to
detect
even
large
treatment
effects.

An
examination
of
the
data
indicates
that
EPA
has
wrongly
determined
that
the
lowest
dose
tested
is
a
NOAEL.
Rather,
there
is
a
clear
dose­
dependent
trend
of
all
measured
endpoints,
at
all
doses
tested.
It
is
incumbent
on
the
agency
to
do
a
statistical
test
for
trend
across
the
doses.
If
the
EPA
intends
to
use
this
study
(
MRID
44152102)
to
determine
a
no­
effect
level
for
atrazine
exposure,
then
EPA
has
two
possible
choices:
either
EPA
must
use
an
uncertainty
factor
to
extrapolate
below
the
lowest
dose
tested,
to
estimate
a
no­
effect
level,
or
the
Agency
must
do
a
benchmark
analysis
to
identify
the
LED10
for
these
endpoints.
It
seems
strange
to
us
that
the
Agency
did
not
do
a
benchmark
analysis
in
this
case,
as
it
is
our
understanding
that
EPA
has
been
moving
toward
incorporating
this
approach
routinely
in
their
non­
cancer
risk
assessments.
In
either
event,
NRDC
asserts
that
the
EPA
has
no
scientific
justification
for
the
claim
that
the
lowest
dose
constitutes
a
no­
effect
level.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

10
V.
AGRICULTURE
AND
LAWN
CARE
RISKS
ARE
UNACCEPTABLY
HIGH,
AND
EPA'S
PROPOSED
MITIGATION
IS
INSUFFICIENT.

Occupational
agricultural
exposure
to
atrazine
exceeds
the
EPA
level
of
concern.
Workers
who
mix,
load,
and
apply
atrazine
to
agriculture,
turf,
and
home
lawns
currently
exceed
the
level
of
concern
presuming
baseline
or
label­
stipulated
personal
protective
equipment
(
PPE).
The
Agency
has
proposed
to
mitigate
these
risks
with
the
following
label
changes:
closed
mixing
and
loading
systems
will
be
required
for
some
aerial
applications;
maximum
PPE
(
long
shirts
and
pants,
protective
eyewear,
dust/
mist
respirator)
will
be
required
for
liquids
and
dry
flowables;
wettable
powders
will
be
packaged
in
water
soluble
bags
for
aerial
and
groundboom
applications;
closed
cockpits
will
be
required
for
aerial
applications;
closed
cabs
will
be
required
for
flaggers.

For
occupational
non­
agricultural
use,
the
following
label
changes
will
be
made:
baseline
PPE
(
long
shirts
and
pants,
shoes
and
socks)
will
be
required
for
granular
formulations;
baseline
PPE
plus
gloves
will
be
required
for
water
dispersable
granules
and
water
soluble
powders;
maximum
PPE
will
be
required
for
liquid
formulations;
maximum
single
application
rates
for
liquid
formulations
will
be
reduced
from
2
to
1
lb
ai/
A;
granular
lawn
products
will
be
required
to
be
watered
in.

Residential
uses
of
atrazine
exceed
the
Agency's
level
of
concern
for
some
uses.
Bellygrinder
applications
of
granular
formulations
are
of
particularly
great
concern
(
MOE=
65).
The
Agency
proposes
the
following
mitigation:
hand­
held
devices
used
for
granular
formulations
will
be
restricted
to
spot
applications
only;
prohibit
granular
products
for
hand
applications;
reduce
the
maximum
one­
time
application
rate
from
2
to
1
lb
ai/
A;
require
granular
lawn
products
to
be
watered
in.
All
homeowner
handler
assessments
for
residential
applicator
risks
are
done
presuming
short­
sleeved
shirts
and
short
pants,
considered
a
reasonable
assumption
by
the
EPA
and
NRDC.

Given
the
reality
of
poor
compliance
and
limited
enforcement
of
regulations
and
labeling,
EPA's
assumption
of
100%
compliance
and
enforcement
leaves
workers
unprotected.
There
is
poor
compliance
with
EPA
regulations
and
label
restrictions,
which
include
personal
protective
equipment,
closed
cab
systems,
lengthened
re­
entry
intervals,
and
wash
facilities.
iii
iv
There
is
almost
no
enforcement
of
EPA
regulations
and
label
restrictions,
making
them
practically
ineffective.
This
is
evident
by
approximately
2,000
pesticide
poisoning
incidents
reported
annually
to
the
CDC,
and
to
the
EPA
FIFRA
6(
a)(
2)
system.
v
In
light
of
evidence
of
poor
compliance
with
EPA
regulatory
standards,
the
inaccurate
assumption
of
full
compliance
will
leave
untold
numbers
of
agricultural
workers
and
residential
users
at
unacceptably
high
risk,
including
some
children,
and
some
pregnant
women.

VI.
ECOLOGICAL
RISKS
ARE
UNACCEPTABLY
HIGH,
AND
NO
EFFECTIVE
MITIGATION
IS
PROPOSED.

In
our
comments
on
the
Revised
Preliminary
Human
Health
Risk
Assessment
for
atrazine,
and
our
comments
on
the
Preliminary
Ecological
Fates
and
Effects
Risk
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

11
Assessment
(
EFEC;
November
2001)
we
urged
EPA
to
take
steps
to
cancel
this
dangerous
pesticide.
EPA
itself
concluded
in
1996
that
"[
b]
ecause
of
[
atrazine
and
four
other
pesticides']
potential
to
contaminate
ground
water,
EPA
has
determined
that
these
pesticides
may
cause
unreasonable
adverse
effects
on
the
environment
in
the
absence
of
effective
management
measures
provided
by"
a
State
Management
Plan
(
SMP).
61
Fed.
Reg.
33,260
(
June
26,
1996).
EPA
has
not
found
that
such
SMPs
have
been
effective
at
reducing
atrazine
levels
below
the
drinking
water
standard,
and
any
change
in
the
agency's
1996
pronouncement
and
findings
is
an
unsupported
and
unwarranted
departure
from
the
agency's
previous
well­
documented
findings.
The
Ecological
Risk
Assessment
makes
the
case
for
cancellation
far
stronger,
considering
EPA's
conclusion
that:

