Page
1
of
16
Overview
of
the
PCNB
Risk
Assessments
August
18,
2004
Introduction
This
document
summarizes
EPA's
human
health
and
ecological
risk
findings
and
conclusions
for
the
fungicide
pentachloronitrobenzene
(
PCNB),
as
presented
fully
in
the
documents,
"
Pentachloronitrobenzene
(
PCNB):
Revised
HED
Chapter
of
the
Reregistration
Eligibility
Decision
Document
(
RED),"
dated
July
27,
2004,
and
the
"
Environmental
Fate
and
Ecological
Risk
Assessment
for
the
Re­
registration
of
Pentachloronitrobenzene,"
dated
July
26,
2004.
The
purpose
of
this
overview
is
to
assist
the
reader
by
identifying
the
key
features
and
findings
of
these
risk
assessments
and
conclusions
reached
in
the
assessments.
This
overview
was
developed
in
response
to
comments
and
requests
from
the
public
which
indicated
that
the
risk
assessments
were
difficult
to
understand,
that
they
were
too
lengthy,
and
that
it
was
not
easy
to
compare
the
assessments
for
different
chemicals
due
to
the
use
of
different
formats.

The
PCNB
risk
assessments
and
supporting
documents
are
posted
on
EPA's
Internet
website
(
http://
www.
epa.
gov/
pesticides/)
and
are
available
in
the
Pesticide
Docket
for
public
viewing.
Meetings
with
stakeholders
will
be
held
to
discuss
the
risk
assessments
and
solicit
input
on
risk
mitigation
strategies,
if
needed.
This
feedback
will
be
used
to
complete
the
Reregistration
Eligibility
Decision
(
RED)
document,
which
will
include
the
resulting
risk
management
decisions.
The
Agency
plans
to
conduct
a
close­
out
conference
call
with
interested
stakeholders
to
describe
the
regulatory
decisions
presented
in
the
RED.

Risks
summarized
in
this
document
are
those
that
result
only
from
the
use
of
PCNB.
The
Food
Quality
Protection
Act
(
FQPA)
requires
that
the
Agency
consider
"
available
information"
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
"
other
substances
that
have
a
common
mechanism
of
toxicity."
The
reason
for
consideration
of
other
substances
is
due
to
the
possibility
that
low­
level
exposures
to
multiple
chemical
substances
that
cause
a
common
toxic
effect
by
a
common
toxic
mechanism
could
lead
to
the
same
adverse
health
effect
as
would
a
higher
level
of
exposure
to
any
of
the
substances
individually.
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
EPA
has
not
made
a
common
mechanism
of
toxicity
finding
for
PCNB
and
any
other
substances;
PCNB
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
this
action,
therefore,
EPA
has
not
assumed
that
PCNB
has
a
common
mechanism
of
toxicity
with
other
substances.
For
information
regarding
EPA's
efforts
to
determine
which
chemicals
have
a
common
mechanism
of
toxicity
and
to
evaluate
the
cumulative
effects
of
such
chemicals,
see
the
policy
statements
released
by
EPA's
Office
of
Pesticide
Programs
concerning
common
mechanism
determinations
and
procedures
for
cumulating
effects
from
substances
found
to
have
a
common
mechanism
on
EPA's
website
at
http://
www.
epa.
gov/
pesticides/
cumulative/.
Page
2
of
16
Use
Profile
$
Fungicide:
PCNB
is
an
organochlorine
fungicide
used
to
control
diseases
on
vegetables
(
predominantly
cole
crops
and
green
beans),
field
crops
(
cotton,
potatoes,
and
peanuts),
turf,
ornamentals
and
seeds
(
seed
treatments
of
barley,
beans,
corn,
cotton,
oats,
peas,
peanut,
potato,
safflower,
sorghum,
soybean,
sugar
beet,
and
wheat).
It
is
applied
to
soil,
foliage
(
for
turf
uses),
and
seeds.

$
Tolerances:
There
is
a
tolerance
of
0.1
ppm
established
for
PCNB
in
or
on
cottonseed.
Regional
tolerances
of
0.2
ppm
are
established
for
the
combined
residues
of
PCNB
and
its
metabolites
PCA
and
MPCPS
(
PCTA)
in
or
on
collards,
kale,
and
mustard
greens
[
40
CFR
180.291].
Interim
tolerances
are
established
for
bean,
broccoli,
brussels
sprouts,
cabbage,
cauliflower,
garlic,
pepper,
potato,
and
tomato
at
0.1
ppm.
There
is
an
interim
tolerance
of
1.0
ppm
for
peanuts
[
40
CFR
180.319].
The
interim
tolerances
are
in
effect
pending
evaluation
of
petitions
for
tolerances
for
negligible
residues.

