1
TABLE
OF
CONTENTS
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1
EXECUTIVE
SUMMARY
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3
OCCUPATIONAL
AND
RESIDENTIAL
TOXICOLOGICAL
ENDPOINTS
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6
4.1
OCCUPATIONAL
/
RESIDENTIAL
EXPOSURE
 
DERMAL
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6
Dermal
Absorption
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6
Short­
Term
Dermal
(
1
day
­
1
month)
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6
Intermediate­
Term
Dermal
(
1
month
to
6
months)
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7
Long­
Term
Dermal
(
greater
than
6
months)
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8
4.1.2
Occupational/
Residential
Exposure
 
Inhalation
(
any
time­
period)
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9
Carcinogenicity
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10
Mutagenicity
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11
4.1.3
FQPA
Considerations
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13
4.1.4
Acute
Toxicology
Categories
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14
4.1.5
Summary
of
Endpoints
of
Concern
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14
4.2
OCCUPATIONAL
HANDLER
EXPOSURES
AND
RISKS
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15
4.2.1
Handler
Data
and
Assumptions
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16
Creosote
Council
II
2001
Study
Synopsis
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17
Pressure
Treatment
Process
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19
Dermal
Exposure
Study
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19
Inhalation
Exposure
Study
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20
4.2.2
Handler
Risk
Assessment
and
Characterization
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21
Handler
Exposure
and
Cancer
Risk
Calculations
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26
4.3
OCCUPATIONAL
POST­
APPLICATION
EXPOSURES
AND
RISKS
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28
4.3.1
Post­
application
Occupational
Data
and
Assumptions,
and
Exposure
and
Risk
Calculations
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30
Dermal
Exposure
Studies
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33
Inhalation
Exposure
Studies
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35
Summary
of
Other
Exposure
Studies
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36
4.3.2
Occupational
Post­
application
Risk
Assessment
and
Characterization
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41
2
4.4
UNCERTAINTIES
AND
LIMITATIONS
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43
4.4.1
Data
Gaps
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43
4.4.2
Creosote
Council
II
2001
Worker
Exposure
Study
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44
4.4.3
Residential
Exposure
Scenarios
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46
4.4.4
Toxicity
Information
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46
4.5
RESULTS
AND
CONCLUSIONS
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47
4.6
REFERENCES
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50
3
CREOSOTE
­
HUMAN
EXPOSURE
EXECUTIVE
SUMMARY
Creosote
is
applied
by
occupational
handlers
only.
Since
it
is
a
restricted­
use
pesticide
that
can
only
be
applied
by
certified
applicators
or
someone
under
their
direct
supervision,
it
is
not
available
for
sale
to
or
use
by
homeowners.
A
recent
voluntary
cancellation
of
all
non
pressure
treatment
uses
restricts
creosote
to
commercial
and
industrial
settings.

The
amount
of
creosote
handled
in
a
given
day
among
pressure
treatment
facilities
depends
on
such
factors
as
the
size
of
the
facility
and
the
number
of
treatment
cylinders
on
site.
In
a
given
facility,
the
amount
of
creosote
handled
per
day
varies
depending
on
the
wood
conditioning
techniques
used
for
a
given
charge,
on
the
type
of
wood
being
treated,
and
the
type
of
product
being
produced
(
e.
g.,
marine
piling
vs
utility
poles).

This
chapter
is
a
revision
of
the
earlier
draft
Human
Exposure
RED
Chapter
for
Creosote
completed
on
January
27,
2000.
EPA
received
an
extensive
creosote­
specific
handler/
post­
application
exposure
study
from
the
Creosote
Council
II
that
was
completed
on
January
30,
2001.
The
study
was
reviewed
and
accepted
by
EPA.
The
new
study
as
well
as
the
earlier
pilot
study
(
completed
July
2,
1998),
estimated
worker
exposure
to
pressure
treated
wood.
The
new
study
entitled
"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
with
Pressure­
Treatment
of
Wood
with
Creosote"
was
submitted
by
the
Creosote
Council
II
for
all
tasks
involving
pressure
treating
wood
with
creosote.
As
a
result
of
these
new
data,
many
of
the
scenarios
and
exposures
in
the
earlier
draft
chapter
were
revised
to
incorporate
the
new
data.

The
earlier
draft
chapter
contained
exposure
data
from
the
pilot
study
which
indicated
that
the
workers
at
the
pressure
treatment
plant
were
the
treatment
operator,
treatment
supervisor,
pressure
treatment
loader,
test
borer,
environmental
compliance
operator,
loader
man,
and
locomotive
driver.
The
exposure
of
the
treatment
operator
and
treatment
supervisor
were
used
to
represent
handler
exposure
and
the
pressure
treatment
loader,
test
borer,
environmental
compliance
operator,
loader
man,
and
locomotive
driver
were
used
to
represent
post­
application
exposure
in
the
earlier
Human
Exposure
RED
Chapter.
However,
worker
titles
in
the
new
exposure
study
were
much
different
although
the
job
functions
were
similar.
Workers
included
the
treatment
operator,
treatment
assistant,
cylinder
area
loader,
cylinder
area
helper,
checker,
drip
pad
loader,
load­
out
area
loader,
load­
out
area
loader
helper,
forklift
operator,
oil
unloader,
test
borer,
and
water
treatment
system
operator.
For
4
this
chapter,
the
treatment
operator
and
treatment
assistant
are
used
to
represent
handler
exposure
during
the
pressure
treatment
process.
Exposure
data
for
the
cylinder
area
loader,
cylinder
area
loader
helper,
checker,
drip
pad
loader,
load­
out
area
loader,
load­
out
area
loader
helper,
load­
out
area
forklift
operator,
oil
unloader,
test
borer,
and
water
treatment
system
operator
are
representative
of
occupational
post­
application
exposure.

The
scenarios
using
the
Pesticide
Handlers
Exposure
Database(
PHED)
and
the
Chemical
Manufactures
Association
(
CMA)
data
from
the
earlier
draft
chapter
(
completed
January,
27,
2000)
have
been
deleted
based
on
the
voluntary
cancellation
of
all
non
pressure
treatments.
Uncertainties
and
limitations
exist
in
available
exposure
data
and
toxicity
information.
Specific
uncertainty
concerns
are
summarized
in
Section
10
of
this
document.

The
results
of
the
post­
application
occupational
exposure
and
risk
assessment
indicate
that
the
creosote
inhalation
exposures
exceed
the
level
of
concern
for
all
post­
application
scenarios.
For
dermal
risks,
some
of
the
short­,
intermediate­
and
long­
term
exposures
also
exceed
the
level
of
concern.
The
target
MOE
is
100
or
more
for
short­
and
intermediate­
term
risks
and
300
for
long­
term
dermal
durations.
In
addition,
cancer
risks
for
all
post­
application
occupational
scenarios
exceed
the
level
of
concern
(
1E­
04);
all
are
greater
than
1E­
03,
except
for
load­
out
area
loader
helpers
who
had
cancer
risks
ranging
from
4E­
04
to
8E­
04.

In
a
recent
submission
dated
November
25,
2003,
the
registrants
submitted
a
probablistic
worker
risk
assessment
for
creosote.
This
probablistic
assessment
has
been
included
in
the
public
docket.
The
methodology
and
data
inputs
in
this
recent
submission
will
be
reviewed
during
the
public
comment
phase.

No
chemical­
specific
data
for
residential
post­
application
exposure
were
submitted.
Therefore,
exposure
could
not
be
estimated.
Data
were
not
adequate
for
use
in
the
exposure
assessment.
5
The
following
table
shows
the
scenarios
and
the
source
of
data
used
to
develop
these
scenarios
for
this
preliminary
risk
assessment.

Table
1.
Summary
of
the
Occupational/
Nonoccupational
Exposure
Scenarios
and
Source
of
Data
Exposure
Scenario
Source
of
Data
Occupational
Handler
(
1a)
Mixing/
Loading/
Applying
Liquids
at
a
Pressure
Treatment
Facility
(
treatment
operator)
Exposure
Study
Data
from
Creosote
Council
II
and
PHED,
1997used
as
a
surrogate
(
1b)
Mixing/
Loading/
Applying
at
a
Pressure
Treatment
Facility
(
treatment
assistant)
Exposure
Study
Data
from
Creosote
Council
II
Occupational
Postapplication
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
No
data
No
data
Non­
Occupational
(
e.
g.,
Residential)

(
1)
homeowner
incidental
ingestion
and
dermal
contact
with
soil
contaminated
with
creosote
(
e.
g.,
soil
contaminated
by
creosote
treated
telephone
poles)
(
child)
No
data
(
2)
outdoor
homeowner
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
posts,
shingles,
fencing,
lumber,
piers,
etc.)
(
adult)
No
data
(
3)
outdoor
homeowner
hand­
to­
mouth
and
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
posts,
shingles,
fencing,
lumber,
piers,
etc.)
(
child)
No
data
6
4.
OCCUPATIONAL
AND
RESIDENTIAL
EXPOSURE
AND
RISK
ASSESSMENT
Occupational
and
Residential
Toxicological
Endpoints
An
occupational
and/
or
residential
exposure
risk
assessment
is
required
for
an
active
ingredient
if
(
1)
certain
toxicological
criteria
are
triggered
and
(
2)
there
is
potential
exposure
to
handlers
(
mixers,
loaders,
applicators,
etc.)
during
use
or
to
persons
entering
treated
sites
after
application
is
complete.
For
creosote,
both
criteria
are
met.
On
April
1,
1999,
the
Hazard
Identification
Assessment
Review
Committee
evaluated
the
toxicology
data
base
of
Creosote
and
selected
the
toxicological
endpoints
for
short­
term,
intermediate­
term,
and
long­
term
occupational/
residential
exposure
risk
assessments
and
for
carcinogenicity
screens.
An
acute
and
chronic
Reference
Dose
(
RfD)
was
not
selected,
as
there
are
no
food
uses
for
creosote
(
USEPA,
1999).
An
acute
or
chronic
dietary
risk
assessment
is
not
required
for
creosote,
as
there
is
no
anticipated
dietary
exposure
to
creosote
(
USEPA,
1999).

4.1
Occupational
/
Residential
Exposure
 
Dermal
Dermal
Absorption:
A
50%
dermal
absorption
value
is
used
for
short
and
longterm
non­
cancer
assessments.
The
value
of
50%
dermal
absorption
was
obtained
by
comparison
of
the
oral
and
dermal
LOAELs
from
the
developmental
toxicity
study
in
rats
(
MRID
#
43584201)
and
the
90­
day
dermal
toxicity
study
in
rats
(
MRID
#
43616101)
using
the
P1/
P13
blend.
The
oral
LOAEL
of
175
mg/
kg/
day
observed
in
the
developmental
toxicity
study,
when
compared
to
the
dermal
LOAEL
of
400
mg/
kg/
day
observed
in
the
dermal
toxicity
study,
yields
an
absorption
factor
of
44%,
which
was
rounded
up
to
50%
by
the
Committee,
taking
into
account
the
dermal
irritation
which
also
occurs
from
dermal
exposure
to
creosote
(
USEPA,
1999).

Short­
Term
Dermal
(
1
day
­
1
month):
An
oral
maternal
NOAEL
of
50
mg/
kg/
day,
based
on
decreased
body
weight
gain
during
the
study,
was
chosen
for
this
endpoint.
Although
a
90­
day
dermal
toxicity
study
was
available,
the
developmental
toxicity
study
was
chosen
for
the
following
reasons:
1)
dermal
toxicity
studies
(
including
the
2­
week
range­
finding
studies)
did
not
measure
developmental
endpoints,
which
are
present
in
both
developmental
toxicity
studies;
and
2)
the
results
of
dermal
toxicity
studies
would
not
be
protective
of
infants
and
children
from
residential
exposure
to
creosote.
An
uncertainty
factor
(
MOE)
of
100
is
applied
to
this
risk
assessment
(
USEPA,
1999).
7
In
a
developmental
toxicity
study
using
P1/
P13
creosote
(
MRID
#
43584201),
pregnant
female
Sprague­
Dawley
rats
(
30/
dose)
were
administered
P1/
P13
creosote
at
dose
levels
of
0,
25,
50,
and
175
mg/
kg/
day
on
gestation
days
6
through
15
inclusive.
Decreased
body
weight
and
food
consumption
were
observed
at
the
175
mg/
kg/
day
dose
level
in
this
study
in
maternal
rats.
Decreased
uterine
weight
was
observed
in
maternal
rats
at
the
high
dose,
which
is
reflected
partly
by
the
decreased
live
fetuses
per
litter
at
the
high
dose
(
although
mean
fetal
weight
was
not
affected).
Cesarean
section
observations
showed
significantly
increased
resorptions
and
post­
implantation
loss
as
well
as
decreased
number
of
live
fetuses
per
litter
at
the
175
mg/
kg/
day
dose.
Based
on
the
results
of
this
study,
the
Maternal
NOAEL
is
50
mg/
kg/
day,
and
the
Maternal
LOAEL
is
175
mg/
kg/
day,
based
on
decreased
body
weight
gain
during
the
study
(
USEPA,
1999).

No
treatment­
related
malformations
(
external,
visceral
or
skeletal)
were
observed
in
any
of
the
fetuses
at
25
mg/
kg
bw/
day.
At
50
mg/
kg
bw/
day,
the
overall
incidence
of
malformations
on
a
fetal
and
litter
basis
were
statistically
elevated
compared
to
controls.
However,
these
individual
malformations
were
not
seen
at
higher
dose
levels
and/
or
fell
within
the
range
of
historical
control
data.
At
175
mg/
kg
bw/
day
there
was
(
i)
an
overall
significant
increased
incidence
of
developmental
malformations,
(
ii)
increased
incidence
of
cardiovascular,
vertebral
and
digital
malformations,
compared
to
lower
dose
levels,
concurrent
controls
or
historical
controls
(
2429
and
2898
fetuses
examined
viscerally
and
skeletally
respectively)
and
(
iii)
an
increased
incidence
of
malformations
at
this
dose
level
in
spite
of
increased
fetal
loss
(
resorptions)
(
Beck
and
Lloyd,
1963)
thus
resulting
in
fewer
fetuses
available
for
teratogenic
examination.
Although
the
incidence
of
fetal
malformations
observed
at
175
mg/
kg
bw/
day
dose
level
in
rats
was
low
and
could
be
related
to
maternal
stress
(
decreased
body
weight
gain
and
food
consumption),
the
teratogenic
potential
of
P1/
P13
Creosote
cannot
be
ruled
out.
Based
on
these
data,
the
developmental
toxicity
LOAEL
can
be
determined
as
175
mg/
kg/
day,
with
the
developmental
toxicity
NOAEL
as
50
mg/
kg/
day
(
USEPA,
1999).

