Document ID: EPA-HQ-OPP-2003-0248-0010
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-11-26T05:00Z

1
CREOSOTE
HUMAN
RISK
CHARACTERIZATION
Background
Creosote
is
a
fungicide,
insecticide,
and
sporicide
used
as
a
wood
preservative
for
above
and
below
ground
wood
protection
treatments
as
well
as
for
treating
wood
in
marine
environments.
All
16
Creosote
products
currently
registered
are
Restricted
Use
Pesticides;
15
are
End­
Use
Products
and
1
is
a
Manufacturing­
Use
Product
for
formulating
industrial
end­
use
wood
preservative
products.
Creosote
wood
preservatives
are
used
primarily
to
pressure
treat
railroad
ties/
crossties
(
represents
close
to
70%
of
all
Creosote
use)
and
utility
poles/
crossarms
(
represents
15
­
20%
of
all
Creosote
use).
Assorted
Creosote­
treated
lumber
products
(
e.
g.,
timbers,
poles,
posts
and
groundline­
support
structures)
represent
the
remaining
uses
for
this
wood
preservative.
The
industry
refers
to
different
blends
of
creosote,
based
on
the
wood
treatment
standards
set
by
the
American
Wood­
Preservers'
Association
(
AWPA),
as
P1/
P13
and
P2.
Typically,
railroad
ties/
crossties
are
treated
with
a
P2
blend,
which
is
more
viscous
than
the
P1/
P13
blend
used
for
treating
utility
poles.

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.
On
September
29,
2003,
in
accordance
with
section
6(
f)(
1)
of
FIFRA,
as
amended,
EPA
issued
a
Notice
of
Receipt
of
Requests
by
Registrants
of
Pesticide
Products
containing
Creosote
to
voluntarily
cancel
non­
pressurized
and/
or
to
amend
to
terminate
non­
pressurized
use
of
affected
products.

The
Antimicrobials
Division
(
AD),
Office
of
Pesticide
Programs
(
OPP),
U.
S.
EPA,
has
evaluated
the
toxicological
database
for
P1/
P13
and
P2
creosote
and
determined
that
the
data
are
adequate
to
support
a
reregistration
eligibility
decision.

Hazard
Profile
The
Toxicology
database
for
Creosote
is
adequate
to
assess
the
hazard
profile
of
creosote
for
use
in
a
Preliminary
Risk
Assessment
(
PRA).
Review
of
the
database
shows
concern
for
the
mutagenicity
and
carcinogenicity
of
creosote
as
well
as
cardiomyopathy
after
inhalation
exposure
and
dermal
inflammation
after
repeated
dermal
exposure.
Results
of
developmental
toxicity
testing
of
creosote
in
experimental
animal
species
shows
qualitative
evidence
of
susceptibility
from
creosote
,
thus
raising
concern
for
creosote
as
a
potential
developmental
toxicant.

Cardiotoxicity
was
observed
in
a
subchronic
inhalation
toxicity
study
in
rats
with
the
P1/
P13
blend
of
creosote
(
MRID
#
43601001).
Diffuse
myocardial
degeneration
affecting
the
right
side
of
the
heart
as
well
as
arterial
medial
hypertrophy
of
the
small
arterioles
of
the
lung
were
observed
after
13
weeks
of
exposure
to
0.049
mg/
L
creosote.
Exposure
to
the
P2
blend
of
creosote
by
inhalation
resulted
in
changes
to
the
olfactory
epithelium
(
inflammation,
hyperplasia,
metaplasia).
2
Follicular
cell
hypertrophy
of
the
thyroid
was
also
observed
as
well
as
increased
thyroid
weight.
Both
blends
produced
granular
pigment
deposition
within
the
lungs,
a
s
shown
by
the
presence
of
granular
pigment
within
the
alveolar
macrophages.
In
90­
day
dermal
toxicity
studies
with
both
blends
of
creosote,
these
effects
were
not
observed,
although
a
significant
dermal
response
(
inflammation)
was
observed
for
both
blends.

The
developmental
and
reproductive
toxicity
of
creosote
was
evaluated.
Developmental
toxicity
studies
in
the
rat
with
both
blends
showed
qualitative
evidence
of
susceptibility
to
offspring.
For
the
P1/
P13
blend,
significantly
increased
resorptions
and
post­
implantation
loss
as
well
as
decreased
live
fetuses
per
litter
were
observed
at
a
dose
of
175
mg/
kg/
day,
while
the
only
maternal
effect
at
this
dose
was
increased
incidence
of
hair
loss.
In
addition,
increased
incidence
of
cardiovascular,
vertebral,
and
digital
malformations
was
observed
which
exceeded
both
concurrent
and
historical
control
incidence.
For
the
P2
blend,
single
incidences
of
malformations
of
the
skull
and
eye
were
considered
treatment
related,
in
the
absence
of
maternal
toxicity.
A
developmental
toxicity
study
in
rabbits
with
P1/
P13
creosote
showed
increased
abortions,
decreased
number
of
live
litters,
and
decreased
mean
implantation
sites
at
a
dose
of
75
mg/
kg/
day
in
maternal
rabbits.
There
were
no
significant
effects
on
fetuses
from
treated
dams
at
any
dose
level.
A
2­
generation
reproduction
study
using
P1/
P13
Creosote
showed
decreased
pre­
mating
body
weights
in
F1
female
rats
and
F1
males
rats
at
a
dose
of
25
mg/
kg/
day,
the
lowest
dose
tested
in
this
study.
At
25
mg/
kg/
day
and
above
there
was
reduced
fertility
and
pregnancy
indices
in
the
F1
generation
in
comparison
to
controls,
but
the
control
fertility
index
was
also
lower
than
expected.
Thus
although
there
was
no
evidence
of
susceptibility
in
this
study,
the
low
fertility
and
pregnancy
indices
for
F1
female
parental
animals
introduced
uncertainty
in
the
interpretation
of
the
results
in
treated
animals.

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.

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
results
of
testing
of
both
the
P1/
P13
blend
and
P2
blend
of
creosote
showed
that,
at
doses
toxic
to
the
dosed
animals
(
330.5
mg/
kg
for
the
P1/
P13
blend,
and
194
mg/
kg
for
the
P2
blend),
there
was
no
evidence
of
a
dominant
lethal
effect
of
either
creosote
blend.

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
3
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.