$
Formulations:
Flowable
concentrate,
water
dispersible
granular,
wettable
powder,
emulsifiable
concentrate,
granular,
dust,
and
ready­
to­
use
formulations.

$
Method
of
Application:
Seed
treatment,
pre­
plant
incorporated
applications,
in­
furrow
applications,
broadcast
applications,
or
banded
applications
using
ground
equipment.

$
Use
Rates:
The
maximum
application
rate
for
turf
is
33
lb.
ai/
A,
at
two
applications/
season.
Maximum
application
rates
for
field
and
vegetable
crops
are
10­
30
lb.
ai/
A
with
one
application/
season.
Ornamental
bulbs
are
dip­
treated
prior
to
planting
at
213
lb.
ai./
A
for
the
highest
yearly
application
rate.

$
Annual
Poundage:
Total
agricultural
usage
between
2000­
2002
was
estimated
at
600,000­
800,000
lbs/
year:

$
Cotton
500,000
lbs/
year,
5%
crop
treated
$
Potatoes
200,000
lbs/
year
(
increasing
recently),
7%
crop
treated
$
Green
Beans
30,000
lbs/
year,
15%
crop
treated
$
Cabbage
10,000
lbs/
year,
<
1%
crop
treated
$
Cauliflower
5,000
lbs/
year,
1%
crop
treated
$
Peanuts
5,000
lbs/
year,
<
1%
crop
treated
$
Brussels
sprouts
4,000
lbs/
year,
6%
crop
treated
Turf
use
was
estimated
at
250,000­
500,000
lbs/
year
(
mostly
golf
courses;
decreasing
recently).

$
Technical
Registrants:
Uniroyal
and
Amvac
are
supporting
registrations
with
soil
and
seed
treatment
applications.
Gustafson
is
the
primary
seed
treatment
registrant.
Page
3
of
16
Human
Health
Risk
Assessment
Acute
Dietary
(
Food)
Risk
(
For
a
compete
discussion,
see
section
4.3.2.1
of
the
Human
Health
Risk
Assessment)

No
adverse
effects
attributed
to
a
single
exposure
(
dose)
were
identified.
Therefore,
no
acute
dietary
risk
assessment
was
conducted.

Chronic
Dietary
(
Food)
Risk
(
For
a
compete
discussion,
see
section
4.3.2.2
of
the
Human
Health
Risk
Assessment)

Chronic
dietary
risk
is
calculated
by
using
the
average
consumption
values
for
food
and
average
residue
values
for
those
foods
over
a
70­
year
lifetime.
A
risk
estimate
that
is
less
than
100%
of
the
chronic
PAD
(
the
dose
at
which
an
individual
could
be
exposed
over
the
course
of
a
lifetime
and
not
expect
an
adverse
health
effect)
does
not
exceed
the
Agency's
level
of
concern.

The
chronic
dietary
risk
(
food
only)
for
PCNB
does
not
exceed
the
Agency's
level
of
concern
(
i.
e.,
less
than
100%
of
the
chronic
PAD
is
utilized).

$
The
toxicological
endpoints
are
liver
and
thyroid
effects,
as
seen
at
the
lowest
observed
adverse
effect
level
(
LOAEL)
of
150
mg/
kg/
day
in
the
chronic/
oncogenicity
feeding
study
in
rats.
The
no
observed
adverse
effect
level
(
NOAEL)
in
this
study
is
1.0
mg/
kg/
day.

$
The
10X
special
FQPA
safety
factor
was
reduced
to
1X
because
there
are
no
residual
uncertainties
for
pre­
and/
or
postnatal
toxicity.

$
A
database
uncertainty
factor
of
10x
(
UF
DB
of
10x)
has
been
applied
to
the
dietary
and
residential/
recreational
risk
assessments
on
the
absence
of
comparative
thyroid
data.

$
The
dietary
exposure
assessment
for
food
includes
the
parent
compound,
pentachloroaniline
(
PCA),
and
pentachlorothioanisole
(
PCTA),
which
are
also
included
in
the
tolerance
expression.
There
is
little
information
available
on
the
metabolites,
and
toxicological
equivalence
to
the
parent
was
assumed.

$
The
chronic
PAD
(
cPAD)
is
calculated
to
be
0.001
mg/
kg/
day
derived
from
a
NOAEL
of
1.0
mg/
kg/
day,
an
Uncertainty
Factor
of
100
that
includes
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation,
1X
for
FQPA,
and
10X
for
database
uncertainty.