Intermediate­
Term
Dermal
(
1
month
to
6
months):
A
dermal
NOAEL
of
40
mg/
kg/
day,
based
on
decreased
body
weight
gain
in
males
at
400
mg/
kg/
day,
is
selected
for
this
endpoint.
An
uncertainty
factor
(
MOE)
of
100
is
applied
to
this
risk
assessment
(
USEPA,
1999).

In
a
90­
day
dermal
toxicity
study
(
MRID
#
43616201),
Charles
River
rats
(
10/
sex/
dose)
were
given
dermal
applications
of
P2
creosote
in
corn
oil
at
dosage
levels
of
0,
4,
40
or
400
mg/
kg
bw/
day.
There
was
no
mortality
observed
in
this
study
at
any
dose
level.
Body
weight
in
high
dose
males
was
decreased
7­
8%
during
weeks
9­
12
of
the
study,
and
body
weight
gain
decreased
15%
in
high
dose
males
for
the
treatment
period.
Food
consumption
in
high
dose
males
was
decreased
during
weeks
2­
4
and
week
6
by
4­
10%
vs
control.
Only
slight
dermal
irritation
was
observed
in
high
dose
males.
No
effects
8
were
observed
on
hematology
or
clinical
chemistry.
Treated
skin
in
the
400
mg/
kg/
day
dose
groups
(
male
and
female)
was
observed
with
increased
incidence
of
dermal
inflamation.
Based
on
the
results
of
this
study,
the
systemic
LOAEL
is
400
mg/
kg/
day,
based
on
decreased
body
weight
gain
in
male
rats.
The
systemic
NOAEL
is
40
mg/
kg/
day.
For
females,
the
NOAEL
is
set
at
400
mg/
kg
bw/
day
since
no
systemic
toxic
effects
were
noted
in
any
of
the
treated
groups
(
USEPA,
1999).

Long­
Term
Dermal
(
greater
than
6
months):
A
parental
oral
LOAEL
of
25
mg/
kg/
day,
based
on
decreased
pre­
mating
body
weight,
was
selected
for
this
endpoint.
An
extra
uncertainty
factor
of
3x
is
applied
for
use
of
a
LOAEL
in
this
study
for
occupational
risk
assessments
(
USEPA,
1999).

In
this
study,
Charles
River
Crl:
CD
rats,
26/
sex/
group,
were
dosed
by
gavage
with
P1/
P13
creosote
in
corn
oil
at
doses
of
0,
25,
75,
and
150
mg/
kg/
day.
Pre­
mating
treatment
phase
lasted
approximately
17
weeks,
which
may
have
contributed
to
the
decreased
fertility
observed
in
this
study.
Systemic
effects
observed
in
this
study
for
parental
animals
included
decreased
body
weight
during
the
pre­
mating
period
at
all
dose
levels,
with
a
dose­
response
noted
for
this
effect.
Salivation
was
also
observed
at
75
mg/
kg/
day
and
above
in
the
F1
generation.
Effects
in
offspring
included
a
dose­
related
decrease
in
growth
of
offspring
of
the
F0
generation
starting
at
25
mg/
kg/
day
(
as
shown
by
decreased
pup
weight).
For
the
F0
pups,
mean
number
of
liver
pups
per
litter
was
decreased
at
75
and
150
mg/
kg/
day,
and
percent
live
pups
at
175
mg/
kg/
day
was
also
decreased.
In
the
F1
pups,
the
percent
live
pups
was
decreased
at
75
and
150
mg/
kg/
day,
but
pup
growth
was
affected
only
at
150
mg/
kg/
day
as
shown
by
decreased
mean
pup
weight.
Decreased
fertility
and
pregnancy
indices
were
observed
in
the
F1
female
parental
rats
at
all
dose
levels,
but
this
was
not
interpreted
as
a
treatment­
related
effect,
as
it
was
more
likely
related
to
the
fact
that
the
critical
weight
for
fertility
was
exceeded
by
the
17­
week
pre­
mating
interval.
Based
on
the
results
of
this
study,
the
Parental
Systemic
NOAEL
is
<
25
mg/
kg/
day,
and
the
Parental
Systemic
LOAEL
is
25
mg/
kg/
day,
based
on
decreased
pre­
mating
body
weight.
The
developmental
NOAEL
in
this
study
is
<
25
mg/
kg/
day,
and
the
developmental
LOAEL
is
25
mg/
kg/
day,
based
on
a
dose­
related
decrease
in
pup
body
weight
for
the
F0
pups
from
days
14­
21.
The
reproductive
NOAEL
is
<
25
mg/
kg/
day,
and
the
reproductive
LOAEL
is
25
mg/
kg/
day,
based
on
reduced
pregnancy
and
fertility
indices
in
F1
female
parental
rats
(
USEPA,
1999).
9
4.1.2
Occupational/
Residential
Exposure
 
Inhalation
(
any
time­
period):

An
NOAEL
of
0.0047
mg/
L,
based
on
decreased
body
weight
gain,
altered
hematology
and
clinical
chemistry,
and
increased
absolute
and
relative
weight
of
the
liver
and
thyroid
observed
at
0.048
mg/
L,
was
selected
for
this
endpoint
(
USEPA,
1999).

In
a
13­
week
inhalation
toxicity
study
(
MRID
#
43600901),
20
Sprague­
Dawley
rats/
sex/
group
were
treated
for
5
days/
week,
6
hours/
day
with
P2
Creosote
CTM
via
whole
body
exposure
at
doses
of
0,
4.7,
48
or
102
mg/
m3
(
0,
0.005,
0.048
or
0.102
mg/
L
)
in
air
measured
gravimetrically.
The
aerosol
size
MMAD
was
between
2.4
and
2.9
microns
with
a
geometric
standard
deviation
between
1.85
and
1.91.
Subsequent
to
the
exposure
period
10
rats/
sex/
group
were
allowed
to
recover
from
treatment
for
6
weeks
(
USEPA,
1999).

During
the
exposure
period,
two
animals
(
low
dose
female;
mid
dose
male)
were
sacrificed
in
extremis
and
the
cause
of
morbidity
was
not
related
to
treatment.
Significant
treatment­
related
findings
in
mid
and
high
dose
animals
included
decreased
terminal
body
weight
and
body
weight
gain
(
m/
f),
altered
hematological
parameters
(
decreased
hemoglobin
content,
hematocrit,
erythrocyte
and
platelet
counts;
increased
reticulocyte
counts
and
mild
poikilocytosis,
m/
f)
and
biochemical
parameters
(
increased
serum
cholesterol
levels,
m/
f).
In
both
sexes
macroscopic
discolouration
of
the
lungs
persisted
through
the
recovery
period
and
correlated
with
the
presence
of
black
pigment
granules
within
alveolar
macrophages.
Both
sexes
showed
increased
absolute
and
relative
liver
and
thyroid
weights
and
increased
lung/
trachea/
body
weight
ratios.
Absolute
and
relative
thyroid
weights
of
high
dose
animals
actually
increased
after
the
recovery
period.
An
increased
incidence
of
lesions
of
the
nasal
cavity
epithelium
(
chronic
inflammation)
was
noted
following
treatment
(
all
treatment
groups,
m/
f)
but
appeared
to
lessen
in
incidence
and
severity
during
the
recovery
period
(
mainly
the
high
dose
group,
m/
f).
During
exposure
an
increased
incidence
of
thyroid
follicular
epithelial
cell
hypertrophy
occurred
in
all
male
groups
including
control
and
in
the
high
dose
female
group.
At
recovery
the
male
incidence
remained
similar
to
that
observed
at
exposure
while
the
incidence
in
females
of
the
high
dose
group
had
declined.
The
incidence
of
thyroid
follicular
cell
hypertrophy
was
slightly
increased
in
low
and
mid
dose
females
after
the
recovery
period.
Slightly
increased
incidence
of
mild
poikilocytosis
was
observed
in
all
treatment
groups
(
m/
f)
including
the
low
dose
group
and
control,
which
persisted
through
the
recovery
period.
Low
dose
animals
exhibited
lesions
of
the
nasal
cavity
epithelium
which
had
resolved
after
the
recovery
period.
Based
on
the
results
of
this
study,
the
systemic
LOAEL
is
48
mg/
m3,
based
on
decreased
body
weight
and
weight
gain,
altered
haematology
ad
clinical
chemistry,
increased
absolute
and
relative
weight
of
the
liver
ad
thyroid,
and
increased
incidence
of
lesions
of
the
nasal
cavity.
The
systemic
NOAEL
is
set
at
4.7
mg/
m3
(
0.0047
mg/
L)
for
P2
Creosote
CTM
in
rats
(
USEPA,
1999).
10
Inhalation
NOAEL
(
mg/
kg/
day)

NOAEL
(
mg/
L)
x
RV
L
hr
x
D
x
A
x
AF
BW
The
short­
intermediate,
and
long­
term
NOAEL
of
1.2
mg/
kg/
day
was
calculated
by
converting
the
inhalation
NOAEL
of
0.0047
mg/
L
in
Sprague­
Dawley
rats.
The
inhalation
endpoint
of
0.0047
mg/
L
was
converted
to
an
oral
equivalent
dose
using
Equation
1
of
the
HED
Route
to
Route
Extrapolations
memo
dated
October
9,
1998
(
USEPA,
1998a)
presented
below:

Equation
1:

where:

NOAEL
=
No­
observed­
adverse­
effect
level
(
NOAEL)
(
0.0047
mg/
L)
RV
=
Respiratory
volume
(
10.26
L/
hr)
D
=
Duration
of
daily
animal
exposure
(
based
on
a
6­
hour/
day
study)
BW
=
Mean
body
weight
in
kg
of
Sprague­
Dawley
rat
(
0.236
kg)
A
=
Absorption
­
the
ratio
of
deposition
and
absorption
in
the
respiratory
tract
compared
to
absorption
by
the
oral
route,
assumed
to
be
1
AF
=
Activity
factor
­
animal
default
is
1
Carcinogenicity
Screen:
Cancer
information
was
not
initially
presented
in
the
initial
draft
of
the
hazard
identification
report
(
USEPA,
1999).
EPA
suggested
using
a
cancer
slope
factor
of
7.3
(
mg/
kg/
day)­
1
for
this
assessment
(
Personal
Communication,
1999).

The
carcinogenicity
data
base
for
creosote
as
required
by
the
Agency
in
the
1988
DCI
consist
of
a
six­
month
dermal
oncogenicity
study
of
creosote
conducted
in
mice.
Creosote
in
this
study
was
tested
both
as
an
initiator
(
5
dermal
applications
per
week
for
2
weeks
at
doses
of
500

g/
mouse,
25
mg/
mouse,
or
56
mg/
mouse
followed
by
TPA
for
26
weeks)
and
as
a
promotor
(
DMBA
as
a
positive
initiator
at
50

g/
mouse
followed
by
twice
weekly
applications
of
creosote
at
the
same
doses
as
used
for
the
initiation
11
protocol).
As
an
initiator,
creosote
did
not
produce
any
increase
in
incidence
of
benign
tumors,
but
at
the
25
and
50
mg
doses,
squamous
cell
carcinomas
were
observed
in
2/
30
mice
at
each
dose.
As
a
promotor
in
DMBA­
initiated
mice,
creosote
produced
doserelated
increases
in
skin
papillomas,
keratoacanthoma,
squamous
cell
carcinoma,
and
basal
cell
carcinoma
at
the
25
and
50
mg
doses.
Increases
in
these
tumor
types
were
also
observed
when
creosote
was
used
as
both
initiator
and
promoter.
This
study
shows
that
creosote
acts
most
effectively
as
a
promoter
but
also
functions
as
a
"
complete"
carcinogen
(
USEPA,
1999).

Mutagenicity:
In
consideration
of
the
available
evidence
that
creosote
is
a
positive
mutagen,
the
Agency
waived
the
requirement
for
the
standard
mutagenicity
battery,
and
instead
required
dominant
lethal
testing
of
both
the
P1/
P13
and
P2
blends.
The
executive
summaries
of
these
studies
are
shown
below
(
USEPA,
1999).

In
a
rat
dominant
lethal
assay
with
P1/
P13
creosote
(
MRID
not
available),
male
Sprague­
Dawley
rats
were
treated
orally
once
per
day
for
five
consecutive
days
with
Creosote
P1/
P13
at
target
doses
of
725,
362.5
or
181.25
mg/
kg
body
weight/
day
in
a
volume
of
2.5
mL/
kg.
Actual
doses
determined
by
chemical
analysis
were
857.5,
330.5
and
230.8
mg/
kg/
day.
Twenty­
one
rats
were
dosed
at
the
two
lower
doses
and
26
rats
at
the
highest
dose.
The
vehicle
was
corn
oil.
Seven
days
after
the
initial
dosing,
each
male
was
mated
with
two
untreated
females
per
week
for
10
weeks
(
USEPA,
1999).