widespread
environmental
exposure
has
serious
implications
when
compared
to
ecotoxicological
endpoints
of
concern.
The
preliminary
ecological
risk
assessment
indicated
that
risk
quotients
exceeded
the
levels
of
concern
for
chronic
effects
on
mammals,
birds,
fish,
aquatic
invertebrates
and
non­
target
plants
are
possible
at
maximum
and
in
some
cases
typical
use
rates.
A
refined
risk
assessment
focusing
on
the
aquatic
environment
and
using
the
extensive
exposure
monitoring
data
as
well
as
additional
ecotoxicological
data
found
in
the
open
literature,
resulted
in
concerns
for
adverse
toxicological
effects
on
freshwater
and
estuarine
plants
and
their
communities
as
well
as
indirect
adverse
effects
on
aquatic
invertebrate
and
fish
populations
at
monitored
atrazine
levels
in
surface
waters.
vi
The
direct
effects
of
atrazine
on
nontarget
aquatic
plants
indicate
a
high
risk,
such
that
routine
peaks
in
atrazine
levels
above
20
ppb
cause
death
of
some
aquatic
flora,
and
complete
loss
of
some
plant
species
(
Reregistration
Eligibility
Science
Chapter
for
Atrazine,
Environmental
Fate
and
Effects
Chapter
[
EFEC],
p.
60;
Kettle
et
al,
1987vii).
As
EPA
acknowledges,
these
direct
effects
of
atrazine
alone
may
devastate
the
aquatic
community
by
reducing
oxygen
levels
and
nutrients
in
the
water,
thereby
risking
further
loss
of
aquatic
plants
and
animals.
EFED
states
that
a
reduction
in
primary
production
of
algae
(
EC50=
1
ppb),
reduction
in
invertebrate
populations
(
EC50=
10
ppb),
and
a
reduction
in
phytoplankton
production
(
EC50=
20
ppb)
are
real­
world
risks
following
seasonal
atrazine
exposures.
The
crippling
effects
on
fish
populations
follow
loss
of
aquatic
vegetation
within
weeks
to
months
(
Atrazine
EFEC
at
21).
Brook
trout,
among
the
most
sensitive
aquatic
animal,
has
a
chronic
NOAEC
value
of
65
ppb,
and
fish
populations
are
likely
to
suffer
reductions
due
to
food
loss
and
habitat
damage
at
20
ppbviii.
At
current
use
rates,
atrazine
may
threaten
the
complex
integrity
of
aquatic
communities;
a
pond
whose
community
is
limited
to
only
the
most
hardy,
atrazineresistant
species
may
be
less
able
to
provide
for
the
waterfowl
and
mammals
who
depend
on
aquatic
environments
for
food
and
reproduction.
EFED
rightly
agrees
with
Kettle
et
al,
1987,
who
maintain
that
at
20
µ
g/
L,
recovery
is
uncertain,
species
diversity
is
very
important,
and
the
combined
effects
of
atrazine
with
other
pesticides
would
lower
the
tolerance
of
the
plants
to
atrazine
toxicity,
making
the
whole
aquatic
community
more
vulnerable.
These
authors
found
that
a
single
application
of
20
µ
g/
L
(
ppb)
of
atrazine
to
a
pond
reduced
vegetation
60%
within
several
months,
and
by
90%
within
a
year.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

12
Bluegill
(
a
very
hardy
species)
was
reduced
96%
in
a
year.
Indirect
community
effects
resulted
from
the
impacts
of
atrazine
on
aquatic
vegetation
(
Atrazine
EFEC
at
21).

The
Agency
has
concluded
that
atrazine
is
toxic
to
non­
target
plants
(
neighbor
crops)
at
levels
that
exceed
the
Agency's
level
of
concern.
It
is
especially
disturbing
that
the
level
of
concern
is
exceeded
from
spray
drift
alone,
or
spray
drift
and
runoff,
even
when
assuming
that
spray
drift
is
5%,
and
runoff
is
2%,
both
likely
underestimates
of
actual
drift
and
runoff.

The
EFED
report
states
that
mammalian
and
avian
reproduction
chronic
levels
of
concern
(
LOC)
are
routinely
exceeded
for
several
use
scenarios
(
Atrazine
EFEC
at
64­
66).
Following
maximum
use
rates
on
sugarcane,
chronic
LOC
is
exceeded
for
mammalian
reproduction
by
as
high
as
90­
fold
(
NOAEL
is
50
ppm
for
adult
body
weight
reduction,
and
10
ppm
for
pup
weight
reduction),
and
4­
fold
for
avian
species
(
NOAEL
is
225
ppm
for
egg
production).
Typical
use
rates
for
sugarcane,
corn,
and
sorghum
all
resulted
in
risk
quotients
which
exceeded
the
LOC
(
Risk
Quotient
(
RQ)=
1)
for
mammalian
and
avian
reproduction
(
RQ=
26­
62).
These
are
extremely
high
RQ's,
and
clearly
represent
a
hazard
for
wildlife
populations.

In
NRDC's
view,
the
fact
that
risk
quotients
exceed
EPA
levels
of
concern
for
chronic
effects
on
mammals,
birds,
and
fish,
as
well
as
other
organisms,
for
maximum
and
in
some
cases
even
typical
atrazine
use
rates
clearly
suggests
that
the
chemical
is
having
adverse
effects
on
the
environment.
Rather
than
an
effective
mitigation
strategy,
EPA
is
requiring
the
manufacturer,
Syngenta,
to
perform
more
aggressive
water
monitoring.
This
passive
strategy
will,
of
course,
have
no
effect
on
reducing
atrazine
levels.
If
an
exceedence
of
37.5
ppb
seasonal
average
is
detected
in
raw
drinking
water,
then
EPA
writes
that
"
further
use
of
atrazine
will
be
prohibited
in
that
watershed"
(
IRED
at
84).
This
strategy
will
allow
continued
use
of
atrazine
in
all
watersheds,
since
no
watershed
currently
exceeds
the
action­
trigger
of
37.5
ppb.
Meanwhile,
aquatic
communities
will
continue
to
suffer
population
declines
and
adverse
effects
because
it
is
clear
that
adverse
effects
occur
at
levels
significantly
below
37.5
ppb.
NRDC
believes
that
this
is
unacceptable.
In
view
of
the
severe
adverse
environmental
consequences
detailed
here
and
in
our
previous
comments,
and
considering
EPA's
obligation
under
FIFRA
to
regulate
pesticides
in
order
to
prevent
"
unreasonable
adverse
effects
on
the
environment,"
FIFRA
§
3(
c)(
5),
we
believe
that
atrazine
can
not
safely
be
reregistered.