$
The
highest
estimated
risks
are
for
children
1­
2
years
of
age
(
34%
cPAD).
The
major
contribution
to
the
risk
came
from
milk
fat,
followed
by
brassica
vegetables.
Page
4
of
16
Cancer
Dietary
(
Food)
Risk
(
For
a
complete
discussion,
see
section
4.3.2.3
of
the
Human
Health
Risk
Assessment.)

PCNB
is
classified
as
a
Group
C
(
possible
human)
carcinogen.
Because
evidence
of
carcinogenic
effects
is
weak,
a
dose
response
assessment
for
cancer
was
not
conducted.

Drinking
Water
Dietary
Risk
Drinking
water
exposure
to
pesticides
can
occur
through
groundwater
and
surface
water
contamination.
Estimated
Drinking
Water
Concentrations
(
EDWCs)
were
calculated
to
estimate
the
potential
contribution
to
acute
and
chronic
dietary
exposures
from
drinking
water.
EDWCs
for
surface
water
bodies
were
determined
using
the
Tier
II
screening­
level
simulation
models
PRZM
(
v.
3.12)/
EXAMS
(
2.98.04).
The
Tier
I
screening
model
SCI­
GROW
was
used
to
calculate
the
groundwater
EDWCs.

EDWCs
for
Drinking
Water
Risk
Assessment
Surface
water
drinking
water
sources
1­
in­
10­
years
(
chronic):
44.2
ug/
L
(
ppb)

Groundwater
drinking
water
sources
30.6
ug/
L
(
ppb)

EDWCs
are
compared
to
Drinking
Water
Levels
of
Concern
(
DWLOCs)
to
determine
if
drinking
water
exposures,
when
added
to
food
exposures,
exceed
dietary
levels
of
concern.

Acute
water
risk:

$
No
adverse
effects
attributed
to
a
single
exposure
were
identified.
Therefore,
no
acute
drinking
water
risk
assessment
was
conducted.

Chronic
water
risk:

$
In
the
absence
of
environmental
fate
data
on
the
metabolites,
their
mobility
into
sources
of
drinking
water
is
assumed
to
be
the
same
as
the
parent.
Only
risks
associated
with
PCNB
and
its
metabolite
pentachloroaniline
(
PCA)
were
quantified
in
the
drinking
water
assessment.

$
Results
of
the
chronic
drinking
water
risk
assessment
are
captured
under
the
section
on
"
Aggregate
Risk"
below.
Page
5
of
16
Residential
Risk
(
For
a
complete
discussion,
see
section
4.5
of
the
Human
Health
Risk
Assessment)

$
PCNB
is
registered
for
use
on
residential
lawns.
It
is
not
a
restricted­
use
chemical;
homeowners
may
obtain
and
apply
PCNB
to
the
lawn
to
treat
fungal
diseases.
Product
labels
recommend
no
more
than
2
applications
per
year.
Screening­
level
assumptions
are
incorporated
into
residential
exposure
assessments
and
result
in
high­
end
estimates.

$
Adults
may
be
exposed
to
PCNB
through
dermal
contact
with
the
lawn,
and
through
application
and
mowing.

$
Children
(
especially
toddlers)
may
be
exposed
through
dermal
contact
with
the
treated
lawn,
and
through
hand
to
mouth,
object
to
mouth,
and
incidental
ingestion
exposures.

Dermal
and
Inhalation
Toxicity
The
following
endpoints
and
factors
were
used
in
estimating
dermal
and
inhalation
risks:

Dermal
Toxicity
$
Short­
(
1­
30
days)
and
intermediate­
term
(
1­
6
months)
dermal
endpoints
are
based
on
a
NOAEL
of
300
mg/
kg/
day
from
a
21­
day
dermal
toxicity
study
in
rats
in
which
adverse
thyroid
effects
were
observed
at
a
LOAEL
of
1000
mg/
kg/
day.

$
The
long­
term
(
6
months­
lifetime)
dermal
endpoint
is
based
on
a
NOAEL
of
1.0
mg/
kg/
day
from
a
chronic
toxicity
study
in
rats
in
which
adverse
liver
and
thyroid
effects
were
observed
(
same
endpoint
used
in
dietary
assessment).

$
Dermal
absorption
was
estimated
at
33%
based
on
comparison
of
the
systemic
LOAEL
(
333
mg/
kg/
day)
from
the
subchronic
oral
toxicity
study
in
male
rats
and
the
LOAEL
(
1000
mg/
kg/
day)
from
the
21­
day
dermal
toxicity
study
in
the
rat.
Thyroid
toxicity
was
the
common
toxic
effect
for
both
routes
of
exposure.

Inhalation
Toxicity
$
No
inhalation
toxicity
studies
are
available.
Absorption
by
the
inhalation
route
is
considered
to
be
equivalent
to
absorption
by
the
oral
route.