A
large
body
of
experimental
evidence
exists
which
shows
a
positive
relationship
between
dermal
exposure
to
creosote
and
development
of
tumors
in
experimental
animals.
In
addition
to
its
tumor­
promoting
potential,
the
ability
of
creosote
to
induce
lung
tumors
after
dermal
application
was
examined.
Dermally
applied
creosote
(
0.25ml
undiluted,
twice
weekly
for
8
months)
induced
5.8
lung
adenomas
per
mouse
in
mice
housed
in
stainless
steel
cages,
while
untreated
controls
showed
0.5
lung
adenomas/
mouse
(
Roe
et
al,
Cancer
Res.
18:
1176­
1178,
1958).
Carcinogenicity
of
two
high­
temperature
derived
creosote
oils
was
studied
by
Poel
and
Kammer
(
JNCI
18:
41­
55,
1957).
The
light
creosote
fraction
is
composed
mainly
of
benzene,
toluene,
xylene,
and
solvent
naphtha,
while
the
blended
oil
is
composed
of
creosote
oil,
anthracene
oil,
and
oil
drained
from
recovery
of
naphthalene.
Oils
were
applied
by
drops
to
the
skin
of
mice
at
concentrations
of
20%,
50%,
or
80%
three
times
a
week
for
life.
By
weeks
21­
26,
both
oils
had
induced
skin
tumors.
Several
mice
exhibited
metastases
to
the
lungs
or
regional
lymph
nodes.
Coal
tar
carcinogenicity
was
studied
by
Culp
et
al.
(
1996)
in
which
female
B6C3F1
mice
(
48/
group)
were
administered
coal
tar
in
the
diet
at
concentrations
of
0,
0.01,
0.03,
0.1,
0.3,
0.6,
and
1%
for
2
years.
The
coal
tar
was
a
mixture
of
samples
from
seven
waste
sites.
Tumors
of
the
forestomach
were
observed
in
all
groups
fed
the
coal­
tar
containing
diet,
as
were
small
intestine
tumors
fed
the
0.6%
or
1.0%
concentrations
of
coal
tar.
In
a
second
study
by
Culp
et
al.
(
1998)
female
B6C3F1
mice
were
given
coal
tar
samples
in
the
diet,
derived
from
manufactured
gas
plant
waste
sites
at
0,
12,
33,
117,
333,
739,
and
1300
mg/
kg/
day
(
coal
tar
sample
1)
or
40,
120,
and
346
mg/
kg/
day
(
coal
tar
sample
2)
for
2
years.
Coal
tar
sample
1
was
a
mixture
of
samples
from
seven
waste
sites
and
coal
tar
sample
2
was
a
mixture
from
two
of
the
waste
sites
plus
a
third
waste
site
with
a
high
benzo(
a)
pyrene
content.
Significant
concentration­
related
increases
in
incidence
of
tumors
of
the
liver,
lung,
forestomach,
and
increased
incidence
of
hemangiosarcoma,
histiocytic
sarcoma,
and
sarcoma
were
observed
for
both
coal
tar
sample
1
and
2.
Tumors
of
the
small
intestine
were
also
observed
in
addition
in
those
mice
receiving
coal
tar
sample1,
similar
to
the
earlier
study.

In
humans,
evidence
for
carcinogenicity
of
creosote
varies.
Several
studies
have
associated
occupational
exposure
to
creosote
with
development
of
skin
cancer,
with
a
latency
period
of
20­
25
years.
These
studies
are
very
old
(
1920'
s
to
1940'
s),
when
occupational
safety
practices
were
much
more
lax
than
today.
More
recent
reports
(
1980)
show
no
increase
in
risk
of
skin,
bladder,
or
lung
cancer
in
wood
treatment
plant
workers,
or
after
treatment
for
4
years
with
coal­
tar
medicinal
therapy
for
treatment
of
dermatitis.
These
reports,
however,
were
limited
in
scope.
Those
reports
associated
with
therapeutic
use
of
coal
tar
did
not
mention
the
fact
that
the
composition
of
the
coal
tar
used
therapeutically
is
different
than
that
used
for
wood
treatment.
In
the
report
on
wood
treatment
workers,
the
population
studied
was
small,
and
the
follow­
up
4
period
was
too
short
to
allow
a
long
enough
latency
for
tumor
development.

The
carcinogenicity
data
base
submitted
to
the
Agency
for
creosote
consists
of
a
six­
month
initiation/
promotion
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
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
dose­
related
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
promotor.
This
study
shows
that
creosote
acts
most
effectively
as
a
promotor
but
also
functions
as
a
"
complete"
carcinogen.

The
Agency
in
1988
acknowledged
limitations
on
conducting
a
quantitative
risk
assessment
from
use
of
a
single
component
of
creosote
(
Guidance
for
the
Reregistration
of
Pesticide
Products
Containing
Coal
Tar/
Creosote
As
the
Active
Ingredient,
USEPA,
1988),
but
it
was
also
observed
that
creosote
mixtures
are
"
complex
mixtures
with
known
synergistic
effects"
on
carcinogenicity.
A
specific
quantitative
risk
assessment
on
carcinogenicity
of
creosote
has
not
been
performed
by
the
Agency,
but
a
cancer
slope
factor
(
q*)
exists
for
one
of
the
more
prominent
components
of
creosote,
benzo(
a)
pyrene,
with
a
q*
value
of
7.3
as
published
in
the
Agency's
IRIS
database.
The
Antimicrobials
Division
proposes
to
use
benzo(
a)
pyrene
as
an
indicator
for
conduct
of
the
cancer
risk
assessment
for
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
the
tumors
observed
from
administration
of
creosote.
Benzo(
a)
pyrene
has
also
been
shown
to
be
a
"
complete"
carcinogen
similar
to
creosote,
and
also
tests
positive
for
mutagenicity
in
a
variety
of
assays.
Cancer
risk
estimates
for
oral
exposure
to
polycyclic
aromatic
hydrocarbon
mixtures
as
well
as
inhalation
exposure
to
coal
tar/
pitch
condensation
aerosol
(
Schenider
et
al.,
J.
Appl.
Toxicol
22(
1),
2002;
Heinrich
et
al.,
Toxicol.
Lett.
72(
1­
3),
1994)
have
been
performed
using
benzo(
a)
pyrene
as
an
indicator.
The
use
of
benzo(
a)
pyrene
as
an
indicator
is
not
felt
to
be
overly
conservative
and
may
underestimate
carcinogenic
risk
of
creosote,
as
other
components
of
creosote
including
naphthalene,
1­
methylnaphthalene,
carbazole,
quinoline,
and
beno[
b]
fluoranthene
have
also
shown
carcinogenic
potential
in
animal
studies
(
Nesnow
et
al.,
Exp.
Lung
Res.
24(
4):
1998;
Murata
et
al.,
Fundam
Appl.
Toxicol.
21(
1):
1993
)
and
could
likely
contribute
additional
potency
over
that
of
benzo(
a)
pyrene
alone.
While
the
Agency
proposes
this
approach,
the
Agency
is
also
aware
of
the
recent
study
of
Culp
et
al.
(
1998)
that
examined
tumors
induced
by
coal
tar
as
well
as
the
recent
publications
by
Gaylor
et
al.
(
2000)
and
Schneider
et
al.
(
2002)
which
analyzed
these
data
for
purposes
of
quantitative
cancer
risk.
The
Agency
is
considering
these
publications
and
their
potential
modification
of
the
approach
proposed
above
for
quantification
of
creosote
carcinogenicity.
The
metabolism
of
Creosote
has
not
been
examined,
due
to
the
extremely
complex
nature
of
the
components
of
creosote.
Information
from
the
Agency
for
Toxic
Substances
and
Disease
5
Registry
indicates
that
some
of
the
components
of
creosote
are
persistent
within
the
body.