VII.
THE
ONGOING
REGISTRATION
OF
ATRAZINE
JEOPARDIZES
ENDANGERED
SPECIES
AND
THEIR
CRITICAL
HABITAT.

Based
on
EPA's
IRED
and
ecological
risk
assessments,
widespread
environmental
exposure
to
atrazine
threatens
endangered
species
throughout
the
country.
Atrazine
exposure
exceeds
EPA's
LOCs
for
endangered
terrestrial
plants,
aquatic
plants,
aquatic
invertebrates,
and
fish,
and
may
indirectly
affect
endangered
birds,
mammals,
amphibians,
reptiles,
and
beneficial
insects.
EPA
has
therefore
acknowledged
 
but
failed
to
take
any
steps
to
remedy
 
that
atrazine
may
threaten
hundreds
of
endangered
species
nationwide.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

13
EPA
acknowledges
that
atrazine
is
highly
toxic,
persistent,
and
mobile,
and
therefore
poses
significant
threats
to
endangered
species
and
other
non­
target
organisms
(
IRED
at
50­
51).
Atrazine
is
transported
via
spray
drift
and
runoff
to
surface
water,
and
it
leaches
into
groundwater
(
IRED
at
50).
EPA
notes
that
atrazine
has
been
"
widely
detected"
in
air
and
rainfall
samples
in
both
high
use
areas
and
areas
far
removed
from
high
use
areas
(
IRED
at
52).
EPA
has
found
that
there
is
"
widespread
environmental
exposure"
to
atrazine
in
aquatic
communities
and
other
ecosystems
that
may
have
many
effects
(
IRED
at
50).
The
laboratory,
microcosm,
mesocosm
and
field
studies
used
by
EPA
"
suggest
that
atrazine
concentrations
measured
in
the
environment
could
reach
levels
that
are
likely
to
have
negative
impact
on
sensitive
aquatic
species
and
communities."
(
IRED
at
61).
The
exposure
of
aquatic
communities
to
atrazine
at
levels
10­
20
ppb
(
significantly
below
the
EPA
proposed
seasonal
average
level
of
concern
of
37.5
ppb)
can
result
in
community­
level
and
population­
level
effects
(
IRED
at
4).
In
addition,
atrazine
exposure
in
aquatic
communities
may
cause
direct
effects
on
aquatic
non­
vascular
plants
that
could
result
in
reductions
in
populations
of
aquatic
macrophytes,
invertebrates,
and
fish
(
Atrazine
EFEC
at
2).
Atrazine
indirectly
affects
aquatic
communities
through
loss
of
species
sensitive
to
atrazine
and
resulting
changes
in
structure
and
functional
characteristics
of
the
affected
communities.
Because
atrazine
is
used
primarily
during
crop
pre­
planting
and
pre­
emergence,
the
levels
of
use
are
highest
during
spring
rainfall.
This
period
is
also
the
breeding
season
for
most
aquatic
organisms.

EPA's
risk
assessment
acknowledges
a
number
of
ways
that
atrazine
may
jeopardize
endangered
species
(
IRED
at
66­
67;
Atrazine
EFEC
at
94­
95).
EPA's
levels
of
concern
for
endangered
terrestrial
plants
and
vascular
aquatic
plants
are
exceeded
(
Atrazine
EFEC
at
94).
Acute
levels
of
concern
for
endangered
species
are
exceeded
for
aquatic
invertebrates,
and
chronic
levels
of
concern
are
exceeded
for
fish
and
aquatic
invertebrate
reproduction
(
Atrazine
EFEC
at
95).
Furthermore,
EPA
acknowledges
that
atrazine
may
indirectly
affect
endangered
birds,
mammals,
and
beneficial
insects
through
loss
of
food
sources
and
habitat
disruption
caused
by
atrazine's
adverse
chronic
effects
on
terrestrial
and
aquatic
plants
(
Atrazine
EFEC
at
94).
Moreover,
adverse
effects
of
atrazine
on
aquatic
vegetation
may
cause
a
loss
of
vegetative
habitat
that
could
affect
populations
of
endangered
aquatic
invertebrates
and
endangered
fish
species
(
Atrazine
EFEC
at
95).

The
U.
S.
Fish
and
Wildlife
Service
submitted
extensive
comments
to
EPA
in
response
to
the
Atrazine
EFEC,
and
FWS
concluded
that
atrazine's
release
into
the
environment
is
problematic
(
FWS
Comments
at
1).
Chronic
exposure
may
occur
to
a
wide
range
of
biota,
because
atrazine
is
persistent
in
aquatic
environments
and
is
transported
via
spray
drift
and
runoff
to
surface
water
(
FWS
Comments
at
2).
FWS
noted
that
EPA's
risk
assessment
 
which
acknowledges
significant
ecological
concerns
 
likely
underestimates
the
"
true
potential
for
ecological
impacts,"
in
part
because
EPA
did
not
consider
sublethal
effects
of
atrazine
exposure,
like
the
altered
reproductive
capacity
of
non­
target
organisms
(
FWS
Comments
at
2­
3).
FWS
also
disagreed
with
EPA's
use
of
surrogate
species
for
toxicity
testing,
pointing
out
that
"
standard
test
species"
are
not
appropriate
surrogates
for
listed
species
because
"
different
species
can
have
different
life
histories,
biological
requirements
and
sensitivities
to
pesticides
.
.
.
."
(
FWS
Comments
at
3).
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

14
FWS
concluded
that
EPA's
atrazine
risk
assessment
process
did
not
effectively
address
impacts
to
endangered
species
and
did
not
appear
to
meet
EPA's
consultation
requirement
under
the
Endangered
Species
Act
(
FWS
Comments
at
7).

Section
7(
a)(
2)
of
the
ESA
requires
that
"
each
federal
agency
shall,
in
consultation
with
and
with
the
assistance
of
the
Secretary,
insure
that
any
action
authorized,
funded,
or
carried
out
by
such
agency
(
hereinafter
in
this
section
referred
to
as
an
`
agency
action')
is
not
likely
to
jeopardize
the
continued
existence
of
any
endangered
species
or
threatened
species
or
result
in
the
destruction
or
adverse
modification
of
habitat
of
such
species
which
is
determined
by
the
Secretary
.
.
.
to
be
critical."
16
U.
S.
C.
§
1536(
a)(
2).
EPA
has
failed
to
consult
with
FWS
and
the
National
Marine
Fisheries
Service
(
NMFS),
as
required
by
Section
7(
a)(
2)
of
the
ESA,
16
U.
S.
C.
§
1536(
a)(
2),
to
ensure
that
its
registration
of
the
pesticide
atrazine
will
not
jeopardize
the
survival
and
recovery
of
endangered
amphibians,
reptiles,
fish,
birds,
mammals,
plants,
aquatic
invertebrates,
and
beneficial
insects
nationwide.