Creosote
P1/
P13
was
tested
to
toxic
doses.
A
preliminary
toxicity
test
was
conducted
with
Creosote
P1/
P13
concentrations
of
625,
1250,
1875
and
2500
mg/
kg/
day
for
five
consecutive
days.
All
rats
in
the
top
three
dosage
groups
were
dead
within
three
days.
No
treatment
related
deaths
occurred
in
the
lowest
dosage
group
although
other
clinical
signs
were
seen
following
dosing
including
decreased
activity,
increased
salivation,
diarrhea
and
anogenital
staining.
In
the
dominant
lethal
study,
all
rats
in
the
top
two
treatment
groups
but
none
in
the
low
dose
group
showed
decreased
activity
following
dosing
and
all
rats
in
the
high
dose
group
had
dyspnea.
Two
animals
in
the
low
dose
group
and
two
in
the
high
dose
group
had
material
around
the
nose
and
mouth.
Other
pharmacotoxic
signs
were
limited
to
a
few
animals
in
the
high
dose
group
and
included
lacrimation,
deposition
of
the
test
material
around
the
eyes,
increased
salivation
and
anogenital
staining.
One
high
dose
rat
died
following
the
fourth
dose.
A
dose­
related
decrease
in
body
weight
in
the
low­,
mid­,
and
high­
dose
animals,
compared
to
the
solvent
controls,
was
seen
during
the
dosing
period,
and
this
initial
weight
loss
was
not
recovered
in
mid­
and
high­
dose
rats
during
the
ten
week
mating
period.
Females
were
sacrificed
13
days
after
the
midweek
of
the
presumptive
mating
day
and
the
following
data
collected:
total
implantations
per
female,
corpora
lutea
per
female,
pre­
implantation
losses
per
female,
live
implantations
per
female,
dead
implantations
per
female,
proportion
of
females
with
one
or
more
dead
implantations,
proportion
of
females
with
two
or
more
dead
12
implantations
and
dead
implantations/
total
implantations
(
expressed
as
a
percentage).
The
fertility
index,
computed
as
the
number
of
fertile
females
(
with
corpora
lutea
present)
per
number
of
mated
females,
was
also
determined.
Statistically
significant
differences
from
control
values
were
seen
in
a
number
of
endpoints
throughout
the
study;
however,
with
the
exception
of
results
from
mating
group
nine,
none
were
endpoints
indicative
of
a
dominant
lethal
effect.
In
mating
group
nine,
statistically
significant
increases
were
seen
in
dead
implantations
per
female,
the
percentage
of
females
with

one
implantation,
the
percentage
of
females
with

two
implantations
and
the
percent
dead
implantations
per
total
implantations.
These
increases
were
seen
at
the
low
and
mid
doses
but
not
at
the
high
dose.
Also,
the
vehicle
control
values
in
mating
group
nine
were
unusually
low
compared
to
those
in
the
other
weekly
mating
groups
(
there
were
fewer
preimplantation
losses
(
0.85
per
female)
and
fewer
dead
implantations
(
0.41
per
female)
than
seen
for
the
vehicle
controls
in
the
other
mating
groups
(
1.53
±
0.37
and
0.85
±
0.20
per
female,
respectively)
and
values
for
percentage
of
females
with

one
and
two
dead
implantations
and
the
percent
dead
implantations
per
total
implantations
were
depressed).
The
results,
although
statistically
significant,
are
thus
not
considered
biologically
significant.
Positive
and
solvent
control
values
were
appropriate
except
where
noted
for
the
vehicle
controls
in
mating
group
nine.
There
was
no
evidence
that
Creosote
P1/
P13
induced
dominantlethals
in
any
germ
cell
stage
in
male
rats
as
tested
in
this
study
(
USEPA,
1999).

In
rat
dominant
lethal
assay
with
P2
creosote
(
MRID
not
available),
male
Sprague­
Dawley
rats
were
treated
orally
once
per
day
for
five
consecutive
days
with
Creosote
P2
at
target
doses
of
775,
387.5
or
193.75
mg/
kg
body
weight/
day
in
a
volume
of
2.5
mL/
kg.
Actual
doses
by
chemical
analysis
were
866.3,
431,
or
199.3
mg/
kg
body
weight/
day.
Twenty­
one
rats
were
dosed
at
the
two
lower
doses
and
26
rats
at
the
highest
dose.
The
vehicle
was
corn
oil.
Seven
days
after
the
initial
dosing,
each
male
was
mated
with
two
untreated
females
per
week
for
10
weeks
(
USEPA,
1999).

Creosote
P2
was
tested
at
an
adequate
dose.
All
rats
in
all
treatment
groups
showed
decreased
activity
following
dosing.
Other
clinical
signs,
limited
to
a
few
animals
in
which
there
was
a
back­
up
of
test
material
during
dosing,
were
lacrimation,
deposition
of
the
test
material
around
the
eyes
and
increased
salivation
in
one
high­
dose
male,
labored
breathing
in
one
low­
dose
male
and
two
high­
dose
males,
and
material
around
nose
and
mouth
in
two
low­
dose,
one
medium­
dose
and
four
high­
dose
males.
Reduced
food
consumption
was
seen
in
all
high­
dose
rats.
No
dosing­
or
test
material­
related
deaths
occurred
during
the
study.
A
dose­
related
decrease
in
body
weight
in
the
low­,
mid­,
and
high­
dose
animals,
compared
to
the
solvent
controls,
was
seen
during
the
dosing
period,
and
this
initial
weight
loss
was
not
recovered
in
mid­
and
high­
dose
rats
during
the
ten
week
mating
period.
Females
were
sacrificed
13
days
after
the
midweek
of
the
presumptive
mating
day
and
the
following
data
collected:
total
implantations
per
female,
corpora
lutea
per
female,
preimplantation
losses
per
female,
live
implantations
per
female,
13
dead
implantations
per
female,
proportion
of
females
with
one
or
more
dead
implantations,
proportion
of
females
with
two
or
more
dead
implantations
and
dead
implantations/
total
implantations
(
expressed
as
a
percentage).
The
fertility
index,
computed
as
the
number
of
fertile
females
(
with
corpora
lutea
present)
per
number
of
mated
females,
was
also
determined.
Statistically
significant
differences
from
solvent
control
values
(
p

0.05)
were
seen
for
a
number
of
endpoints
during
the
first
nine
weekly
mating
intervals
but,
with
one
exception,
not
in
endpoints
considered
indicative
of
dominant
lethality.
The
one
exception
was
a
significant
increase
in
the
number
of
dead
implants
over
the
solvent
control
value
in
the
sixth
mating
group
at
the
lowest
Creosote
P2
dose.
This
increase
was
not
considered
biologically
relevant
because
no
significant
increases
were
seen
at
higher
doses
or
in
other
endpoints
concerning
dead
implants.
In
the
tenth
mating
group
(
exposure
to
the
test
material
at
the
spermatogonial
stem
cell
stage),
an
apparently
dose­
related
increase
was
seen
in
the
number
of
dead
implantations
per
female,
the
percentage
of
females
with

1
dead
implant,
the
percentage
of
females
with

2
dead
implants
and
the
percentage
of
dead
implantations
per
total
implantations.
The
increases
reached
statistical
significance
at
the
highest
dose
for
the
first
two
endpoints.
Lack
of
a
dominant
lethal
effect
in
the
eighth
and
ninth
mating
groups,
which
also
test
spermatozoa
that
were
exposed
at
the
spermatogonial
stem
cell
stage,
may
possibly
indicate
treatment­
related
cell
cycle
delay.
Positive
and
solvent
control
values
were
appropriate.

There
was
no
evidence
of
a
dominant
lethal
effect
in
the
first
nine
weeks
following
treatment;
however,
significant
differences
between
the
control
group
and
the
treated
group
were
seen
in
week
ten
with
respect
to
dead
implantations
per
female,
the
percentage
of
females
with

1
dead
implantation
and
the
percentage
of
dead
implantations
per
total
implantations
(
USEPA,
1999).

4.1.3
FQPA
Considerations
As
there
are
no
existing
tolerances
or
other
clearances
for
residues
of
creosote
in
food,
an
FQPA
assessment
is
not
necessary.
Potential
post­
application
exposures
to
residents,
including
children
(
e.
g.,
from
use
of
railroad
ties
by
homeowners),
could
not
be
assessed
due
to
lack
of
exposure
data.
The
available
evidence
on
developmental
and
reproductive
effects
of
creosote
was
assessed
by
the
Health
Effects
Division
(
HED)
Hazard
Identification
Assessment
Review
Committee
on
April
1,
1999
The
committee
expressed
concern
for
potential
infants
and
children's
susceptibility
of
creosote,
based
on
the
severity
of
offspring
vs.
maternal
effects
observed
with
testing
of
creosote
in
the
P1/
P13
blend
developmental
toxicity
study
in
rats
at
the
175
mg/
kg/
day
dose
level
as
well
as
deficiencies
observed
in
the
2­
generation
reproduction
toxicity
study
in
rats.
14
Although
there
are
no
current
Agency
guideline
neurotoxicity
studies
available
for
creosote,
the
existing
studies
on
creosote
indicate
no
evidence
of
neurotoxicity
for
either
the
P1/
P13
or
P2
blends
of
creosote
(
ATSDR,
2002).
Based
on
the
above,
and
realizing
that
creosote
is
currently
registered
only
for
non
­
food
use
and
is
a
restricted
use
pesticide,
no
additional
neurotoxicity
testing
will
be
required
at
this
time.

4.1.4
Acute
Toxicology
Categories
Table
1
provides
the
acute
toxicity
categories
for
creosote.
It
also
provides
the
results
of
the
toxicity
tests.

Table
1.
Acute
Toxicity
Categories
for
Creosote
Test
Results
Toxicity
Category
Acute
Oral
Toxicity
LD50
=
2,451
mg/
kg
(
M);
1,893
mg/
kg
(
F)
III
Acute
Dermal
Toxicity
LD50
>
2,000
mg/
kg
III
Acute
Inhalation
Toxicity
LC50
>
5
mg/
L
IV
Primary
Eye
Irritation
Irritation
clearing
in
8­
12
days
II
Primary
Dermal
Irritation
Erythema
to
day
14
III
Dermal
Sensitization
Study
unacceptable
NA
NA
­
Not
applicable,
no
toxicological
endpoint.

4.1.5
Summary
of
Endpoints
of
Concern
Endpoints
for
assessing
occupational
and
residential
risks
are
presented
in
Table
2.
The
results
of
the
exposure
tests
are
also
provided.

Table
2.
Endpoints
for
Assessing
Occupational
and
Residential
Risks
for
Creosote
Test
Results
MOE
Acute
Dietary
Exposure
Not
required
NA
Chronic
Dietary
Exposure
­
Reference
Dose
(
RfD)
Not
required
NA
Short­
term
Dermal
Exposure
(
1
to
30
days)
Oral
developmental
rat
study
NOAEL
50
mg/
kg/
day
based
on
maternal
effects
+
50%
dermal
absorption
100
Intermediate­
term
Dermal
Exposure
(
1
to
6
months)
Dermal
90­
day
dermal
toxicity
study
in
rats
NOAEL
40
mg/
kg/
day
based
on
decrease
in
body
weight
gain
100
Long­
term
Dermal
Exposure
(
greater
than
6
months)
Oral
two
generation
reproduction
study
in
rats
LOAEL
25
mg/
kg/
day
based
on
decreased
pre­
mating
body
weight
+
50%
Dermal
absorption
300
Short­,
Intermediate­,
and
Longterm
Inhalation
Exposure
NOAEL
0.0047
mg/
L
based
on
decreased
body
weight
gain,
altered
hematology,
and
increased
weight
of
liver
and
thyroid
(
converted
to
1.2
mkd)
100
Test
Results
MOE
15
Oral
Cancer
Slope
Factor*
7.3
(
mg/
kg/
day)­
1+
50%
dermal
abs.
NA
NA­
not
applicable,
no
toxicological
endpoint.
*
Slope
factor
is
for
benzo(
a)
pyrene,
a
component
of
creosote,
and
used
as
an
indicator
of
carcinogenic
potential
of
creosote.

The
short­
term,
long­
term,
and
cancer
endpoints
are
based
on
toxicity
endpoints
from
oral
studies.
A
dermal
absorption
rate
of
50
percent
was
applied
to
oral
exposure
estimates
to
establish
risks
reflective
of
a
dermal
endpoint
as
recommended
in
the
report
of
the
Hazard
Identification
Assessment
Review
Committee
(
USEPA,
1999).
The
intermediate­
term
dermal
endpoint
is
based
on
the
results
of
a
dermal
study.
Thus,
no
dermal
absorption
rate
is
required.

4.2
Occupational
Handler
Exposures
and
Risks
EPA
has
determined
that
there
are
potential
exposures
to
mixers,
loaders,
applicators,
and
other
handlers
during
typical
use­
patterns
associated
with
creosote
and
from
use
in
commercial
and
industrial
settings.
The
following
types
of
handler
exposures
have
been
identified:

(
1a)
mixing/
loading/
applying
liquids
at
a
pressure
treatment
facility
(
treatment
operator);
(
1b)
mixing/
loading/
applying
liquids
at
a
pressure
treatment
facility
(
treatment
assistant);

Table
3
provides
a
description
of
exposure
scenarios
for
occupational
handlers.

Table
3.
Exposure
Scenarios
for
Occupational
Handlers
Exposure
Scenario
Scenario
Description
(
1a)
Mixing/
loading/
applying
liquids
at
a
pressure
treatment
facility
(
treatment
operator)
Scenario
pertains
to
a
wood
pressure
treatment
plant.
Liquid
ready­
to­
use
creosote
is
prepared
from
concentrate
and
loaded
into
the
retort
using
a
mechanical
pump.
Exposure
occurs
while
pumping
liquid
into
the
retort
and
pumping
liquid
from
retort
back
into
holding
tank.
Exposure
data
from
the
Creosote
Council
II
study
for
the
treatment
operator
(
TO)
were
used
in
this
assessment
(
Creosote
Council
II,
2001).
TOs
operated
and
monitored
application
system
valves
and
controls,
they
sometimes
opened
and
closed
cylinder
doors,
and
they
supervised
the
insertion
and
removal
of
charges
(
loaded
dried,
debarked
poles
or
untreated
ties)
of
poles
from
the
treatment
cylinders.