Dose­
Response
Assessment
On
April
1,
1999,
the
Health
Effects
Division's
Hazard
Identification
Assessment
Review
Committee
(
HIARC)
evaluated
the
toxicological
endpoints
selected
for
occupational
and
residential
(
dermal
and
inhalation)
exposure
risk
assessments
for
Creosote.
On
September
3,
2003,
the
Antimicrobials
Division
Toxicity
Endpoint
Selection
Committee
(
ADTC)
met
to
verify
the
selected
endpoints
for
long­
term
dermal
risk
assessments
for
creosote
and
inhalation
risk
assessment,
and
also
discussed
whether
dermal
and
inhalation
Margins
of
Exposure
should
becombined
for
creosote
risk
assessment.
The
toxicological
endpoints
selected
for
various
exposure
scenarios
are
summarized
in
the
table
below.
6
Table
1
Toxicology
Endpoint
Selection
for
Creosote
EXPOSURE
SCENARIO
DOSE
(
mg/
kg/
day)
ENDPOINT
STUDY
Acute
and
Chronic
Dietary
Acute
and
Chronic
Dietary
risk
assessment
not
required
Carcinogenicity
(
Dietary)
Creosote
has
been
shown
to
exert
positive
mutagenic
effects
in
vitro,
and
has
been
shown
to
be
positive
for
carcinogenicity
in
an
initiation/
promotion
study.
Creosote
has
been
classified
as
a
B1
carcinogen
in
IRIS.
Oral
cancer
slope
factor
for
benzo(
a)
pyrene,
a
component
of
creosote,
used
as
indicator
for
carcinogenic
potential
of
creosote:
7.3
(
mg/
kg/
day)­
1
+
50%
dermal
absorption.

Short­
Term
Dermal
(
1­
30
days)
Oral
NOAEL=
50
decreased
body
weight
gain
at
175
mg/
kg/
day
Developmental
Toxicity
­
Rat
MOE
=
100
(
50%
dermal
absorption)

Intermediate­
term
Dermal
(
1­
6
months)
Dermal
NOAEL
=
40
Decreased
body
weight
gain
at
400
mg/
kg/
day
90­
Day
Dermal
Toxicity
Study
in
the
Rat
MOE
=
100
Long­
Term
Dermala
(>
6
months)
Oral
LOAEL
=
25
mg/
kg/
day
decreased
pre­
mating
body
weight
2­
generation
reproduction
study
­
Rat
MOE
=
300
(
10x,
10x,
3x
for
use
of
a
LOAEL)

Inhalationb
(
any
time
period)
NOAEL
=
0.0047mg/
L
MOE
=
100
decreased
body
weight,
body
weight
gain,
altered
hematology
90­
day
Inhalation
Study
in
the
Rat
Dermal
absorption
c
50%,
estimated
from
ratio
of
oral/
dermal
LOAEL
aafter
re­
examination
of
the
toxicology
data,
the
ADTC
concluded
that
the
2­
generation
reproduction
toxicity
study
was
appropriate
for
long­
term
dermal
risk
assessment
for
the
following
reasons:
the
duration
of
the
2­
generation
reproduction
study
is
more
representative
of
the
time
frame
(
i.
e.
long­
term)
than
the
90­
day
dermal
study,
and
is
consistent
with
OPP
policy
regarding
duration
of
the
study
vs.
route
of
exposure;
body
weight
gain
decreases
in
the
2­
generation
reproduction
toxicity
study
were
observed
in
the
F2
generation,
supporting
the
time
frame
for
the
long­
term
endpoint
(
i.
e.
>
6
months).
The
90­
day
dermal
study
effects
are
not
as
representative
of
the
time
frame
for
the
long­
term
dermal
risk
assessment.
However,
the
two
studies
can
be
considered
co­
critical
studies
for
this
endpoint.
Correction
of
the
LOAEL
from
the
2­
generation
reproduction
toxicity
study
for
dermal
absorption
(
50%)
and
use
of
a
LOAEL
(
3x
extra
UF)
yields
a
MOE
and
endpoint
(
300
and
50
mg/
kg/
day)
similar
to
the
90­
day
dermal
toxicity
study
(
40
mg/
kg/
day
and
MOE
of
300
[
extra
3x
to
extrapolate
to
long­
term
endpoint]).

bthe
ADTC
re­
examined
the
use
of
the
inhalation
toxicity
study
selected
for
inhalation
risk
assessment
for
creosote
and
concluded
that
a
developmental
toxicity
study,
as
used
for
the
oral
and
dermal
risk
assessments
of
creosote,
is
not
appropriate
for
inhalation
risk
assessment
because:
(
1)
the
inhalation
toxicity
study
showed
significant
effects
on
body
weight
gain
early
in
the
study
(
one
week)
and
is
therefore
relevant
for
short­
term
assessment
(
2)
it
is
also
a
route­
specific
study;
and
(
3)
the
inhalation
NOAEL
is
more
sensitive
than
the
developmental
NOAEL.
Therefore,
the
inhalation
study
will
remain
as
the
study
for
the
short­
term
inhalation
endpoint.

CNo
dermal
absorption
studies
for
creosote
are
available.
The
HIARC
estimated
a
dermal
absorption
of
50%
based
on
the
results
of
an
oral
developmental
toxicity
in
rats
and
a
90­
day
dermal
toxicity
studies
in
the
same
species
(
rats)
with
similar
endpoints
(
e.
g.,
decrease
in
body
weight
gains).
Benzo(
a)
pyrene
has
also
shown
a
similar
extent
of
dermal
absorption
(
Ng
et
al.,
Toxicol.
Appl.
Pharamcol.
115:
216­
223,
1992)
and
supports
the
HIARC's
decision
for
creosote.
7
An
acute
and
chronic
Reference
Dose
value
were
not
selected
for
creosote,
as
there
are
no
food
uses
for
creosote
and
a
dietary
risk
assessment
is
not
needed.