VIII.
ATRAZINE
HAS
BEEN
ASSOCIATED
WITH
AN
INCREASED
RISK
OF
CANCER
IN
SEVERAL
STUDIES.

There
is
evidence
from
both
epidemiology
studies
and
laboratory
studies
suggesting
that
atrazine
may
be
associated
with
an
increased
risk
of
cancer.
Several
laboratory
studies
have
demonstrated
that
rats
and
mice
exposed
to
atrazine
had
increased
rates
of
uterine
cancers,
mammary
tumors,
and
combined
leukemia
/
lymphoma
cancersix
(
note
that
these
results
are
debated
as
to
their
significance
to
human
risk).
Several
field
studies
of
human
exposure
to
triazine
pesticides,
including
atrazine,
find
that
exposure
is
associated
with
an
increase
in
several
cancer
types:
Hodgkins
and
Non­
Hodgkins
lymphoma,
x
colon
cancer,
xi
brain
cancer,
xii
testicular
cancer,
xiii
and
childhood
cancers.
xiv
This
is
particularly
disturbing
given
that
childhood
cancers
(
age
0­
14
yrs)
have
risen
26%
from
1975­
1999.
xv
NRDC
insists
that
EPA
provide
a
proper
review
of
the
available
evidence
suggesting
an
association
between
atrazine
and
cancer.

A.
The
St.
Gabriel
Study
Sponsored
by
Syngenta
Is
Suggestive
of
a
Cancer
Link.

EPA
concludes
that
an
epidemiology
study
of
workers
at
the
Syngenta
atrazine
manufacturing
plant
(
St.
Gabriel
study)
was
"
insufficiently
large
and
has
limitations
that
prevent
ruling
out
atrazine
as
a
potential
contributor
to
the
increase
observed."
(
IRED
at
49).
In
other
words,
despite
Syngenta's
efforts,
the
study
fails
to
disprove
the
apparent
link
between
atrazine
exposure
and
increased
cancer
cases
among
workers.
This
is
supported
by
further
suggestive
evidence,
acknowledged
by
EPA
in
the
IRED
(
at
49):
"
atrazine
has
also
been
tied
to
inflammation
of
the
prostate
in
laboratory
animals
and
changes
in
testosterone
at
high
doses";
"
other
cancers
besides
prostate
were
found
to
have
an
elevated,
though
not
statistically
significant,
increase
in
risk
at
the
St.
Gabriel
plant";
"
other
studies
have
suggested
an
increased
risk
for
ovarian,
breast,
and
other
cancers,
including
non­
Hodgkin's
lymphoma."
NRDC
agrees
that
the
study
is
likely
underpowered,
but
points
out
that
insufficient
statistical
power
predictably
results
in
an
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

15
underestimate
of
the
magnitude
of
an
association
between
an
exposure
and
disease.
In
addition,
the
"
healthy
worker
effect"
predictably
results
in
lower
rates
of
chronic
diseases
such
as
cancer
among
active
workers,
making
these
results
all
the
more
unusual.

The
St.
Gabriel
study
was
sent
by
the
EPA
to
four
reviewers,
and,
while
one
reviewer
(
Giovannucci)
accepted
the
industry­
authors
suggestion
that
the
excess
in
cancer
was
due
to
the
company's
PSA­
screening
initiative,
the
other
three
(
Hayes,
Morrison,
Blair)
were
not
so
easily
convinced.
In
fact,
in
contrast
to
Giovannucci,
the
other
three
epidemiologists
all
point
out
that
no
definite
conclusions
can
be
drawn,
positive
or
negative,
from
such
a
weak
study,
and
suggest
improvements
by
which
it
might
be
more
informative.
xvi
1.
Study
summary.

The
findings
of
the
Syngenta/
Novartis
study
of
the
atrazine
manufacturing
plant
are
presented
in
the
Table
below.
All
data
is
from
the
company
study
submitted
to
the
EPA.
Note
that
the
company
divided
the
cohort
of
workers
into
active
and
inactive
employees,
to
designate
whether
they
were
currently
employed
by
the
plant,
or
former
employees.
The
cohort
was
also
divided
into
company
and
contract
employees.
Note
that
the
excess
in
prostate
cancers
(
11
v.
1.8)
is
in
the
active
company
employees,
the
same
group
that
also
received
intensive
PSA­
screening.
.
Note
also
that
the
efforts
to
locate
inactive
employees
and
contract
employees
were
exceptionally
poor
in
this
study.
For
example,
the
researchers
made
no
efforts
to
locate
inactive
employees
if
they
had
moved
out
of
Louisiana.
This
makes
it
quite
possible,
or
even
likely,
that
cases
were
missed
in
the
inactive
worker
groups.

Observed/
expected
number
of
prostate
cancers,
by
employee
group,
1985­
1999.
Expected
values
are
derived
from
comparison
with
the
industrial
corridor.
xvii
ACTIVE
INACTIVE
TOTAL
COMPANY
11/
1.8
3/
3.7
14/
5.5
CONTRACT
1/
1.1
2/
3.0
3.0/
4.1
TOTAL
12/
2.9
5/
5.6
17/
9.5
2.
Syngenta
downplays
atrazine's
risks.

Although
industry
makes
much
of
the
fact
that
IARC
has
recently
down­
graded
atrazine
from
group
2B
(
possible
human
carcinogen)
to
group
3
(
unable
to
be
classified),
Dr.
Morrison
correctly
points
out
the
fact
that
this
"
hasn't
been
without
controversy."
Morrison
refers
to
a
published
scientific
article
by
NIEHS
senior
scientist
James
Huff,
suggesting
that
atrazine
is
a
victim
of
an
increased
reliance
on
industry
data
and
increased
industry
representation
on
evaluation/
advisory
panels,
resulting
in
a
trend
towards
disregarding
evidence
of
carcinogenesis.
xviii
Morrison
challenges
the
industry
assertion
that
there
are
no
data
to
suggest
carcinogenicity,
stating,
"
to
say
that
there
is
no
prior
biological
or
eidemiological
evidence
that
atrazine
is
a
human
carcinogen
is
misleading.
For
an
example
of
the
non­
existent
epidemiological
evidence,
see
[
Schroeder
et
al,
1991].
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

16
Many
other
examples
of
positive
epidemiological
literature
are
cited
by
the
review
by
the
Natural
Resources
Defense
Council."
Morrison
also
points
out
that
"[
t]
he
[
NRDC]
review
makes
much
of
the
finding
of
11
cases,
when
1.2
were
expected,
among
company
employees
actively
working
at
diagnosis.
This
is
a
curious
and
suggestive
finding,
which
isn't
adequately
dealt
with
in
the
paper
by
MacLennan
et
al."
(
emphasis
added).
And,
although
the
industry
provides
very
little
exposure
history
of
the
cases,
and
none
for
the
controls,
they
suggest
that
the
lack
of
a
clear
dose­
response
should
be
interpreted
as
a
lack
of
a
causal
association.
Morrison
disagrees,
and
asks,
"[
j]
ust
how
much
could
you
say
about
dose­
response
when
you[
r]
study
only
has
11
cases?"