(
1b)
Mixing/
loading/
applying
liquid
formulation
at
a
pressure
treatment
facility
(
treatment
assistant)
Scenario
pertains
to
a
wood
pressure
treatment
plant.
Liquid
ready­
to­
use
creosote
is
prepared
from
concentrate
and
loaded
into
the
retort
using
a
mechanical
pump.
Exposure
occurs
while
pumping
liquid
into
the
retort.
Exposure
data
from
the
Creosote
Council
II
study
for
the
treatment
assistant
(
TA)
were
used
in
this
assessment
(
Creosote
Council
II,
2001).
TAs
performed
many
of
the
same
functions
as
the
TOs
and
sometimes
assisted
the
TO
in
charge
preparation,
cylinder
cleaning
and
maintenance,
filter
cleaning,
mixing
of
treatment
solution,
and
also
participated
in
some
loader
operations
moving
charges.
16
Creosote
is
used
by
occupational
handlers
only.
Since
it
is
a
restricted­
use
pesticide
that
can
only
be
applied
by
certified
applicators
or
someone
under
their
direct
supervision,

it
is
not
available
for
sale
to
or
use
by
homeowners.
Creosote
is
now
to
be
used
exclusively
in
industrial
settings.

4.2.1
Handler
Data
and
Assumptions
In
the
course
of
development
of
this
risk
assessment,
data
from
the
chemical­
specific
handler
study
was
exclusively
used
to
assess
potential
risks
to
workers
at
pressure
treatment
facilities.

The
Agency
used
a
worker
exposure
study
on
pressure
treatment
use
submitted
by
the
Creosote
Council
II
to
provide
chemical­
specific
handler
dermal
and
inhalation
exposure
data
in
support
of
the
re­
registration
of
pressure
treatments
of
creosote
(
Creosote
Council
II,
2001).
These
data
were
used
to
support
scenarios
1a
and
1b
of
the
assessment.
These
data
were
reviewed
internally
by
EPA
(
USEPA,
2001).

No
dermal
exposure
studies
were
identified
in
the
available
literature.
This
is
consistent
with
EPA
statements
in
the
most
recent
re­
registration
position
document
entitled
Wood
Preservative
Pesticides:
Creosote,
Pentachlorophenol,
and
Inorganic
Arsenicals:
Position
Document
4
(
USEPA,
1984).
"
There
are
no
quantitative
data
on
dermal
exposure
to
these
workers."
Since
EPA
currently
wishes
to
pursue
estimation
of
quantitative
exposures
to
creosote,
the
Creosote
Council
II's
2001
study
was
used
in
order
to
estimate
dermal
exposure
information
for
occupational
handlers
exposed
during
the
pressure
treatment
process.

Inhalation
exposure
data
were
also
sparse.
In
the
document
entitled
Wood
Preservative
Pesticides:
Creosote,
Pentachlorophenol,
and
Inorganic
Arsenicals:

Position
Document
4
(
USEPA,
1984),
EPA
states
that
"
the
Agency
still
has
no
definitive
data
on
the
identity
of
the
airborne
component
chemicals
of
creosote
to
which
workers
are
exposed
in
wood
treatment
plants
where
creosote
is
used."
In
addition,
there
are
apparently
no
exact
methods
to
develop
inhalation
exposure
data
through
personal
monitoring
of
creosote.

Because
of
the
overall
variability
in
the
composition
of
creosote
(
e.
g.,
over
100
known
chemicals
are
components
of
creosote),
it
is
difficult
to
characterize
its
exact
nature.
Since
neither
the
characterization
of
airborne
creosote
or
the
development
of
inhalation
sampling
17
methods
are
specific
for
creosote,
there
exists
a
high
variability
in
the
creosote
inhalation
data
presented
in
the
literature.
Most
of
the
studies
presented
in
the
literature
were
conducted
by
industrial
hygienists
using
methods
approved
by
the
National
Institute
for
Occupational
Safety
and
Health
(
NIOSH)
and
Occupational
Safety
and
Health
Administration
(
OSHA)
for
polycyclic
aromatic
hydrocarbons
(
PAHs),
phenols/
creosols,

and
the
individual
constituents
of
the
PAHs
(
i.
e.,
naphthalene,
phenanthrene,
anthracene,

etc).
Since
the
Creosote
Council
study
is
the
most
recent
study
presented
on
creosote
exposure
and
presents
both
dermal
and
inhalation
exposure,
it
was
used
to
provide
exposure
estimates.
Other
studies
found
in
the
available
literature
are
also
presented
in
the
post­
application
section.

This
chemical­
specific
information
is
believed
to
provide
a
more
accurate
estimation
of
actual
exposures
than
surrogate
data
currently
available
from
PHED
or
CMA.
Since
the
actual
mixing/
loading/
applying
of
creosote
is
an
entirely
mechanical
process,
dermal
and
inhalation
exposures
to
the
handlers
that
participate
in
the
pressure
treatment
process
(
e.
g.,
treatment
operators
and
)
were
used
to
estimate
total
handler
exposure
during
the
pressure
treatment
process.
These
handlers
are
selected
because
they
are
representative
of
the
population
of
handlers
that
would
be
loading
the
wood
preservative
and
operating
the
retort.
A
description
of
their
duties
is
provided
in
Table
3.
The
study
examined
exposure
to
handlers
for
four
to
five
days.

Creosote
Council
II
2001
Study
Synopsis:

The
handlers
monitored
include
a
treatment
operator
and
treatment
assistant.
Handlers
performed
typical
tasks
related
to
these
activities
and
were
monitored
during
a
full
work
cycle
beginning
at
7
AM
and
ending
at
3
PM.
The
following
are
descriptions
of
the
tasks:
18

Treatment
operator
­
TOs
operated
and
monitored
application
system
valves
and
controls,
occasionally
opened
and
closed
cylinder
doors,
and
supervised
the
insertion
and
removal
of
charges
(
loads
of
dried,
debarked
poles
or
untreated
ties)
of
poles
from
the
treatment
cylinders.


Treatment
assistant
­
TAs
performed
many
of
the
same
functions
as
the
TOs
and
sometimes
assisted
the
TO
during
charge
preparation,
cylinder
cleaning
and
maintenance,
filter
cleaning,
mixing
of
treatment
solution,
and
also
participated
in
some
of
the
loader
operations
for
moving
charges.


Loader
operator
­
LOs
stacked
untreated
wood
onto
charge
trams,
moved
charges
into
and
out
of
treatment
cylinders,
distributed
treated
wood
to
loadout
area,
and
loaded
treated
wood
for
shipment.


Cylinder­
area
helpers
(
CHs
in
the
cylinder
area,
and
LHs
in
the
loadout
areas)
­
CHs/
LHs
aided
the
LOs
by
opening/
closing
cylinder
doors,

cleaning
door
debris
and
performing
door
maintenance,
handling
charge
leads
and
cables,
and
banding
stacked
wood.


Checker
(
CK)
­
CKs
performed
many
of
the
duties
of
a
CH.


Test
borers
(
TBs)
­
TBs
took
cores
from
freshly
treated
poles
or
ties
to
be
tested
for
creosote
content
and
penetration
depth.


Load­
out
area
helpers
(
LHs)
­
LHs
aided
their
LOs
by
banding
treated
wood
and
removing
culls.


Oil
unloaders
(
OUs)
­
OUs
operated
the
equipment
that
transferred
creosote
from
rail
tank
cars
to
treating
system
tanks.


Drip
pad
laborer
(
DP)
­
DPs
steam­
cleaned
drip
pads
and
tracks.
They
also
picked
up
and
disposed
of
treated
wood
waste
and
performed
various
labor
clean­
up
duties
in
treatment
areas.


Water
treatment
system
operators
(
WOs)
­
WOs
controlled
equipment
that
collected
drip­
pad
effluent
water,
and
removed
creosote
and
other
contaminants.
19
Pressure
Treatment
Process:
Pressure
treatment
is
often
required
because
of
the
resistance
of
wood
to
deep
penetration
by
preservatives.
The
pressure
treatment
process
begins
when
untreated
wood
is
loaded
onto
small
rail/
tram
cars
that
are
pushed
into
the
treating
cylinder
using
locomotives,
forklifts,
or
similar
equipment.
The
cylinder
door
is
sealed
via
a
pressure­
tight
door
and
the
operation
remains
a
closed
system
during
the
entire
treatment
process.
Treating
solutions
are
then
pumped
into
the
cylinder
and
the
inside
pressure
is
raised.
At
the
end
of
the
treatment
process,
the
excess
treating
solution
is
pumped
out
of
the
treating
cylinder
and
back
to
storage
for
reuse.
The
cylinder
is
opened,
and
the
rail/
tram
cars
holding
the
treated
wood
are
pulled
out
of
the
cylinder
using
a
locomotive,
forklift,
or
similar
equipment.

According
to
information
provided
by
industry
sources
(
Krygsman,
1994),
wood
pressure
treatment
of
railroad
ties
in
a
retort
may
last
anywhere
from
4
to
24
hours.
A
typical
retort
cylinder
has
a
diameter
of
about
8
feet
and
a
length
of
about
120
feet.
About
16
rail/
tram
cars
can
be
placed
in
a
retort
at
one
time.
The
rail/
tram
cars
usually
are
connected
together
and
are
pushed
in
and
out
of
the
retort
on
railroad
tracks
using
a
locomotive.
Wood
preservative
is
loaded
into
the
wood
pressure
treatment
retort
facilities
from
rail
tank
cars
using
hoses
and
metered
pumps.
The
wood
preservative
is
stored
in
two
or
three
holding
tanks
that
may
be
as
large
as
60,000
gallons.
During
the
wood
treatment
process
the
wood
is
sprayed
under
pressure
in
the
enclosed
retort.
In
the
retort,

a
"
charge"
of
liquid
preservative
is
pumped
into
the
trams
and
then
later
pumped
out.

After
the
wood
preservative
is
pumped
out,
the
wood
is
dried
through
a
vacuum
treatment
and
the
tram
cars
containing
wood
(
e.
g.
railroad
ties)
are
then
pulled
out.
Since
the
wood
in
the
tram
cars
is
pulled
by
mechanical
means
there
is
very
little
direct
human
contact
with
the
exposed
wood.
Likely
contact
is
through
dermal
contact
with
equipment
that
was
previously
in
the
retort,
removing
cables
that
separated
layers
of
ties,
dermal
and
inhalation
contact
to
vapors
inside
the
retort
before
and
after
pressure
treatment,
cleaning
the
retort,
and
inspecting
wood
pieces
by
coring
the
wood.

Dermal
Exposure
Study:
Since
creosote
is
a
complex
mixture
of
over
100
chemicals
including
phenols,
creosol,
and
aromatic
hydrocarbons,
it
is
difficult
and
expensive
to
identify
all
of
the
chemicals
in
the
mix.
In
addition,
creosote
cannot
be
measured
directly
because
of
its
complex
mixture.
Dermal
exposure
to
"
total
creosote"
was
estimated
by
measuring
the
levels
of
ten
individual
polynuclear
aromatic
hydrocarbon
(
PNA)

compounds.
Each
analyte
was
determined
in
each
whole­
body
dosimeter
(
WBD)
and
glove
sample
as
if
it
represented
total
creosote.
The
goal
was
to
use
these
marker
compounds
to
represent
"
total
creosote".
20
Dermal
Exposure
Monitoring:
The
creosote
dermal
exposure
to
each
worker
was
determined
using
a
WBD,
consisting
of
a
100%
cotton
thermal
shirt
and
long
pants.
Each
worker
at
Sites
A,
C,
or
D
wore
his
WBD
under
a
fresh
work
uniform
consisting
of
a
cotton
long­
sleeved
work
shirt
and
cotton
work
trousers
(
or
one­
piece
cotton
coverall)

provided
by
the
test
site.
The
workers
at
Site
B
were
not
provided
uniforms
therefore,
for
the
purpose
of
this
study,
each
worker
wore
a
WBD
under
a
fresh
lightweight
cotton/
polyester
sweat
shirt
and
pants
purchased
locally
by
study
personnel.
The
workers
at
all
four
sites
wore
a
lightweight
100%
cotton
glove
dosimeter
on
each
hand
under
his
chemical­
resistant
or
work
gloves,
as
appropriate.
Each
of
these
analytes
were
determined
in
each
WBD
and
glove
sample
as
if
it
represented
total
creosote.
The
averaged
analyte
concentrations
were
used
to
estimate
the
level
of
total
creosote
present
in/
on
the
individual
sample.

Inhalation
Exposure
Study:
Inhalation
exposures
for
each
worker
was
estimated
by
active
dosimetry.
Inhalation
exposure
was
estimated
for
11
individual
PNA
compounds
as
well
as
for
benzene­
soluble
PNAs
and
related
compounds
collectively
known
as
coal
tar
pitch
volatiles
(
CTPVs).
The
Polytetrafluroethylene
(
PTFE)
filter
retained
the
CTPVs,

while
the
PNAs
were
retained
in
the
XAD­
2
resin
tubes.
Each
worker
wore
a
sampling
train
consisting
of
a
PTFE
filter
upstream
from
two
in­
line
XAD­
2
resin­
filled
air
sampling
tubes.
(
However,
there
was
no
attempt
by
the
study
sponsors
to
relate
inhalation
levels
found
for
PNAs
and
CTPVs
to
"
total
creosote"
­­
a
significant
weakness
with
the
study.)

Inhalation
Exposure
Monitoring:
Handler
inhalation
exposure
for
a
pressure
treatment
facility
was
examined
using
the
creosote­
specific
data
for
the
treatment
operator
and
the
treatment
assistant.