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.

Human
Exposure
Dietary
Exposure
Based
upon
its
classification
as
a
restricted
use
pesticide
and
restrictions
on
use
sites
since
1984,
dietary
exposure
to
creosote
is
not
expected
through
food.
In
drinking
water,
the
Agency
has
determined
that
the
use
pattern
of
Creosote
is
not
expected
to
impact
water
resources
through
labeled
uses.
In
light
of
this
finding,
EPA
believes
that
Creosote's
use
will
not
impact
ground
or
surface
water
and
therefore
is
not
expected
to
lead
to
exposure
to
humans
through
drinking
water.

Non­
Dietary
Exposure
Occupational
uses
of
creosote
are
restricted
to
pressure
treatments.
To
estimate
handler
and
postapplication
exposure
at
pressure
treatment
facilities,
the
Agency
used
dermal
and
inhalation
exposure
data
from
a
worker
exposure
study
(
MRID
453234­
01)
submitted
by
the
Creosote
Council
II:

1.
This
study
was
designed
to
estimate
the
exposure
to
creosote
of
individuals
performing
job
functions
involved
in
commercial
pressure
treatment
of
lumber,
utility
poles,
and
railroad
ties
at
four
typical
commercial
treatment
facilities
in
the
United
States
and
Canada
(
referred
to
as
Sites
A
through
D).
Three
end
use
products
for
coal
tar
creosote
were
used.
Twenty­
five
workers
and
11
job
functions
(
tasks)
were
monitored
for
up
to
4
or
5
consecutive
work
days
each
(
8
hour
shifts).
Many
of
the
job
functions
may
have
been
performed
by
one
or
more
worker(
s).
Where
a
single
worker
performed
the
duties
of
more
than
one
job
function,
the
title
of
the
job
function
which
represented
the
majority
of
their
work
efforts
was
used
to
identify
the
worker.
Employee
positions
monitored
were:
treatment
operator,
treatment
assistant,
cylinder
area
loader
operator,
cylinder
area
loader
helper,
checker,
drip
pad
laborer,
load­
out
area
loader
operator,
load­
out
area
loader
helper,
load­
out
area
forklift
operator,
oil
unloader,
test
borer,
and
water
treatment
system
operator.

2.
Dermal
and
inhalation
exposure
levels
were
estimated.
Dermal
exposure
levels
were
8
estimated
by
passive
dosimetry
using
whole
body
dosimeters
(
WBDs)
and
cloth
dosimeter
gloves.
The
WBDs
and
cloth
dosimeter
gloves
were
worn
under
the
workers'
protective
clothing
and
chemical
resistant
gloves.
Inhalation
exposure
levels
were
estimated
by
active
dosimetry
using
a
sampling
train
(
placed
in
the
worker's
breathing
zone)
that
consisted
of
a
PTFE
air
filter
upstream
from
two
in­
line
XAD­
2
resin
filled
air
sampling
tubes.
The
air
was
pulled
through
the
sampling
train
by
a
portable
air
sampling
pump.

3.
Creosote
cannot
be
measured
directly
because
it
is
a
mixture
of
many
component
compounds.
In
this
study
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
WBD
and
glove
sample
as
if
it
represented
total
creosote.
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
PTFE
filter
retained
the
CTPVs,
while
the
PNAs
were
retained
in
the
XAD­
2
resin
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.)

4.
The
creosote
worker
exposure
study
(
MRID
No.
453234­
01)
used
personal
air
samplers
to
determine
air
concentrations
of
11
PNAs
in
the
breathing
zone
of
the
workers.
The
samplers
worn
by
the
workers
consisted
of
PTFE
filters
(
2­

m
pore
size)
backed
by
XAD­
2
sorbent
tubes.
Analyzes
were
performed
for
11
PNAs.
Of
the
11
PNAs,
naphthalene
was
detected
in
100
percent
of
the
samples.
Because
naphthalene
was
present
in
all
samples
for
each
of
the
12
job
classifications,
it
has
been
selected
to
indicate
potential
risks
to
workers
exposed
to
creosote.

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
data.

Risk
Characterization
Summary
Dietary
Risk­
food
Based
upon
its
classification
as
a
restricted
use
pesticide
and
restrictions
on
use
sites
since
1984,
dietary
risk
assessment
is
is
not
applicable
to
currently
registered
uses
of
creosote.

Dietary
Risk
­
drinking
water
The
Agency
has
determined
that
the
use
pattern
of
Creosote
is
not
expected
to
impact
water
resources
through
labeled
uses.
In
light
of
this
finding,
EPA
believes
that
Creosote's
use
will
not
impact
ground
or
surface
water
and
therefore
is
not
expected
to
lead
to
exposure
to
humans
through
drinking
water.
If
new
uses
are
added
in
the
future,
the
Agency
will
reassess
the
9
potential
impacts
of
creosote
on
drinking
water
as
a
part
of
the
aggregate
risk
assessment
for
this
chemical.

Occupational
Risk
AD
has
determined
that
Short
and
Intermediate­
term
Occupational
Handler
dermal
risk
estimates
do
not
exceed
AD's
level
of
concern
(
i.
e.
MOEs
are
greater
than
100)

AD
has
determined
that
Chronic
Occupational
Handler
dermal
risk
estimates
exceed
AD's
level
of
concern
(
i.
e.
MOE
<
300)
for
the
treatment
operator.
The
MOE
for
the
treatment
assistant
does
not
exceed
the
target
MOE
For
inhalation
exposure
to
creosote,
AD
has
determined
that
Occupational
Handler
Inhalation
risk
estimates
exceed
AD's
level
of
concern
(
i.
e.
MOEs
<
100)
for
both
the
treatment
operator
and
treatment
assistant.

Cancer
risks
from
dermal
and
inhalation
exposure
exceed
the
level
of
1
x
10­
4
for
all
handler
scenarios
described.