$
Short­
and
intermediate­
term
incidental
oral
and
inhalation
endpoints
are
based
on
a
LOAEL
of
1.0
mg/
kg/
day
and
NOAEL
of
less
than
1.0
mg/
kg/
day,
from
a
90­
day
oral
study
in
rats
in
which
thyroid
effects
were
observed.

$
The
long­
term
inhalation
endpoint
is
based
on
a
NOAEL
of
1.0
mg/
kg/
day,
from
a
chronic
oral
toxicity
study
in
rats
in
which
adverse
liver
and
thyroid
effects
were
observed.
Page
6
of
16
Residential
Handler
(
mixer/
loading/
applying)

$
Target
dermal
and
inhalation
Margins
of
Exposure
(
MOE)
for
short­
term
exposures
are
both
1000.
MOE's
below
1000
are
a
concern.

$
Calculated
MOEs
for
residential
applicators
using
PCNB
on
lawns
are
provided
in
the
table
below.

Scenario
Dermal
MOE
Inhalation
MOE
Hand
application
of
granules
65
200
Mixing/
Loading/
Applying
Liquids
for
Low
Pressure
Handwand
application
280
3100
Mixing/
Loading/
Applying
Liquids
for
Backpack
sprayer
application
5500
3100
Mixing/
Loading/
Applying
Liquids
for
Garden
hose­
end
sprayer
(
ORETF
­
RTU)
application
490
390
Mixing/
Loading/
Applying
Liquids
for
Garden
hose­
end
sprayer
(
ORETF
­
conventional)
application
120
250
Loading/
Applying
Granulars
for
Belly
Grinder
application
12
69
Loading/
Applying
Granulars
for
Push­
type
spreader
(
ORETF)
application
1900
4900
Loading/
Applying
Granulars
for
Push­
type
spreader
(
ORETF)
application
1400
3700
$
Residential
risks
are
of
concern
for
several
scenarios,
including
hand
application
of
granules,
mixing/
loading/
applying
liquids
with
a
low
pressure
handwand
and
hose­
end
sprayers,
and
loading/
applying
granules
with
a
belly
grinder.

Residential
and
Recreational
Post­
application
$
The
scenarios
likely
to
result
in
residential
post­
application
exposures
are
dermal
contact
for
adults
and
toddlers
to
treated
turf
and
lawns,
and
oral
exposure
to
toddlers
from
ingestion
of
grass,
soil,
or
hand­
to­
mouth
contact.
Inhalation
exposure
is
expected
to
be
negligible
for
non­
handlers
due
to
its
moderate
volatility
and
dilution
of
vapor
outdoors.
Exposures
are
believed
to
be
primarily
of
short­
and
intermediate­
term
because
PCNB
is
applied
no
more
than
twice
a
year.

$
The
target
Margin
of
Exposure
(
MOE)
for
residential
post­
application
is
1000.
MOE's
below
1000
are
a
concern.
Page
7
of
16
$
PCNB
is
used
on
golf
courses,
where
golfers
may
be
exposed.
Two
application
rates
of
32.67
lbs
active
ingredient
per
acre
(
ai/
A)
and
43.56
lbs
ai/
A
were
chosen.
The
target
MOE
for
both
dermal
and
oral
non­
dietary
activities
is
1000.

$
MOEs
for
residential
and
recreational
post­
application
scenarios
at
high
application
rates
are
provided
in
the
table
below.

Activity
MOE
on
day
of
application
high
contact
lawn
activities
B
adult
30
high
contact
lawn
activities
B
toddler
80
hand­
to­
mouth
transfer
from
treated
turf
B
toddler
2
turfgrass
mouthing
B
toddler
6
ingestion
of
soil
from
treated
lawns
B
toddler
460
mowing
B
turf
860
golfing
575­
430
$
All
post­
application
scenarios
yield
MOEs
of
concern.

Bystander
Exposure
Measurable
levels
of
PCNB
have
been
detected
in
an
ambient
air
monitoring
study
conducted
by
CalEPA's
Department
of
Pesticide
Regulation
(
CDPR)
in
Lompoc,
California
(
Santa
Barbara
County)
in
2000
(
http://
www.
cdpr.
ca.
gov/
docs/
dprdocs/
lompoc.
pdf).
PCNB
was
detected
in
72%
of
the
air
samples
taken
between
May­
August
2000.
Since
this
information
raised
concerns
for
potential
risks
to
bystanders
and
workers
in
adjacent
fields,
a
screening
level
assessment
was
conducted
by
the
USEPA.
The
Agency
subsequently
determined
that
these
potential
exposures
result
in
risks
that
are
not
of
concern
(
i.
e.
>
MOE
1000).
It
is
not
clear
how
the
California
data
relate
to
other
measures
of
volatility.