Inhalation
exposure
monitoring
at
Site
A
was
unsuccessful
because
a
single
XAD­
2
tube
was
used
along
with
a
non­
solvent­
resistant
filter
cassette.
Therefore,
the
sampling
methodology
was
changed
to
include
the
use
of
a
second
XAD­
2
resin
tube
in
the
sampling
train
prior
to
sampling
at
Sites
B,
C,
and
D.
Inhalation
exposure
monitoring
was
performed
successfully
at
these
sites.
Each
worker
at
Sites
B,
C,
and
D
was
equipped
with
an
air
sampling
train
consisting
of
a
PTFE
filter
in
an
opaque,
solvent­
resistant
plastic
cassette
connected
upstream
from
two
in­
line
XAD­
2
resin­
filled
air
sampling
tubes.
The
intake
orifice
of
the
filter
was
placed
in
the
worker's
breathing
zone,
directed
downward.

Air
was
pulled
through
the
sampling
train
by
a
portable
air
sampling
pump
attached
to
the
worker's
belt.
The
pump
drew
air
through
the
sampling
tube
at
approximately
1
L/
minute
21
while
the
worker
performed
his
tasks.
Pumps
were
calibrated
immediately
prior
to
and
after
each
monitoring
period
using
a
mass
flow
meter
or
bubble
calibrator.
The
pumps
were
turned
on
at
the
beginning
of
each
work
cycle
and
were
left
running
during
restroom,

coffee,
or
other
short
breaks,
but
were
turned
off
or
set
on
"
hold"
during
lunch
breaks.

The
pumps
and
samplers
were
removed
from
the
worker
during
the
lunch
break.
At
the
conclusion
of
the
lunch
break,
the
pump
and
sampling
train
were
reinstalled
and
the
pump
restarted.
All
start
and
stop
times
for
breaks
were
recorded.

During
each
work
cycle,
start
times
and
end
times
of
each
task
performed
by
the
worker
were
recorded.
Pump
parameters
during
use
were
also
recorded.
At
the
end
of
each
work
cycle,
the
pumps
and
sample
trains
were
collected.
Each
filter
cassette
and
sampling
tube
were
capped,
labeled,
bagged,
and
placed
on
dry
ice
for
shipment
to
USX
Engineers
and
Consultants,
Inc.
(
UEC)
for
extraction
and
analysis.
After
the
collection
of
the
air
samples,
the
air
sampling
pump
was
re­
calibrated.

4.2.2
Handler
Risk
Assessment
and
Characterization
The
handler
exposure
assessment
is
based
on
the
Creosote
Council's
worker
exposure
study.
Tables
4
and
5
present
the
exposure/
risk
calculations
for
each
exposure
scenario.

The
short­
term
dermal
endpoint
is
based
on
a
maternal
toxicological
endpoint;

therefore,
the
body
weight
of
a
typical
woman
(
60
kg)
was
used
for
the
dose
calculation.

The
adult
body
weight
of
70
kg
was
used
for
the
intermediate­
term,
long­
term,
and
cancer
endpoints.
Short­
term,
long­
term,
and
cancer
endpoints
are
all
based
on
oral
administrations.
A
50
percent
absorption
factor
was
used
to
develop
a
dermal
dose
based
on
an
oral
administration.
Intermediate­
term
endpoints
are
based
on
a
dermal
administration;
therefore,
no
absorption
factor
was
used.
22
Daily
Inh.
Dose
mg
ai
kg/
day

Daily
Exposure
Data
(
mg/
day)
x
1
Body
Weight
(
kg)
x
ABS
(%)
Creosote­
specific
inhalation
data
were
available.
For
these
scenarios,
specific
inhalation
studies,
which
measured
air
concentrations
in
pressure
treatment
facilities,
were
used
to
derive
an
inhalation
dose.
The
inhalation
dose
from
an
air
concentration
was
calculated
as
follows:

=
Values
obtained
from
studies
Body
Weight
(
kg)
=
70
kg
for
short,
intermediate
and
chronic
ABS
=
100
percent
23
Table
4.
Handler
Exposure/
Dose
for
Creosote
Exposure
Scenarioa
Dermal
Inhalation
Combined
Dermal
&
Inhalation
Lifetime
Average
Daily
Doseg
(
mg/
kg/
day)

Exposure
Study
Data
(

g/
kg/
day)
b
Daily
Exposure
(
mg/
day)
c
Short­
term
Daily
Dose
(
mg/
kg/
day)
d
Int.­
term
Daily
Dose
(
mg/
kg/
day)
d
Long­
term
Daily
Dose
(
mg/
kg/
day)
d
Lifetime
Average
Daily
Dose
(
mg/
kg/
day)
e
Daily
Exposure
c
(
mg/
day)
Daily
Dose
d
(
mg/
kg/
day)
Lifetime
Average
Daily
Dose
e
(
mg/
kg/
day)

Mixer/
Loaders
(
1a)
Mixing/
Loading/

Applying
Liquids
at
a
Pressure
Facility
(
treatment
operator)

(
1b)
Mixing/
Loading/

Applying
Liquids
at
a
Pressure
Treatment
Facility
(
treatment
assistant)

a
Exposure
scenarios
based
on
review
of
available
labels
and
LUIS
report.

b
c
d
Daily
Dose
(
mg/
kg/
day)
=
Daily
Dermal
Exposure
(
mg/
day)
/
Body
Weight
(
kg).
Short­
term
uses
a
60
kg
body
weight
and
a
50%
dermal
absorption,
intermediate­
term
uses
a
70
kg
body
weight
with
no
absorption,
and
long­
term
uses
a
70
kg
body
weight
with
50%
dermal
absorption.
Inhalation
uses
a
70
kg
body
weight
with
100%
absorption.

e
Lifetime
Average
Daily
Creosote
Dose
(
mg/
kg/
day)=
Daily
Exposure
(
mg/
day)
/
Body
Weight
(
70
kg)
*
ABS
(
50%)
*
[
Exposure
Frequency
(
250
days/
year)
*
Exposure
Duration
(
40
yrs)]
/
[
365
days/
yr
*
Lifetime
(
75
yrs)].

f
Based
on
the
study
submitted
by
Creosote
Council
II
entitled"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
with
Pressure­
Treatment
of
Wood
with
Creosote"
(
Creosote
Council
II,
2001).
Note:
Inhalation
exposure
was
estimated
for
11
individual
PNA
compounds
as
well
as
for
benzene­
soluble
PNAs
and
related
compounds
collectively
known
as
coal
tar
pitch
volatiles
(
CTPVs).

g
Combined
dermal
and
inhalation
lifetime
average
daily
dose
(
LADD)
=
dermal
LADD
+
inhalation
LADD.

NA
­
Not
available.

GM
­
Geometric
mean.
The
study
provided
the
geometric
mean
creosote
exposure
based
on
multiple
replicates
from
multiple
sites
presented
in
the
study
submitted
by
Creosote
Council
II
(
2001).
The
geometric
mean
exposure
is
used
to
represent
a
typical
exposure.
24
Table
5.
Handler
Short­
term,
Intermediate­
term,
and
Long­
term
Risks
for
Creosote
Exposure
Scenarioa
Risk
Mitigation
b
Dermal
MOEs
Inhalation
MOE
f
Cancer
Risks
Based
on
0.5­
1.0%

Benzo[
a]
Pyreneg
Short­
term
c
Intermediate­
term
d
Longterm
e
Mixer/
Loaders
a
Exposure
scenarios
based
on
review
of
available
labels
and
LUIS
report.

b
Risk
mitigation
is
per
each
facility
in
the
pressure
treatment
exposure
study.

c
Short­
term
Dermal
MOE=
Short­
term
NOAEL
(
50
mg/
kg/
day)
/
Short­
term
Dose
(
see
Table
4).

d
Intermediate­
term
Dermal
MOE=
Intermediate­
term
NOAEL
(
40
mg/
kg/
day)
/
Intermediate­
term
Dose
(
see
Table
4).

e
Long­
term
Dermal
MOE=
Long­
term
LOAEL
(
25
mg/
kg/
day)/
Long­
term
Dose
(
see
Table
4).

f
Inhalation
MOE=
Inhalation
NOAEL
(
1.2
mg/
kg/
day)/
Inhalation
Dose
(
see
Table
4).

g
Cancer
Risk=
Combined
Lifetime
Average
Daily
Dose
(
LADD)
(
see
Table
4)
x
Q1
*
(
7.3
(
mg/
kg/
day)­
1)
x
(
0.5%
or
1.0%
benzo[
a]
Pyrene).
25
Daily
Dermal
Dose
mg
ai
Kg/
Day

Daily
Dermal
Exposure
mg
ai
day
x
1
Body
Weight
(
Kg)
x
ABS
(%)
Creosote­
specific
dermal
data
were
available
for
scenarios
1a
and
1b.
The
dermal
dose
was
calculated
as
follows:

Daily
Dermal
Exposure
=
Exposure
study
data
(
ug/
kg/
day)
x
Study's
Body
Weight
(
71.8
kg)

Body
Weight
(
kg)
=
60
kg
for
short­
term
and
70
kg
for
intermediate­
term
and
chronic
Table
4
uses
exposure
study
data
from
the
Creosote
Council
II,
2001,
exposure
assessment
entitled
"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
With
Pressure­
Treatment
of
Wood
with
Creosote."
This
source
provides
a
geometric
mean
dermal
dose
of
360
µ
g/
kg/
day
(
note:
the
maximum
dermal
dose
is
49,573
µ
g/
kg/
day)
for
a
treatment
operator
(
scenario
1a,
Table
4)
and
a
geometric
mean
dermal
dose
of
27
µ
g/
kg/
day
(
note:
the
maximum
dermal
dose
is
33
µ
g/
kg/
day)
for
a
treatment
assistant
(
scenario
1b,
Table
4).
Because
EPA
traditionally
uses
an
adult
body
weight
of
70
kg
and
female
body
weight
of
60
kg
in
its
exposure
assessments
which
is
slightly
different
then
the
71.8
kg
body
weight
used
in
the
Creosote
Council
II
exposure
assessment,
the
doses
used
in
this
assessment
had
to
be
normalized
back
to
daily
dermal
exposures.
The
normalization
was
performed
by
multiplying
the
exposure
dose
times
the
71.8
kg
body
weight.

ABS
=
50
percent
absorption
for
short­
term
and
chronic,
100
percent
for
intermediate­
term
The
calculations
of
the
daily
dermal
dose
of
creosote
received
by
handlers
were
used
to
calculate
the
short­
term,
intermediate­
term,
and
chronic
MOEs.
The
daily
dermal
MOE
was
calculated
using
an
NOAEL
of
50
mg/
kg/
day
for
short­
term
exposure,
an
NOAEL
of
40
mg/
kg/
day
for
intermediate­
term
exposures,
and
an
LOAEL
of
25
mg/
kg/
day
for
chronic
exposures.
26
Dermal
MOE

NOAEL
(
mg/
kg/
day)
Dermal
Dose
(
mg/
kg/
day)

Inhalation
MOE

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

LADD
(
mg/
kg/
day)

Daily
Exp.
(
mg/
day)/
Body
Weight
(
kg)

ABS
(%)

Exp.
Frequency
(
days)

Exp.
Duration
(
yrs)
365
days/
yr

Lifetime
(
yrs)
Risk
Calculations:
The
following
formula
describes
the
calculation
of
a
dermal
MOE:

The
target
MOE
for
short­
and
intermediate­
term
dermal
exposure
is
100
and
the
target
MOE
for
long
term
exposure
is
300.

The
following
formula
describes
the
calculation
of
an
inhalation
MOE:

The
target
MOE
for
total
short­
term,
intermediate­
term,
and
long­
term
inhalation
exposure
is
100.

Handler
Exposure
and
Cancer
Risk
Calculations:
For
the
handler
exposure
and
cancer
risk
calculations
the
lifetime
average
daily
dose
was
calculated
by
adding
the
chronic
dermal
and
inhalation
doses
and
accounting
for
exposure
frequency,
exposure
duration,
and
lifetime.
Exposure
duration
was
assumed
to
be
40
years
and
is
the
standard
value
used
by
EPA
Office
of
Pesticide
Programs
to
represent
a
working
lifetime.
This
is
assumed
to
be
a
high
end
value.
Lifetime
is
assumed
to
be
75
years.
This
is
the
recommended
value
for
the
U.
S.

population
as
cited
in
EPA's
Exposure
Factors
Handbook
(
USEPA,
1997).
All
handler
scenarios
assume
an
exposure
frequency
of
250
days
per
year
(
i.
e.,
5
days
per
week,
50
weeks
per
year).
This
is
a
standard
Agency
assumption
for
days
worked
per
year.
Table
5
details
the
handler
cancer
risk
estimates.
The
following
formula
describes
the
calculation
of
the
lifetime
average
daily
dose
(
LADD):
27
Risk

LADD
mg
ai
kg/
day
x
Cancer
Slope
Factor
1
(
mg/
kg/
day)
Risks
are
calculated
by
multiplying
the
lifetime
average
daily
dose
times
the
cancer
slope
factor
of
7.3
(
mg/
kg/
day)
­
1
using
the
following
formula:

Creosote
is
rated
as
a
B1
probable
human
carcinogen
based
on
limited
evidence
of
the
association
between
occupational
creosote
contact
and
subsequent
tumor
formation.
Further,

while
a
specific
quantitative
risk
assessment
on
carcinogenicity
of
creosote
has
not
been
performed
by
the
Agency,
a
quantitative
cancer
risk
assessment
exists
for
benzo(
a)
pyrene,
one
of
the
components
of
creosote.
Administration
of
benzo(
a)
pyrene
by
inhalation
has
been
shown
to
result
in
respiratory
tract
tumors,
and
administration
by
the
dermal
route
results
in
skin
tumor
production,
similar
to
creosote.
Benzo(
a)
pyrene
has
also
been
shown
to
be
a
"
complete"

carcinogen
similar
to
creosote,
and
also
tests
positive
for
mutagenicity
on
a
variety
of
assays.

Therefore,
the
Anitmicrobials
Division
is
using
the
cancer
slope
factor
for
benzo(
a)
pyrene
[
7.3
(
mg/
kg/
day)­
1
]
as
an
indicator
of
worker
risk
in
conducting
the
cancer
risk
assessment
for
creosote.