3.
Tellingly,
the
authors
of
the
Syngenta
study
have
not
attempted
to
provide
quantitative
estimates
of
the
impact
of
PSA
screening
on
prostate
cancer
incidence.

Dr.
Hayes
provides
a
suggestion
for
better
quantifying
the
impact
of
PSA
screening
on
prostate
cancer
incidence
among
this
cohort,
since
the
issue
is
germane
to
the
interpretation
of
the
data.
He
suggests
that
"
further
analysis
of
risk
by
calendar
period,
comparing
PSA
screening
v.
non­
screening
time­
periods,
could
provide
some
insight
into
this
important
issue."
Dr.
Blair
supports
the
need
for
this
information
by
saying,
"
a
few
additional
analyses
of
prostate
cancer
risk
before
and
after
initiation
of
screening
would
also
provide
direct
information
on
the
impact
of
the
screening."
NRDC
suggests
that
it
is
both
significant
and
curious
that
the
manufacturer
has
made
no
attempt
to
quantify
the
impact
of
PSA
screening
on
the
cancer
incidence,
despite
its
confident
assertions
that
PSA
screening
accounts
for
all
the
excess
in
prostate
cancers.

4.
Quantitative
exposure
assessment
should
be
done
for
cases
and
controls.

Syngenta,
after
requests
from
NRDC
and
the
EPA,
provided
some
limited
qualitative
estimates
of
exposure
for
the
prostate
cancer
cases.
Dr.
Aaron
Blair
states,
"[
t]
o
clearly
understand
the
issue
of
prostate
cancer
and
atrazine
exposure
in
this
cohort
it
is
essential
that
a
quantitative
exposure
assessment
be
added."
Blair
challenges
the
company
to
provide
this
information,
saying,
"[
I]
f
it
is
possible
to
reconstruct
possible
atrazine
exposure
for
cases,
as
was
done
for
this
report,
it
could
be
done
for
controls
also."
xix
Without
proper
case­
control
comparisons,
Dr.
Blair
points
out
that
the
information
about
exposure
among
cases
is
not
very
informative.
Morrison
also
raises
concern
about
the
lack
of
this
critical
information,
stating,
"[
t]
he
[
NRDC]
has
correctly
identified
the
lack
of
exposure
histories
of
workers
as
both
significant
and
curious."
(
emphasis
added).

5.
The
industry­
proposed
nested
case­
control
study
is
likely
to
be
uninformative.

The
reviewers
expressed
concern
that
the
industry­
proposed
nested
case­
control
study,
would
likely
be
uninformative
due
to
the
small
number
of
cases,
and
without
some
design
corrections.
Dr.
Blair
states
that
"
the
small
number
of
cases
would
be
a
severe
limitation"
to
any
case­
control
comparisons.
Morrison
states
that
"[
t]
he
[
industry]
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

17
proposed
nested
case­
control
study
lacks
any
discussion
of
the
abysmal
lack
of
power
the
study
will
realistically
have.
It
would
be
a
great
study
for
the
company
to
have
conducted,
given
that
it
has
little
likelihood
of
observing
a
statistically
significant
effect
because
it
will
be
underpowered."
Hayes
suggests
that
while
"
comparisons
of
exposure
history
of
prostate
cases
and
non­
cases
 
coupled
with
individual
data
on
PSA
screening
 
could
provide
insight "
the
Exponent
proposal
will
be
compromised
from
the
small
number
of
cases.
Hayes
suggests
using
the
full
cohort,
or
a
random
sample,
to
reconstruct
risks.

6.
The
reviewers
concluded
that
the
study
is
underpowered
and
suffers
methodological
limitations,
so
that
the
contribution
of
atrazine
to
the
observed
excess
cancers
cannot
be
ruled
out.

While
the
reviewers
are
clearly
disappointed
in
the
lack
of
effort
to
provide
such
important
information
as
exposure
histories
for
both
cases
and
controls,
they
conclude
that
the
study
cannot
rule
out
the
possible
association
of
atrazine
with
the
observed
excess
in
cancers.
Morrison
concludes,
"
while
there
was
almost
definitely
some
increased
prostate
cancer
case
finding
because
of
the
increased
PSA
screening,
there
was
a
suggestion
that
this
might
not
be
the
entire
explanation."
xx
Hayes
states
"[
w]
hile
PSA
screening
may
account
for
much
of
the
excess
of
prostate
cancer
in
this
Triazine
manufacturing
facility,
it
would
be
premature
to
reject
a
potential
role
of
occupational
exposure
to
triazines
as
a
contributing
factor
to
the
observed
excess
of
this
disease."
xxi
NRDC
concurs
with
the
conclusions
of
the
reviewers,
that
the
study
is
underpowered
and
has
some
significant
design
problems.
However,
we
do
not
think
that
these
flaws
are
justification
to
completely
ignore
the
results
of
this
study.
Instead,
we
believe
the
Agency
must
make
every
effort
to
work
with
Syngenta
to
update
the
new
cancer
cases
through
2002,
gather
the
additional
exposure
data
on
these
workers,
and
to
patch
some
of
the
other
gaps
in
this
study.
In
addition,
EPA
must
consider
this
study
in
the
context
of
all
the
evidence
related
to
atrazine
and
cancer
NRDC
again
insists
that
the
EPA
must
consider
all
the
evidence,
as
required
by
the
2003
Draft
Cancer
Guidelines,
in
evaluating
atrazine.
While
one
or
two
weak
studies
may
not
be
conclusive,
the
2003
Guidelines
dictate
that
a
handful
of
weak
epidemiology
studies
suggesting
an
association,
coupled
with
evidence
in
animal
studies,
and
with
the
evidence
that
there
are
at
least
two
possible
modes
of
action
(
LH
disruption,
aromatase
activation),
dictate
that
atrazine
must
be
classified
as
a
likely
or
suggested
carcinogen.

B.
Consistent
with
the
2003
Draft
Cancer
Guidelines,
Atrazine
Is
a
"
Likely"
or
"
Suggested"
Human
Carcinogen.

Atrazine
has
sufficient
evidence
of
carcinogenicity
in
animal
data,
but
insufficient
evidence
in
humans,
according
to
the
International
Agency
for
Research
on
Cancer
(
IARC).
xxii
A
demonstrated
mode
of
action
is
attenuation
of
leutenizing
hormone
(
LH),
which
is
hypothesized
to
explain
the
observed
tumor
response
in
rats,
but
is
unlikely
to
induce
tumor
formation
in
humans.
However,
the
recent
decision
by
the
EPA
to
classify
it
as
"
not
likely"
a
human
carcinogen
is
inconsistent
with
the
2003
Guidelines,
and
with
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

18
the
IARC
criteria.
The
IARC
states
that
the
classification
of
"
not
a
human
carcinogen"
requires
a
wealth
of
data,
including
multiple,
mutually
consistent,
adequately
powered
studies
covering
the
full
range
of
human
exposures
that
exclude
with
reasonable
certainty
bias,
confounding,
and
chance
to
provide
individual
and
pooled
estimates
of
risk
near
unity
with
narrow
confidence
intervals.
xxiii
Importantly,
IARC
cautions
that
latent
periods
substantially
shorter
than
30
years
cannot
provide
evidence
for
lack
of
carcinogenicity
(
workers
in
the
St.
Gabriel
study
have
a
median
of
18
years
follow­
up).
In
no
way
should
the
absence
of
data
be
considered
an
absence
of
carcinogenicity.