Aggregate
Risk
(
For
a
complete
discussion,
see
section
5.0
of
the
Human
Health
Risk
Assessment)

Aggregate
risk
combines
risk
estimates
from
exposure
through
food,
drinking
water,
and
residential
uses
of
a
pesticide.
Generally,
combined
risks
from
these
exposures
must
occupy
less
than
100
percent
of
the
PAD
to
be
below
the
Agency's
level
of
concern.

$
For
PCNB
and
its
metabolites,
quantitative
aggregate
exposure
assessments
that
include
dietary
(
food
and
drinking
water),
and
incidental
dermal,
inhalation,
and
oral
exposures
were
not
performed,
since
potential
risks
from
the
individual
sources
of
non­
dietary
Page
8
of
16
exposure
were
already
of
concern,
particularly
for
children.

$
Chronic
aggregate
risk
estimates
which
include
only
dietary
pathways
of
exposure
(
food
+
water)
were
calculated.
The
chronic
dietary
risk
without
the
inclusion
of
water
is
below
the
Agency's
level
of
concern;
i.
e.,
<
100%
cPAD.
When
exposures
from
drinking
water
are
added,
chronic
aggregate
risks
for
most
of
the
exposed
population
subgroups,
particularly
infants
(
313%
cPAD)
and
children
1­
2
years
old
(
173%
cPAD)
are
above
the
Agency's
level
of
concern.

$
PCNB
is
classified
as
a
Group
C
(
possible
human)
carcinogen.
A
separate
assessment
of
aggregate
cancer
risk
has
not
been
conducted
because
the
carcinogenic
potential
of
PCNB
has
not
been
quantified.

$
Chronic
dietary
(
food
only),
as
modeled
using
DEEM­
FCID,
and
aggregate
dietary
(
food
+
water)
risks
are
summarized
in
the
table
below.

Population
Subgroup
Crops
only
(
no
water)
%
cPAD
Risk
from
all
crops
plus
water
%
cPAD
U.
S.
Population
12%
105%

All
infants
(<
1
yr)
7%
313%

Children
1­
2
yrs
34%
173%

Children
3­
5
yrs
25%
155%

Children
6­
12
yrs
16%
105%

Youth
13­
19
yrs
10%
78%

Adults
20­
49
yrs
10%
97%

Adults
50+
yrs
10%
102%

Females
13­
49
yrs
10%
96%

$
Chronic
dietary
risks
of
concern
are
shown
in
boldface.

Occupational
Risk
(
For
a
compete
discussion,
see
section
7.0
of
the
Human
Health
Risk
Assessment)

Workers
can
be
exposed
to
a
pesticide
through
mixing,
loading,
or
applying
the
pesticide,
treating
seed
with
the
pesticide
or
handling
treated
seed,
and
through
reentering
a
treated
site.
Worker
risk
is
measured
by
a
Margin
of
Exposure
(
MOE)
which
determines
how
close
the
occupational
exposure
comes
to
the
NOAEL
taken
from
animal
studies.
Generally,
MOEs
that
are
greater
than
100
do
not
exceed
the
Agency's
level
of
concern.
Page
9
of
16
No
chemical­
specific
exposure
data
are
available
for
occupational
exposure
scenarios
for
PCNB.
Estimates
from
available
databases,
primarily
the
Pesticide
Handlers
Exposure
Database
(
PHED),
and
standard
assumptions
were
used
to
calculate
potential
exposures.

Agricultural
Handlers
(
excluding
seed
treatment
and
treated
seed)

$
Potential
handler
exposures
are
assessed
using
the
appropriate
toxicological
endpoints
and
uncertainty
factors
associated
with
the
active
ingredient.
Exposures
specific
to
a
level
of
Personal
Protective
Equipment
(
PPE)
or
Engineering
Controls
are
determined
independently
from
what
is
required
by
product
labels
because
label
requirements
vary
depending
on
the
acute
toxicity
of
the
end­
use
product.

The
following
exposure
scenarios
were
modeled:


Chemigation

Ground
boom
sprayer

Airblast
sprayer

Push
type
spreader

Tractor
drawn
spreader

Aerial
application
$
Handler
MOEs
were
calculated
for
short­
and
intermediate­
term
durations.
For
dermal
exposures,
the
NOAEL
of
300
mg/
kg/
day
from
a
21­
day
dermal
study
in
rats
showing
thyroid
effects
was
used.
For
inhalation
exposures,
the
NOAEL
of
1.0
mg/
kg/
day
from
a
non­
guideline
subchronic
oral
toxicity
study
in
rats
showing
thyroid
effects
was
used.
The
short­
term
duration
is
believed
to
be
most
representative
of
private
growers
and
the
intermediate­
term
duration
represents
commercial
applicators
who
may
repeatedly
apply
PCNB
for
1
to
6
months.