The
results
of
the
post­
application
occupational
exposure
and
risk
assessment
indicate
that
the
short­
term
non­
cancer
margins
of
exposure
for
dermal
exposures
do
not
exceed
the
level
of
concern
for
most
post­
application
scenarios
with
the
exception
of
the
oil
unloader
(
MOE=
93).
Intermediate­
term
dermal
margins
of
exposure
are
for
most
scenarios
not
of
concern
with
the
exception
of
the
cylinder
area
loader
helper,
checker,
and
oil
unloader.
Long­
term
dermal
margins
of
exposure
are
of
concern
with
the
exception
of
the
load­
out
area
loader
operator
and
helper.
Inhalation
margins
of
exposure
were
all
of
concern
for
all
exposure
druation
(
i.
e.
MOEs
less
than
100).
In
addition,
cancer
risks
for
all
post­
application
occupational
scenarios
exceed
the
level
of
concern
(
1E­
04);
all
are
greater
than
1E­
02.

Combined
Occupational
Margins
of
Exposure
Separate
Margins
of
Exposure
were
calculated
for
dermal
and
inhalation
routes
of
exposure
for
occupational
scenarios.
The
Antimicrobials
Division's
ADTC
committee
determined
that
the
MOEs
for
dermal
and
inhalation
exposure
should
not
be
combined.
First,
effects
are
observed
in
the
90­
day
inhalation
study
that
are
not
observed
in
the
90­
day
dermal
study
and
include
hematological
changes,
serum
biochemistry,
thyroid
follicular
cell
hypertrophy,
lesions
of
the
nasal
epithelium,
and
increased
absolute
and
relative
liver
weights.
Only
decreased
body
weight
and
dermal
irritation
were
observed
in
the
90­
day
dermal
toxicity
study.
Thus,
MOEs
will
not
be
combined
for
the
dermal
and
inhalation
routes
of
exposure.
10
Data
Needs
There
are
no
additional
toxicology
data
requirements
for
creosote
at
this
time.
However,
additional
toxicological
data
requirements
may
be
identified
as
the
PRA
is
refined.
In
addition,
risk
mitigation
measures
(
e.
g.,
engineering
controls)
need
to
be
discussed
with
the
Creosote
Council
prior
to
requiring
any
potential
exposure
data
for
occupational
workers.
Additional
data
are
needed
to
assess
exposure
and
risks
to
railroad
workers,
utility
pole
installers,
and
residential
exposure
to
utility
poles
and/
or
railroad
ties.

Cumulative
Exposure
Section
408(
b)(
2)(
D)(
v)
of
FFDCA
requires
that,
when
considering
whether
to
establish,
modify,
or
revoke
a
tolerance,
the
Agency
consider
available
information
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
other
substances
that
have
a
common
mechanism
of
toxicity.
As
there
are
no
tolerances
for
creosote,
the
Agency
is
not
considering
whether
creosote
has
a
common
mechanism
of
toxicity
with
any
other
chemicals.
However,
based
on
the
complex
nature
of
the
creosote
mixture,
components
of
this
mixture
may
act
in
similar
ways
to
produce
the
adverse
effects
noted
for
creosote.

Endocrine
Disruption
EPA
is
required
under
FFDCA,
as
amended
by
FQPA,
to
develop
a
screening
program
to
determine
whether
certain
substances
(
including
all
active
pesticides
or
other
ingredients)
"
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen,
or
other
such
endocrine
effects
as
the
Administrator
may
designate."
Following
the
recommendations
of
its
Endocrine
Disruptor
Screening
and
Testing
Advisory
Committee
(
EDSTAC),
the
EPA
has
determined
that
there
was
scientific
bases
for
including,
as
part
of
the
program,
the
androgen
and
thyroid
hormone
systems,
in
addition
to
the
estrogen
hormone
system.
EPA
also
adopted
EDSTAC
recommendation,
that
program
include
evaluations
of
potential
effects
in
wildlife
may.
For
pesticide
chemicals,
EPA
will
use
FIFRA
and,
to
some
extent
that
effects
in
wildlife
may
help
determine
whether
a
substance
may
have
an
effect
on
humans,
FFDCA
authority
to
require
the
wildlife
evaluations.
As
the
science
develops
and
resources
allow,
screening
additional
hormone
systems
may
be
added
to
the
Endocrine
Disruptor
Screening
Program.

When
the
appropriate
screening
and/
or
testing
protocols
being
considered
under
the
Agency's
EDSP
have
been
developed,
creosote
may
be
subjected
to
additional
screening
and/
or
testing
to
better
characterize
effects
related
to
endocrine
disruption.
11
Risk
Characterization
Overview
Dermal
Margin
of
Exposures
(
MOEs)
­
Summary:
Toxicological
endpoints
for
short­,
intermediate­,
and
long­
term
dermal
exposures
to
creosote
have
been
selected
A
Margin
Of
Exposure
(
MOE)
of
greater
than
100
for
creosote
is
considered
to
indicate
no
risk
concern
for
short­
term
(
1
day
to
1
month)
and
intermediate­
term
(
1
to
6
months)
exposures,
and
a
MOE
of
greater
than
300
for
creosote
is
considered
to
indicate
no
risk
concern
for
long­
term
(
6
months
or
longer)
exposures.

Inhalation
MOEs
­
Summary:
Toxicological
endpoints
for
short­,
intermediate­,
and
long­
term
inhalation
exposure
have
been
selected
for
creosote
as
well
as
naphthalene.
Naphthalene
has
been
selected
as
an
indicator
or
worker
risks
because
it
was
detectable
in
all
worker
inhalation
exposure
samples.
For
creosote,
a
MOE
of
greater
than
100
is
considered
to
indicate
no
risk
concern.
For
naphthalene,
the
Antimicrobials
Division
used
the
inhalation
reference
concentration
(
RfC)
for
naphthalene
published
in
the
EPA's
IRIS
database.
The
RfC
was
derived
from
a
2
year
chronic
inhalation
study
in
the
mouse
in
which
exposure
was
for
6
hours/
day,
5
days/
week.
The
ACGIH
documentation
for
recommending
the
TLV
cited
the
same
2
year
mouse
study
as
EPA.
However,
the
RfC
value
of
0.0031
mg/
m3
differs
dramatically
from
the
TLV's
8­
hr
TWA
value
of
52
mg/
m3.
The
RfC
was
derived
by
adjusting
the
inhalation
mouse
study's
6
hour/
day
5
day/
week
LOAEL
of
52
mg/
m3
to
a
24
hour/
day
7
day/
week
value
of
9.3
mg/
m3
and
then
dividing
by
an
uncertainty
factor
of
3000
(
10x
intra
species
variability,
10x
inter
species
extrapolation,
10x
for
a
lack
of
a
NOAEL,
and
3x
for
data
base
deficiencies).
On
the
other
hand,
the
TLV
recommendation
of
52
mg/
m3
was
based
on
reviewing
human
poisoning
incidents
and
other
animal
studies,
including
the
inhalation
mouse
study.
For
the
purposes
of
using
naphthalene
as
an
indicator
of
inhalation
risk
concerns
for
workers
exposed
to
creosote,
EPA
is
using
the
inhalation
route­
specific
LOAEL
of
52
mg/
m3
with
a
target
MOE
of
300
(
10x
intra
species
variability,
10x
inter
species
extrapolation,
and
3x
for
a
lack
of
a
NOAEL).
While
EPA
recognizes
that
the
24
hour/
day
7
day/
week
adjustment
to
the
RfC
is
not
representative
of
a
typical
work
day,
uncertainty
factors
are
warranted
to
account
for
inter
species
extrapolation
and
variability
among
workers.
Therefore,
a
inhalation
MOE
of
greater
than
300
is
considered
to
indicate
no
risk
concern.