Non­
cancer
acute,
sub­
chronic,
and
chronic
toxicity
endpoints
related
to
dermal
exposures
to
creosote
have
also
been
identified.
A
MOE
of
greater
than
100
for
creosote
is
considered
to
indicate
no
risk
concern
for
short­
term
and
intermediate­
term
exposures,
and
a
MOE
of
greater
than
300
for
creosote
is
considered
to
indicate
no
risk
concern
for
chronic
exposures.
The
results
were
presented
in
Table
5
and
are
summarized
as
follows:

The
calculations
of
short­
and
intermediate­
term
risks
indicate
that
dermal
MOEs
are
more
than
100
(
i.
e.,
not
of
concern)
with
additional
engineering
controls
for
the
following
scenarios:


28
The
calculations
of
long­
term
risks
indicate
that
dermal
MOEs
are
less
than
300
with
additional
engineering
controls
for
the
following
scenarios:

The
calculations
of
long­
term
risks
indicate
that
dermal
MOEs
are
more
than
300
with
additional
engineering
controls
for
the
following
scenarios:

One
inhalation
endpoint
(
acute,
sub­
chronic,
and
chronic)
related
to
inhalation
exposures
has
been
identified.
A
MOE
of
greater
than
100
for
creosote
is
considered
to
indicate
a
no­
risk
exposure.
The
creosote
inhalation
MOEs
for
the
TO
and
TA
are
of
concern
(
MOEs
=
10
and
17,
respectively).

All
of
the
handler
scenarios
exceed
the
1E­
04
cancer
risk
levels.
All
of
the
handler
scenarios
are
expected
to
pose
a
risk
concern.

4.3
Occupational
Post­
application
Exposures
and
Risks
The
Agency
is
concerned
about
potential
post­
application
exposures
to
creosote.

Since
coal
tar
creosote
is
a
blend
of
over
100
compounds,
degradation
is
complicated.
These
compounds
include
volatile
and
semi­
volatiles.
The
volatiles
are
the
single
ring
compounds
and
the
semi­
volatiles
are
the
two
to
six
ring
compounds.
The
vapor
pressure
tends
to
become
larger
as
aromatic
rings
are
added
to
the
compound.
The
more
soluble
compounds
in
creosote
include
phenols,
creosol,
and
N­
heterocyclics.
The
high
molecular
weight
PAHs
tend
to
have
low
aqueous
solubilities
("
The
Environmental
Degradation
of
Creosote",
1998).

Potential
post­
application
exposure
may
occur
following
creosote
applications
in
commercial,
industrial,
and
residential
settings.
Post­
application
concerns
exist
in
residential
settings
when
pressurized
treated
wood
(
railroad
crossties,
cross
planks,
cross
arms)
is
used
for
29
block
flooring,
and
fence
posts
in
residential
areas.
Although
homeowner
handler
use
is
prohibited
by
the
label,
post­
application
exposures
to
creosote­
treated
wood
are
a
potential
homeowner
concern.

The
potential
post­
application
exposures
to
homeowners
include:

(
1)
homeowner
incidental
ingestion
and
dermal
contact
with
soil
contaminated
with
creosote
(
e.
g.,
soil
contaminated
by
creosote
treated
telephone
poles)
(
child)

(
2)
outdoor
homeowner
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
piers,
etc.)
(
adult)

(
3)
outdoor
homeowner
incidental
hand­
to­
mouth
and
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
posts,
decks,
shingles,
fencing,

lumber,
piers,
etc.)
(
child)
30
4.3.1
Post­
application
Occupational
Data
and
Assumptions,
and
Exposure
and
Risk
Calculations
In
the
course
of
development
of
this
RED,
chemical­
specific
post­
application
data
identified
from
pertinent
literature
sources
were
used
in
conjunction
with
both
industry
and
Agency
estimates
of
exposure
parameters
to
predict
exposures.
Tables
6
and
7
include
the
exposure/
risk
calculations
for
non­
cancer
and
cancer
risks
for
each
exposure
scenario.
31
Table
6.
Post­
application
Exposure/
Dose
for
Creosote
Exposure
Scenarioa
Dermal
Inhalation
Combined
Dermal
&
Inhalation
Lifetime
Average
Daily
Dose
f
(
mg/
kg/
day)

Exposure
Study
Data
b
(

g/
kg/
day)
Daily
Exposure
c
(
mg/
day)
Short­
term
Daily
Dosed
(
mg/
kg/
day)
Int.­
term
Daily
Dosed
(
mg/
kg/
day)
Long­
term
Daily
Dosed
(
mg/
kg/
day)
Lifetime
Average
Daily
Dermal
Dose
e
(
mg/
kg/
day)
Daily
Exposure
c
(
mg/
day)
Daily
Dosed
(
mg/
kg/
day)
Lifetime
Average
Daily
Dose
e
(
mg/
kg/
day)

(
1)
Cylinder
Area
Loader
Operator
313
22
0.19
0.32
0.16
0.059
11
0.16
0.057
0.12
(
2)
Cylinder
Area
Loader
Helper
626
45
0.37
0.64
0.32
0.12
22
0.31
0.11
0.23
(
3)
Checker
638
46
0.38
0.65
0.33
0.12
3.1
0.044
0.016
0.14
(
4)
Drip
Pad
Labor
271
19
0.16
0.28
0.14
0.051
4.4
0.063
0.023
0.074
(
5)
Load­
out
Area
Loader
Operator
69
5
0.041
0.071
0.035
0.013
4.4
0.063
0.023
0.036
(
6)
Load­
out
Area
Loader
Helper
25
1.8
0.015
0.026
0.013
0.0047
1.3
0.019
0.007
0.011
(
7)
Load­
out
Area
Forklift
Operator
208
15
0.12
0.21
0.11
0.039
8.3
0.12
0.043
0.082
(
8)
Oil
Unloader
901
65
0.54
0.92
0.46
0.17
13
0.19
0.068
0.24
(
9)
Test
Borer
385
28
0.23
0.39
0.2
0.072
11
0.16
0.057
0.13
(
10)
Water
Treatment
System
Operator
108
7.8
0.065
0.11
0.055
0.02
7.7
0.11
0.040
0.06
(
11)
Railroad
Worker
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
(
12)
Pole
Installer
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
No
Data
a
Exposure
scenarios
based
on
review
of
available
labels
and
LUIS
report.
32
d
Daily
dose
(
mg/
kg/
day)
=
daily
exposure
/
body
weight
(
kg).
Short­
term
uses
a
60
kg
body
weight
and
a
50
percent
dermal
absorption;
intermediate­
term
uses
a
70
kg
body
weight
(
no
absorption
factor
is
necessary);
and
long­
term
uses
a
70
kg
body
weight
with
50
percent
dermal
absorption.
Inhalation
uses
a
70
kg
body
weight
with
100
percent
inhalation
absorption.

e
Lifetime
average
daily
dose
=
daily
dose
(
mg/
kg/
day)
*
[
exposure
frequency
(
250
days/
year)
*
exposure
duration
(
40
years)]
/
[
365
days/
year
*
lifetime
(
75
years)].

f
Combined
LADD
=
dermal
LADD
+
inhalation
LADD.

Table
7.
Post­
application
Short­
term,
Intermediate­
term,
and
Long­
term
Risks
for
Creosote
Exposure
Scenarioa
Dermal
MOEs
Inhalation
MOE
e
Target
MOE=
100
Cancer
Risk
based
on
0.5%­
1.0%
Benzo
[
a]
Pyrenef
Short­
term
b
Target
MOE=
100
Intermediate­
term
c
Target
MOE=
100
Long­
term
d
Target
MOE=
300
(
1)
Cylinder
Area
Loader
Operator
270
120
160
7.6
4.3E­
03­
8.5E­
03
(
2)
Cylinder
Area
Loader
Helper
130
62
78
3.8
8.5E­
03­
1.7E­
02
(
3)
Checker
130
61
76
27
5.0E­
03­
9.9E­
03
(
4)
Drip
Pad
Labor
310
140
180
19
2.7E­
03­
5.4E­
03
(
5)
Load­
out
Area
Loader
Operator
1200
570
710
19
1.3E­
03­
2.6E­
03
(
6)
Load­
out
Area
Loader
Helper
3300
1600
1900
65
4.2E­
04­
8.4E­
04
(
7)
Load­
out
Area
Forklift
Operator
400
190
230
10
3.0E­
03­
6.0E­
03
(
8)
Oil
Unloader
93
43
54
6.5
8.5E­
03­
1.7E­
02
(
9)
Test
Borer
220
100
130
7.6
4.7E­
03­
9.4E­
03
(
10)
Water
Treatment
System
Operator
770
360
450
11
2.2E­
03­
4.4E­
03
(
11)
Railroad
Worker
No
Data
No
Data
No
Data
No
Data
No
Data
(
12)
Pole
Installer
No
Data
No
Data
No
Data
No
Data
No
Data
a
Exposure
scenarios
based
on
review
of
available
labels
and
LUIS
report.

b
Short­
term
Dermal
MOE=
Short­
term
NOAEL
(
50
mg/
kg/
day)
/
Short­
term
Dose
(
see
Table
6).

c
Intermediate­
term
Dermal
MOE=
Intermediate­
term
NOAEL
(
40
mg/
kg/
day)
/
Intermediate­
term
Dose
(
see
Table
6).

d
Long­
term
Dermal
MOE=
Long­
term
LOAEL
(
25
mg/
kg/
day)/
Long­
term
Dose
(
see
Table
6).

e
Inhalation
MOE=
Inhalation
NOAEL
(
1.2
mg/
kg/
day)/
Chronic
Dose
(
see
Table
6).

f
Cancer
risk
=
combined
LADD
(
see
Table
6)
*
cancer
slope
factor
(
7.3
mg/
kg/
day)­
1
x
(
0.5%
or
1.0%
Benzo[
a]
Pyrene).
33
Dermal
Exposure
Studies:
The
Creosote
Council
II
exposure
study
data
that
were
used
for
handler
exposure
were
also
used
for
post­
application
dermal
exposure
(
Creosote
Council
II,
2001).
No
other
data
for
dermal
post­
application
exposure
were
identified
in
the
available
literature.
The
difference
between
the
reported
data
for
the
handler
and
the
post­
application
assessment
was
that
the
exposure
data
for
the
treatment
operator
and
treatment
assistant
were
used
as
representative
of
handler
exposures,
and
the
exposure
data
for
cylinder
area
loader,
cylinder
area
loader
helper,
checker,
drip
pad
loader,
load­
out
area
loader,
load­
out
area
loader
helper,
load­
out
area
forklift
operator,

oil
unloaders,
test
borers,
water
treatment
system
operator,
railroad
worker
and
pole
installer
were
assumed
to
be
representative
of
dermal
post­
application
exposure
to
creosote
at
a
pressure
treatment
facility.
The
individuals
are
representative
of
postapplication
exposures
because
they
were
exposed
to
pressure
treated
wood
following
treatment
with
creosote.
The
methods
and
deficiencies
of
the
dermal
exposure
study
as
well
as
a
brief
description
of
the
pressure
treatment
process
were
fully
described
in
Section
4.2.
a.
A
description
of
the
scenarios
are
listed
below:

1)
Loader
operators
(
CLOs
in
the
cylinder
area,
and
LLOs
in
the
load­
out
areas)
­
LOs
stacked
untreated
wood
onto
charge
trams,
moved
charges
into
and
out
of
treatment
cylinders,
distributed
treated
wood
to
load­
out
area,
and
loaded
treated
wood
for
shipment.

2)
Cylinder­
area
helpers
(
CHs
in
the
cylinder
area,
and
LHs
in
the
loadout
areas)
­
CHs/
LHs
aided
the
LOs
by
opening/
closing
cylinder
door,

cleaning
door
debris
and
performing
door
maintenance,
handling
charge
leads
and
cables,
and
banding
stacked
wood.

3)
Checker
(
CK)
­
CKs
performed
many
of
the
duties
of
a
CH.

4)
Load­
out
area
helpers
(
LHs)
­
LHs
aided
their
LOs
by
banding
treated
wood
and
removing
culls.

5)
Test
borers
(
TBs)
­
TBs
took
cores
from
freshly
treated
poles
or
ties
to
be
tested
for
creosote
content
and
penetration
depth.
34
Daily
Dermal
Dose
mg
ai
Kg/
Day

Daily
Dermal
Exposure
mg
ai
day
x
1
Body
Weight
(
Kg)
x
ABS
(%)
6)
Oil
unloaders
(
OUs)
­
OUs
operated
the
equipment
that
transferred
creosote
from
rail
tank
cars
to
treating
system
tanks.

7)
Drip
pad
laborer
(
DP)
­
DPs
steam­
cleaned
drip
pads
and
tracks.
They
also
picked
up
and
disposed
of
treated
wood
waste
and
performed
various
labor
clean­
up
duties
in
treatment
areas.

8)
Water
treatment
system
operators
(
WOs)
­
WOs
controlled
equipment
that
collected
drip­
pad
effluent
water,
and
removed
creosote
and
other
contaminants.

9)
Railroad
worker­
This
individual
is
assumed
to
become
exposed
during
the
mechanical
and
manual
installation
of
pressure
treated
railroad
crossties
as
well
as
during
inspection
procedures
(
ATSDR,
1990).
No
dermal
exposure
data
were
available
for
this
scenario.

10)
Pole
installers­
This
individual
was
expected
to
become
exposed
while
attaching
fittings
on
telephone
poles,
installing
new
telephone
poles,

conducting
groundline
treatment
of
telephone
poles,
and
maintaining
and
repairing
existing
telephone
poles
(
ATSDR,
1990).
No
dermal
exposure
data
were
available
for
this
scenario.