$
For
most
scenarios,
risk
estimates
for
short­
and
intermediate­
term
dermal
exposures
are
greater
than
or
equal
to
the
target
MOE
of
100,
with
use
of
PPE
or
engineering
controls.
The
following
scenarios
had
MOEs
<
100
at
all
levels
of
PPE
and
engineering
controls,
and
represent
risks
of
concern:

$
mixing/
loading
dry
flowable
for
chemigation
application
(
sod
farms)

$
sprays
for
high
pressure
handwand
application
(
ornamentals)

$
mixing/
loading/
applying
liquid
for
handgun
(
lawn)
sprayer
application
$
mixing/
loading/
applying
granular
for
belly
grinder
application
(
ornamentals)

$
mixing/
loading/
applying
wettable
powders
for
low
pressure
handwand
application
(
ornamentals
­
woody
shrubs
and
vines,
herbaceous
plants,
and
shade
trees)­
shade
trees)
Page
10
of
16
$
All
the
risk
estimates
for
short­
and
intermediate­
term
inhalation
exposures
are
greater
than
or
equal
to
the
target
MOE
of
100,
although
some
scenarios
require
the
addition
of
PPE
or
engineering
controls
to
achieve
that
level.
These
scenarios
include:

$
mixing/
loading
dry
flowable
for
chemigation
application
(
sod
farms)

$
mixing/
loading
liquids
for
chemigation
and
aerial
applications
$
mixing/
loading
wettable
powder
for
chemigation
application
(
cole
crops
and
sod
farms)

$
mixing/
loading
wettable
powders
for
groundboom
application,

$
sprays
for
high
pressure
handwand
applications
$
mixing/
loading/
applying
wettable
powders
for
low
pressure
handwand
application
(
ornamentals
­
woody
shrubs
and
vines,
herbaceous
plants,
and
shade
trees)

Seed
Treatment
and
Handlers
$
Seed
may
be
treated
at
commercial
facilities
or
on
the
farm
where
it
is
to
be
planted.
On­
farm
seed
treatment
is
considered
to
represent
a
relatively
small
proportion
of
the
total
use
of
treated
seed
in
the
U.
S.

$
The
results
of
the
short­
and
intermediate­
term
seed
handler
assessments
indicate
that,
for
all
formulations,
the
majority
of
the
potential
exposure
scenarios
result
in
total
MOEs
>
100
with
long
pants,
long
sleeved
shirts,
gloves,
and
no
respirator
while
using
open
systems.

$
Seed
handlers
working
in
a
smaller
facility,
performing
multiple
activities
(
such
as
in
an
on­
farm
situation)
might
require
a
respirator
to
reduce
risks
below
the
levelof
concern
(
above
the
MOE
of
100).

Occupational
Postapplication
Exposures
and
Risk
$
There
is
a
low
potential
for
occupational
post­
application
exposure
when
a
pre­
plant
or
at
planting
fungicide
such
as
PCNB
is
used.
The
Agency
conducted
a
risk
assessment
for
potential
post­
application
exposures
where
PCNB
is
applied
to
foliage,
i.
e.,
to
turf
at
golf
courses
and
sod
farms.

$
The
short­
and
intermediate­
term
risks
to
golf
course
workers
or
sod
farm
workers
performing
hand­
harvesting
of
sod
on
the
day
of
application
are
equal
to
or
greater
than
the
target
MOE
of
100
and
are
not
of
concern.
Page
11
of
16
Incident
Data
A
number
of
accidental
human
poisonings
from
exposure
to
PCNB
in
both
occupational
and
residential
settings
have
been
reported.
Though
the
data
from
these
sources
often
lacked
specific
information
on
the
extent
of
exposure
and
the
circumstances
of
exposure,
the
incidence
information
indicate
potential
poisoning
risks
from
misuse
of
products
that
contain
PCNB,
or
from
not
wearing
PPE.

Ecological
Risk
To
estimate
potential
ecological
risk,
EPA
integrates
the
results
of
exposure
and
ecotoxicity
studies
using
the
risk
quotient
method.
Risk
quotients
(
RQs)
are
calculated
by
dividing
exposure
estimates
by
ecotoxicity
values,
both
acute
and
chronic,
for
various
wildlife
species.
RQs
are
then
compared
to
levels
of
concern
(
LOCs).
Generally,
the
higher
the
RQ,
the
greater
the
potential
risk.
Risk
characterization
provides
further
information
on
the
likelihood
of
adverse
effects
occurring
by
considering
the
fate
of
the
chemical
in
the
environment,
communities
and
species
potentially
at
risk,
their
spatial
and
temporal
distributions,
and
the
nature
of
the
effects
observed
in
laboratory
studies.