Carcinogenicity
­
Summary:
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
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
dose­
related
increases
in
skin
papillomas,
keratoacanthoma,
squamous
cell
carcinoma,
and
basal
cell
carcinoma
at
the
25
and
50
mg
doses.
12
Increases
in
these
tumor
types
were
also
observed
when
creosote
was
used
as
both
initiator
and
promotor.
This
study
shows
that
creosote
acts
most
effectively
as
a
promotor
but
also
functions
as
a
"
complete"
carcinogen.

The
Agency
proposes
to
use
benzo(
a)
pyrene
as
an
indicator
for
carcinogenic
potential
of
creosote,
but
is
also
examining
new
published
data
on
carcinogenicity
of
creosote
itself
to
determine
whether
these
data
will
modify
the
current
proposal.
This
approach
has
been
discussed
in
the
Hazard
Profile
section
of
this
document.

Creosote
Worker
Exposure
Study:
Although
there
are
issues
with
the
analytical
portion
of
this
study,
the
Agency
has
relied
heavily
on
this
study
to
assess
dermal
and
inhalation
exposures
and
cancer
and
non­
cancer
risks
to
workers
in
creosote
pressure
treatment
plants.
A
brief
summary
of
this
study
was
presented
earlier.

An
in­
depth
discussion
of
exposures
(
excluding
naphthalene)
can
be
found
in
the
human
exposure
chapter,
but
a
summary
of
our
findings
for
application
(
handler)
and
post­
application
scenarios
is
presented
here:

Handler
Exposures
and
Risks
Handler
Scenarios
with
Non­
Cancer
Dermal
Risk
Concerns
(
Short­
and
Intermediate­
term
Risk)

Short­
and
intermediate­
term
non­
cancer
dermal
risks
for
handlers
(
mixing/
loading
applying
liquids
at
a
pressure
treatment
facility­
treatment
operators
and
treatment
assistant)
are
not
of
concern
(
i.
e.
MOEs
are
>
100)
with
additional
engineering
controls
utilized.

Handler
Scenarios
with
Non­
Cancer
Dermal
Risk
Concerns
(
Long­
term
Risk)

A
risk
of
concern
(
i.
e.
MOE
<
300)
was
identified
for
the
non­
cancer
long
term
dermal
exposure
of
treatment
operators
mixing/
loading/
applying
liquids
at
a
pressure
treatment
facility
(
long­
term
MOE
of
140)
with
engineering
controls.

In
addition
to
reporting
creosote
inhalation
non
cancer
risks,
naphthalene
has
been
selected
to
indicate
worker
risk
concerns.
Naphthalene
has
been
selected
because
it
was
detected
in
all
samples
for
each
of
the
12
job
classifications
in
the
creosote
worker
exposure
study.
The
geometric
mean
air
concentrations
of
naphthalene
for
the
12
job
classifications
are
reported
in
Table
2.
Table
2
presents
these
air
concentrations
as
a
percent
of
the
TLV
value
(
i.
e.,
worker
air
concentration
/
TLV
air
concentration).
Although
the
measured
naphthalene
air
concentrations
in
13
the
worker's
breathing
zone
represents
only
from
0.1
to
2.5
percent
of
the
TLV,
EPA
considers
additional
uncertainty
factors
in
the
risk
assessment.
Table
2
also
presents
MOEs
as
which
indicate
a
risk
concern
for
the
creosote
workers.
The
target
MOE
is
300.
The
MOEs
range
from
the
highest
potential
risk
of
12
for
the
cylinder
area
loader
helper
(
CH)
to
the
lowest
potential
risk
of
390
for
the
load­
out
area
loader
helper
(
LH)
activity.
The
MOEs
are
estimated
using
the
following
equation:

MOE
=
(
LOAEL
52
mg/
m3
x
6
hr/
day
mouse
study)
/
(
worker
air
conc
mg/
m3
x
8
hr/
day
workday
x
(
1
m3/
hour
working
breathing
rate
/
0.4
m3/
hour
resting
breathing
rate)

where:
1
m3/
hour
working
breathing
rate
represents
for
light
activity;
and
0.4
m3/
hour
resting
breathing
rate
to
account
for
the
fact
that
the
mouse
was
"
at
rest"
during
the
toxicity
testing.

Table
2.
Naphthalene
Air
Concentrations
as
an
Indicator
of
Creosote
Risks.

Job
Classification
a
Naphthalene
Air
Conc.(
mg/
m3)
Geo
Mean
(
range)
b
%
of
TLV
c
MOE
(
Target
300)
d
Cylinder
area
loader
helper
(
CH)
1.291
(
0.0794
to
5.918)
n=
10
2.5
12
Oil
unloader
(
OU)
0.896
(
0.701
to
1.399)
n=
5
1.7
17
Test
borer
(
TB)
0.778
(
0.514
to
1.648)
n=
5
1.5
20
Water
treatment
system
operator
(
WO)
0.763
(
0.500
to
1.987)
n=
5
1.5
20
Cylinder
area
loader
operator
(
CLO)
0.596
(
0.105
to
2.696)
n=
14
1.1
26
Treating
operator
(
TO)
0.595
(
0.133
to
2.624)
n=
14
1.1
26
Load­
out
area
forklift
operator
(
LLO
(
F))
0.433
(
0.0750
to
1.259)
n=
5
0.8
36
Drip
pad
labor
(
DP)
0.255
(
0.142
to
0.874)
n=
4
0.5
61
Load­
out
area
loader
operator
(
LLO)
0.138
(
0.0282
to
1.540)
n=
14
0.3
110
Checker
(
CK)
0.083
(
0.0308
to
0.268)
n=
5
0.2
190
Load­
out
area
loader
helper
(
LH)
0.04
(
0.0269
to
0.0612)
n=
4
0.1
390
Treating
assistant
(
TA)
0.346
(
0.117
to
0.575)
n=
4
0.7
45
a
Job
classifications
are
based
on
the
descriptions
provided
in
MRID
No.
453234­
01).
b
Geometric
mean
air
concentration
are
used
to
estimate
MOEs
from
MRID
No.
453234­
01.
c
%
TLV
=
(
air
conc
mg/
m3
/
TLV
52
mg/
m3)
*
100.
d
MOE
=
(
LOAEL
52
mg/
m3
x
6
hr/
day
mouse
study)
/
(
air
conc
mg/
m3
x
8
hrs/
day
working
x
(
1
m3
work
activity
/
0.4
m3
resting))
14
Short­
term,
intermediate­
term,
and
long­
term
15
16
17
Note:
Exposure
data
were
not
available
for
assessing
short­
term
non­
cancer
risks
for
the
following
two
scenarios:

a.
Railroad
worker;
and
b.
Pole
installer.

Post­
Application
Cancer
Risks
from
Dermal
and
Inhalation
Exposures
to
Creosote
The
Agency
has
determined
that
all
of
the
post­
application
scenarios
exceed
the
1E­
04
cancer
risk
levels.
This
is
based
upon
calculated
dermal
and
inhalation
residues
from
the
Creosote
Council's
worker
exposure
study.
Therefore,
all
of
the
post­
application
scenarios
are
expected
to
pose
a
risk
concern.

Note
that
the
Agency
has
adjusted
cancer
risk
calculations
by
factors
of
0.005
and
0.01.
This
was
done
because:

a.
The
cancer
risk
assessment
is
based
upon
benzo(
a)
pyrene,
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
has
assumed
that
levels
of
benzo(
a)
pyrene
may
occur
from
0.5%
to
1%
of
total
creosote
formulations.

Even
with
use
of
the
0.005
and
0.01
adjustment
factors
the
1E­
04
cancer
risk
level
of
concern
is
exceeded.
18
Post­
Application
Non­
Occupational
(
Residential)
Scenarios
Potential
post­
application,
non­
occupational
exposure
scenarios
likely
include
the
following:

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

(
2)
Dermal
contact
with
pressure
treated
wood
products
(
e.
g.,
utility
poles,
railroad
ties
used
in
home
settings,
posts)
(
adult);
and
(
3)
Hand­
to­
mouth
and
dermal
contact
with
industry
pressure
treated
wood
products
(
e.
g.,
utility
poles,
railroad
ties
used
in
home
settings,
posts)
(
child).

However,
adequate
data
are
not
available
to
assess
these
post­
application
exposures
and
risks.

Risk
Mitigation
The
majority
of
the
calculated
non­
cancer
and
cancer
risks
are
based
upon
the
results
of
the
Creosote
Council
II's
2001
worker
exposure
study
which
examined
workers
under
actual
creosote
use
conditions
in
wood
treatment
plants.
Since
each
NAFTA
partner
(
PMRA
and
CALDPR
has
questions
and
issues
associated
with
this
study
(
e.
g.,
analytical
issues),
further
discussion
among
NAFTA
partners,
as
well
as
with
the
Creosote
Council
II
and
study
authors,
is
required
to
determine
if
there
are
any
appropriate
risk
mitigation
measures
that
can
be
taken
to
reduce
non­
cancer
and
cancer
risks.
Additionally,
PMRA
has
indicated
that
they
have
videotapes
from
several
of
the
sites
studied;
NAFTA
partners
have
view
of
these
tapes
to
assist
in
identifying
any
further
risk
mitigation
measures
that
could
be
taken.

Data
Gaps,
Uncertainties,
and
Limitations
Data
Gaps
1.
Occupational
Exposures:
Although
the
Creosote
Council
II
submitted
a
worker
exposure
study
which
addresses
worker
exposures
in
creosote
pressure
treatment
plants,
no
data
are
available
to
assess
railroad
workers
and
utility
pole
installers.

2.
Non­
occupational
(
Residential)
Exposures:
Data
are
not
adequate
to
characterize
nonoccupational
(
residential)
post­
application
exposures.
19
Uncertainties/
Limitations
With
The
Occupational
Handler
and
Post­
Application
Data
Issues
with
the
Creosote
Council
II's
worker
exposure
study
(
MRID
45323401):

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

b.
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;

c.
Air
samplers
did
not
show
quantifiable
levels
for
several
of
the
PNAs
monitored:
(
e.
g.,
benzo(
a)
pyrene
was
not
detected
in
any
of
the
worker
samples);

d.
Inhalation
field
fortification
percent
recoveries
for
CTPVs
were
poor:
overall
recoveries
ranged
from
51
%
­
57%.

Uncertainties/
Limitations
With
Agency
Cancer
Risk
Estimates
A
specific
quantitative
cancer
assessment
on
the
carcinogenicity
of
creosote
has
not
been
performed
by
the
Agency,
but
a
cancer
potency
factor
exists
for
one
of
the
components
of
creosote,
benzo(
a)
pyrene,
with
a
Q1*
value
of
7.3(
mg/
kg/
dy)­
1.
The
Agency
proposes
to
use
the
risk
assessment
for
benzo(
a)
pyrene
as
an
indicator
for
carcinogenic
potential
of
creosote.

Considering
the
above,
EPA
adjusted
creosote
cancer
risk
calculations
by
factors
of
0.005
and
0.01.
This
was
done
because:

a.
The
cancer
risk
assessment
is
based
upon
benzo(
a)
pyrene,
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.

However,
it
should
be
noted
that
although
corrections
to
cancer
risk
estimates
were
made,
data
from
the
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.
20
Aggregate
risk
assessments
Acute
Aggregate
Risk
Under
the
current
policy
of
the
Office
of
Pesticide
Programs,
acute
aggregate
risk
assessment
determines
the
acute
risk
from
combined
dietary
consumption
of
pesticide
residues,
separate
from
residential
exposures
(
Health
Effects
Division,
Standard
Operating
Procedure
97.2,
April
1998).
In
the
case
of
creosote,
an
acute
aggregate
(
food
+
water)
risk
estimate
was
not
performed
for
creosote.
Creosote
is
not
registered
for
any
food
use,
and
it
has
also
been
determined
that
creosote
is
not
likely
to
impact
the
diet
or
drinking
water.