The
2003
Cancer
Guidelines
provide
a
framework
for
"
judging
whether
available
data
support
a
mode
of
carcinogenic
action
hypothesized
for
an
agent."
xxiv
This
framework
incorporates
the
criteria
for
causality
used
in
epidemiological
studies,
as
stated
by
Bradford
Hill
(
1965),
with
subsequent
modifications.
The
author
and
those
who
use
these
criteria
understand
that
each
criterion
support
the
determination
of
causality,
and
the
more
criteria
that
are
satisfied,
the
stronger
the
evidence
for
causality.
However,
it
is
not
necessary,
and
not
likely,
that
all
criteria
are
satisfied
to
demonstrate
causality.
xxv
Further,
the
Guidelines
remind
the
user
that
support
for
one
mode
of
action
does
not
limit
the
possibility
of
other
modes
of
action.
Rather,
the
Agency
is
obligated
to
consider
the
highly
likely
possibility
of
other
modes
of
action
that
may
be
consistent
with
tumor
formation
in
humans.
For
example,
atrazine
has
been
shown
in
animals
and
in
humanderived
cell
cultures
to
stimulate
aromatase
activity,
resulting
in
conversion
of
testosterone
to
estrogen.
Might
this
mode
of
action
cause
or
contribute
to
observed
mammary
tumors
in
male
atrazine­
exposed
animals?
The
possibility,
coupled
with
all
existing
experimental
and
epidemiological
data,
xxvi
would
suggest
that
atrazine
would
more
appropriately
be
classified
as
a
"
likely"
or
"
suggested"
human
carcinogen,
according
to
the
2003
Guidelines,
and
confirmed
in
conversations
with
EPA
scientists
W.
Wood,
W.
Farland,
and
J.
Cogliano.

IX.
SUBSTANTIAL
DATA
DEMONSTRATE
THAT
ATRAZINE
IS
AN
ENDOCRINE
DISRUPTOR.

In
establishing
a
tolerance
for
atrazine,
EPA
is
expressly
required
to
consider
any
effect
"
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen
or
other
endocrine
effects."
FFDCA
§
408(
c)(
2)(
D)(
viii),
21
U.
S.
C.
§
346(
c)(
2)(
D)(
viii).
The
evidence
in
laboratory
animals
of
atrazine
as
an
endocrine
disruptor
is
particularly
troublesome
given
that
the
highest
tumor
incidence
among
the
U.
S.
population,
regardless
of
race,
is
now
prostate
and
breast
cancers,
both
cancers
of
endocrine
glands,
and
both
showing
increasing
incidence
trends.
xxvii
Dr.
Hayes
of
the
National
Cancer
Institute
points
out
in
his
review
for
the
EPA
of
the
excess
prostate
cancers
among
workers
in
the
atrazine
manufacturing
plant,
that,

[
s]
teroidal
hormones
are
believed
to
play
a
role
[
in
prostate
cancer]
because
of
their
importance
in
prostate
development,
prostate
cancer
management,
and
their
successful
use
in
experimental
disease
induction.
While
testosterone
and
its
metabolites
are
the
prime
suspects,
inter­
relationships
in
prostate
carcinogenesis
with
estrogenic
compounds
may
also
be
important.
Atrazine
and
related
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

19
compounds
have
profound
estrogen
disrupting
capacity
in
amphibians
at
a
very
low
dose
[
Hayes
et
al,
2002]
xxviii
Atrazine
disrupts
sexual
development
in
experimental
animals.
When
nursing
rats
were
treated
with
atrazine
the
male
offspring
developed
prostate
gland
inflammationxxix
(
note,
this
study
was
done
by
EPA
staff
scientists).
It
is
not
known
if
prostatitis
will
proceed
to
prostate
cancer.
Treatment
of
rats
with
atrazine
from
weaning
until
puberty
resulted
in
delayed
sexual
maturityxxx
(
note,
this
study
was
done
by
EPA
staff
scientists).
Atrazine
reduced
the
ability
of
active
testosterone
to
bind
to
its
receptor
in
the
prostate
gland,
thus
reducing
its
effectiveness.
xxxi
Atrazine
reduced
the
ability
of
testosterone
to
convert
to
its
active
form
in
rat
prostate
gland.
xxxii
Atrazine
has
been
shown
to
be
toxic
to
sperm,
and
reduced
sperm
motility
in
exposed
rats.
xxxiii
Atrazine
acts
in
amphibians
to
disrupt
reproductive
organ
development.
The
following
summary
of
supporting
data
is
excerpted
from
unpublished
notes
compiled
by
Dr.
Tyrone
Hayes,
Berkeley
Univ,
CA.
Following
exposure
to
21
ppb
(
µ
g/
L)
for
only
48
hours,
atrazine­
exposed
Xenopus
laevis
(
frog)
males
suffered
from
testicular
resorption
that
resulted
in
gonadal
dysgenesis
(
small
underdeveloped
testis
with
decreased
germ
cell
numbers).
xxxiv
Effects
were
quite
significant
and
included
a
57%
reduction
in
testicular
volume,
a
70%
reduction
in
primary
spermatogonial
cell
nests
(
which
represent
the
germ
cells
for
the
life
of
the
organism),
a
74%
reduction
in
the
nurse
cells
(
which
represent
the
pool
of
sperm­
nourishing
cells
for
the
organism's
life),
testicular
resorption
in
70%
of
the
exposed
males,
and
failure
of
full
development
in
10%
of
the
exposed
males.
Atrazine
induced
feminization
of
male
gonads
in
X.
laevis;
hermaphroditism
and
gonadal
dysgenesis
occurred
in
16­
20%
of
the
exposed
frogs
(
32­
40%
of
the
males).
xxxv
In
similar
studies
in
wild
Rana
pipiens
(
frogs),
testicular
oocytes
were
observed
at
0.1
and
25
µ
g/
L
atrazine
at
all
sites
where
water­
concentrations
of
atrazine
was
measured
in
excess
of
0.1
µ
g/
L.
xxxvi
xxxvii
The
observed
gonadal
abnormalities
associated
with
atrazine
exposure
in
amphibians
are
of
great
concern:
32­
40%
of
the
males
in
X.
laevis,
up
to
29%
of
the
male
Rana
pipiens
in
the
laboratory
and
up
to
92%
of
the
males
in
some
wild
populations.
Further,
Syngenta­
funded
researchers
James
Carr
and
others
treated
X.
laevis
larvae
throughout
development.
xxxviii
"
Carr
et
al.
(
2003)
report
a
concentrationdependent
relationship
between
atrazine
and
total
incidence
of
gonadal
abnormalities
males."
xxxix
Another
recent
study
funded
by
Syngenta
found
hermaphroditic
Bufo
marinus
(
cane
toads)
in
sugarcane
fields
treated
with
atrazine,
but
no
hermaphroditism
at
reference
sites
free
of
atrazine.
xl
In
fact,
males
in
contaminated
areas
had
female­
typical
skin
coloration,
had
measurable
vitellogenin
in
the
plasma
and
some
had
eggs.
xli
It
was
reported
that
this
work
"
lends
credence
to
University
of
Berkeley
endocrinologist
Tyrone
Hayes'
hypothesis
that
atrazine
is
affecting
sexual
development
of
amphibians,"
and
Syngenta­
funded
researcher
Tim
Gross
was
cited
"
adding
that
the
findings
are
consistent
with
the
previous
work
of
both
Hayes
and
Texas
Tech
experimental
toxicologist
James
Carr,
`
Carr
finds
an
effect
at
atrazine
concentrations
that
are
similar
to
what
we
see
in
the
field
and
to
what
we
think
the
toads
are
exposed.'"
xlii
Thus,
there
is
compelling
evidence
for
endocrine
effects
from
multiple,
mutuallyconsistent
studies
in
multiple
species,
with
sufficient
statistical
power.
There
is
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