Environmental
Fate
and
Transport
(
For
a
complete
discussion,
see
the
Environmental
Fate
and
Ecological
Risk
Assessment.)

PCNB
has
a
large
number
of
potential
degradates
and
metabolites;
six
of
these
are
considered
to
be
predominant:

$
pentachloroaniline
(
PCA)

$
pentachlorothioanisole
(
PCTA)

$
pentachlorothioanisole
sulfoxide
$
pentachloroanisole
sulfone
$
pentachlorophenol
(
PCP)

$
pentachlorobenzene
(
PCB)

The
parent
and
these
degradates
are
likely
to
be
persistent.
The
exact
conditions
that
favor
the
formation
of
PCP
are
uncertain.
It
is
routinely
detected
in
water
and
sediment
monitoring
studies.
PCP,
as
a
pesticidal
active
ingredient,
is
also
used
as
a
wood
preservative,
and
the
origin
of
the
PCP
as
detected
in
these
studies
is
unclear.

PCNB
is,
in
general,
expected
to
be
a
persistent,
moderately
volatile
compound
that
will
be
immobile
in
most
soils.
It
can
be
expected
to
dissipate
through
volatilization;
dissipation
from
the
soil
through
volatilization
should
be
reduced
by
incorporation
of
the
pesticide
into
the
soil
at
application.
Volatilization
may
also
be
an
important
environmental
fate
process
for
PCA,
PCTA,
Page
12
of
16
PCB
and
PCP.

The
primary
degradation
pathway
for
PCNB
is
aqueous
photodegradation
when
the
compound
is
present
in
an
unsorbed
state
in
clear
and
shallow
surface
water
under
favorable
light
conditions.
Photodegradation
of
PCNB
in
surface
water
is
moderately
rapid,
with
half­
lives
on
the
order
of
a
few
days
or
less.

PCNB
has
a
very
high
potential
to
bioaccumulate
in
fish,
but
is
metabolized
and
will
undergo
moderately
rapid
depuration
when
the
fish
are
no
longer
exposed
to
the
compound.

PCNB
is
stable
to
hydrolysis
and
is
effectively
stable
to
photodegradation
on
soil
(
half­
life
of
80
days).
PCNB
biodegrades
slowly
in
aerobic
soils,
showing
half­
lives
of
77
and
189
days.

Risks
to
Terrestrial
Wildlife
Chronic
and
acute
exposure
from
multiple
applications
of
PCNB
were
estimated
using
a
35­
day
foliar
half­
life,
a
default
value
used
for
terrestrial
assessments
in
the
absence
of
total
foliar
residue
data.
The
use
of
the
default
likely
results
in
overestimates
of
exposure.

Although
screening­
level
models
indicate
that
terrestrial
exposure
to
PCNB
is
likely
through
consumption
of
treated
seed
and
foliar
residues,
the
likelihood
of
acute
risk
to
birds
and
mammals
is
considered
to
be
low
because
PCNB
is
practically
nontoxic
to
both
birds
and
mammals
on
an
acute
exposure
basis.

Chronic
risk
levels
of
concern
are
exceeded
for
birds
and
mammals.
Chronic
effects
such
as
reductions
in
the
number
of
eggs
laid,
number
of
viable
embryos,
and
numbers
of
14­
day
survivors
may
result
from
chronic
exposure
of
birds
to
PCNB.
Although
chronic
exposure
to
PCNB
did
not
result
in
reproductive
effects
in
mammals,
toxic
effects
on
the
liver
and
thyroid
were
noted
in
laboratory
studies
on
rodents.
The
relevance
of
these
endpoints
on
wildlife
are
not
clear.
The
chronic
reproductive
effects
observed
in
birds
and
thyroid
effects
in
mammals
may
be
indicative
of
PCNB's
capacity
to
impact
endocrine­
mediated
processes.
The
open
literature
indicates
that
PCNB,
PCA,
and
PCA
have
estrogen­
binding
abilities.

Risks
to
terrestrial
wildlife
are
summarized
along
with
risks
to
aquatic
species
in
the
table
which
follows
the
section
on
aquatic
wildlife,
below.
Page
13
of
16
Risks
to
Aquatic
Wildlife
PCNB
is
highly
toxic
to
freshwater
fish
and
invertebrates
and
is
very
highly
toxic
to
estuarine/
marine
fish
and
invertebrates
on
an
acute
exposure
basis.