Chemical­
specific
data
were
available
for
all
scenarios
except
for
the
Railroad
worker
and
Pole
installer
scenarios.
The
dermal
dose
was
calculated
as
follows:

Daily
Dermal
Exposure
=
Exposure
Study
data
(
ug/
kg/
day)
x
Study
Body
Weight
(
71.8
kg).
35
Daily
Inh.
Creosote
Dose
mg
ai
kg/
day

Daily
Inhalation
Creosote
Exposure
mg
day
x
1
Body
Weight
(
kg)
The
column
entitled
Exposure
Study
Data
in
Table
6
presents
the
dermal
doses
calculated
by
the
Creosote
Council
II,
1998
in
an
exposure
assessment
entitled
"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
With
Pressure­
Treatment
of
Wood
with
Creosote".
Because
EPA
traditionally
uses
an
adult
body
weight
of
70
kg
and
female
body
weight
of
60
kg
in
its
exposure
assessments
which
is
slightly
different
then
the
71.8
kg
body
weight
used
in
the
Creosote
Council
II
exposure
assessment,
the
doses
used
in
this
assessment
had
to
be
normalized
back
to
daily
dermal
exposures.
The
normalization
was
performed
by
multiplying
the
exposure
dose
times
the
71.8
kg
body
weight
Body
Weight
(
kg)
=
60
kg
for
short­
term,
70
kg
for
intermediate­
term
and
chronic
ABS
=
50
percent
absorption
for
short­
term
and
chronic;
100
percent
absorption
for
intermediate­
term
The
calculations
of
the
daily
dermal
dose
of
creosote
received
by
handlers
were
used
to
calculate
the
short­
term,
intermediate­
term,
and
chronic
MOEs.

Inhalation
Exposure
Studies:
The
scenarios
for
inhalation
post­
application
exposure
are
identical
to
that
of
the
dermal
data.
The
data
from
the
Creosote
Council
II
were
used
for
this
assessment
and
used
to
estimate
inhalation
doses.

Creosote
inhalation
dose
was
calculated
from
an
air
concentration
as
follows:

Daily
exposure
inhalation
creosote
=
mg/
day
Body
Weight
(
kg)
=
70
kg
for
short­
and
intermediate­
term
and
chronic
exposure
The
daily
inhalation
MOE
was
calculated
using
a
NOAEL
of
1.2
mg/
kg/
day.
36
Summary
of
Other
Exposure
Studies:
Additional
creosote
exposure
studies
in
the
literature
are
summarized
below
and
in
Table
8.
Todd
and
Timbie
(
NIOSH;
1980)

estimated
occupational
exposures
of
workers
to
creosote
in
a
railroad
tie
treatment
plant
in
Sommervile,
Texas.
Petroleum
oil/
creosote
solutions
of
70/
30
and
50/
50
were
used
respectively
to
treat
the
cross
ties
and
bridge
timbers
in
the
plant.
The
concentrations
of
creosote
(
i.
e.,
coal­
tar
pitch
volatiles;
CTPV)
in
personal
air
samples
over
a
two­
day
monitoring
period
ranged
from
0.002
to
1.211
mg/
m3.
37
Table
8.
Summary
of
Occupational
Inhalation
Exposure
Studies
of
Creosote
Study
Setting/
Subjects
Components
Reported
(
Analyzed)
Concentration
NIOSH;
1980
(
Todd
&
Timbie)
railroad
tie
treatment
plant
coal­
tar
pitch
volatiles
(
CTPV)
0.002­
1.211
mg/
m3
NIOSH;
1981a
(
Todd
&
Timbie)
wood
treatment
facility
CTPV
0.0004­
0.112
mg/
m3
NIOSH;
1981b
(
Baker
&
Fannick)
dock
builder
CTPV
(
cyclohexane
extractables)
0­
0.059
mg/
m3
Markel
et
al.

(
1977)
and
SRI
(
1993)
wood
treatment
facility
polycyclic
organic
materials
(
PPOM)
<
0.1
mg/
m3
Hiekkila
et
al.

(
1987)
creosote
impregnation
plant;
average
total
vapor
(
naphthalene
being
the
major
component)
0.5­
71
mg/
m3
Hiekkila
et
al.

(
1987)
handling
impregnated
wood
average
total
vapor
(
naphthalene
being
the
major
component)
0.1­
11mg/
m3
Flickenger
and
Lawrence,
1982
wood
pressure
treatment
plants
total
vapor
(
naphthalene
being
the
major
component)
0.92­
6.5
mg/
m3
Another
NIOSH
study
of
occupational
exposure
to
creosote
at
a
wood­
treatment
facility
in
Tacoma,
Washington
reported
CTPV
concentrations
in
personal
air
samples
ranging
from
less
than
0.0004
to
0.112
mg/
m3
with
the
highest
concentration
found
at
the
end
of
the
treatment
process
when
the
cylinder
was
opened
(
NIOSH;
1981a).
NIOSH
also
reported
creosote
exposures
of
dock
builders
ranging
from
zero
to
0.059
mg/
m3
based
on
cyclohexane
extractable
fraction
of
CTPV
(
NIOSH;
1981b).

Studies
conducted
by
Markel
et
al.
(
1977)
and
SRI
(
1993)
indicated
that
particulate
polycyclic
organic
materials
(
PPOM)
was
within
0.1
mg/
m3,
the
NIOSH
permissible
level
for
CTPV,
when
estimating
occupational
exposure
to
creosote
in
wood
38
treatment
plants.
The
concentrations
of
naphthalene,
methylnaphthalene,
and
acenaphthene
(
the
only
components
in
the
vapor­
phase
fractions
that
could
be
reliably
measured)
ranged
from
0.54
to
2.0
mg/
m3.
Benzene­
soluble
particulates
(
PPOM)
ranged
from
0.02
to
0.10
mg/
m3.

Hiekkila
et
al.
(
1987)
conducted
an
occupational
study
in
Finland
estimating
workers'
exposure
to
creosote
in
the
creosote
impregnation
plants
and
when
they
were
handling
the
impregnated
wood.
The
average
vapor
concentrations
(
naphthalene
being
the
major
component)
ranged
from
0.5
to
71
mg/
m3
in
the
impregnation
plants;
while
the
vapor
concentrations
ranged
from
0.1
to
11
mg/
m3
in
the
handling
of
impregnated
wood.

Most
of
the
airborne
contaminants
in
workers'
breathing
zones
were
in
the
vapor
phase;

the
proportion
of
particulate
polycyclic
aromatic
hydrocarbons
(
PAHs)
to
total
concentration
of
vapors
was
less
than
0.5
to
3.7
percent.

A
German
study
by
Rotard
and
Mailahn
(
1987)
reported
high
levels
of
carcinogenic
PAHs,
such
as
benzo[
a]
pyrene,
benzo[
b]­
fluoranthene,
and
benzo[
j]
fluoranthene,
and
cocarcinogenic
PAHs
in
samples
of
wooden
sleepers
(
railroad
cross
ties)
installed
in
playgrounds.

A
study
entitled
"
Occupational
Health
Experience
in
the
Wood
Preserving
Industry"
MRID
447595­
02
was
submitted
to
the
U.
S.
Environmental
Protection
Agency
(
EPA)
by
industry
for
review
as
a
possible
source
of
handler
and
post­
application
inhalation
information
for
the
Creosote
Reregistration
Eligibility
Decision
Document
(
RED)
exposure
chapter
(
Flickinger
and
Lawrence,
1982).
This
study
assessed
the
daily
inhalation
exposure
of
workers
involved
in
the
wood
pressure
treatment
industry.
The
requirements
for
inhalation
exposure
are
normally
specified
by
the
U.
S.
Environmental
Protection
Agency
under
Series
875.1300
Group
A
Occupational
and
Residential
Exposure
Test
Guidelines
and
Series
875.2500
Group
B
­
Post
Application
Exposure
Monitoring
Test
Guidelines.
The
EPA
reviewed
this
study
and
concluded
that
the
study
does
not
meet
the
minimum
Series
875
guidelines
and
has
several
issues
of
technical
merit.

The
major
issues
of
technical
merit
are
listed
below:


A
thorough
description
of
the
inhalation
sampling
equipment
(
e.
g.,
type
of
personal
sampling
pumps
and
attached
collection
devices),
sampling
technique
39
(
e.
g,
duration
of
time
the
samples
were
collected),
equipment
calibration,
air
flows,
EPA
sampling
method
numbers
were
not
provided.


The
detectable
concentrations
have
a
wide
range
of
variability.


The
study
appeared
to
be
too
old
(
e.
g.,
the
study
was
written
in
1982
and
the
sampling
analysis
results
were
performed
in
1977
)
to
represent
current
conditions
at
a
creosote
pressure
treatment
facility
and
does
not
begin
to
address
all
of
the
issues
presented
in
the
Series
875
guidelines.


The
study
does
not
assess
dermal
exposure.


The
study
does
not
specify
whether
the
creosote
was
a
P2
or
P1/
P13
formulation.


Background
creosote
air
concentrations
were
not
provided.


Limits
of
detection
and
quantification
limits
were
not
clearly
identified.


Personal
protection
methods
and
engineering
controls
were
apparently
used,

but
not
described.

The
following
is
a
brief
description
of
the
Series
875
compliance
issues:


Series
875
requires
tests
on
laboratory
recovery,
field
recovery,
or
method
recovery
to
evaluate
the
overall
quality
of
the
analysis.
A
study
must
have
a
recovery
percent
of
between
70­
120%
with
a
standard
deviation
of
one
to
be
acceptable.
Since
the
study
does
not
discuss
recovery,
it
is
impossible
to
determine
extraction
and
analysis
efficiency.
If
the
recovery
is
not
acceptable,

the
data
must
be
corrected
to
determine
the
actual
concentrations.


The
study
does
not
discuss
storage
stability
issues.
Storage
stability
issues
discuss
how
long
between
collection
and
analysis
and
possible
degradation
of
the
compound
in
question.
40

Series
875
requires
that
the
study
identify
the"
typical
end
use
product
of
the
active
ingredient
used."
The
study
identifies
the
end
use
product
as
Koppers
70/
30
creosote/
coal
tar
solution;
however,
the
study
does
not
reference
a
label,

provide
an
analysis
of
the
batch,
or
identify
typical
uses.


It
was
not
clear
how
many
sites
were
evaluated.
Series
875
guidelines
recommend
that
at
least
three
representative
sites
should
be
selected.


Series
875
guidelines
require
that
"
for
exposure
monitoring
at
least
five
replicates
(
e.
g.,
individuals)
at
each
of
three
monitoring
periods
be
assessed
(
e.
g.,
`
n'
days
after
application)."
The
replicates
of
the
workers
were
not
reported
and
all
workers
were
monitored
on
just
one
day.


Series
875
guidelines
recommend
that
"
monitoring
period
is
sufficient
to
collect
measurable
residues,
but
not
excessive
so
that
residue
loss
occurs."

Sampling
duration
was
not
discussed.


Series
875
guidelines
requires
that
"
inhalation
exposures
be
monitored
by
validated
methodologies".
Methods
were
briefly
discussed,
but
no
specified
method
numbers
were
referenced.


Series
875
guidelines
requires
that
"
quantity
of
active
ingredient
handled
and
duration
of
monitoring
period
should
be
reported
for
each
replication."
This
was
not
reported.


Series
875
guidelines
require
that
quantitation
of
level
of
detection
be
reported.


Series
875
guidelines
require
that
"
at
least
one
field
fortification
sample
per
worker
per
monitoring
period
per
fortification
level
for
each
matrix.
At
least
one
field
blank
per
worker
per
monitoring
period
for
each
matrix."
No
field
blanks
or
fortification
samples
were
reported.

This
study
was
rejected
in
favor
of
the
more
recent
Creosote
Council
II
study
(
Creosote
Council
II,
2001).
The
major
reasons
include:
(
1)
the
study
would
better
represent
more
current
conditions
at
wood
preservative
plant;
(
2)
the
study
included
an
41
analysis
of
field,
lab
and
method
recoveries;
(
3)
the
pilot
study
also
assessed
dermal
exposure;
(
4)
the
study
addressed
important
Series
875
issues
such
as
number
of
replicates,
sampling
methodologies,
fortifications,
and
levels
of
detection
and
quantitation;

and
(
5)
the
Creosote
Council
II
study
is
more
recent.

Post­
application
Cancer
Risk
Calculations:
Post­
application
cancer
risks
were
calculated
in
the
same
manner
as
for
handlers.
The
exposure
durations
and
lifetime
values
used
were
the
same
as
for
handlers.
Exposure
frequency
was
assumed
to
be
250
days/
year
(
i.
e.,
standard
annual
working
frequency)
for
all
scenarios.

Estimated
cancer
risks
from
dermal
and
inhalation
post­
application
exposures
are
presented
in
Table
8.

4.3.2
Occupational
Post­
application
Risk
Assessment
and
Characterization
The
calculations
of
short­
term
dermal
non­
cancer
risks
indicate
that
dermal
MOEs
are
more
than
100
(
i.
e.,
not
of
concern)
for
the
following
scenarios:

Note:
Scenario
8,
oil
unloader,
the
MOE
is
93.
42
The
calculations
of
intermediate­
term
risks
indicate
that
dermal
MOEs
are
more
than
100
(
i.
e.,
not
of
concern)
for
the
following
scenarios:

The
calculations
of
long­
term
risks
indicate
that
dermal
MOEs
are
more
than
300
(
not
of
concern)
for
the
following
scenarios:

The
calculations
of
short­,
intermediate­,
and
long­
term
inhalation
non­
cancer
risks
indicate
that
inhalation
MOEs
are
more
than
100
for
the
following
scenarios:

For
dermal
and
inhibitor
cancer
risks
all
of
the
post­
application
scenarios
(
except
for
scenarios
11
and
12
­
see
below)
exceed
the
1E­
04
risk
levels.
All
of
these
scenarios
are
expected
to
pose
a
risk
concern.