Short­
and
Intermediate­
Term
Aggregate
Risks
Aggregate
short
and
intermediate
term
risk
assessments
are
designed
to
provide
estimates
of
risk
likely
to
result
from
exposures
to
the
pesticide
or
pesticide
residues
in
food,
water,
and
from
residential
(
or
other
non­
occupational)
pesticide
uses.
Due
to
the
lack
of
exposure
through
food
or
water,
short
and
intermediate
term
aggregate
risks
were
not
performed.
Residential
exposures
to
creosote
residues
may
occur,
but
data
are
not
available
to
assess
these
risks.

Chronic
(
Non­
Cancer)
Aggregate
Risk
Based
on
the
lack
of
potential
for
chronic
exposure
to
creosote
through
food
and
water,
a
chronic
(
non­
cancer)
aggregate
risk
assessment
was
not
performed.
21
References
MRID
REFERENCE
453234­
01
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.

None
Agency
for
Toxic
Substances
and
Disease
Registry
(
1995):
Toxicological
Profile
for
Polycyclic
Aromatic
Hydrocarbons.
U.
S.
Department
of
Health
and
Human
Services:
Public
Health
Service.

None
Agency
for
Toxic
Substances
and
Disease
Registry
(
2002):
Toxicological
Profile
for
Creosote
(
update).
U.
S.
Department
of
Health
and
Human
Services:
Public
Health
Service.

None
Butala,
J.
H.
1999.
Creosote
Council
II
memorandum
with
attachment
to
Nader
Elkassabany,
U.
S.
Environmental
Protection
Agency,
Antimicrobials
Division.
February,
1999.

None
Murata
et
al.
1993.
Chronic
Toxicity
and
Carcinogenicity
Studies
of
1­
methylnapthalene
in
B6C3F1
mice.
Fundam
Appl.
Toxicol.
21(
1):
1993.

None
McMahon,
Timothy
F.
1999.
Creosote:
Report
of
the
Hazard
Identification
Assessment
Review
Committee.
May,
1999.
HED
document
no.
013375.
Unpublished.

None
National
Toxicology
Program.
TR
410.
Toxicology
and
Carcinogenesis
Studies
of
Naphthalene
in
B6C3F1
Mice
(
Inhalation
Studies).

None
National
Toxicology
Program.
TR
500.
Toxicology
and
Carcinogenesis
Studies
of
Naphthalene
in
F344/
N
Rats
(
Inhalation
Studies).

None
Nesnow
et
al.
1998.
Mechanistic
relationships
between
DNA
adducts,
oncogene
mutations,
and
lung
tumorigenesis
in
strain
A
mice.
Exp.
Lung
Res.
24(
4):
1998.

None
USEPA,
1984:
Wood
Preservative
Pesticides:
Creosote,
Pentachlorophenol,
Inorganic
Arsenicals.
Position
Document
4.

None
USEPA,
1997.
FIFRA
Science
Advisory
Panel.
A
Set
of
Scientific
Issues
Being
Considered
by
the
Agency
to
Discuss
and
Evaluate
the
Inhalation
Risk
22
Assessments
and
the
Combining
of
Margins
of
Exposure.
Transmittal
of
the
Final
Report
of
the
FIFRA
Scientific
Advisory
Panel
Meeting
for
March
19
and
20,
1997.
April
28,
1997.

None
Whalen,
John
E.
vand
Hugh
M.
Pettigrew.
Inhalation
Risk
Characterizations
and
the
Aggregate
Risk
Index
(
ARI).
USEPA.
Health
Effects
Division.
November
25,
1998.

None
York,
Raymond
G.
(
1994):
Developmental
Toxicity
Study
in
New
Zealand
White
Rabbits.
Study
conducted
by
IRDC,
Mattawan,
MI
for
Koppers
Inductries,
Pittsburgh,
PA.
Report
no.
672­
002.
Unpublished.

None
York,
Raymond
G.
(
1995):
Two
Generation
Reproduction/
Fertility
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
Koppers
Inductries,
Pittsburgh,
PA.
Report
no.
672­
006.
Unpublished.

43032101
North
American
P1/
P13
Creosote:
Acute
Oral
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032102
North
American
P1/
P13
Creosote:
Acute
Dermal
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032103
North
American
P1/
P13
Creosote:
Acute
Inhalation
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032104
North
American
P1/
P13
Creosote:
Eye
Irritation
Study
in
Rabbits.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032105
North
American
P1/
P13
Creosote:
Primary
Dermal
Irritation
Test
in
Rabbits.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032106
North
American
P1/
P13
Creosote:
Dermal
Sensitization
Study
(
Buehler)
in
the
Albino
Guinea
Pig.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032301
North
American
P2
Creosote:
Acute
Oral
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.
23
43032302
North
American
P2
Creosote:
Acute
Dermal
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.

43032303
North
American
P2
Creosote:
Acute
Inhalation
Toxicity
Evaluation
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032304
North
American
P2
Creosote:
Eye
Irritation
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032305
North
American
P2
Creosote:
Primary
Dermal
Irritation
Test
in
Rabbits.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43032306
North
American
P2
Creosote:
Dermal
Sensitization
Study
(
Buehler)
in
the
Albino
Guinea
Pig.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Unpublished.
HED
document
no.
011033.

43601001
North
American
P1/
P13
Creosote:
Thirteen
Week
Subchronic
Inhalation
Toxicity
Study
on
North
American
P1/
P13
Creosote
CTM
in
Rats:
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
016
(
1995).
Unpublished.

43600901
North
American
P2
Creosote:
Thirteen
Week
Subchronic
Inhalation
Toxicity
Study
on
North
American
P2
Creosote
CTM
in
Rats:
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
018
(
1995).
Unpublished.

43616101
North
American
P1/
P13
Creosote:
90­
Day
Subchronic
Dermal
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
013
(
1995).
Unpublished.

43616201
North
American
P2
Creosote:
90
Day
Subchronic
Dermal
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
014
(
1993).
Unpublished.

43584201
North
American
P1/
P13
Creosote:
Developmental
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
020
(
1995).
Unpublished.

43584202
North
American
P2
Creosote:
Developmental
Toxicity
Study
in
Rats.
Study
conducted
by
IRDC,
Mattawan,
MI
for
the
Creosote
Council
II.
Report
No.
671­
022
(
1995).
Unpublished.
24
44844401
A
6­
Month
Dermal
Oncogenicity
Study
of
Creosote
in
Mice.
Study
conducted
by
WIL
Research
Laboratories,
Ashland,
OH
for
Koppers
Industries,
Pittsburgh,
PA.
Report
no.
WIL­
100005.
Unpublished.

45323401
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.