Chronic
risk
levels
of
concern
were
exceeded
for
freshwater
fish
and
invertebrates;
chronic
effects
include
reduced
number
of
eggs
produced
and
reductions
in
the
number
of
young
surviving.
Data
are
lacking
on
chronic
effects
in
estuarine/
marine
fish
and
invertebrates.

PCNB
and
its
degradates
persist
in
the
aquatic
environment
and
tend
to
bioconcentrate
(
bioconcentration
factors
as
high
as
22,000Xin
algae).
The
presence
of
PCNB
and
degradate
in
benthic
(
bottom)
sediments
is
expected
to
serve
as
a
likely
route
of
exposure
to
bottom­
dwelling
fauna.
This
may
also
serve
as
a
means
of
entry
into
aquatic
food
chains
where
the
compound
and/
or
its
degradates
may
biomagnify.

$
Ecological
risks
to
terrestrial
and
aquatic
wildlife
are
summarized
in
the
table
below.

Wildlife
type
Acute
Risk
Quotient
range
Chronic
Risk
Quotient
range
Soil
application
avian
(
nongranular)
<
0.01­
0.24
0.05­
22
mammalian
0.00­
2.5
0.2­
65
freshwater
fish
0.22­
2.60
0.8­
8.3
freshwater
invertebrates
0.03­
0.34
0.6­
6.0
Estuarine/
marine
fish
<
0.01­
0.03
data
not
available
Estuarine/
marine
invertebrates
1.8­
22
data
not
available
Seed
treatment
avian
<
0.01
0.03­
4.2
mammalian
<
0.01­<
0.06
0.8­
13
$
Risk
Quotients
which
exceed
Levels
of
Concern
for
acute
and
chronic
risk
are
shown
in
boldface.

Nontarget
Plant
Risk
$
Data
are
not
available
on
the
effects
of
PCNB
on
either
aquatic
or
terrestrial
plants
and
will
be
required.
Page
14
of
16
Endangered
Species
$
Endangered
species
lists
have
been
developed
for
PCNB
of
five
modeled
crops
by
removing
species
not
likely
to
be
impacted.
Based
on
a
preliminary
screen,
a
list
of
of
potentially
impacted
species
has
been
developed
which
includes
28
birds,
13
mammals,
91
fish,
and
91
invertebrates
(
clams,
snails,
crustaceans).

Summary
of
Data
Needs
Environmental
Fate
and
Ecological
Effects
Data
Needs
The
following
data
would
be
useful
in
refining
our
understanding
of
the
environmental
fate
and
ecological
effects
of
PCNB
and
its
degradates:

$
Additional
data
on
whether
the
formation
of
PCP
from
PCNB
is
likely
in
the
field
$
Data
on
the
long­
range
atmospheric
transport
of
PCNB
and
degradates
$
Volatility
data,
to
assist
in
determining
the
foliar
dissipation
half
life
of
PCNB
$
Endocrine
disruption
$
Toxicity
of
PCNB
to
benthic
invertebrates
$
Chronic
toxicity
of
PCNB
to
estuarine/
marine
fish
and
invertebrates
$
Toxicity
of
PCNB
to
terrestrial,
semi­
aquatic,
and
aquatic
plants
Human
Health
Data
Needs
The
following
data
would
be
useful
in
refining
our
understanding
of
the
human
health
risks
associated
with
PCNB.

Toxicology
$
Data
on
thyroid
toxicity
in
adults
and
its
relationship
to
functional
development
in
offspring
$
Data
to
explore
the
origin
and
significance
of
dose­
dependent
decreases
in
certain
liver
enzyme
values
in
studies
in
rats
and
dogs..

$
A
guideline
metabolism
study
of
PCNB
(
including
a
mass
balance
of
radioactivity
in
excreta,
tissues,
and
carcass),
including
a
Tier
II
study
of
blood
kinetics,
to
determine
metabolic
half­
life
$
An
in
vivo
cytogenetic
assay
examining
clastogenicity.

$
A
90­
day
inhalation
toxicity
study
of
PCNB
to
facilitate
occupational
risks
Page
15
of
16
Product
Chemistry
$
Generic
data
on
UV/
visible
absorption
(
OPPTS
830.7050)

$
Some
data
are
still
need
on
preliminary
analysis
(
OPPTS
830.1700)
Page
16
of
16
Residue
Chemistry
$
Metabolism
data
$
Analytical
reference
standards
$
Field
trial
data
(
root
and
tuber
vegetables
group,
legume
vegetables
group,
cotton,
peanuts,
ginseng),
and
processed
commodities
(
cottonseed,
peanut,
soybean,
meat)