20
compounding
and
compelling
evidence
for
multiple
mechanisms
of
action
of
atrazine
and
all
are
consistent
with
the
observed
effects
of
atrazine
on
reproductive
development
and
function
in
mammals
and
amphibians.
Many
agencies
have
identified
atrazine
as
an
endocrine
disruptor,
including
the
United
Kingdom's
Environmental
Agency,
the
European
Union,
the
Oslo
and
Paris
Commission
Convention
for
the
Protection
of
the
Marine
Environment
of
the
North­
East
Atlantic,
and
the
State
of
Illinois.
These
findings,
along
with
the
evidence
noted
above,
compel
a
finding
of
unreasonable
adverse
effects
on
the
environment
under
FIFRA,
and
cancellation
of
atrazine.

Under
FFDCA
§
408,
moreover,
EPA
cannot
determine
a
"
safe"
level
of
atrazine
at
which
there
is
a
"
reasonable
certainty
of
no
harm"
to
infants,
children,
and
vulnerable
populations
from
the
endocrine
disrupting
effects
of
atrazine,
and
therefore
the
agency
simply
cannot
leave
in
effect
any
tolerances
for
atrazine
under
FFDCA
§
408.
If
there
is
a
threshold
for
atrazine's
endocrine
effects,
EPA
has
not
found
it,
and
therefore
EPA
can
allow
no
greater
than
a
1
in
1
million
risk
of
any
endocrine
disrupting
effect
to
exposed
individuals
under
the
FFDCA.
If
EPA
had
found
a
threshold
for
atrazine's
endocrine
effects,
the
agency
would
have
to
scientifically
explain
and
justify
that
threshold
determination,
and
apply
that
in
determining
whether
any
tolerance
could
legally
issue,
using
appropriate
safety
factors
(
including
the
statutory
tenfold
safety
factor
to
protect
infants
and
children).

X.
CONCLUSION.

EPA's
Atrazine
IRED
is
significantly
flawed.
The
IRED
both
understates
legitimate
risks
from
atrazine
exposure
(
such
as
the
endocrine
effects)
and
ignores
the
risks
that
it
does
acknowledge
(
such
as
the
ecological
harm
and
jeopardy
to
endangered
species).
In
light
of
the
above
comments,
EPA
cannot
reregister
atrazine
without
violating
the
Agency's
obligation
under
FIFRA
to
prevent
unreasonable
adverse
effects
on
human
health
and
the
environment.
FIFRA
§
§
3(
c)(
5)
&
4(
g)(
2).

EPA
and
NRDC
resolved
litigation
in
NRDC
v.
Whitman,
No.
C­
99­
3701
WHA
(
N.
D.
Cal.),
through
a
consent
decree.
Pursuant
to
the
amended
consent
decree
between
EPA
and
NRDC
in
that
case,
affirmed
by
court
order
on
January
24,
2003,
EPA
must
sign
a
revised
Atrazine
IRED
by
October
31,
2003.
The
consent
decree
also
obligates
EPA
to
submit
a
paper
to
the
FIFRA
Scientific
Advisory
Panel
(
SAP)
for
review
and
comment
concerning
(
1)
the
significance
of
amphibian
risk
data;
(
2)
whether
there
is
a
need
for
additional
data
to
characterize
more
fully
atrazine's
potential
risks
to
amphibians;
and
(
3)
other
scientific
issues
concerning
atrazine,
including
"
the
significance
of
data
bearing
on
the
association
between
atrazine
exposure
and
the
incidence
of
prostate
or
other
cancer
in
humans."
EPA
must
develop
this
paper
and
submit
it
to
the
SAP
for
review
and
comment
by
July
31,
2003
 
three
months
before
the
October
31
revised
IRED
deadline.
NRDC
fully
expects
that
EPA
will
do
so,
and
we
will
treat
any
failure
to
do
so
as
a
breach
of
the
consent
decree
in
contempt
of
court.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

21
Please
feel
free
to
contact
us
at
(
202)
289­
6868
should
you
have
any
questions
about
these
comments.
Thank
you
for
the
opportunity
to
comment,
and
thank
you
in
advance
for
your
consideration.

Respectfully
submitted,

Jennifer
Sass,
Ph.
D.
Senior
Scientist
Aaron
Colangelo
Staff
Attorney
Erik
D.
Olson
Senior
Attorney
Gina
Solomon,
M.
D.
Senior
Scientist
i
Atrazine:
Response
to
Public
Comments
on
the
EPA's
April
16,
2002
Revised
Human
Health
Risk
Assessment
and
Associated
Documents
for
the
Reregistration
Eligibility
Decision
(
RED).
PC
Code:
080803.
DP
Barcode:
284707.
January
31,
2003
ii
NRDC
comments
to
EPA
on
the
revised
human
health
assessment
for
atrazine.
July,
2002.
Docket
#
OPP­
34237C
iii
Katten,
A.
California
Rural
Legal
Assistance
Foundation.
Presentation.
A
view
from
the
field:
Use
and
limitations
of
incident
data.
Worker
Risk
Seminar,
October,
2002.