Data
gaps
exist
for
the
following
scenarios:

°
(
11)
Railroad
workers
°
(
12)
Pole
installers
43
The
Agency
also
has
is
concerns
that
there
are
potential
exposure
concerns
relating
to
post­
application
exposure
to
individuals
following
the
use
of
creosote­
treated
wood
in
residential
settings.
The
potential
residential
post­
application
exposure
pathways
are
outlined
below:

(
1)
homeowner
incidental
ingestion
and
dermal
contact
with
soil
contaminated
with
creosote
(
e.
g.,
soil
contaminated
by
creosote
treated
telephone
poles)

(
child)

(
2)
outdoor
homeowner
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
railroad
ties
used
in
home
settings,
posts)
(
adult)

(
3)
outdoor
homeowner
hand­
to­
mouth
and
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
railroad
ties
used
in
home
settings,

posts)
(
child)

No
chemical­
specific
data
for
residential
post­
application
exposure
was
submitted.

Therefore,
exposure
doses
could
not
be
calculated.
Data
were
not
adequate
for
use
in
the
exposure
assessment.

4.4
Uncertainties
and
Limitations
4.4.1
Data
Gaps
At
this
time,
information
from
creosote
labels,
from
EPA's
LUIS
database,
and
from
industry
sources
has
been
used
to
identify
probable
use
scenarios
for
creosote.
These
may
have
to
be
adjusted
if
more
specific
use
information
is
received
from
industry
sources.

Dermal
and
inhalation
data
gaps
exist
for
the
following
post­
application
exposure
scenarios:


Railroad
Worker,
and

Pole
Installer.

Data
are
not
adequate
to
characterize
residential
post­
application
exposure.
44
4.4.2
Creosote
Council
II
2001
Worker
Exposure
Study
This
section
summarizes
key
compliance
concerns
with
using
the
Creosote
Council
II
worker
exposure
study
(
Creosote
Council
II,
2001)
which
replaces
the
data
from
the
pilot
study
(
Creosote
Council
II,
1998).
The
Agency
used
a
worker
exposure
study
submitted
from
the
Creosote
Council
II
to
provide
chemical
specific
handler
and
exposure
data
post­
application
in
support
of
re­
registration
of
creosote
(
Creosote
Council
II,
2001).
The
Creosote
Council
II
study
was
judged
to
be
of
better
quality
than
the
other
currently
existing
exposure
studies
available
at
this
time
(
NIOSH,
1980;
NIOSH
1981a;

NIOSH
1981b;
Markel
et
al.,
1977;
SRI,
1993;
Heikkila
et
al.,
1987;
and
Flickenger
and
Lawrence,
1982).
Compliance
concerns
for
the
Creosote
Council
(
2001)
study
are
the
following:

°
It
should
be
noted
that
the
Creosote
Council
II
(
2001)
exposure
study
data
were
used
for
dermal
and
inhalation
handler
exposure
and
also
for
postapplication
dermal
and
inhalation
exposure.
The
difference
between
the
reported
data
for
the
handler
and
the
post­
application
assessment
was
that
the
exposure
data
for
the
treatment
operator
and
treatment
assistant
were
used
as
representative
of
handler
exposures,
and
the
exposure
data
for
cylinder
area
loader,
cylinder
area
loader
helper,
checker,
load­
out
area
loader,
load­
out
area
loader
helper,
load­
out
area
forklift
operator,
oil
unloader,
test
borer,
water
treatment
system
operator,
railroad
worker,
and
pole
installer
were
assumed
to
be
representative
of
post­
application
exposure
to
creosote
at
a
pressure
treatment
facility.
These
individuals
are
representative
of
post­
application
exposures
because
they
were
exposed
to
pressure
treated
wood
following
treatment
with
creosote.

°
The
amount
of
product
applied
and
the
amount
of
active
ingredient
handled
by
each
worker
was
not
calculated
because
the
creosote
was
applied
in
a
closed
system
which
recovered
and
retained
excess
treatment
solution
from
the
wood
and
treatment
vessel
while
sealed.

°
The
number
of
field
fortification
samples
collected
at
the
sites
were
less
than
the
required
number
to
satisfy
Series
875
guidelines.
According
to
the
guidelines,
there
should
be
at
least
one
fortification
sample
per
worker
per
monitoring
period
(
8
hour
shift)
per
fortification
level
(
three
levels)
for
each
45
matrix
and
at
least
one
field
blank
per
worker
per
monitoring
period
for
each
matrix.
There
were
more
workers
monitored
than
there
were
field
fortifications
and
field
blank
samples
collected.

°
The
overall
inhalation
field
fortification
percent
recoveries
for
the
coal
tar
pitch
volatiles
(
CTPVS)
were
poor.
The
overall
recovery
for
Site
B
was
57%.
The
overall
recoveries
for
Sites
C
and
D
were
51%
and
57%,

respectively.
All
inhalation
fortification
recoveries
below
70%
should
be
considered
unacceptable
according
to
Series
875
guidelines
and
therefore
undermines
the
validity
of
the
results.

°
There
were
some
dermal
fortification
levels
with
extremely
high
recoveries
for
WBD's
and
some
with
unacceptable
low
recoveries
for
gloves.
As
an
example,
for
a
60
µ
g/
sample
"
total
creosote"
fortification
for
Site
B,
the
recoveries
for
the
WBD's
were
as
high
as
150%
and
recoveries
for
the
gloves
as
low
as
52.3%.
There
were
measurable
amounts
of
total
creosote
found
in
each
of
the
control
samples
prepared
at
each
facility.
All
dermal
fortification
recoveries
above
120%
and
below
70%
are
outside
of
the
range
recommended
in
Series
875
guidelines
and
undermine
the
validity
of
the
results.

°
The
study
sponsors
made
no
attempt
to
relate
inhalation
levels
found
for
PNAs
and
CTPVs
to
"
total
creosote"
­­
a
significant
weakness
with
the
study.

°
PMRA
has
indicated
that
there
are
calculation
mistakes
with
inhalation
data
in
the
study.

°
There
were
inconsistencies
in
raw
data
and
examples
provided
by
the
study
authors:
e.
g.,
inhalation
raw
data
did
not
reflect
data
found
in
bar
graphs.
46
4.4.3
Residential
Exposure
Scenarios
No
chemical­
specific
data
for
residential
post­
application
exposure
were
submitted
and
exposures
were
not
calculated.
No
chemical­
specific
data
for
residential
exposure
were
identified
in
the
available
literature.

4.4.4
Toxicity
Information
Cancer
information
was
not
initially
presented
in
the
initial
draft
of
the
Hazard
Identification
report
(
USEPA,
1999).
Toxicity
experts
at
the
EPA
recommended
using
the
BAP
cancer
slope
factor
of
7.3
(
mg/
kg/
day)­
1
as
an
indicator
of
worker
risk
concerns
for
creosote.
This
recommendation
was
based
on
the
Agency's
decision
to
use
benzo(
a)
pyrene,
a
component
of
creosote,
as
a
surrogate
for
identifying
potential
worker
cancer
risk
concerns
for
creosote.
Also,
it
is
noted
that
creosote
is
classified
as
a
B1
carcinogen,
whereas
benzo(
a)
pyrene
is
classified
as
a
B2
carcinogen.

As
indicated
above,
the
Agency
uses
the
risk
assessment
for
benzo(
a)
pyrene
as
an
indicator
of
worker
risks
for
creosote.
Considering
this,
the
Agency
adjusted
calculated
creosote
handler
and
post­
application
cancer
risk
calculations
by
factors
of
0.005
and
0.01.
This
was
done
because:
(
a)
benzo(
a)
pyrene
is
a
component
found
in
creosote
formulations;
and
(
b)
available
information
indicates
that
benzo(
a)
pyrene
occurs
as
a
component
in
creosote
at
levels
of
0.5%.
(
However,
in
order
to
provide
a
conservative
assessment
the
Agency
assumed
that
levels
of
benzo(
a)
pyrene
may
occur
from
0.5%
to
1%
of
total
creosote
formulations.)

It
should
also
be
noted
that
although
these
corrections
to
cancer
risk
estimates
were
made,
data
from
the
Creosote
Council
II's
2001
worker
exposure
study
were
not
provided
on
the
actual
amount
of
benzo(
a)
pyrene
found
as
dermal
residues.
Further,
in
this
study
all
inhalation
samples
of
benzo(
a)
pyrene
were
found
to
be
at
levels
below
the
Level
of
Detection
(
LOD).
These
factors,
therefore,
increase
the
uncertainty
of
the
cancer
risk
assessment.
47
4.5
Results
and
Conclusions
The
results
of
the
handler
exposure
and
risk
assessment
indicate
that
the
risk
drivers
are
the
long­
term
dermal
MOEs,
inhalation
MOEs,
and
the
cancer
assessment
with
the
cancer
risks
of
most
concern.
Cancer
risks
for
all
handler
scenarios
exceed
the
level
of
concern
(
1E­
04)
for
occupational
handlers.
Table
9
summarizes
each
exposure
pathway
in
the
RED;
the
overall
results
of
the
MOE
and
cancer
risk
evaluations;
and
identification
of
any
additional
data
that
would
prove
useful
in
reducing
the
uncertainties
of
the
MOE
and
cancer
risk.

Table
9.
Summary
of
the
Occupational/
Nonoccupational
Exposure
Scenarios
Data
Exposure
Scenario
Source
of
Data
Occupational
Handler
(
1a)
Mixing/
Loading/
Applying
Liquids
at
a
Pressure
Treatment
Facility
(
treatment
operator)
Exposure
Study
Data
from
Creosote
Council
II
and
PHED,
1997used
as
a
surrogate
(
1b)
Mixing/
Loading/
Applying
at
a
Pressure
Treatment
Facility
(
treatment
assistant)
Exposure
Study
Data
from
Creosote
Council
II
Occupational
Postapplication
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
Exposure
Study
Data
from
Creosote
Council
II
No
data
No
data
Non­
Occupational
(
e.
g.,
Residential)

(
1)
homeowner
incidental
ingestion
and
dermal
contact
with
soil
contaminated
with
creosote
(
e.
g.,
soil
contaminated
by
creosote
treated
telephone
poles)
(
child)
No
data
(
2)
outdoor
homeowner
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
posts,
shingles,
fencing,
lumber,
piers,
etc.)
(
adult)
No
data
(
3)
outdoor
homeowner
hand­
to­
mouth
and
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
posts,
shingles,
fencing,
lumber,
piers,
etc.)
(
child)
No
data
48
In
summary,
the
handler
and
post
application
MOEs
and
cancer
risk
are
presented
below:

Occupational
Handler
°

°
Scenario
1b
exceeds
only
inhalation
MOEs
and
cancer
risk
criteria.

Occupational
Postapplication
.

°
Scenario
4
°
Scenario
5
.

°
Scenario
6
exceeds
the
inhalation
MOE
and
cancer
risk
criteria.

°
Scenario
7
°
Scenario
8
exceeds
all
MOE
and
cancer
risk
criteria.

°
Scenario
9
°
Scenario
10
exceeds
the
inhalation
MOE
and
cancer
risk
criteria.

°
Scenario
11
There
are
no
data
for
railroad
worker
exposure.

°
Scenario
12
There
are
no
data
for
utility
pole
installers.
49
Non­
occupational
Post­
application
No
data
were
submitted
to
characterize
the
residential
scenarios.
Site
specific
exposure
data
would
be
helpful
to
rectify
the
lack
of
data
for
the
following
occupational
postapplication
scenarios.

°
incidental
ingestion
and
dermal
contact
with
soil
contaminated
with
creosote
(
e.
g.,

soil
contaminated
by
creosote
treated
telephone
poles)
(
child)

°
hand­
to­
mouth
and
dermal
contact
with
pressure
treated
wood
products
(
e.
g.,

utility
poles,
posts,
shingles,
fencing,
lumber,
piers,
etc.)
(
adult)
50
4.6
References
Agency
for
Toxic
Substances
and
Disease
Registry
(
ATSDR,
1990).
Toxicological
Profile
for
Creosote.
U.
S.
Public
Health
Service.
February
16,
1990.

Agency
for
Toxic
Substances
and
Disease
Registry
(
ATSDR,
1995).
Toxicological
Profile
for
Creosote.
U.
S.
Public
Health
Service.

Butala
J.
H.
February,
1999.
Creosote
Council
II
memorandum
with
attachment
to
Nader
Elkassabany,
U.
S.
Environmental
Protection
Agency,
Antimicrobial
Division.

Creosote
Council
II,
1998.
"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
with
Pressure­
Treatment
of
Wood
with
Creosote."

Submitted
by
John
H.
Buttala,
Creosote
Council
II.
Field
work
by
George
M.

Singer,
Ph.
D,
American
Agricultural
Services
Inc.
Analytical
work
by
David
A.

Winkler,
EN­
CAS
Laboratories.

Creosote
Council
II,
2001.
"
Assessment
of
Potential
Creosote
Inhalation
and
Dermal
Exposure
Associated
with
Pressure
Treatment
of
Wood
with
Creosote."

Submitted
by
John
H.
Butala,
Creosote
Council
II.
Field
work
by
Mark
G.

Bookbinder,
Ph.
D,
c/
o
American
Agricultural
Services
Inc.
Analytical
work
by
Bert
Clayton,
EN­
CAS
Laboratories
and
Stephanie
Guilyard,
USX
Engineers
and
Consultants.
MRID
453234­
01.

Flickinger
and
Lawrence,
1982.
Occupational
Health
Experience
in
the
Wood
Preserving
Industry.
Koppers
Company,
Inc.
MRID
447595­
02.

Heikkila
PR,
Hameila
M,
Pyy
L,
et
al.
1987.
Exposure
to
Creosote
in
the
Impregnation
and
Handling
of
Impregnated
Wood.
Scand
J
Work
Environ
Health
13:
431­
437.
51
Krygsman,
Adrian
1994.
"
Wood
Preservation.
An
Overview
of
Biocide
Use
and
Application."
NIOSH
(
1980a).
Industrial
Hygiene
Report,
Comprehensive
Survey
of
Wood
Preservative
Treatment
Facility
at
Santa
Fe
Centralized
Tie
Plant,

Somerville,
Texas.
National
Institute
for
Occupational
Safety
and
Health,
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