Fenske,
R.
Univ
Washington.
Towards
more
accurate
assessments
of
occupational
pesticide
exposure.
Worker
Risk
Seminar,
October,
2002.

iv
California
Environmental
Protection
Agency,
Department
of
Pesticide
Regulation.
Compliance
Assessment
Report
(
Pesticide
Handler
and
Field
Worker
Safety
Survey,
June
1997­­
March
2001).
http://
www.
cdpr.
ca.
gov/
docs/
enfcmpli/
cmpasses.
pdf
v
Blondell,
J.
EPA.
Presentation.
Use
of
incident
data
in
exposure
evaluation.
Worker
Risk
Seminar,
October,
2002.

Calvert,
GM.
NIOSH­
CDC.
Presentation.
An
overview
of
SENSOR­
pesticides
tracking
acute
occupational
pesticide­
related
illness
in
the
US.
Worker
Risk
Seminar,
October,
2002.

vi
Reregistration
Eligibility
Science
Chapter
for
Atrazine,
Environmental
Fate
and
Effects
Chapter,
p.
1
(
Jan.
26,
2001).

vii
Kettle
WD,
deNoyelles
F
Jr,
Heacock
BD,
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AM.
Diet
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of
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from
experimental
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1987
Jan;
38(
1):
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52.
MRID
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viii
Kettle
et
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ix
Pinter
A,
Torok
G,
Borzsonyi
M,
et
al.
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term
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of
the
herbicide
atrazine
in
F344
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1990;
37(
5):
533­
44.
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
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22
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JT,
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L.
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A,
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13­
month
study
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albino
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intraperitoneal
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Ital
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x
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SK,
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risk
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tissue
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1986;
256(
9):
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7.

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SH,
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PA,
Blair
A.
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in
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Hodgkin's
lymphoma.
Epidemiology.
2001;
12(
6):
701­
9.

xi
Hoar
SK,
Blair
A,
Holmes
FF,
Boysen
C,
Robel
RJ.
Herbicides
and
colon
cancer.
Lancet.
1985;
1(
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1277­
8.

xii
Mills
PK.
Correlation
analysis
of
pesticide
use
data
and
cancer
incidence
rates
in
California
counties.
Arch
Environ
Health.
1998;
53(
6):
410­
3.

xiii
Mills
PK.
Correlation
analysis
of
pesticide
use
data
and
cancer
incidence
rates
in
California
counties.
Arch
Environ
Health.
1998;
53(
6):
410­
3.

xiv
Daniels
JL,
Olshan
AF,
Savitz
DA.
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and
childhood
cancers.
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105(
10):
1068­
77.

xv
SEER
Cancer
Statistics
Review
1973­
1999.
National
Cancer
Institute.
Section
XXVII,
Childhood
cancer
by
site,
incidence,
survival,
and
mortality.

xvi
Blondell,
J.
EPA.
Review
of
additional
data
on
potential
atrazine
exposure
and
review
comments
submitted
by
Syngenta
and
NRDC
on
atrazine
cancer
epidemiology
study:
"
Follow­
up
study
of
cancer
incidence
among
workers
in
triazine­
related
operations
at
the
Novartis
St.
Gabriel
plant"
by
Elizabeth
Delzell
et
al.
DP
Barcode
D287278,
MRID#
455184­
01.
January
15,
2003
xvii
Delzell
E,
Sathiakumar
N,
MacLennan
P,
Grizzle
W,
Cheng
H.
2001.
A
follow­
up
study
of
cancer
incidence
among
workers
in
triazine­
related
operations
at
the
Novartis
St.
Gabriel
plant.
Syngenta
Number
2207­
01.
Data
taken
from
Tables
17,
18.

xviii
Huff
J.
IARC
monographs,
industry
influence,
and
upgrading,
downgrading,
and
under­
grading
chemicals:
a
personal
point
of
view.
International
Agency
for
Research
on
Cancer.
Int
J
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Environ
Health.
2002;
8(
3):
249­
70
xix
op
cit.
Blondell,
2003.
p.
27
xx
op
cit.
Blondell,
2003.
p.
17
xxi
op
cit.
Blondell,
2003.
p.
23
NRDC
comments
on
the
Atrazine
IRED.
April,
2003.
Docket
OPP­
2003­
0072.

23
xxii
IARC.
Atrazine.
International
Agency
for
Research
on
Cancer
Monogr
Eval
Carcinog
Risks
Hum.
Vol
73,
1999.

xxiii
Melnick
RL,
Kamel
F,
Huff
J.
2003.
Declaring
chemicals
"
not
carcinogenic
to
humans"
requires
validation,
not
speculation.
Environ
Health
Perspect,
111
(
4);
A204
xxiv
Draft
Cancer
guidelines.
2003.
p.
2­
31.
Section
2.5.3
xxv
Draft
Cancer
guidelines.
2003.
p.
2­
31,
lines
30­
32
xxvi
Hoar
SK,
Blair
A,
Holmes
FF,
Boysen
CD,
Robel
RJ,
Hoover
R,
et
al.
Agricultural
herbicide
use
and
risk
of
lymphoma
and
soft­
tissue
sarcoma.
Jama
1986;
256(
9):
1141­
7.

Zahm
SH,
Weisenburger
DD,
Saal
RC,
Vaught
JB,
Babbitt
PA,
Blair
A.
The
role
of
agricultural
pesticide
use
in
the
development
of
non­
Hodgkin's
lymphoma
in
women.
Arch
Environ
Health
1993;
48(
5):
353­
8.

Schroeder
JC,
Olshan
AF,
Baric
R,
Dent
GA,
Weinberg
CR,
Yount
B,
et
al.
Agricultural
risk
factors
for
t(
14;
18)
subtypes
of
non­
Hodgkin's
lymphoma.
Epidemiology
2001;
12(
6):
701­
9.

Hoar
SK,
Blair
A,
Holmes
FF,
Boysen
C,
Robel
RJ.
Herbicides
and
colon
cancer.
Lancet
1985;
1(
8440):
1277­
8
Mills
PK.
Correlation
analysis
of
pesticide
use
data
and
cancer
incidence
rates
in
California
counties.
Arch
Environ
Health
1998;
53(
6):
410­
3.

MacLennan
PA,
Delzell
E,
Sathiakumar
N,
Myers
SL,
Cheng
H,
Grizzle
W,
Chen
VW,
Wu
XC.
Cancer
incidence
among
triazine
herbicide
manufacturing
workers.
J
Occup
Environ
Med.
2002
Nov;
44(
11):
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